Journal of Healthcare Systems and Innovations
Journal of Healthcare Systems and Innovations (JHSI) is a triple-blind peer-reviewed academic journal published by ELITE PATH EDUCATIONAL ACADEMY (SMC-PRIVATE) LIMITED. The journal provides a scholarly platform for researchers, healthcare professionals, and academics to publish high-quality research related to healthcare systems, medical innovations, and clinical practices. The journal is published semiannually and aims to promote the dissemination of impactful research in the medical and healthcare fields. Articles published in the journal are indexed and visible through Google Scholar, increasing global accessibility and academic reach. Scope The journal covers a wide range of topics related to healthcare and medical sciences, including but not limited to: Healthcare Systems and Policy Clinical Medicine and Medical Research Public Health and Epidemiology Healthcare Management and Administration Medical Technology and Innovation Digital Health and Telemedicine Nursing and Allied Health Sciences Healthcare Quality and Patient Safety Health Informatics and Data Management Global Health and Community Medicine Biomedical Research and Healthcare Solutions
ELITE PATH EDUCATIONAL ACADEMY (SMC-PRIVATE) LIMITED
MATERNAL NUTRITION AND PREGNANCY OUTCOMES: A SYSTEMATIC LITERATURE REVIEW
Moral nutrition during pregnancy is a determinant factor of the pregnancy outcome, which has both short-term and long-term implications of not only the maternal and baby health, but also the risk of disease in the future generations. Despite the massive advancement of the specific effects of nutrients, gaps remain in the comparative efficacy of different nutritional interventions, the adherence effect, and the mechanistic aspect of nutrition in terms of how nutrition attains its effects. It is a system review of the correlation between maternal nutrition and pregnancy outcome in the past five years with precise reference to dietary patterns, micronutrient supplementation and biological processes in the same. According to the requirements of the PRISMA 2020, a system search was conducted on PubMed, Scopus, Web of Science, Embase, and Cochrane Library of all articles published between January 2019 and December 2024. Search terms were the words which were combination of maternal nutrition, pregnancy diet, micronutrient supplementation, pregnancy outcomes, birth outcomes and gestational outcomes. The criteria used to include the studies included randomised controlled trials, prospective cohort studies and systematic reviews of maternal nutritional status or interventions and their association with defined outcome of pregnancy. The quality assessment tools were Cochrane Risk of Bias tool of randomised trials and Newcastle-Ottawa Scale of observational studies. A total of 2,847 records were identified, 47 studies were selected by including the study, and 28 randomised controlled trials, 12 prospective cohort studies, and 7 meta-analysis systematic reviews were included. It had four important thematic areas, which were; dietary patterns and pregnancy outcomes (n=15 studies); micronutrient supplementation effects (n=18 studies); the placental-mediated mechanisms of nutritional interventions (n=8 studies); and the role of adherence and timing in intervention effectiveness (n=6 studies). Compliance on Mediterranean and DASH diets was associated with reduced risk of gestational diabetes mellitus (OR 0.60, 95% CI 0.450.80), and excessive gestational weight gain. Multifunctional micronutrient supplementation (as compared to iron-folic acid alone) improved birth weight (mean difference 56 g) and also reduced the risk of low birth weight, small-gestationally-age and stunting at six months of age. It is increasingly being evidenced that nutritional interventions do play a role in influencing placental development and placental functions and that placental adaptations are associated with improved maternal and offspring outcomes. The direct provision of nutrients and placental reactions indirectly play the role of determining the outcome of pregnancy and are dependent on the nutritional status of motherhood and diet intake. Early intervention, high compliance and combination of dieting patterns with the rightful supplementation are most likely to produce the best results. The individualised nutrition strategies, effects intergeneration, and effective methods to optimize maternal nutrition throughout the world are the areas that should be taken into consideration in the future research.
Copyright (c) 2025 Seemi Tanvir (Author) https://creativecommons.org/licenses/by/4.0
PSYCHOLOGICAL ADAPTATION AND COPING MECHANISMS IN ADVANCED CANCER PATIENTS RECEIVING PALLIATIVE CARE
This research examines the psychological adaptation and coping of older cancer patients under palliative care, focusing on the interaction between the emotional distress and symptom burden, coping styles, spiritual well-being and social support. The study investigated quantitative indices (anxiety, depression, coping frequencies, pain/distress correlations, and quality-of-life domains) using a mixed-methods design, which was supplemented by qualitative knowledge of the emotional account and existential issues of patients. Findings revealed moderate and high anxiety and depression rates were common and highly correlated with symptom severity especially unmanaged pain. Positive coping strategies such as acceptance, positive reframing, spiritual activities and problem-oriented coping were also associated with better emotional stability, distress, and well-being. On the other hand, the maladaptive coping patterns were associated with worse psychological outcomes. The latter spiritual well-being proved to be one of the most important protective factors with a steady negative correlation with the depressive symptoms, whereas robust familial and social support proved to be instrumental in reducing the emotional burden and increasing the level of resilience. The results highlight the necessity of interdisciplinary, holistic models of palliative care, which combine physical, emotional, social, and spiritual interventions to assist patients in adapting psychologically throughout terminal disease. These findings indicate that adaptive coping should be reinforced, symptom burden treated proactively, and family and culturally sensitive care practices should be integrated to improve the quality of life and improve emotional dignity in end-of-life care.
Palliative care; Advanced cancer; Psychological adaptation; Coping mechanisms; Anxiety; Depression; Spiritual well-being; Social support; Quality of life; Terminal illness
Copyright (c) 2025 https://creativecommons.org/licenses/by/4.0
MOTOR AND COGNITIVE REHABILITATION STRATEGIES FOR STROKE SURVIVORS: A MULTIDISCIPLINARY EVALUATION
This study evaluated the effectiveness of integrated motor and cognitive rehabilitation strategies in improving functional outcomes among stroke survivors using a multidisciplinary, mixed-methods design. A cohort of participants underwent a structured 12-week rehabilitation program incorporating physiotherapy, occupational therapy, computerized cognitive training, and psychosocial support. Quantitative measures included motor performance assessments, gait-speed analysis, upper-limb kinematic tracking, and standardized cognitive evaluations, while qualitative data were collected through semi-structured interviews exploring motivational and emotional dimensions of recovery. Results demonstrated notable improvements in motor function, including enhanced coordination, balance, and limb control, alongside significant gains in attention, executive functioning, and processing speed. Advanced statistical modeling revealed strong correlations between motor and cognitive recovery trajectories, emphasizing the interconnected nature of neuroplastic adaptation post-stroke. Furthermore, early-phase improvement and psychosocial resilience emerged as significant predictors of long-term outcomes. The integrated Motor–Cognitive Recovery Index developed in this study successfully captured multidimensional progress, supporting its potential utility as a clinical evaluation tool. Qualitative themes reinforced that emotional stability, self-efficacy, and therapeutic engagement were critical facilitators of rehabilitation adherence. Collectively, the findings underscore the value of multidisciplinary, personalized, and neuroplasticity-based rehabilitation approaches in accelerating functional restoration and improving quality of life for stroke survivors. This study contributes robust evidence supporting the expansion of integrated therapeutic models in stroke care and provides a foundation for future clinical and translational research.
