Caffeic acid (3,4-dihydroxy cinnamic acid) (CA) is naturally found in fruits, vegetables, olive oil, and coffee. This study was undertaken to evaluate the anticancer effect of caffeic acid on HT-1080 human fibrosarcoma cell line. The antiproliferative effect of caffeic acid was determined by MTT assay, and the oxidative stress was determined by lipid peroxidation, changes in the enzymatic, and non-enzymatic antioxidant status. To understand the mode of antiproliferative effect of CA, the authors observed intracellular ROS levels by DCFH-DA method, mitochondrial membrane potential alterations by Rh-123 staining, oxidative DNA damage by comet assay, and apoptotic morphological changes by AO/EtBr-staining method. The results show that caffeic acid enhances lipid peroxidative markers such as TBARS, CD, and LHP in HT-1080 cell line. Caffeic acid enhances the ROS levels, which is evidenced by the increased DCF fluorescence. Further, caffeic acid treatment altered the mitochondrial membrane potential in HT-1080 cells. Similarly, the authors observed increased oxidative DNA damage (% Tail DNA, % Tail length, Tail moment, and olive tail moment), and apoptotic morphological changes in caffeic acid-treated groups. These data suggest that caffeic acid exhibits potent anticancer effect in HT-1080 cell line, and that it may be used as an anticancer agent.

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The present review has been focused largely on the sex type differences in beef quality among heifers, cows, steers and bulls in various feeding environments. Genetic groups, feeding systems and gender are the major factors that change carcass characteristics and fatty acid profiles of cattle. Studies identified that heifer beef has super characteristics in eating quality and a better healthy composition in fatty acids than steer, cow and bull. Diet influences the variation of fatty acid profile; particularly the level of polyunsaturated fatty acids (PUFA) interacts with breed and sex. Animals finished in pasture systems were reported to show better ratios of PUFA/ saturated fatty acids and n-6/n-3. Carcasses of roughage-fed beef are lighter and have less marbling and lower quality grades but have higher cutability than carcasses of grain-fed bulls. Heifers and cows are reported to deposit more fat than steers and bulls. Among males, lower production of testosterone by steers favors more fat thickness compared with bulls. Marbling greatly varies among cattle belonging to different sexes, and particularly, females have genetic makeup that efficiently controls deposition. The current review identified that heifers can be a premium beef brand, while steer beef currently take a large part of market share across the world.

Myocardial infarction is a pathological state which occurs due to severe abrogation of the blood supply (ischemia) to a part of heart, which can cause myocardial damage. The short intermittent cycles of sub-lethal ischemia and reperfusion has shown to improve the tolerance of the myocardium against subsequent prolonged ischemia/reperfusion (I/R)-induced injury, which is known as ischemic preconditioning (IPC). Although, IPC-induced cardioprotection is well demonstrated in various species, including human beings, accumulated evidence clearly suggests critical abrogation of the beneficial effects of IPC in diabetes mellitus, hyperlipidemia and hyperhomocysteinemia. Various factors are involved in the attenuation of the cardioprotective effect of preconditioning, such as the reduced release of calcitonin gene-related peptide (CGRP), the over-expression of glycogen synthase kinase-3β (GSK-3β) and phosphatase and tensin homolog (PTEN), impairment of mito-KATP channels, the consequent opening of mitochondrial permeability transition pore (MPTP), etc. In this review, we have critically discussed the various signaling pathways involved in abrogated preconditioning in chronic diabetes mellitus, hyperlipidemia and hyperhomocysteinemia. We have also focused on the involvement of PTEN in abrogated preconditioning and the significance of PTEN inhibitors.

The aim of the study was to develop PVA-CS hydrogel scaffolds using glutaraldehyde as a cross-linking agent by chemical crosslinking method in order to obtain biomimetic scaffolds for articular cartilage regeneration. The introduction of PVA enhances the mechanical and bioadhesive properties to the native tissue while chondroitin sulphate enhances the glycosaminoglycan content of extracellular matrix. The role of hydrogel as cartilage regeneration scaffold was evaluated by swelling study, porosity, rheological behaviour, in vitro degradation, and quantification of released chondroitin sulphate. In vivo results showed that cross-linked hydrogels repaired defects with no sign of inflammation as it was well anchored to tissue in the formation of new articular surface. It may be concluded that the addition of chondroitin sulphate to the PVA polymer develops a novel composite with significant applications in cartilage tissue engineering.

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Diabetes and smoking have been considered as major health problems individually and their seriousness related to health hazard has been well reported. The role of nicotine in causing or worsening effect on diabetes is not well understood. The aim of our study was to investigate the effect of nicotine on experimental diabetes and to analyze the effect of bis-1,7-(2-hydroxyphenyl)-hepta-1,6-diene-3,5-dione a bisdemethoxy curcumin analog (BDMCA) in streptozotocin and nicotine induced toxicity. Group I: control rats; Group II: nicotine (2.5 mg/kg b.wt); Group III: streptozotocin (STZ) (40 mg/kg b.wt); Group IV: STZ (40 mg/kg b.wt) + nicotine (2.5 mg/kg b.wt); Group V: STZ + nicotine + BDMCA (40 mg/kg b.wt); Group VI: STZ + nicotine + BDMCA (80 mg/kg b.wt). Efficacy of BDMCA was determined by evaluating blood glucose, thiobarbituric acid reactive substances (TBARS), hydroperoxides (HP), activities of marker enzymes alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) and activities of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). From our study, we have observed that nicotine not only aggravates diabetic complications but also increased the risk for diabetes. BDMCA, at a dose 80 mg/kg body weight was found to be more effective in decreasing toxic effects induced by nicotine and STZ.