Objective To observe the distribution of parvalbumin immunoreactive neurons in the hippocampal formation of human fetuses. Methods The distribution of parvalbumin immunoreactive neurons in the hippocampal formation of human fetuses at 30 week were investigated by ABC immunocytochemical technique. Results The abundant parvalbumin immunoreactive neurons were localized in all regions of hippocampal formation, especially in the stratum pyramidale. In the stratum oriens of CA1\|3, the triangle or shuttle parvalbumin immunoreactive neurons with some processes were smaller and scattered in this layer. In the stratum pyramidale, the parvalbumin immunoreactive neurons distributed densely, and the processes run out to the stratum oriens and stratum moleculare. In the stratum moleculare the parvalbumin immunoreactive neurons were sparser than in the stratum oriens and stratum moleculare. The parvalbumin immunoreactive neurons in hilus were denser in the hippocampal formation, compared with the other regions, however, delamination of them was not distinct. The processes of parvalbumin immunoreactive neurons run out to the dentate gyrus. The parvalbumin immunoreactive neurons in the dentate gyrus were mainly localized in the stratum granule. Few immunoreactive neurons distributed in the other layers, which were lightly stained and with no processes. In the subicular complex, the lightly stained neurons with few processes were mainly localized in the stratum pyramidale. Conclusion The abundant parvalbumin immunoreactive neurons presented in all regions of the hippocampal formation, especially in the stratum pyramidale. However, the ripe time of these neurons might be different, neurons in CA3 and hilus were earlier than in the dentate gyrus and subicular complex.

Learning and memory dysfunction caused by diabetes is gaining an increased attention. Diabetes can significantly increasethe risk of dementia, including vascular dementia and Alzheimer's disease; and diabetes itself can lead to mild or moderate cognition decline.Many clinical and experimental datas indicated that deficiency of insulin or insulin resistance can significantly reduce the threshold of cognitivedysfunction and accelerate the progress of cognitive decline. This paper reviewed the effect of insulin and insulin resistance on cognitivefunction in diabetes.

Objective To evaluate the safety of simultaneous transurethral green laser vaporization therapy in benign prostatic hyperplasia (BPH) and nonmuscle-invasive bladder transitional cell carcinoma (NMIBT).Methods The clinical data of 27 patients (observation group) who had undergone simultaneous transurethral green laser vaporization therapy in BPH and NMIBT between May 2004 and October 2010 were analyzed retrospectively.Meanwhile 27 patients(control group) only had undergone green laser vaporization therapy in NMIBT during the same period were selected.Clinicopathologic parameters,rate of recurrence and progression,rate of recurrence in the bladder neck and prostatic urethra were determined and compared.Results The time of follow-up in observation group and control group were (28.61 ± 19.53) and (30.20 ± 21.46) months.The rates of recurrence,progression and recurrence in the bladder neck and prostatic urethra between observation group and control group had no significant differences [ 18.5％ (5/27) vs.25.9％ (7/27),3.7％ (1/27) vs.0,0 vs.0] (P ＞0.05).Conclusion Simultaneous transurethral green laser vaporization of NMIBT and BPH can be safely performed without increasing the risk of tumor recurrence in the prostatic urethra.

Objective MiRNA-10b is an important member of the MiRNA family , which has been proven that miRNA-10b can promote the growth and invasion of a variety of tumor cells .The aim of this study was to to investigate the effect and mechanism of miR-NA-10b on proliferation and invasion of low metastasis of lung cancer cell line (95-C). Methods The recombinant of miRNA-10b was transfected into 95-C by lipofectin method .The experiment set up 3 groups:blank control group , negative control group and miRNA-10b expression plasmid transfected group .MiRNA-10b expression level and KLF4mRNA expression level were detected by real-time fluores-cence quantitative PCR ( RTFQ-PCR) .The cell proliferation was detected by cell proliferation assay .The invasive ability of cell was de-tected by Transwell experiment .The expression of KLF4 protein was assessed by Western blot . Results At 48 hours after transfection, compared with blank control group (1.01 ±0.08) and negative control group (0.86 ±0.07), the miRNA-10b expression level in miRNA-10b expression plasmid transfected group (1.61 ±0.12) increased significantly (P<0.05) and there was no statistical difference between blank control group and negative control group (P>0.05).From the growth curve, the cell proliferation rate was obviously increased in miRNA-10b expression plasmid transfected group ([188.0 ±15.1]/HP) compared with the other two groups ([151.0 ±11.3]/HP), ([136.0 ±10.8]/HP) (P <0.05) and there was no statistical difference between these two groups ( P >0.05 ).Transwell result showed more cells transferred to the other side of Transwell compared with the other two groups ( P <0.05 ) and there was no statistical difference between these two groups (P >0.05).The expression of KLF4 protein decreased in miRNA-10b expression plasmid transfected group compared with the other two groups ( P<0.05).KLF4mRNA expression decreased, but the difference had no statistical significance (P>0.05). Conclusion MiRNA-10b might promote the pro-liferation and invasion of 95-C through down-regulation of KLF4 protein expression .

