Multimorbidity and its associated risk factors among older adults in India.

BACKGROUND: Health at older ages is a key public health challenge especially among the developing countries. Older adults are at greater risk of vulnerability due to their physical and functional health risks. With rapidly rising ageing population and increasing burden of non-communicable diseases older adults in India are at a greater risk for multimorbidities. Therefore, to understand this multimorbidity transition and its determinants we used a sample of older Indian adults to examine multimorbidity and its associated risk factors among the Indian older-adults aged 45 and above. METHODS: Using the sample of 72,250 older adults, this study employed the multiple regression analysis to study the risk factors of multimorbidity. Multimorbidity was computed based on the assumption of older-adults having one or more than one disease risks. RESULTS: Our results confirm the emerging diseases burden among the older adults in India. One of the significant findings of the study was the contrasting prevalence of multimorbidity among the wealthiest groups (AOR = 1.932; 95% CI = 1.824- 2.032). Similarly women were more likely to have a multimorbidity (AOR = 1.34; 95% CI = 1.282-1.401) as compared to men among the older adults in India. CONCLUSION: Our results confirm an immediate need for proper policy measures and health system strengthening to ensure the better health of older adults in India.

Sinapic Acid Ameliorates Oxidative Stress, Inflammation, and Apoptosis in Acute Doxorubicin-Induced Cardiotoxicity via the NF-κB-Mediated Pathway.

In the present study, we explored SA's activity against DOX-induced cardiotoxicity and revealed its underlying mechanisms. Male Wistar rats (weight, 190-210g; n = 6) were randomly divided into four groups: group I, normal control; group II, DOX 15 mg/kg via intraperitoneal (ip) route; group III, administered DOX+SA 20 mg/kg; and group IV, administered DOX+captopril (CAP 30 mg/kg). SA and CAP were administered orally for seven days, and DOX (15 mg/kg) was injected intraperitoneally an hour before SA treatment on the fifth day. Forty-eight hours after DOX administration, animals were anesthetized and sacrificed for molecular and histology experiments. SA significantly mitigated the myocardial effects of DOX, and following daily administration, it reduced serum levels of lactate dehydrogenase (LDH) and creatine kinase isoenzyme-MB to near normal values. Levels of oxidative stress markers, glutathione-peroxidase, superoxide dismutase, and catalase, in the cardiac tissue were significantly increased, whereas malondialdehyde levels decreased after SA treatment in DOX-administered rats. Furthermore, DOX caused an inflammatory reaction by elevating the levels of proinflammatory cytokines, tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and endothelin- (ET-) 1, as well as nuclear factor kappa-B (NF-κB) expression. Daily administration of SA significantly repressed TNF-α, IL-1ß, ET-1, and NF-κB levels. caspase-3 and Bax expression, bcl-2-like protein and caspase-3 activities and levels. Overall, we found that SA could inhibit DOX-induced cardiotoxicity by inhibiting oxidative stress, inflammation, and apoptotic damage.

Nanoparticles-mediated drug delivery approaches for cancer targeting: a review.

Cancer has become the leading cause of death among different populations of the world. The treatment is limited to chemotherapy, radiation, and surgery. Selective targeting to the tumor cells is possible by nanoparticles-based drug delivery system. It maximizes the drug concentration at the desired target and protects the surrounding healthy tissues at the same time. To improve the targeting potential of the anticancer drugs, nanoparticles were optimized for the size and surface characteristics to enhance their circulation time and targeting efficiency. Passive targeting involves surface modification with polyethylene glycol to avoid its elimination by natural body defense mechanism. Active targeting involves chemical interaction with certain antigen, receptors, and genes which are over expressed during progression of disease. In addition, the article highlights recent developments in "smart"-stimulus-responsive-drug carriers designed to enhance the localization and efficacy of therapeutic payloads as compared with free drug. Enhanced targeting potential, imaging, and controlled release of drugs or therapeutic molecules could be possible through multi-functional nanocarrier. Such multi-faceted, versatile nanocarriers and drug delivery systems promise a substantial increase in the efficacy of diagnostic and therapeutic applications in pharmaceutical sciences.

Protective effects of Pycnogenol on hyperglycemia-induced oxidative damage in the liver of type 2 diabetic rats.

