Objective To investigate the clinical effects of laparoscopic repair of esophageal hiatal hernia using Bard CruraSoft PTFE/ePTFE Mesh combined with Toupet partial fundoplication.Methods From August 2006 to April 2007,13 patients with esophageal hiatal hernia(typeⅠin 6 and type Ⅲ in 7)were treated by laparoscopy in our hospital.Under a laparoscope,esophageal hiatal hernia was separated by ultrasonic scalpel,and then repaired using Bard CruraSoft PTFE/ePTFE Mesh with Ethicon Endopath Multifieed Stapler.Afterwards,Toupet partial fundoplication was performed.Results The operation was completed in all the cases without converting to open surgery.The mean operation time was 142 min(115-185 min);mean intraoperative blood loss was 75 ml(25-120 ml);mean time to the first flatus and oral feeding was 32 h(26-37 h);and mean postoperative hospital stay was 4 d(3-6 d).The patients were followed up for 4-11 mon(mean 6.5 mon).The symptoms disappeared in 1 month.Three months after the operation,barium examination found no recurrence of the hernia in the 13 cases.Conclusions Laparoscopic repair of esophageal hiatal hernia with mesh combined with Toupet partial fundoplication is a safe and minimally invasive operation.The method is worth being widely used.

AIM: To study the effect of sphingosine 1-phosphate (S1P) on the increase in microvessel permeability induced by platelet activating factor (PAF). METHODS: The microvessel permeability was assessed by measuring hydraulic conductivity (Lp). To observe the effect of S1P and PAF on vascular endothelial-cadherin (VE-Cadherin), the microvessels were stained with immunofluorescence and examined by laser confocal microscopy. RESULTS: After giving PAF at concentration of 10 nmol/L, the Lp value of rat mesentery microvessel was significantly increased. However, after pretreatment with S1P, PAF did not give rise to a further significant change. The effect of PAF on microvascular endothelial cells could be seen: the formation of endothelial gap was induced, the microvascular fluorescence intensity significantly increased, a large number of fluorescent microspheres (FMs) distributed in the space among the endothelial cells. However, after pretreated with S1P, no obvious gap opening and the FMs accumulation were observed. Compared to normal control, no significant difference of the microvascular fluorescence intensity was found. CONCLUSION: PAF changes the structure of VE-Cadherin, leading to detachment of adherent junction, formation of intercellular gaps, which contributes to the increase in the permeability. S1P improves the increase in the microvessel permeability caused by PAF, which might be mediated by strengthening adherent junction and inhibiting the formation of endothelial gaps.

In order to understand the alcohol's toxicity to the quantitative alternations of synapses in mouse visual cortex, the expression of synaptophysin after prenatal alcohol exposure was investigated. In present study, the experimental mice at P0, P7, P14 and P30 were grouped, as control, 2 g x kg(-1) alcohol treatment and 4 g x kg(-1) alcohol treatment. The pre-synaptic elements which were used to represent synapses were marked with synaptophysin (a synaptic vesicle associated protein) by immunocytochemistry technique. The synaptophysin positive boutons in layer VI of visual cortex were imaged under laser confocal microscope. With stereological methods, the number cal density of synapse in visual cortex was calculated in different groups at various ages. Moreover, Western blotting was carried out to detect the expression of synaptophysin in visual cortex. The results showed that prenatal alcohol exposure could cause synaptic loss with long-term effect and in a dose dependent manner. For instance, there were significant difference among the different treatment groups of P0, P14 and P30 as well (P < 0.05). Western blotting supported the results of immunofluorescent labeling. In conclusion, prenatal alcohol exposure can induce the synaptic loss dose dependently and with long-term effect. Our findings implicate that the synaptic loss with long-term effect in CNS probably contributes to the lifelong mental retardation and memorial lowliness associated with childhood FAS.

The effect of bee pollen of Brassica campestris L. and its alcohol extract on lipid peroxidation was observed in vivo and in vitro.The results showed that the production of lipid peroxides in normal liver hotnogenate of mice and elevation of production of lipid peroxides induced by cysteine and FeSO4 in homogenate were found to be inhibited significantly by in vitro addition of alcohol extract of bee pollen.The elevation of lipid peroxides in serum and liver in adult mice induced by alloxan 75 mg/kg(iv)or by administration of peroxidized corn oil 0.2 ml/mouse was markedly inhibited by oral administration of bee pollen (10 g? kg-1?d-1)for 20 days as compared with respective control groups.The level of lipid peroxide in geriatric mice was also markedly lowered by oral administration of bee pollen (10 g?kg-1?d-1)for 3 months as compared to non-treated geriatric mice.Based on the above in vitro and in vivo experimental results, it may be suggested that bee pollen and its alcohol extract protect tissues against destruction by lipid peroxides.

