The letter, authored by Barina Khan of Karachi Medical and Dental College and published on 3 September 2026 as Volume 29, article number 59 of the journal, is written in direct response to a pilot study by Tran and colleagues that documented dynamic platelet dysfunction in patients undergoing extracorporeal membrane oxygenation. That pilot work, which appeared in the same journal earlier in 2026, used platelet function testing to follow how platelet performance changed over the course of ECMO support and explored whether those changes tracked with clinically significant bleeding. The new letter does not dispute that platelet dysfunction is real and important in ECMO patients. Instead, it questions whether the specific instrument and protocol used can reliably detect it in this population.

The core of the concern lies in what laboratory scientists call a ceiling effect. The PFA-200 measures the time it takes for platelets, under controlled high shear conditions, to form a plug that occludes a microscopic aperture in a cartridge coated with platelet agonists such as collagen and epinephrine or collagen and adenosine diphosphate. When platelet function is severely impaired, the plug simply never forms, and the instrument reports a result at or above the maximum assay limit, typically a value greater than 300 seconds. In profoundly thrombocytopenic or platelet-exhausted patients, which many ECMO patients quickly become, large numbers of test results pile up at this artificial ceiling. Once a value has been censored at the upper limit, the assay can no longer distinguish between moderately severe and catastrophic platelet failure, compressing exactly the range of dysfunction that matters most for predicting bleeding.

Khan’s letter argues that this censoring problem is particularly acute during ECMO, where platelet counts fall progressively, platelets become activated and exhausted through continuous contact with the oxygenator membrane and circuit tubing, and acquired platelet defects accumulate over days of support. If a study correlates closure times with bleeding episodes in such a cohort, the relationship may be flattened or distorted by the many results that read simply as greater than 300 seconds. Statistical associations computed on censored data risk either underestimating the true strength of the link between platelet failure and hemorrhage or, depending on how the ceiling values are handled in the analysis, producing misleading conclusions about when platelet dysfunction begins to matter clinically.

The second confounder the letter highlights is hematocrit, the proportion of blood volume occupied by red blood cells. It is a long-standing observation in hematology that the PFA-100 and PFA-200 are exquisitely sensitive to the hematocrit of the sample. Red cells are not passive bystanders in primary hemostasis; they physically push platelets toward the vessel wall in flowing blood and contribute chemical signals, including adenosine diphosphate released from erythrocytes, that amplify platelet activation. When the hematocrit drops below roughly 30 percent, closure times lengthen even if platelets themselves are functioning normally, and severe anemia can push closure times beyond the assay limit on its own. Conversely, elevating the hematocrit can shorten closure times and mask genuine platelet defects, an effect documented decades ago in studies of uremic and cirrhotic patients evaluated on the platelet function analyzer.

This sensitivity is a serious problem in the ECMO population specifically. Patients on extracorporeal support are frequently anemic, whether from hemodilution caused by circuit priming, hemolysis within the circuit, repeated blood sampling, gastrointestinal bleeding, or the suppressed red cell production that accompanies critical illness. In such patients, a prolonged closure time may reflect the red cell deficit rather than intrinsic platelet failure, and the degree of prolongation may bear little relationship to the true functional capacity of the platelets. Khan’s letter suggests that unless hematocrit is either matched across study groups or formally adjusted for in the statistical model, the association reported between PFA-200 closure times and bleeding in ECMO patients may be confounded from the outset, with anemia masquerading as platelet dysfunction.

The letter places these concerns in a broader and somewhat sobering context. The clinical utility of closure times on the platelet function analyzer has been debated for more than two decades. Studies in cardiac surgery patients have repeatedly questioned whether the device predicts blood loss after cardiopulmonary bypass, another setting in which acquired platelet defects, hemodilution and anemia coexist. A comprehensive review in the American Journal of Hematology catalogued the assay’s utility across bleeding disorders while also documenting its susceptibility to hematologic variables, and a worldwide survey of platelet function testing practices conducted under the auspices of the International Society on Thrombosis and Haemostasis underscored how much variability exists in how platelet function is assessed even among expert laboratories. Against that backdrop, applying the PFA-200 to the uniquely harsh environment of extracorporeal circulation demands particular caution about the assay’s known limitations.

