农村小型水利工程老损情况评价原则与方法

结合工作实际,针对农村小型水利工程老损情况评价原则与方法进行了论述。

双牌灌区渡槽槽身老损处理

双牌灌区已运行 34年 ,渡槽槽身自然老化 ,混凝土碳化、裂缝、钢筋裸露、过水断面破损、渗水严重。为延长使用寿命 ,采用丙乳硅粉水泥砂浆进行补强处理 。

洪山灌区渠系及建筑物老损评价研究

文中通过对洪山灌区节水改造设计中渠系及建筑物的老损程度评价的阐述,提出了一个全新的、较系统完善的评价办法,为灌区改造提供了一个良好的模式。

微循环血流不畅是引起疾病有碍健康促进衰老损寿的早期主要原因（列题）

微循环血流不畅是引起疾病有碍健康促进衰老损寿的早期主要原因（列题）中国蛇协急危重症医学研究所林可干微循环血流不畅是引起疾病有碍健康促进衰老损寿的早期主要原因（列题）@林可干$中国蛇协急危重症医学研究所...

农用变压器如何防止火灾

近年来,全国各地尤其广大农村、集镇、许多变压器都已接近更新年限,故障不断.而部分检修人员业务水平低,难以及时消除设备故障,使得变压器火灾时有发生.

Master Curve Method of Cumulative Damage for Prediction of Service Life

Aim To study the theory and method for the prediction of service life of solid rocket propellant grain. Methods With the aid of discontiguous diagnostic technology and method of accumulated damage using accelerated aging or heat air oven, the aging isotherms for void content versus aging time were determined. According to the principle of time temperature equivalence the viscoelastic master curve for the prediction of service life were obtained. Results and Conclusion The service life of HMX CMDB solid rocket propellant grain were obtained. Because the critical storage life is measured, the accuracy of predicting the service life of the grain has been increased greatly.

中药离子导入治疗足跟痛

目的 观察中药离子导入治疗足跟痛的临床疗效。方法 采用中药离子导入治疗足跟痛患者 76例。 结果 治愈显效率为 93%。结论 中药离子导入治疗足跟痛疗效显著 ,值得推广应用。

Development of a novel rat model of heterogeneous hepatic injury by injection with colchicine via the splenic vein

AIM To develop a novel rat model of heterogeneous hepatic injury.METHODS Seventy male Sprague-Dawley rats were randomly divided into a control group(n = 10) and a colchicine group(n =60). A 0.25% colchicine solution(0.4 mL/kg) was injected via the splenic vein in the colchicine group to develop a rat model of heterogeneous hepatic injury. An equal volume of normal saline was injected via the splenic vein in the control group. At days 3, 7, and 14 and weeks 4, 8, and 12 after the operation, at least seven rats of the colchicine group were selected randomly for magnetic resonance imaging(MRI) examinations, and then they were euthanized. Ten rats of the control group underwent MRI examinations at the same time points, and then were euthanized at week 12. T2-weighted images(T2 WI) and diffusion weighted imaging(DWI) were used to evaluate the heterogeneous hepatic injury. The heterogeneous injury between the left and right hepatic lobes was assessed on liver sections according to the histological scoring criteria, and correlated with the results of MRI study. RESULTS Obvious pathological changes occurred in the hepatic parenchyma in the colchicine group. Hepatic injury scores were significantly different between the left and right lobes at each time point(P < 0.05). There was a significant difference in apparent diffusion coefficient(ADC) of DWI and liver-to-muscle ratio(LMR) of T2 WI between the left and right lobes of rats in the colchicine group(P < 0.05) at each time point, and similar results were observed between the colchicine and control groups. Besides, there was a significant correlation between hepatic injury scores and ADC values or LMR(r =-0.682, P = 0.000; r =-0.245, P = 0.018).CONCLUSION Injection with colchicine via the splenic vein can be used to successfully develop a rat model of heterogeneous hepatic injury. DWI and T2 WI may help evaluate the heterogeneous injury among liver lobes.