Stroke rehabilitation; Motor recovery; Cognitive retraining; Neuroplasticity; Multidisciplinary therapy; Gait speed; Executive function; Kinematic analysis; Patient motivation; Functional outcomes
IMPACT OF ANTIHYPERTENSIVE DRUG ADHERENCE ON LONG-TERM CARDIOVASCULAR OUTCOMES: A PREVENTIVE MEDICINE PERSPECTIVE
The long-term cardiovascular outcomes strongly depend on the adherence to antihypertensive medication, which is still a common global issue that is not eliminated. This was a preventive-medicine trial that tested the relationship between the level of adherence and the occurrence of major cardiovascular events by a mixed-method design by combining quantitative clinical indicators, medication-possession ratios, the tracking of long-term outcomes, and qualitative measurement of behavioral barriers. A total cohort of hypertensive adults was assessed on high-, medium-, and low-adherence levels, and the concept of adherence was measured by means of the Medication Possession Ratio (MPR) and self-reports scales. Monitored cardiovascular outcomes, such as myocardial infarction, stroke, heart failure hospitalization, and cardiovascular mortality, were followed up over a multi-year follow-up period. Findings revealed that excellent compliance was closely linked to better blood pressure management, reduced LDL-C and fasting glucose, reduced acute cardiovascular, and significantly less mortality in the long term. On the contrary, low-adherence patients reported a much higher event rate, worse metabolic and hemodynamic status, and risk and responses in predictive modeling. A qualitative analysis of the data conducted revealed forgetfulness, medication fatigue, financial strain, and low perceived necessity as the key contributors to non-adherence. Combining clinical data with behavioral and predictive data proved that adherence is a modifiable and independent predictive variable of cardiovascular outcomes. These data support the importance of adherence-strengthening measures, such as patient education, electronic reminder tools, and simplified regimens as a solution to decrease cardiovascular morbidity and mortality that can be prevented. In general, the paper has made it clear that the optimization of the adherence to antihypertensives is one of the most effective preventive measures existing in contemporary cardiovascular medicine.
Antihypertensive adherence; Medication Possession Ratio (MPR); Cardiovascular outcomes; Preventive medicine; Hypertension control; Myocardial infarction risk; Stroke prevention; Long-term mortality; Behavioral barriers; Treatment compliance
Copyright (c) 2026 https://creativecommons.org/licenses/by/4.0
GENETIC AND HORMONAL INTERACTIONS IN POLYCYSTIC OVARY SYNDROME: A TRANSLATIONAL RESEARCH APPROACH
Polycystic ovary syndrome (PCOS) is a multifactorial endocrine disorder characterized by complex interactions between genetic susceptibility, hormonal dysregulation, and metabolic disturbance. This translational research aimed to investigate the interplay between SNP-level genetic variations and hormonal profiles to understand how these factors collectively influence PCOS severity and phenotypic expression. Using an integrated mixed-methods approach combining genomic analysis, endocrine biomarker quantification, metabolic assessment, and ultrasound-based ovarian morphology evaluation, the study identified significant associations between high-risk genotypes and elevated androgen levels, disrupted LH/FSH ratios, and increased AMH concentrations. Metabolic indicators such as fasting insulin, glucose, and HOMA-IR further correlated with specific genetic clusters, suggesting that metabolic dysfunction amplifies hormonally driven reproductive abnormalities. Additionally, qualitative lifestyle and menstrual history analyses revealed that psychosocial stressors and environmental factors further worsen endocrine imbalance. Hybrid statistical models demonstrated that combined genetic–hormonal burdens, rather than isolated biomarkers, serve as stronger predictors of PCOS severity. The findings highlight the necessity of considering multidimensional biological inputs for diagnosis and management, supporting a precision-medicine framework that incorporates genetic screening, hormonal monitoring, and metabolic profiling. Overall, this study reinforces that PCOS is a heterogeneous disorder requiring integrative assessment and opens pathways for targeted, individualized therapeutic strategies that may significantly improve clinical outcomes.
Polycystic Ovary Syndrome (PCOS); Genetic Polymorphisms; Hormonal Dysregulation; LH/FSH Ratio; Hyperandrogenism; AMH Levels; Insulin Resistance; Metabolic Dysfunction; Ovarian Morphology; Translational Research
NUTRITIONAL STATUS AND LIVER FUNCTION INTERPLAY IN PATIENTS WITH NON-ALCOHOLIC FATTY LIVER DISEASE
Non-Alcoholic Fatty Liver Disease (NAFLD) has emerged as one of the most prevalent chronic liver conditions worldwide, strongly linked to metabolic dysfunction and dietary imbalances. This study investigated the relationship between nutritional status and liver function parameters among clinically confirmed NAFLD patients using a mixed-methods approach that integrated anthropometric evaluation, dietary intake assessment, biochemical profiling, and ultrasound-based steatosis grading. Nutritional patterns were analyzed through detailed macronutrient and micronutrient intake evaluations, while liver dysfunction was assessed using liver enzyme levels, lipid markers, glucose–insulin indices, and hepatic fat grades. Findings revealed a strong association between elevated BMI, increased body fat percentage, excessive carbohydrate and fat consumption, and significant elevations in ALT, AST, and GGT levels. Micronutrient deficiencies, particularly vitamin D and antioxidant insufficiency, were highly prevalent and correlated with higher steatosis grades and worsening metabolic indicators. The integrated nutrition–liver dysfunction index demonstrated that patients with poor dietary quality and nutritional inadequacies exhibited more severe biochemical and imaging abnormalities, emphasizing the synergistic effect of metabolic and nutritional risk factors on disease progression. Qualitative lifestyle insights further validated the quantitative findings by highlighting irregular eating patterns, sedentary behavior, and high consumption of processed foods as major contributors to hepatic deterioration. Overall, the study underscores the pivotal role of nutritional health in modulating NAFLD severity and highlights the necessity of structured nutritional interventions, weight optimization, and lifestyle modifications as essential components of NAFLD management. These findings provide critical evidence supporting the integration of nutritional assessment into routine clinical evaluation to improve long-term hepatometabolic outcomes.
