Objective To explore the magnetic resonance spectroscopy characteristics of prefrontal white matter in bipolar Ⅱ disorder and its relation with executive function.Methods Thirty bipolar Ⅱ disorder patients and twenty healthy controls were evaluated with Multi-Voxel proton magnetic resonance spectroscopy (1H-MRS)scans on prefrontal white matter to assess the N-acetyl-aspartate (NAA),Choline (Cho),Creatine (Cr) and myoinositol (MI),and then the ratios of NAA/Cr,Cho/Cr,MI/Cr,NAA/Cho and NAA/Cho + Cr were calculated.All subjects were assessed for executive function using the Wisconsin Card Sorting Test (WCST).Results NAA/Cr in right prefrontal white matter(1.43 ± 0.26) and NAA/Cr,NAA/Cho,NAA/Cho + Cr in left prefrontal white matter (separatelyl.40 ± 0.29,1.13 (1.53,0.24),0.62 ± 0.12) were lower than healthy controls (separately 1.58 ±0.18,1.59,0.23,1.30 (0.53 ± 0.29),0.71 ± 0.08) (P ＜ 0.05).The correct trials and the number of categories of WCST in Bipolar Ⅱ disorder (separately 26.97 ± 8.97,3(6,3)) were less than in healthy controls(separately 36.35±4.85,5 (3,2)),and perseverative errors and random errors were more in patients (separately 12.77 ±5.73,7 (21,5)) than healthy controls (separately 7.35 ± 3.01,4 (13,2)).NAA/Cho and NAA/Cho + Cr in left prefrontal white matter were positively correlated with correct trials,number of categories,and negatively related with perseverative errors (P＜0.05).Conclusions Bilateral prefrontal white matter fiber damage occurs to bipolar Ⅱ disorder.And left prefrontal white matter fiber damage in bipolar Ⅱ disorder may lead to executive impairment.

Objective To investigate the effect of shRNA-mediated down-regulation of the receptor for activated C kinase 1 (RACK1) gene on the chemotherapeutic sensitivities in human lung adenocarcinoma cell line A549.Methods The shRNA recombinant plasmid targeting to human RACK1 gene was designed and transferred into A549 cells by lipofectin technique.The protein level of RACK1 was measured by Western blot to confirm the function of shRNA plasmid.Drug sensitivities of A549 cells to cisplatin,gemcitabine,pemetrexed and paclitaxel were analyzed by MTT assay.The protein expression of LRP and MRP were detected by Western blot.Results After 24 hours transfection,the relative expression quantity of RACK1 protein in RACK1-shRNA group was 0.267± 0.470,which was significantly lower than that in vector-shRNA group (0.821±0.109) and control group (0.842±0.060) (F =54.438,P ＜ 0.05).The results of MTT showed that the growth of A549 cells in the RACK1-shRNA group was markedly inhibited.The sensitivities of A549 cells to cisplatin and paclitaxel were significantly enhanced compared with that in the vector-shRNA group and control group (P ＜ 0.05).The relative expression quantity of LRP and MRP protein in RACK1-shRNA group were 0.163±0.056 and 0.246±0.050,which were lower than that in vector-shRNA group and control group (F LRP =19.430,F MRP =61.548,both P ＜ 0.05).Conclusion Targeted gene silencing of RACK1 improves the sensitivity of A549 cells to the ascisplatin and paclitaxel medicines,which might be achieved through down-regulation of the expression of LRP and MRP.

PURPOSE: The objective of this study was to observe the neurodevelopmental outcomes of the surviving very low birth weight infants (VLBWIs) and to identify the perinatal risk factors having influences on to poor neurodevelopmental outcomes . METHODS: The VLBWIs weighing 500 to 1,499 g at birth who had survived to discharge from one NICU during about a 2 year period were followed-up and assessed with using the Baley Scales of Infant Development-Second Edition (BSID-II) test and neurologic examinations when the infants corrected age was between 12 and 24 months. Developmental delay was defined as a MDI less than 70 or a PDI less than 70. The birthweight specific rates of developmental delay and cerebral palsy were examined. The perinatal data were retrospectively collected from the medical records to identify peinatal risk factors that had an influence on poor neurologic outcomes. RESULTS: Thirty three (42.9%) of the 77 VLBWIs were assessed with the BSID-II and neurologic examination, when their corrected age was between 12 and 24 months. The rate of developmental delay and cerebral palsy in the assessed infants was 15.2% and 21.2%, respectively. Extremely low birth weight infants (ELBWIs) had high rates of developmental delay (30.8%) and cerebral palsys (30.8%). Maternal old age (>35 years, odds ratio=18.0, 95% CI, 1.2-262.7, P=0.035) and periventricular leukomalacia (PVL, odds ratio=12.6, 95% CI, 1.1-148.1, P=0.044) were independently associated with developmental delay and cerebral palsy, respectively. CONCLUSION: Significant poor neurodevelopmental outcome for the VLBW infants needs a more extended follow-up study for development, and especially for the ELBWIs.
Cerebral Palsy ; Follow-Up Studies ; Humans ; Infant* ; Infant, Low Birth Weight ; Infant, Newborn ; Infant, Very Low Birth Weight* ; Leukomalacia, Periventricular ; Medical Records ; Neurologic Examination ; Parturition ; Retrospective Studies ; Risk Factors ; Weights and Measures