PROTECTIVE EFFECT OF TETRAMETHYLPYRAZINE ON LEARNING AND MEMORY FUNCTION IN D-GALACTOSE-LESIONED MICE

To explore the protective effect of tetramethylpyrazine (TMP) on the learning and memory function in D-galactose (D-gal)-lesioned mice. Methods C57BL/6 mice were injected (s.c.) 2% D-gal for 40 days (100 mg·kg-1·d-1). Normal saline, TMP, and Huper-zine A were respectively given by intragastric administration in different groups from the third week. Learning and memory ability was tested with Morris water maze for 5 days at the sixth week. After completion of behavioral test, the mice were sacrificed by decapitation. The brain was rapidly removed, and the cortex and hippocampus were separated. The superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in the cortex were determined. At the same time, the activity of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE), the binding sites (Bmax) and the affinity (KD) of M-cholinergic receptor in the cortex, and Bmax and KD of N-methyl-D-aspartate (NMDA) receptor in the hippocampus were determined. Results In this model group, (1) The deficit of learning and memory ability, (2) elevated MDA content and lowered SOD activity, (3) decreased AChE activity and M-cholinergic receptor binding sites in the cortex, and (4) lowered NMDA receptor binding sites were observed in the hippocampus, as compared with the normal control. TMP could markedly (1) attenuate cognitive dysfunction, (2) lower MDA content and elevate SOD activity, (3) increase the activity of ChAT and AChE, and M-cholinergic receptor binding sites in the cortex in the mice treated with D-gal. NMDA receptor binding sites were also increased in the hippocampus in the treated mice. Conclusion TMP can significantly strengthen antioxidative function, improve central cholinergic system function, protect NMDA receptor activity, and thus enhance the learning and memory ability in D-gal-lesioned mice.

Peripheral nerve regeneration and intraneural revascularization

Peripheral nerves are particularly vulnerable to injuries and are involved in numerous pathologies for which specific treatments are lacking. This review summarizes the pathophysiological features of the most common traumatic nerve injury in humans and the different animal models used in nerve regeneration studies. ~Ihe current knowledge concerning Wallerian degeneration and nerve regrowth is then described. Finally, the involvement of intraneural vascularization in these processes is addressed. As intraneural vascularization has been poorly studied, histological experiments were carried out from rat sciatic nerves damaged by a glycerol injection. The results, taken together with the data from literature, suggest that revascularization plays an important role in peripheral nerve regeneration and must therefore be studied more carefully.

Management of carbon tetrachloride-induced acute liver injury in rats by syngeneic hepatocyte transplantation in spleen and peritoneal cavity

AIM:Acute hepatitis may seldom have a fulminant course. In the treatment of this medical emergency,potential liver support measure must provide immediate and sufficient assistance to the hepatic function.The goal of our study was to study the adequacy of hepatocyte transplantation (HCTx)in two different anatomical sites,splenic parenchyma and peritoneal cavity,in a rat model of reversible acute hepatitis induced by carbon tetrachloride(CCl_4). METHODS:After CCl_4 intoxication,84 male Wistar rats used as recipients were divided in to four experimental groups accordingly to their treatment:Group A(n=-24):intrasplenic transplantation of 10×10~6 isolated hepatocytes,Group B(n=24): intraperitoneal transplantation of 20×10~6 isolated hepatocytes attached on plastic microcarriers,Group C(n=-18):intrasplenic injection of 1 mL normal saline(sham-operated controls), Group D(n=-18):intraperitoneal injection of 2.5 mL normal saline(sham-operated controls).Survival,liver function tests (LFT)and histology were studied in all four groups,on d 2, 5 and 10 post-HCTx. RESULTS:The ten-day survival(and mean survival)in the 4 groups was 72.2%(8.1±3.1),33.3%(5.4±3.4),0% (3.1±1.3)and 33.3%(5.4±3.6)in groups A,B,C,D, respectively(P_(AB0<0.05,P_(AC)<0.05,P_(BD)=NS).In the final survivors,LFT(except alkaline phosphatase)and hepatic histology returned to normal,independently of their previous therapy.Viable hepatocytes were identified within splenic parenchyma(in group A on d 2)and both in the native liver and the fatty tissue of abdominal wall(in group B on d 5). CONCLUSION:A significantly better survival of the intrasplenically transplanted animals has been demonstrated. Intraperitoneal hepatocytes failed to promptly engraft.A different timing between liver injury and intraperitoneal HCTx may give better results and merits further investigation.

