Cancer is one of the major causes of deaths in developed countries and is emerging as a major public health burden in developing countries too. Changes in cancer prevalence patterns have been noticed due to rapid urbanization and changing lifestyles. One of the major concerns is an influence of dietary habits on cancer rates. Approaches to prevent cancer are many and chemoprevention or dietary cancer prevention is one of them. Therefore, nutritional practices are looked at as effective types of dietary cancer prevention strategies. Attention has been given to identifying plant-derived dietary agents, which could be developed as a promising chemotherapeutic with minimal toxic side effects. Naringenin, a phytochemical mainly present in citrus fruits and tomatoes, is a frequent component of the human diet and has gained increasing interest because of its positive health effects not only in cancer prevention but also in noncancer diseases. In the last few years, significant progress has been made in studying the biological effects of naringenin at cellular and molecular levels. This review examines the cancer chemopreventive/therapeutic effects of naringenin in an organ-specific format, evaluating its limitations, and its considerable potential for development as a cancer chemopreventive/therapeutic agent.

Introduction: Type 2 diabetes (T2DM), which is more prevalent (more than 90% of all diabetes cases) and the main driver of the diabetes epidemic, now affects 5.9% of the world’s adult population, with almost 80% of the total in developing countries. At present, 537 million adults (20–79 years) are living with diabetes—1 in 10. This number is predicted to rise to 643 million by 2030 and 783 million by 2045. In India, reports show that 69.2 million people are living with diabetes (8.7%) as per 2015 data. Long-term metformin treatment is a known pharmacological cause of vitamin B12 (Vit B12) deficiency, as was evident within the first 10–12 years after it started to be used. Methods: This was a cross-sectional study conducted in the Postgraduate Department of Medicine in one of the tertiary hospitals in Kashmir. A total of 1600 consecutive patients with T2DM were taken for the study. Out of which 700 patients met the inclusion criteria. These 700 patients were divided into two groups: those taking metformin, and those who were not on metformin. Cumulative metformin doses were recorded in patients taking metformin, using history of dose and duration of treatment. Serum Vit B12 levels were taken for all patients. Based on the results of Vit B12 levels, patients were classified into normal levels (20 pmol/L), possible B12 deficiency (150–220 pmol/l), and definite deficiency (<150 pmol/L). Results: Our results depicted that patients on prolonged metformin therapy showed an increase in Vit B12 deficiency by 11.16%. The prevalence of clinical neuropathy in the metformin-exposed group was 45%, whereas, a prevalence of 31.8% was found in the non-metformin group. The mean age of patients with neuropathy was higher than those without neuropathy (59.01 ± 7.14 vs. 49.95 ± 7.47) (p-value < 0.514, statistically insignificant). Conclusions: In our study, we found that metformin use is associated with Vit B12 deficiency, which is dependent upon the cumulative dose of metformin. Importantly, prolonged metformin use is also associated with an increase in the prevalence of clinical neuropathy.

Introduction: Rheumatoid arthritis (RA) is a common autoimmune illness that manifests mostly as chronic, symmetric, and progressive polyarthritis with a global frequency of 0.3–1.0%. RA is a disease that affects people all over the world. In India, the prevalence is estimated to be 0.7%, with around 10 million persons suffering from RA. Most people with rheumatoid arthritis experience fatigue on most days, with over 70% experiencing symptoms similar to chronic fatigue syndrome. Patients rate fatigue as a top priority and believe this unmanageable symptom is ignored by clinicians; a systematic review shows the biological agents for RA inflammation have only a small effect on fatigue. Fatigue predicts and reduces the quality of life, and it is as difficult to cope with as pain. Physicians have traditionally concentrated on the inflammatory aspects of the illness (e.g., synovitis), whereas RA patients have prioritized pain, exhaustion, sleep difficulties, and other quality-of-life issues. Aims and Objectives: The basic aim of the study was to access the incidence of fatigue in rheumatoid arthritis and evaluate its impact on the quality of life in these patients using the MAF scale (multidimensional assessment of fatigue) after prior permission for the first time in an Asian population. Results: A total of 140 subjects and 100 controls were included in the study. Age was closely matched between the study subjects and controls. Among study subjects with the disease, 94 (67%) had a disease duration ≤ 5 years, 26 (19%) had a disease duration between 6–10 years, 10 (7%) had a duration of 11–15 years and 10 (7%) had >10 years disease duration. Among the sample, 31 (25%) study subjects had a DAS score ≤ 4.0, 63 (50%) study subjects had a DAS score (disease activity score) between 4.01 and 6.0, and in the remaining 31 (25%) study subjects, the DAS score was >6.0. The mean DAS score among study subjects was 4.96, and the study subjects had a mean activity of daily living (ADL) score of 11.64; controls had a mean score of 2.42 with a statistically significant p-value. The global fatigue index was higher in study subjects, with a mean of 33.16 in contrast with a mean of 14.41 in the controls with a significant p-value. Conclusion: Our study fatigue was a persistent problem, despite treatment. The median level of fatigue experienced by study subjects with RA was high. Therefore, as persistent fatigue is associated with functional loss, fatigue in RA remains an ‘unmet need’ and continues to be ignored by clinicians.

