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Since the discovery of the dystrophin gene (DMD gene) thirty years ago, several therapeutic approaches have been investigated to treat Duchenne muscular dystrophy (DMD). This includes cell therapy, exon jumping, exonic knockout, and the CinDel method. In this article, we present the challenges of developping a treatment for DMD and the advances of these various approaches. We included the new CRISPR-Cas9 system, which permits not only major progress in the development of new treatments based on genome editing but also the production of new animal models.

Bipolar disorder (formerly called manic-depressive illness or manic depression) is a mental disorder that causes unusual shifts in mood, energy, activity levels, concentration, and the ability to carry out day-to-day tasks. During mood swings, there may be features of psychosis (delusions and hallucinations) that are mood-congruent. Although psychotic symptoms are seen only in a minority of patients, they explain the early terminology of manic–depressive psychosis. Stage 1a is defined as mild or non-specific symptoms of mood disorder and intervened as formal mental health literacy; family psychoeducation; substance abuse reduction; cognitive behavioral therapy. Euphoric means the experience of pleasure or excitement and intense feelings of well-being and happiness. Certain natural rewards and social activities, such as aerobic exercise, laughter, listening to or making music, and dancing, can induce a state of euphoria. Racing thoughts are consistent, persistent, often intrusive thoughts that come in rapid succession. There is a direct link between depression and anxiety and racing thoughts. Whereas jumping from topic to topic as in the flight of ideas can be observed by others, ascertainment of racing thoughts requires asking the child whether his or her thoughts seem to be going too fast.

Introduction: Candidiasis is more frequent in human immunodeficiency virus (HIV)-infected patients and knowledge about the distribution and antifungal susceptibility of oral Candida species is important for effective management of candidiasis. Material and Methods: An oral rinses sample collected from hundred HIV-infected patients with and without clinical evidence of oral candidiasis in this study at the Infectious Department/Tripoli Medical Center, Libya. Species identified by standard phenotypic and conventional methods and in vitro susceptibility testing of the yeast isolates to antifungals were performed using the Disc diffusion method protocol as recommended by the Clinical Laboratory Scientific Institute. Results: Oral Candida colonization is detected in all patients with and without clinical syndromes, and Candida albicans were accounted for (74%), C. dubliniensis (11%) and C. glabrata (6%). A high proportion of Candida species (42%) showed decreased susceptibility to fluconazole. Among C., albicans more than 30% of isolate were resistant to most new azole antifungal including fluconazole, itraconazole, posoconazole and voriconazole. Conclusions: A significant number of oral Candida species particular Candida albicans exhibiting decreased susceptibility to fluconazole were isolated from colonized HIV-infected individual, given the high incidence and severity of fungal infections in HIV-infected individuals. The results of this study reinforce the importance of antifungal susceptibility testing, which contributes to the therapeutic strategies and highlights the need for continuous surveillance of Candida colonization in this population.

The present study aimed to investigate and identify the association between the intake of allium vegetables and colorectal cancer (CRC) in population. A hospital‐based matched case‐control study was conducted between June 2009 and November 2011 in three hospitals. Eight hundred thirty three consecutively recruited cases of CRC were frequency matched to 833 controls by age (within 2.5 years of difference), sex, and residence area (rural/urban). Demographic and dietary information were collected via face‐to‐face interviews using a validated food frequency questionnaire. Adjusted odds ratios (aORs) and 95% confidence intervals (CIs) were estimated by using unconditional logistic regression.

Acute pulmonary damage and vascular coagulopathy appear to be frequent in patients with SARS-CoV-2 infection relation to corona-virus. The inflammatory process accompanying the infection and excessive coagulation state is one of the most important causes of patient loss.