Review:DNA-damage response network at the crossroads of cell-cycle checkpoints, cellular senescence and apoptosis

Tissue homeostasis requires a carefully-orchestrated balance between cell proliferation, cellular senescence and cell death. Cells proliferate through a cell cycle that is tightly regulated by cyclin-dependent kinase activities. Cellular senescence is a safeguard program limiting the proliferative competence of cells in living organisms. Apoptosis eliminates unwanted cells by the coordinated activity of gene products that regulate and effect cell death. The intimate link between the cell cycle, cellular senes- cence, apoptosis regulation, cancer development and tumor responses to cancer treatment has become eminently apparent. Extensive research on tumor suppressor genes, oncogenes, the cell cycle and apoptosis regulatory genes has revealed how the DNA damage-sensing and -signaling pathways, referred to as the DNA-damage response network, are tied to cell proliferation, cell-cycle arrest, cellular senescence and apoptosis. DNA-damage responses are complex, involving “sensor” proteins that sense the damage, and transmit signals to “transducer” proteins, which, in turn, convey the signals to numerous “effector” proteins implicated in specific cellular pathways, including DNA repair mechanisms, cell-cycle checkpoints, cellular senescence and apoptosis. The Bcl-2 family of proteins stands among the most crucial regulators of apoptosis and performs vital functions in deciding whether a cell will live or die after cancer chemotherapy and irradiation. In addition, several studies have now revealed that members of the Bcl-2 family also interface with the cell cycle, DNA repair/recombination and cellular senescence, effects that are generally distinct from their function in apoptosis. In this review, we report progress in understanding the molecular networks that regulate cell-cycle checkpoints, cellular senescence and apoptosis after DNA damage, and discuss the influence of some Bcl-2 family members on cell-cycle checkpoint regulation.

Failure of P-selectin blockade alone to protect the liver from ischemia-reperfusion injury in the isolated blood-perfused rat liver

AIM： To determine if blockade of P-selectin in the isolated blood-perfused cold ex vivo rat liver model protects the liver from ischemia-reperfusion injury. METHODS： The effect of P-selectin blockade was assessed by employing an isolated blood-perfused cold ex vivo rat liver with or without P-selectin antibody treatment before and after 6 h of cold storage in University of Wisconsin solution. RESULTS： In our isolated blood-perfused rat liver model, pre-treatment with P-selectin antibody failed to protect the liver from ischemia-reperfusion injury, as judged by the elevated aspartate aminotransferase activity. In addition, P-selectin antibody treatment did not significantly reduced hepatic polymorphonuclear leukocyte accumulation after 120 min of perfusion. Histological evaluation of liver sections obtained at 120 min of perfusion showed significant oncotic necrosis in liver sections of both ischemic control and P-selectin antibody-treated groups. However, total bile production after 120 rain of perfusion was significantly greater in P-selectin antibody-treated livers, compared to control livers. No significant difference in P-selectin and ICAM-1 mRNAs and proteins, GSH, GSSG, and nuclear NF-kB was found between control and P-selectin antibody-treated livers. CONCLUSION： In conclusion, we have shown that blockade of P-selectin alone failed to reduced polymorphonuclear leukocyte accumulation in the liver and protect hepatocytes from ischemia-reperfusion injury in the isolated blood-perfused cold-ex vivo rat liver model.

Prostacyclin inhibition by indomethacin aggravates hepatic damage and encephalopathy in rats with thioacetamide-induced fulminant hepatic failure

AIM: Vasodilatation and increased capillary permeability have been proposed to be involved in the pathogenesis of acute and chronic form of hepatic encephalopathy. Prostacyclin (PGI2) and nitric oxide (NO) are important contributors to hyperdynamic circulation in portal hypertensive states. Our previous study showed that chronic inhibition of NO had detrimental effects on the severity of encephalopathy in thioacetamide (TAA)-treated rats due to aggravation of liver damage. To date, there are no detailed data concerning the effects of PGI2 inhibition on the severity of hepatic encephalopathy during fulminant hepatic failure. METHODS: Male Sprague-Dawley rats weighing 300-350 g were used. Fulminant hepatic failure was induced by intraperitoneal injection of TAA (350 mg/(kg·d) for 3 d. Rats were divided into two groups to receive intraperitoneal injection of indomethacin (5 mg/(kg·d), n = 20) or normal saline (N/S, n = 20) for 5 d, starting 2 d before TAA administration. Severity of encephalopathy was assessed by the counts of motor activity measured with Opto-Varimex animal activity meter. Plasma tumor necrosis factor-α (TNF-α, an index of liver injury) and 6-keto-PGF1α (a metabolite of PGI2) levels were measured by enzyme-linked immunosorbent assay. RESULTS: As compared with N/S-treated rats, the mortality rate was significantly higher in rats receiving indomethacin (20% vs5%, P<0.01). Inhibition of PGI2 created detrimental effects on total movement counts (indomethacin vs N/S: 438±102 vs 841±145 counts/30 min, P<0.05). Rats treated with indomethacin had significant higher plasma levels of TNPa (indomethacin vs N/S: 22±5 vs 10±1 pg/mL, P<0.05) and lower plasma levels of 6-keto-PGF1α (P<0.001), but not total bilirubin or creatinine (P>0.05), as compared with rats treated with N/S. CONCLUSION: Chronic indomethacin administration has detrimental effects on the severity of encephalopathy in TAA-treated rats and this phenomenon may be attributed to the aggravation of liver injury. This study suggests that PGI2 may provide a protective role in the development of fulminant hepatic failure.

