The Journal of Translational Research is a leading peer-reviewed academic journal published by BIOMED INSTITUTE FOR SCIENTIFIC RESEARCH (SMC-PRIVATE) LIMITED. The journal is dedicated to the advancement of translational science by integrating basic scientific research with clinical and public health applications. It serves as a scholarly platform to bridge the gap between laboratory discoveries and real-world clinical implementation, with the ultimate goal of improving healthcare outcomes and advancing medical practice. The journal promotes interdisciplinary collaboration among scientists, clinicians, researchers, and healthcare professionals by publishing high-quality research that translates scientific knowledge into practical solutions for disease prevention, diagnosis, and treatment. Scope: The Journal of Translational Research welcomes submissions in the following areas, but not limited to: Translational and Clinical Research Molecular and Cellular Biology Pharmacology and Drug Development Biotechnology and Biomedical Engineering Clinical Trials and Evidence-Based Medicine Genomics, Proteomics, and Precision Medicine Public Health and Preventive Medicine Diagnostic Technologies and Medical Innovations Health Systems Research and Implementation Science Regenerative Medicine and Therapeutic Development The journal publishes original research articles, clinical studies, review papers, commentaries, and opinion pieces that contribute to the advancement of translational science. It emphasizes ethical research practices, scientific rigor, and interdisciplinary collaboration to support innovation in healthcare. Publication Frequency: Biannual (Two issues per year)
BIOMED INSTITUTE FOR SCIENTIFIC RESEARCH (SMC-PRIVATE) LIMITED
TELEMEDICINE IN PRIMARY HEALTHCARE DELIVERY: A SYSTEMATIC LITERATURE REVIEW
Telemedicine has emerged as a transformative strategy for strengthening primary healthcare delivery by improving access, continuity, and system efficiency. The rapid expansion of telemedicine during the COVID-19 pandemic accelerated its integration into routine care; however, questions remain regarding its long-term sustainability, equity implications, and impact on clinical outcomes in diverse healthcare contexts.This systematic literature review synthesizes contemporary evidence on the effectiveness, implementation challenges, equity implications, and sustainability of telemedicine in primary healthcare settings, with particular emphasis on post-2020 developments. A systematic search of multiple electronic databases was conducted in accordance with established review guidelines and the Population–Concept–Context framework. Studies published from January 1, 2020 onward were screened using predefined inclusion and exclusion criteria. Two independent reviewers performed title, abstract, and full-text screening. Data were extracted using a standardized form and synthesized thematically to identify trends related to telemedicine modalities, patient outcomes, provider experiences, cost-effectiveness, and health equity. Sixty-eight studies met the inclusion criteria. Telemedicine interventions were predominantly delivered through synchronous video consultations and telephone visits, with increasing adoption of hybrid and remote monitoring models. Across chronic disease management, mental health care, and preventive services, telemedicine demonstrated clinical outcomes comparable to traditional face-to-face consultations while improving access to care and reducing indirect patient costs. Patient satisfaction was generally high; however, disparities persisted among older adults, low-income populations, and individuals with limited digital literacy. Provider experiences reflected improved flexibility and outreach but highlighted workflow disruption and diagnostic limitations. Sustainability was strongly associated with policy support, reimbursement reform, digital infrastructure, and targeted strategies to address the digital divide. Telemedicine has evolved from a crisis-response mechanism into a core component of primary healthcare delivery. While evidence supports its effectiveness and feasibility, equitable and sustainable integration requires continued investment in digital infrastructure, regulatory clarity, workforce training, and targeted interventions to mitigate health inequities. Policymakers and healthcare leaders must adopt context-sensitive strategies to ensure telemedicine strengthens rather than exacerbates disparities in primary care systems globally.
, COVID-19 pandemic, virtual care, health system sustainability, healthcare policy, remote monitoring
Copyright (c) 2025 https://creativecommons.org/licenses/by/4.0
INTERLINKING DIABETIC CARDIOMYOPATHY AND RENAL DYSFUNCTION: A MULTISYSTEMIC PERSPECTIVE
Diabetic cardiomyopathy and renal dysfunction are increasingly recognized as interconnected complications of long-standing diabetes, sharing overlapping metabolic, inflammatory, and hemodynamic pathways. This study investigates the multisystemic association between cardiac structural impairment and renal functional decline using an integrated mixed-methods experimental design. Quantitative biochemical profiling, echocardiographic assessment, and renal filtration measurements were combined with qualitative clinical interpretation to construct a unified model of the cardio-renal axis in diabetes. Results demonstrated a consistent relationship between decreasing estimated glomerular filtration rate (eGFR) and worsening global longitudinal strain (GLS), accompanied by elevations in NT-proBNP, inflammatory cytokines, and oxidative stress biomarkers. Cardiac deformation indices and renal dysfunction stages showed parallel progression, supporting the hypothesis that both organs deteriorate through shared mechanisms involving microvascular injury, endothelial dysfunction, and mitochondrial stress. Scatter and trend analyses further revealed clustering patterns of multisystemic risk, indicating that early abnormalities in one organ predict subsequent impairment in the other. The integrated cardio-renal model developed in this study underscores the need for clinical frameworks that evaluate cardiovascular and renal systems jointly rather than independently. These findings highlight the importance of early multisystemic screening and holistic intervention strategies to mitigate progression and improve outcomes in diabetic populations. Overall, the study strengthens the understanding that diabetic cardiomyopathy and renal dysfunction represent a continuous, interconnected disease spectrum driven by metabolic and inflammatory cross-talk rather than separate pathological entities.
Copyright (c) 2025 Shazia Khalid, Humayun Ali (Author) https://creativecommons.org/licenses/by/4.0
GUT MICROBIOTA DYSBIOSIS AND COLORECTAL CARCINOGENESIS: A HISTOPATHOLOGICAL STUDY
Gut microbiota dysbiosis is increasingly recognized as a critical factor influencing colorectal carcinogenesis, yet the mechanistic relationship between microbial imbalance and tissue-level pathological alterations remains incompletely understood. This study investigates the correlation between dysbiosis and colorectal tumor development by integrating high-throughput 16S rRNA microbial profiling with detailed histopathological examination of colorectal tissue samples. A mixed-methods experimental approach was employed, allowing quantitative microbial abundance, diversity indices, and dysbiosis scores to be analyzed alongside qualitative assessments of epithelial dysplasia, architectural distortion, inflammatory infiltration, and tumor grading. Results revealed significant enrichment of pro-carcinogenic taxa, particularly Fusobacterium nucleatum, mucin-degrading species, and inflammation-associated bacteria, in samples exhibiting advanced tumor grades. Diversity analyses demonstrated a marked decline in protective commensals, including butyrate-producing organisms, suggesting ecological collapse within the gut microbiome as lesions progressed. Statistical modeling further confirmed that higher dysbiosis scores strongly correlated with increased histopathological severity, supporting a dose-dependent microbial influence on neoplastic transformation. The integration of molecular and morphological findings provides robust evidence that dysbiosis contributes both to the initiation and progression of colorectal cancer. These findings highlight the potential of microbial signatures as early diagnostic biomarkers and emphasize the importance of microbiome-targeted strategies in risk prediction, prevention, and personalized therapeutic intervention.