A series of isoindoline derivatives were designed, synthesized, and evaluated for their double inhibitory activities. All of them were new compounds, and their structures were confirmed by 1H NMR and HR-MS. Preliminary in vitro pharmacological tests showed that all compounds exhibited 5-HT or NE reuptake inhibition activity. Among the tested compounds, compound I-3 exhibited potent inhibitory activity against 5-HT and NE reuptake in vitro, and exhibited potent antidepressant activity in vivo. These compounds designed can be further optimized for finding more potent 5-HT/NE dual reuptake inhibitors and antidepressant candidates as well.
Antidepressive Agents ; chemical synthesis ; chemistry ; Biological Transport ; Drug Design ; Isoindoles ; chemical synthesis ; chemistry ; Serotonin Uptake Inhibitors ; chemical synthesis ; chemistry ; Structure-Activity Relationship

10.3969/j.issn.1007-3969.2013.04.00X

OBJECTIVETo study the effect of medicines for activating blood and reinforcing Qi on the number of new micro-vessels and the protein expressions of VEGF and bFGF in the infarcted myocardium edge area of acute myocardial infarction (AMI) model in rats.

METHODThe AMI model of rats was established. After the successful model establishment, rats were randomly divided into the sham-operated group, the model group, the Danshen-Huangqi (1 : 2) group, the Danshen-Huangqi (1 : 1) group, the Chuanxiong-Huangqi (1 : 2) group, the Danshen group, the Chuanxiong group, the Chishao group and the Shexiang Baoxin pill group, with five rats in each group. Rats in each medicated group were orally administered with drugs as per 13.5 g x kg(-1) x d(-1) once everyday for three weeks. The immunohistochemical SP method was adopted to detect the expression of vWF in myocardial tissues, and count the number of micro-vessels (MVC). The protein expression of VEGF and bFGF in myocardial tissues were determined by Western blot.

RESULTThe new micro-vessels stained by vWF factor could be found in the infarcted myocardium edge area of the sham-operated group, the model group and all of medicated groups. The sham-operated group show unobvious new micro-vessels in myocardial tissues. A small amount of new micro-vessels could be seen in the infarcted myocardium edge area of the model group. Whereas a larger number of micro-vessels could be seen in the infarcted myocardium edge area of all of medicated groups. The differences between the sham-operated group and the model group had statistical significance (P < 0.05). The differences between each medicated group and the model group had statistical significance as well (P < 0.05 or P < 0.01). The lowest protein expression of VEGF and bFGF was found in myocardium of the sham-operated group, with the statistical significance compared with the model group (P < 0.05). Compared with the model group, each medicated group showed significant increase in the protein expression of VEGF and bFGF, with the statistical significance between them (P < 0.05 or P < 0.01).

CONCLUSIONThe Danshen group, the Chuanxiong group, the Chishao group, the Danshen-Huangqi (1 : 2) group, the Danshen-Huangqi (1 : 1) group and the Chuanxiong-Huangqi (1 : 2) group show the effect in promoting angiogenesis. Their mechanism for promoting angiogenesis may be related to the improvement of the protein expressions of VEGF and bFGF, so as to increase the contents of VEGF and bFGF and promote the angiogenesis of new vessels.

Animals ; Drugs, Chinese Herbal ; administration & dosage ; Fibroblast Growth Factor 2 ; genetics ; metabolism ; Humans ; Male ; Microcirculation ; drug effects ; Microvessels ; drug effects ; physiopathology ; Myocardial Infarction ; drug therapy ; physiopathology ; Neovascularization, Pathologic ; drug therapy ; genetics ; metabolism ; Qi ; Rats ; Rats, Sprague-Dawley ; Vascular Endothelial Growth Factor A ; genetics ; metabolism

Objective To identify gene mutations in two families with epidermolytic hyperkeratosis (EHK).Methods Clinical data were collected from two families with EHK.Peripheral blood was isolated from the probands and unaffected family members in the families as well as from 50 healthy controls.PCR was performed to amplify the encoding exons and flanking intron regions of KRT1 and KRT10 genes followed by direct DNA sequencing.Results Two mutations in the KRT10 gene,including a heterozygous acceptor splice site mutation in intron 4 (c.1030-2 A＞G) and a heterozygous missense mutation c.467 G＞A,were identified in the probands of both families,but absent in the unaffected family members or healthy controls.ConclusionThe splice site mutation c.1030-2 A＞G and missense mutation c.467 G＞A might be responsible for the phenotype of EHK in the two families.

