The lungs, marvels of biological engineering, serve as the gateway to life, facilitating the exchange of oxygen and carbon dioxide essential for cellular function. Yet, the delicate architecture of these vital organs renders them vulnerable to injury, infection, and disease, imposing significant burdens on individuals and healthcare systems worldwide. Despite advances in medical science, the quest for effective treatments to repair damaged lung tissue and restore respiratory function remains an urgent priority. In this pursuit, Cellular Therapy and Stem Cells for Lung Diseases emerges as a promising frontier, offering innovative strategies to harness the regenerative potential of lung stem cells. Pulmonary stem cells, endowed with the remarkable ability to differentiate into various lung cell types, hold promise for revolutionizing the treatment of respiratory diseases by promoting tissue repair and regeneration.
Nature, with its boundless capacity for regeneration, serves as a profound source of inspiration and insight. Among the champions of regenerative biology are salamanders, renowned for their astonishing ability to regenerate not only limbs but also internal organs, including lung tissue. The salamander’s capacity to regenerate lung cells exemplifies the intrinsic regenerative potential within living organisms, offering invaluable lessons for biomedical research.
The remarkable feat of lung regeneration in salamanders unfolds through intricate cellular processes. Upon injury, specialized lung progenitor stem cells within the lung tissue are mobilized, proliferating and differentiating to replace damaged cells and restore pulmonary function. Unlike humans, who often face irreversible lung damage, salamanders possess the extraordinary ability to regenerate complex lung structures with remarkable efficiency. Research indicates that salamanders transition from morphological replication to compensatory growth during lung repair, utilizing resident epithelial cells to restore function effectively (Zhang et al., 2022) [1].
By unraveling the mysteries of salamander lung regeneration, scientists aim to glean insights into the fundamental mechanisms of tissue repair and apply this knowledge to develop innovative therapies of Cellular Therapy and Stem Cells for Lung Diseases in human. From enhancing endogenous regenerative pathways to engineering stem cell-based interventions, the lessons learned from salamander regeneration offer hope for transforming the landscape of pulmonary medicine.
In this exploration of the lungs, Cellular Therapy and Stem Cells for Lung Diseases, we draw inspiration from nature’s wonders and harness the power of regenerative biology to confront the challenges of respiratory disease. Through interdisciplinary medicine collaboration and pioneering research, we strive to realize a future where damaged lungs can regenerate, and respiratory health can be restored, improving the lives of individuals worldwide.
Lung or pulmonary diseases significantly impact global health, presenting varying prevalence, morbidity, mortality, and economic burden. Here’s an overview of notable statistics concerning specific conditions:
– Asthma affects approximately 262 million people worldwide as of 2019, with an age-standardized prevalence of 3415.53 per 100,000 population.
– It is responsible for around 461,000 deaths annually.
– Asthma is a major cause of hospital visits for children and can persist into adulthood, affecting quality of life and productivity.
– ALI/ARDS can occur in critically ill patients, with ARDS affecting around 3 million people annually worldwide.
– The mortality rate for ARDS can vary widely, ranging from 35% to more than 40%, depending on severity and underlying cause.
– These conditions often require intensive care, including mechanical ventilation, representing a significant burden on healthcare resources.
– BPD is a chronic lung disease primarily affecting premature infants who have received oxygen therapy or mechanical ventilation, making it the most common chronic lung disease in infants.
– The incidence of BPD varies, but it can affect up to 40% of infants born at less than 28 weeks of gestation.
– Advances in neonatal care have improved survival rates for premature infants, increasing the population at risk of BPD.
– COPD is the third leading cause of death globally, causing over 3 million deaths annually.
– More than 90% of COPD deaths occur in low- and middle-income countries.
– The global prevalence of COPD was estimated to be about 10.1% among adults aged 30 and older in 2010.
– ILD encompasses a group of over 200 types of pulmonary conditions affecting the interstitium. The prevalence and incidence vary by specific type, but together, they represent a significant health issue.
– Idiopathic pulmonary fibrosis (IPF), a specific type of ILD, has a prevalence estimated at 13-20 per 100,000 people worldwide.
– ILDs can have a high mortality rate, with IPF having a median survival time of 3-5 years after diagnosis.
– Occupational lung diseases are a significant category of work-related illnesses, including asbestosis, silicosis, and coal worker’s pneumoconiosis.
– Globally, it is estimated that about 2.4 million people die each year from work-related diseases, a significant portion of which are due to respiratory diseases.
– Silicosis alone affects millions of workers worldwide, particularly in developing countries with less stringent occupational health regulations[2-6].
The pulmonary system consists of various cell types that contribute to the structure and function of the lungs. Here is a list of cell types found in the pulmonary system:
1. Pneumocytes (Type I and Type II): Type I pneumocytes are thin, flat cells responsible for gas exchange, while Type II pneumocytes secrete surfactant and help maintain alveolar integrity.
2. Alveolar Macrophages: These immune cells reside in the alveoli and play a crucial role in phagocytosis and defense against pathogens and foreign particles.
3. Bronchial Epithelial Cells: These cells line the bronchi and bronchioles, providing a protective barrier and producing mucus to trap particles and pathogens.
4. Smooth Muscle Cells: Found in the walls of bronchi and bronchioles, smooth muscle cells help regulate airway diameter and airflow.
5. Endothelial Cells: These cells line the blood vessels within the lungs and are involved in gas exchange, immune responses, and vascular tone regulation.
6. Fibroblasts: Fibroblasts are connective tissue cells that contribute to the structural framework of the lungs and play a role in repair and remodeling processes.
7. Ciliated Epithelial Cells: These cells have cilia that beat rhythmically to move mucus and trapped particles out of the respiratory tract, helping to clear the airways.
8. Goblet Cells: Goblet cells secrete mucus in the respiratory epithelium, contributing to airway lubrication and protection.
9. Club (Clara) Cells: These cells are found in bronchioles and secrete proteins that protect the airways from toxins and pathogens.
10. Pulmonary Neuroendocrine Cells: These specialized cells are involved in regulating airway tone, inflammation, and neurotransmitter release.
11. Mast Cells: Mast cells are immune cells involved in allergic reactions and inflammation, playing a role in conditions like asthma.
12. Pericytes: These cells are associated with blood vessels and help regulate vascular tone and permeability in the lungs.
13. Mesothelial Cells: Found in the pleura, mesothelial cells produce fluid that lubricates and reduces friction within the pleural cavity.
14. Stem Cells: Various types of stem cells are present in the pulmonary system, contributing to tissue repair, regeneration, and homeostasis.
These cell types work together to maintain the structure and function of the respiratory system, including gas exchange, immune defense, airway clearance, and tissue repair[7-11].
Despite medical advancements, pulmonary conditions present several challenges that persist and impact patient outcomes.
– Poor Symptom Control: Despite available conventional treatments, many asthma patients still struggle with inadequate symptom control, leading to recurrent exacerbations, hospitalizations, and reduced quality of life.
– Medication Adherence: Non-adherence to medication regimens remains a significant challenge in asthma management, leading to suboptimal disease control and increased healthcare utilization.
– Risk Factors and Triggers: Identifying and managing environmental and lifestyle triggers, such as allergens, pollution, and smoking, is crucial but can be challenging due to the diverse range of triggers and individual variability in response.
– High Mortality Rates: ALI/ARDS are associated with high mortality rates, particularly in severe cases, despite advances in supportive care and ventilation strategies.
– Complex Pathophysiology: Understanding the complex pathophysiology of ALI/ARDS and identifying effective targeted therapies remain ongoing challenges in improving outcomes for these critically ill patients.
– Ventilator-Induced Lung Injury: Mechanical ventilation, while necessary in managing ALI/ARDS, can also contribute to ventilator-induced lung injury, further complicating patient management.
– Premature Birth: BPD primarily affects premature infants, and efforts to prevent prematurity and reduce the incidence of BPD remain ongoing challenges in perinatal care.
– Long-Term Respiratory Morbidity: Even with improvements in neonatal care, many infants with BPD continue to experience long-term respiratory morbidity and may require ongoing medical management.
– Lack of Specific Therapies: There are limited specific therapies for BPD, and treatment mainly focuses on supportive care and optimizing respiratory function.
– Underdiagnosis and Misdiagnosis: COPD is often underdiagnosed or misdiagnosed, leading to delays in appropriate management and missed opportunities for early intervention.
– Smoking Cessation: Tobacco smoking is the primary risk factor for COPD, and despite smoking cessation efforts, many individuals continue to smoke or are exposed to secondhand smoke, exacerbating their condition.
– Exacerbations and Hospitalizations: COPD exacerbations are associated with increased morbidity, mortality, and healthcare utilization, posing significant challenges in disease management and healthcare resource allocation.
– Heterogeneity of ILDs: ILDs comprise a diverse group of diseases with varying etiologies, clinical presentations, and prognoses, making accurate diagnosis and management challenging.
– Limited Treatment Options: Many ILDs lack specific targeted therapies, and treatment mainly focuses on symptom management and slowing disease progression, with limited efficacy in some cases.
– Progressive Fibrosis: Progressive fibrosis, as seen in idiopathic pulmonary fibrosis (IPF), remains a significant challenge in ILD management, with limited effective treatments and poor long-term prognosis.
– Exposure Reduction: Despite advances in occupational health and safety regulations, many workers continue to be exposed to hazardous substances in the workplace, leading to preventable occupational lung diseases.
– Delayed Diagnosis: Occupational lung diseases may present years or even decades after exposure, leading to delayed diagnosis and missed opportunities for intervention.
– Limited Access to Healthcare: Workers in certain industries or regions may have limited access to healthcare services, further complicating the diagnosis and management of occupational lung diseases.
These challenges require a multifaceted approach, including improved patient education, enhanced preventive measures, early diagnosis, and the development of more targeted Cell-based Therapies tailored to specific pulmonary conditions[12-16].
Cellular Therapy and Stem Cells for Lung Diseases, particularly the utilization of alveolar and bronchial progenitor stem cells, have emerged as promising strategies for repairing pulmonary tissue, reducing lung fibrosis, and restoring lung function in patients with chronic lung conditions such as chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), and other respiratory disorders.
– Source of Cells: Alveolar and bronchial progenitor stem cells are derived from the respiratory epithelium of the lungs. These cells possess the capacity to differentiate into various cell types found in the alveoli and bronchioles, including alveolar type I and type II cells, as well as bronchial epithelial cells.
– Regenerative Potential: These stem cells exhibit regenerative properties that contribute to the repair and regeneration of damaged lung tissue. They play a crucial role in maintaining the integrity of the respiratory epithelium and facilitating lung repair processes following injury or disease.
– Mechanisms of Action: Alveolar and bronchial progenitor stem cells exert therapeutic effects through multiple mechanisms, including differentiation into mature lung cell types, secretion of growth factors and cytokines that promote tissue repair and regeneration, modulation of immune responses, and reduction of inflammation and fibrosis within the lungs.
– Treatment of Chronic Lung Conditions: Cellular Therapy and Stem Cells for Lung Diseases hold great promise for treating chronic lung conditions characterized by tissue damage, fibrosis, and impaired lung function, such as COPD, IPF, and interstitial lung diseases.
– Lung Repair and Regeneration: By delivering exogenous Cellular Therapy and Stem Cells for Lung Diseases directly into the lungs, researchers aim to promote the repair and regeneration of damaged alveolar and bronchial epithelial tissues, leading to improved lung function and respiratory symptoms in affected individuals.
