Administrative Personnel ; psychology ; Burnout, Professional ; Female ; Humans ; Male ; Reproducibility of Results ; Research Personnel ; psychology ; Surveys and Questionnaires

Objective To investigate the correlation between the characteristics of intracranial lesions and the level of cognitive function in patients with an initial diagnosis of brain metastases.Methods A retrospective analysis was performed in 51 patients with an initial diagnosis of brain metastases who were admitted to The Second Hospital Affiliated to Suzhou University from January 2015 to April 2016.CT and (or) MRI were used to determine the characteristics of intracranial lesions and the Montreal Cognitive Assessment was used to evaluate the cognitive function of patients.Comparison between groups was made by Mann-Whitney U test.The correlation between ranked data was analyzed by Spearman rank correlation test.Results Of the 51 patients with an initial diagnosis of brain metastases,47(92%) had cognitive impairment,including mild cognitive impairment in 31(61%) and dementia in 16(31%).There was no significant difference in level of cognitive function between the patients with involvement of the left hemisphere alone and those with involvement of the right hemisphere alone (P=0.425).The patients with involvement of both hemispheres had a significantly lower level of cognitive function than those with involvement of the left hemisphere alone (P=0.042).The patients with involvement of three or more brain lobes had a significantly lower level of cognitive function than those with involvement of one or two brain lobes (P=0.015,0.024).The intracranial lesion volume and edema volume had no significant effect on the overall cognitive function of patients (P=0.077,0.178).The patients with>3 intracranial lesions had a significantly lower level of cognitive function than those with 1-3 intracranial lesions (P=0.010).Conclusions More than 90% of patients with an initial diagnosis of brain metastases have cognitive impairment.Cognitive impairment is mainly associated with lesion site,involvement of brain lobes,and number of lesions,but not with lesion volume and edema volume.

Objective To explore the effects of pretreatment with different doses of curcumm on the expression of p-CREB and PGC-1α in hippocampus after global cerebral ischemia-reperfusion (IR) injury in rats.Methods Three hundred male SD rats weighing 200-250 g were randomly divided 5 groups ( n = 60 each): sham operation group (group S), IR group, low, median and high dose curcumin group (group LC, MC, HC). Global cerebral ischemia was produced by occlusion of 4 vessels (cauterization of bilateral vertebral arteries and 15 min occlusion of bilateral common carotid arteries) according to the method described by Finkbeiner. Bilateral common carotid arteries were only exposed but not ligated in group S. Intraperitoneal curcumin 30, 100 and 300 mg/kg were injected at 1 h before ischemia in group LC, MC and HC respectively. Equal volume of dimethylsulfoxide (DMSO) was injected intraperitoneally in group S and IR. The rats were killed at 2, 6, 24 and 72 h and 7 d after reperfusion (12 at each time point). Brains were immediately removed and hippocampus was isolated. The number of apoptosis neurons was counted using TUNEL. The expression of p-CREB and PG C-1α protein in hippocampus was detected by Western blot. Results The number of apoptosis neurons, p-CREB and PG C-1α protein expression were significantly higher at each time point in the other 4 groups than in group S ( P ＜ 0.05). The number of apoptosis neurons was significantly lower at T2-4 in group LC and MC, while p-CREB and PG C-Ⅰα protein expression wes significantly higher at T1-4 in group LC, MC and HC than in group IR (P ＜ 0.05). The number of apoptosis neurons was significantly higher, while p-CREB and PGC-1α protein expression was significantly lower at T2-4 in group LC and HC than in group MC ( P ＜ 0.05). Conclusion Curcumin can inhibit neuronal apoptosis in hippocampus and reduce global cerebral IR injury by up-regulating p-CREB and PG C-1α expression in rats and the effect was dose-related.

Objective To observe the changes of abdominal oxygen saturation in very low birth weight infants (VLBWI)with feeding intolerance (FI)within 1 4 days after birth monitored by near infrared spectroscopy (NIRS).Methods VLBWI fitting entry criteria were enrolled into this study.NIRS monitoring was carried out to detect cerebral oxygen saturation (ScO2 )and abdominal oxygen saturation (SsO2 ).Data were analyzed between FI infants and feeding tolerance (FT)infants.FI was defined as follows:gastric residual of more than 50% of the previous feeding volume;emesis or abdominal distention or both;decrease,delay or discontinuation of enteral feedings. Results 93 VLBWI were enrolled.52 cases(55.91 %)presented with FI,including 29 cases(31 .1 9%)of gastric residual increasing and 23 cases(24.73%)of emesis with or without abdominal distention within 1 4 days after birth. The levels of SsO2 and SsO2 /ScO2 showed no differences in infants with FT and with FI within 24h after birth (P >0.05).The change rates of the median of SsO2 and SsO2 /ScO2 in FT infants were similar during 1 4 days (P >0.05).While both the change rates of SsO2 and SsO2 /ScO2 were markedly decreased 1 day before and the day of FI (P <0.01 ).The decreasing degree of SsO2 was similar between infants with gastric residual increasing and infants with emesis with or without abdominal distention[(1 6.2 ±5.1 )vs (1 7.4 ±3.6)%,t =0.733,P =0.476]. Conclusion Abdominal oxygen saturation measured by NIRS may be a useful method for infants adjusting the feeding plan.

