[A Case Report of Rectal MiNEN Laparoscopic Resection].

A 74-year-old woman underwent colonoscopy for positive fecal occult blood test. A colonoscopy revealed a Type 1 tumor in the rectosigmoid region. The tumor was diagnosed as well-differentiated adenocarcinoma(tub1)by biopsy.

Planar catechin increases bone mass by regulating differentiation of osteoclasts in mice.

Objectives: While catechins have been reported to exhibit potential to benefit osteoporosis patients, the effects of planar catechin (PCat), synthesized during the development of drugs for Alzheimer's disease, have not been clearly elucidated. Here, we examined the effects of PCat on mouse bone metabolism both in vivo and in vitro.

Methods: Six week old female mice were orally administered PCat (30 mg/kg) every other day for four weeks, and their femurs were analyzed using micro-computed tomography imaging.

Cholesterol and fat in diet disrupt bone and tooth homeostasis in mice.

Dyslipidemia is a condition of high levels of triglycerides and cholesterol in the blood, and high levels of cholesterol is associated with a variety of systemic diseases. The effects of a high-fat diet on bone have been reported, however, it is not clear which components of a high-fat diet affect bone. This study was conducted to examine the effects of dietary lipids and cholesterol on bone homeostasis maintenance.

Licochalcones extracted from Glycyrrhiza inflata inhibit platelet aggregation accompanied by inhibition of COX-1 activity.

Licochalcones extracted from Glycyrrhiza inflata are known to have a variety of biological properties such as anti-inflammatory, anti-bacterial, and anti-tumor activities, but their action on platelet aggregation has not yet been reported. Therefore, in this study we investigated the effects of licochalcones on platelet aggregation. Collagen and U46619, a thromboxane A2 receptor agonist, caused rabbit platelet aggregation, which was reversed by pretreatment with licochalcones A, C and D in concentration-dependent manners.

Indoxyl sulfate down-regulates SLCO4C1 transporter through up-regulation of GATA3.

The accumulated uremic toxins inhibit the expression of various renal transporters and this inhibition may further reduce renal function and subsequently cause the accumulation of uremic toxins. However, the precise mechanism of the nephrotoxicity of uremic toxins on renal transport has been poorly understood. Here we report that indoxyl sulfate, one of the potent uremic toxins, directly suppresses the renal-specific organic anion transporter SLCO4C1 expression through a transcription factor GATA3.