None of this means the assay should be abandoned in the ECMO setting, the letter’s argument implies, but rather that its results must be interpreted with an awareness of when the instrument can and cannot see. Practical strategies exist. Researchers can report the proportion of censored results explicitly and use statistical methods designed for data with detection limits rather than treating the ceiling value as a genuine number. Studies can stratify closure times by hematocrit, exclude samples with severe anemia from platelet-focused analyses, or measure closure times only after red cell transfusion has stabilized the hematocrit. Complementary tests that are less dependent on shear, hematocrit and sample handling, such as light transmission aggregometry, flow cytometric markers of platelet activation, or other point-of-care viscoelastic and platelet-mapping devices, can help triangulate the true state of platelet function. The pilot study’s central observation, that platelet dysfunction evolves dynamically during ECMO, remains valuable; the question is whether the PFA-200, as deployed, is measuring that dysfunction or partly measuring the anemia around it.

The stakes are far from academic. Bleeding remains one of the most feared complications of ECMO, occurring in a substantial fraction of patients and driving decisions about anticoagulation intensity, transfusion thresholds and circuit management. If closure times on the PFA-200 are adopted as a bedside guide without accounting for ceiling effects and hematocrit, clinicians risk both false reassurance, when an apparently normal result is actually capped by the assay limit in a patient with profound platelet exhaustion, and false alarm, when a prolonged result in an anemic patient triggers unnecessary platelet transfusion. Given that platelet transfusions carry their own risks, including allergic reactions, transfusion-associated circulatory overload and the theoretical promotion of thrombosis in a patient group already prone to circuit clotting, refining which patients truly need platelet support is a matter of real clinical consequence.

Khan’s letter is a compact methodological intervention, but it lands at a moment when interest in platelet function testing during extracorporeal support is growing rapidly. As devices for measuring closure times, aggregometry and platelet activation migrate from hematology laboratories to the intensive care unit bedside, the letter serves as a reminder that the validity of any such measurement depends on the biology of the sample as much as the precision of the instrument. In ECMO patients, where thrombocytopenia, platelet exhaustion and anemia march together, closure times must be read with both eyes open. Whether future studies can confirm a robust, hematocrit-independent association between PFA-200 results and bleeding in this population will determine whether the assay earns a genuine place in the ECMO management toolkit, or remains a test whose ceiling it cannot see above and whose red cell context it cannot escape.

Subject of Research: The reliability of PFA-200 platelet function closure times for assessing bleeding risk during extracorporeal membrane oxygenation

Article Title: PFA-200 closure times in ECMO: Are ceiling effects and hematocrit confounding the bleeding association?

Article References: Khan, B. (2026). PFA-200 closure times in ECMO: Are ceiling effects and hematocrit confounding the bleeding association?. Journal of Artificial Organs, 29(4), Article 59. https://doi.org/10.1007/s10047-026-01589-0

Image Credits: AI Generated

DOI: 10.1007/s10047-026-01589-0

Keywords: ECMO, PFA-200, platelet function, closure time, bleeding risk, hematocrit, coagulation, extracorporeal membrane oxygenation, platelet dysfunction, anemia, point-of-care testing, Journal of Artificial Organs

ARDS entered medical history in 1967, when Ashbaugh and colleagues described adults with severe hypoxemia, diffuse pulmonary infiltrates, reduced lung compliance and a clinical picture resembling the “shock lung” previously recognized after trauma. The syndrome is now understood as a form of acute inflammatory lung injury in which the alveolar-capillary barrier becomes abnormally permeable. Fluid floods the air spaces, surfactant function deteriorates, areas of lung collapse, and blood continues to pass through poorly ventilated regions. The result is profound impairment of oxygen transfer. Mechanical ventilation can sustain gas exchange, but excessive pressures and volumes may stretch vulnerable lung tissue, producing ventilator-induced lung injury. Extracorporeal support emerged as a way to interrupt that cycle by transferring part of the work of gas exchange from the damaged lungs to an external circuit.

The earliest systems were technically demanding and associated with substantial complications. In the 1970s, investigators used membrane lungs to oxygenate blood outside the body for patients with severe post-traumatic respiratory failure. A landmark randomized study published in 1979, however, failed to demonstrate a clear survival advantage for extracorporeal membrane oxygenation in severe adult respiratory failure. At the time, equipment limitations, high anticoagulation requirements and inadequate ventilation strategies constrained the therapy. ECMO subsequently declined in adult practice for several decades, even as it became an important treatment for selected newborns and children. The field began to change when improved pumps, polymethylpentene oxygenators, safer vascular cannulation and more protective ventilator strategies made prolonged support more feasible.