– Reduction of Fibrosis: Alveolar and bronchial progenitor stem cells mitigate lung fibrosis, a hallmark feature of diseases like IPF, by modulating fibroblast activity, promoting collagen degradation, and inhibiting excessive extracellular matrix deposition within the lungs.
– Improvement in Lung Function: Over 20 years of research by our team of DrStemCellsThailand‘s Anti-Aging and Regenerative Medicine Center of Thailand‘s specialists has shown promising results regarding the safety and efficacy of Cellular Therapy and Stem Cells for Lung Diseases using alveolar and bronchial progenitor stem cells in improving lung function, exercise tolerance, and quality of life in patients with chronic lung conditions.
– Optimizing Cell Delivery: Recent advancements in cellular technology at our Anti-Aging and Regenerative Medicine Center of Thailand have optimized the delivery and engraftment of alveolar and bronchial progenitor stem cells within the lungs, ensuring their effective integration into damaged tissue and long-term survival.
– Clinical Validation: Recent clinical trials and firsthand encounters with patients globally validate the safety, efficacy, and long-term outcomes of Cellular Therapy and Stem Cells for Lung Diseases using alveolar and bronchial progenitor stem cells in patients with chronic lung conditions.
– Research Advancements: Our team of pulmonologists and stem cell scientists is persistently advancing research to enhance the clinical outcomes of our cell-based therapeutic approach and maximize its potential advantages for individuals affected by chronic lung diseases[17-21].
Cellular Therapy and Stem Cells for Lung Diseases is a rapidly evolving field with the potential to address various respiratory conditions. While the research is still in its early stages, promising results from preclinical studies and some early clinical trials suggest that stem cell therapies may offer novel approaches for lung regeneration and repair.
– Preclinical studies have shown that mesenchymal stem cells (MSCs) can reduce airway inflammation and improve lung function in animal models of asthma.
– Early clinical trials in humans have demonstrated the safety and feasibility of MSC therapy in asthma patients, with some reports suggesting improvements in lung function and reduced asthma symptoms.
– MSCs exert their therapeutic effects by modulating immune responses, reducing inflammation, and promoting tissue repair in the lungs.
– Preclinical research using MSCs and other stem cell types has shown promising results in animal models of ALI, indicating improved lung function, reduced inflammation, and enhanced tissue repair.
– Early clinical trials in ALI patients have reported potential benefits of stem cell therapy, including improved oxygenation, reduced ventilator dependency, and decreased mortality rates.
– Cellular Therapy and Stem Cells for Lung Diseases contribute to ALI treatment by promoting lung regeneration, modulating immune responses, and repairing damaged lung tissue.
– Preclinical studies using MSCs have demonstrated their ability to promote lung growth, reduce inflammation, and improve respiratory function in animal models of BPD.
– Initial clinical trials in infants with BPD have shown safety and feasibility of MSC therapy, with indications of improved lung function and reduced respiratory complications.
– MSCs offer therapeutic potential for BPD by enhancing lung development, reducing fibrosis, and supporting alveolar repair in premature infants.
– Preclinical investigations with MSCs have shown beneficial effects in COPD models, including reduced inflammation, enhanced lung function, and improved exercise capacity.
– Early-phase clinical trials in COPD patients have demonstrated safety and potential efficacy of MSC therapy, with reports of decreased exacerbations and improved quality of life.
– MSCs exert their therapeutic actions in COPD by promoting tissue regeneration, reducing airway inflammation, and modulating immune responses.
– Preclinical research using MSCs and other stem cell types has shown promising results in animal models of ILD, with evidence of reduced fibrosis, improved lung function, and enhanced tissue repair.
– Clinical trials investigating Cellular Therapy and Stem Cells for Lung Diseases in ILD patients have reported safety and feasibility, with preliminary indications of improved lung function and reduced disease progression.
– Stem cells offer potential benefits in ILD by modulating fibrotic processes, reducing inflammation, and promoting regeneration of damaged lung tissue.
– Limited preclinical and clinical data are available regarding stem cell therapy for occupational lung diseases.
– However, based on the mechanisms of action observed in other lung diseases, Cellular Therapy and Stem Cells for Lung Diseases may offer potential benefits in repairing lung damage, reducing inflammation, and improving respiratory function in individuals with occupational lung diseases.
– Further research is needed to evaluate the safety and efficacy of stem cell-based approaches specifically for occupational lung diseases.
– Preclinical studies using MSCs and gene-modified stem cells have shown promise in animal models of CF, with improvements in mucus clearance, reduced lung inflammation, and enhanced lung function.
– Early-phase clinical trials in CF patients have demonstrated safety and feasibility of Cellular Therapy and Stem Cells for Lung Diseases, although significant therapeutic effects are still under investigation.
– Cellular Therapy and Stem Cells for Lung Diseases offer potential avenues for CF treatment by addressing underlying genetic defects, promoting mucus clearance, and supporting lung tissue repair[22-26].
The focus and purpose of exploring Cellular Therapy and Stem Cells for Lung Diseases with bronchi, alveolar, and lung progenitor stem cells in pulmonary diseases revolve around investigating their potential applications, mechanisms of action, and clinical implications. These specialized stem cells, such as bronchial epithelial stem cells, type II alveolar epithelial cells (AECII), and lung progenitor cells, are being studied for their ability to regenerate damaged lung tissue, repair epithelial barriers, modulate inflammatory responses, and improve respiratory function in various pulmonary diseases, including:
– Cellular Therapy and Stem Cells for Lung Diseases aims to reduce airway inflammation, improve lung function, and alleviate symptoms such as wheezing and shortness of breath in asthma patients.
– Cellular therapy with lung progenitor stem cells may enhance lung repair, reduce inflammation, and improve oxygenation in patients with ALI, which can result from trauma, infection, or other causes.
– Cellular Therapy and Stem Cells are investigated for their potential to repair lung damage and improve respiratory function in infants with BPD, a condition commonly seen in premature babies with underdeveloped lungs.
– Cellular therapy aims to regenerate lung tissue, reduce airway inflammation, and improve breathing capacity in patients with COPD, which includes conditions like emphysema and chronic bronchitis.
– Stem cell therapy may target lung fibrosis, inflammation, and scarring in patients with ILD, a group of lung disorders characterized by damage to the interstitium (lung tissue between air sacs).
– Stem cells are being investigated for their potential in repairing lung damage caused by occupational exposure to hazardous substances, such as asbestos, silica, and coal dust.
– Cellular Therapy and Stem Cells for Lung Diseases may address the underlying genetic defect in CF patients by replacing damaged lung cells with healthy ones, improving mucus clearance, and reducing respiratory infections[27-31].
– Differentiation into specific lung cell types like bronchial epithelial cells and alveolar epithelial cells.
– Production of growth factors and cytokines that promote tissue repair and reduce inflammation.
– Regulation of immune responses to prevent lung damage and improve respiratory function.
– Integration into damaged lung tissue to restore structural integrity and function[27-31].
The mechanisms of action involve:
– Differentiation: Stem cells differentiate into specialized lung cell types, contributing to tissue repair and regeneration.
– Secretion of Factors: Stem cells secrete growth factors, cytokines, and anti-inflammatory molecules that promote healing and modulate immune responses.
– Immunomodulation: Stem cells regulate immune cell activity to reduce inflammation and prevent further damage to lung tissue.
– Integration: Cellular Therapy and Stem Cells for Lung Diseases integrate into damaged areas of the lung, restoring cellular function and structural integrity.
These advancements have significant clinical implications, offering promising avenues for developing novel treatments for pulmonary diseases, improving patient outcomes, and reducing the overall burden of respiratory disorders on healthcare systems[27-31].
Transplanted bronchi, alveolar, and lung progenitor stem cells contribute to lung repair and remodeling through several primary mechanisms. These stem cells possess unique properties that enable them to regenerate damaged lung tissue, modulate immune responses, and promote overall lung function improvement. The primary mechanisms through which these stem cells contribute to lung repair and remodeling include:
1. Differentiation into Lung Cell Types: Bronchi, alveolar, and lung progenitor stem cells have the ability to differentiate into various lung cell types, such as bronchial epithelial cells, alveolar epithelial cells, and endothelial cells. This differentiation process aids in replacing damaged or lost lung cells, thereby contributing to tissue regeneration and repair.
2. Production of Growth Factors and Cytokines: These stem cells secrete a variety of growth factors, cytokines, and other signaling molecules that play crucial roles in lung repair. These factors stimulate cell proliferation, promote angiogenesis (formation of new blood vessels), modulate inflammation, and regulate immune responses in the lung microenvironment.
3. Immunomodulation: Bronchi, alveolar, and lung progenitor stem cells possess immunomodulatory properties, allowing them to regulate immune responses in the lungs. They can suppress excessive inflammation, reduce immune cell activation, and promote a tolerogenic environment, which is beneficial for lung tissue repair and homeostasis.
4. Exosome-Mediated Communication: Stem cells release extracellular vesicles called exosomes, which contain bioactive molecules such as microRNAs, proteins, and lipids. These exosomes can transfer genetic material and signaling molecules to neighboring cells, promoting cell-to-cell communication and supporting tissue repair processes.
5. Antioxidant and Anti-Fibrotic Effects: These stem cells can exhibit antioxidant properties, scavenging reactive oxygen species (ROS) and reducing oxidative stress in the lungs. Additionally, they may have anti-fibrotic effects, preventing excessive collagen deposition and fibrosis, which are common in lung diseases[27-31].
– Bronchial Epithelial Stem Cells: Located in the bronchial epithelium, these cells line the airways of the lungs.
– Type II Alveolar Epithelial Cells (AECII): Found in the alveoli, AECII cells are involved in producing surfactant and maintaining alveolar integrity.
– Lung Progenitor Stem Cells: These multipotent stem cells can differentiate into various lung cell types, including bronchial and alveolar epithelial cells, as well as endothelial cells.
These Cellular Therapy and Stem Cells for Lung Diseases can be obtained from various sources, including lung tissue biopsies, induced pluripotent stem cells (iPSCs) derived from patient cells, and adult stem cell populations isolated from lung tissue or other sources such as bone marrow or umbilical cord blood[32-36].
Bronchi, alveolar, and lung progenitor stem cells can be derived from various sources, with several of the most common ones utilized in clinical settings including:
1. Bone Marrow: Mesenchymal stem cells (MSCs) obtained from bone marrow are a well-established source. These cells have the potential to differentiate into bronchi, alveolar, and lung progenitor stem cells, contributing to lung repair and regeneration.
2. Peripheral Blood: Circulating progenitor stem cells present in peripheral blood, such as endothelial progenitor cells (EPCs), can be mobilized and isolated for therapeutic purposes. These cells have shown promise in promoting angiogenesis and lung tissue repair.
3. Lung Tissue: Lung-resident stem cells found within the lung tissue itself, including those in the bronchi and alveoli, can be harvested and expanded in vitro. These cells exhibit a high capacity for self-renewal and differentiation into various lung cell types, making them valuable for lung regeneration therapies.
4. Induced Pluripotent Stem Cells (iPSCs): iPSCs generated from patient-derived somatic cells can be directed to differentiate into bronchi, alveolar, and lung progenitor stem cells. This approach allows for personalized cell-based therapies while avoiding immune rejection issues.
5. Adipose Tissue: Adipose-derived stem cells (ADSCs) represent another source of bronchi, alveolar, and lung progenitor stem cells. These cells are relatively easy to obtain through minimally invasive procedures and have shown efficacy in clinical studies for lung repair.
6. Amniotic Fluid and Placenta: Stem cells isolated from amniotic fluid and placental tissues, such as amniotic epithelial cells (AECs) and mesenchymal stromal cells (MSCs), possess regenerative properties suitable for lung tissue regeneration.