Spontaneous intestinal perforation is characterized by isolated mucosal ulceration with acute inflammation, submucosal edema and serosal inflammation, and considered as a separate clinical entity from necrotizing enterocolitis. The causes of spontaneous intestinal perforation are administration of indomethacin, dexamethasone, umbilical artery catheterization, defect of intestinal musculature, and systemic candidasis. Intestinal perforation caused by defects of intestinal musculature is rare, and its pathogenesis remains uncertain. The authors report one case of a premature infant with defect in intestinal musculature confirmed through postoperation biopsy who was misdiagnosed as intestinal perforation due to necrotizing enterocolitis.
Biopsy ; Catheterization ; Catheters ; Dexamethasone ; Edema ; Enterocolitis, Necrotizing ; Humans ; Indomethacin ; Infant, Newborn ; Infant, Premature ; Inflammation ; Intestinal Perforation* ; Ulcer ; Umbilical Arteries

PURPOSE: To investigate whether growth hormone (GH) has a protective effect on neurons in hippocampal slice cultures of neonatal rats exposed to oxygen-glucose deprivation (OGD). METHODS: Cultured hippocampal slices of 7-day-old rats were exposed to OGD for 60 min. Then, the slices were immediately treated with three doses of GH (5, 50, or 500 micrometer) in media. The relative fluorescent densities of propidium iodide (PI) uptake in the slices and relative lactate dehydrogenase (LDH) activities in the media were determined and compared between each GH-treated group of slices and untreated slices (control) at 12 and 24 h after OGD. Immunofluorescent staining for caspase-3 and TUNEL staining were performed to observe the effect of GH on apoptotic neuronal death. RESULTS: The relative fluorescent densities of PI uptake in CA1 and dentate gyrus (DG) of the hippocampal slices in each GH-treated group were not significantly different from those in the untreated slices at 12 and 24 h after OGD (P>0.05). Treatment with GH could reduce the relative LDH activities in the media of the GH-treated groups only at 12 h after OGD (P<0.05). Expression of caspase-3 and TUNEL positivity in CA1 and DG of the slices treated with 50-iM GH were not different from those of the untreated slices at 12 and 24 h after OGD. CONCLUSION: Treatment of hippocampal slice cultures with GH after OGD does not show a definitive protective effect on neuronal death but can reduce the LDH efflux of the slices in media at 12 h after OGD.
Animals ; Apoptosis ; Caspase 3 ; Dentate Gyrus ; Growth Hormone ; In Situ Nick-End Labeling ; L-Lactate Dehydrogenase ; Neurons ; Propidium ; Rats

PURPOSE: To investigate whether growth hormone (GH) has a protective effect on neurons in hippocampal slice cultures of neonatal rats exposed to oxygen-glucose deprivation (OGD). METHODS: Cultured hippocampal slices of 7-day-old rats were exposed to OGD for 60 min. Then, the slices were immediately treated with three doses of GH (5, 50, or 500 micrometer) in media. The relative fluorescent densities of propidium iodide (PI) uptake in the slices and relative lactate dehydrogenase (LDH) activities in the media were determined and compared between each GH-treated group of slices and untreated slices (control) at 12 and 24 h after OGD. Immunofluorescent staining for caspase-3 and TUNEL staining were performed to observe the effect of GH on apoptotic neuronal death. RESULTS: The relative fluorescent densities of PI uptake in CA1 and dentate gyrus (DG) of the hippocampal slices in each GH-treated group were not significantly different from those in the untreated slices at 12 and 24 h after OGD (P>0.05). Treatment with GH could reduce the relative LDH activities in the media of the GH-treated groups only at 12 h after OGD (P<0.05). Expression of caspase-3 and TUNEL positivity in CA1 and DG of the slices treated with 50-iM GH were not different from those of the untreated slices at 12 and 24 h after OGD. CONCLUSION: Treatment of hippocampal slice cultures with GH after OGD does not show a definitive protective effect on neuronal death but can reduce the LDH efflux of the slices in media at 12 h after OGD.
Animals ; Apoptosis ; Caspase 3 ; Dentate Gyrus ; Growth Hormone ; In Situ Nick-End Labeling ; L-Lactate Dehydrogenase ; Neurons ; Propidium ; Rats

