Fourteen critical patients were treated by total parenteral nutrition(TPN) or en- teral nutrition(EN) and good results were achieved.Among the1 4patients,1 0 cases were suffered from MSOF.The results suggest thatnutritional support is very im- portant for the critical patients,especially for their rehabilitation and prognosis.The use of TPN is not limited by the gastroin- testinal function.TPN should be sellected preferably when a patient is critical and se- rious.EN should be used when gastroin- testinal function have recovered in order to reduce the translocation of bacteria and en- dotoxin in the gut and decrease gastroin- testinal bleeding.

Tuberous sclerosis complex (TSC) is a genetic disorder affecting every organ system, but disease manifestations vary significantly among affected individuals.The diverse and varied presentations and progression can be life-threatening with significant impact on quality of life.The 2012 international Tuberous Sclerosis Complex Consensus Recommendations provide an evidence-based, standardized approach for optimal clinical care provided for individuals with TSC.

Objective To present one case of bronchial artery aneurysm successfully treated with endovascular interventional procedure and review literature. Methods A 67-year-old man was diagnosed with mediastinal bronchial artery aneurysm accompanied with tuberculous pleurisy by chest imaging. The aneurysm was treated via transcatheter bronchial artery embolization combined with endovascular stent-graft placement in the thoracic aorta under DSA guidance. Results Postprocedural angiography showed satisfactory exclusion of the aneurysm and no endolead. Conclusion Interventional therapeutic management of bronchial artery aneurysm is feasible and accurate.

Objective To explore the dynamic expression of ROCK-Ⅰ,p-MBS Thr-697,α-SMA protein and their mRNA in the hepatic fibrogenesis and the changes of actin cytoskeleton.Methods ROCK-Ⅰ and p-MBS Thr-697 protein in liver were determined by Western blot and their mRNA was examined by reverse transcription-polymerase chain reaction (RT-PCR),while the distribution of ROCK-Ⅰ and α-SMA in liver was assessed immunohistochemis-tically.The change of actin cytoskeleton was shown by fluorescence.Results With the development of hepatic fi-brosis,the positive areas in model groups at week 1 to 4 of ROCK-Ⅰ and α-SMA of the rat livers were larger than that in control group respectively(P <0.05).ROCK-Ⅰ,p-MBS Thr-697 ,α-SMA protein and mRNA were increased than that in control group respectively.ROCK-Ⅰ mRNA expression correlated with α-SMA (r =0.718,P <0.05).With the development of liver fibrosis,the images of fluorescence were inhanced.Conclusion With the develop-ment of liver fibrosis,both protein and mRNA of ROCK-Ⅰ increased.

BACKGROUND:It remains controversial in term of efficacy for the lightweight mesh and heavyweight mesh in inguinal hernia repair.
OBJECTIVE:To compare the clinical therapeutic effects of lightweight mesh and heavyweight mesh in open methods of inguinal hernia repair with Meta-analysis.
METHODS:Comprehensive electronic search strategies were developed using the fol owing electronic databases:PubMed, Cochrane Library, EMBASE, Medline, Ovid, CNKI, VIP, Wanfang and FMJS. The Literature published before February 2013 was searched. The randomized control ed trials about comparing lightweight mesh and heavyweight mesh in open methods of inguinal hernia repair were included. A data-extraction sheet was developed based on the preset standards. The data from eligible studies were pooled using RevMan5.1 software through Meta-analysis.
RESULTS AND CONCLUSION:Eighteen trials with a total of 4 450 hernias met the inclusion criteria. The meta-analysis showed that there was a statistical difference between lightweight mesh group and the heavyweight mesh group on short-term pain [odd ratio (OR)=0.57, 95%confidence interval (CI) (0.43, 0.74), P<0.05] and a reduced risk of developing foreign body sensations [OR=0.49, 95%CI (0.35, 0.69), P<0.05]. No significant differences were found between the two groups in recurrence rate, testicular atrophy, seroma, hematoma, wound infection, urine retention (P>0.5). According to limited evidence, there are some findings as fol ows:the lightweight mesh is of feasibility, safety and effectiveness for inguinal hernia repair. Because of the limits of sample and quality, more large-sample and high-quality trials are required to make a definite clinical evidence to use lightweight mesh for inguinal hernia repair.

