Replication stress promotes cell elimination by extrusion.

Cell extrusion is a mechanism of cell elimination that is used by organisms as diverse as sponges, nematodes, insects and mammals. During extrusion, a cell detaches from a layer of surrounding cells while maintaining the continuity of that layer. Vertebrate epithelial tissues primarily eliminate cells by extrusion, and the dysregulation of cell extrusion has been linked to epithelial diseases, including cancer.

Neurohormonal signaling via a sulfotransferase antagonizes insulin-like signaling to regulate a Caenorhabditis elegans stress response.

Insulin and insulin-like signaling regulates a broad spectrum of growth and metabolic responses to a variety of internal and environmental stimuli. For example, the inhibition of insulin-like signaling in C. elegans mediates its response to both osmotic stress and starvation.

Protective role of ceftriaxone plus sulbactam with VRP1034 on oxidative stress, hematological and enzymatic parameters in cadmium toxicity induced rat model.

We investigated the protective role of ceftriaxone plus sulbactam with VRP1034 (Elores) on hematological, lipid peroxidation, antioxidant enzymatic activities and Cd levels in the blood and tissues of cadmium exposed rats. Twenty-four male rats were divided into three groups of eight rats each. The control group received distilled water whereas group II received CdCl2 (1.

Sub-acute toxicity study of a new aminoglycoside etimicin sulphate in swiss albino mice.

Etimicin sulfate, an ethylization derivative of gentamicin, is a new soluble wide-spectrum synthetic aminoglycoside drug. It has wide antibacterial spectrum with high effect and less cross resistance as compared to other aminoglycosides. In order to further explore its safety and tolerance, we have conducted a subactute toxicity study on swiss albino mice.

Pharmacokinetic study of sulbactomax.

We have evaluated pharmacokinetics of a fixed dose combination (FDC) of ceftriaxone and sulbactam (2:1) or sulbactomax in eight healthy volunteers. A 1.5 g dose of sulbactomax, 1 g dose of ceftriaxone and 0.

Ceftriaxone-vancomycin drug toxicity reduction by VRP 1020 in Mus musculus mice.

Drug toxicity is a common cause of liver injury and kidney failure. This study was designed to elucidate whether administration of high doses of Ceftriaxone or Vancomycin induce oxidative stress in liver as well as kidney, and to investigate the protective effects of VRP 1020 with fixed dose combination of ceftriaxone-vancomycin (Immunox-V). Twenty four Mus musculus mice (weighing 30 +/- 5 g) were divided into four groups containing six mice in each group.

Fixed dose combination of cefepime plus amikacin prevent oxidative stress in liver of Mus musculus mice.

Oxidative stress and free radical are causative factors for aminoglycoside induced tissue injury. The objective of present study was to evaluate effect of fixed dose combination of cefepime + amikacin on antioxidant enzymes such as superoxide dismutase (SOD), catalase along with malonaldialdehyde (MDA) levels in liver of Mus musculus mice. Our findings showed that the activities of the antioxidant enzymes such as superoxide dismutase (p<0.

Effect of vitamin E on platelet enzymatic anti-oxidants in the patients of myocardial infarction.

Effect of administration of 600 mg. vitamin E each day, for six days, was observed on activity of some of the anti-oxidant enzymes and levels of malondialdehyde (as an index of free radical mediated damage) in the platelets of patients reperfused after myocardial infarction. It has been found that vitamin E administration significantly lowers the level of malondialdehyde in the patients.