Objective To evaluate the role of alpha4 beta2 neuronal nicotinic acetylcholine receptor in the inhibition of synaptic long-term potentiation (LTP) by isoflurane in the CA1 area of rat hippocampal slices.Methods Hippocampal slices (400 μm thick) were prepared from the brains of adult male SD rats, 2 months old, weighing 200-250 g, anesthetized with ether and decapitated. The slices were incubated in artificial cerebrospinal fluid (aCSF) at room temperature for at least 2 h before use. Seventy slices were randomly divided into 10 groups ( n = 7 each): Ⅰ LTP group in which the slices were perfused with aCSF; Ⅱ , Ⅲ and Ⅳ group in which the slices were perfused with aCSF containing isoflurane 0.125, 0.25 and 0.5 mmol/L respectively (group Ⅰ1-3 );Ⅴ and Ⅵ group in which the slices were perfused with aCSF containing epibatidine 0.1 and 1.0 μmol/L respectively (group E1.2 ); Ⅶ group epibatidine 0.1 μmol/L + isoflurane 0.25 mmol/L (group E1 + I2 ); Ⅷgroup epibatidine 1.0 μmol/L + isoflurane 0.25 mmol/L (group E2 + I2); Ⅸ group DHβE 0.1 μmol/L (group D); Ⅹ group DHβE 0.1 μmol/L + isoflurane 0.125 mmol/L (group D + I1 ). Population spikes (PS) were recorded for at least 30 min before LTP in each group. For LTP induction, high-frequency stimulation (HFS) was applied to the Schaffer collateral-commissural pathway of hippocampus and maintained for 15 min using a stimulating electrode.The changes in PS amplitude were analyzed at 5, 10, 15, 20, 25, 30, 40, 50 and 60 min after HFS in each group. Results Compared with group LTP, the PS amplitude was significantly decreased after HFS in group I1 ,I2, I3 , D, D + I1 and E1 + I2 ( P ＜ 0.05), while increased after HFS in group E1 .2 ( P ＜ 0.05 ), but no significant change was found after HFS in group E2 + I2 ( P ＞ 0.05). The PS amplitude was significantly decreased after HFS in group D + I1 compared with group I1 (P ＜ 0.05). The PS amplitude was significantly increased after HFS in group E1 + I2 and F2 + I2 compared with group I2 ( P ＜ 0.01 ). Conclusion Isoflurane inhibits LTP induction via inhibiting the activation of alpha4 beta2 nicotinic acetylcholine receptor in rat hippocampus.

Objective To determine the risk factors for postoperative respiratory complications and establish a preoperative risk scoring system.Methods Patients,aged ≥ 18 yr,scheduled for elective surgery or undergoing emergency operation under total intravenous anesthesia or field block anesthesia,were studied.The general data of patients,preoperative SpO2,and conditions of respiratory infection,anemia or cough tests within 1 month before surgery were recorded.The operative sites (thorax,upper abdomen,other sites),duration of operation,type of surgery (emergency operation/elective operation),and methods of anesthesia (general anesthesia/field block) were also recorded.According to the development of respiratory complications within 1-7 days after operation,the patients were divided into either postoperative respiratory complication group or non-postoperative respiratory complication group.The risk factors of which P values were less than 0.05 would enter the multivariate logistic regression analysis to pick out the risk factors for postoperative respiratory complications and to establish a preoperative risk scoring system.Results Two thousand and thirty-seven patients completed the study.A total of 493 patients developed postoperative pulmonary complications,and the incidence was 24.20％.Statistical analysis showed that the risk factors associated with postoperative respiratory complications included age ＞ 50 yr,preoperative SpO2 ≤90％,high ASA physical status,duration of smoking ＞ 1 yr,positive cough tests,respiratory infections at one month before operation,preoperative anemia,upper abdominal and intrathoracic operations,duration of operation ＞ 2 h.A preoperative risk scoring system was established for postoperative respiratory complications based on 6 independent risk factors:preoperative SpO2,anemia,respiratory infections,age,duration of operation and operative sites.The incidence of postoperative respiratory complications was 61.9 ％,52.8 ％ and 17.2 ％ in high-risk,medium-risk and low-risk groups,respectively,and there was significant difference between the three groups (P ＜ 0.01).Area under the ROC curve was 90％ for subsamples and 87％ for the validation subsamples.Conclusion Age ＞ 50 yr,high ASA physical status,duration of smoking ＞ 1 yr,positive cough tests,preoperative SpO2 ≤90％,anemia,respiratory infections at one month before operation,duration of operation ＞ 2 h,upper abdominal and intrathoracic operations are risk factors for postoperative respiratory complications.A preoperative risk scoring system is successfully established for postoperative respiratory complications based on preoperative SpO2,anemia,respiratory infections,age,duration of operation and operative sites.