ObjectiveTo study the suppressive role of emodin on the growth and its effect on the proliferation cycle and apoptosis of human bladder cancer cell line BIU87.MethodsThe effect of different concentration of emodin at different time point on cell proliferation of BIU87 were measured with methylthiazole (MTT) chromatometry, the cell proliferation cycle were detected with flow cytometry, expressions of bc1-2 and caspase-3 were detected by SP of immunohistochemistry.ResultsWithin a certain range, the higher concentration of emodin (10 ～ 80 μg/ml) and the longer action time are positive related the more significant inhibition of tumor cell growth and the higher apoptosis rate [(9.84 ± 1.13)％, (18.32 ±2.14)％ ,(29.73+1.42)％ ,(42.13 +2.36)％ ,respectively].Compared with control group [(2.01 ±0.92)％], the differences were statistically significant(F =531.85, P ＜0.01).Emodin could inhibit the proliferation of human bladder cancer cell BIU87 by blocking BIU87 cell in G0/G1 stage, thus cut down cell proportion in stage of S [(33.27 +1.26)％ ,(29.17 ±1.39)％, (16.94 ±0.86)％ ,(10.85 ± 1.47)％,respectively], compared with the control group [(35.45 ± 0.38) ％], the differences were statistically significant(F =524.64, P ＜0.01).After 48 h of emodin treatment, the bc1-2 expression(Grayscale values:122.65 + 2.12,131.37 ± 1.62,134.81 ± 1.36,145.55 ± 2.01, respectively) was decreased and the caspase-3 expression(Grayscale values : 135.26 + 1.41,130.22 ± 1.74,126.11 ± 1.77,118.36 + 1.53, respectively) was increased in a dose dependent manner.Compared with control group (Grayseale values:108.42 + 3.73,149.35 ± 1.82, respectively), the differences were statistically significant (F = 216.23,224.83, P ＜0.01).ConclusionsEmodin could significantly inhibit the growth and induce apoptosis of BIU87 cells in vitro, which may be through down regulation of bc1-2, and up regulation of caspase-3, and blocking BIU87 cell in G0/G1 stage.

Objective To investigate the inhibitory effect of emodin on hetertransplanted human bladder cancer in nude mice and explore its mechanism.Methods Heterotransplanted models of human bladder cancer cell line BIU87 cells in nude mice were established.The mice were randomly divided into 4 groups during the experiment:blank control group,Z-VAD-FMK group,emodin group and emodin combined with Z-VAD-FMK group.The growth of tumors was observed and the growth curve was mapped.The nude mice were sacrificed 4 weeks later,the tumors were isolated and weighed.The pathological changes of tumor were observed after HE staining,the cells apoptosis were detected with flow cytometry,and the expression of AIF and Endo G were examined by reverse transcription PCR (RT-PCR) and Western blot.Results The tumor growth rate in emodin group was lower than that in the other three groups.The tumor quality in emodin group [(0.41 ± 0.05 ) g] and emodin combined with Z-VAD-FMK group [( 0.69 ±0.07)g]were lighter than that in the other two groups[(1.08 ±0.13,1.04 ±0.09)g,],and the differences were statistically significant( F =90.56,27.49,P ＜0.01 ).The quality difference in emodin group and emodin combined with Z-VAD-FMK group was statistically significant ( t =10.01,P ＜ 0.01 ).The apoptosis rate in emodin group [(42.71 ±2.69)％]was significantly higher than that in emodin combined with Z-VAD-FMK group[(34.38 ± 1.73)％] ( t =6.38,P ＜0.01 ).The expression of AIF and Endo G in emodin combined with Z-VAD-FMK group was significantly increased than other groups [( 1.65 ±0.12)vs(1.24±0.08),(0.51 ±0.07),(0.48 ±0.04);(2.12 ±0.16)vs(1.75 ±0.13),(0.57 ±0.06),(0.59±0.07);(2.42±0.13)vs(1.73 ±0.11),(0.78 ±0.07),(0.75 ±0.08);(3.13 ±0.25)vs(2.15± 0.18 ),(0.85 ± 0.09 ),(0.81 ± 0.14 )],and the differences were significant ( F =303.22,319.32,409.38,258.53,P ＜ 0.01 ).Conclusions Emodin could significantly inhibit the growth of hetertransplanted human bladder cancer in nude mice.The mechanism might be partly due to the expression increase of AIF and Endo G in bladder cancer cells,which might induce apoptosis through Caspase-independent pathway.

Objective To study the effects of emodin on apoptosis and mRNA and protein of apoptosis inducing factor (AIF) and Endonuclease G (Endo G) in human bladder cancer cells BIU87,and to investigate the anticancer mechanism of emodin. Methods The BIU87 cells were divided into 4 groups,control group,Z-VAD-FMK group,emodin group,emodin combined with Z-VAD-FMK group.The effects of different concentrations of emodin at different action time on cells proliferation of BIU87 in vitro culture were measured by methylthiazole (MTT) chromatometry,the cells apoptosis were detected by flow cytometry,and expression of AIF and Endo G were examined by reverse transcription PCR (RT-PCR) and Western blot.Results MTT assay demonstrated that the higher concentration of emodin and the longer action time,the more significant inhibition of tumor cell growth.Based on the IC50 value,80 μmol/L and 72 h of emodin intervention were selected as an intervention condition.The apoptosis rate in emodin group (44.57 ± 1.52 ) ％was significantly higher than that in emodin combined with Z-VAD-FMK group (35.58 ± 1.61 ) ％ ( P ＜0.01).RT-PCR and Western blot showed that the mRNA and protein of AIF in emodin combined with Z-VAD-FMK group,emodin group,control group,Z-VAD-FMK group were ( 1.74 ± 0.11 ) and (2.59 ±0.13),(1.36±0.08) and (1.89±0.14),(0.37 ±0.02) and (0.53±0.11),(0.42 ±0.06) and (0.44 ± 0.07),respectively.There were significant differences between emodin group and the other groups (P ＜0.01 ).The mRNA and protein of Endo G in emodin combined with Z-VAD-FMK group,emodin group,control group,Z-VAD-FMK group were (2.28±0.15) and (3.31 ±0.36),(1.85 ±0.13) and (2.15 ±0.27),(0.53 ±0.07) and (0.71 ±0.16),(0.61 ±0.04) and (0.67 ±0.22),respectively.The differences were significant between emodin group and the other groups ( P ＜ 0.01 ). Coneltusion Emodin can upgrade the expression of AIF and Endo G in bladder cancer cells BIU87,which can induce apoptosis through Caspase-independent pathway.

