Based on summing up the mainstream opinion of the reasons of the failure of medical health reform and analyzing typical cases,this article promulgates the following content.The medical health reform' s failure are due to the clinical decision-made in seeking interest and the health policy of exuding the commercialization.The forming mechanism is the two reasons work together.The essence is the medical health service is not suited to people's healthy demand which grows day by day and the level of economic development.This refracts the absentation of the government responsibility ethics,which does not present or work.The basic goal of the medical health service to maxi mize the public benefit,which is the dominant value orientation in the medical health service.Certainly it is also the right orientation of the government responsibility ethics in medical health reform.

Objective:To investigate the effect of the intact parathyroid hormone (iPTH) on residual renal function (RRF). Methods: The relationship between iPTH and calcium, phosphorum, product Ca?P, hypertension, triglycende, cholesterol,left ventricular mass index(LVMI) and RRF in 120 hemodialysis patients with chronic renal failure. Results: The results showed that 95. 9% of the hemodialysis patients with chronic renal failure had secondary parathyroldism. It was found that iPTH was positively correlated with SBP,DBP, product Ca?P, triglycende and LVMI, and negatively correlated with endogenous creatinine clearance rate and KT/V. RRF had positive correlation with KT/V and SBP,DBP, calcium, product Ca?P, triglyceride, cholesterol and LVMI. Conclusion: iPTH level is elevated in hemodialysis patients, which may lead to RRF loss.

Objective To explore the correlation between characteristics of surface electromyography (sEMG) from biceps brachii (BB)and triceps brachii (TB) and the Modified Ashworth Scale (MAS) during a passive movement of the spastic elbow in patients with hemiplegiaafter brain lesion. Methods 37 hemiplegics were assessed the elbow spasticity with MAS by a same therapist. Their sEMG of BB andTB were recorded synchronously. Results The Spearman analysis showed that the root mean square (RMS) of sEMG from BB (r=0.651),TB (r=0.912), TB+BB (r=0.905), TB-BB (r=0.903) correlated with MAS (P<0.001) when elbows were flexed, as well as elbows were extended(r=0.848, r=0.518, r=0.850, r=0.711, P<0.001). Conclusion sEMG can present the electrical activities of agonist and antagonist duringpassive movements of both elbow flexion and extension, which may help for the spasticity assessment.

ObjectiveTo detect BAG1 expressions in digestive tract cancer by tissue microarray and to evaluate its clinical significance.MethodsTissue microarray of digestive tract cancer and normal tissues were analyzed by DAKO Envision system immunohistochemical staining for apoptosis related gene BAG-1 expression.ResultsThe positive rate of BAG-1 expression among esophagus cancer,gastric cancer and rectal cancer were higher than that of normal tissues respectively(P<0.01).ConclusionThere is an overexpression of BAG-1 in digestive tract cancer,which suggest that apoptosis related gene BAG-1 may be related to these cancer.

Objective To observe the clinical effect of Chuanxiong-Chatiao San in treatment hemicrania. Methods All patients were randomly recruited into a control group (75cases) and a treatment group (78 cases). The control group was treated with Gastrodin injection, Ligustrazine injection and Mailuoning injection; on this basis, the treatment group was treated with Chuanxiong-Chatiao powder. Both groups were treated for 14 days with a 7 days interval. Results The excellent rate and effective rate were 91.03% and 96.08% in the treatment group respectively; and 70.66% and 94.67% in the control group respectively. The difference between the two groups was significant (χ2= 12.7143,P<0.01) . Conclusion Chuanxiong-Chatiao powder combined with western medicine is effective in treating hemicrania.

The basic premise of syndrome essence discussion is the standardization of traditional Chinese medicine (TCM) syndrome type. However, there still exists confusion regarding the standardization of TCM syndrome differentiation treatment, and the guidelines for TCM syndrome differentiation could not really be used for guiding clinical treatment. This is mainly due to the inappropriate use of research ideas and methods. The fundamental research of TCM syndrome based on the differentiation and classification of diseases is the main method for studying the standardization of TCM syndrome type. The accuracy quantification of symptoms is the powerful guarantee for authenticity and reliability of the results from standardization study of syndrome type. The correct choice for statistical methods gives powerful technical support to determine the differentiation threshold. The unified scales, expert discussions and complex scientific theories are the best methods for current research on standardization of syndrome type. The correlation study of syndrome type and physicochemical indexes cannot reflect the syndrome type completely. It is supposed to establish the treatment principles according to the main pathological changes of diseases on the basis of the standardization of TCM syndrome differentiation.

