Insulin resistance (IR) is a significant factor in the development and progression of metabolic-related diseases like dyslipidemia, T2DM, hypertension, nonalcoholic fatty liver disease, cardiovascular and cerebrovascular disorders, and cancer. The pathogenesis of IR depends on multiple factors, including age, genetic predisposition, obesity, oxidative stress, among others. Abnormalities in the insulin-signaling cascade lead to IR in the host, including insulin receptor abnormalities, internal environment disturbances, and metabolic alterations in the muscle, liver, and cellular organelles. The complex and multifaceted characteristics of insulin signaling and insulin resistance envisage their thorough and comprehensive understanding at the cellular and molecular level. Therapeutic strategies for IR include exercise, dietary interventions, and pharmacotherapy. However, there are still gaps to be addressed, and more precise biomarkers for associated chronic diseases and lifestyle interventions are needed. Understanding these pathways is essential for developing effective treatments for IR, reducing healthcare costs, and improving quality of patient life.

Insulin resistance (IR) is a significant factor in the development and progression of metabolic-related diseases like dyslipidemia, T2DM, hypertension, nonalcoholic fatty liver disease, cardiovascular and cerebrovascular disorders and cancer. The pathogenesis of IR depends on multiple factors including age, genetic predisposition, obesity, oxidative stress and other factors. Abnormalities in the insulin signaling cascade lead to IR in the host, including insulin receptor abnormalities, internal environment disturbances, and metabolic alterations in the muscle, liver and cellular organelles. The complex and multifaceted characteristics of insulin signaling and insulin resistance envisage its thorough and comprehensive understanding at the cellular and molecular level. Therapeutic strategies for IR include exercise, dietary interventions and pharmacotherapy. However, there are still gaps to be addressed, and more precise biomarkers for associated chronic diseases and lifestyle interventions are needed. Understanding these pathways is essential for developing effective treatments for IR, reducing healthcare costs and improving quality of patient life.

Bronchogenic cyst usually presents along the tracheobronchial tree. Rarely, it is found inside peritoneal cavity. Here is a case of 30-year-old man who presented with concerns of abdominal pain. On evaluation, contrast-enhanced CT scan showed hypodense cystic lesion in epigastric region related to right crus of diaphragm. The patient underwent laparoscopic marsupialization/deroofing of cyst. Histopathological examination of resected specimen showed respiratory epithelium. Postoperative period was uneventful.

Objective: To investigate the effect of Camellia (C.) sinensis in mitigating oxidative damage and reproductive toxicity in testis induced by sodium fluoride in a rat model. Methods: Twenty-four adult male Wister rats were divided into 4 groups, with 6 rats in each group. Group 1 orally received distilled water (1 mL/100 g body weight) daily and served as the control group, while group 2 received drinking water with 100 ppm sodium fluoride per day for 21 consecutive days, group 3 was administered with only C. sinensis extract by gavage at a dose of 100 mg/kg body weight and group 4 received drinking water with 100 ppm sodium fluoride and 100 mg/kg body weight C. sinensis leaf extract per day for 21 consecutive days. At the end of the treatment, the rats were sacrificed under light ether anesthesia. The gonado-somatic index, sperm count and motility, serum level of luteinizing hormone and testosterone were assayed. Lipid peroxidation [malondialdehyde (MDA) level], nitric oxide (NO) production, and activities of antioxidant enzymes - superoxide dismutase (SOD), catalase, and reduced glutathione level (GSH) were also analysed. Results: Sodium fluoride treatment significantly decreased gonado-somatic index, sperm count and motility as well as the serum level of luteinizing hormone and testosterone (P<0.05). The histological examination of testes revealed atrophy and degenerative changes in several seminiferous tubules, along with enhanced interstitial space and a reduced number of Leydig cells. There was a highly significant increase in NO and MDA production (P<0.05), while SOD, catalase activities and GSH level decreased significantly (P<0.05). However, C. sinensis significantly restored testicular weight, sperm parameter, hormonal level (P<0.05), and also reversed MDA and NO generation and antioxidant enzymes activities in the testicular tissue (P<0.05). Conclusions: C. sinensis may have an ameliorative role against sodium fluoride-induced oxidative damage in the testis probably because of its antioxidant property.

Prostate cancer remains one of the most biologically heterogeneous malignancies in men and continues to present major therapeutic challenges despite advances in androgen receptor-targeted therapy and molecular stratification. Increasing evidence suggests that prostate cancer progression is influenced not only by tumor-intrinsic genetic alterations but also by complex interactions involving androgen receptor signaling, inflammatory pathways, metabolic reprogramming, oxidative stress, epigenetic remodeling, immune dysregulation, and gut microbiome-associated signaling. Within this evolving systems-level framework, natural products have attracted increasing attention because of their ability to modulate multiple interconnected molecular pathways. This review examines the molecular basis of prostate cancer progression with particular emphasis on crosstalk among androgen receptor signaling, microbiome-associated regulation, epigenetic adaptation, inflammatory signaling, and tumor microenvironment remodeling. The emerging role of the gut microbiome in androgen metabolism, microbial metabolite production, immune regulation, and endocrine resistance is critically discussed, together with current evidence describing the biological effects of selected phytochemicals including curcumin, epigallocatechin-3-gallate, resveratrol, sulforaphane, quercetin, and genistein. These compounds may influence prostate cancer-associated pathways through modulation of inflammatory signaling, oxidative stress, metabolic adaptation, chromatin remodeling, and microbiome dynamics. Major translational limitations including poor bioavailability, pharmacokinetic variability, microbiome heterogeneity, inconsistent clinical evidence, and incomplete mechanistic understanding are additionally discussed. Rather than considering natural products as isolated anticancer agents, this review adopts a systems-level perspective in which dietary bioactive compounds may function as modulators of interconnected regulatory networks relevant to prostate cancer biology and therapeutic responsiveness.