This paper reviews the current status of health education intervention, health education intervention model and evaluation indicators of intervention effect in noninvasive positive pressure ventilation in China.By analysing the existing problems in the health education of noninvasive positive pressure ventilation, this artical will provide the basis for exploring the new health education mode ,so as to improve the effect of non-invasive positive pressure ventilation and the patients′quality of life.

Objective To assess the incidence rate of postoperative nausea and vomiting (PONV) after total intravenous anesthesia (TIVA) with propofol versus sevoflurane-based anesthesia with or without ondansetron in patients undergone gynecological laparoscopy. Methods Totally 138 patients were randomly divided into three groups: sevoflurane group (Sev group) sevoflurane-ondansetron group (Sev-O group),and propofol TIVA group (TIVA group),with 46 cases in each. In the Sev and Sev-O groups,anesthesia was maintained by inhalation of 50% N2O and sevoflurane;in the Sev-O group,8 mg of prophylactic ondansetron was given intravenously 30 minutes prior to the end of the operation. In the TIVA group,target-controlled infusion of propofol and remifentanil were used. In each group,the incidence of nausea and vomiting and use of antiemetic drugs in 24 hours after the surgery were recorded. Results In 0 to 2 hours after the operation,the incidence rate of nausea and vomiting in the TIVA group was significantly lower than that in the Sev group [22% (10/46) vs 54% (25/46),?2=10.376,P=0.001] and Sev-O group [50% (23/46),?2=7.986,P=0.005]. In 2-6 hours,the rate in the Sev-O group was lower than that in the Sev group [22% (10/46) vs 46% (21/46),?2=5.887,P=0.015]. The total incidence rate of nausea and vomiting in 24 hours after the operation was 57% (26/46) in the TIVA group,which was significantly lower than that in the Sev group [80% (37/46),?2=6.093,P=0.014]. In the Sev,Sev-O,and TIVA groups,there were 13 (28%),6 (13%),and 6 (13%) cases respectively received antiemetic drugs after the surgery. Conclusions Compared with sevoflurane-based anesthesia,propofol TIVA results in a lower rate of PONV after gynecological laparoscopy.

Alzheimer's disease is a common neurodegenerative disease. One of the main pathology is neurofibrillary tangles in neurons,in which principal component is the phosphorylation of tau protein. Previous studies focused on senile plaques and Aβ levels. Recent studies indicated that the development of tau protein closely associated with Alzheimer's disease, especially the abnormal phosphorylation. This paper reviewed the relationship between tau protein phosphorylation and Alzheimer's disease based on the perspective of protein kinases and phosphatases.

AIM: To investigate the possibility that hepatocyte growth factor (HGF) directly induces differentiation of human embryonic stem cells (hESCs) into neural progenitors (NPs). METHODS: hESCs colonies were induced to form the embryoid body (EB). Four-day-old EBs were randomly divided into 4 groups: control group (EBs were cultured in neural induction medium);G5 supplement group (EBs were cultured in neural induction medium supplied with G5 supplement);HGF group (EBs were cultured in neural induction medium supplied with 10 mg/L HGF), and HGF+G5 group (EBs were cultured in neural induction medium supplied with 10 mg/L HGF and G5 supplement). After induced in suspension system for 7 days, EBs with various treatments were cultured in poly-D-lysine/laminin-coated plates for 7-10 days for selection of NPs. NPs were gathered by 0.3 g/L dispase treatment and characterized by immunofluorescence staining. The percentages of the nestin+ cells in NPs in various groups were detected by fluorescent activated cell sorter (FACS). The multipotency of NPs was determined by immunofluorescence staining after the NPs were cultured without G5 and HGF for 7 days. The expression of region markers of neural progenitors treated with sonic hedgehog (Shh) protein (one of the neural inductive signals), was detected by RT-PCR. RESULTS: HGF+G5 supplement induced hESCs differentiation into neural progenitors. Immunofluorescence staining indicated that NPs differentiated from hESCs expressed NP markers including nestin, Pax6 and musashi-1. FACS data showed that the proportion of nestin positive cells in HGF+G5 supplement group (87.3%±3.9%) was the highest in all treatment groups. The time of HGF and G5 supplement treatment was important to differentiate into NPs, the maximal effect was observed at 7th day. After treated with Shh, the expression of ventral forebrain/hindbrain marker genes (Nkk2.1, and Nkk2.2) and hindbrain progenitor marker gene Gbx2 in NPs were upregulated, while the forebrain progenitor marker genes Otx2 and Bf1 were downregulated. CONCLUSION: The neural induction system containing HGF and G5 supplement effectively induces the differentiation of hESCs into NPs, which might be a potent model for investigating the mechanism of neural development and differentiation.

The atherogensis was involved in a complex pathological process. Injury to endothelial cells of blood vessels was confirmed to be the in itial stage of this process. Migration to subendothelial layer and accumulation and proliferation of smooth muscle cells were attributed to various cytokines an d adhesive molecules secreted by activated endothelial cells, subsequently resul ting in aggregation of lymphocytes,platelets, monocytes and macrophages in the i ntima of artery. These cellular components ultimatedly led to the formation of a mature atherosclerotic plaque. Its quite acknowledged that a better understan ding of the atherogenic events might promise us the development of new chemical entities of anti-atherosclerotic therapies. A large body of evidence has demons trated that sulfated polysaccharides played a critical role in the development o f atherosclerosis. The underlying mechanisms of the anti-atherosclerotic activi ty of sulfated polysaccharides were reported to contribute to protecting against endothelial cells injury,inhibiting migration and proliferation of vascular smo oth muscle cells, and reducing the adhesion of inflammatory cells, platelets and lymphocytes. And also, the prevention of complement activation by sulfated poly saccharides could not be excluded. On the other hand,the promoting effects of su lfated polysaccharides atherosclerosis was also reported. Its therefore conclu ded that the relationships between atheriosclerosis and sulfated polysaccharides remained to be further elucidated.