It is first time to use dextren T-40 oxidative method to conjugate anti-gastric cancer mono-colonal antibody(McAb)with anti-tumor medicines of daunorubicin(DNR)and methotrexate(MTX)together.Cytotoxicity of conjugates was measured by MTT method and ~3H-TdR incor-poration method respectively.Both sensitivity is similar.The results have showed that this conju-gate exhibited selective cytotoxicity on human gastric cancer cells in vitro.

OBJECTIVETo further study the binding character of hepatitis B surface antigen (HBsAg) and beta 2-glycoprotein I (beta2GP I) and to explore whether beta2GP I plays an important role in the hepatotropism of hepatitis B virus.

METHODSUsing Western blot technique, we observed the binding character of the HBsAg with reduced and non-reduced beta2GP I.

RESULTSrHBsAgs with reduced and non-reduced beta2GP I showed identical binding activity.

CONCLUSIONSThe binding activity of HBsAg is dependent on tandem residues, but not on conformational structures of beta2GP I. There is a specific binding between HBV and beta2GP I, which may play an important role in HBV infection and is one of the reasons of hepatotropism of HBV.

Hepatitis B ; virology ; Hepatitis B Surface Antigens ; metabolism ; Hepatitis B virus ; pathogenicity ; Humans ; Viral Envelope Proteins ; blood ; beta 2-Glycoprotein I ; blood

OBJECTIVETo investigate serum procalcitonin (PCT) concentrations in premature infants with different gestational ages at different times after birth.

METHODSA total of 217 neonates without infection, including 102 premature infants and 115 full-term infants, were enrolled in this study. The premature infants were further divided by gestational age into three subgroups: 30-32 weeks (n=30), 33-34 weeks (n=35) and 35-36 weeks (n=37). All the infants were studied to evaluate serum PCT concentrations at 0-12, 13-24, 25-36, 37-48, 49-72, 73-96, 97-120 and 121-144 hours after birth.

RESULTSIn the newborns, serum PCT concentrations increased gradually after birth, reached peak values at about 24 hours after birth, and then gradually declined and dropped to normal values for children at about 96 hours after birth. In the premature infants, serum PCT concentrations reached peak values at about 36 hours after birth, later than in the full-term infants, then declined slowly and dropped to levels similar to the full-term infants at 96 hours after birth. Serum PCT concentrations in the 30-32 week subgroup remained at low levels after birth, and increased gradually, later than in other premature infants, at 37-48 hours after birth.

CONCLUSIONSEarly after birth, neonates have a changing serum PCT concentration, increasing first and then decreasing. Peak serum PCT levels appear later in premature infants than in full-term infants. Serum PCT concentrations of premature infants with a gestational age of under 32 weeks remain at relatively low levels within 36 hours after birth.

Calcitonin ; blood ; Calcitonin Gene-Related Peptide ; Gestational Age ; Humans ; Infant, Newborn ; Infant, Premature ; blood ; Protein Precursors ; blood ; Time Factors