OBJECTIVE:To provide reference for promoting rational use of essential medicines. METHODS:Combined with the actual situation of our hospital,a set of risk prevention and control system on essential medicine was constructed on the basis of relevant laws and regulations and support of information,and then implemented. RESULTS:The implementation of the system greatly promoted cognition of all medical staffs on reasonable,economical and safe use of essential drugs,standardized medication behavior and improved essential medicine use more reasonable. After the implementation of risk prevention and control system on essential medicines,medicine ratio of whole hospital decreased from 34.62% to 32.64%,inpatient medicine ratio decreased from 33.02% to 27.89%;essential medicine ratio of whole hospital rose from 31.22% to 43.34%,inpatient essential medicine ratio in-creased from 23.46%to 39.17%;the proportion of outpatient antibiotics prescriptions decreased from 15.04%to 13.46%,the utili-zation of inpatient antibiotics decreased from 62.11% to 48.47%. Various early warning were sent out 104 times in total,and 23 medical staff were punished due to irrational drug use. The prescription form and rationality of drug use were improved gradually. CONCLUSIONS:The construction of risk prevention and control system on essential medicine is one of the keys to the success of health care reform. It is suggested to make full use of thesystem+technologymeans,establish long-term mechanism for risk pre-vention and control,and constantly improve the system.

Child ; Female ; Humans ; Lymphoma, Extranodal NK-T-Cell

BACKGROUND: More recently,repair of skull defect with computer-designed prosthesis contributes to the revolutionary development of skull reconstruction technique. OBJECTIVE: To individually molded titanium mesh by computer-aided design (CAD) technique,and to observe the clinical application value of the titanium mesh in the repair of large-area skull defects in the fronto- temporo-parietal lobes. DESIGN,TIME AND SETTING: A retrospective case analysis was performed at the Department of Neurosurgery,Liuzhou People's Hospital between January 2006 and August 2007.PARTICIPANTS: A total of 16 patients comprising 12 males and 4 females,aged 16-52 years,suffered from skull defects in the fronto-temporo-parietai lobes following standard large trauma craniotomy and were recruited into this stud Two of these patients were complicated by hydrocephalus and received ventriculoperitoneal shunt. Skull defect area ranged between 9. 2 cm ×11.2 cm and 12.2 cm×14.6 cm. Skull defect neoplasty was performed in all patients 3-8months following standard large trauma craniotomy. METHODS: Titanium mesh patches were individually modeled by CAD,computer-aided manufacturing (CAM) and rapid shaping techniques and implanted into skull defect region. In addition,defect edge was fastened with titanium nails. MAIN OUTCOME MEASURES: Moulding effects and complications following skull defect neoplasty. RESULTS: A small amount of subcutaneous effusion was found in one patient and disappeared after liquid extraction and pressure dressing. Titanium mesh was firmly fixed with no loosening. Patients exhibited left-right symmetry,appropriate lateral curvature,no irregular umbilication or chewing dysfunction. All patients were followed for 3-18 months postoperatively and were satisfied with good resuRs,Le.,no complications,infection,material exposure,loosening,or collapse. CONCLUSION: CAD technique used for repair of skull defects is convenient,effective,and safe. This method can. reduce postoperative complications and improve repair effects.