Copyright (c) 2025 Zia Ur Rehman, Mashal Shahzadi (Author) https://creativecommons.org/licenses/by/4.0
PHARMACOTHERAPEUTIC ADVANCES IN AUTOIMMUNE SKIN DISORDERS: NOVEL BIOLOGICS
Autoimmune skin disorders represent a significant clinical and socioeconomic burden due to their chronicity, relapsing nature, and impact on patient quality of life. This study evaluates emerging pharmacotherapeutic advances with a specific focus on novel biologic agents targeting key immunologic pathways involved in autoimmune dermatologic disease. Using a mixed-methods approach that integrates quantitative clinical outcomes with qualitative clinician insights, the study analyzes efficacy trends, biomarker responsiveness, adverse-event profiles, and molecular selectivity across multiple biologic classes. Quantitative assessments demonstrate robust improvements in remission rates, inflammatory biomarker reduction, and dose–response performance, particularly among IL-17 and IL-23 inhibitors. Qualitative data from dermatologists reveal strong support for personalized therapy models, emphasizing mechanistic precision, patient acceptability, and long-term safety advantages over traditional immunosuppressants. Triangulated findings highlight the superiority of targeted biologics in both clinical and molecular dimensions, while also identifying persistent challenges, including heterogeneous response patterns, treatment fatigue, and cost-related barriers. The study concludes that novel biologics have transformed the therapeutic landscape of autoimmune skin disorders by providing more effective, durable, and pathway-specific treatment options. Continued advancements in biomarker-guided therapy selection, patient stratification, and equitable access strategies will be essential for optimizing future clinical outcomes and ensuring the widespread benefits of these pharmacotherapeutic innovations.
Copyright (c) 2025 Rabia Kiran, Shahzad Rafiq (Author) https://creativecommons.org/licenses/by/4.0
EFFECTIVENESS OF NATIONAL IMMUNIZATION POLICIES ON VACCINE-PREVENTABLE DISEASES IN LOW-INCOME REGIONS
This study evaluates the effectiveness of national immunization policies in reducing vaccine-preventable diseases (VPDs) across low-income regions by employing a mixed-methods research design that integrates epidemiological trend analysis with qualitative policy assessment. Quantitative data from national surveillance systems, immunization registries, and disease reporting platforms were used to measure changes in vaccination coverage, incidence patterns, and policy-driven reductions in disease burden. Qualitative insights from policy reviews and implementation reports provided essential context regarding operational challenges, such as cold-chain limitations, workforce shortages, funding constraints, and sociocultural barriers affecting uptake. Results revealed a consistent inverse relationship between vaccination coverage and VPD incidence, demonstrating that regions with stronger policy implementation achieved significantly greater disease reductions. However, notable disparities remained, especially in geographically isolated or socioeconomically disadvantaged districts, which continued to exhibit lower coverage and higher dropout rates. Statistical associations confirmed that increased coverage strongly predicted incidence declines, while qualitative triangulation highlighted governance effectiveness, community trust, and health-system resilience as key determinants of policy success. Overall, the study concludes that national immunization policies are effective mechanisms for reducing VPD burden in low-income settings, but their full potential depends on equitable implementation, improved infrastructure, targeted community engagement, and adaptive policy reforms that respond to local needs. These findings provide actionable insights for strengthening immunization strategies and enhancing long-term public health outcomes in resource-constrained environments.
Copyright (c) 2025 Shahzad Rafiq, Muhammad Rehan (Author) https://creativecommons.org/licenses/by/4.0
DIAGNOSTIC ACCURACY OF MRI IN DETECTING MICROFRACTURES IN POLYTRAUMA PATIENTS
The research paper assesses the diagnostic validity of Magnetic Resonance Imaging (MRI) in detecting microfractures on polytrauma patients, which is one of the clinical issues contributing to delayed therapy when fractures are still occult on other imaging modalities. The study employed a mixed-method experimental study, which compared the results of MRI and a composite reference standard, high-resolution computed tomography and intraoperative observations. A wide range of MRI sequences was used to determine changes in marrow edema, disruption of trabecular structure, and cortical changes: T1, T2, STIR, and gradient-echo. The quantitative findings presented that MRI was highly sensitive to identify marrow-based microfractures, especially in the areas of the anatomy rich in the trabecular structures, but denser cortical structures had higher patterns of false-negative. Specificity depended on the parameters of sequence, with the STIR sequence and the gradient- echo sequence being the most suitable structures to provide the best contrast. Trends of predictive value, and inter-rater reliability assessments also supported the strong performance of MRI, and significant consensus between radiologists was achieved when standardized reporting criteria were employed. The results of regression analysis showed that the intensity of edema and clinical symptom severity were significantly detectable, and the use of clinical markers in the imaging workflow is justified. All in all, the study confirms that MRI is a necessary diagnostic method in trauma cases, especially in case early detection can affect treatment planning, morbidity, and long-term complications. These results underpin the necessity of streamlined multi-sequence MRI sequences and point to the opportunities of utilizing advanced imaging analytics to improve microfracture imaging in different trauma groups.
Copyright (c) 2025 Younas Rehman, Muska Hayat (Author) https://creativecommons.org/licenses/by/4.0
THE ROLE OF RECURRENT OTITIS MEDIA IN COGNITIVE DEVELOPMENT DELAY: A LONGITUDINAL PEDIATRIC STUDY
Otitis media is one of the most common pediatric infections and has been implicated in adverse developmental outcomes, yet few studies have quantified its long-term impact on cognitive trajectories. In this prospective cohort study, 300 infants (mean age 6 months at enrollment) were followed over 48 months to examine how the frequency, duration, and severity of recurrent otitis media influence neurocognitive development. Otitis media episodes were diagnosed by pediatric otolaryngologists and confirmed via tympanometry and audiometry at six-month intervals. Cognitive function was evaluated at 12, 24, 36, and 48 months using the Bayley Scales of Infant and Toddler Development, Third Edition, and at 48 months with the Wechsler Preschool and Primary Scale of Intelligence. Multilevel linear mixed-effects models adjusted for sex, socioeconomic status, parental education, and baseline development. Children experiencing three or more infection episodes exhibited progressively lower Bayley-III composite scores, declining from a mean of 95 ± 12 at 12 months to 88 ± 15 at 48 months, compared with gains from 100 ± 10 to 108 ± 12 among non-recurrence peers (p ≤ 0.01 at each timepoint). Each additional episode corresponded to a 1.5-point reduction in cognitive score (SE = 0.5; p = 0.002), and longer episode duration produced an independent −0.8-point effect (SE = 0.3; p = 0.01). At 48 months, full-scale IQ averaged 95 ± 12 in the recurrence group versus 110 ± 10 in the non-recurrence group. Nearly 30% of children with recurrent infections fell below the clinical threshold for cognitive delay (<85), compared with 10% of their counterparts. Executive function trajectories diverged significantly over time (p < 0.005), and cumulative hearing loss was negatively correlated with memory scores (r = –0.42; p < 0.001). Early tympanostomy tube placement was associated with a 15-point increase in mean cognitive score at 48 months.These findings establish a dose-dependent, deleterious effect of recurrent otitis media on early cognitive and executive function, highlighting the importance of prompt diagnosis, audiological monitoring, and timely medical or surgical intervention to protect neurodevelopmental outcomes.
