[Study of pancreases ß-cell function in first-degree relatives of type 2 diabetes patients].

AIM: To investig the pancreases ß-cell function in no-diabetic first-degree relatives of type 2 diabetes mellitus( FDR) patients. METHODS: Collect T2DM first-degree relatives, and divided them into three groups:no-diabetes group with normal sugar tolerance (NGT); no-diabetes with abnormal sugar tolerance (IGT); new-confirmed T2DM. apart from that three group patients, 30 normal people with no-related disease risks were also collected as normal control (NC). All four groups of patients were experienced with intravenous glucose tolerance test (IVGTT) and counting the first phase of pancreases function by statistic AIR35 and insulin sensitive index (ISI). RESULTS: New-confirmed T2DM patients with the significantly abnormal statistic results about AIR3.5 and ISI, while NGT patients had the abnormal results compared with normal control group but better than T2DM patients. CONCLUSION: Compared with normal group patients, NGT group appeared decrease of pancreases first phase secretes and insulin resistance but not aggravate enough to induce type 2 diabetes.

Madecassoside reduces ischemia-reperfusion injury on regional ischemia induced heart infarction in rat.

Madecassoside (MA), one of the principle terpenoids in Centella asiatica, has shown protect effect on isolated rat hearts and isolated cardiomyocytes against reperfusion injury in our previous studies. The aim of this study is to investigate if MA also protected against myocardial ischemia-reperfusion injury in vivo. The ischemia infarction model was established in rats. Left ventricular function was monitored during the ischemia-reperfusion period by a multi-channel recorder. After the ischemia-reperfusion process the infarcted areas were assessed. The levels of lactate dehydrogenase (LDH), creatinephosphokinase (CK), malondialdehyde (MDA), super-oxide dismutase (SOD) and C-reactive protein (CRP) in serum were determined. Cardiomyocytic apoptosis was measured by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining. Pre-treatment with MA (50, 10 mg/kg) attenuated myocardial damage characteristic of decreasing infarct size, decreasing LDH and CK release. Activities of SOD were increased and MDA level increased obviously in control group whereas pretreatment with MA blunted the decrease of SOD activity, markedly reduced the level of MDA and the activity of CRP, and relieved myocardial cell apoptosis. These results suggest that MA has the protective effect on myocardial ischemia-reperfusion injury. This protection ability possibly due to its anti-lipid peroxidation, anti-inflammation and anti-apoptosis function and the enhancement of SOD activity.

Radioimmunotherapy of carcinoma of colon with [131I]-labeled recombinant chimeric monoclonal antibodies to carcinoembryonic antigen.

AIM: To study the distribution of [(131)I]-labeled anti-CEA MoAbs and its therapeutic effect on the human colonic cancer model in nude mice. METHODS: A nude mice model of human colonic cancer was established. [(131)I]-labeled anti-CEA MoAbs were injected intravenously into mice. The distribution of the MoAbs was then determined and the effect of RIT on human colonic cancer was observed. RESULTS: The [(131)I]-labeled anti-CEA MoAbs had a specific distribution after injection. Tumor/non-tumor ratios for [(131)I]-labeled anti-CEA MoAbs were 10-20 times higher than [(131)I]-labeled IgG 96 h after injection. Thirty days after injection, significant inhibition of the volume and weight of tumor was observed in the treated mice compared with the control. The tumor growth inhibition rate of 3.1 mCi/kg CEA MoAbs group (LS180, LS174T, SW1116) was 47.8%-64.0%. This was 69.6%-78.6% in the 6.25 mCi/kg CEA MoAbs group, and 81.8%-86.2% in the 12.5 mCi/kg [(131)I]-labeled anti-CEA MoAbs group. The plasma CEA level was also lower in treated mice. CONCLUSION: The results indicate that [(131)I]-labeled anti-CEA MoAbs can be effective in RIT on colonic cancers.