Objective To investigate rite effects of loag-term exposure to low-level sevoflurane on reproductive function in mice.Method F0ny male ICR mice,aged 60 d,weighlag 20-25 g,were randomly divided into 4 groups(n=10 each):control group received no sevoflunme(C);group S1-3 were exposed to 0.003%.0.01% and 0.03% sevoflurane 2 h per day for 5 consecutive days per week for 8 weeks respectively. The mice were then sacrificed at the end of the 8 weeks.The testes and epididymis were emoved and sampled for determination of the activities of total lactic dehydregenase(LDH)and lactic dehydrogenase-X(LDH-X),and the motility rate,amount,and aberration rate of sperm.Testicular uhrastructure were observed by transmission electron microscopy.Results The sperm motifity nne were significantly lower.the sperm aberration rate higher and the activity of LDH-X lower in group S3 than in group C(P<0.05),but there was no significant difference in the above parametem between group SI and group S2(P>0.05).The pathology changed of testes occurred only in group S3 among the 3 groups.Conclusion Long-term exposure to 0.03% sevoflurane can result in the abnormality of the reproductive function in male mice but exposure to≤0.01%sevoflurane dose not.

Objective To investigate the effect of curcumin on apoptosis in hippocampal neurons and the expression of c-Jun N-terminal kinase 3 (JNK3) and postsynaptic density protein 95 (PSD95) in hippocampus during cerebral ischemia-reperfusion (I/R) in rats with spontaneous hypertension (SH) .Methods One hundred and thirty-five male rats (homologous with WKY) with SH and 90 male normotensive WKY rats, weighing 275-325 g,were used in this study. The WKY rats were randomized into 2 groups ( n = 45 each) : sham operation group (WS group) and cerebral I/R group (W-I/R group) . The rats with SH were randomly divided into 3 groups ( n = 45each) : sham operation group (S-S group), cerebral I/R group (S-I/R group) and curcumin group (S-C group) .Global cerebral ischemia was produced by 4 vessel-occlusion method. The bilateral common carotid arteries were only exposed but not ligated in W-S and S-S groups. Intraperitoneal corn oil 10 ml/kg was injected at 30 min of reperfusion in W-I/R and S-I/R groups. Intraperitoneal curcumin 100 mg/kg was injected at 30 min of reperfusion in S-C group. Three animals in each group were sacrificed at 2 h, 6 h, 1 d, 3 d and 7 d of reperfusion and their brains were harvested for determination of apoptosis in hippocampal neurons and the expression of JNK3 and PSD95in hippocampus. Results The number of apoptotic neurons was significantly increased in S-S group compared with W-S group ( P < 0.05) . The number of apoptotic neurons was significantly increased and the expression of JNK3was up-regulated in S-I/R group compared with S-S group ( P < 0.05) . The number of apoptotic neurons was significantly decreased and the expression of JNK3 was down-regulated in S-C group compared with S-I/R group (P <0.05) . There was no significant difference in the expression of PSD95 among all the groups ( P > 0.05) . Conclusion Curcumin can inhibit apoptosis in hippocampal neurons and the mechanism is related to down-regulation of the expression of JNK3 in hippocampus. The mechanism by which curcumin down-regulates the expression of JNK3in hippocampus may not be related to PSD95 pathway.

Objective To investigate the effect of curcumin pretreatment on endoplasmic reticulum stress induced by global cerebral ischemia-reperfusion (I/R) in rats. Methods One hundred forty-four male SD rats weighing 200-250 g were randomly divided into 4 groups (n = 36 each): sham operation group (group S) ; I/Rgroup; curcumin group (group Cur) and vehicle control group (group VC). Global cerebral I/R was produced by four-vessel occlusion technique in S, I/R, Cur, VC groups. Bilateral vertebral arteries were cauterized. Bilateral common carotid arteries were occluded by clipping for 15 min. Curcumin 200 mg/kg was injected intraperitoneally (IP) at 1 h before cerebral ischemia. Global cerebral ischemia was confirmed by unconsciousness and disappearance of papillary and righting reflex. Animals were sacrificed at 12 h, 1,3 and 7 d of reperfusion. Neuronal apoptosis in hippocampal CA1 region was detected by TUNEL assay. Apoptosis index (AI) was calculated. The expression of glucose regulated protein 78 (GRP78) ,growth arrest and DNA damage inducible gene 153 (GADD153) and caspase-12 protein in hippocampal region was assessed by Western blot analysis. Results Cerebral I/R significantly increased AI and GRP78 and caspase-12 protein expression in hippocampus as compared with group S( P <0.05) . Curcumin pretreatment significantly decreased AI, increased GRP78 protein expression and decreased caspase-12 protein expression as compared with group I/R ( P < 0.05) . There was no significant difference in the GADD153 protein expression among Cur, VC and I/R groups ( P > 0.05) . Conclusion Curcumin pretreatment can significantly reduce global cerebral I/R-induced neuronal apoptosis in hippocampus by increasing GRP78 expression and decreasing easpase-12 expression in hippocampus.