Effect of 2-amino-2-[2-(4-octylphenyl) ethyl] propane- 1,3-diol hydrochloride (FTY 720) on immune liver injury in mice

AIM: To investigate the protective effect against two immune liver injury models in mice by 2-amino-2-[2-(4-octylphenyl) ethyl] propane-l,3-diol hydrochloride and its possible mechanisms in Con A-induced liver damage. METHODS: Liver tissue or hepatocyte injury was monitored biochemically by measuring alanine aminotransferase (sALT) and aspartate aminotransferase (sAST) activity. Hematoxylin & eosin (HE) staining was used for histopathological examination. To evaluate the role of IFN-γ and IL-4 in the liver injury, serum levels of IFN-γ and IL-4 were determined using commercially available ELISA kit at 12 h after Con A challenge. We also determined FTY 720-induced spleen cell apoptosis by flow cytometry analysis or spleen cell proliferation test. RESULTS: Different doses of FTY 720 treatment dramatically reduced circulating markers of hepatocyte injury in two kinds of immunological liver injury models. FTY 720 dramatically reduced the elevated serum IFN-γ and IL-4 levels after Con A injection. Effect of spleen cell supernatants treated with Con A or FTY 720 on hepatocytes showed that ALT activities in cultured hepatocyte supernatants in Con A treatment group increased markedly and FTY 720 could reduce this elevated ALT activities in FTY 720 treatment group. FTY 720 dose-dependently increased the percentage of apoptotic cells in T cells and inhibited splenocyte proliferation induced by Con A. CONCLUSION: Pretreatment with FTY 720 was shown to produce protective effect on the immune liver injury in mice. The possible mechanism of FTY 720 on Con A-induced liver damage is that it could inhibit lymphocyte proliferation and induce lymphocyte apoptosis, resulting in the reduction of IL-4 or IFN-γ release, and subsequently protecting liver from being damaged by Con A.

Effect of resveratrol on microcirculation disorder and lung injury following severe acute pancreatitis in rats

AIM: To investigate the mechanism of resveratrol underlying the microcirculation disorder and lung injury following severe acute pancreatitis (SAP). METHODS: Twenty-four rats were divided into 3 groups (SAP, sham and resveratrol groups) randomly. SAP model was established by injecting 4% sodium taurocholate l mL/kg through puncturing pancreatic ducts. Sham (control) group (8 rats) was established by turning over the duodenum. Resveratrol was given at 0.1 mg/kg b.m. intraperitoneally. Rats were sacrificed 9 h after SAP was induced. Blood samples were obtained for hemorrheological examination. Lung tissues were used for pathological observation, and examination of microvascular permeability, dry/wet ratio and myeloperoxidase (MPO) activity. Gene expression of intercellular adhesion molecule-1 (ICAM-1) was detected by RT-PCR. RESULTS: Compared with SAP group, resveratrol relieved the edema and infiltration of leukocytes in the lungs. Resveratrol improved markers of hemorrheology: high VTB (5.77±1.18 mPas vs9.49±1.34 mPas), low VTB (16.12±3.20 mPas vs30.91±7.28 mPas), PV (4.69±1.68 mPas vs 8.00±1.34 mPas), BSR (1.25±0.42 mm/h vs50.03±0.03 mm/h), VPC (54.67±3.08% vs 62.17±3.39%), fibrinogen (203.2?7.8 g/ L vs 51.3±19.1 g/L), original hemolysis (0.45±0.02 vs 0.49±0.02), and complete hemolysis (0.41±0.02 vs 0.43±0.02) (P<0.05). Resveratrol decreased the OD ratio of ICAM-1 gene (0.800±0.03 vs 1.188±0.10), dry/wet ratio (0.74±0.02 vs 0.77±0.03), microvascular permeability (0.079±0.006 vs 0.112±0.004) and MPO activity (4.42±0.32 vs 5.03±0.51) significantly (P<0.05). CONCLUSION: Resveratrol can improve the microcirculation disorder of the lung by decreasing leukocyte-endothelial interaction, reducing blood viscosity, improving the decrease of blood flow, and stabilizing erythrocytes in SAP rats. It may be a potential candidate to treat SAP and its severe complications (ALI).