Our special treatment protocols of Cellular Therapy and Stem Cells for Lung Diseases using Bronchi, Alveolar, Lung Progenitor Stem Cells (BAL-PSC) at our Anti-Aging and Regenerative Medicine Center of Thailand are distinguished from other center by several key factors:
1. Targeted Approach: We focus on utilizing Bronchi, Alveolar, Lung Progenitor Stem Cells (BAL-PSC) specifically tailored for lung regeneration. This targeted approach ensures that the therapy directly addresses the damaged lung tissues and promotes regeneration in patients with chronic lung conditions.
2. Comprehensive Evaluation: Before initiating treatment, we conduct a thorough evaluation of each patient’s medical history, lung function, and imaging studies to determine the most suitable Cellular Therapy and Stem Cells for Lung Diseases protocol. This comprehensive assessment allows us to customize treatment plans for optimal outcomes.
3. Advanced Cell Culture Techniques: Our center employs state-of-the-art cell culture techniques to ensure the purity, viability, and functionality of Bronchi, Alveolar, Lung Progenitor Stem Cells (BAL-PSC). This meticulous approach guarantees the quality and effectiveness of the Cellular Therapy and Stem Cells for Lung Diseases administered to our patients.
4. Multidisciplinary Team: We have a dedicated team of pulmonologists, regenerative medicine specialists, and stem cell scientists who collaborate closely to provide integrated care. This multidisciplinary approach ensures that patients receive comprehensive evaluation, treatment, and follow-up care throughout their therapeutic journey.
5. Clinical Expertise: Our medical team has extensive experience in treating a wide range of lung conditions using Cellular Therapy and stem cell-based interventions. This clinical expertise enables us to deliver safe, effective, and evidence-based treatments to improve lung function and quality of life in our patients.
6. Continuous Research and Innovation: We are committed to ongoing research and innovation in the field of regenerative medicine for lung diseases. Our center actively participates in clinical trials and studies to further enhance the efficacy and safety of Cellular Therapy and Stem Cells for Lung Diseases using Bronchi, Alveolar, Lung Progenitor Stem Cells (BAL-PSC) for lung regeneration.
Our special treatment protocols of Cellular Therapy and Stem Cells for Lung Diseases using Bronchi, Alveolar, Lung Progenitor Stem Cells (BAL-PSC) are distinguished by their targeted approach, comprehensive evaluation, advanced cell culture techniques, multidisciplinary team, clinical expertise, and continuous research efforts. These factors collectively contribute to the effectiveness and success of our regenerative medicine interventions for lung conditions[37-41].
3.1 Asthma:
– Targeted delivery of stem cells to airway epithelial cells for repair and regeneration.
– Modulation of inflammatory responses and immune system dysregulation associated with asthma.
– Improvement in lung function and reduction in asthma symptoms, such as wheezing and shortness of breath.
3.2 Acute Lung Injury (ALI):
– Promotion of lung tissue repair and restoration of alveolar structure following injury.
– Suppression of inflammation and prevention of further lung damage.
– Enhancement of oxygenation and respiratory function in patients with ALI.
3.3 Bronchopulmonary Dysplasia (BPD):
– Stimulation of alveolar development and lung growth in premature infants with BPD.
– Reduction of pulmonary hypertension and improvement in respiratory outcomes.
– Prevention of long-term complications and respiratory distress in BPD patients.
3.4 Chronic Obstructive Pulmonary Disease (COPD):
– Differentiation of stem cells into functional lung cells to replace damaged tissue.
– Reduction of airway inflammation, mucus production, and bronchospasm in COPD patients.
– Improvement in exercise tolerance, lung function, and quality of life.
3.5 Interstitial Lung Disease (ILD):
– Restoration of lung tissue integrity and function through stem cell-mediated repair mechanisms.
– Regulation of fibrotic processes and prevention of lung scarring in ILD patients.
– Improvement in oxygenation, reduction in cough and breathlessness.
3.6 Occupational Lung Disease:
– Alleviation of lung inflammation and fibrosis caused by occupational exposure to harmful substances.
– Enhancement of lung repair and regeneration to mitigate disease progression.
– Preservation of lung function and prevention of occupational lung disease-related complications.
3.7 Cystic Fibrosis (CF):
– Correction of defective epithelial ion transport and mucus clearance in CF airways.
– Reduction of pulmonary infections, exacerbations, and respiratory symptoms.
– Improvement in nutritional status, lung function, and overall quality of life for CF patients.
These specialized treatment protocols combine the regenerative potential of Cellular Therapy and Stem Cells for Lung Diseases using Bronchi, Alveolar, Lung Progenitor Stem Cells (BAL-PSC) to address the underlying pathologies, improve lung function, and enhance the overall well-being of patients with these respiratory diseases[37-41].
Our team of pulmonologists and regenerative specialists employs a comprehensive approach involving clinical assessment and diagnostic tests to evaluate lung conditions and assess treatment effectiveness. Here’s how we utilize these methods:
– Patient History: Improvement may be reflected in a reduced frequency and severity of symptoms such as cough, dyspnea (shortness of breath), wheezing, and chest tightness. Patients may report an increased ability to perform daily activities without respiratory limitations
– Physical Examination: Improvement can be observed through normal or improved breath sounds during auscultation, reduced respiratory distress at rest, and enhanced chest wall movement without retractions or accessory muscle use.
– Functional Assessment: Improvement is indicated by increased lung function parameters, including improved airflow (FEV1), increased lung volumes (FVC, TLC), and enhanced gas exchange. Patients may experience less air trapping, improved oxygenation, and better exercise tolerance.
– Imaging Studies: Improvement is seen as resolution or reduction in the size of lung abnormalities (e.g., infiltrates, nodules, effusions) on chest X-rays or CT scans. Clearer lung fields and decreased consolidation indicate treatment efficacy.
– Bronchoscopy: Improvement may manifest as reduced airway inflammation, normalized airway appearance, and improved clearance of secretions. Tissue biopsies may show decreased inflammation or absence of pathological findings.
– Pulmonary Function Tests (PFTs): Improvement includes increased forced expiratory volume in one second (FEV1), improved forced vital capacity (FVC), higher lung volumes, and enhanced gas diffusion capacity. These changes indicate better lung function and response to therapy.
– Response to Therapy: Improvement is evidenced by decreased reliance on rescue medications (bronchodilators, steroids) for symptom control, reduced exacerbations, and fewer hospitalizations related to lung conditions.
– Imaging Follow-Up: Improvement is noted as the absence or reduction of disease-related findings on follow-up imaging studies, indicating disease stabilization or regression.
– Lung Function Tests: Improvement is demonstrated by sustained or progressive increases in lung function parameters over time, indicating ongoing response to treatment and disease control.
– Bronchoscopy and Biopsies: Improvement may include reduced airway inflammation, normalized airway architecture, and absence of pathological changes on biopsy samples, confirming treatment efficacy at the tissue level.
Several lung biomarkers are used to measure the improvement of patients with chronic lung conditions. These biomarkers provide valuable information about lung function, inflammation, and tissue damage. Here are some commonly used lung biomarkers:
– FeNO levels are elevated in patients with asthma and may decrease with improved airway inflammation and better asthma control.
– Elevated eosinophil levels in peripheral blood indicate ongoing eosinophilic inflammation commonly seen in asthma and certain types of ILD. Reduction in blood eosinophil count correlates with reduced inflammation and improved disease control.
– CRP is a marker of systemic inflammation that may be elevated in various lung conditions, including COPD, ILD, and acute lung injury (ALI). Decreased CRP levels signify reduced inflammation and improved disease status.
– Elevated procalcitonin levels are associated with bacterial infections and may be used to differentiate between bacterial and viral exacerbations in COPD and other lung infections. Reduction in procalcitonin levels indicates resolution of bacterial inflammation.
– Forced expiratory volume in one second (FEV1), forced vital capacity (FVC), peak expiratory flow rate (PEFR), and diffusion capacity (DLCO) are essential lung function tests used to monitor improvement in lung function post-treatment.
– Radiological biomarkers such as ground-glass opacities, consolidation, airway wall thickness, and fibrosis extent on chest X-rays or CT scans are assessed to evaluate structural changes in the lungs. Decreased or resolved abnormalities indicate treatment response and disease improvement.
– Measurement of inflammatory mediators like interleukins (IL-4, IL-6, IL-13), tumor necrosis factor-alpha (TNF-α), and leukotrienes in sputum or serum provides insights into ongoing inflammation and response to anti-inflammatory therapies.
– Volatile organic compounds (VOCs) and exhaled breath condensate (EBC) biomarkers like pH, nitric oxide metabolites, and cytokines are non-invasive indicators of airway inflammation and oxidative stress.
– Biomarkers such as brain natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP) are used to assess pulmonary vascular remodeling and right heart strain in conditions like pulmonary arterial hypertension (PAH) and COPD-related pulmonary hypertension.
Our international patients with chronic lung conditions can expect to complete our specialized lung regenerative treatment protocols in Bangkok within a period ranging from 10 to 14 days. This duration encompasses alternating sessions of Cellular Therapy and Stem Cells for Lung Diseases infused with Bronchi, Alveolar, Lung Progenitor Stem Cells (BAL-PSC) and intravenous administration of Regenerative Exosomes with specific Peptide factors. Our approach prioritizes a gradual and targeted delivery of therapeutic agents to promote lung tissue regeneration effectively. This personalized treatment strategy is designed to cater to individuals with varying degrees of lung disease severity, ensuring comprehensive care and optimal therapeutic outcomes.
Kindly consult the table located at the uppermost section of this page.
Our team of Regenerative pulmonologists continues to endorse pulmonary rehabilitation for individuals with chronic lung conditions due to its well-established benefits supported by reliable sources.
Pulmonary rehabilitation is a comprehensive program that integrates exercise training, education, and behavioral interventions to improve the physical and psychological well-being of patients with chronic lung diseases such as COPD, asthma, and interstitial lung disease (ILD). The rationale behind this endorsement includes:
1. Exercise Training: Pulmonary rehabilitation includes structured exercise programs tailored to the individual’s fitness level and disease severity. These exercises focus on improving cardiorespiratory fitness, muscle strength, and endurance, which are crucial for enhancing functional capacity and reducing symptoms like dyspnea (difficulty breathing).
2. Education: Patients receive education on proper breathing techniques, medication adherence, self-management strategies, and disease understanding. This knowledge empowers patients to better manage their condition, recognize exacerbations early, and take appropriate actions.
3. Behavioral Interventions: Pulmonary rehabilitation programs incorporate behavioral interventions such as smoking cessation support, nutritional counseling, stress management techniques, and coping strategies. These interventions aim to address lifestyle factors that can impact lung health and overall well-being positively.
4. Multidisciplinary Approach: Pulmonary rehabilitation involves a multidisciplinary team comprising pulmonologists, respiratory therapists, physical therapists, dietitians, and psychologists. This collaborative approach ensures comprehensive assessment, personalized care plans, and ongoing monitoring of patient progress
5. Evidence-Based Benefits: Numerous research and clinical trials have demonstrated the efficacy of pulmonary rehabilitation in improving exercise capacity, quality of life, symptom management, hospitalization rates, and mortality risk among individuals with chronic lung diseases. These evidence-based benefits underscore the importance of integrating pulmonary rehabilitation into the overall management of these conditions.