Abnormal regulation of glucose and impaired carbohydrate utilization that result from a defective or deficient insulin are the key pathogenic events in type 2 diabetes mellitus (T2DM). Experimental and clinical studies have shown the antidiabetic effects of Pycnogenol (PYC). However, the protective effects of PYC on the liver, a major metabolic organ which primarily involves in glucose metabolism and maintains the normal blood glucose level in T2DM model have not been studied. The present study evaluated the beneficial effect of PYC, French maritime pine bark extract, on hyperglycemia and oxidative damage in normal and diabetic rats. Diabetes was induced by feeding rats with a high-fat diet (HFD; 40%) for 2 weeks followed by an intraperitoneal (IP) injection of streptozotocin (STZ; 40 mg/kg; body weight). An IP dose of 10mg/kg PYC was given continually for 4 weeks after diabetes induction. At the end of the 4-week period, blood was drawn and the rats were then sacrificed, and their livers dissected for biochemical and histopathological assays. In the HFD/STZ group, levels of glycosylated hemoglobin (HbA1c), significantly increased, while hepatic glycogen level decreased. PYC supplementation significantly reversed these parameters. Moreover, supplementation with PYC significantly ameliorated thiobarbituric reactive substances, malonaldehyde, protein carbonyl, glutathione and antioxidant enzymes [glutathione-S-transferase, catalase, superoxide dismutase, glutathione peroxidase and glutathione reductase] in the liver of HFD/STZ rats. These results were supported with histopathological examinations. Although detailed studies are required for the evaluation of the exact protective mechanism of PYC against diabetic complications, these preliminary experimental findings demonstrate that PYC exhibits antidiabetic effects in a rat model of type 2 DM by potentiating the antioxidant defense system. These finding supports the efficacy of PYC for diabetes management.

Nephroprotective action of tocotrienol-rich fraction (TRF) from palm oil against potassium dichromate (K 2 Cr 2 O 7)-induced acute renal injury in rats.

Industrial and occupational exposure to chromium compounds, particularly hexavalent chromium (Cr(VI))-containing compounds are often known to cause acute renal injury (ARI) in humans and animals. Its nephrotoxicity is associated with an increased formation of reactive oxygen species and lipid peroxidation in renal tissue. Recent studies suggest that antioxidants of the vitamin E family have protective effects against metal toxicity. Tocotrienols are known to have greater antioxidant activity than tocopherols and protect more efficiently against some free radical-related diseases than does tocopherols. In the present study, ARI induced by potassium dichromate (K(2)Cr(2)O(7)) has been used as a model to investigate the possible nephroprotective effect of tocotrienol-rich fraction (TRF) from palm oil. Wistar male rats having an average body weight (bw) of 210 g were divided into four groups. The first group was taken as control and injected with vehicle alone while the second group was drug control and ingested with TRF (200mg/kg, bw, orally, once daily for 21 days); the third group served as toxicant and was pre-treated with saline, followed by a single subcutaneous (SC) injection of K(2)Cr(2)O(7) (15 mg/kg bw). The fourth group was pre-treated with TRF and subsequently injected with K(2)Cr(2)O(7) (same dose as for the third group). Renal functions, oxidative and nitrosative stress were evaluated on days 0, 1, 2, 4, 7, 11 and 14 after treatment with K(2)Cr(2)O(7). The results revealed altered proximal tubular function; decreased glomerular filtration accompanied by oxidative damage 48 h after exposure to dichromate; while in the TRF-treated group proximal reabsorptive function, glomerular function and the cellular redox status were sustained. These results were further supported and confirmed by histological findings. The study suggests that TRF is effective in preventing K(2)Cr(2)O(7)-induced acute renal injury, but more studies are needed to confirm the effects of TRF as a nephroprotective agent.

Pycnogenol prevents potassium dichromate K2Cr2O7-induced oxidative damage and nephrotoxicity in rats.

Environmental and occupational exposure to chromium compounds, especially hexavalent chromium [Cr(VI)], is widely recognized as a potential nephrotoxic in humans and animals. Its toxicity is associated with overproduction of free radicals, which induces oxidative damage. Recent evidence indicates that Pycnogenol (PYC), French maritime pine bark extract, exhibits antioxidant potential and protects against various oxidative stressors. The aim of the present study was to examine the modulating impacts of PYC on potassium dichromate K2Cr2O7-induced oxidative damage and nephrotoxicity in rats. Male Wistar rats were divided into four groups. The first group was control, the second group was control plus pre-treated with PYC (10 mg/kg, body weight; in saline; intraperitoneally; once daily for 3 weeks) as drug control and the third group was saline pre-treated plus treated with a single injection of K2Cr2O7 (15 mg/kg, body weight; in saline; intraperitoneally) as toxicant group. The fourth group was PYC pre-treated plus K2Cr2O7 injected. Forty-eight hours after K2Cr2O7-treatment, blood was drawn for estimation of renal injury markers in serum. Rats were then sacrificed, and their kidneys were dissected for biochemical and histopathological assays. K2Cr2O7-treated rats showed significant increases in markers of renal injury in serum, including blood urea nitrogen (BUN), serum creatinine (Scr), and alkaline phosphatase (ALP), which were significantly (P < 0.05) decreased by PYC pre-treatment. Moreover, prophylactic pre-treatment of rats with PYC significantly (P < 0.05) ameliorated increased thiobarbituric reactive substances (TBARS), malonaldehyde (MDA) and protein carbonyl (PC), and decreased levels of glutathione (GSH) and catalase activity in the kidney homogenate of K2Cr2O7-treated rats. These results were also supported and confirmed with histopathological findings. The study suggests that PYC is effective in preventing K2Cr2O7-induced oxidative mediated nephrotoxicity, but more studies are needed to confirm the effects of PYC as a nephroprotective agent.