Objective To investigate the genotype-phenotype correlation between TSC1 and TSC2 associated tuberous sclerosis complex(TSC).Methods Nineteen infants with TSC were enrolled in the study.Their clinical manifestations and mutations of TSC gene were analyzed by chip capturing and next-generation sequencing.Results Among the total of 19 patients with TSC,13 TSC2 mutations and 4 TSC1 mutations were detected.The ratio of TSC2/TSC1 mutation-positive cases was 3.4/1.Six mutations were novel.There were epilepsy in 10 cases carrying TSC2 mutations,including 4 cases (31％) with refractory to antiepileptic treatment,and 3 cases carrying TSC1 mutations,including 1 case (25 ％)with refractory to antiepileptic treatment.The incidence and severity (grade 2)of epilepsy,brain imaging were not different in TSC2 and TSC1 patients(P =0.480 7,0.462 2).Compared with clinical manifestations,incidence of mental retardation (grade 1 or grade 2) was higher in TSC2 patients (85 ％,11/13 cases) than TSC1 patients (50 ％,2/4 cases).Also,the incidence of moderate and severe mental retardation (grade 2) was higher in TSC2 patients (54％,7/13 cases) in comparison with TSC1 patients(25％,1/4 cases).Compared with the phenotype of TSC2 and TSC1 patients,the frequencies of skin,renal and cardiac lesions were significantly higher in TSC2 patients than TSC1 patients.Conclusions TSC2 mutation may be the prominent molecular pathogenesis in Han population with TSC.TSC2 patients have much profound muhisystemitc leisions than TSC1 patients,including mental retardation,epilepsy,facial angiofibromas and renal angiomyolipomas etc,which should be confirmed further in domestic multicenter and large samples.

Objective To explore the potential changes of connexin Cx36 in hippocampus and cortical neurons of rats with hyperthermia -induced convulsion.Methods Rats were divided into 2 groups according to the random number table method:normal control group and experimental group.Febrile convulsion model was elicited through im-mersion in warm water.The experimental group was generated following febrile convulsion model:hyperthermia group and febrile convulsion group.Among normal control group,hyperthermia group and febrile convulsion group,western blot analysis and immunofluorescence labeling techniques were used to examine the expression of Cx36 protein in the hippo-campus and cortex area.One -Way ANOVA was used to compare the mean of multiple sample,the LSD test was used to compare the two means.Tamhane′s test was used when variance were uneven.Results The incubation period,seizure duration and temperature were (4.39 ±0.08)min,(5.38 ±0.07)min,(41 .87 ±0.06)℃ after hyperthermia-in-duced convulsion,respectively.Western blot analysis showed that the expression of Cx36 protein in the hippocampus and cortex area decreased gradually after 1 0 times of seizure in normal control group,hyperthermia group and febrile convulsion group,and the febrile convulsion group decreased most obviously.Compared with normal control group and hyperthermia group,respectively,in febrile convulsion group Cx36 expression obviously decreased in the hippocampus and cortex in rats with 1 ,5,1 0 seizure times induced by hyperthermia,and with the increase of number of induced con-vulsion,the expression of Cx36 was significantly decreased in the cortex (0.1 04 ± 0.01 2)and CA1 (0.091 ± 0.01 1 ),CA3 (0.090 ±0.01 1 )and DG (0.092 ±0.01 2)areas of hippocampal neurons compared with the normal control group (0.21 2 ±0.01 7,0.1 67 ±0.01 3,0.1 59 ±0.01 4,0.1 71 ±0.01 3)and the hyperthermia group (0.1 89 ± 0.006,0.1 44 ±0.008,0.1 29 ±0.005,0.1 65 ±0.01 1 )(all P <0.05).Furthermore,the extent of reduction in Cx36 expression seemed to correlate with the number of seizures.Conclusion With the increase of thermal seizure frequen-cy,Cx36 expression of rats was decreased obviously which may lower convulsion threshold and lead to recurrent seizures.