NEUROENDOCRINE-IMMUNE INTERACTIONS IN AUTOIMMUNE DISEASES: A CROSS-SPECIALTY PERSPECTIVE
Autoimmune diseases are becoming known to reflect highly complicated relations between neuro endocrine- immune systems but the clinical research is very fragmented among specialties. This paper uses a mixed-methods experimental design to examine these interactions through a combination of biomarker measurements to include patient-derived qualitative perspectives. A group of autoimmune patients was selected in rheumatology and endocrinology departments. Quantitative data incorporated serum cytokines (IL-6, TNF-alpha), cortisol and ACTH concentrations and others as indicators of autonomic functioning-ie, the heart rate variability. Findings showed that there were statistically significant reciprocals between increased pro-inflammatory cytokines and diminished autonomic performance, and imbalanced cortisol regulation, which indicates HPA axis dysfunction. The above biomarkers passed the test of multivariate regression as predictive of severity of symptoms in the various types of diseases. Parallel to them, qualitative interviews were conducted to investigate patient experiences of flares of their symptoms, aspects perceived as triggering stress, and emotional load. Thematic analysis identified a number of recurrent themes of psychological stress followed by physiological aggravation indicating a duplicating neuroimmune feedback system. The cross-specialty management systems that take into account the molecular and experiential aspects of disease were outlined by the combination of quantitative and qualitative information. These outcomes demonstrate the importance of cross-discipline collaboration when it comes to the improvement of patient-centred care, patient monitoring, and diagnostic accuracy in autoimmunity.
Copyright (c) 2024 https://creativecommons.org/licenses/by/4.0
CARDIOPULMONARY IMPLICATIONS OF LONG COVID: PULMONOLOGY MEETS CARDIOLOGY
Although there is growing evidence regarding severe, long-term cardiopulmonary damage in survivors of COVID, limited knowledge is available regarding cardiopulmonary consequences of long-term COVID. This study applied a mixed-methods experimental design and utilized Previously SARS-CoV-2 positive individuals who were still presenting with the effects of cardiopulmonary sequelae (excess symptoms) 12 weeks later. Biomarker analysis was used to assess the participants, which was done by pulmonologists and cardiologists in collaboration with one another. The values of diffusion capacity of the lungs to carbon monoxide (DLCO) and left ventricular diastolic heart functioning were established to be significantly diminished, and the associations between the indicators of cardiac and pulmonary dysfunctions were quite significant, depending on the quantitative data. The statistical modeling using the generalized estimating equations displayed interaction effect of FEV1 and LVEF on fatigue and dyspnea scores (p < 0.01). The qualitative data obtained through structured interviews was used to highlight the physical constraints, the increased anxiety marking cardiopulmonary manifestations and the uncertainties in the event of establishing long-term recovery. Individualized treatment was designed on the basis of integrated care teams and therapeutic strategies involved beta-blockers, anticoagulation, pulmonary rehabilitation, and psychosocial therapeutic modalities. Three- and six-month follow-ups showed improvement in physiological and quality-of-life results in patients. An interdisciplinary cooperation is also a possibility and the visual workflow (Fig. 1) reflects the full cycle of customized management following the hiring. To be able to manage these sequelae significantly, the study highlights the importance of integrative diagnostic and treatment paradigms and suggests the fact that Long COVID has multidisciplinary cardiac impacts.
MULTIMODAL MANAGEMENT OF PEDIATRIC EPILEPSY: NEUROLOGY-PSYCHIATRY COLLABORATION
The efficacy of multimodal management with combined neurology and psychiatry is observed in this study to treat paediatric epilepsy. The research itself involved children with clinically diagnosed epilepsy between 3 and 16 in terms of a mixed-methods experimental approach. At baseline and in the middle of the treatment and after treatment, the quantitative descriptive data was collected, like the frequency of the seizures and behavioural results (CBCL, SDQ). At the same time, there was a qualitative approach through semi-structured interviews with carers to record psychosocial impacts and care satisfaction. The integrated treatment approach involved cognitive behavioural therapy (CBT), antiepileptic medications (AEDs), and regular case reviews at that interdisciplinary level. Statistically significant outcomes included changes in behavioural ratings in the positive direction with repetition of the measures of ANOVA, and reductions in seizure frequency (p < 0.01). The effect estimation of the difference between two conditions proved clinically significant alterations to be true. Qualitative findings indicated better family coping mechanisms, better control of emotions in children and parent satisfaction. The collaborative model made it easier to provide individualised care because treatment plans were always revised based on mental and neurological information. The results of the study indicated that an integrated approach of neurology and psychiatry is beneficial in order to enhance neurological outcome as well as psychosocial functioning resulting in superior management of paediatric epilepsy. In tertiary care, the present paradigm proposes the provision of patient-centered care by adopting the multidisciplinary approach in a scaled down manner.
AI-GUIDED SURGICAL PATHOLOGY FOR PERSONALIZED ONCOLOGY
This study using deep learning-based histopathological image analysis with the ability to learn in an iterative manner of clinical returns will develop and test an AI-guided surgical pathology paradigm to achieve personalised oncology treatment. High-resolution WSIs of cancer tissue biopsies were interpreted within convolutional neural networks, due to prior annotation as done by pathologists via a mixed-methods experimental design. Quantitative analysis also demonstrated the good diagnostic performance with high sensitivity and specificity across the tumour subtypes of the models. The HAP analysis confirmed the independent relevance of morphological features like nuclear pleomorphism and mitotic activity, and the subjective pathologist and oncologist input was incorporated to assess the interpretability and clinical utility. In over 90 percent of test conditions, the clinical decision support component recommended personalised therapy that was in agreement with expert consensus. A feedback integration loop allowed continuous improvement of models with respect to practical observations and contributed to a higher dependability and contextual flexibility of the system. Fig. 1 indicates the visual methodology workflow, and they show the full process of tissue sample to feedback-driven AI enhancement. So, taking everything into consideration, the proposed framework paves the way toward scalable structure of next-generation clinical decision-making systems and describes how AI can advance the diagnostic accuracy and personalisation of therapy in oncology.
INTEGRATIVE APPROACHES TO CARDIO-ONCOLOGY: MANAGING HEART HEALTH IN CANCER PATIENTS
Cardiovascular complications are considered one of the chief reasons of morbidity among the cancer patients undergoing treatments that are suspected to be cardiotoxic. This study evaluated the success of the integrative cardio-oncology approaches, which involve the combination of biomarker-based surveillance with both clinical risk stratification and self-report construction as the mixed-methods experimental design. In Breast cancer patients who were receiving various types of cancer treatment, 100 patients received measurement of biomarkers including NT-proBNP, Troponin and ejection fraction, the Framingham risk scores as well as quality-of-life indicators. It revealed that 30 percent of the patients presented with cardiotoxicity symptoms, and increased values of NT-proBNP and reduced ejection fractions were also eminent mostly in patients subjected to combination treatment and those with co-morbidly diabetes and hypertension. Regression models identified age, status of comorbidity, treatment modality, and NT-proBNP as the significant predictors of cardiovascular decline. The qualitative interviews of cardiologists and patients were used to identify such barriers to early detection as disjointed communication and absence of standardised screening procedures. Statistical relationships were supported with regression visuals, heatmaps, trajectory line, scatterplot, and other visual analytics to see how cardiac risks were moving. One of the key clinical implications of quantitative and qualitative insights is that cardio-oncology has to shift towards being proactive and interdisciplinary. By setting the foundation of early intervention, this research will likely enhance the survivorship rate by urging the use of standard cardiac monitoring and risk profiling, which has proven to be of immense worth to oncology treatments.
