Prenatal X-irradiation increases GFAP- and calbindin D28k-immunoreactivity in the medial subdivision of the nucleus of solitary tract in the rat

Glial fibrillary acidic protein- (GFAP) and calbindin D28k-immunoreactivity (IR) were investigated in the medial subdivision of the nucleus of the solitary tract (mNST) of prenatally X-irradiated rats. Pregnant rats were exposed to a single whole-body X-irradiation on day 11 or 16 of gestation at a dose of 1. 3 Gy. The offspring were killed at 7-14 days of age for the immunohistochemical observations. Rat pups showed strong GFAP-IR at the level rostral to the obex when receiving X-rays on day 11 of gestation, with hypertrophy of astrocyte cell bodies and cytoplasmic processes, but weak GFAP-IR when receiving X-rays on day 16 of gestation. Calbindin D28k-IR was stronger in the animals receiving X-rays on day 11 or 16 of gestation compared to that in the control animals. In the present study, the increase of GFAP- and calbindin D28k-IR cells in the mNST might indicate that adaptative mechanisms are taking place to preserve integrated nervous system function and possibly, to provide neuroprotection.     

内皮素受体拮抗剂治疗充血性心衰一项meta分析

目的初步评价内皮素拮抗剂治疗心衰的效果和安全性。方法借助循证医学检索途径和方法筛选出临床随机对照试验(RCTs),数据用Revman4.2软件进行分析。结果共入选13个临床随机对照试验(RCT)4137名患者,其中3个试验评价了心脏指数改善情况,5个试验评价死亡和心衰恶化,4个试验评价其它副作用。心脏指数改善的总效应为:WMD(加权均数差)0.47,95%可信区间(CI)[0.36,0.57](P<0.00001)。Tezosentan<50mg/h、50mg/h和100mg/h三组比较具有相似的效果及副作用,而副作用有随剂量增加的趋势。作为主要终点指标死亡率和心衰恶化两组相似(RR=1.00,95%CI[0.89,1.13](P=0.89),而其它副作用事件发生率则存在明显差异(RR=1.28,95%CI[1.13,1.44](P<0.0001)。结论内皮素拮抗剂可改善心衰患者的心脏指数,但长期效应尚未得到证实。治疗组患者副作用发生常见,并呈剂量依赖性。内皮素拮抗剂的长期效果还需要设计更完善、纳入例数更多的临床随机对照试验加以阐明。     

Protein kinase C iota protects neural cells against apoptosis induced by amyloid beta-peptide

Protein kinase C (PKC) isoforms are increasingly recognized as playing important roles in the regulation of neuronal plasticity and survival. Recent findings from studies of non-neuronal cells suggest that atypical isoforms of PKC can modulate apoptosis in various paradigms. Because increasing data support a role for neuronal apoptosis in the pathogenesis of Alzheimer's disease (AD), we tested the hypothesis that PKCiota (PKCiota) can modify vulnerability of neural cells to apoptosis induced by amyloid beta-peptide (ABP), a cytotoxic peptide linked to neuronal degeneration in AD. Overexpression of PKCiota increased the resistance of PC12 cells to apoptosis induced by ABP. Associated with the increased resistance to apoptosis were improved mitochondrial function and reduced activity of caspases. In addition, ABP-induced increases in levels of oxidative stress and intracellular calcium levels were attenuated in cells overexpressing PKCiota. These findings suggest that PKCiota prevents apoptosis induced by ABP by interrupting the cell death process at a very early step, thereby allowing the cells to maintain ion homeostasis and mitochondrial function.     

Why the prevention strategies are in low priority？

It is a puzzle to many researchers that with so extensive resources, so advanced technology, and so urgent need the world over, so little has been done to alleviate the suffering of the people. Why is it so difficult to develop the prevention and health promotion strategies？ This paper tries to discuss the issue.     

The expression of TRPA1 mRNA in the rat brain

Objective： To investigate the distribution of TRPA1 （one kind of the TRP-like ion channel family） channel in the hippocampus and cerebral cortex of rat. Methods： RT-PCR was used to amplify the fragment of TRPA1 in the DRG （dorsal root ganglion）, hippocampus and cerebral cortex of adult SD rat. In situ hybridization staining was used to show the distribution of TRPA1 mRNA in the hippocampus and cerebral cortex of adult rat brain. Results： Both RT-PCR and in situ hybridization staining showed that TRPA1 mRNA was expressed in hippocampus and cerebral cortex of the adult rat brain. Conclusion： Our results suggest that there is expression of TRPA1 mRNA both in the hippocampus and cerebral cortex of the adult rat brain.     