Copyright (c) 2024 https://creativecommons.org/licenses/by/4.0
THE IMPACT OF ANESTHETIC TECHNIQUES ON TUMOR RECURRENCE IN CANCER SURGERY: A META-ANALYSIS ACROSS MULTIPLE ONCOLOGICAL SUBTYPES
This meta-analysis investigates the impact of anesthetic techniques—regional anesthesia (RA) versus general anesthesia (GA)—on tumor recurrence across multiple oncological subtypes. A total of 32 studies, including randomized controlled trials, cohort, and case-control designs, were systematically analyzed, covering breast, prostate, colorectal, lung, and ovarian cancers. Data from over 15,000 patients were synthesized to evaluate recurrence rates, hazard ratios (HR), and methodological quality. RA and cancer were repeatedly associated with a risk of tumour recurrence that was lower than with GA in all cancer types. The rate of cancer coming back was lower after surgery for breast cancer (8.2% vs. 12.5%) and colorectal cancer (12.7% vs. 17.4%) in the RA groups. The combined hazard ratios for breast (HR = 0.74) and colorectal cancer (HR = 0.77) showed a notable drop in patients with RA. Following the removal of studies with high risk of bias, additional testing showed the results were still valid. The effect sizes in RCTs, cohort studies and case-control studies remained similar after being examined individually by design. Most papers (more than 85%) showed a low risk in major research methods and there were no signs of severe imbalance or missing studies in the results of bias analysis. They suggest that RA might reduce the chances of cancer coming back after surgery by possibly lowering perioperative immune system weakening, the level of inflammation, opioid intake and exposure to volatile anaesthetics. This study justifies including RA in the multidisciplinary plan for oncologic surgeries even though larger trials need to confirm its cause and effect. If anaesthetic planning is added to cancer treatment, it could be a simple and cost-effective approach to boost long-term satisfaction.
INVESTIGATING CYTOKINE STORM MARKERS IN SEVERE COVID-19-RELATED ARDS CASES
In a prospective observational cohort of 100 mechanically ventilated adults with RT-PCR–confirmed SARS-CoV-2 infection, peripheral blood was sampled on days 0, 3, and 7 following intubation to quantify eight key cytokines (IL-6, IL-1β, TNF-α, IL-8/CXCL8, IP-10/CXCL10, IL-18, GM-CSF, M-CSF) via multiplex bead–based immunoassay. Mixed‐effects linear regression revealed that IL-18 and IP-10 concentrations were highest at enrollment (median 120 pg/mL and 100 pg/mL, respectively), peaked on day 3 (180 pg/mL and 150 pg/mL), and declined by day 7 (140 pg/mL and 110 pg/mL), and that elevated IP-10 and IL-6 levels exhibited the strongest inverse correlations with ventilator‐free days (r = –0.65 and r = –0.60; p < 0.001 for both). Receiver operating characteristic analysis demonstrated that IP-10 (AUC 0.88; 95% CI 0.84–0.92; sensitivity 82%; specificity 85%) and IL-6 (AUC 0.85; 95% CI 0.80–0.90; sensitivity 80%; specificity 75%) were the most accurate predictors of 28-day mortality. Semi-structured interviews with 20 treating clinicians underscored “patient heterogeneity” and “timing of sampling” as primary barriers to routine cytokine monitoring. These data therefore delineate a reproducible cytokine signature—particularly IP-10, IL-6, and IL-18—that correlates with disease severity and mortality in severe COVID-19–related ARDS, suggesting that their integration into adaptive immunomodulatory protocols, with careful attention to sampling timing and patient stratification, may enhance therapeutic targeting and improve clinical outcomes.
COMPARATIVE OUTCOMES OF ROBOTIC VS. OPEN SURGERY IN PROSTATE CANCER PATIENTS
This study provides a comprehensive comparative analysis of robotic-assisted radical prostatectomy (RARP) and open radical prostatectomy (ORP) in the treatment of localized prostate cancer, with a focus on perioperative safety, functional recovery, and oncological efficacy. Utilizing a retrospective quantitative design, clinical data from 300 patients were analyzed, equally divided between RARP and ORP groups. Results demonstrated that RARP was significantly associated with reduced intraoperative blood loss, lower transfusion rates, and shorter hospital stays compared to ORP. Functional outcomes were notably improved in the RARP cohort, with higher rates of urinary continence and erectile function recovery at 3, 6, and 12 months postoperatively. Additionally, oncological measures such as positive surgical margin rates and biochemical recurrence were more favorable in the robotic group. Quality-of-life assessments revealed superior patient-reported outcomes in urinary and sexual domains following RARP. Subgroup analysis further confirmed that the benefits of robotic surgery extended across various age brackets, with particularly strong functional recovery observed in younger patients. While both techniques demonstrated efficacy in cancer control, the overall advantages of RARP in terms of precision, reduced morbidity, and faster recovery support its growing adoption as the preferred surgical modality. These findings underscore the importance of integrating advanced surgical technologies to optimize patient outcomes in prostate cancer management, while also emphasizing the need for surgeon expertise and patient-specific decision-making in clinical practice.
ROLE OF NEUTROPHIL EXTRACELLULAR TRAPS IN ATHEROSCLEROTIC PLAQUE INSTABILITY
Atherosclerosis remains a leading cause of morbidity and mortality worldwide, driven by a complex interplay of chronic inflammation, endothelial dysfunction, and oxidative stress. This study investigated the molecular and cellular mechanisms underlying atherosclerosis progression with a particular focus on inflammatory cytokines, oxidative biomarkers, endothelial injury, and neutrophil extracellular traps (NETs). A total of 100 participants, including clinically diagnosed atherosclerosis patients and healthy controls, were assessed through biochemical, immunological, and molecular analyses. Results demonstrated significantly elevated levels of TNF-α, IL-6, and IL-1β in the atherosclerosis group, indicating a heightened pro-inflammatory state. Oxidative stress markers showed increased malondialdehyde (MDA) and reduced antioxidant enzymes such as superoxide dismutase (SOD) and glutathione (GSH), confirming oxidative imbalance. Endothelial dysfunction was evident from upregulated vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1), along with decreased nitric oxide levels. Importantly, NETs biomarkers—citrullinated histone H3 (CitH3) and myeloperoxidase-DNA complexes—were significantly higher in patients, highlighting the role of NETosis in plaque instability. Correlation analysis revealed strong associations between NETs and pro-inflammatory cytokines (r > 0.69, p < 0.001), and logistic regression identified CitH3, TNF-α, MDA, and VCAM-1 as independent predictors of plaque vulnerability. These findings provide a multidimensional view of atherosclerosis pathogenesis, integrating immune, oxidative, and vascular markers. The results underscore the potential of NETs and inflammatory mediators as novel biomarkers and therapeutic targets for early intervention. This study advances our understanding of the disease’s mechanistic underpinnings and supports the need for targeted strategies beyond lipid-lowering therapies, focusing instead on inflammation and endothelial repair to prevent plaque rupture and associated cardiovascular events.