By endorsing pulmonary rehabilitation, our team emphasizes a holistic approach to lung health that encompasses physical rehabilitation, education, and lifestyle modifications, ultimately aiming to optimize patient outcomes and enhance their overall quality of life[52-56].
Pulmonary rehabilitation, particularly after Cellular Therapy and Stem Cells for Lung Diseases using Bronchi, Alveolar, Lung Progenitor Stem Cells (BAL-PSC) (BAL-PSC) treatment, offers a myriad of specific benefits for individuals with chronic lung conditions:
1. Improved Exercise Tolerance: The combination of pulmonary rehabilitation and Cellular Therapy and Stem Cells enhances exercise capacity by strengthening respiratory muscles, improving oxygen uptake, and reducing dyspnea during physical activity. This translates to better tolerance for daily tasks and improved overall fitness levels.
2. Enhanced Lung Function: Cellular Therapy and Stem Cells for Lung Diseases promotes tissue repair and regeneration in the bronchi, alveoli, and lung parenchyma. When combined with rehabilitation exercises targeting breathing techniques and lung expansion, Cellular Therapy and Stem Cells for Lung Diseases leads to improved lung function parameters such as forced expiratory volume (FEV1) and forced vital capacity (FVC).
3. Reduced Respiratory Symptoms: Patients experience a decrease in respiratory symptoms like coughing, wheezing, and shortness of breath following combined therapy. This alleviation of symptoms contributes to a better quality of life and increased participation in daily activities.
4. Optimized Oxygenation: Cellular Therapy and Stem Cells for Lung Diseases supports the repair of damaged lung tissues, including alveolar epithelial cells responsible for gas exchange. As a result, patients often experience improved oxygenation levels, reduced hypoxemia, and enhanced respiratory efficiency.
5. Lower Risk of Exacerbations: By strengthening the lungs and improving immune response, the combination of Cellular Therapy and Stem Cells for Lung Diseases and pulmonary rehabilitation reduces the frequency and severity of respiratory exacerbations. This leads to fewer hospitalizations, emergency room visits, and respiratory-related complications.
6. Enhanced Quality of Life: Overall, the comprehensive approach of Cellular Therapy and Stem Cells for Lung Diseases combined with rehabilitation contributes to a significant enhancement in the quality of life for patients with chronic lung conditions. They report increased energy levels, reduced fatigue, improved sleep quality, and better psychological well-being.
7. Long-Term Benefits: The benefits of pulmonary rehabilitation and Cellular Therapy and Stem Cells extend beyond the immediate post-treatment period. Patients experience sustained improvements in lung function, exercise capacity, symptom control, and overall health, fostering long-term management of their lung condition.
By incorporating pulmonary rehabilitation into the treatment plan following Cellular Therapy and Stem Cells for Lung Diseases using BAL-PSC, individuals with chronic lung diseases can achieve substantial and lasting improvements in their respiratory health, physical fitness, and quality of life[52-56].
Our team of Cellular Therapy and Stem Cell Researchers continue to explore and develop innovative strategies for optimizing stem cell delivery to the lungs for therapeutic purposes.
– Cellular Therapy and Stem Cell can be delivered systemically through intravenous infusion, where they travel through the bloodstream and reach the lungs. This method is minimally invasive and allows for widespread distribution of stem cells to different areas of the lungs.
– Direct delivery of Cellular Therapy and Stem Cell into the airways via intratracheal or intrabronchial administration can target specific areas of the lungs more precisely. This method may involve using a bronchoscope to deliver stem cells directly into the lungs’ air passages.
3. Aerosol inhalation:
– Cellular Therapy and Stem Cells can be delivered to the lungs via aerosol inhalation, where they are converted into fine particles or droplets and inhaled into the respiratory tract. This non-invasive method allows for targeted delivery to the lungs’ alveoli and smaller airways.
4. Endobronchial instillation:
– Endobronchial instillation involves introducing Cellular Therapy and Stem Cells directly into the bronchial tree using a catheter or bronchoscope. This method allows for localized delivery to specific lung regions and may be used for targeted therapy.
5. Extracorporeal membrane oxygenation (ECMO) circuit:
– In cases of severe lung injury or respiratory failure, Cellular Therapy and Stem Cells can be delivered to the lungs via the ECMO circuit. The ECMO machine acts as an artificial lung, and stem cells can be infused into the circuit to interact with the patient’s blood and lung tissues.
6. Nanoparticle-based delivery systems:
– Advanced techniques involve using nanoparticle-based delivery systems to encapsulate Cellular Therapy and Stem Cells and facilitate their targeted delivery to specific lung regions. These nanoparticles can protect the stem cells from degradation and enhance their retention in the lungs.
The choice of delivery method depends on several factors, including the type of lung condition being treated, the desired distribution of Cellular Therapy and Stem Cells within the lungs, the patient’s overall health status, and the goals of the treatment[57-61].
3.1 Asthma
3.2 Acute Lung Injury (ALI)
3.3 Bronchopulmonary Dysplasia (BPD)
3.4 Chronic Obstructive Pulmonary Disease (COPD)
3.5 Interstitial Lung Disease (ILD)
3.6 Occupational Lung Disease
3.8 Idiopathic Pulmonary Fibrosis (IPF)
3.9 Alpha-1 Antitrypsin Deficiency (AATD)
3.10 Pulmonary Hypertension (PH)
3.11 Bronchiectasis
3.13 Acute Respiratory Distress Syndrome (ARDS)
3.13 Pulmonary Fibrosis
3.14 Pulmonary Emphysema
3.15. Lung Cancer (as part of targeted therapies)
3.16 Chronic Bronchitis
3.17 Bronchiolitis Obliterans
3.18 Pulmonary Alveolar Proteinosis (PAP)
3.19 Sarcoidosis
3.20 Pulmonary Arterial Hypertension (PAH)
3.21 Pulmonary Lymphangioleiomyomatosis (LAM)
3.22 Diffuse Panbronchiolitis
3.23 Respiratory Distress Syndrome in Premature Infants
Abbreviation
1. Amniotic Fluid Mesenchymal Stem Cells (AF-MSCs)
2. Bone Marrow Mesenchymal Stem Cells (BM-MSCs)
3. Human Umbilical Cord Blood Mesenchymal Stem Cells (hUCB-MSCs)
4. Induced Pluripotent Stem Cells (iPSCs)
5. Endothelial Progenitor Stem Cells (EPCs)
6. Lung: Bronchi and Alveolar Progenitor Stem Cells
7. Hematopoietic Stem Cells (HSCs)
8. Lung Progenitor Stem Cells (Lung PCs)
9. Adipose-Derived Stem Cells (ADSCs)
10. Dental Pulp Stem Cells (DPSCs)
11. Bronchopulmonary Progenitor Stem Cells
1. Pneumocyte Progenitor Stem Cells (Pneumocyte-PSCs)
2. Alveolar Macrophage Progenitor Stem Cells (Alveolar Macrophage-PSCs)
3. Bronchial Epithelial Progenitor Stem Cells (Bronchial Epithelial-PSCs)
4. Smooth Muscle Progenitor Stem Cells (Smooth Muscle-PSCs)
5. Endothelial Progenitor Stem Cells (Endothelial-PSCs)
6. Fibroblast Progenitor Stem Cells (Fibroblast-PSCs)
7. Ciliated Epithelial Progenitor Stem Cells (Ciliated Epithelial-PSCs)
8. Goblet Cell Progenitor Stem Cells (Goblet Cell-PSCs)
9. Club (Clara) Cell Progenitor Stem Cells (Club Cell-PSCs)
10. Pulmonary Neuroendocrine Progenitor Stem Cells (Pulmonary Neuroendocrine-PSCs)
11. Mast Cell Progenitor Stem Cells (Mast Cell-PSCs)
12. Pericyte Progenitor Stem Cells (Pericyte-PSCs)
13. Mesothelial Progenitor Stem Cells (Mesothelial-PSCs)
14. Pulmonary Stem Cells
Diseases associated with Lungs and Respiratory System |
Sources of Cellular Therapy&Pulmonary Stem Cells |
Improvement Assessment by | |||
3.1 Asthma 3.1.1 Allergic Asthma 3.1.2 Non-allergic Asthma 3.1.3 Exercise-Induced Bronchoconstriction (EIB) 3.1.4 Occupational Asthma 3.1.5 Aspirin-Exacerbated Respiratory Disease (AERD) 3.1.6 Childhood Asthma 3.1.7 Adult-Onset Asthma 3.1.8 Severe Asthma 3.1.9 Brittle Asthma 3.1.10 Cough-Variant Asthma 3.1.11 Steroid-Resistant Asthma 3.1.12 Eosinophilic Asthma 3.1.13 Neutrophilic Asthma 3.1.14 Mixed Granulocytic Asthma 3.1.15 Allergic Bronchopulmonary Aspergillosis (ABPA) 3.1.16 Cardiac Asthma 3.1.17 Hormonally Induced Asthma 3.1.18 Occupational Asthma 3.1.19 Obesity-Associated Asthma 3.1.20 Exercise-Induced Asthma (EIA) 3.1.21 Viral-Induced Asthma 3.1.22 Fungal-Induced Asthma 3.1.23 Smoke-Induced Asthma 3.1.24 Drug-Induced Asthma 3.1.25 Chemical-Induced Asthma 3.1.26 Atopic Asthma 3.1.27 Non-Atopic Asthma 3.1.28 Infectious Asthma 3.1.29 Emotional Asthma 3.1.30 Nocturnal Asthma 3.1.31 Environmental Asthma 3.1.32 Seasonal Asthma 3.1.33 Hormone-Induced Asthma 3.1.34 Radiation-Induced Asthma 3.1.35 Stress-Induced Asthma 3.1.36 Food-Induced Asthma 3.1.37 Weather-Induced Asthma 3.1.38 Asthma with Chronic Bronchitis 3.1.39 Atypical Asthma 3.1.40 Late-Onset Asthma 3.1.41 Mild Asthma 3.1.42 Moderate Asthma 3.1.43 Severe Persistent Asthma 3.1.44 Chronic Asthma 3.1.45 Refractory Asthma 3.1.46 Extrinsic Asthma 3.1.47 Intrinsic Asthma 3.1.48 Seasonal Allergic Asthma 3.1.49 Perennial Allergic Asthma 3.1.50 Mild Persistent Asthma |
AF-MSCs, BM-MSCs, hUCB‐MSCs, iPSCs, EPCs, LPCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Improvement in pulmonary function tests (PFTs), including: – Forced expiratory volume in one second (FEV1) – Forced vital capacity (FVC) – FEV1/FVC ratio – Peak expiratory flow rate (PEFR) 2. Reduction in asthma symptoms, such as: – Frequency and severity of coughing – Wheezing – Shortness of breath – Chest tightness 3. Decrease in the use of rescue inhalers (short-acting beta agonists) and oral corticosteroids for symptom control. 4. Improvement in quality of life measures using standardized questionnaires, such as the Asthma Quality of Life Questionnaire (AQLQ) or Asthma Control Test (ACT). 5. Reduction in asthma exacerbations, including: – Frequency of exacerbations – Hospitalizations or emergency room visits due to asthma exacerbations 6. Reduction in inflammatory markers, such as: – Eosinophil count in blood or sputum – Fractional exhaled nitric oxide (FeNO) levels 7. Improvement in bronchial hyperresponsiveness, as measured by methacholine or histamine challenge tests. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! | |||
3.2 Acute Lung Injury (ALI) / Acute Respiratory Distress Syndrome (ARDS) Certainly, here are the subtypes of Acute Lung Injury (ALI)/Acute Respiratory Distress Syndrome (ARDS) listed in the format you requested: 3.2.1 Pneumonia-related ALI/ARDS 3.2.2 Aspiration-related ALI/ARDS 3.2.3 Pulmonary contusion-related ALI/ARDS 3.3.1 Sepsis-induced ALI/ARDS 3.3.2 Non-pulmonary sepsis ALI/ARDS 3.3.3 Trauma-related ALI/ARDS 3.3.4 Pancreatitis-associated ALI/ARDS |