Objective To explore the effect of Jinmaitong (JMT) on expression of Bax, Bcl-2 and Caspase-3 in hippocampal neurons culturedwith high glucose. Methods Hippocampal neurons were primarily cultured and purified from the hippocampus of new-born SpragueDawley rats. Neuron-specific enolase immunocytochemical method was adopted for the identification of the neurons. They were divided intonormal control group, high glucose group, high-dose JMT (JH) group, middle-dose JMT (JM) group, low-dose JMT (JL) group and a positivecontrol group. 72 hours later, Western blotting was adopted to detect the expression of Bax, Bcl-2 and Caspase-3. Results Comparedwith the normal control group, the expression of Bax and Caspase-3 in the high glucose group significantly increased (P<0.01), and the expressionof Bcl-2 significantly decreased (P<0.05). Compared with the high glucose group, the expression of Caspase-3 and Bax in the positivecontrol group and JH, JM, and JL groups significantly decreased (P<0.01), and the expression of Bcl-2 significantly increased (P<0.05).Compared with the positive control group, the expression of Caspase-3 and Bax significantly decreased in JH, JM, and JL groups (P<0.05),and the expression of Bcl-2 significantly increased in JH and JM groups (P<0.05). Conclusion JMT may reduce apoptosis by inhibiting theexpression of Bax and Caspase-3 and promoting the expression of Bcl-2.

Objective To evaluate a new computer-aided technique applicable for myocardial contrast echocardiography(MCE) to quantitate automatically calibrated myocardial contrast intensity(CD and to test the feasibility of calibrated CI in assessing myocardial perfusion. To analyze the relationship on myocardial perfusion,regional contractile function and cell apoptosis in stunned myocardium. Methods According to coronary occlusion and reperfusion at different times, rabbits were divided into three groups: 15 min occlusion/30min reperfusion (group Ⅰ ),30 min occlusion / 60min reperfusion (group Ⅱ ) and 120 min occlusion / 60min reperfusion (group Ⅲ ). MCE was performed on all rabbits at baseline,occlusion and after reperfusion,and its images were analyzed by a new computer-aided technique. Myocardial calibrated CI of each segment was measured automatically by software. Percentage wall thickening (WT) of each risk segment at each stage were also measured by echocardiography. The apoptotic index(AI) in regional left myocardial dysfunction was calculated by terminal deoxynucleotidyl transferease-mediated biotinylated deoxyuridine triphosphate nick end labeling(TUNEL ). Results (1) During occlusion, WT in the areas at risk decreased to zero or negative and the calibrated CI values were significantly lower than those at baseline ( P ＜0.01 ). After reperfusion, WT in all risk segment remained depressed, but calibrated CI significantly improved in group Ⅰ and Ⅱ while those remained unchanged in group Ⅲ. (2)AI in risk myocytes were (13. 70 ± 5.48 ) %, (36.25 ± 5.55 ) % and ( 62.06 ± 6. 70 ) %, respectively, both statistically significant difference between the two groups ( P ＜0.05 or P ＜ 0.01 ). AI were negatively correlated to WT and calibrated CI ( r = - 0. 87 and r = - 0. 77, P ＜0.05). Conclusions MCE with computer-aided technique can assess quantitatively myocardial perfusion and regional contractile function. Short-term ischemiareperfusion does not cause myocardial necrosis, but it will lead to myocardial cell apoptosis and the phenomenon of myocardial stunning. Prolonged ischemia, even if given sufficient reperfusion, can lead to apoptosis and necrosis simultaneously.