THE IMPACT OF ANTIOXIDANTS ON OXIDATIVE STRESS AND AGING
Oxidative stress, a condition arising from an imbalance between reactive oxygen species (ROS) and antioxidant defense systems, is a pivotal factor contributing to aging and the onset of numerous age-related diseases. The damage induced by ROS affects key cellular components including DNA, lipids, and proteins, leading to impaired cellular function, mitochondrial dysfunction, and genomic instability over time.This study investigates the role of various dietary and endogenous antioxidants in mitigating oxidative stress and their potential to modulate the biological mechanisms underlying aging. A literature-based experimental model was employed, integrating comparative analyses of antioxidant impact on biomarkers such as telomere length, lipid peroxidation, gene expression, and mitochondrial integrity. The results demonstrate that antioxidant treatment significantly reduces ROS levels, enhances mitochondrial membrane potential, preserves telomere length, and upregulates protective genetic pathways such as Nrf2 signaling. Moreover, notable reductions in DNA oxidative damage and apoptosis rates were observed in antioxidant-administered groups compared to controls, supporting the hypothesis that antioxidants improve cellular resilience against age-related deterioration.These findings underscore the therapeutic potential of antioxidants in promoting healthy aging and reducing the burden of neurodegenerative, cardiovascular, and oncological diseases. By protecting cellular structures, modulating gene expression, and maintaining redox balance, antioxidants contribute meaningfully to the preservation of physiological function. Future clinical research is warranted to optimize antioxidant formulations and validate their long-term efficacy in aging populations.
MECHANISMS OF NEUROPLASTICITY: INSIGHTS FROM ANIMAL MODELS
Neuroplasticity, the brain’s intrinsic ability to reorganize its structure and function, plays a vital role in learning, memory, and recovery from neurological damage. Understanding the mechanisms that govern neuroplasticity has profound implications for therapeutic interventions in stroke, Alzheimer’s disease, and spinal cord injury. Animal models, particularly rodents, offer a robust platform for investigating the cellular, molecular, and environmental determinants of neuroplasticity. This study synthesizes evidence from controlled experiments in rodent and primate models to examine how synaptic plasticity, neurogenesis, and neurotrophic signaling contribute to brain reorganization. Experimental interventions included physical exercise, environmental enrichment, and stress modulation, assessed through electrophysiological recordings, behavioral tasks, and molecular assays.Results demonstrated that environmental enrichment and voluntary exercise significantly enhance synaptic strength and neurogenesis, primarily in the hippocampus. Elevated levels of brain-derived neurotrophic factor (BDNF) were observed under these conditions, supporting increased synaptic density and cognitive performance. Conversely, chronic stress suppressed neuroplastic responses, highlighting the dual impact of lifestyle factors on brain adaptability. Therapeutic strategies leveraging these mechanisms have shown promise in promoting functional recovery post-stroke and in mitigating cognitive decline in neurodegenerative conditions.In conclusion, neuroplasticity emerges as a dynamic and modifiable process with considerable translational potential. The interplay between genetic, molecular, and environmental factors offers a multifaceted target for neurological rehabilitation. Future advancements in imaging, genetic editing, and personalized medicine are poised to enhance the efficacy of neuroplasticity-based therapies in clinical settings.
EXPLORING THE EFFECT OF ENVIRONMENTAL TOXINS ON GENE EXPRESSION IN MAMMALIAN CELLS
Environmental toxins, including heavy metals, pesticides, and industrial pollutants, have emerged as critical threats to human health due to their ability to induce molecular disturbances within biological systems. These toxicants disrupt normal gene regulatory mechanisms, potentially leading to carcinogenesis, neurodegeneration, reproductive dysfunction, and other chronic diseases. Understanding how these compounds influence gene expression in mammalian cells is essential for elucidating their pathological effects and guiding public health interventions. This study investigates the impact of various environmental toxins on gene expression dynamics by employing high-throughput RNA sequencing and quantitative PCR techniques. The experimental approach included exposing mammalian cell lines to cadmium, arsenic, lead, and pesticide mixtures, followed by transcriptomic profiling and epigenetic analysis. Data were evaluated using fold change calculations, pathway enrichment, and miRNA expression modulation, offering a comprehensive assessment of transcriptional and post-transcriptional alterations. Results revealed substantial gene expression changes in response to toxin exposure, particularly the upregulation of stress-related genes and downregulation of DNA repair pathways. The study also identified significant epigenetic modifications, such as altered DNA methylation patterns and shifts in histone acetylation, as well as deregulation of miRNA profiles. These molecular disruptions were shown to be dose-dependent and tissue-specific, indicating complex regulatory responses that extend beyond acute toxicity.The findings demonstrate that environmental toxins exert both immediate and persistent effects on gene expression, thereby increasing disease susceptibility over time. This research highlights the utility of gene expression profiling as a biomarker for toxic exposure and supports the development of predictive and preventive models for toxin-induced diseases. By elucidating the molecular mechanisms underlying these effects, the study contributes to more informed environmental health policies and targeted therapeutic strategies.
THE ROLE OF EPIGENETICS IN CELLULAR ADAPTATION TO STRESS
Cellular stress is a universal biological phenomenon that disrupts homeostasis and compels cells to activate adaptive mechanisms for survival. Epigenetic regulation plays a central role in these adaptations by enabling reversible changes in gene expression without altering the DNA sequence. This study investigates the contribution of key epigenetic mechanisms—including DNA methylation, histone modifications, and non-coding RNAs—in modulating stress responses across different biological systems. A combination of in vivo rodent models and in vitro cultured cell lines was employed to explore the dynamics of epigenetic remodeling under oxidative, nutritional, and psychological stress conditions. Epigenetic profiling and transcriptomic analyses were used to evaluate the impact of these stressors on gene expression and chromatin state. The results reveal significant shifts in DNA methylation patterns, with stress-induced hypomethylation activating survival pathways and hypermethylation silencing regulatory genes involved in differentiation and apoptosis. Histone acetylation was generally increased in stressed cells, facilitating transcription of stress-response genes, while context-specific histone methylation changes contributed to either gene repression or activation. Furthermore, non-coding RNAs such as miR-21 and lncRNAs were differentially expressed and shown to regulate inflammation, repair, and apoptosis networks under stress conditions.The findings suggest that epigenetic modifications not only orchestrate short-term cellular responses but also establish a molecular memory of stress, influencing long-term adaptation and disease susceptibility. These insights provide a mechanistic foundation for the development of epigenetic therapies targeting stress-related pathologies. By elucidating the regulatory interplay between environmental stress and the epigenome, this study contributes to the emerging field of stress epigenetics and opens new avenues for personalized medicine and therapeutic intervention.