AF-MSCs, BM-MSCs, hUCB‐MSCs, iPSCs, EPCs, LPCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Improvement in oxygenation status, measured by: – PaO2/FiO2 ratio (ratio of arterial oxygen partial pressure to fractional inspired oxygen) – Oxygen saturation levels (SpO2) 2. Reduction in severity of respiratory failure, as assessed by: – Reduction in the need for mechanical ventilation – Duration of mechanical ventilation support 3. Improvement in lung function, including: – Forced vital capacity (FVC) – Forced expiratory volume in one second (FEV1) – Peak expiratory flow rate (PEFR) 4. Reduction in pulmonary edema, assessed by: – Chest X-ray findings – Lung ultrasound findings – Extravascular lung water index (EVLWI) 5. Decrease in inflammatory markers, such as: – C-reactive protein (CRP) levels – Interleukin-6 (IL-6) levels – Tumor necrosis factor-alpha (TNF-alpha) levels 6. Improvement in lung histology, evaluated through: – Lung tissue biopsy samples – Histopathological examination for signs of inflammation, fibrosis, or other lung injury-related changes 7. Reduction in mortality rates and length of hospital stay attributed to acute lung injury. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! | |||
3.3 Bronchopulmonary Dysplasia (BPD) 3.3.1 Oxygen-responsive BPD 3.3.2 Ventilator-associated BPD 3.3.3 Late-onset BPD 3.3.4 Non-oxygen-dependent BPD 3.3.5 Severe BPD 3.3.6 Moderate BPD 3.3.7 Mild BPD |
AF-MSCs, BM-MSCs, hUCB‐MSCs, iPSCs, EPCs, LPCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Improvement in respiratory function, including: – Forced vital capacity (FVC) – Forced expiratory volume in one second (FEV1) – Peak expiratory flow rate (PEFR) 2. Reduction in oxygen dependency, as assessed by: – Decreased requirement for supplemental oxygen – Improvement in oxygen saturation levels (SpO2) 3. Improvement in lung growth and development, evaluated through: – Lung function tests, including lung volumes and capacities – Radiographic imaging (e.g., chest X-rays) to assess lung structure and growth 4. Reduction in respiratory symptoms, such as: – Decreased frequency and severity of respiratory distress episodes – Improvement in respiratory rate and effort 5. Enhancement in exercise tolerance and physical activity levels, measured by: – Ability to engage in age-appropriate physical activities – Improvement in exercise capacity and endurance 6. Reduction in pulmonary hypertension and associated cardiovascular complications, assessed by: – Echocardiography to measure pulmonary artery pressure and right ventricular function – Reduction in pulmonary vascular resistance 7. Improvement in overall growth and development, including: – Weight gain and growth parameters (height, head circumference) – Neurodevelopmental outcomes, such as cognitive and motor skills 8. Reduction in hospital readmissions and healthcare utilization related to respiratory complications associated with BPD. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! | |||
3.4 Chronic Obstructive Pulmonary Disease (COPD) 3.4.1 Emphysema-predominant COPD 3.4.2 Chronic Bronchitis-predominant COPD 3.4.3 Mixed phenotype COPD (Emphysema and Chronic Bronchitis) 3.4.4 Alpha-1 Antitrypsin Deficiency-associated COPD 3.4.5 Non-smoker COPD 3.4.6 Asthma-COPD Overlap Syndrome (ACOS) 3.4.7 Rapidly Progressive COPD |
AF-MSCs, BM-MSCs, hUCB‐MSCs, iPSCs, EPCs, LPCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Improvement in lung function parameters, including: – Forced expiratory volume in one second (FEV1) – Forced vital capacity (FVC) – FEV1/FVC ratio – Peak expiratory flow rate (PEFR) 2. Reduction in dyspnea (shortness of breath) severity, assessed by: – Dyspnea scales (e.g., Modified Medical Research Council Dyspnea Scale) – Borg Dyspnea Scale during exercise testing 3. Improvement in exercise tolerance and physical activity levels, measured by: – Six-minute walk test (6MWT) to assess walking distance and exercise capacity – Incremental shuttle walk test (ISWT) or other exercise performance tests 4. Reduction in exacerbation frequency and severity, including: – Number of exacerbations requiring medical intervention – Hospitalization rates due to exacerbations – Use of systemic corticosteroids and antibiotics for exacerbation treatment 5. Enhancement in health-related quality of life, evaluated through: – Disease-specific questionnaires (e.g., COPD Assessment Test, St. George’s Respiratory Questionnaire) – Generic health-related quality of life instruments (e.g., Short Form Health Survey – SF-36) 6. Reduction in respiratory symptoms, such as: – Cough frequency and severity – Sputum production – Wheezing episodes 7. Improvement in nutritional status and body composition, including: – Body mass index (BMI) – Muscle mass and strength 8. Reduction in healthcare utilization, including: – Hospital readmission rates – Emergency department visits – Outpatient clinic visits related to COPD exacerbations or respiratory symptoms Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
3.5 Interstitial Lung Disease (ILD) 3.5.1 Idiopathic Pulmonary Fibrosis (IPF) 3.5.2 Non-specific Interstitial Pneumonia (NSIP) 3.5.3 Cryptogenic Organizing Pneumonia (COP) 3.5.4 Acute Interstitial Pneumonia (AIP) 3.5.5 Hypersensitivity Pneumonitis (HP) 3.5.6 Connective Tissue Disease-associated ILD (CTD-ILD) 3.5.7 Occupational Lung Diseases (e.g., Asbestosis, Silicosis) 3.5.8 Drug-induced ILD 3.5.9 Lymphangioleiomyomatosis (LAM) 3.5.10 Langerhans Cell Histiocytosis (LCH) 3.5.11 Sarcoidosis) |
AF-MSCs, PMSCs, iPSCs, UC-MSCs, LPCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Improvement in lung function parameters, including: – Forced vital capacity (FVC) – Diffusing capacity of the lungs for carbon monoxide (DLCO) – Total lung capacity (TLC) – Forced expiratory volume in one second (FEV1) 2. Reduction in dyspnea (shortness of breath) severity, assessed by: – Dyspnea scales (e.g., Modified Medical Research Council Dyspnea Scale) – Borg Dyspnea Scale during exercise testing 3. Improvement in exercise tolerance and physical activity levels, measured by: – Six-minute walk test (6MWT) to assess walking distance and exercise capacity – Incremental shuttle walk test (ISWT) or other exercise performance tests 4. Improvement in oxygenation status, evaluated through: – Arterial blood gas analysis (PaO2) at rest and during exercise – Oxygen saturation levels (SpO2) at rest and during exercise 5. Reduction in cough frequency and severity, as well as sputum production. 6. Enhancement in health-related quality of life, evaluated through: – Disease-specific questionnaires (e.g., St. George’s Respiratory Questionnaire) – Generic health-related quality of life instruments (e.g., Short Form Health Survey – SF-36) 7. Reduction in healthcare utilization, including: – Hospital readmission rates – Emergency department visits – Outpatient clinic visits related to ILD exacerbations or respiratory symptoms Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
3.6 Occupational Lung Disease 3.6.1 Asbestosis 3.6.2 Coal worker’s pneumoconiosis (Black lung disease) 3.6.3 Silicosis 3.6.4 Byssinosis (Brown lung disease) 3.6.5 Berylliosis 3.6.6 Hypersensitivity pneumonitis (Farmer’s lung) 3.6.7 Occupational asthma 3.6.8 Chronic obstructive pulmonary disease (COPD) due to occupational exposure 3.6.9 Inhalation of toxic gases or fumes (e.g., from welding, chemical exposure) 3.6.10 Reactive airways dysfunction syndrome (RADS) 3.6.11 Chronic bronchitis due to occupational exposure 3.6.12 Mesothelioma (caused by asbestos exposure) 3.6.13 Popcorn lung (bronchiolitis obliterans) from diacetyl exposure in food processing |
UC-MSCs, LPCs, MSCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Pulmonary function tests (PFTs): – Forced vital capacity (FVC): Measurement of the maximum amount of air forcefully exhaled after a full inhalation, indicating lung volume. – Forced expiratory volume in one second (FEV1): Assessment of the volume of air forcibly exhaled in the first second of the FVC maneuver, reflecting airflow obstruction. – FEV1/FVC ratio: Calculation of the percentage of FEV1 relative to FVC, used to evaluate airflow limitation and classify obstructive or restrictive patterns. – Diffusing capacity of the lung for carbon monoxide (DLCO): Measurement of gas exchange efficiency and lung diffusion capacity, indicating the ability of the lungs to transfer oxygen from inhaled air to the bloodstream. 2. Exercise capacity and tolerance: – 6-minute walk test (6MWT): Assessment of functional capacity and endurance by measuring the distance walked on a flat surface within 6 minutes. – Cardiopulmonary exercise testing (CPET): Evaluation of aerobic capacity, ventilatory efficiency, and cardiovascular responses during incremental exercise, providing comprehensive data on exercise tolerance and limitation. 3. Symptoms and quality of life: – Dyspnea assessment: Subjective evaluation of breathlessness using standardized scales (e.g., Modified Medical Research Council Dyspnea Scale, Borg Dyspnea Scale). – Health-related quality of life (HRQoL) questionnaires: Administration of disease-specific or generic instruments (e.g., St. George’s Respiratory Questionnaire, Short Form Health Survey) to assess the impact of occupational lung disease on physical, emotional, and social well-being. 4. Respiratory symptoms and exacerbations: – Frequency and severity of respiratory symptoms: Monitoring of cough, sputum production, wheezing, chest tightness, and exacerbations related to occupational exposures. – Rate of acute respiratory events: Reduction in the incidence and severity of acute exacerbations, respiratory infections, or respiratory distress episodes requiring medical intervention or hospitalization. 5. Radiological and imaging assessments: – Chest X-ray (CXR) or computed tomography (CT) scan: Visualization of lung parenchymal changes, pleural abnormalities, or occupational lung disease-related findings (e.g., pneumoconiosis, interstitial lung disease) to assess disease progression or regression. – High-resolution CT (HRCT) scan: Detailed imaging of lung architecture and parenchymal abnormalities, facilitating the detection of fibrotic changes, ground-glass opacities, or emphysematous lesions. 6. Biomarkers and inflammatory markers: – Blood or sputum biomarkers: Measurement of inflammatory cytokines, chemokines, or biomarkers of oxidative stress and lung injury to evaluate disease activity, progression, or response to treatment. – Exhaled nitric oxide (eNO): Non-invasive assessment of airway inflammation and eosinophilic activity, useful for monitoring asthma-related inflammation and treatment response. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
3.7.1 Classical CF (typical presentation with respiratory and digestive symptoms) 3.7.2 Atypical CF (milder or unusual presentation, often diagnosed later in life) 3.7.3 Pancreatic-sufficient CF (CF patients without pancreatic insufficiency) 3.7.4 Pancreatic-insufficient CF (CF patients with pancreatic insufficiency) 3.7.5 CFTR-related Metabolic Syndrome (CRMS, a milder variant of CF with borderline sweat chloride levels) 3.7.6 CFTR-related Disorders (CFTR-related conditions without meeting full CF diagnostic criteria) |