重型颅脑损伤救治的临床伦理学问题探析

重型颅脑损伤病人病情危急，致残率、死亡率高，而医护人员的医德修养直接影响危重病人的治疗效果．也关系着医疗卫生行业的社会声誉，因而对临床伦理学有着更高、更严的要求，作者对在救治重型颅脑损伤病人过程中的伦理学问题进行了探讨。     

Cloning, distribution and functional analysis of the type III sodium channel from human brain

The type III voltage-gated sodium channel was cloned from human brain. The full-length cDNA has 89% identity with rat type III, and the predicted protein (1951 amino acids) has 55 differences. The expression pattern of human type III mRNA was determined in adult brain tissue and, in contrast to rat, was detected in many regions, including caudate nucleus, cerebellum, hippocampus and frontal lobe. The human type III channel was stably expressed in Chinese hamster ovary (CHO) cells and its biophysical properties compared to the human type II channel using identical conditions. The voltage dependence and kinetics of activation were found to be similar to that of type II. The kinetics of inactivation of the two human subtypes were also similar. However, type III channels inactivated at more hyperpolarized potentials and were slower to recover from inactivation than type II. When expressed in human embryonic kidney (HEK293T) cells, type III channels produced currents with a prominent persistent component, which were similar to those reported for rat type II [Ma et al. (1997) Neuron, 19, 443-452]. However, unlike type II, this was prominent even in the absence of coexpressed G-proteins, suggesting type III may adopt this gating mode more readily. The distinct properties of the channel, together with its wide distribution in adult brain, suggest that in humans, type III may have important physiological roles under normal, and perhaps also pathological conditions.     

疏肝健脾法治疗纤维肌痛综合征56例临床观察

目的:观察疏肝健脾法治疗纤维肌痛综合征(FMS)的临床疗效.方法:56例FMS患者分为A组38例(原发性)和B组18例(合并其他风湿病),给予逍遥散加减治疗,疗程12周.结果:A组总有效率为92.11%,B组总有效率为72.22%.两组比较,A组疗效优于B组(P<0.05),疼痛、压痛、僵硬、疲乏及睡眠障碍等明显改善(P<0.01).结论:疏肝健脾法治疗FMS具有较好的临床疗效,对原发性FMS作用尤为明显.     

p53 Codon 72 polymorphism predicts the pathologic response to neoadjuvant chemotherapy in patients with breast cancer.

PURPOSE: Recent studies have highlighted that the p53 codon 72 polymorphism plays a crucial role in modulating wild-type p53 apoptotic capacity, and as such may influence the response to chemotherapy. Thus, the purpose of this study was to investigate whether the p53 codon 72 polymorphism might influence pathologic response to neoadjuvant chemotherapy in primary breast cancer. EXPERIMENTAL DESIGN: One hundred and ten operable breast cancer patients received anthracycline-based neoadjuvant chemotherapy and p53 codon 72 polymorphism status was analyzed by PCR-RFLP. RESULTS: The distribution of initial clinical stage, tumor size, estrogen receptor or progesterone receptor status, menopausal status, or erbB2 expression was not significantly different among the polymorphic variants. However, we found that only 13% (3 of 23) of patients with the Pro/Pro variant had a good pathologic response, defined as a complete pathologic response or minimal residual disease. In comparison, 40% (22 of 55) or 37.5% (12 of 32) of patients with the Pro/Arg or Arg/Arg variant had a good pathologic response (P = 0.019). Moreover, patients with the Pro/Pro variant were more likely to have a positive axillary lymph node status than those with the Pro/Arg or Arg/Arg variant (P = 0.007). Furthermore, in multivariate analysis, p53 codon 72 polymorphism was found to be a strong predictor of pathologic response (odds ratio 6.7, 95% confidence interval, 1.4-31.2; P = 0.016). CONCLUSION: Our study indicates that breast cancer patients with the Pro/Pro variant may be less sensitive to anthracycline-based treatment than those with the Pro/Arg or Arg/Arg variant and suggests that analysis of p53 codon 72 polymorphism may provide a simple predictive marker for selecting the right breast cancer patients to anthracycline-based neoadjuvant chemotherapy in clinical setting.