INVESTIGATING THE MOLECULAR MECHANISMS OF STEM CELL DIFFERENTIATION: IMPLICATIONS FOR REGENERATIVE MEDICINE
Stem cell differentiation is a fundamental biological process that underpins tissue development, maintenance, and repair, making it central to advances in regenerative medicine. Understanding the molecular mechanisms that guide stem cell fate decisions is crucial for developing safe and effective therapies for degenerative diseases and tissue injuries. This study investigates the genetic, epigenetic, and environmental factors influencing stem cell differentiation, with a particular focus on transcriptional regulators, signaling pathways such as Wnt, Notch, and TGF-β, and the microenvironmental niche. A literature-driven analytical framework was employed to map the dynamic interplay among these regulatory systems, incorporating transcription factor analysis, epigenetic modification tracking, and pathway-specific impact assessments on cell lineage outcomes. Results indicate that the suppression of pluripotency genes such as Oct4 and Sox2 initiates lineage specification, while epigenetic mechanisms like DNA methylation and histone modification stabilize the differentiated states. Differentiation efficiencies varied significantly across conditions involving hypoxia, matrix stiffness, and cytokine exposure. Analysis showed that environmental cues combined with pathway-specific modulation yielded high-fidelity differentiation into cardiac, neural, hepatic, and mesenchymal lineages. The use of CRISPR-based gene regulation and tailored culture conditions further enhanced lineage precision and reduced undesired outcomes. The study concludes that stem cell fate is governed by a tightly regulated, multifactorial network of intrinsic and extrinsic signals. Optimizing the interactions among transcriptional, epigenetic, and microenvironmental elements holds the key to developing robust, personalized regenerative therapies. These insights not only deepen our biological understanding but also pave the way for safer clinical applications in tissue engineering, disease modeling, and cell replacement strategies.
Copyright (c) 2024 Journal of Healthcare Systems and Innovations https://creativecommons.org/licenses/by/4.0
PULMONARY MICROTHROMBOSIS IN SEVERE COVID-19: AUTOPSY-BASED STUDY
Pulmonary microthrombosis has emerged as a significant contributor to respiratory failure and mortality in severe COVID-19. This autopsy-based study aimed to characterize the extent, distribution, and clinical associations of pulmonary microthrombi in patients who succumbed to SARS-CoV-2 infection. Autopsies were conducted on 40 deceased COVID-19 patients. Lung tissues were examined histologically and immunohistochemically to identify and quantify microthrombi. Clinical data, including coagulation biomarkers, comorbidities, and anticoagulation therapy, were retrospectively analyzed. Statistical analyses and multivariate logistic regression were performed to explore associations between thrombotic burden and clinical variables. Most of the time, microthrombi formed in the small blood vessels of the lungs and the lower lobes had the most. According to histological observation, pathological changes included swelling of endothelial cells, development of hyaline membranes, thick fibrin that stuck platelets in the blood and lung oedema. Using immunohistochemistry, researchers found excess expression of von Willebrand factor and tissue factor in the endothelium near areas of high thrombus deposits. The amount of microthrombus found was increased when fibrinogen and D-dimer levels were higher (P < 0.01). Microthrombi were found less frequently in patients on prophylactic or therapeutic anticoagulants (p = 0.04), however, patients with diabetes and hypertension had a greater number of thrombi. Technology confirmed that 29% of patients with COVID-19 triggered blood clots in their brains, 42% in their hearts and 68% in their kidneys. According to logistic regression, increased D-dimer (OR 3.2), high CRP (OR 2.4) and findings of endotheliitis in tissues (OR 2.7) were linked to the development of microthrombosis in the lungs. Both clinically and in the long term, severe COVID-19 can increase the risk of dying by causing microthrombosis in the lungs. COVID-19 is classified as a thromboinflammatory illness because of the activation of endothelial cells and widespread thrombi. It is apparent from these results that finding and treating coagulopathy in high-risk COVID-19 patients is important as soon as possible.
Copyright (c) 2025 Abdul Ghaffar , Humayun, Ali Jawad Ali (Author) https://creativecommons.org/licenses/by/4.0
ROLE OF NEUTROPHIL EXTRACELLULAR TRAPS IN ACUTE EXACERBATIONS OF COPD
Acute exacerbations of chronic obstructive pulmonary disease (AECOPDs) represent pivotal events in the disease progression of COPD, significantly influencing patient morbidity and mortality. While traditionally attributed to infectious agents and environmental pollutants, emerging evidence highlights a central role of neutrophil extracellular traps (NETs) in exacerbation pathogenesis.For this reason, this study reviews and connects recent work on NETs’ correlation with AECOPDs. When a neutrophil undergoes NETosis, it releases a network of DNA, histones and enzymes that surround pathogens and trigger events that damage lung tissue. Markers of inflammation have been found to increase in the lungs and airways of COPD patients when they experience NETs. In the study, it is noted that NETs like histones, neutrophil elastase and matrix metalloproteinases contribute to airway changes, break down the extracellular matrix and cause harm to both epithelial and endothelial cells. Following NET’s formation, complement activation and inflammasome generation enable neutrophils to continue inflammation. According to studies, NETs increase local inflammation after the first stimulus by producing more oxidative stress, drawing in more immune cells and increasing nearby cytokines. NETs have a harmful effect in leading to small airway disease, fibrosis and emphysema which signal that COPD is becoming more severe. This shows that NETs or their components might be useful in managing and preventing AECOPDs. Moreover, this research finds that how neutrophils act in the lung may have a major role in COPD and that controlling NET formation may shape upcoming COPD treatments.
Copyright (c) 2025 Dr Syeda Iram Batool , Muhammad Inam Farooq (Author) https://creativecommons.org/licenses/by/4.0
ROLE OF INTESTINAL MICROBIOTA IN PERSISTENT TYPHOID CARRIERS
Persistent Salmonella enterica serovar Typhi (S. Typhi) carriage represents a significant public health concern, particularly in endemic regions, as asymptomatic carriers continue to shed the pathogen long after clinical recovery. This study aimed to investigate the role of intestinal microbiota and gut virome in sustaining S. Typhi persistence post-infection.People from areas where S. Typhi infections are common and remain for a long time, along with non-carrier people, took part in a type of case-control study. The stool samples were analyzed using viral metagenomics and 16S rRNA gene sequencing. To analyze diversity, composition and phage infection, QIIME2, LEfSe and PICRUSt were applied; the acceptable threshold was p < 0.05. Persistent carriers had a significantly lower Shannon index for Alpha diversity (2.71 compared to 3.85, p < 0.001). Different community structures could be seen through the beta diversity method. The study identified that there was a fewer number of Lactobacillus and Bifidobacterium in carriers, even though LEfSe found more Desulfovibrio, Enterobacteriaceae and Bacteroides fragilis in them. Research of the function showed that the sulphur metabolism and lipopolysaccharide production pathways were turned on more. Due to an increase in virulence and resistance genes coming from tendentially integrated prophages, the study indicated a higher number and richness of Myoviridae and Siphoviridae viruses. We observed that specific virulence-associated phages tend to be present with pathogenic bacteria in the carrier group. Fun fact: Changes in the gut’s bacteria microbiota and more phages, possibly leading to higher bacterial virulence and survival in the body, are associated with persistent S. Typhi carriage. The findings suggest that the microbiota-virome-immune axis greatly influences long-term possession and suggest different ways to treat it, including controlling phage activity or restoring the microbiome.