Effect of Batroxobin on Neuronal Apoptosis During Focal Cerebral Ischemia and Reperfusion in Rats

We have found that Batroxobin plays a protective role in ischemic brain injury, which attracted us to investigate the effect of Batroxobin on apoptosis of neurons during cerebral ischemia and reperfusion. The apoptotic cells in ischemic rat brains at different reperfusion intervals were tested with method of TdT-mediated dUTP-DIG nick end labeling (TUNEL) and the effect of Batroxobin on the apoptosis of neurons was studied in left middle cerebral artery (LMCA) occlusion and reperfusion in rat models (n = 18). The results showed that few scattered apoptosis cells were observed in right cerebral hemispheres after LMCA occlusion and reperfusion, and that a lot of apoptosis cells were found in left ischemic cortex and caudoputamen at 12 h reperfusion, and they reached peak at 24 h-48 h reperfusion. However, in the rats pretreated with Batroxobin, the number of apoptosis cells in left cerebral cortex and caudoputamen reduced significantly and the neuronal damage was much milder at 24 h reperfusion than that of saline-treated rats. The results indicate that administration of Batroxobin may reduce the apoptosis of neurons induced by cerebral ischemia and reperfusion and afford significant cerebroprotection in the model of focal cerebral ischemia and reperfusion.

Protective Effects of Jin Bai Mei Yan Prescription on Oxidative Damage and Photoaging Induced by Ultraviolet B in HaCaT Cells

Objective Ultraviolet B(UVB)mainly acts on the skin epidermis,causing oxidative damage and apoptosis of keratinocytes.Jin Bai Mei Yan Prescription(JBMYP)comprises a variety of antioxidant traditional Chinese medicines(TCM).In this study,we aimed to evaluate the effects of JBMYP on the oxidative damage induced by UVB in human immortalized epidermal keratinocytes(HaCaT)cells.Methods HaCaT cells were divided into six groups:control group,model(UVB)group,positive(UVB+vitamin E)group,UVB+JBMYP low dose group(160μg/mL),UVB+JBMYP moderate dose group(800μg/mL),and UVB+JBMYP high dose group(1600μg/mL).HaCaT cells were irradiated with UVB and treated with JBMYP for 24 h.Methyl thiazolyl tetrazolium(MTT)assay and real-time unlabeled cell function analyzer were used to assess the cell survival and proliferation rates,respectively.At the same time,the levels of intracellular reactive oxygen species(ROS),lipid peroxide malondialdehyde(MDA),glutathione(GSH),and hydroxyproline(HYP),as well as the activities of antioxidant enzyme superoxide dismutase(SOD)and catalase(CAT)were evaluated using enzyme linked immunosorbent assay(ELISA).Results Compared with the model group,the survival rate of HaCaT cells in each dosage group of JBMYP was significantly improved(P<0.05).Further,JBMYP could promote the proliferation of HaCaT cells,leading to a reduction in the contents of MDA and ROS,and increase in the contents of SOD,CAT,GSH and HYP in HaCaT cells.Conclusions JBMYP has enhanced protective effect on oxidative damage induced by UVB in HaCaT cells.

Caloric Restriction and Litter Size Do Not Compromise Renal Function of Male Wistar Rats

This work had the purpose of comparing some renal parameters of Wistar rats raised in small litters either freely-fed （G3L） or subjected to 30% caloric restriction （G3R） with those of rats from normal litters （Gg） at the age of 90 days. The results showed that the relative weight of the kidneys and urinary flow were not significantly different. All the groups had GFR （glomerular filtration rate） and proteinuria within normal values, despite group G3R having values statistically lower. However, group G3R had diminished glomerular area and increased numbers of renal corpuscles. Group G3L did not exhibit differences compared with controls （G9）. The effects of caloric restriction did not compromise kidney structure and function in 90-day-old rats.