Objective To evaluate the effect of zinc deficiency factor on cognitive function after isoflurane anesthesia in mice with Alzheimer's disease (AD).Methods One hundred and forty-four APP/ PS1 transgenic mice with AD,weighing 22-28 g,aged 8-10 months,were divided into 6 groups (n=24 each) using a random number table:zinc adequate group (group ZA),zinc adequate plus isoflurane anesthesia group (group ZA+Iso),zinc deficiency group (group ZD),zinc deficiency plus isoflurane anesthesia group (group ZD+Iso),zinc treatment group (group ZT) and zinc treatment plus isoflurane anesthesia group (group ZT+Iso).The mice were fed a diet adequate in zinc and deionized water for 2 months in ZA and ZA+Iso groups.The mice were fed a diet low in zinc (0.01‰ zinc) and deionized water for 1 month in ZD and ZD+Iso groups.The mice were fed a diet adequate in zinc and 0.12‰ ZnSO4 · 7H2O water for 2 months in ZT and ZT+Iso groups.The mice underwent 2 h of anesthesia with 1.4％ isoflurane starting from the end of feeding in ZA+Iso,ZD+Iso and ZT+Iso groups.At 24 h after anesthesia,the mice were sacrificed and hippocampal tissues were obtained for determination of the contents of soluble amyloid beta protein 40 (Aβ40) and Aβ42 and insoluble Aβ40 and Aβ42 (using enzyme-linked immunosorbent assay) and expression of total Aβ,Aβ40,Aβ42,tau pSer396,tau pSer262 and tau pThr231 (by Western blot).Morris water maze test was performed at 24 h after anesthesia.Results There was no significant difference in each parameter between group ZA and group ZA+Iso and between group ZT and group ZT+Iso (P＞0.05).Compared with group ZD or group ZT+Iso,the escape latency was significantly prolonged,the space exploration time was shortened,the expression of hippocampal Aβ42,tau pSer396,tau pSer262 and tau pThr231 was up-regulated,and the contents of soluble and insoluble Aβ42 were increased in group ZD+Iso (P＜0.05 or 0.01).Conclusion Zinc deficiency can aggravate the impairment of cognitive function after isoflurane anesthesia in mice with AD,and the mechanism is related to the promotion of hippocampal Aβ aggregation and tau protein phosphorylation.

OBJECTIVETo study the relationship between the degree of white matter damage and changes in brain function in premature infants early after birth according to amplitude-integrated electroencephalogram (aEEG) and raw EEG (with burst-suppression patterns).

METHODSThirty-eight premature infants of less than 32 weeks' gestational age and with white matter damage, including 20 cases of mild white matter damage and 18 cases of severe white matter damage, were included in the study. Forty-two premature infants without white matter damage were selected as a control group. After birth, they were examined using aEEG and brain ultrasound once a week until four weeks after birth or a corrected gestational age of 32 weeks. The white matter damage and control groups were compared in terms of aEEG patterns and amplitudes and burst suppression ratio (BSR) on EEG.

RESULTSThe white matter damage and control groups had highly discontinuous patterns and had no complete sleep cycles. The lower amplitude was significantly smaller in the severe white matter damage subgroup than in the mild white matter damage subgroup and control group. There was alternating burst-suppression activity on the raw EEG in the white matter damage and control groups; and the severe white matter damage subgroup had a significantly longer suppression time and a significantly higher BSR on EEG compared with the mild white matter damage subgroup and control group.

CONCLUSIONSBrain function monitoring should be performed in premature infants with white matter damage early after birth so as to detect cases of severe white matter damage in time.

Brain ; pathology ; Electroencephalography ; Humans ; Infant, Newborn ; Infant, Premature ; physiology ; Leukomalacia, Periventricular ; physiopathology

A boy aged 2 months (born at 36 weeks of gestation) was admitted due to cough and dyspnea. After admission, he was found to have persistent hypertension, proteinuria, and persistent convulsion, and imaging examination showed extensive calcification of the aorta and major branches and stenosis of local lumens of the abdominal aorta and the right renal artery with increased blood flow velocity. The boy was admitted during the neonatal period due to wet lung and pulmonary arterial hypertension and was found to have hypertension and proteinuria. High-throughput whole-exome sequencing was performed and found two compound heterozygous mutations in the ENPP1 gene from his parents, c.130C>T (p.Q44X) and c.1112A>T (p.Y371F). c.130C>T was a nonsense mutation, which could cause partial deletion of protein from 44 amino acids, and was defined as a primary pathogenic mutation. c.1112A>T was a missense mutation which had been reported as a pathogenic mutation associated with idiopathic infantile arterial calcification (IIAC). Therefore, he was diagnosed with IIAC. He was given phosphonate drugs, antihypertensive drugs, anticonvulsion treatment, and respiratory support. Blood pressure was maintained at the upper limit of normal value. There was no deterioration of arterial calcification. It is concluded that IIAC should be considered for infants with persistent hypertension and extensive vascular calcification, and imaging and genetic examinations should be performed as early as possible to make a confirmed diagnosis.
Humans ; Hypertension ; Infant ; Infant, Premature ; Male ; Mutation ; Vascular Calcification