The modern revival of adult ECMO was strongly influenced by the CESAR trial, published in 2009, which compared conventional treatment with referral to an ECMO-capable specialist center. The study showed a higher probability of survival without severe disability among patients managed through the specialist pathway, although the trial evaluated referral to a comprehensive center rather than ECMO alone. The 2009 H1N1 influenza pandemic then provided an unexpected global test of the technology. Hospitals in Australia, the United Kingdom, Italy and elsewhere reported that selected patients with otherwise fatal viral pneumonia could survive with ECMO. During the COVID-19 pandemic, international registry studies further demonstrated that VV-ECMO could support patients with severe viral ARDS, although outcomes worsened when systems became overwhelmed and patients were referred after prolonged mechanical ventilation or extensive secondary organ injury.

Venovenous ECMO is designed primarily for respiratory failure. Blood is drained from the venous circulation, propelled through an artificial lung where carbon dioxide diffuses out and oxygen enters, and returned to the right side of the heart. The patient’s own heart then circulates the oxygenated blood through the body. Unlike venoarterial ECMO, which can provide both cardiac and respiratory support, VV-ECMO does not directly replace the pumping function of the heart. Its principal value in ARDS is that it can maintain oxygen delivery while allowing clinicians to reduce ventilator intensity. Lower tidal volumes, lower driving pressures and reduced respiratory rates can limit mechanical stress on the remaining functional lung. In some patients, ECMO also permits prone positioning, spontaneous breathing strategies or carefully controlled near-apneic ventilation, although each approach requires specialized monitoring.

The review emphasizes that ECMO is not a universal treatment for every patient with hypoxemia. Candidates generally have severe, potentially reversible respiratory failure despite optimized conventional care, including lung-protective ventilation, prone positioning and appropriate treatment of the underlying cause. Clinicians must also consider the duration of mechanical ventilation, age, frailty, neurological status and the presence of irreversible disease affecting other organs. Registry analyses and prognostic models such as RESP, PRESERVE and ECMOnet can help structure assessment, but they cannot determine an individual patient’s outcome with certainty. Obesity alone should not automatically exclude a patient, and selected people with cancer or other complex conditions may benefit. Conversely, advanced multisystem organ failure, devastating brain injury or an inability to recover from the underlying disease may make ECMO medically inappropriate.

Once support begins, management extends far beyond the circuit itself. Ventilator settings must be adjusted to avoid continuing injury while ensuring sufficient gas exchange and preventing dangerous derecruitment. Blood flow, sweep gas, oxygen transfer, carbon dioxide removal and recirculation must be assessed together rather than treated as isolated variables. Anticoagulation is usually required because blood contacts artificial surfaces, yet anticoagulation increases the risk of bleeding. Large international studies have documented frequent hemorrhagic and thrombotic events, including cannula-site bleeding, gastrointestinal hemorrhage, intracranial bleeding, oxygenator clotting and circuit thrombosis. Neurological complications are particularly serious; rapid changes in carbon dioxide after ECMO initiation may alter cerebral blood flow and have been associated with brain injury. Infection, limb ischemia, hemolysis, kidney failure, pressure injuries and profound muscle weakness add to the burden of prolonged support.

Liberation from ECMO is another area in which practice is evolving. As the lungs recover, clinicians gradually reduce sweep gas and test whether the patient can maintain acceptable oxygenation and carbon dioxide levels with less extracorporeal assistance. Successful weaning depends on improving pulmonary compliance, gas exchange, respiratory muscle function and the condition of other organs. There is no single universally accepted weaning protocol, and an international survey published in 2026 highlighted continued variation between centers. The review also notes that prone positioning during VV-ECMO remains an active subject of research. The PRONECMO randomized trial found that prone positioning could be performed safely in experienced centers, but broader questions remain about which patients benefit most and whether the strategy improves survival rather than simply oxygenation.

ECCO₂R represents a different concept. Instead of providing enough blood flow to replace most pulmonary gas exchange, ECCO₂R uses a lower-flow extracorporeal circuit primarily to remove carbon dioxide. Because carbon dioxide is more easily removed than oxygen is added, the technology can operate through smaller vascular catheters and may be less invasive than full ECMO. The proposed benefit is “ultra-lung-protective” ventilation: clinicians could reduce tidal volume or airway pressure beyond conventional protective targets while using the circuit to prevent carbon dioxide accumulation. Early studies, including Xtravent and SUPERNOVA, demonstrated technical feasibility and the ability to lower ventilator intensity in selected patients. Yet physiological improvement has not consistently translated into better outcomes. In the REST randomized trial, ECCO₂R-facilitated lower tidal-volume ventilation did not reduce 90-day mortality in patients with acute hypoxemic respiratory failure, and bleeding and other device-related risks remained important concerns.