CELLULAR MECHANISMS OF DNA REPAIR IN RESPONSE TO GENOTOXIC STRESS
Genotoxic stress, resulting from physical, chemical, or biological agents, poses a significant threat to genomic integrity by inducing various forms of DNA damage, including single- and double-strand breaks, base modifications, and bulky lesions. To maintain cellular homeostasis and prevent mutagenesis, cells rely on sophisticated DNA repair mechanisms that identify, signal, and rectify these lesions with high specificity and fidelity.This study systematically investigates the four principal DNA repair pathways—base excision repair (BER), nucleotide excision repair (NER), double-strand break repair (DSBR), and mismatch repair (MMR)—highlighting their molecular components, mechanisms, and context-specific activation under genotoxic conditions. The research further explores the roles of key proteins such as PARP1, ATM, BRCA1/2, RAD51, and XPA in orchestrating pathway-specific responses.The findings reveal elevated BER and HR activity in metabolically active and proliferative tissues, respectively, while a marked decline in NER and MMR efficiency was observed in aging and cancerous cells. Additionally, the therapeutic efficacy of PARP inhibitors in homologous recombination-deficient tumors was confirmed, along with the successful application of CRISPR-Cas9 for correcting BRCA1/2 mutations in targeted models.These results underscore the central role of DNA repair in both disease progression and treatment. By demonstrating the pathway-specific vulnerabilities in cancer and the age-related decline in repair capacity, this study supports the advancement of targeted therapies, including gene editing and synthetic lethality approaches. Understanding the cellular mechanisms of DNA repair in response to genotoxic stress provides a foundation for the development of precision medicine strategies and opens new avenues for combating cancer, neurodegenerative disorders, and premature aging.
EXPLORING THE ROLE OF INFLAMMATION IN THE PATHOGENESIS OF AUTOIMMUNE DISEASES
Autoimmune diseases (AIDs) are chronic conditions characterized by the immune system's misdirected attack on self-tissues, resulting in sustained inflammation and progressive organ damage. Central to this pathological process is a complex interplay of genetic, environmental, and immunological factors that drive persistent activation of inflammatory pathways.This study aimed to dissect the molecular and cellular mechanisms underlying inflammation in AIDs by profiling key cytokines—TNF-α, IL-6, and IFN-γ—and evaluating the functional roles of dysregulated immune cells including T-cells, B-cells, macrophages, and dendritic cells. A structured methodology involving patient immune profiling, cytokine quantification, and comparative analysis was employed to assess variations in inflammatory markers across disease subtypes and treatment responses. Results revealed consistently elevated levels of TNF-α and IL-6 across patient cohorts, correlating with disease severity and treatment resistance. IFN-γ was notably increased in patients with central nervous system involvement, reinforcing its association with neuroinflammatory autoimmune conditions. Visual analysis through line plots, scatter distributions, and hybrid visualizations provided strong evidence for biomarker clustering and therapeutic differentiation. The study concludes that TNF-α, IL-6, and IFN-γ are robust indicators of inflammatory burden and serve as viable therapeutic targets in AIDs. The integration of cytokine profiling with immune cell analysis offers a valuable framework for developing precision medicine approaches tailored to individual inflammatory signatures. These findings contribute to a deeper understanding of autoimmune pathogenesis and highlight the importance of targeted immunomodulation in improving patient outcomes.
Copyright (c) 2024 Rabia Kiran, Hassan Yar Mahsood (Author) https://creativecommons.org/licenses/by/4.0
INVESTIGATING THE EFFECT OF DIET ON GUT MICROBIOME COMPOSITION AND IMMUNE FUNCTION
The human gut microbiome plays a central role in maintaining physiological and immune homeostasis, with growing evidence indicating its modulation by dietary patterns. Disruptions in microbial composition, known as dysbiosis, are increasingly linked to chronic diseases such as inflammatory bowel disease, obesity, and autoimmune disorders. Understanding how specific dietary components influence microbial diversity and immune function is therefore essential for preventive and therapeutic strategies.This study investigated the impact of various dietary interventions—including fiber-rich, probiotic, and high-fat diets—on gut microbiome composition and immune modulation. High-throughput sequencing techniques, including 16S rRNA and metagenomic analysis, were employed to profile microbial communities from fecal samples, while immune biomarkers were quantified using ELISA and flow cytometry. Microbial diversity metrics, SCFA concentrations, and cytokine profiles were analyzed and correlated with dietary intake using multivariate statistical models.The findings revealed that fiber- and probiotic-enriched diets significantly enhanced microbial diversity and increased the abundance of beneficial taxa such as Bifidobacterium and Lactobacillus. These shifts were associated with higher levels of short-chain fatty acids and anti-inflammatory cytokines, such as IL-10, while high-fat and high-sugar diets correlated with reduced microbial richness, elevated pro-inflammatory markers, and impaired gut barrier integrity.Overall, the study demonstrates that targeted dietary interventions can meaningfully alter gut microbial ecosystems and modulate immune responses. These results emphasize the potential of nutritional strategies to enhance gut and immune health, reduce systemic inflammation, and prevent chronic disease onset. Future longitudinal studies and personalized nutrition approaches will be essential to optimize dietary recommendations based on individual microbiome profiles.
THE MOLECULAR BASIS OF MUSCLE ATROPHY: INSIGHTS FROM MYOCYTE MODELS
Muscle atrophy, characterized by a progressive decline in muscle mass and strength, is a debilitating condition associated with aging, prolonged inactivity, cancer cachexia, and chronic inflammatory diseases. Understanding the molecular underpinnings of muscle wasting is essential for the development of effective therapeutic strategies targeting its diverse etiologies.This study investigates the cellular mechanisms of muscle atrophy using differentiated myocyte models subjected to stressors such as pro-inflammatory cytokines (TNF-α, IL-6), oxidative conditions, and nutrient deprivation. Experimental conditions were designed to mimic pathological muscle loss in vitro, while molecular responses were analyzed through qPCR, Western blotting, immunofluorescence, and viability assays. Mathematical modeling of protein degradation kinetics was employed to simulate the rate of muscle protein turnover.The findings reveal significant upregulation of ubiquitin-proteasome system components, including atrogin-1 and MuRF-1, under inflammatory and nutrient-deficient conditions. Concurrently, autophagy-related genes such as LC3 and Beclin-1 were markedly elevated, confirming hyperactivation of catabolic pathways. IGF-1 treatment partially restored protein synthesis rates, while gene knockdown of MuRF-1 reduced cellular degradation and improved myotube morphology. Pharmacological interventions targeting proteasome and autophagy pathways exhibited therapeutic potential, particularly when combined with anabolic stimulation.In conclusion, this study highlights the central role of myocyte-based experimental platforms in dissecting the molecular cascades of muscle atrophy. By elucidating the coordinated regulation of UPS, autophagy, and cytokine signaling, and by testing therapeutic modulators in a controlled setting, the research lays a foundation for future preclinical and clinical efforts aimed at preserving muscle integrity and function across diverse atrophic conditions.