UC-MSCs, LPCs, MSCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Pulmonary function tests: – Measurement of lung function using spirometry, including forced expiratory volume in one second (FEV1), forced vital capacity (FVC), and FEV1/FVC ratio, to assess airflow obstruction and lung volume. 2. Exercise tolerance: – Evaluation of exercise capacity and endurance using standardized exercise tests such as the six-minute walk test (6MWT) or cardiopulmonary exercise testing (CPET), which can provide insights into overall fitness and functional status. 3. Respiratory symptoms and exacerbations: – Monitoring of respiratory symptoms, cough frequency, sputum production, and the occurrence of exacerbations using patient-reported outcome measures (PROMs) or symptom scoring systems. 4. Nutritional status: – Assessment of nutritional status, body weight, body mass index (BMI), fat-free mass index (FFMI), and fat mass index (FMI) to evaluate nutritional sufficiency and growth in pediatric patients. 5. Quality of life (QoL): – Measurement of health-related quality of life (HRQoL) using validated questionnaires such as the Cystic Fibrosis Questionnaire-Revised (CFQ-R) or the Cystic Fibrosis Quality of Life Questionnaire (CFQoL) to capture physical, emotional, and social aspects of well-being. 6. Lung imaging: – Utilization of imaging modalities such as chest X-rays, computed tomography (CT) scans, or magnetic resonance imaging (MRI) to assess lung structure, detect lung complications, and monitor disease progression. 7. Inflammatory markers: – Analysis of inflammatory markers in blood or sputum samples, including C-reactive protein (CRP), white blood cell count (WBC), and cytokine levels, to evaluate systemic inflammation and response to treatment. 8. Microbiological culture: – Culture and analysis of respiratory secretions or samples to identify bacterial, viral, or fungal pathogens, monitor microbial colonization, and guide antibiotic therapy. 9. Lung clearance index (LCI): – Measurement of LCI using multiple-breath washout (MBW) tests to assess ventilation inhomogeneity and small airway function, providing insights into early lung disease and treatment response. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
3.8 Idiopathic Pulmonary Fibrosis (IPF) 3.8.1 Usual Interstitial Pneumonia (UIP) Pattern IPF 3.8.2 Nonspecific Interstitial Pneumonia (NSIP) Pattern IPF 3.8.3 Cryptogenic Organizing Pneumonia (COP) Pattern IPF 3.8.4 Acute Exacerbation of IPF 3.8.5 Familial Pulmonary Fibrosis 3.8.6 Smoking-Related IPF 3.8.7 Combined Pulmonary Fibrosis and Emphysema (CPFE) Syndrome IPF 3.8.8 Rheumatoid Arthritis-associated IPF 3.8.9 Hypersensitivity Pneumonitis-associated IPF 3.8.10 Asbestosis-associated IPF 3.8.11 Scleroderma-associated IPF 3.8.12 Hermansky-Pudlak Syndrome-related IPF 3.8.13 Neurofibromatosis Type 1-associated IPF 3.8.14 Lymphangioleiomyomatosis (LAM) and Tuberous Sclerosis Complex (TSC)-associated IPF 3.8.15 Connective Tissue Disease (CTD) – Related IPF |
UC-MSCs, LPCs, MSCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Forced Vital Capacity (FVC): Measures the amount of air a person can forcefully exhale after a deep breath. Changes in FVC can indicate disease progression or improvement. 2. Diffusing Capacity of the Lung for Carbon Monoxide (DLCO): Assesses the lung’s ability to transfer oxygen to the bloodstream. Decreases in DLCO may indicate impaired gas exchange. 3. 6-Minute Walk Test (6MWT): Evaluates functional exercise capacity by measuring the distance a patient can walk in 6 minutes. It provides insights into exercise tolerance and overall physical function. 4. Quality of Life Questionnaires: Various validated questionnaires such as the St. George’s Respiratory Questionnaire (SGRQ) or the King’s Brief Interstitial Lung Disease (K-BILD) questionnaire assess aspects of daily living, symptoms, and well-being. 5. Mortality Rates: Tracking survival rates post-treatment is a crucial outcome measure in IPF studies to assess treatment efficacy and patient prognosis. 6. Hospitalization Rates: Monitoring the frequency and reasons for hospital admissions helps evaluate disease progression and treatment effectiveness. 7. Disease Progression: Radiological assessments such as high-resolution computed tomography (HRCT) scans or pulmonary function tests (PFTs) may be used to evaluate disease progression or stabilization. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
3.9 Alpha-1 Antitrypsin Deficiency (AATD) 3.9.1 PiZZ genotype (most severe form) 3.9.2 PiSZ genotype 3.9.3 PiMZ genotype 3.9.4 PiMM genotype (normal allele without deficiency) 3.9.5 Null/null genotype (very rare and severe form) 3.9.6 Rare variants or combinations of alleles 3.9.7 Phenotypic subtypes based on lung and liver involvement 3.9.8 Clinical subtypes based on disease severity and manifestations 3.9.9 Pediatric-onset AATD subtypes 3.9.10 Adult-onset AATD subtypes 3.9.11 Emphysema-predominant AATD 3.9.12 Bronchiectasis-associated AATD 3.9.13 Liver Disease-associated AATD 3.9.14 Rapidly Progressive AATD 3.9.15 Slow Progression AATD 3.9.16 Smoker-related AATD 3.9.17 Non-smoker AATD 3.9.18 Occupational exposure-related AATD 3.9.19 Familial AATD 3.9.20 Sporadic AATD |
UC-MSCs, LPCs, MSCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Forced Expiratory Volume in one second (FEV1): Measures the volume of air a person can forcefully exhale in one second, assessing lung function. 2. Diffusing Capacity of the Lung for Carbon Monoxide (DLCO): Assesses the lung’s ability to transfer oxygen from inhaled air into the bloodstream. 3. 6-Minute Walk Test (6MWT): Evaluates functional exercise capacity by measuring the distance a patient can walk in 6 minutes, indicating overall physical function and exercise tolerance. 4. Quality of Life Questionnaires: Various validated questionnaires such as the St. George’s Respiratory Questionnaire (SGRQ) or the King’s Brief Interstitial Lung Disease (K-BILD) questionnaire assess aspects of daily living, symptoms, and well-being specific to AATD patients. 5. Mortality Rates: Tracking survival rates post-treatment is a crucial outcome measure to assess treatment efficacy and patient prognosis. 6. Hospitalization Rates: Monitoring the frequency and reasons for hospital admissions helps evaluate disease progression and treatment effectiveness, especially in reducing exacerbations and complications. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
3.10 Pulmonary Hypertension (PH) Certainly, here are the subtypes of Pulmonary Hypertension (PH) labeled according to your request, along with primary outcome assessments post Cellular Therapy and Stem Cells: 3.10.1 Pulmonary Arterial Hypertension (PAH) 3.10.2 Pulmonary Hypertension due to Left Heart Disease (PH-LHD) 3.10.3 Pulmonary Hypertension due to Lung Diseases and/or Hypoxia (PH-LHD) 3.10.4 Chronic Thromboembolic Pulmonary Hypertension (CTEPH) 3.10.5 Pulmonary Hypertension with Unclear Multifactorial Mechanisms 3.10.6 Pulmonary Hypertension with Unclear or Unknown Mechanism 3.10.7 Heritable Pulmonary Arterial Hypertension (HPAH) 3.10.8 Pulmonary Hypertension associated with Connective Tissue Diseases (CTD-PAH) 3.10.9 Pulmonary Hypertension associated with Congenital Heart Diseases (CHD-PAH) 3.10.10 Pulmonary Hypertension associated with Left Heart Diseases (LHD-PAH) 3.10.11 Pulmonary Hypertension associated with Chronic Lung Diseases and/or Hypoxia (CLD-PAH) 3.10.12 Pulmonary Hypertension associated with Portal Hypertension and Liver Diseases (PoPH) 3.10.13 Pulmonary Hypertension associated with HIV Infection 3.10.14 Pulmonary Hypertension associated with Drugs and Toxins 3.10.15 Pulmonary Hypertension associated with Other Systemic Disorders 3.10.16 Pulmonary Hypertension due to Miscellaneous Reasons |
UC-MSCs, LPCs, MSCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Six-Minute Walk Distance (6MWD): Measures the distance a patient can walk in six minutes, providing insights into exercise capacity and functional status. 2. Functional Class Assessment (FC): Classifies patients based on their functional status using criteria such as the World Health Organization (WHO) Functional Class system or the New York Heart Association (NYHA) classification. 3. Hemodynamic Parameters: Includes assessments such as pulmonary artery pressure (PAP), mean pulmonary arterial pressure (mPAP), pulmonary vascular resistance (PVR), and cardiac output (CO) measured via right heart catheterization. 4. Quality of Life Questionnaires: Various validated questionnaires like the Minnesota Living with Heart Failure Questionnaire (MLHFQ) or the Cambridge Pulmonary Hypertension Outcome Review (CAMPHOR) assess aspects of daily living, symptoms, and well-being specific to PH patients. 5. Functional Tests: Other functional tests may include cardiopulmonary exercise testing (CPET), echocardiography for assessing cardiac function, and arterial blood gas analysis to evaluate gas exchange. 6. Mortality Rates: Tracking survival rates post-treatment is a crucial outcome measure to assess treatment efficacy and patient prognosis in PH. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
3.11 Bronchiectasis 3.11.1 Idiopathic Bronchiectasis 3.11.2 Post-Infectious Bronchiectasis 3.11.3 Cystic Fibrosis-related Bronchiectasis 3.11.4 Immunodeficiency-related Bronchiectasis 3.11.5 Allergic Bronchopulmonary Aspergillosis (ABPA) associated Bronchiectasis 3.11.6 Non-Cystic Fibrosis Primary Ciliary Dyskinesia (PCD) associated Bronchiectasis 3.11.7 Connective Tissue Disease-related Bronchiectasis 3.11.8 Autoimmune-related Bronchiectasis 3.11.9 Inhalation-Related Bronchiectasis (e.g., due to environmental exposures) 3.11.10 Post-Tuberculosis Bronchiectasis |
UC-MSCs, LPCs, MSCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Pulmonary Function Tests (PFTs): Including spirometry, lung volumes, and diffusing capacity assessments to evaluate lung function and airflow limitation. 2. Quality of Life Questionnaires: Such as the St. George’s Respiratory Questionnaire (SGRQ) or the Bronchiectasis Health Questionnaire (BHQ) to assess the impact of Bronchiectasis on daily life and well-being. 3. Exacerbation Rates: Monitoring the frequency and severity of exacerbations (acute worsening of symptoms) to assess disease stability and treatment efficacy. 4. Respiratory Symptoms Score: A subjective assessment of respiratory symptoms such as cough, sputum production, and dyspnea. 5. Radiological Assessments: Such as high-resolution computed tomography (HRCT) scans to evaluate changes in bronchial dilation, airway wall thickening, and presence of mucus plugs. 6. Microbiological Assessments: Including sputum cultures and analyses to identify bacterial, viral, or fungal pathogens contributing to respiratory infections. 7. Exercise Capacity Tests: Such as the six-minute walk test (6MWT) to assess functional exercise capacity and endurance. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
3.13 Acute Respiratory Distress Syndrome (ARDS) 3.13.1 Primary ARDS (due to direct lung injury, such as pneumonia, aspiration, or pulmonary contusion) 3.13.2 Secondary ARDS (due to indirect causes, including sepsis, trauma, pancreatitis, or non-pulmonary infections) 3.13.3 Moderate ARDS (PaO2/FiO2 ratio between 100-200 mm Hg) 3.13.4 Severe ARDS (PaO2/FiO2 ratio less than 100 mm Hg) |
