Translational Health Science and Technology Institute

To evaluate the impact of maxillary advancement by distraction osteogenesis (DO) on the pharyngeal airway including the following parameters in patients with cleft lip and palate (CLP), with a secondary focus on long-term changes ≥1 year: palatal pharyngeal space, superior posterior pharyngeal space, middle pharyngeal space, inferior pharyngeal space, epiglottic pharyngeal space, velar angle, velar length, and need ratio. A comprehensive search was conducted in Medline through PubMed, Scopus, Cochrane databases, Embase, and Directory of Open Access Journals through October 2024. Studies were assessed for pharyngeal airway changes at three time points: pre-DO (T1), post-DO (T2), and ≥1-year post-DO (T3). Quality was assessed using the National Institute of Health tool for before-after (pre-post) studies with no control group. Meta-analysis was conducted using Cochrane Review Manager (RevMan) Version 5.3. A random effect model assessed the mean difference (MD) in parameters representing the pharyngeal airway at T1, T2, and T3. GRADE criterion assessed the certainty of evidence. The protocol is officially registered with PROSPERO (CRD42023444533). In this systematic review, we followed Preferred Reporting Items for Systematic Reviews and Meta-Analysis guidelines. The meta-analysis included 10 studies with 135 patients. The included studies ranged from fair to good quality. Significant increases were observed in pharyngeal space post-DO, particularly in superior and middle pharyngeal regions. Slight relapse was noted after 1 year, but overall, airway improvement remained significant. Evidence certainty by GRADE assessment revealed high to moderate evidence except for need ratio (low). Maxillary advancement by DO significantly improves pharyngeal airway in CLP patients, with minimal relapse after 1 year.

Sepsis remains one of the most diagnostically challenging syndromes due to its clinical heterogeneity, overlapping host-pathogen responses, and lack of a singular biomarker. Biosensors are redefining this landscape by moving beyond slow, culture-based methods toward real-time, multiplexed, and clinically validated diagnostic platforms. In this review, we synthesize advances across substrate engineering, nanomaterial-enabled amplification, and next-generation biorecognition elements, including aptamers, AMPs, PNAs, XNAs, and CRISPR systems, supported by real-world case studies that demonstrate clinical feasibility. Furthermore, the role of artificial intelligence in augmenting sepsis diagnostics is delineated by distinguishing models that enhance biosensor signal interpretation from broader EHR-driven prediction frameworks. A dedicated section consists of the translational bottlenecks: analytical-to-clinical performance gaps, regulatory barriers, diagnostic coding mismatches, and reimbursement challenges under DRG and NTAP pathways. Finally, we propose a forward-looking blueprint for accelerating biosensor deployment in sepsis care, emphasizing the need for harmonized clinical validation, design-for-deployment strategies, and collaborative innovation ecosystems. Unlike generic biosensor or AI reviews, this work advances explicitly against sepsis's diagnostic heterogeneity, offering a disease-centered translational roadmap.

Cerebral malaria (CM) is associated with dysregulated immune response against the blood stage of malaria parasite that often leads to serious organ damage, ultimately causing fatal pathological complications. Conventional treatments, although effective in controlling the parasite, often fail to address the severe immunopathology associated with the disease. Herein, we investigated the therapeutic potential of Mesenchymal stem cells (MSCs) in managing the excess proinflammatory response and maintaining immune homeostasis in Plasmodium berghei ANKA (PbA) infected C57BL/6 mice, an experimental cerebral malaria (ECM) disease model. Parasitemia and survival were monitored regularly, along with the neurological complications associated with the disease. Immunophenotyping, along with programmed cell death analysis of splenocytes, was also done via flow cytometry, and cytokine levels were analyzed at different time points in serum, as well as spleen, through bioplex assay and qRT-PCR. It was found that MSC effectively reduced parasitemia, increased survival, and decreased hemozoin accumulation in spleens of PbA-infected mice, along with improving brain pathology by preventing vascular leakage and protecting the blood-brain barrier (BBB). MSCs not only rescued the lymphocytes from apoptosis by downregulating PD-1/PD-L1 and ROS levels but also effectively modulated the Th17/Treg imbalance and maintained immune homeostasis by downregulating Interleukin-6 (IL-6) and Interleukin-17 (IL-17) cytokines and upregulating Interleukin-10 (IL-10) cytokine in infected mice. For the first time, we reported that MSCs were able to induce a dual phenotype effector Treg cell subset (Tr17), which are known to express both RoRγt and Foxp3 transcription factors, which were highly suppressive against pathogenic Th17 cells as they significantly downregulated IL-17 expression in Th17 cells. In conclusion, our findings offer insight into how the infusion of MSCs reduces the severity of experimental CM by modulating Th17/Treg balance and inducing Tr17 effector Treg response against Th17 cells. Thus, MSCs could potentially be used as an adjunct therapy for addressing the immunopathological complications of CM.