CELLULAR RESPONSES TO HYPOXIA: PATHOPHYSIOLOGICAL IMPLICATIONS FOR TISSUERE GENERATION
Hypoxia, characterized by reduced oxygen availability in tissues, plays a critical role in both physiological development and pathological conditions. Emerging evidence underscores its significance in orchestrating cellular mechanisms that drive tissue regeneration and repair. Central to this process are hypoxia-inducible factors (HIFs), transcription factors that regulate genes involved in angiogenesis, metabolism, stem cell activation, and extracellular matrix remodeling.This study systematically explored the cellular and molecular responses to hypoxia using a comprehensive literature synthesis, computational modeling, and visual analytics of hypoxia-driven gene expression, protein signaling, and regenerative outcomes. The methodology integrated data from experimental studies on endothelial cells, fibroblasts, stem cells, and ischemic tissue models to evaluate the role of hypoxic signaling in modulating regenerative mechanisms.The results demonstrated that hypoxia robustly upregulates angiogenic factors such as VEGF, enhances glycolytic pathway activity, and promotes stem cell proliferation and differentiation across tissue types. Hypoxia-mimetic agents and preconditioned stem cell therapies exhibited improved regenerative performance in both in vitro and in vivo contexts. Furthermore, ECM remodeling was shown to be tightly regulated under hypoxic conditions, contributing to efficient wound closure and structural restoration.In conclusion, hypoxia serves as a master regulator of tissue repair by activating key signaling pathways that coordinate metabolic adaptation, vascular remodeling, and cellular regeneration. While therapeutic strategies such as hypoxia mimetics and hypoxic preconditioning hold substantial promise, precise modulation of these responses is essential to avoid adverse outcomes like fibrosis or uncontrolled cell proliferation. These findings offer a compelling foundation for future clinical applications of hypoxia-based interventions in regenerative medicine.
EVALUATING HYPERINSULINEMIA-INDUCED COGNITIVE DECLINE IN PRE-DIABETIC PATIENTS
Hyperinsulinemia, a hallmark of insulin resistance and a precursor to type 2 diabetes, has been increasingly implicated in cognitive dysfunction. This study aimed to evaluate the impact of hyperinsulinemia on cognitive performance and inflammatory markers in pre-diabetic individuals. Fasting insulin levels and HOMA-IR indices helped classify 150 pre-diabetic adults into hyperinsulinemic (75) and normoinsulinemic (75) groups. Memory, executive function and processing speed were tested in standardised ways, making it possible for the researchers to study participants’ metabolism and intellect in great detail. Neuroinflammation activity was measured by detecting levels of TNF-α and IL-6 in the serum with ELISA. Samples were matched using t-test analyses and both ANCOVA and Pearson correlation tests were run to assess group differences and relationships in insulin, inflammation and cognition. Hyperinsulinemic participants had significantly higher fasting insulin (27.43 ± 4.79 µGI/mL) and HOMA-IR scores (7.19 ± 1.52) compared to people whose insulin levels were normal (9.90 ± 1.86 µGI/mL and 2.58 ± 0.88). Those with hyperinsulinemia scored lower than others in memory (60.21 ± 10.12 vs. 70.18 ± 7.85), executive function (54.89 ± 9.05 vs. 66.22 ± 6.74) and processing speed (49.76 ± 6.89 vs. 63.03 ± 5.98) (p < 0.01). When insulin was raised, the levels of inflammatory biomarkers – TNF-α and IL-6 – often increased greatly, compared to the control group (TNF-α: 7.51 ± 1.21 pg/mL; IL-6: 6.78 ± 1.04 pg/mL). Fasting insulin levels were strongly related to worse memory performance, with r = –0.62 and p = 0.001. People with pre-diabetes have hyperinsulinemia and often face serious cognitive problems as well as more neuroinflammation. They show early management of metabolism is needed to protect thinking abilities and highlight that good insulin control is essential in pre-diabetes.
Copyright (c) 2025 Hassan Yar Mahsood , Sami Ullah (Author) https://creativecommons.org/licenses/by/4.0
IDENTIFYING GENETIC RISK FACTORS FOR EARLY-ONSET TYPE 1 DIABETES
Early-onset type 1 diabetes mellitus (T1D) is an autoimmune condition primarily affecting children and adolescents, characterised by the destruction of pancreatic β-cells. While environmental triggers are known contributors, genetic predisposition remains a pivotal determinant in disease development. This study aimed to identify and quantify key genetic risk factors associated with early-onset T1D. For the study, one hundred people with early-onset T1D and one hundred healthy participants matched by age and sex were used. Paired genomic DNA samples for T1D-associated alleles including HLA-DR3, HLA-DR4, INS (rs689), CTLA4 (rs231775), PTPN22 (rs2476601), IL2RA (rs2104) and IFIH1 (rs1990760) were analyzed by examining how many times each allele occurred in each group. Additionaly, I collected information regarding autoimmune illnesses in people’s families. The T1D group had a significantly higher rate of HLA-DR3 (68%) and HLA-DR4 (60%) alleles than the controls did. Interesting findings were a hike in the INS AA version (55% vs. 20%), CTLA4 GG version (48% vs. 22%) and PTPN22 TT version (50% vs. 18%) in T1D. In addition, we observed higher frequencies of IL2RA AA (52%) than IFIH1 CC (19%) and IL2RA AA (21%) for IFIH1 CC (45%). More than 60 percent of those living with T1D said they had relatives with some form of autoimmune disease. T1D group participants were found to carry much higher genetic risk, suggesting their genes make them more likely to develop T1D. We saw a statistically significant relationship in all the associations (p < 0.01). This study explains that particular HLA and non-HLA genetic markers have an important role in early-onset T1D. As a result, it becomes necessary to screen genes and classify individuals by risk level to begin interventions that try to control or stop the beginning of diseases early.
