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We present a novel laboratory setup for studying the fluid dynamics in liquid metal batteries (LMBs). LMBs are a promising technology suited for grid-scale energy storage, but flows remain a confounding factor in determining their viability. Two important drivers of flow are thermal gradients, caused by internal heating during operation, and electrovortex flow (EVF), induced by diverging current densities. Our setup explores thermal gradients and electrovortex flow separately and in combination in a cylindrical layer of liquid gallium, simulating the behavior in a single layer of an LMB. In this work, we discuss the design principles underlying our choices of materials, thermal control, and current control. We also detail our diagnostic tools - thermocouple measurements for temperature and Ultrasonic Doppler Velocimetry (UDV) probes for velocities - and the design principles which go into choosing their placement on the setup. We also include a discussion of our post-processing tools for quantifying and visualizing the flow. Finally, we validate convection and EVF in our setup: we show that scaling relationships between the nondimensional parameters produced by our data agree well with theory and previous studies., 13 pages, 9 figures

Summary We have developed an ultrasound probe through the centre of which an epidural needle can pass, intended to reduce the rate of contact between bone and needle during epidural insertion. We tested the ability of this probe to identify the lumbar interspace, using A-mode ultrasound, in a submerged plastic model, a porcine phantom and five human volunteers. In the plastic model, the minimum echo representing the interspace was only 8.8% of the maximum echo from the ‘bone’. In the porcine model, the echo variations between the interspace and L3 were up to 48% and the needle was safely inserted into the interspace without bone contact under guidance. The human study also showed that the maximum bone echo was at least three times stronger than the interspace echo. Axial ultrasound guidance, with the needle passing through the probe, offers a method for reducing bone contact during epidural insertion.

The erosion under a spillway can be a long-term issue that threatens the structural integrity of a water reservoir. The heavy rainfall associated with storms or typhoons could cause a serious flood if the spillways do not function properly. The spillway under investigation was suspected to be defective after they had been commissioned in 1987. Potholes and subsurface cavities were confirmed in the safety assessment using various NDT techniques including ground penetrating radar and impact echo. The engineering team applied the repair project that aimed to remedy the deteriorating concrete structure. The GPR inspection was able to differentiate the repaired region from the cavities under concrete slabs. The results were verified against other measurement data obtained independently. Hence, the GPR technique is effective for quality check of grouting repair of spillways. Repetitive GPR scans were also carried out after the rehabilitation of spillways. Not only the quality of repair can be evaluated, but the scans were also provided as the baseline record for long-term condition assessment of the spillway-reservoir system in the future.

The temperature field analysis of electromagnetic rail launcher is an important basis for studying the launching stability and life. Aiming at the rail groove erosion phenomenon, the launching initial segment is selected as the research site. The heat generation mechanism of Joule heat and friction heat is analyzed, the heat source model is established, the three-dimensional finite element simulation model is established and the position, velocity and current waveform of the launching initial section are determined according to the circuit simulation, the finite element simulation results show that the heat in the initial stage of launching mainly concentrates on the contact surface between armature and rail. The friction heat is the main factor affecting the temperature rise of the contact surface, and the uneven distribution of the current density will lead to the uneven temperature distribution of the contact surface.

Through-thickness cone cracking is one of major failures which needs to be considered in the safety calculations and assessment of containment structures in a nuclear power plant. In this paper, numerical study is performed on the through-thickness cone cracking of reinforced concrete slabs subjected to impact by flat-ended projectiles at normal incidence. First, a recently proposed 3D meso-mechanical model together with a recently developed computational concrete constitutive model are briefly described and then employed to study numerically the problem. The present numerical predictions are compared with some available experimental results. Furthermore, the 3D meso-mechanical model predictions are also compared with the numerical results obtained from FEM (finite element method) model. It transpires that the present numerical simulations are in good agreement with available experimental observations for the through-thickness cone cracking of reinforced concrete slabs struck normally by flat-nosed missiles. It also transpires that the 3D meso-mechanical model can predict more accurately than the FEM model in terms of the details of crack patterns though these two models produce similar results for relatively low velocities.

