Objective To discuss the nursing for the different postoperative residual urine of patient with pelvic floor dysfunction.Method To evaluate the nursing for the postoperative residual urine of patient with pelvic floor dysfunction and the time of urinary catheters inserted,We completed a retrospective review of 138 adult patients.Results ①Toally 138 participants were categorized into 3 groups:74 (53.6％) patients carried a residual volume ＜ 100ml,53 (38.4％) patient did 100～300ml,11 (8.0％)did ＞300ml.②About11 patients who were able to void but carried a residual volume ＞300ml required indwelling catheterization.In these cases,100％ carried a residual volume ＜ 100ml after indwelling urinary catheter extraction (IUCE) after 4～5 days.③About 53 patients who were able to void but carried a residual volume between 100ml to 300ml received urine nursing,phychological nursing and bladder function exercise.Two days after IUCE 41 (77.4％) patients' residual volume was ＜100ml;three days after IUCE 11 (20.7％) patients' residul volume was ＜100ml;five days 1 patiens' residul volum was ＜100ml.Conclusion When a postvoid residual＞300ml,the patient should be performed catheterization,When a postvoid residual between 100ml to 300ml,the nurse should give the patient mental easing and teach them to perform pelvic floor muscle exercise.This can reduce the suffering of patients.

Objective To screen out single chain variable fragment antibody (scFv)specific to vascular cell adhesion mole‐cule 1(Vcam‐1)from phage recombinant antibody library ,and to evaluate its activity and compare its activity with full‐length monoclonal antibody.Methods Amplification of Vcam‐1 was performed by PCR and Vcam‐1 gene plasmid was transferred into eukaryotic cells to express Vcam‐1 antigen protein.Immune cuvette was coated with purified Vcam‐1 antigen ,and the positive clones were screened out by 4 rounds of “adhesion‐elution‐proliferation” process with gradually increasing pressure.The posi‐tive clones were tested by ELISA method and high titer clones were chosen for gene sequencing.Then the high‐titer clones were transferred into E.coli ,and the clone with the highest expression was regarded as the final requisite one.Competent cells were infected by the final requisite clone and scFv was expressed.After purification ,the activity of scFv was tested by ELISA and its affinity was evaluated.Results Molecular weight of Vcam‐1 antigen protein was 85-90 kD.Positive clones were screened out by taking Vcam‐1 protein as the antigen ,and 9 high titer clones were obtained by single phage ELISA.Gene sequencing of these clones was carried out and 3 sequences were obtained ,1 of which got the highest expression.Molecular weight of the expressed scFv was about 30 kD.The scFv got high affinity to Vcam‐1 antigen according to ELISA ,in spite of its lower activity than full‐length monoclonal antibody.Conclusion scFv antibody specific to Vcam‐1 was successfully obtained from phage display librar‐y ,which laid the foundation of subsequent in vivo diagnosis and therapy.

Objective To explore the effects of maternal hypercholanemia on the myocardium changes in rat fetus. Methods Thirty clean SD female rats were equally randomized to three groups after mating successfully.From the 13th to 20th day of gestation,group A and B were injected injected with sodium chloride(NS) as control.Total bile acid(TBA) and cardiac troponin I(cTnI) were measured in the maternal and fetal serum on the 21st day when all rats were killed.Fetal cardiac muscle cells were also collected for examination with light microscope and electronic microscope.Results (1)TBA in maternal and fetal serum were(22.32±8.12)μmol/L and(28.84±8.06) μmol/L,respectively in group A,(9.77±3.56)/μmol/L and(9.34±3.54) μmol/L in group B,and (3.60±1.78) μmol/L and(3.95±1.19) μmol/L in group C.Significant differences were found among groups(P<0.01).(2)Fetal death rates were significantly different among the three groups (P<0.05),with 30.11%,16.85%,and 7.05%,respectively.(3)Fetal cTnl were also found significant difference among groups(P<0.01),with(19.98±7.75)ng/ml,(11.41±3.64)ng/ml and(4.38±1.19)ng/ml,respectively.(4)The integrated scores of fetal necrosis area were significantly different in three groups(P<0.05),with 1.92±0.43,1.36±0.37 and 0.44±0.12,respectively.(5)Under electronic microscope,the number density of mitochondria in group A was lower than that in group C(P<0.05)while the average volume of mitochondria was larger in group A (P<0.05).The average volume of mitoehondria in group B was larger than that in group C(P<0.05) while no difference was found with regard to the number density between the two groups.The number density and average volume of myofibril in group A were lower than those in group C(P<0.05).The number density of myofibril in group B was higher than that in group C(P<0.05) while no difference was found with the average volume.(6)Positive correlations were found in maternal TBA,fetal TBA,fetal cTnI and the integrate of fetal necrosis area when comparing every two of the above factors. Conclusions Fetal myocardium is impaired obviously in hypercholanemia rats.The serum level of TBA and cTnI in fetal rats are positively correlated with each other.