The future of extracorporeal lung support will therefore depend less on simply building more powerful machines than on identifying the right patient at the right moment. Newer ECCO₂R platforms are being evaluated in mild-to-moderate ARDS, while studies are exploring support before invasive mechanical ventilation, advanced imaging, biological phenotyping and artificial-intelligence-assisted prediction. Researchers are also examining right-ventricular injury, a complication of severe pulmonary vascular stress that may improve when VV-ECMO reduces hypoxemia and unloads the heart. At the same time, long-term follow-up is revealing that survival is only the beginning of recovery. Survivors may experience persistent weakness, impaired cognition, post-traumatic stress, depression, anxiety and new mental-health diagnoses. The central lesson of six decades is therefore both promising and cautionary: ECMO can create time for injured lungs to heal, but it cannot replace careful critical care, and its success must ultimately be measured by meaningful recovery after the circuit is removed.

Subject of Research: Extracorporeal lung support for acute respiratory distress syndrome, including venovenous ECMO and ECCO₂R

Article Title: 60 years of ARDS and the evolution of extracorporeal lung support – from ECMO to ECCO₂R

Article References: Fernando SM, Brodie D, Slutsky AS, et al. “60 years of ARDS and the evolution of extracorporeal lung support – from ECMO to ECCO₂R.” Intensive Care Medicine (2026).

Image Credits: AI Generated

DOI: 10.1007/s00134-026-08533-z

Keywords: Acute respiratory distress syndrome; extracorporeal life support; venovenous ECMO; extracorporeal membrane oxygenation; ECCO₂R; respiratory failure; lung-protective ventilation

Extracorporeal membrane oxygenation has emerged as a critical lifesaving intervention for patients suffering from severe respiratory failure. The VV ECMO system, which involves the removal, oxygenation, and return of blood to the patient’s body, relies heavily on the design of the drainage cannula. Traditional models have often overlooked the impact that side holes can have on blood flow and oxygenation levels, which may lead to inadequate patient care and higher mortality rates in unstable patients. Togo’s research aims to fill this gap in knowledge and establish new guidelines for optimal cannula design.

Through a series of meticulous in vitro experiments, the study assessed various configurations of drainage cannulas, meticulously noting the differences in blood flow dynamics. Each setup was designed to simulate conditions reflective of a clinical environment, allowing the researcher to accurately measure the effects of distinct side hole placements on blood oxygenation. By focusing on these variables, Togo was able to identify specific patterns that correlate particular cannula designs with improved oxygenation metrics, thus paving the way for more effective clinical practices.

Oxygenation efficiency in VV ECMO is paramount for patient survival, and Togo’s findings highlight the role of side holes in facilitating or inhibiting this process. The presence of strategically placed side holes was found to enhance the mixing of oxygen-rich blood with deoxygenated blood, thereby improving overall oxygen delivery to the patient. This is especially crucial in the context of patients who are hemodynamically unstable, where the immediate availability of well-oxygenated blood can make a critical difference in survival rates.

Additionally, the study conducted by Togo emphasizes that not only the quantity, but also the quality of side holes plays a significant role in efficient drainage. Larger, well-distributed side holes showed a more favorable impact on overall blood flow rates when compared to smaller or poorly placed ones. Understanding these dynamics is essential for the design and selection of cannulas best suited for VV ECMO, as improper configurations can lead to complications such as thrombosis or inadequate oxygenation.

Togo’s research also explores the implications of cannula design on the overall ECMO circuit. An efficient drainage cannula reduces the risk of complications and enhances the effectiveness of the entire ECMO system. This reinforces the idea that advancements in cannula technology and design can lead to better clinical outcomes, emphasizing the need for continuous innovation within this field. The results could encourage manufacturers to revisit and possibly redesign their existing products based on Togo’s findings.

As the medical community strives to enhance the efficacy of life-support technologies, insights from this study will prove invaluable. It presents an opportunity for healthcare professionals and engineers to collaborate more closely, ensuring that designs of circulatory support devices are informed by evidence-based research, such as Togo’s. This relationship can lead to improved patient care standards and ultimately save more lives.