Copyright (c) 2025 Dr. Sajjad Mehdi, Muska Hayat (Author) https://creativecommons.org/licenses/by/4.0
THE IMPACT OF COINFECTION OF DENGUE AND COVID-19 ON CLINICAL OUTCOMES
The concurrent circulation of dengue virus and SARS-CoV-2 in tropical and subtropical regions has raised concerns about the clinical implications of coinfection. Overlapping symptomatology and immunopathological mechanisms pose diagnostic and therapeutic challenges, yet evidence on the clinical outcomes of coinfection remains limited. To evaluate the impact of dengue and COVID-19 coinfection on clinical presentation, laboratory findings, treatment modalities, and patient outcomes compared to monoinfection. Three groups of 900 patients—300 with dengue alone, 300 with COVID-19 alone, and 300 with dengue-COVID-19 coinfection—were included in a retrospective, multi-center observational analysis. Analysis was done on imaging results, laboratory results, clinical data, treatment plans, and results. Mortality predictors were found using multivariate logistic regression. Compared to dengue (4%) and COVID-19 (11%) monoinfection groups, coinfected patients showed noticeably greater rates of ICU hospitalisation (28%), mechanical ventilation (19%), and mortality (12%). Coinfection was linked to greater D-dimer levels (2.3 mg/L), higher CRP (56 mg/L), and lower platelet counts (mean 98 ×10³/μL), indicating a compounded inflammatory and coagulopathic profile. Ground-glass opacities and lung infiltrates were common radiological findings, while rash and gastrointestinal symptoms complicated the diagnosis. Coinfection status (OR 2.17, 95% CI: 1.31–3.61), advanced age, high CRP, and low platelet count were all found to be independent predictors of death using logistic regression. Cross-reactivity in serological assays (42%) and delayed RT-PCR results hindered prompt diagnosis, making diagnostic difficulties prevalent. To increase accuracy, the use of integrated clinical scoring systems and multiplex assays was recommended. The co-occurrence of dengue with COVID-19 leads to worse clinical outcomes, longer hospital stays, and higher fatality rates. Improving the prognosis for coinfected patients requires early detection, quick diagnostics, and vigorous supportive care. In order to properly manage this newly developing dual illness burden, the study emphasises the necessity of region-specific protocols and improved surveillance systems.
Copyright (c) 2025 Rida Naz, Shahzad Rafiq (Author) https://creativecommons.org/licenses/by/4.0
GENETIC SUSCEPTIBILITY TO CEREBRAL MALARIA: A GWAS STUDY
Cerebral malaria is a life-threatening neurological complication of Plasmodium falciparum infection, predominantly affecting children in sub-Saharan Africa. While many individuals are exposed to the parasite, only a subset develops cerebral malaria, suggesting a pivotal role for host genetic susceptibility. This study aimed to identify genetic variants associated with susceptibility to cerebral malaria using a genome-wide association study (GWAS) approach. A total of 1,000 children (500 cases with cerebral malaria and 500 controls with uncomplicated malaria) were genotyped using high-density SNP arrays. Rigorous quality control procedures were applied, and population stratification was corrected using principal component analysis. To assess the SNPs and illness link, a logistic regression method was applied while also considering age, sex and ancestry. After looking at replication results in a Ghanaian cohort, we used gene ontology enrichment to determine the significance of the genes. Several, but specifically ten, DNA variations were discovered by the GWAS on chromosomes 6, 9 and 11 and these variations were found to play important roles in immune stimulation and endothelial health. Because the odds ratios ranged from 1.4 to 2.5, it was clear that these SNPs might become genetic markers of risk. In other locations, evidence of a connection was also uncovered (p < 1 x 10⁻⁵). Nominal significance was seen in four SNPs, whereas seven SNPs were confirmed to be associated by the replication study in Ghana. In gene ontology analysis, significant details were found in pathways involving leukocyte adhesion, cytokine behavior and barrier breakdown for the brain, all of which are related to the symptoms of cerebral malaria. After principal component analysis, we found only little population substructure bias and this did not affect the performance of the logistic regression models. Apart from explaining molecular pathways related to severe malaria, this research proposes genes that put people at risk of cerebral malaria and suggests areas for consideration in risk assessment and treatment.
Copyright (c) 2025 Journal of Healthcare Systems and Innovations https://creativecommons.org/licenses/by/4.0
ASSOCIATION BETWEEN ALLERGIC RHINITIS AND SLEEP APNEA: A CROSS-SECTIONAL ANALYSIS OF SLEEP QUALITY
Objective: To evaluate the association between allergic rhinitis (AR) and obstructive sleep apnea (OSA) severity and their combined impact on sleep quality in a cross-sectional adult cohort. Methods: Between January and June 2024, 300 consecutive patients (mean age 45.2 ± 12.1 years; 54% male) presenting for sleep evaluation underwent standardized AR assessment (ARIA criteria, Total Nasal Symptom Score), full‐night attended polysomnography (apnea–hypopnea index [AHI], arousal index, sleep efficiency), and subjective sleep measures (Pittsburgh Sleep Quality Index [PSQI], Epworth Sleepiness Scale [ESS]). Nasal nitric oxide and peripheral eosinophil counts were obtained to quantify allergic inflammation. Multivariable linear and logistic regressions adjusted for age, sex, BMI, and smoking status. Results: AR was present in 160 participants (53.3%). Compared to non‐AR individuals, those with AR exhibited significantly higher mean AHI (15.3 ± 8.6 vs. 9.8 ± 6.4 events/hour; p < 0.001), worse PSQI scores (8.2 ± 3.1 vs. 5.6 ± 2.4; p < 0.001), and greater daytime sleepiness (ESS 11.5 ± 4.2 vs. 7.4 ± 3.3; p < 0.001). AR symptom severity independently predicted increased AHI (β = 0.34; p = 0.002), PSQI (β = 0.29; p = 0.001), and ESS (β = 0.25; p = 0.003). Persistent AR phenotype demonstrated higher nasal nitric oxide (340 ± 60 vs. 220 ± 45 ppb) and eosinophil counts (780 ± 200 vs. 450 ± 120 cells/µL) than intermittent AR (both p < 0.001). Conclusions: AR significantly exacerbates OSA severity and subjective sleep disturbances, with biomarker levels indicating a dose–response relationship. These findings support routine AR screening in sleep clinics and integrated management strategies to improve patient outcomes.