Copyright (c) 2025 Shahzad Rafiq , Jawad Ali (Author) https://creativecommons.org/licenses/by/4.0
THE ROLE OF GUT-DERIVED GLP-1 IN HYPOGLYCEMIA UNAWARENESS
Hypoglycemia unawareness is a dangerous complication of diabetes, marked by a diminished perception of low blood glucose levels and an impaired counter-regulatory response. Emerging evidence suggests that gut-derived glucagon-like peptide-1 (GLP-1), a key incretin hormone, may play a role in modulating hypoglycemia awareness through its influence on hormonal and autonomic pathways.To study how levels of GLP-1 are linked to hypoglycemia unawareness among people with diabetes and whether higher GLP-1 causes people to lose the ability to fight low blood sugar. People with diabetes separated into two groups, one aware of hypoglycemia and one not and were examined in a cross-sectional study. Among the other important counter-regulating hormones (glucagon, cortisol, epinephrine) and insulin, glucose readings and the frequency of low blood sugar detected by CGM, I also examined GLP-1 levels both while fasting and after meals. A statistical approach was used to check for similarities between groups of awareness and groups of unawareness. Those with hypoglycemia unawareness had much higher fasting GLP-1 (29.93 ± 5.50 pmol/L) and more GLP-1 AUC (2402 ± 342) compared to conscious participants and their glucagon (50.12 ± 12.03 pg/mL), cortisol (9.03 ± 3.12 µg/dL) and epinephrine (59.84 ± 20.04 pg/m Moreover, people without awareness had about four times as many hypoglycemia episodes (6.49 ± 1.96 vs. 2.53 ± 1.12, p < 0.01). The frequency of hypoglycemia increased as GLP-1 levels in the blood went up, as seen during the study. The study suggests that when GLP-1 acts too much, people may become unaware of hypoglycemia because their hormones cannot balance it properly. These findings suggest it is necessary to design custom diabetes treatment plans, mainly for GLP-1-based medications.
Copyright (c) 2025 Wesam Taher Almagharbeh , Humayun Ali (Author) https://creativecommons.org/licenses/by/4.0
INVESTIGATING LEPTIN RESISTANCE IN MORBID OBESITY AND TYPE 2 DIABETES
Leptin resistance has emerged as a critical factor in the pathogenesis of type 2 diabetes mellitus (T2DM), particularly in the context of morbid obesity. This study aimed to investigate the associations between leptin resistance, metabolic markers, and inflammatory parameters in individuals with T2DM and varying degrees of obesity. Patients who had both T2DM and morbid obesity (BMI greater than 40), those with T2DM but not morbidly obese (BMI below 40) and non-diabetic controls were all part of the study. Serum leptin, glucose, insulin, HOMA-IR, CRP, IL-6 and HbA1c were looked at using blood samples taken after a fast and anthropometric measurements. To perform the analyses, I used both group comparisons and correlation studies. When comparing to only T2DM or control participants, participants with morbid obesity along with T2DM had higher average levels of leptin (60.37 ± 9.75 ng/mL), insulin (24.87 ± 5.12 µIU/mL) and HOMA-IR score (11.01 ± 1.93). Records from the morbidly obese diabetes group also indicted rise in inflammatory factors: CRP (9.91 ± 2.13 mg/L) and IL-6 (8.03 ± 2.07 pg/mL.). Because the HbA1c level in this group was the highest (9.02 ± 1.04%), there were clear difficulties in ongoing glucose control. By examining the results, we noticed that there were strong favorable correlations among leptin, insulin, HOMA-IR and BMI. In addition, it was pointed out that resistance to leptin can hurt insulin and its function. Even more connections were found between parenting and behavior by using visual graphs. This finding suggests that morbid obesity markedly reduces leptin levels which also increases insulin resistance, inflammation in the body and hyperglycaemia in those with T2DM. Such discoveries demonstrate that including leptin-based treatments may benefit the therapy of obese diabetic populations.
Copyright (c) 2025 Muska Hayat , Rabia Nasir (Author) https://creativecommons.org/licenses/by/4.0
EXPLORING SURFACTANT PROTEIN DEFICIENCY IN NEONATAL RESPIRATORY DISTRESS
Neonatal respiratory distress syndrome (RDS) remains a leading cause of morbidity and mortality among preterm infants, primarily due to surfactant protein deficiency. This study investigates the relationship between surfactant protein levels—specifically SP-A, SP-B, and SP-C—and the clinical severity of RDS, examining their potential role as diagnostic and prognostic biomarkers. A quantitative observational study was conducted on 100 neonates admitted with respiratory distress within the first 48 hours of life. Clinical parameters including gestational age, birth weight, ventilation modality, NICU stay, and oxygen therapy duration were recorded. Surfactant protein levels were measured using ELISA.Researchers looked at data to find links between deficiencies in surfactants and clinical results, in particular BPD development and death. The fetuses were born after a 30.1-week pregnancy and their average birth weight was 1497 grammes. The study revealed that newborns requiring breathing help through tubes had many times fewer surfactant proteins than did infants getting help with regular breathing. Things like SP-A, SP-B and SP-C all decreased in relationship to the seriousness of the disease as seen on X-ray. BPD-affected infants were found with lower levels of SP-A (42.0 ng/mL) and needed more oxygen compared to healthy newborns. A lower birth weight, an early gestational period and longer stays in the intensive care unit were linked to increased risk of death for neonates. To prove these points, visual studies were done with bar graphs, histograms, boxplots and violin plots. This research proves that an inadequacy of surfactant proteins is related to more serious illness, the need for greater medical support and bad results for babies with RDS. A diagnosis given early and plain management choices made with SP-A assessment are most valuable. Using predictive modelling, non-invasive support and measuring surfactant could help treat newborns more effectively.
Copyright (c) 2025 Younas Rehman , Syeda Iram Batool (Author) https://creativecommons.org/licenses/by/4.0
ADVANCED WOUND HEALING: PLASTIC SURGERY AND INFECTIOUS DISEASES
Surgical and medical complications in wound healing become huge obstacles in the procedures of surgeons and doctors particularly plastic and reconstructive surgeons. In this case study plastic surgery and control of infectious diseases are examined as factors that aid in the healing process of patients. It employs a sample of 180 individuals that have various wounds and the severity of infection. Nine elaborate tables and 12 intricate visualizations indicate that early surgery combined with customised antibiotic medication has a massive effect on wound healing. The rapidity of recovery of worry patients given Vancomycin and Ceftriaxone was found to be quicker in the case of clean of moderately infected wounds. Conversely, non-healing wounds were larger than and healed more slowly than necrotic, severely infected wounds. Scatter plots and regression overlay indicated strong negative relation between the size of wound and the rate at which the wound healed. The pie and bar charts indicated the spreading of the disease and the successfully working of therapy on various categories of patients. Demographic and seasonal tendencies were also noted, and they revealed that wound care treatments must be tailored to an individual. This approach that couples the accuracy of surgery with infective control is a holistic solution to the question of how to treat complex wounds. The results provide physicians with the method to make decisions concerning the care of wounds and employ predictive analysis in the future.
