Objective To explore the pathological changes of the livers from hepatic failure (HF)patients and its association with clinical disease stages.Methods Thirty-nine patients with liver failure caused by HBV infections were investigated,and none accompanied with hepatocellular carci- noma.The sections of tissue were taken from the liver after liver transplantation and stained with he- matoxylin eosin(H&E)or RT(reticular fiber)staining.The pathological features were analyzed and compared between the clinical and pathological diagnosis.Results 1.The range and the grade of the pathological changes were all well-proportioned in the whole liver but quite asymmetrical in the same spicemen.2.4 cases with clinical diagnosis of cirrhosis(active stage)were in accordance with the pathological diagnosis.Only 17 in 35cases can be pathologically diagnosed as chronic severe hepatitis (SH),while the other 18 cases were pathologically diagnosed as cirrhosis(active stage).Conclu- sion There were a great inconsistency between the clinical and pathological diagnosis.

Objective To investigate effects and safety of dexmedetomidine on the prevention of abnormal mental in patients after liver transplantation.Methods 160 patients after liver transplantation were randomly divided into the two groups using the drawing method:midazolam group(n =80),dexmedetomidine group(n =80),compared the two groups of patients with general,mental abnormality and the occurrence of adverse reactions.Results There were no significant differences in the general situation (gender,age,postoperative ventilator time,ICU stay time,oper-ation time,blood FK506 concentration,APACHEII score 24 hours after operation)of the two groups of patients (P >0.05),the spirit of the abnormal rate of the observation group was lower than that of the control group (P =0.009), incidence of hypotension and hypertension in the observation group was higher than that in the control group (P =0.035,0.029).Conclusion Dexmedetomidine can effectively reduce the postoperative mental disorders in patients in the early stage after liver transplantation.

Objective:To observe the changes of visual evoked potential(VEP)in diabetic rats and the influence of nerve growth factor(NGF)and aminoguanidine(AG)on VEP.Methods:Diabetes was induced in adult male Wistar rats with streptozotocin(STZ).Rats were divided into normal control group(CON),diabetes model group(DM).NGF-treated group(D +N)and AG-treated group(D+A).VEP was measured during the 3~(rd)month,6~(th)month,9~(th)month,and 12~(th)month.Results: Compared with the CON group,all rest groups had longer latencies and lower amplitudes(P

Objective:　To explore the variant processes of c ell apoptosis and the inhibiting effect of moderate hypothermia on cell apoptosi s after diffuse brain injury. 　　Methods:　Models of diffuse brain injury were induced by the tra uma device reported by Marmarou.1 A total of 128 Wistar rats were divided into 4 groups: the uninjured group (Group A, n=8), the severely i njured group (Group B, n=60), the mildly injured group (Gr oup C, n=30) and the mild hypothermia group (Group D, n=30). In Group D, the severely injured rats were treated with moderate hypothermia to keep the rectal temperature at 32℃ (standard deviation for 0.1℃) for 6 hours. Then the morphosis, the characteristics and the qua ntity of apoptotic cells in the cerebral cortex and in the hippocampus regions a fter different severities of craniocerebral injuries were observed and compared under an electronic microscope, with terminal deoxynucleotidyl nick end labeling (TUNEL) in DNA fragmentation and with agarose gel electrophoresis. 　　Results:　TUNEL showed apoptotic cells increased according to t he injury severity, and they peaked at 48 hours after injury and then declined. In Group C, apoptosis was located in the CA2 and CA3 areas of the hippocampu s. And in Group B, apoptosis increased evidently, and located in the whole hippo campus and in the frontal and parietal cortex regions. The hypothermia-treated rats had some apoptotic cells, too. However, even at 24, 48 and 72 hours after i njury there were significantly fewer apoptotic cells in the cortex and in the hi ppocampus in Group D than that in the non-treated groups. Electron microscopy s howed that the apoptotic cells were round and shrunken in morphology and the nuc lei were round and condensed at 24 and 48 hours after injury. And the apoptosis at 48 hours was more severe than that at 24 hours. The hypothermia-treated rats had no apoptotic cells. Gel electrophoresis showed that characteristic DNA “la dders” were observed in the cortex and in the hippocampus at 48 hours after sev ere injury. But there was no DNA “ladder” at other time points in the severely injured group, in the mildly injured group and in the hypothermia-treated grou p. 　　Conclusions:　It suggests that apoptosis occurs after diffuse br ain injury and apoptotic cells increase with the injury severity. Moderate hypot hermia has a specific inhibiting effect on cell apoptosis after diffuse brain in jury in rats.