Objective To study effect and mechanism of fungus polysaccharide PSM-a of Polyporus sp.M05 on S180 bearing mice. Methods MTT method was used to detect the inhibiting role of PSM-a on S180 cells proliferation in vitro. S180 mice model was established,and was administered by gavage. Tumor volume was detected, and the ratio of tumor to mile weight and inhibiting tumor rate. The activity of NK and LAK cells on the target cells was analyzed by MTT colorimetric assay ;HE stain was used to detect the necrosis of tumor cells. Results PSM-a could inhibit S180 cells grouth in vitro. PSM-a could decrease the tumor weight and increase the ratio of tumor volume and mice weight; Tumor inhibiting rate reached 80% and above when treated with 250 μg/nml PSM-a. PSM-a could increase the activity of NK and LAK cells, and necrosis happened. Conclusion PSM-a could significantly inhibit the growth of S180 cells, and the mechanism bnay be related with the increased killing activity of immunne cells to tumor cells.

Objective To study the role of manganese-enhanced MRI(MEMRI) in the depiction of cortical architecture of rat brain after systemic administration of Mn~(2+) through caudal vein and compare the effects of normal or opened blood-brain barrier on the manganese-enhanced MRI. Methods Fifteen SD rats were randomly divided into three groups according to ranked list of random. Blood-brain barrier was opened in short time by the injection of 30% mannitol via the right internal carotid artery, in group A, then 100 mmol/L MnCl_2 physiologic saline solution was delivered through vena caudalis, and MRI was performed 12 hours later. In group B, 100 mmol/L MnCl_2 physiologic saline solutions was administrated through vena caudalis, following normal saline injection into the right internal carotid artery, and MRI was performed 12 hours later. The group C served as normal control group. All images were acquired with a 7.0 T microMR scanner. Signal-to-noise ratios (SNR) in regions of interest were measured by Paravision 4.0 and the differences of three groups were compared by using one-way ANOVA. The differences of SNR on both sides of hemispheres were compared by using paired t test. Results MEMRI could show the gray matter and white matter of rat brain and the anatomy borders between somatosensory cortex and motor cortex clearly. Periventricular structures such as hippocampus, dentate gyms, habenula united, and olfactory bulb could also be showed clearly. Symmetrical enhancement on both sides of the cortex and banded structures was shown clearly in group B. The SNR increased and the differences were significant in right cerebral cortex, both sides of cerebellar cortex, hippocampus and pituitary, among three groups (right cerebral cortex 35.2±7.0,30.1±2.4,26.6±2.8,F =4.36,P=0.038;left cerebellar cortex 27.1±5.2,29.4±3.8,19.4±4.5, F=6.66, P=0.011;right cerebellar cortex 27.8±3.8,28.5±4.2,20.4±4.8, F=5.84, P=0.017; left hippocampus 34.5±4.9,38.1±5.3,24.5±3.6, F=11.38, P=0.002; right hippocampus 35.3±5.5, 37.6±4.7,25.6±3.0,F=9.93,P=0.003;pituitary 39.5±3.8,52.6±9.1,26.2±4.2,F=22.80, P=0.001) after systemic administration of Mn~(2+). Asymmetric enhancement on two sides of cortex was shown in group A. The mannitol-infused side was enhanced obviously but displayed blurring banded structures. However,the SNR differences of both sides of hemispheres in group A and B were not significant (P >0.05). Conclusions After systemic administration of MnCl_2 through vena caudalis, MEMRI could map the laminar architectures and the anatomy border of functional zone of somatosensory cortex specifically. High concentration of mannitol could open blood brain barrier(BBB) effectively and have distinct impacts on the architectures displayed in MEMRI. Opening or maintaining BBB in MEMRI had respective characteristics, and it should be selected according to practical needs.