Objective Through investigate dissection of 14v group lymph node of patients with gastric cancer and its metastasis , to explore the influence factors and prognosis of dissection of 14v group lymph node .Methods 120 cases of gastric cancer patients who underwent radical gastrectomy and dissected 14v group lymph node since Mar .2004 to Mar .2012 were analyzed ,through his-topathological and immunohistochemical examination to detect the 14v group lymph node metastasis and calculation .Results Gas-tric antrum carcinoma were detected 176 nodes ,29 nodes were metastasis ,but there were none in other places .About TNM classifi-cation ,14v group lymph node metastasis among patients in stage Ⅳ(5 cases) was 50 .0% ,in stage ⅢC(7 cases)was 33 .3% ;About Borrmann classification ,14v group lymph node metastasis among patients in borrmann type Ⅳ (4cases) was 80 .0% ,in stage Ⅲ(11cases) was 30 .6% ,which were higher than that of other types(P<0 .05) .Among the 18 cases which had 14v group lymph node metastasis ,15 cases(83 .3% )invaded serosa ,invading the surrounding organs .The 5 year rate of 14v group metastasis patients was 7 .7% .Conclusion Gastric carcinoma tumor size ,tumor stage ,Borrmann classification ,invading the surrounding organs and tissues and metastasis in 14v group lymph node have a certain relationship .14v lymph node dissection for lately TNM stage gastric tumor has no certain significance .

0.05. Fixed effect model analysis showed that the summary RR was 1.43 (95%CI, 1.36 to 1.90), indicating a higher risk of future coronary heart disease in individuals with periodontal disease compared with those without. Conclusion This result suggests that periodontal disease is significantly related with coronary heart disease, they may be a risk indicator for each other. However, we should strengthen the prevention and cure of PD and control the probability of CHD.

The atherogensis was involved in a complex pathological process. Injury to endothelial cells of blood vessels was confirmed to be the initial stage of this process. Migration to subendothelial layer and accumulation and proliferation of smooth muscle cells were attributed to various cytokines and adhesive molecules secreted by activated endothelial cells, subsequently resulting in aggregation of lymphocytes, platelets, monocytes and macrophages in the intima of artery. These cellular components ultimatedly led to the formation of a mature atherosclerotic plaque. It's quite acknowledged that a better understanding of the atherogenic events might promise us the development of new chemical entities of anti-atherosclerotic therapies. A large body of evidence has demonstrated that sulfated polysaccharides played a critical role in the development of atheroscle- rosis. The underlying mechanisms of the antiatherosclerotic activity of sulfated polysaccharides were reported to contribute to protecting against endothelial cells injury, inhibiting migration and proliferation of vascular smooth muscle cells, and reducing the adhesion of inflammatory Cells, platelets and lymphocytes. And also, the prevention of complement activation by sulfated polysaccharides could not be excluded. On the other hand, the promoting effects of sulfated polysaccharides atherosclerosis was also reported. It's therefore concluded that the relationships between atherioscierosis and sulfated polysaccharides remained to be further elucidated.

Two aberrant structures, extracellular senile plaques (SP) and intracellular neurofibrillary tangles (NFTs) are the characteristic neuropathological hallmarks of Alzheimers disease (AD). Amyloid ? protein (A?) and hyperphosphorylated tau protein are the major components of SP and NFTs respectively. A large body of evidence has highlighted the pivotal role of sulfated polysaccharides in the amyloidogenesis and formation of NFTs. The underlying mechanisms of the involvement of sulfated polysaccharides in the development of AD were reported to contribute to their high affinity for both A? and tau protein. Sulfated polysaccharides not only promoted the ? secretase cleavage of APP and the increased production of A? and induced the aggregation and deposition of A?, but also facilitated the phosphylation of tau and promoted tau polymerization into fibrils and tangle formation. On the other hand, the neurotrophic effects exerted by sulfated polysaccharides were also demonstrated. These notions were probably due to the inhibition of the formation of A? fibrils or to the counteraction of the abnormal phosphorylation of tau by promoting the protein phosphatase2B activity, which has been speculated to be attributed to the variation in either structural backbone or degree of sulfation or position of sulfation. Putting together, the appropriate structural modification of sulfated polysaccharides may be effective as therapeutic agents for AD.

This study is to investigate the effect of baicalin (BL) against oxidative injury stress of SH-SY5Y cells induced by H2O2 and the possible mechanism. SH-SY5Y cells were pre-incubated with baicalin (25, 50, and 100 micromol x L(-1)) for 12 h prior to exposure to H2O2 (150 micromol x L(-1)) for 24 h. The viability of SH-SY5Y cells was measured by MTT assay. The contents of LDH and NO were determined. The percentage of apoptotic cells was assessed by flow cytometry (FCM). The content of Caspase-3 was tested by immunofluorescence histochemical method. BL at 50 and 100 micromol x L(-1) separately increased the cell viability and up-regulated SIRT1, reduced the contents of LDH, NO, Caspase-3 and the apoptotic percentage of SH-SY5Y cells. This study results suggest that baicalin could inhibit the H2O2-induced neuronal apoptosis. The further mechanism studies show that baicalin inhibit apoptosis via reducing Caspase-3 expression and up-regulating SIRT1.