0.05).Conclusion Febrile seizures seldomly cause severe neurological damage.

This paper is discussed about course system construction of Microbiology, teaching method, in- struction means and experimental teaching mode. Teaching practice indicated that reform the pattern of Mi- crobiology educational mode can stimulate students’ interest in studying the course, cultivate their inde- pendent ability to solve questions, develop their creative thinking. It is an important way to train high-caliber talents.

Animals ; Fatty Liver, Alcoholic ; drug therapy ; Female ; Male ; Phytotherapy ; Rats ; Rats, Wistar ; Saponins ; therapeutic use ; Trigonella

OBJECTIVETo explore the relationship between angiotensin converting enzyme (ACE) gene single nucleotide polymorphisms (SNP) and premature coronary heart disease (PCHD) patients with blood stasis syndrome (BSS).

METHODSrs4343, rs4293, and rs4267385 were selected at SNP from ACE gene. Allele and genotype were detected. Frequencies of allele and genotype were compared by using time-of-flight mass spectrometry technique (TOF-MS).

RESULTSCompared with the healthy control group, genotype of rs4293 and rs4267385 in ACE gene were similar, but there was statistical difference in polymorphisms and allele frequencies of rs4343 in the I and II group (P < 0.05, P < 0.01). The frequency of G allele was higher in the 3 groups than in the healthy control group (P < 0.05, P < 0.01). The relative risk analysis showed that the risk for PCHD occurrence in G allele carriers at rs4343 (GG +AG) was 3. 6 times the risk in non-G allele carriers (95% CI: 1.224-10.585, P = 0.02). There was also statistical difference in sex, age, TC, and TG after adjusted Logistic regression analysis (OR = 3.994, 95% CI: 1.230-12.974, P = 0.021).

CONCLUSIONThe polymorphism at rs4343 (G2350A) might be one of risk factors for PCHD occurrence, but not a predisposing factor for PCHD patients of BSS.

Alleles ; Case-Control Studies ; Coronary Artery Disease ; genetics ; Gene Frequency ; Genotype ; Humans ; Medicine, Chinese Traditional ; Peptidyl-Dipeptidase A ; genetics ; Polymorphism, Single Nucleotide ; Risk Factors

Acupuncture Therapy ; California ; International Cooperation ; Medicine, Chinese Traditional ; methods ; trends ; United States

Heat shock protein 27 ( HSP27 ) is an endogenous protein that plays an important role in a great variety of physio-logical and pathological processes. It can express a large number under body stress conditions. Recent studies have shown estro-gen upregulates the expression of HSP27 through a number of ways, playing a perfect “triple protection” role. In the early stage of atherosclerosis, estrogen induces the phosphorylation of HSP27 via PI3K/Akt signaling pathway. Phosphorylation of HSP27 can resist the injury of vascular endothelial cells( VECs) through an antioxidant and anti-apoptotic pathway as well as the inhibition of cytochrome C. In the stage of forming foam cells, estrogen induces the expression and release of HSP27 from mac-rophages by stimulating the estrogen receptor β ( ERβ) , then HSP27 inhibits the LDL uptake and the release of proinflammato-ry cytokine by binding scavenger receptor A ( SR-A) . During the proliferation and migration of vascular smooth muscle cells ( VSMCs) , estrogen induces estrogen receptor α ( ERα) and protein phosphatase 2 ( PP2A) to form a complex that enhances the activity of PP2A, then it can lead to the dephosphorylation of HSP27 and finally inhibit cells proliferation and migration. In summary, the anti-atherosclerotic effect of estrogen is closely re-lated to the role of HSP27. Given the side effects of estrogen re-placement therapy( MHT) , regulating HSP27 may provide a no-vel therapy for the prevention and treatment of cardiovascular dis-eases in menopausal women clinically.