Copyright (c) 2023 Hassan Yar Mahsood, Abdul Ghaffar, Roohan Ahmad (Author) https://creativecommons.org/licenses/by/4.0
PSORIASIS AND CARDIOVASCULAR RISK: AN INTEGRATIVE CARDIO-DERMATOLOGY PERSPECTIVE
Psoriasis is a chronic unstable skin illness that is gaining prominence in the effect it caused in the entire human body particularly increasing the chances of heart illness. This is a mixed-methods experimental research that examines clinical and pathophysiological associations between psoriasis and cardiovascular disease (CVD). Adults included in the study were 180 and were categorized into three groups; psoriasis-only, CVD-only and comorbid. The severity of the skin condition was measured by using the Psoriasis Area and Severity Index (PASI), and the score used to measure the risk of heart disease was Framingham Risk Scale (FRS), carotid intima-media thickness (cIMT) and high-sensitivity C-reactive protein (hs-CRP). The results of the analysis of biomarkers indicated elevated concentrations of TNF-alpha and IL-17 in individuals constituting the comorbid group. Regression models demonstrated also that PASI was significantly predictive of increased cardiovascular load. In addition as well, interviews done, semi structured with a few comorbid patients revealed that they spoke a lot about psychological problems like they felt miserable about the state of their condition, how angry they were and how scared they were of heart problems. The quantitative and qualitative findings support the notion of similarity in the rate of inflammation and the psychosomatic pathways of psoriasis and CVD. The integrative clinical approach proposed in the study gives priority to the early screening and the care of numerous disciplines to enhance the long-term outcomes. These findings complement the emerging literature that cardiovascular screening ought to be included in the dermatologic treatment of patients with moderate-to-severe psoriasis.
Copyright (c) 2023 Rabia Nasir, Rabia Kiran (Author) https://creativecommons.org/licenses/by/4.0
AI-DRIVEN PREDICTIVE MODELING FOR GERIATRIC ONCOLOGY OUTCOMES
Implementing artificial intelligence (AI) in geriatric oncology is a game-changing approach to predicting the outcomes of treatment and customizing the care of geriatric cancer patients. A mixed-methods research was conducted to develop Machine Learning models capable of predicting the possibility of hospitalization, treatment toxicity, and survival 12 months after the onset of cancer in persons above the age of 65. In the dataset consisting of 412 patients with clinical, geriatric, and genomic data, we trained and tested such models as logistic regression, random forest, support vector machines, and XGBoost. XGBoost fared the best with an AUC score of 0.87, F1-score of 0.79 and a balanced accuracy of 0.81. SHAP analysis revealed the best predictors of survival were age, hemoglobin level, mutation burden and ECOG status. Together with quantitative modeling, qualitative interviews with 30 patients identified significant themes such as anxieties related to therapy and functional independence and emotional resilience. Such themes were employed in enhancing the interpretation and application of the model to real world. The model was also tested outwardly by an independent group of individuals (n = 98), and it has been identified that it was strong (AUC = 0.83). The findings indicate the significance of AI-driven tools to segregate risks, assist physicians in decision-making, and inculcate the values of patient-centredness into cancer treatment of the aged. This research is based on a paradigm that can be applied repetitively and comprehended which is the rigour in computer science and compassion in health science.
Copyright (c) 2023 Muhammad Inam Farooq, Syeda Iram Batool (Author) https://creativecommons.org/licenses/by/4.0
METABOLIC SYNDROME AND NEUROPSYCHIATRIC COMORBIDITIES
A trend emanating in the recent past is a connectedness between metabolic syndrome (MetS), a set of associated metabolic disorders, and neuropsychiatric issues such as melancholy, anxiety and cognitive loss. With clear criteria in diagnosing MetS and verified psychological assessment instruments (PHQ-9, GAD-7, MoCA), the mixed-methods research examined the shared experiences of 312 individuals aged 25-65 who are experiencing some form of neuropsychiatric load. The measuring of mental and cognitive discomfort has resulted in a new scoring called Neuropsychiatric Burden Score (NPBS). Quantitative data indicated that high fasting glucose and central adiposity were the most appropriate predictors of high NPBS (p < 0.01). Regression models also indicated that the higher the number of MetS-related factors an individual had, the poorer his/ her mental health outcomes became. Individuals with HOMA-IR of 2.5 or higher had significantly higher NPBS very low MoCA score, so it demonstrates the consequences of insulin resistance in the brain. Emotional exhaustion, sleep disorders, weight-related stigma, and reported cognitive failures theme were singled out by a qualitative analysis of 22 patient interviews. These thematics form a suitable pattern with the biomarker and the psychometric findings. Individuals with elevated NPBS were frequently receiving issues with cortisol levels as well as elevated levels of hs-CRP. This confirms the conception that neuroinflammation and HPA dysfunction is present. The integrated design of the study integrated into Figure 1 was able to merge both the metabolic diagnostics and psychiatric profiling hence forging a complete biopsychosocial map of comorbidity. These findings indicate that we require generalizable screening procedures and treatments that are interdisciplinary and take care of plans to control metabolism and psychological robustness in individuals with MetS
Copyright (c) 2023 Younas Rehman, Wesam Taher Almagharbeh (Author) https://creativecommons.org/licenses/by/4.0
MULTISYSTEM INFLAMMATORY SYNDROME IN CHILDREN: A RHEUMATOLOGY-PULMONOLOGY COLLABORATION
Digital health and telemedicine would constitute a fine idea to implement in rural emergency medicine to make clinical work more efficient, faster responsive, and reduce patient outcomes in regions that lack sufficient medical attention. The qualitative and quantitative methods applied in this study examined the impacts of utilising real-time tele-consultations on six rural emergency departments, looking at those cases that required urgent care, such as stroke, sepsis, myocardial infarction. A quantitative investigation (studying 284 encounters that were made possible by telemedicine) revealed that an average of thirty-four percent or forty-two percent of the time (respectively) was saved upon initiating the system correspondingly in order to get-a-treatment and a consultation. The calculated efficiency gain (E gain) and logistic regression modeling indicated that the shorter response time was related closely and significantly to the improved patient stabilization and a lower number of 30-day readmissions (p < 0.01). Meanwhile, interviews based on qualitative research with 48 physicians working in rural settings identified similar themes of improved cooperation across disciplines, increased trust in clinical expertise or issues such as the inability to use technology or internet access. Thematic analysis revealed that the perceptions of the providers and trends of the outcomes aligned with one another. That is why it is critical to align work and train employees. The methodological illustration of the working process (Figure 1) presents all triage and clinical data and feedback systems and how they combine to ensure the success of telehealth. This conclusion reveals the way, in which the telemedicine may transform the situation during a rural emergency and provides a model of expanding the use of digital medical care in resource-poor locations.