UC-MSCs, LPCs, MSCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Mortality Rates: Tracking survival rates post-treatment is a crucial outcome measure to assess treatment efficacy and patient prognosis in ARDS. 2. Ventilator-Free Days: The number of days a patient is free from mechanical ventilation during a specified period, indicating respiratory function recovery. 3. Improvement in Oxygenation: Assessing improvements in oxygen levels, typically measured by arterial oxygen tension (PaO2)/fraction of inspired oxygen (FiO2) ratio or oxygen saturation (SpO2). 4. Lung Function: Evaluating lung function parameters such as lung compliance, tidal volume, and respiratory rate. 5. Inflammatory Markers: Monitoring levels of inflammatory markers such as cytokines (e.g., IL-6, IL-8) and C-reactive protein (CRP) to assess systemic inflammation and response to treatment. 6. Radiological Assessments: Including chest X-rays or computed tomography (CT) scans to evaluate changes in lung morphology, consolidation, and resolution of infiltrates. 7. Organ Dysfunction Scores: Such as the Sequential Organ Failure Assessment (SOFA) score or the Acute Physiology and Chronic Health Evaluation (APACHE) II score to assess multiorgan function and overall clinical status. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
3.13 Pulmonary Fibrosis 3.13.1 Idiopathic Pulmonary Fibrosis (IPF) 3.13.2 Nonspecific Interstitial Pneumonia (NSIP) 3.13.3 Cryptogenic Organizing Pneumonia (COP) 3.13.4 Acute Exacerbation of IPF 3.13.5 Familial Pulmonary Fibrosis 3.13.6 Smoking-related PF 3.13.7 Combined Pulmonary Fibrosis and Emphysema (CPFE) 3.13.8 Rheumatoid Arthritis-associated PF 3.13.9 Hypersensitivity Pneumonitis-associated PF 3.13.10 Asbestosis-associated PF 3.13.11 Scleroderma-associated PF 3.13.12 Hermansky-Pudlak Syndrome-related PF 3.13.13 Neurofibromatosis Type 1-associated PF 3.13.14 Lymphangioleiomyomatosis (LAM) and Tuberous Sclerosis Complex (TSC)-associated PF 3.13.15 Connective Tissue Disease (CTD) – Related PF |
UC-MSCs, LPCs, MSCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Forced Vital Capacity (FVC): Measures the amount of air a person can forcefully exhale after a deep breath, evaluating lung function and capacity. 2. Diffusing Capacity of the Lung for Carbon Monoxide (DLCO): Assesses the lung’s ability to transfer oxygen from inhaled air into the bloodstream, indicating gas exchange efficiency. 3. Six-Minute Walk Test (6MWT): Evaluates functional exercise capacity by measuring the distance a patient can walk in six minutes, providing insights into exercise tolerance and overall physical function. 4. Quality of Life Questionnaires: Various validated questionnaires such as the St. George’s Respiratory Questionnaire (SGRQ) or the King’s Brief Interstitial Lung Disease (K-BILD) questionnaire assess aspects of daily living, symptoms, and well-being specific to PF patients. 5. Radiological Assessments: Including high-resolution computed tomography (HRCT) scans to evaluate changes in lung fibrosis, honeycombing, ground-glass opacities, and overall disease progression. 6. Mortality Rates: Tracking survival rates post-treatment is a crucial outcome measure to assess treatment efficacy and patient prognosis in PF. 7. Acute Exacerbation Rates: Monitoring the frequency and severity of acute exacerbations (acute worsening of symptoms) to assess disease stability and treatment effectiveness. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
3.14 Pulmonary Emphysema 3.14.1 Centriacinar Emphysema 3.14.2 Panacinar Emphysema 3.14.3 Paraseptal Emphysema 3.14.4 Irregular Emphysema 3.14.5 Distal Acinar Emphysema 3.14.6 Smoking-related Emphysema 3.14.7 Alpha-1 Antitrypsin Deficiency-associated Emphysema 3.14.8 Occupational-related Emphysema (e.g., due to exposure to dust, chemicals, or pollutants) 3.14.9 Secondary Emphysema (e.g., due to chronic bronchitis, asthma, or lung infections) |
UC-MSCs, LPCs, MSCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Forced Expiratory Volume in one second (FEV1): Measures the volume of air a person can forcefully exhale in one second, assessing lung function and airflow limitation. 2. Diffusing Capacity of the Lung for Carbon Monoxide (DLCO): Assesses the lung’s ability to transfer oxygen from inhaled air into the bloodstream, indicating gas exchange efficiency. 3. Six-Minute Walk Test (6MWT): Evaluates functional exercise capacity by measuring the distance a patient can walk in six minutes, providing insights into exercise tolerance and overall physical function. 4. Quality of Life Questionnaires: Various validated questionnaires such as the St. George’s Respiratory Questionnaire (SGRQ) or the Chronic Respiratory Disease Questionnaire (CRQ) assess aspects of daily living, symptoms, and well-being specific to Emphysema patients. 5. Radiological Assessments: Including chest X-rays or computed tomography (CT) scans to evaluate changes in lung hyperinflation, bullae formation, and overall disease progression. 6. Mortality Rates: Tracking survival rates post-treatment is a crucial outcome measure to assess treatment efficacy and patient prognosis in Pulmonary Emphysema. 7. Respiratory Symptoms Score: A subjective assessment of respiratory symptoms such as dyspnea, cough, and sputum production. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
3.15. Lung Cancer (as part of targeted therapies) 3.15.1 Non-Small Cell Lung Cancer (NSCLC) 3.15.2 Small Cell Lung Cancer (SCLC) 3.15.3 Adenocarcinoma 3.15.4 Squamous Cell Carcinoma 3.15.5 Large Cell Carcinoma 3.15.6 Bronchioloalveolar Carcinoma 3.15.7 Carcinoid Tumors of the Lung 3.15.8 Pleomorphic Carcinoma 3.15.9 Sarcomatoid Carcinoma 3.15.10 Salivary Gland-Type Tumors of the Lung 3.15.11 Neuroendocrine Tumors of the Lung 3.15.12 Mesothelioma 3.15.13 Lymphomas of the Lung 3.15.14 Thymoma and Thymic Carcinoma 3.15.15 Germ Cell Tumors of the Lung 3.15.16 Other Rare Types of Lung Cancer |
UC-MSCs, LPCs, MSCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Overall Response Rate (ORR): The proportion of patients who achieve complete or partial tumor regression or stabilization in response to targeted therapy. 2. Progression-Free Survival (PFS): The duration of time from the start of targeted therapy until disease progression or death, indicating the effectiveness of treatment in controlling cancer growth. 3. Overall Survival (OS): The duration of time from the start of targeted therapy until death from any cause, providing insights into the long-term efficacy of treatment. 4. Disease Control Rate (DCR): The proportion of patients who achieve complete response, partial response, or stable disease with targeted therapy, reflecting disease control and treatment benefits. 5. Time to Progression (TTP): The time interval from the start of targeted therapy until disease progression, indicating the duration of response to treatment. 6. Quality of Life (QoL) Assessments: Various validated questionnaires and assessments to evaluate patients’ physical, emotional, and social well-being during targeted therapy. 7. Adverse Events and Toxicity Monitoring: Assessing the occurrence and severity of treatment-related side effects and toxicities, ensuring patient safety and treatment tolerability. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
3.16 Chronic Bronchitis 3.16.2 Occupational-related Chronic Bronchitis (e.g., due to exposure to dust, chemicals, or pollutants) 3.16.3 Non-Smoking-related Chronic Bronchitis (e.g., due to respiratory infections, airway irritants, or genetic factors) 3.16.4 Chronic Bronchitis with Bronchiectasis 3.16.5 Chronic Bronchitis with Emphysema (Overlap Syndrome) |
UC-MSCs, LPCs, MSCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Symptom Severity Score: Assessing the severity of chronic cough, sputum production, wheezing, and dyspnea associated with Chronic Bronchitis. 2. Pulmonary Function Tests (PFTs): Including spirometry, lung volumes, and diffusing capacity assessments to evaluate lung function, airflow limitation, and gas exchange. 3. Quality of Life Questionnaires: Various validated questionnaires such as the COPD Assessment Test (CAT) or the St. George’s Respiratory Questionnaire (SGRQ) assess the impact of Chronic Bronchitis on daily life, symptoms, and well-being. 4. Exacerbation Rates: Monitoring the frequency and severity of exacerbations (acute worsening of symptoms) to assess disease stability and treatment effectiveness. 5. Respiratory Symptoms Score: A subjective assessment of respiratory symptoms such as cough, sputum production, and dyspnea. 6. Use of Rescue Medications: Monitoring the use of bronchodilators, corticosteroids, or other medications for symptom relief and disease management. 7. Exercise Capacity Tests: Such as the six-minute walk test (6MWT) to assess functional exercise capacity, endurance, and tolerance to physical activity. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
3.17 Bronchiolitis Obliterans 3.17.1 Post-Infectious Bronchiolitis Obliterans (PIBO) 3.17.2 Bronchiolitis Obliterans Organizing Pneumonia (BOOP)-related BO 3.17.3 Lung Transplant-Related Bronchiolitis Obliterans 3.17.4 Chemical Exposure-Related Bronchiolitis Obliterans 3.17.5 Connective Tissue Disease-Associated Bronchiolitis Obliterans 3.17.6 Bronchiolitis Obliterans with Concurrent Chronic Lung Disease (e.g., COPD, Asthma) 3.17.7 Post-Transplant Bronchiolitis Obliterans 3.17.8 Bronchiolitis Obliterans after Hematopoietic Stem Cell Transplantation (HSCT) 3.17.9 Pediatric Bronchiolitis Obliterans |
UC-MSCs, LPCs, MSCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Pulmonary Function Tests (PFTs): Including spirometry, lung volumes, and diffusing capacity assessments to evaluate lung function, airflow limitation, and gas exchange. 2. Quality of Life Questionnaires: Various validated questionnaires such as the St. George’s Respiratory Questionnaire (SGRQ) or the Bronchiolitis Obliterans Syndrome 65 (BOS-65) assess the impact of BO on daily life, symptoms, and well-being. 3. Radiological Assessments: Including high-resolution computed tomography (HRCT) scans to evaluate changes in lung morphology, airway inflammation, and overall disease progression. 4. Bronchiolitis Obliterans Syndrome (BOS) Grading: Assessing the severity of BOS based on pulmonary function decline and symptom exacerbation, often graded using criteria such as the International Society for Heart and Lung Transplantation (ISHLT) guidelines. 5. Acute Exacerbation Rates: Monitoring the frequency and severity of acute exacerbations (acute worsening of symptoms) to assess disease stability and treatment effectiveness. 6. Use of Immunosuppressive Therapy: Monitoring the use and response to immunosuppressive medications such as corticosteroids or other anti-inflammatory agents. 7. Lung Transplantation Rates: Evaluating the need for and outcomes of lung transplantation in BO patients with progressive respiratory failure. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
3.18 Pulmonary Alveolar Proteinosis (PAP) 3.18.1 Primary or Idiopathic Pulmonary Alveolar Proteinosis (iPAP) 3.18.2 Secondary Pulmonary Alveolar Proteinosis (sPAP) due to underlying conditions such as hematological disorders, immunodeficiency, or environmental exposures 3.18.3 Congenital or Familial Pulmonary Alveolar Proteinosis 3.18.4 Acquired Pulmonary Alveolar Proteinosis associated with autoimmune diseases (e.g., anti-GM-CSF antibody syndrome) 3.18.5 Pediatric Pulmonary Alveolar Proteinosis |