Furthermore, a wide array of variables requires attention when considering the design and implementation of drainage cannulas. This research sheds light on the need for continuous evaluation and iteration in the engineering process. Rigorous testing coupled with real-world feedback will help ensure that the devices used meet the demands of clinical practice, especially in high-stakes environments encountered in intensive care units.

Togo’s research adds to a growing body of literature advocating for evidence-based approaches in medical device innovation. By illuminating the significance of drainage cannula design features that affect oxygenation, the study provides a solid foundation for further investigations into related fields. The findings encourage ongoing discourse around optimal practices and highlight the importance of multidisciplinary approaches to enhance patient care in critical scenarios.

Ultimately, as we progress in understanding the intricate mechanics of VV ECMO, the pivotal role of the drainage cannula cannot be overstated. This study underscores the importance of reevaluating existing clinical standards in light of new evidence, and it calls for a proactive approach to adopting changes that can lead to better patient outcomes. The ripple effect of such research can have a transformative impact on both technology development and clinical practices surrounding ECMO.

In conclusion, K. Togo’s investigation into the impact of drainage cannula design on blood oxygenation offers vital insights that could revolutionize practices in respiratory support technologies. This research opens the door for enhanced efficacy in ECMO systems, ultimately leading to improved survival rates for patients in critical condition. As healthcare continues to evolve, the intersection of innovative engineering and clinical application will be paramount in advancing the future of medical treatments.

Subject of Research: Optimal drainage cannula design for venovenous extracorporeal membrane oxygenation.

Article Title: Investigating optimal drainage cannula for venovenous extracorporeal membrane oxygenation: impact of side holes on blood oxygenation – an in vitro study.

Article References:

Togo, K. Investigating optimal drainage cannula for venovenous extracorporeal membrane oxygenation: impact of side holes on blood oxygenation – an in vitro study.
J Artif Organs (2025). https://doi.org/10.1007/s10047-025-01525-8

Image Credits: AI Generated

DOI: 10.1007/s10047-025-01525-8

Keywords: venovenous ECMO, drainage cannula, blood oxygenation, medical device design, critical care.

ECMO, an advanced life-support system, temporarily assumes the role of the lungs and heart by oxygenating the blood outside the body, effectively providing a bridge to recovery or transplantation in cases of severe respiratory failure. While ECMO sustains life, it simultaneously complicates therapeutic interventions, especially those involving intravenous cell infusions. Traditional systemic administration of mesenchymal stromal cells (MSCs) risks obstructing the delicate gas-exchange membranes of the ECMO circuit, potentially jeopardizing the system’s function and, consequently, patient survival. Until now, this hazard has largely barred the exploration of stem cell therapies in this vulnerable patient group.

The CIBA method creatively circumvents this barrier by employing a bronchoscope—a slender, flexible tube inserted directly into the airways—to deliver stem cells precisely into the pulmonary alveoli. This targeted, fractionated intrabronchial administration bypasses the bloodstream and the ECMO circuit, ensuring that the therapeutic cells reach the damaged lung tissue without compromising the extracorporeal oxygenation machinery. This controlled, localized delivery maximizes therapeutic potential while safeguarding the integrity of life support, an achievement deemed a technical milestone in critical care medicine.

At the cellular level, the therapeutic agents are Wharton’s jelly-derived mesenchymal stromal cells (WJ-MSCs), known for their immunomodulatory and regenerative properties. Unlike specialized lung cells, these MSCs possess plasticity that allows them to migrate into damaged tissue, modulate inflammatory responses, and promote tissue repair. Upon reaching the alveolar spaces, these cells engage with resident immune populations—including alveolar macrophages and regulatory T cells—stimulating the release of anti-inflammatory cytokines such as interleukin-10 (IL-10) while attenuating pro-inflammatory cytokines like tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). This nuanced immunological interaction helps modulate the excessive lung inflammation characteristic of end-stage lung diseases and severe respiratory distress.

The initial application of the CIBA technique was carried out under compassionate use in a critically ill two-year-old patient suffering from end-stage interstitial lung disease, a devastating condition marked by progressive scarring and respiratory compromise that left no option for lung transplantation. Despite prolonged ECMO support and aggressive immunosuppression, the child’s condition showed minimal improvement. Following regulatory approval by the Spanish Agency of Medicines and Medical Devices (AEMPS), clinicians administered a carefully titrated single dose of WJ-MSCs via the CIBA method. Remarkably, the procedure was well tolerated with no immediate adverse effects, and the patient was successfully extubated within 72 hours—a promising sign of clinical stability.