Copyright (c) 2023 Sami Ullah, Humayun Ali, Jawad Ali (Author) https://creativecommons.org/licenses/by/4.0
INTERSECTION OF KIDNEY DISEASE AND CANCER: SHARED PATHWAYS AND CLINICAL CHALLENGES
The convergence of kidney disease and cancer presents a growing clinical challenge, particularly as global populations age and the burden of chronic diseases escalates. This study explores the shared pathophysiological pathways, clinical outcomes, and therapeutic complications arising from the co-existence of chronic kidney disease (CKD) and malignancies. Through an integrated quantitative and qualitative methodology, we analyzed data from patients with dual diagnoses, focusing on disease prevalence, biomarker trends, treatment responses, and survival outcomes. The results highlight that renal cell carcinoma and bladder cancer are most prevalent among CKD patients, with significantly higher mortality observed in those with compromised renal function. Elevated nephrotoxicity was closely associated with agents such as cisplatin and methotrexate, while biomarkers like creatinine and NGAL demonstrated consistent trends of renal deterioration across various cancer treatments. Our figures captured critical patterns including the inverse relationship between glomerular filtration rate (GFR) and chemotherapy cycles, multi-dimensional survival-biomarker plots, and comparative quality-of-life scores. These findings underline the pressing need for integrated, interdisciplinary approaches in managing patients facing both renal and oncologic conditions. Furthermore, the visualizations and complex data tables enhance our understanding of predictive indicators and therapeutic implications. This research contributes a structured framework for clinicians and policymakers to anticipate risks, personalize treatment regimens, and improve long-term outcomes in this high-risk population.
Copyright (c) 2023 Ranya Mohammed Elmagzoub, Zafar Aleem Suchal (Author) https://creativecommons.org/licenses/by/4.0
HEAD AND NECK CANCER SURVIVORSHIP: NEUROLOGICAL AND CARDIOVASCULAR LONG-TERM EFFECTS
Head and neck cancer (HNC) survivors are increasingly facing long-term health complications beyond tumor remission, particularly in the domains of neurological and cardiovascular health. This study comprehensively investigates the persistence and incidence of these late effects in HNC survivors by integrating both quantitative analysis and clinical records across multiple care centers. A cohort of 420 post-treatment survivors, monitored for up to 10 years, was analyzed using both cross-sectional and longitudinal methods. The results highlight that approximately 34% of patients developed mild to moderate cognitive impairments, with memory loss and decreased executive functioning being most prevalent. Neurological assessments indicated significantly increased risks of peripheral neuropathy and radiotherapy-induced demyelination, particularly in patients who received concurrent chemoradiation therapy. On the cardiovascular side, 41% of participants experienced complications ranging from hypertension to ischemic heart disease. Statistical modeling revealed that radiation exposure to carotid arteries and long-term systemic inflammation were major predictive factors for cardiovascular disease (CVD) development post-treatment. A notable correlation was found between neurocognitive decline and elevated inflammatory biomarkers (p < 0.01), underscoring a possible mechanistic overlap between neurological and cardiovascular effects. Additionally, socioeconomic disparities played a significant role in post-treatment follow-up adherence and management outcomes. Figures and tables included in the study provide detailed breakdowns of prevalence, risk stratification, and comparative outcomes by treatment modality, age, and comorbidity index. Overall, the findings underscore the need for a cross-specialty survivorship model that includes routine neurocardiac monitoring, integrated rehabilitation services, and individualized survivorship care planning to improve long-term quality of life for HNC survivors.
Copyright (c) 2023 Muska Hayat, Shahzad Rafiq (Author) https://creativecommons.org/licenses/by/4.0
PULMONARY TOXICITIES OF TARGETED CANCER THERAPIES: A CROSS-SPECIALTY REVIEW
Targeted cancer therapies have transformed treatment paradigms across multiple malignancies, yet pulmonary toxicities represent a critical barrier to their safe application. This cross-specialty review employed a mixed-methods approach, integrating quantitative synthesis of clinical datasets and qualitative insights from oncology and pulmonology experts, to evaluate the incidence, presentation, and management of pulmonary adverse events. Analysis of nine comprehensive datasets revealed that interstitial lung disease, pneumonitis, pleural effusions, and pulmonary arterial hypertension occurred in up to 40% of patients, with variable severity across therapy classes including EGFR-TKIs, mTOR inhibitors, BCR-ABL TKIs, and monoclonal antibodies. Severity stratification demonstrated that higher grades of toxicity were frequently associated with combination regimens and longer treatment duration. Thirteen figures—including line, bar, scatter, hybrid, and heatmap visualizations—highlighted demographic trends, therapy-specific risk distributions, and correlations between age, cancer subtype, and pulmonary complications. Notably, chronic toxicities persisted in subsets of patients, emphasizing the need for prolonged monitoring. Qualitative analysis reinforced these findings, identifying recurrent clinical challenges such as diagnostic ambiguity, delayed referral to pulmonology, and gaps in standardized management protocols. Integration of these findings underscores the necessity of cross-specialty collaboration, early imaging and biomarker evaluation, and tailored surveillance strategies. Collectively, this study advances current understanding of pulmonary toxicities in targeted therapy, offering a multidimensional evidence base to support personalized management approaches and improved patient outcomes
Copyright (c) 2023 Shazia Khalid, Rida Naz (Author) https://creativecommons.org/licenses/by/4.0
INTEGRATING RHEUMATOLOGY AND ONCOLOGY: AUTOIMMUNE COMPLICATIONS OF IMMUNOTHERAPY
Immune checkpoint inhibitors (ICIs) have revolutionized oncology but carry the risk of inducing autoimmune complications that necessitate an integrated rheumatology–oncology approach. This study employed a mixed-methods design to examine rheumatic immune-related adverse events (irAEs) among patients undergoing ICI therapy. Quantitative analyses were performed on patient cohorts receiving PD-1, PD-L1, CTLA-4, or combination therapies, capturing demographic variables, cancer subtypes, and autoimmune manifestations. Incidence rates revealed that up to 40% of patients developed irAEs, with arthritis, myositis, and vasculitis representing the most frequent complications. Logistic regression identified preexisting autoimmune disease and combination therapy as significant predictors of higher severity scores. Qualitative interviews with oncologists and rheumatologists highlighted challenges in early recognition, interdisciplinary communication, and balancing cancer control with autoimmune toxicity management. Results across nine structured tables and twenty-two figures—including line, bar, pie, scatter, hybrid, radar, heatmap, and bubble charts—demonstrated demographic variation, therapy patterns, severity distributions, and inter-variable correlations. Notably, chronic irAEs persisted in a subset of patients, emphasizing the need for long-term follow-up strategies. The methodological workflow (Figure 1) underscores the integration of patient monitoring, statistical modeling, and thematic analysis. Collectively, findings confirm that autoimmune events are not only prevalent but also diverse in presentation, reinforcing the necessity of multidisciplinary care models and personalized monitoring strategies. This study contributes to evolving frameworks for safer immunotherapy deployment, ensuring both sustained oncologic benefit and preservation of patient quality of life.
Copyright (c) 2023 Jawad Ali, Sajjad Mehdi (Author) https://creativecommons.org/licenses/by/4.0