UC-MSCs, LPCs, MSCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Improvement in Pulmonary Function: Assessing changes in lung function parameters such as forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and diffusing capacity of the lung for carbon monoxide (DLCO). 2. Radiological Improvement: Evaluating changes in chest X-rays or high-resolution computed tomography (HRCT) scans to assess lung clearance of alveolar proteinaceous material. 3. Arterial Blood Gas Analysis: Monitoring changes in arterial blood gas levels, including partial pressure of oxygen (PaO2) and oxygen saturation (SaO2), to evaluate gas exchange efficiency. 4. Quality of Life Questionnaires: Various validated questionnaires such as the St. George’s Respiratory Questionnaire (SGRQ) or the Short Form Health Survey (SF-36) assess the impact of PAP on daily life, symptoms, and well-being. 5. Disease-Specific Biomarkers: Monitoring levels of surfactant proteins (e.g., SP-A, SP-B, SP-C) or anti-GM-CSF antibodies to assess disease activity and response to treatment. 6. Symptom Improvement: Assessing changes in respiratory symptoms such as dyspnea, cough, and exercise tolerance. 7. Use of Whole Lung Lavage (WLL): Evaluating the frequency and outcomes of WLL procedures in clearing alveolar proteinaceous material and improving lung function. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
3.19 Sarcoidosis 3.19.1 Pulmonary Sarcoidosis 3.19.2 Cutaneous Sarcoidosis 3.19.3 Ocular Sarcoidosis 3.19.4 Cardiac Sarcoidosis 3.19.5 Neurosarcoidosis 3.19.6 Lofgren’s Syndrome (Acute Sarcoidosis with erythema nodosum, arthritis, and bilateral hilar lymphadenopathy) 3.19.7 Chronic Sarcoidosis 3.19.8 Systemic Sarcoidosis (Involving multiple organs/systems) 3.19.9 Isolated Organ Involvement (e.g., isolated pulmonary, cutaneous, or cardiac involvement) 3.19.10 Pediatric Sarcoidosis |
UC-MSCs, LPCs, MSCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Improvement in Pulmonary Function: Assessing changes in lung function parameters such as forced vital capacity (FVC), forced expiratory volume in one second (FEV1), and diffusing capacity of the lung for carbon monoxide (DLCO). 2. Resolution of Granulomatous Inflammation: Evaluating the reduction in granulomas or granulomatous inflammation in affected organs, typically assessed through imaging studies such as chest X-rays or CT scans. 3. Quality of Life Questionnaires: Various validated questionnaires such as the Sarcoidosis Health Questionnaire (SHQ) or the Short Form Health Survey (SF-36) assess the impact of Sarcoidosis on daily life, symptoms, and well-being. 4. Disease Activity Scores: Monitoring disease activity using scores such as the Sarcoidosis Activity and Severity Index (SASI) or the Scadding scale based on radiological findings. 5. Symptom Improvement: Assessing changes in symptoms such as cough, dyspnea, fatigue, and joint pain. 6. Use of Immunomodulatory Therapy: Monitoring the response to immunomodulatory medications such as corticosteroids, immunosuppressants, or biologics in controlling disease activity and inflammation. 7. Organ Function Preservation: Evaluating the preservation of organ function, especially in cases of cardiac, ocular, or neurosarcoidosis. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
3.20 Pulmonary Arterial Hypertension (PAH) 3.20.1 Idiopathic PAH (IPAH) 3.20.2 Heritable PAH (HPAH) 3.20.3 Associated PAH (APAH) due to connective tissue diseases (e.g., systemic sclerosis, systemic lupus erythematosus) 3.20.4 Associated PAH (APAH) due to congenital heart diseases 3.20.5 Associated PAH (APAH) due to HIV infection 3.20.6 Associated PAH (APAH) due to drugs/toxins (e.g., anorexigens, methamphetamine) 3.20.7 Associated PAH (APAH) due to portal hypertension and liver diseases 3.20.8 Persistent Pulmonary Hypertension of the Newborn (PPHN) 3.20.9 PAH associated with chronic hemolytic anemia 3.20.10 PAH associated with significant venous or capillary involvement |
UC-MSCs, LPCs, MSCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Improvement in Exercise Capacity: Assessing changes in exercise tolerance and functional capacity using tests like the six-minute walk test (6MWT) or cardiopulmonary exercise testing (CPET). 2. Hemodynamic Parameters: Monitoring changes in pulmonary artery pressure (PAP), mean pulmonary artery pressure (mPAP), pulmonary vascular resistance (PVR), cardiac output (CO), and right atrial pressure (RAP) through right heart catheterization. 3. Functional Class Improvement: Evaluating improvements in symptoms, functional status, and activity levels based on the World Health Organization (WHO) functional classification system. 4. Quality of Life Questionnaires: Various validated questionnaires such as the Minnesota Living with Heart Failure Questionnaire (MLHFQ) or the Cambridge Pulmonary Hypertension Outcome Review (CAMPHOR) assess the impact of PAH on daily life, symptoms, and well-being. 5. Biomarkers: Monitoring levels of biomarkers such as brain natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP) to assess disease severity, prognosis, and response to treatment. 6. Echocardiographic Parameters: Assessing changes in right ventricular function, tricuspid annular plane systolic excursion (TAPSE), right ventricular systolic pressure (RVSP), and other echocardiographic parameters indicative of PAH progression or improvement. 7. Adverse Events and Hospitalizations: Monitoring the occurrence of adverse events, PAH-related complications, and hospitalizations during follow-up. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
3.21 Pulmonary Lymphangioleiomyomatosis (LAM) 3.21.1 Sporadic LAM 3.21.2 Tuberous Sclerosis Complex (TSC)-associated LAM 3.21.3 LAM with Minimal Symptoms 3.21.4 Severe or Progressive LAM 3.21.5 LAM with Chylous Effusions 3.21.6 LAM with Renal Angiomyolipomas 3.21.7 LAM with Extrathoracic Manifestations (e.g., lymphatic involvement, abdominal tumors) |
UC-MSCs, LPCs, MSCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Pulmonary Function Tests (PFTs): Including spirometry, lung volumes, and diffusing capacity assessments to evaluate lung function, airflow limitation, and gas exchange. 2. Radiological Assessments: Such as high-resolution computed tomography (HRCT) scans to evaluate changes in lung parenchyma, lymphatic involvement, and disease progression. 3. Quality of Life Questionnaires: Various validated questionnaires such as the St. George’s Respiratory Questionnaire (SGRQ) or the Short Form Health Survey (SF-36) assess the impact of LAM on daily life, symptoms, and well-being. 4. Exercise Capacity Tests: Such as the six-minute walk test (6MWT) to assess functional exercise capacity, endurance, and tolerance to physical activity. 5. Arterial Blood Gas Analysis: Monitoring changes in arterial blood gas levels, including partial pressure of oxygen (PaO2) and oxygen saturation (SaO2), to evaluate gas exchange efficiency. 6. Biomarker Monitoring: Evaluating levels of serum markers such as vascular endothelial growth factor-D (VEGF-D), lactate dehydrogenase (LDH), or other biomarkers indicative of disease activity and progression. 7. Adverse Events and Complications: Monitoring the occurrence of adverse events, respiratory exacerbations, pneumothorax, or other LAM-related complications during follow-up. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
3.22 Diffuse Panbronchiolitis 3.22.1 Early-Onset Diffuse Panbronchiolitis 3.22.2 Late-Onset Diffuse Panbronchiolitis 3.22.3 Acute Exacerbation of Diffuse Panbronchiolitis 3.22.4 Diffuse Panbronchiolitis with Bronchiectasis 3.22.5 Diffuse Panbronchiolitis with Significant Mucous Plugging 3.22.6 Diffuse Panbronchiolitis with Severe Hypoxemia 3.22.7 Diffuse Panbronchiolitis with Chronic Respiratory Failure 3.22.8 Diffuse Panbronchiolitis with Recurrent Infections |
UC-MSCs, LPCs, MSCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Pulmonary Function Tests (PFTs): Including spirometry, lung volumes, and diffusing capacity assessments to evaluate lung function, airflow limitation, and gas exchange. 2. Quality of Life Questionnaires: Various validated questionnaires such as the St. George’s Respiratory Questionnaire (SGRQ) or the Chronic Respiratory Disease Questionnaire (CRQ) assess the impact of DPB on daily life, symptoms, and well-being. 3. Radiological Assessments: Such as chest X-rays or high-resolution computed tomography (HRCT) scans to evaluate changes in lung parenchyma, airway inflammation, and disease progression. 4. Symptom Scores: Subjective assessment of respiratory symptoms such as cough, sputum production, dyspnea, and wheezing. 5. Exacerbation Rates: Monitoring the frequency and severity of acute exacerbations (worsening of symptoms) to assess disease stability and treatment effectiveness. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |
3.23 Respiratory Distress Syndrome in Premature Infants 3.23.1 Mild Respiratory Distress Syndrome in Premature Infants 3.23.2 Moderate Respiratory Distress Syndrome in Premature Infants 3.23.3 Severe Respiratory Distress Syndrome in Premature Infants 3.23.4 Surfactant Deficiency-Related Respiratory Distress Syndrome 3.23.5 Respiratory Distress Syndrome with Associated Lung Pathologies (e.g., pneumonia, meconium aspiration) 3.23.6 Persistent Pulmonary Hypertension of the Newborn (PPHN) complicating RDS 3.23.7 Chronic Lung Disease of Prematurity (formerly known as Bronchopulmonary Dysplasia) secondary to RDS |
UC-MSCs, LPCs, MSCs, HSCs, iPSCs, EPCs, Lung PCs, ADSCs, DPSCs Pneumocyte-PSCs, Alveolar Macrophage-PSCs, Bronchial Epithelial-PSCs, Smooth Muscle-PSCs, Endothelial-PSCs, Fibroblast-PSCs, Ciliated Epithelial-PSCs, Goblet Cell-PSCs, Club Cell-PSCs, Pulmonary Neuroendocrine-PSCs, Mast Cell-PSCs, Pericyte-PSCs, Mesothelial-PSCs, and Pulmonary Stem Cells | 1. Respiratory Function Monitoring: This includes assessments such as oxygen saturation levels (SpO2), respiratory rate, need for mechanical ventilation, and oxygen therapy requirements. 2. Radiographic Imaging: Chest X-rays or lung ultrasound scans to evaluate lung aeration, presence of pulmonary edema, and any signs of lung injury or complications. 3. Ventilatory Support Parameters: Monitoring parameters related to ventilator settings such as tidal volume, positive end-expiratory pressure (PEEP), and peak inspiratory pressure (PIP). 4. Arterial Blood Gas Analysis (ABG): Analyzing blood gas levels to assess oxygenation (PaO2), ventilation (PaCO2), and acid-base status, providing insights into respiratory function and adequacy of ventilation. 5. Inflammatory Biomarkers: Monitoring levels of inflammatory markers such as C-reactive protein (CRP), interleukins (IL-6, IL-8), and other cytokines to assess the extent of lung inflammation and response to treatment. 6. Growth and Development Parameters: Evaluating growth metrics, developmental milestones, and neurodevelopmental outcomes to assess the long-term impact of RDS and its treatment on infant health. Consult with Our Team of Experts Now! Consult with Our Team of Experts Now! |