Copyright (c) 2023 Muhammad Rehan, Rabia Nasir (Author) https://creativecommons.org/licenses/by/4.0
BIOCHEMICAL MECHANISMS OF OXIDATIVE DNA DAMAGE AND ITS ROLE IN CANCER: CHEMICAL APPROACHES TO REPAIRING DNA DAMAGE
Oxidative DNA damage has a major role in the initiation of carcinogenesis by inducing mutagenesis, genomic instability, and cellular dysfunction. Most of the time, reactive oxygen species (ROS), which are produced from various metabolic processes and from environmental influences, cause DNA lesions such as strand breaks, base modifications, and DNA-protein crosslinks. If not repaired, these oxidative lesions can then lead to permanent changes in the DNA introducing oncogenic pathways, as well as the silencing or impairment of tumor suppressive functions. DNA repair mechanisms such as base excision repair (BER), nucleotide excision repair (NER), and mismatch repair (MMR) are thus important for the maintenance of genomic integrity, with their compromised functions being noted to occur very commonly in cancer cells, further increasing mutation rates and resistance to therapy. The goal of this study is to provide an overview of the biochemical mechanisms underlying oxidative DNA damage, while also evaluating chemical approaches to DNA repair enhancement. The efficacy of small-molecule inhibitors, synthetic base analogs, and antioxidants to modulate DNA repair processes was assessed using in vitro and in vivo models. Importantly, results show that targeting key enzymes of repair increases repair rates and enhance cellular survival under oxidative stress. Also, DNA repair inhibitors could sensitize cancer cells to chemotherapeutic agents by taking advantage of their repair-deficient states. Overall, our findings reaffirm the potential therapeutic applicability of the modulation of DNA repair pathways toward preventing cancer and treating it once established. Further refinement of chemical strategies that target cancer-specific repair weaknesses is vital to curtail potential side effects. This study proposes that integration of DNA repair modulation with precision oncology holds promise to benefit patient outcomes and pave the way for new onco-drugs.
Copyright (c) 2023 Zia Ur Rehman, Zia Ur Rehman (Author) https://creativecommons.org/licenses/by/4.0
ROLE OF METAL IONS IN NEURODEGENERATION: INVESTIGATING THE CHEMISTRY OF COPPER, IRON, AND ZINC IN ALZHEIMER'S AND PARKINSON'S DISEASES
Alzheimer's disease (AD) and Parkinson's disease (PD), well-known neurodegenerative disorders, are related to the progressive loss of neuronal functions and to the accumulation of pathologically aggressive proteins. Recent evidence has shown that metal ions play an important role in the pathogenesis of these disorders, involving metal ions like copper (Cu), iron (Fe), and zinc (Zn). These ions create oxidative stress, induce protein aggregation, and invoke neurotoxicity, furthering the progression of these diseases. On one hand, Cu and Fe take part in free radical generation through redox reactions, while on the other, they induce oxidative damage; Zn, however, acts in a manner to alter protein interactions and aggregation. An imbalance of these metal ions has been observed in postmortem brain specimens from AD and PD subjects, implicating these metal ions in disease etiology. The perturbation of metal homeostasis means an alteration not only in oxidative stress but also in other pivotal biological pathways, including mitochondrial dysfunction, synaptic signaling, and neuroinflammation. Increased accumulation of Fe in the PD patient substantia nigra and of Cu in the AD patient amyloid plaques underlines their pathological significance. Moreover, Zn has also been implicated in modulating amyloid-beta (Aβ) aggregation, playing either a protective role or detrimental role depending on its level of availability and binding state. Herein, we investigate the chemistry of Cu, Fe, and Zn in the context of neurodegeneration, their involvement in oxidative stress, and also some potential therapeutic interventions such as chelation and ionophores to alleviate their detrimental effects. With a complete knowledge of metal ions-neurodegeneration interactions, new therapeutic approaches can be developed to target metal-induced toxicity and restore neuronal homeostasis.
Copyright (c) 2023 Rida tariq, Abdul Waheed Shah (Author) https://creativecommons.org/licenses/by/4.0
NANOPARTICLE-MEDIATED DRUG DELIVERY: A REVOLUTIONARY ADVANCEMENT IN CANCER AND INFECTIOUS DISEASE TREATMENT
Nanoparticle-based drug delivery systems have evolved as a revolutionary approach to targeted cancer and infectious disease treatment. This work discusses the synthesis, functionalization, and assessment of different types of nanoparticles such as polymeric, lipid, and metal oxide nanoparticles. Some of the findings highlighted that polymeric nanoparticles attained maximum encapsulation efficiency (85%) and controlled release profiles, thereby providing long-term therapeutic activity. Lipid nanoparticles showed increased stability in plasma and effective targeting properties, especially using PEGylation and ligand conjugation techniques. pH-responsive nanoparticles showed controlled release under acidic conditions, increasing localized drug delivery. Magnetic dextran-functionalized nanoparticles effectively accumulated in cancer tissues, showing promise in magnetically guided therapies. The research validated enhanced cellular uptake, decreased systemic toxicity, and increased hemocompatibility in all nanoparticle formulations. In vivo experiments showed increased circulation half-lives and targeted localization in tumor tissues through the EPR effect. These results point toward the promise of multifunctional nanoparticles to advance therapeutic efficacy, minimize side effects, and extend clinical use. Future studies will need to prioritize scalable synthesis methods and hybrid nanoparticle system design to further maximize targeted therapies.
Copyright (c) 2023 Sumaiya Sundus, Rizwan Ullah (Author) https://creativecommons.org/licenses/by/4.0
MECHANISMS OF DRUG-RESISTANT CANCER CELLS: ROLE OF CHEMORESISTANCE MEDIATED BY CELLULAR EFFLUX PUMPS AND TARGET MUTATIONS
Chemoresistance is a potent barrier in effective cancer treatment due to various cellular and molecular processes that lower the efficacy of drugs. In this study, the contribution of cellular efflux pumps, genetic mutations, DNA repair pathways, and the tumor microenvironment in drug resistance mediation is explored. Using in vitro assays, CRISPR-Cas9 gene editing, and molecular analytical methods, the study detected significant resistance mechanisms in chemoresistant breast (MCF-7R), lung (A549R), and colorectal (HCT116R) cancer cell lines. Findings confirmed enhanced expression of MDR1, MRP1, and BCRP efflux transporters, which actively decreased intracellular drug levels. Western blot analysis validated higher levels of MGMT and ERCC1, reflecting improved DNA repair capabilities. In addition, the co-culture system demonstrated that tumor microenvironment-induced fibroblast interactions and hypoxia conditions highly increased levels of HIF-1α, which augments resistance. CRISPR-Cas9 knockout of MDR1 and ERCC1 using CRISPR-Cas9 restored drug sensitivity and improved apoptotic responses. The findings emphasize the need for conjugated therapies involving efflux pumps, DNA repair mechanisms, and tumor microenvironment targets to effectively deliver cancer therapy. The next area of study would be incorporating nanotechnology-derived delivery systems with targeted treatment planning to deliver optimum therapeutic effects against drug-resistant malignancies.