With the development of higher education reform, cultivating students' practice ability and innovation consciousness has become the key task of experimental teaching . Aimed at training innovative talent, human anatomy department of Mudanjiang Medical University took mea-sures to reform practical contents of human anatomy such as introduction of animal organs, development of scientific research, and by setting the abundant practical teaching content and appraisal method, constructed the anatomy practice teaching system based on cultivating the innovation ability of medical students, which stimulated the enthusiasm of students for anatomy and improved quality of human anatomy teaching.

[ ABSTRACT] AIM:To investigate the damage in human umbilical vein endothelial cells ( HUVECs) induced by recombinant soluble human CD40 ligand (rshCD40L).METHODS:The cultured HUVECs were treated with rshCD40L for 12 h.The survival activity of the HUVECs was observed by MTS assay.The expression of E-selectin, intercellular ad-hesion molecule (ICAM)-1, tissue factor (TF) and tissue factor pathway inhibitor (TFPI) was measured by ELISA.The activity of superoxide dismutase ( SOD) and the level of malondialdehyde ( MDA) were detected by the methods of thibabi-turic acid (TBA) .RESULTS:Compared with normal group, different concentrations of rshCD40L (0.5, 1, 2, 3 mg/L) had no obvious effect on the survival activity of the HUVECs (P>0.05).rshCD40L at concentration of 0.5 mg/L promo-ted the secretion of E-selectin, sICAM-1, TF and TFPI in the HUVECs (P<0.01).rshCD40L at concentration of 0.5 mg/L also increased MDA content and reduced the activity of SOD in the HUVECs (P<0.05).CONCLUSION:0.5~3mg/L rshCD40L has no obvious effect on endothelial cell survival, but already causes endothelial dysfunction by increas-ing endothelial inflammation and exogenous coagulation reaction, inducing lipid peroxides injury and reducing antioxidant capacity.

BACKGROUND:It is unclear whether hydrogen-rich water can be used to protect skeletal muscle injury induced by eccentric exercise, as wel as the relative mechanism. OBJECTIVE:To observe the effect of hydrogen-rich water on the mitochondrial oxidative stress and inflammation in rat skeletal muscle after eccentric exercise, and to investigate the relative signaling pathway of hydrogen-rich water. METHODS:Forty Sprague Dawley rats were randomly divided into four groups: control group, eccentric exercise group, eccentric exercise+saline group, and eccentric exercise+hydrogen-rich water group. Rats in three eccentric exercise groups were exercised on a motor-driven rodent treadmil at a speed of 16-18 m/min and a slope of-16° for 90 minutes per day. Rats in the eccentric exercise+hydrogen-rich water group were subjected to intraperitoneal injection of hydrogen-rich water (10 mL/kg) immediately after exercise; and rats in the eccentric exercise+saline group were administrated with normal saline after exercise. Al the interventions lasted for 5 days. RESULTS AND CONCLUSION:Hydrogen-rich water intervention after eccentric exercise could markedly enhance the mitochondrial Sirtuin-3 expression, improve the mitochondrial membrane potential and activity of manganese superoxide dismutase, down-regulate the mitochondrial reactive oxygen species generation and mitochondrial DNA oxidative damage, thus inhibiting inflammatory cytokines expression, such as NLRP3 and interleukin-1β. The results indicated that hydrogen-rich saline could directly scavenge reactive oxygen species. In addition, hydrogen-rich water could improve mitochondrial energy metabolism and antioxidant capacity through up-regulation of Sirtuin-3, which in turn inhibits eccentric exercise-induced mitochondrial oxidative stress and secondary inflammation in the skeletal muscle.