Metabolic syndrome (MS) is a cluster of conditions including central obesity, hypertriglyceridemia, low HDL cholesterol, hyperglycaemia, and hypertension with a prevalence rate of 20–25% of the world’s adult population. Metabolic syndrome is often characterized by insulin resistance, which some have suggested is a major supportive connection between physical inactivity and MS. Various studies suggest that moderately elevated iron and ferritin levels are associated with an increased prevalence of metabolic syndrome and are markers of insulin resistance. Increased body iron stores are associated with the development of glucose intolerance, type 2 diabetes mellitus, and insulin resistance syndrome (IRS). This is a hospital-based cross-sectional observational study, which was conducted in the department of internal medicine of a tertiary care hospital in northern India. The study was conducted from 1 January 2019 to 30 June 2020 and included 100 patients and 100 controls. All subjects in the age group of 35–65 years were enrolled and investigated as per the study design. Metabolic syndrome patients were diagnosed according to the modified National Cholesterol Education Program Adult Treatment Panel-III (NCEP ATP-III) with BMI >23 kg/m2. All baseline investigations were undertaken, including serum ferritin levels. Insulin resistance (IR) was calculated using the homeostasis model assessment IR (HOMA-IR) formula. We found a positive association between an increase in serum ferritin with the prevalence of metabolic syndrome and its clinical parameter. The serum ferritin level was positively correlated with the level of insulin resistance and inversely correlated with the insulin level of the patients.

Purpose: Doxorubicin (DOX) is a commonly used chemotherapeutic agent to treat several malignancies, including aggressive tumors like triple negative breast cancer (TNBC) lacking hormonal receptors and HER2 amplification. It has a limited therapeutic index owing to its extreme toxicity and the emergence of drug resistance. As a result, there is a pressing need to find innovative drugs that enhance the effectiveness of doxorubicin while minimizing its toxicity. Recently, the third-generation retinoid adapalene (ADA) was reported as an effective anticancer agent in several malignancies. This study aimed to determine the anticancer activity of ADA in TNBC cells and its effectiveness in combination with DOX and the mechanistic pathways in inhibiting tumorigenicity.Methods: Cell viability was evaluated using the 3-(4,5-Dimethylthiazol-2-Yl)-2,5-Diphenyltetrazolium (MTT) and pharmacodynamic interactions (synergism, antagonism, or additivity) by Chou-Talalay's method. Flow cytometry and fluorimetry were used to determine apoptosis, cell cycle and reactive oxygen species (ROS). Western blotting was utilized to analyze the molecular mechanism and apoptotic protein levels.Results: We found that ADA in synergistic manner with doxorubicin inhibits growth, colony formation, and migration of TNBC cells. Moreover, ADA as single agent or in combination with DOX resulted in ROS accumulation triggering hyperphosphorylation of Erk1/2 and activating caspase 3 and apoptosis. N-acetyl-L-cysteine (NAC) pre-treatment inhibited ROS accumulation triggered by DOX-ADA and substantially reduced Erk1/2 phosphorylation.Conclusions: Our results demonstrate that ADA is a potent antitumor agent that may be used as a single agent or combined with present therapeutic regimens for TNBC treatment.