BACKGROUND: Pulmonary microvascular endothelial cells (PMVECs) were not complex, and the endothelial barrier was destroyed in the pathogenesis progress of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Previous studies have demonstrated that hepatocyte growth factor (HGF), which was secreted by bone marrow mesenchymal stem cells, could decrease endothelial apoptosis. We investigated whether mTOR/STAT3 signaling acted in HGF protective effects against oxidative stress and mitochondria-dependent apoptosis in lipopolysaccharide (LPS)-induced endothelial barrier dysfunction and ALI mice. METHODS: In our current study, we introduced LPS-induced PMEVCs with HGF treatment. To investigate the effects of mammalian target of rapamycin (mTOR)/signal transducer and activator of transcription 3 (STAT3) pathway in endothelial oxidative stress and mitochondria-dependent apoptosis, mTOR inhibitor rapamycin and STAT3 inhibitor S3I-201 were, respectively, used to inhibit mTOR/STAT3 signaling. Moreover, lentivirus vector-mediated mTORC1 (Raptor) and mTORC2 (Rictor) gene knockdown modifications were introduced to evaluate mTORC1 and mTORC1 pathways. Calcium measurement, reactive oxygen species (ROS) production, mitochondrial membrane potential and protein, cell proliferation, apoptosis, and endothelial junction protein were detected to evaluate HGF effects. Moreover, we used the ALI mouse model to observe the mitochondria pathological changes with an electron microscope in vivo. RESULTS: Our study demonstrated that HGF protected the endothelium via the suppression of ROS production and intracellular calcium uptake, which lead to increased mitochondrial membrane potential (JC-1 and mitochondria tracker green detection) and specific proteins (complex I), raised anti-apoptosis Messenger Ribonucleic Acid level (B-cell lymphoma 2 and Bcl-xL), and increased endothelial junction proteins (VE-cadherin and occludin). Reversely, mTOR inhibitor rapamycin and STAT3 inhibitor S3I-201 could raise oxidative stress and mitochondria-dependent apoptosis even with HGF treatment in LPS-induced endothelial cells. Similarly, mTORC1 as well as mTORC2 have the same protective effects in mitochondria damage and apoptosis. In in vivo experiments of ALI mouse, HGF also increased mitochondria structural integrity via the mTOR/STAT3 pathway. CONCLUSION In all, these reveal that mTOR/STAT3 signaling mediates the HGF suppression effects to oxidative level, mitochondria-dependent apoptosis, and endothelial junction protein in ARDS, contributing to the pulmonary endothelial survival and barrier integrity.
Animals ; Apoptosis ; Calcium/metabolism* ; Endothelial Cells/metabolism* ; Endothelium/metabolism* ; Hepatocyte Growth Factor/metabolism* ; Lipopolysaccharides/pharmacology* ; Mammals/metabolism* ; Mechanistic Target of Rapamycin Complex 1/metabolism* ; Mechanistic Target of Rapamycin Complex 2/metabolism* ; Mice ; Mitochondria/metabolism* ; Oxidative Stress ; Reactive Oxygen Species/metabolism* ; Respiratory Distress Syndrome ; Sirolimus/pharmacology* ; TOR Serine-Threonine Kinases/metabolism*

ObjectiveTo study the changes of primary metabolites and phenols in the fruits of Acanthopanax senticosus at different development stages, so as to provide a theoretical basis for the rational utilization of A. senticosus fruit resources. MethodThe primary metabolites and phenols in the fruits at different development stages were determined via gas chromatography-mass spectrometry (GC-MS) and liquid chromatography-mass spectrometry (LC-MS) and then compared by multivariate statistical analysis. ResultA total of 274 chromatographic peaks were obtained by GC-MS-based non-targeted metabonomics and 24 differential metabolites were screened out by multivariate statistical analysis. The differential metabolites were mainly concentrated in pentose phosphate pathway, galactose metabolism, ascorbic acid and aldose metabolism pathways. After color conversion, the pentose phosphate pathway and galactose metabolism were activated and increasing sugars were accumulated. The ascorbic acid and aldose metabolism pathways were active before color conversion, with high accumulation of the end product ascorbic acid. The ultra-high liquid chromatography-mass spectrometry (UPLC-MS) identified 28 phenols in the fruits at different development stages. Flavonoids were accumulated mainly at the green ripening stage before color conversion, and phenolic acids were accumulated mainly after color conversion. ConclusionThe accumulation of primary metabolites and phenols in A. senticosus fruits varies significantly among different development stages