~(131)I uptake by thyroid were assayed in 64 patients with Graves′ disease (GD) and 69 patients with non-GD hyperthyroidism. GD group had higher rate of ~(131)I uptake than non-GD group at 2, 6 and 24 h, and there was no overlap between the two groups at these 3 time points.~(131)I uptake at 2 and 6 h could differentiate GD fromlow ~(131)I uptakehyperthyroidism.

AIM and METHODS: to elucidater the effect of poly(ADP-ribose) polymerase(PARP) on tracheal hyperreactivity of guinea - pig induced by peroxynitrite, the responses of guinea pig tracheas to histamine af- ter incubation with peroxynitrite in the absence and presence of 3 - aminobenzamide(3 - AB), a highly selective inhibitor for PARP, were observed in vitro. RESULTS: The exposure of tracheal strips to peroxynitrite led to epithelial damage and hyperreacitivity to histamine, both of which were reversed by 3 - AB(l mmol/L or 5mmol/L), whereas incubation of tracheal strips with 3 - AB(5 mmol/L) had no effect on the reponses. CONCLUSION:PARP is involved in the epithelial damage and hyperreactivity of guinea - pig tracheas induced by peroxynitrite. The results suggested that inhibition of excessive activation of PARP may represent a novel strategy for the prevention and therapy of airway hyperreactivity in asthma.

AIM: To study the role of polymorphonuclear neutrophile(PMN) in lipopolysaccharide (LPS)- induced acute lung injury (ALI) and the protective effect of interleukin - 10(IL - 10) on ALI. METHODS: LPS alone (100 ?g) or LPS+ IL-10 (l ug) was instilled intratracheally into rats. PMN numbers, protein content and malondialdehyde (MDA) content in bronchoalveolar lavage fluid (BALF) were measured. Histological change of lung was also observed. RESULTS: LPS increased significantly PMN numbers, protein content and MDA content in BALF. Histological finding shows PMN accumulation in lung. IL - 10+LPS reduced remarkably PMN numbers ,pro- tein content and MDA content in BALF than those caused by LPS. PMN decreasing was also identified by light microscopy. CONCLUSION: LPS instilled intratracheally causes PMN accumulation in lung and ALI, while IL - 10 could alleviate ALI through reducing PMN accumulation.

AIM and METHODS: The animal model of acute lung injury (ALI) caused by intratracheal instillation of lipopolysaccharides(LPS) in vivo and human peripheral blood polymorphonuclear neutrophil (PMN) in vitro were used to study the effects of sodium nitroprusside (SNP), nitric oxide (NO) donor, on LPS-induced PMN accumulation, microvascular permeability and PMN apoptosis. RESULTS: ① In vivo , PMN accumulation in lung, the protein content in bronchoalveolar lavage fluid (BALF) and the Evans blue dye and monastral blue dye extravasation in lung tissue of LPS group were markedly higher than those of both sham operation group and LPS+SNP group. ② In vitro, the apoptotic percentage of SNP group was much higher than that of control group, while compared with LPS group, SNP+LPS group has significantly higher apoptotic percentage. CONCLUSIONS: SNP intratracheal instillation attenuated LPS-induced microvascular permeability and alleviated ALI. PMN apoptosis induced by SNP may be one of the potential mechanisms underlying the decrease of PMN accumulation in lung tissue.