Copyright (c) 2023 Saad Abdullah, Usama Raza (Author) https://creativecommons.org/licenses/by/4.0
VASCULAR COMPLICATIONS IN HEAD AND NECK CANCER THERAPY: AN OVERLOOKED BURDEN
Background: Head and neck cancer (HNC) therapy has advanced considerably, yet its long-term vascular complications remain an underappreciated determinant of survivorship. This study investigated the incidence, spectrum, and patient-reported burden of vascular complications arising from multimodal HNC treatment. Methods: A mixed-methods design was employed, integrating quantitative vascular imaging and outcome data with qualitative patient narratives. Quantitative analyses included carotid ultrasonography, CT/MR angiography, and clinical endpoints such as carotid artery stenosis, stroke, carotid blowout syndrome, and venous thrombosis. Qualitative data were obtained through semi-structured interviews, thematically analyzed to contextualize the quantitative findings. Results: Among survivors, clinically significant carotid artery stenosis (>70%) was detected in a notable proportion, with higher cumulative radiation doses and cisplatin exposure strongly associated with stenotic progression. Carotid blowout syndrome, although infrequent, demonstrated catastrophic outcomes with high morbidity and mortality. Venous complications, particularly jugular thrombosis, were more common in patients undergoing extensive surgery or combined chemoradiotherapy. Longitudinal data indicated a rising incidence of ischemic stroke with extended follow-up, emphasizing the chronic nature of vascular injury. Reconstructive flap analysis revealed compromised microvascular integrity in patients with higher vascular burden. Importantly, quality-of-life assessments and patient interviews highlighted significant declines in physical functioning, autonomy, and psychosocial well-being among those affected by vascular events. Integration of both data strands confirmed a consistent pattern in which treatment intensity correlated with vascular risk, while qualitative accounts underscored the overlooked humanistic dimension of these complications. Conclusions: Vascular complications represent a critical yet underrecognized outcome of HNC therapy, significantly impacting survival and quality of life. Structured vascular surveillance, preventive strategies, and multidisciplinary survivorship care are urgently needed to address this burden.
Copyright (c) 2023 Rabia Kiran, Hassan Yar Mahsood (Author) https://creativecommons.org/licenses/by/4.0
THE ROLE OF SLEEP DISORDERS IN THE DEVELOPMENT OF CARDIOMETABOLIC AND ONCOLOGIC DISEASES
Sleep disorders have emerged as significant contributors to the development of cardiometabolic and oncologic diseases in recent years. This study investigates the association between sleep disturbances and chronic health conditions, focusing on how alterations in sleep architecture, duration, and quality influence the pathophysiology of cardiovascular, metabolic, and cancerous conditions. Using a mixed-methods approach, including both qualitative evaluations and quantitative data from patient populations, the research reveals that sleep disorders such as insomnia, obstructive sleep apnea, restless leg syndrome, and circadian rhythm disruptions are strongly correlated with increased incidences of hypertension, myocardial infarction, type 2 diabetes, breast cancer, and colorectal cancer. Mechanistically, these associations are driven by systemic inflammation, oxidative stress, neurohormonal changes, and immune suppression. The study also examines behavioral, environmental, and genetic contributors that exacerbate sleep-related risks. Results from clinical data, predictive models, and patient-reported outcomes suggest that early identification and management of sleep disorders can play a vital role in reducing the burden of these chronic diseases. The findings advocate for integrated healthcare models that incorporate sleep assessments into routine cardiometabolic and oncologic screenings. Furthermore, it underscores the necessity of interdisciplinary collaboration between sleep medicine, oncology, endocrinology, and cardiology to enhance patient care and preventive strategies. Ultimately, this research emphasizes that sleep health is not a peripheral concern but a central pillar in the prevention and management of chronic illnesses in modern clinical practice.
Copyright (c) 2023 Syeda Iram Batool, Younas Rehman (Author) https://creativecommons.org/licenses/by/4.0
IMPACT OF DIABETES AND ENDOCRINE DISORDERS ON BREAST CANCER PROGRESSION AND OUTCOMES
The complex interplay between metabolic dysregulation and oncogenic pathways has positioned endocrine disorders, particularly diabetes mellitus and thyroid dysfunction, as critical modifiers of breast cancer progression and outcomes. This study employed a mixed-methods experimental design integrating clinical, biochemical, and behavioral data from 354 breast cancer patients, 42% of whom had confirmed endocrine comorbidities. Our quantitative analysis demonstrated that patients with type 2 diabetes exhibited a significantly higher incidence of advanced tumor grade (p < 0.001), greater lymph node involvement (p = 0.004), and reduced progression-free survival, particularly among postmenopausal women. Cox regression models revealed a 1.8-fold increased hazard ratio for mortality in diabetic patients after adjusting for age, stage, and receptor status. Additionally, thyroid dysfunction correlated with variability in estrogen receptor (ER) expression and tumor heterogeneity. Figures 2 through 13 visually captured critical associations between HbA1c levels, survival outcomes, hormonal profiles, and treatment toxicity using hybrid models including bar-line composites, scatter trends, and pie-plot distributions. Qualitative data from structured interviews revealed high rates of treatment non-adherence, increased psychological distress, and polypharmacy-induced side effects among patients with dual diagnoses. The results affirm that endocrine dysregulation significantly impacts breast cancer biology and therapy outcomes. These findings underscore the urgent need for integrated oncologic-endocrine clinical models to optimize care pathways, personalize treatment strategies, and improve survival rates for patients navigating the dual burden of breast cancer and metabolic-endocrine disorders.
Copyright (c) 2023 Muhammad Rehan, Muhammad Inam Farooq (Author) https://creativecommons.org/licenses/by/4.0
NEUROVASCULAR DYSFUNCTION IN PATIENTS WITH HEMATOLOGIC MALIGNANCIES
Neurovascular dysfunction is an increasingly recognized but insufficiently understood complication among patients with hematologic malignancies. This study utilized a mixed-methods approach to examine the prevalence, patterns, and predictors of neurovascular compromise in individuals diagnosed with leukemia, lymphoma, and multiple myeloma. Quantitative data included biomarker profiles, neurocognitive scoring, advanced neuroimaging, and clinical outcomes, while qualitative elements captured patient-reported neurological symptoms and functional impairments. Results from over 500 patients revealed that 62% exhibited measurable neurovascular abnormalities, with endothelial biomarkers such as sVCAM-1 and von Willebrand factor significantly elevated in affected cohorts (p < 0.01). MRI-based lesion mapping identified ischemic changes predominantly in subcortical regions, with white matter hyperintensities and microbleeds more prevalent in leukemia patients compared to lymphoma and myeloma. Notably, 73% of high-dose chemotherapy recipients experienced worsening perfusion metrics and neurocognitive scores post-treatment. Multivariate modeling demonstrated that comorbid hypertension and diabetes independently predicted neurovascular injury, while unsupervised clustering revealed three distinct neurovascular phenotypes with varying prognostic implications. Visualization of these trends via scatter plots, hybrid charts, and density maps confirmed statistically significant associations between biomarker elevation, lesion burden, and functional decline. Collectively, these findings highlight a pervasive and heterogeneous neurovascular burden in hematologic malignancy populations, emphasizing the need for early surveillance, risk stratification, and integrative care approaches. This study is one of the first to consolidate imaging, biochemical, and clinical data into a unified model of neurovascular pathology in this vulnerable patient group.
Copyright (c) 2023 Abdul Ghaffar, Roohan Ahmad (Author) https://creativecommons.org/licenses/by/4.0