Although the child’s ultimate clinical course culminated in withdrawal of ECMO support after 127 days due to irreversible progression, this pioneering case demonstrated, for the first time, the feasibility and safety of delivering stem cell therapies directly into the lungs during ECMO support. This breakthrough paves the way for expanded research and clinical trials to explore repeated dosing regimens, dose optimization, and long-term efficacy in larger cohorts.

Technically, the CIBA procedure represents a synthesis of pulmonology, bioengineering, and cell therapy. The delicate act of "drip-feeding" MSCs into the alveolar spaces demands precise control over cell suspension volume, distribution timing, and delivery pressure to prevent airway injury or inadvertent redistribution into the systemic circulation. Professor Soria likens the technique metaphorically to watering a fragile plant with the gentlest possible drip, ensuring nourishment without flooding. This analogy emphasizes the finesse required when working with severely compromised lungs under ECMO.

Scientifically, this research addresses an unmet need in the treatment of respiratory failure complicated by critical illness and advanced life support. Intravenous administration of stem cells has been explored for diverse pulmonary conditions but remained impractical in ECMO patients due to technical risks. By circumventing these risks, the CIBA method opens a new therapeutic avenue rooted in regenerative medicine that might complement or even enhance existing ECMO protocols.

This safety and feasibility study constitutes a proof-of-concept investigation under the DECODE clinical project, funded by Spain’s Instituto de Salud Carlos III. The collaborative effort engaged 28 clinicians spanning four premier Spanish institutions—including Hospital 12 de Octubre in Madrid, Banc de Sang i Teixits in Catalonia, the Institute of Bioengineering at UMH, and the Institute for Health and Biomedical Research of Alicante (ISABIAL)—reflecting a concerted national commitment to translational science with tangible clinical impact.

Notably, the team behind CIBA has chosen not to pursue patent protection for the technique. This open-science approach aims to remove financial barriers, facilitating rapid dissemination and adoption of CIBA within public healthcare systems globally. Given the escalating costs of advanced therapies, this decision underscores an ethical commitment to equitable healthcare access and innovation sharing.

The biological rationale for intrabronchial MSC delivery benefits from an intricate understanding of pulmonary immunology and regenerative mechanisms. MSCs sourced from Wharton’s jelly in the umbilical cord offer advantages due to their relative abundance, ease of harvesting, low immunogenicity, and potent immunomodulatory effects compared to other MSC sources like bone marrow or adipose tissue. Concentrating these cells directly in the lungs postulates augmented local effects, including amelioration of alveolar epithelial damage, inhibition of fibrotic pathways, and restoration of vascular integrity, processes critical in end-stage pulmonary diseases.

Looking ahead, comprehensive randomized controlled trials will be necessary to validate CIBA’s efficacy, optimize dosing protocols, and assess long-term safety. Explorations into repeated administrations and combining MSC therapy with adjunct treatments may yield synergistic benefits. Moreover, extending this methodology to adult patients and diverse pulmonary pathologies could revolutionize regenerative strategies in critical care.

In summary, the CIBA technique represents a remarkable convergence of clinical innovation and biomedical science, overcoming formidable technical challenges to deliver life-sustaining cell therapies directly where they are most needed. As critical care medicine continues to grapple with the complexities of respiratory failure, interventions like CIBA herald a new era in which regenerative medicine can be safely integrated into life-supporting platforms, ultimately improving outcomes for the most vulnerable patients.

Subject of Research: People

Article Title: Consecutive intrabronchial administration of Wharton’s jelly-derived mesenchymal stromal cells in ECMO-supported pediatric patients with end-stage interstitial lung disease: a safety and feasibility study (CIBA method)

News Publication Date: 5-Apr-2025

Web References: http://dx.doi.org/10.1186/s13287-025-04289-3

References: CIBA Method and the Rationale for MSC Administration. Stem Cell Res Ther. 2025. doi: 10.1186/s13287-025-04289-3

Image Credits: CIBA Method and the Rationale for MSC Administration. Stem Cell Res Ther. 2025. doi: 10.1186/s13287-025-04289-3

Keywords: Respiratory failure, Stem cell therapy, Medical tests, Pulmonary alveoli