BACKGROUND: Nitric oxide in the central nervous system is involved in controlling the sympathetic outflow. The authors' recent data show that the reduction of nitric oxide in the rostral ventrolateral medulla (RVLM)enhanced the cardiac sympathetic afferent reflex (CSAR) evoked by stimulating the cardiac sympathetic afferent nerves in rats with chronic heart failure (CHF).OBJECTIVE: To further investigate the effect of nitric oxide in the RVLM on modulating the CSAR evoked by epicardial chemical stimulation in rats with CHF.DESIGN: Randomized controlled experiment.SETTING: Department of Physiology, Nanjing Medical University, and Department of Cellular and Integrative Physiology, University of Nebraska College of Medicine.MATERIALS: This study was carried out in the Department of Physiology, Nanjing Medical University from July 2003 to May 2004. A total of 52male Sprague-Dawley rats weighing 360-420 g were used, and were randomly divided into chronic heart failure group and control group with 23 in each group.METHODS: The rats were carried out either sham surgery or the left coronary artery ligation. Six to eight weeks later, all rats were anesthetized with α-chloralose and urethane and baroreceptor denervated and vagotomized. The CSAR was evoked by epicardial application of bradykinin (BK, 0.04 μg and 0.4 μg in 2.0 μL) to mimic the effect of chemical stimulation on the heart in the CHF state. The renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP) and heart rate (HR) were recorded at baseline and during elicitation of the CSAR. Cannulae were inserted into the RVLM for microinjections.croinjection of MeTC, a nitric oxide synthase inhibitor, into the RVLM on Effects of epicardial pretreatment with lidocaine on the CSAR in CHF rats.infarction of (30.6±2.0) % of the left ventricular (LV) surface. The systolic arterial pressure, pulse pressure, left ventricle peak systolic pressure and maximum of the first differentiation of left ventricular pressure were decreased and the left ventricular end-diastolic pressure was significantly ininto the RVLM had no significant effects on the CSAR in rats with CHF,of SNAP (50 nmol) into the RVLM inhibited the CSAR in both sham rats ventricle abolished the CSAR evoked by epicardial application ofBK on the same area.CONCLUSION: Nitric oxide in the RVLM inhibits the CSAR evoked by epicardial application of BK in normal rats and CHF rats, and the reduction of nitric oxide in the RVLM led to the augmentation of the CSAR in CHF rats.

Objective To investigate function of collapsin response mediator protein 5 ( CRMP5 ) on neurite outgrowth.Methods The CRMP5 eukaryotic expression vector was constructed and transfected into hippocampal neurons . The gene transfection, Real-time quantitative PCR and Western blotting were used to detect expression of CRMP 5 protein. The lapse-time imaging and neurite extraction were utilized to show neurite outgrowth and differentiation and 3 double-pored were performed, compared with the vector without CRMP5 gene.Results It was successful to construct the CRMP5 eukaryotic expression vector with an EGFP tag .The lipofectamine effectually transfected CRMP 5 into cultured neurons , and the CRMP5 protein was expressed successfully more than the control cells .CRMP5 protein was abundant in cell body , initiation and end of neurites .Overexpression of CRMP5 in neuronal cells significantly promoted outgrowth neurites , and led to the formation of longer neurites with more branches .Accompanying rapid outgrowth of neurites , branches from original neurites were contributed to form a network .The results of neurite length and extraction showed that neurons overexpressing CRMP5 were possessed more and longer neurites (P<0.01), compared with control cells .Conclusion The results suggest that CRMP5 accelerates not only axonal growth but also branching .

Objective To understand the malignancy hospitalization expense of malignancy in Shanxi Cancer Hospital and provide a reference for the effective control of hospitalization expense.Methods 89 716 malignancy hospitalization cases in Shanxi Cancer Hospital from 2003 to 2010 were reviewed.Hospital costs of top six malignant tumors were analyzed.Results The hospitalization expense of 6 kinds of malignancy increased in varying degrees.In all cancer patients,the top six number of cases were lung cancer,cervical cancer,stomach cancer,breast cancer,esophageal cancer and colon cancer,there were a total of 89 716 passengers.The growth rate of cervix malignancy' s expense was the fastest.Conclusion Malignancy hospitalization is expensive,comprehensive measures need to be used to control the expense and make full use of health resources.

Objective To explore a new pathogenic gene mutationin in COL4A3 and COL4A4 genes of a family with thin-basement-membrane nephropathy (TBMN), and explain its mechanism.Methods Genomic DNA was extracted from blood samples.Mutation screening for all the exons in COL4A3 and COL4A4 of the proband was carried out by direct PCR sequencing.The sequences of the proband were compared with standard sequences in GenBank.After identifying the mutation in COL4A4, screening for the mutation site in 200 healthy controls and the rest of family members were conducted.RNA sequence of the proband was analyzed by reverse transcription PCR and TA cloning.The positive clones were sequenced for RNA screening.Results There was a G to A mutation in the 1459 site of COL4A4 (c.1459+G ＞ A) in the proband, her mother, and the elder sister, whereas the mutation was not found in other family members and healthy people.RNA screening showed that the COL4A4 (c.1459+G ＞ A) mutation was a heterozygous substitution in position + 1 of exon 21, in the splicing region.This mutation leaded to eliminating of exon 21 from the COL4A4 mRNA, causing the exon 21 deletion and frameshift mutation following the exon 20 in its amino acids sequence.Conclusions It is described that COL4A4 (c.1459+G ＞ A) is a new pathogenic mutation in TBMN, which further help understanding the pathogenesis and clinical diagnosis of TBMN.