Background: Nicotinamide adenine dinucleotide (NAD⁺) is a pivotal coenzyme and signaling substrate that integrates redox balance with mitochondrial energy production, DNA repair, epigenetic control, and cellular stress resilience. Declines in NAD⁺ availability—frequently observed with ageing, chronic inflammation, and metabolic stress—have intensified interest in NAD⁺ restoration as a potential strategy to influence disease biology across multiple organ systems.Objective: This narrative review summarizes contemporary mechanistic and translational evidence on NAD⁺ biosynthesis and turnover, highlighting the de novo kynurenine pathway and vitamin B3–dependent salvage routes (nicotinic acid, nicotinamide, nicotinamide riboside, and nicotinamide mononucleotide). We also examine how major NAD⁺ consumers and sensors, sirtuins, poly(ADP-ribose) polymerases (PARPs), and CD38 link NAD⁺ status to inflammation, oxidative stress, and tissue dysfunction in diverse clinical contexts.Methods: Peer-reviewed literature on NAD⁺ metabolism, NAD⁺-dependent signaling, and preclinical/clinical studies of NAD⁺ precursors was evaluated and organized into: (i) core biochemical functions in cellular energetics, (ii) NAD⁺ consumption in genome maintenance and immune signaling, and (iii) organ-focused evidence relevant to skin disorders, infertility and reproductive health, osteoarthritis, hearing loss, vision decline, gut barrier dysfunction, cardiovascular and renal metabolism, hepatic steatosis, neurological diseases, and skeletal muscle health.Results: NAD⁺ supports glycolysis, the tricarboxylic acid cycle, and oxidative phosphorylation, while acting as an essential substrate for PARP-driven DNA repair and sirtuin-mediated deacylation programs that shape mitochondrial fitness, inflammatory tone, and metabolic flexibility. Across experimental models, impaired NAD⁺ homeostasis repeatedly associates with mitochondrial dysfunction, heightened oxidative injury, and dysregulated immune–barrier responses, features shared by intestinal inflammation, neurodegeneration and ischemic injury, cardiometabolic disease, kidney injury, and fatty liver disease. Supplementation with NAD⁺ precursors (notably NR and NMN) reliably elevates NAD⁺ in preclinical systems and increases circulating NAD⁺ metabolites in humans, with early signals of pathway engagement; however, clinical outcomes remain heterogeneous across populations, dosing regimens, and endpoints. Evidence for intravenous NAD⁺ “drip” therapy is comparatively limited and insufficiently standardized, with constraints related to tolerability, dose consistency, and cost, underscoring the need for controlled trials.Conclusion: NAD⁺ occupies a central position at the interface of energy metabolism, genome integrity, and immunometabolic signaling, providing a coherent framework for understanding how cellular stress can propagate multisystem dysfunction. Although NAD⁺-boosting strategies are biologically plausible and mechanistically supported, definitive clinical benefit across skin, fertility, osteoarthritis, sensory decline, gut disorders, cardiovascular and hepatic disease, neurological conditions, and muscle health will require well-designed human studies with standardized biomarkers, safety surveillance, and clinically meaningful endpoints.

We report a rare case of 62-year-old South Asian women who visited the Molecular Pathology and Genomics Department for hereditary germline cancer genetic testing after being diagnosed with oesophageal cancer, reported as invasive keratinizing squamous cell carcinoma metastasized to the lymph nodes. Her personal history revealed that she was diagnosed with triple-negative breast cancer five years before oesophageal cancer. Germline cancer testing showed pathogenic variants in BRCA1 gene c.68_69delAG, which proved it a hereditary breast and ovarian cancer syndrome. She was started on PARP inhibitors but developed some secondary respiratory failure and succumbed to death. Less than 10 cases have been reported in the literature of the association of germline BRCA1 and Squamous cell Carcinoma – the esophagus. The article focuses on the probable pathogenesis of BRCA1 mutation with non-classic malignancies and the response of Poly adenosine diphosphate ribose polymerase inhibitors (PARP) inhibitors in such a scenario. We report an unusual manifestation of the BRCA1 gene with second primary oesophageal squamous cell cancer occurring five years later to triple-negative breast cancer.

The spleen plays a pivotal role in our immune system by facilitating the proliferation and differentiation of lymphocytes and monocytes. Typically located in the left upper quadrant retroperitoneally, splenic tissue found outside of its usual position is termed ectopic spleen. When the tissue maintains its histological architecture and encapsulation and receives blood supply from splanchnic vessels, it is called an accessory spleen. Although it commonly presents near the splenic hilum or pancreatic tail, rare instances have been reported in the gastric, liver, gastrosplenic/lienorenal ligaments, as well as thoracic and gonadal regions. However, the case of an accessory spleen, mimicking a hepatic lesion in the right diaphragm represents a novel observation.

The incidence of heart failure with preserved ejection fraction (HFpEF) continues to rise, and obesity continues to be a predominant comorbid condition affecting patients with HFpEF. Recent research sheds light on the important pathophysiologic role that obesity plays in the development of HFpEF, with many areas of opportunity existing for future developments in understanding the etiology and management of the disease. Crucial in these pathophysiologic developments are studies that clearly characterize the obesity phenotype in HFpEF and compare it to presentations of HFpEF in patients without obesity. This paper reviews the existing literature on the obesity phenotype within HFpEF and discusses some of the prevailing ideas behind the pathophysiologic interplay between the conditions, as well as the existing treatments demonstrating improved outcomes in HFpEF.

The integration of deep learning and genetic analysis has transformed the assessment of elite sports performance, particularly in competitive swimming. This study examines the fusion of deep learning techniques with DNA markers, physiological biometrics, and performance analytics to enhance the prediction and optimization of swimmer performance. A structured dataset comprising genetic sequences, physiological parameters, and biomechanical attributes was utilized to train a neural network model capable of categorizing swimmers based on genetic predisposition and athletic potential. The model achieved high classification accuracy, demonstrating a strong link between genetic markers, physiological traits, and competitive swimming outcomes. The findings emphasize the potential of AI-driven analytics in talent identification, customized training adaptations, and injury prevention. Furthermore, the study highlights the effectiveness of deep learning in analyzing complex genomic and physiological data to generate meaningful insights for performance enhancement. While the results validate the feasibility of using genetic and AI-based models for performance prediction, further studies are needed to broaden dataset diversity, integrate epigenetic influences, and test the model across varied athlete populations. This research contributes to the expanding field of AI-driven sports science and provides a solid foundation for incorporating genomics with deep learning to enhance elite athletic performance.