PURPOSE: We intended to observe cell death and apoptotic changes in neurons in organotypic hippocampal slice cultures following oxygen-glucose deprivation (OGD), using propidium iodide (PI) uptake, Fluoro-Jade (FJ) staining, TUNEL staining and immunofluorescent staining for caspase-3. METHODS: The hippocampus of 7-day-old rats was cut into 350 micrometer slices. The slices were cultured for 10 d (date in vitro, DIV 10) and and exposed to OGD for 60 min at DIV 10. They were then incubated for reperfusion under normoxic conditions for an additional 48 h. Fluorescence of PI uptake was observed at predetermined intervals, and the cell death percentage was recorded. At 24 h following OGD, the slices were Cryo-cut into 15 micrometer thicknesses, and Fluoro-Jade staining, TUNEL staining, and immunofluorescence staining for caspase-3 were performed. RESULTS: 1) PI uptake was restricted to the pyramidal cell layer and DG in the slices after OGD. The fluorescent intensities of PI increased from 6 to 48 h during the reperfusion stage. The cell death percentage significantly increased time-dependently in CA1 and DG following OGD (P< 0.05). 2) At 24 h after OGD, many FJ positive cells were detected in CA1 and DG. Some neurons had distinct nuclei and processes while others had fragmented nuclei and disrupted processes in CA1. TUNEL and immunofluorescent staining for caspase-3 showed increased expression of TUNEL labeling and caspase-3 in CA1 and DG at 24 h after OGD. CONCLUSION: The numerous dead cells in the slice cultures after OGD tended to display apoptotic changes mediated by the activation of caspase-3.
Animals ; Anoxia ; Apoptosis ; Brain ; Caspase 3 ; Cell Death ; Fluoresceins ; Fluorescence ; Fluorescent Antibody Technique ; Hippocampus ; In Situ Nick-End Labeling ; Ischemia ; Neurons ; Propidium ; Pyramidal Cells ; Rats ; Reperfusion

No abstract available.

Objective To study the relationships between microscopic marginal extensions and tumor types ,and ultrasonic characteristics of malignant liver tumors . Methods Two‐dimensional ultrasonography , contrast‐enhanced ultrasonography and ultrasound‐guided biopsy of hepatic tumors and surrounding hepatic tissues were performed in 78 patients with malignant liver tumor . Pathological microscopic extensions were observed after hematoxylin‐eosin staining of biopsy specimens . Results T he microscopic marginal extension rates of hepatocellular carcinoma ( HCC) ,intrahepatic cholangiocarcinoma ( ICC) and metastatic liver cancer ( M LC) were 62 .5% ( 30/48 ) ,87 .5% ( 7/8 ) ,and 91 .0% ( 20/22 ) ,respectively . For tumors with well‐defined and poorly‐defined two‐dimensional ultrasound boundary ,microscopic marginal extension rates were 50% ( 14/28) ,and 86% ( 43/50) . T umor type and two‐dimensional ultrasound boundary were independent predictors for microscopic extension rate ( P ＜ 0 .05 ) . T he median microscopic extension distances of HCC ,ICC and M LC were 1 .0 ( 0 ,3 .0 ) mm ,4 .0 ( 2 .3 ,4 .0 ) mm ,and 2 .0 ( 1 .8 ,4 .0 ) mm ,respectively . T he distance of microscopic extension increased with tumor size . T umor type and tumor size were independent predictors for the distance of microscopic extension ( P ＜0 .05) . Conclusions ICC ,MLC ,and tumors with larger diameter or poorly‐defined two‐dimensional ultrasound boundary have a larger distance of microscopic extension .

Objective: To study the relationships between microscopic marginal extensions and tumor types, and ultrasonic characteristics of malignant liver tumors. Methods: Two-dimensional ultrasonography, contrast-enhanced ultrasonography and ultrasound-guided biopsy of hepatic tumors and surrounding hepatic tissues were performed in 78 patients with malignant liver tumor. Pathological microscopic extensions were observed after hematoxylin-eosin staining of biopsy specimens. Results: The microscopic marginal extension rates of hepatocellular carcinoma (HCC), intrahepatic cholangiocarcinoma (ICC) and metastatic liver cancer (MLC) were 62.5%(30/48), 87.5%(7/8), and 91.0% (20/22), respectively. For tumors with well-defined and poorly-defined two-dimensional ultrasound boundary, microscopic marginal extension rates were 50%(14/28), and 86%(43/50). Tumor type and two-dimensional ultrasound boundary were independent predictors for microscopic extension rate (P<0.05). The median microscopic extension distances of HCC, ICC and MLC were 1.0(0, 3.0)mm, 4.0(2.3, 4.0)mm, and 2.0(1.8, 4.0)mm, respectively. The distance of microscopic extension increased with tumor size. Tumor type and tumor size were independent predictors for the distance of microscopic extension (P<0.05). Conclusions ICC, MLC, and tumors with larger diameter or poorly-defined two-dimensional ultrasound boundary have a larger distance of microscopic extension.