Background: Prolonged hyperglycemia in diabetes activates platelets and immune cells, forming platelet-immune complexes that damage blood vessels in the retina. However, the role of platelet-neutrophil interactions and neutrophil extracellular traps(NETs) in diabetic retinopathy (DR) has not been explored. Present study investigated the mechanisms underlying platelet-mediated NET formation in DR. Methodology: Platelet activation markers, platelet-neutrophil aggregates(PNA), and NETs markers were assessed by flowcytometry in healthy control(HC), type 2 diabetes mellitus(T2DM), non-proliferative DR(NPDR) and proliferative DR(PDR) subjects, followed by immunofluorescence assay. Proteomics analysis identified the mechanistic regulators of platelet-induced NETs in DR. Platelet pellet and plasma CXCL7 were quantified using Western blot and ELISA, respectively. The role of the CXCL7/CXCR2 axis in inducing NETs formation was examined using recombinant CXCL7, anti-CXCL7 antibody and CXCR2 antagonist(SB225002). Results: Elevated platelet activation markers (p-selectin & PF4), PNA, and NETs markers (%NETs, proteinase-3(PR3), neutrophil elastase(NE)) observed in the DR group compared to T2DM and HC-platelets. Furthermore, platelet activation and NETs markers were positively correlated with pro-angiogenic(ANGPT2,VEGFA) and inflammatory markers(IL18,ICAM1). In vitro studies reveal that NETs induce inflammation, endothelial dysfunction, disrupt the endothelial monolayer and exacerbate angiogenesis in RF/6A endothelial cell spheroids. Proteomics analysis of platelet-induced NETs in DR revealed dysregulation of proteins involved in platelet activation and NET formation, including CXCL7. Furthermore, increased CXCL7 levels were observed in platelet pellet and plasma samples from the DR group. Additionally, CXCL7-treated neutrophils formed NETs via the CXCR2 receptor, and inhibition of NETosis was observed in neutrophils exposed to an anti-CXCL7 antibody and a CXCR2 antagonist. Conclusion: Our findings revealed that platelets released CXCL7 induce NETs formation via the CXCL7/CXCR2 axis and blockade of CXCL7/CXCR2 axis inhibits the NETosis in DR, thereby inhibiting the pathogenesis of DR. Circulating CXCL7 serves as a potential prognostic marker, and the CXCL7/CXCR2 axis may be a therapeutic target for the treatment of DR.

Rabies is a neglected tropical zoonotic disease caused by rabies-virus (RV) infection and is responsible for almost 60,000 annual deaths globally, largely affecting the socio-economically disadvantaged population. Although fatality is preventable by immunization either before or after exposure with therapeutic antibodies, the high cost of prophylaxis or treatment limits their accessibility for the affected population. However, due to the almost 100% fatality rate in symptomatic individuals, almost 29 million annual vaccinations are performed, imposing high financial burden. Human transmission occurs principally through bites from infected dogs and although multiple mammalian species are permissive to RV, transmission from them or from symptomatic humans is rare. To overcome the limitations posed by the requirement of biosafety level-3 (BSL-3) containment for live virus culture, we established a replication-deficient vesicular stomatitis virus (VSV) pseudovirus expressing the Rabies-G (RV-G) protein and a multiplexed Luminex immunoassay for quantifying anti-rabies antibodies in equine sera. The purified pseudovirus exhibited robust luciferase activity and was able to infect multiple mammalian cell lines, although with variable efficiency. Using hyper-immunized equine serum, we observed a strong correlation (ρ > 0.9, p < 0.001) between binding antibody titers measured by the Luminex assay with neutralizing antibody titers determined using the pseudovirus-based neutralization assay. These assays provide a safe, quantitative, and BSL-2-compatible platform for rabies serological evaluation and vaccine testing.

Infertility affects about 16.5% of adults in low- and middle-income countries, according to the World Health Organization, and represents a major global public health concern. Despite this burden, population-level estimates from South Asia remain limited. To address this gap, we conducted a systematic review and meta-analysis to estimate the pooled prevalence of infertility in South Asia and to assess the quality of existing studies. We systematically searched PubMed, Scopus and Embase from inception to 12 April 2025 for studies reporting infertility prevalence in South Asia, excluding studies that did not report the total population from which the prevalence was calculated. Two reviewers independently screened studies, extracted data and assessed study quality using the Joanna Briggs Institute checklist. A random-effects meta-analysis of proportions was performed, and heterogeneity was assessed using I² and Cochran's Q statistics. Of 4326 records screened, 16 studies met the inclusion criteria and were included in the systematic review, of which five were eligible for primary analysis. Except for one study from Nepal, the remaining studies were from India. The pooled prevalence of infertility was 8% (95% confidence interval [CI]: 5%-13%; I² = 98.6%). Community and hospital-based studies showed a prevalence of 10% and 8%, respectively. Primary infertility prevalence was 7% (95% CI: 2%-14%), while secondary infertility was 3% (95% CI: 0%-12%). The review shows a pooled prevalence that is lower than recent global estimates, highlighting the need for robust region-specific data. Considerable variation in infertility definitions contributed to substantial heterogeneity and reduced comparability across studies. About one-third of the included studies were clinic-based, which are not ideal for estimating population prevalence. PROSPERO Registration: CRD42024623937.