Background Nerve conduction block using high-intensity focused ultrasound (HIFU) has been conducted with nerves of mixed fibres in normal animal models. This study tested the feasibility and safety of HIFU for sensory nerve conduction block in diabetic neuropathic nerves to determine its potential for pain relief. Methods Diabetes was induced in Sprague–Dawley rats using streptozotocin, and HIFU at 2.68 MHz was used for the block. This study consisted of two sections, in vitro and in vivo. For the in vitro experiments, the entire contiguous sciatic–sural nerves were obtained. Compound action potentials and sensory action potentials were recorded in the sciatic and sural nerves, respectively. For the in vivo experiments, compound muscle action potentials (CMAPs) were recorded from the gastrocnemius muscles. All data were expressed as median (range). Results The in vitro results showed that HIFU temporarily inhibited sensory action potentials of the control and diabetic rat nerves to 33.9 (8.2) and 14.0 (10.7)% of the baseline values, respectively, whereas the compound action potentials were suppressed to 53.6 (8.4) and 76.2 (7.5)% of baseline, respectively. The in vivo results showed that HIFU acutely blocked CMAPs to 32.9 (12.6) and 19.9 (10.9)% of baseline in control and diabetic rat nerves, respectively. Measurements of CMAPs and histological exanmination were used for indirect assessment of the safety of the HIFU technique. Conclusions High-intensity focused ultrasound safely and reversibly suppressed nerve conduction in diabetic rat nerves when the stimulation parameters were appropriate. The results suggest that HIFU may have potential to block sensory nerves reversibly and provide peripheral pain relief.

This study investigated the effect of the anti-anginal drug, fendiline, on intracellular free Ca2+ levels ([Ca2+]i)inHA/ 22 human hepatoma cells by using fura-2 as a fluorescent Ca2+ dye. Fendiline (1-100 μM) increased [Ca2+]i with an EC50 of 25 μM. Removal of extracellular Ca2+ reduced the [Ca2+]i signals by 51-5%. Fendiline (10 μM)-induced Ca2+release was abolished by pretreatment with 1 μM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor). Inhibition of phospholipase C with 2 μM 1-(6-((17β 3 methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H pyrrole-2,5-dione (U73122) did not alter 10 μM fendilineinducedCa2+ release.Severalothercalmodulinantagonists, such as phenoxybenzamine (100-200 μM), trifluoperazine (5-50 μM),andfluphenazine N-chloroethane(2-100 μM), hadno effect on[Ca2+]i. Together, it wasfound that fendiline increased [Ca2+]i in human hepatoma cells by discharging Ca2+ from the endoplasmic reticulum in an inositol 1,4,5 trisphosphate-independent manner and by inducing Ca2+entry. This effect of fendiline does not appear to be via antagonism of calmodulin.

Capillary electrophoresis (CE) has been employed for the separation of monoamine transmitters (MAs) and tyrosine (Tyr), combined with electrochemical detection (ED) at a carbon disc electrode. The effects of several factors such as the acidity and concentration of running buffer, the separation voltage, the potential applied to the working electrode and the injection time were investigated to find the optimum conditions. Detection limits (S/N=3) ranged from 48.8 to 315.4 nmol·L−1, and the response was linear over 3 order of magnitude for MAs and Tyr. The proposed method was successfully applied to determine MAs and Tyr in the cerebral cortex, thalamus and spinal cord of rats with satisfactory assay results.

Being in a refuge has benefits in terms of predator avoidance and costs in terms of lost feeding opportunities. We investigated how the relative importance of these costs and benefits changes with increasing body length in two sympatric fish species, the minnow, Phoxinus phoxinus, and the stickleback, Gasterosteus aculeatus, which differ in their morphological anti-predator adaptations. Minnows were slower to emerge after taking refuge than sticklebacks, and spent less time outside it, which is consistent with the idea that minnows, which lack the morphological defences (such as spines) of sticklebacks, are more cautious of predators than the latter. Food-deprivation experiments indicated that the costs of missed feeding opportunities in terms of relative weight loss were lower for minnows than sticklebacks. Therefore hiding in a refuge comes at a lower metabolic cost for minnows than sticklebacks. Both species reduced their hiding time when food deprived and increased it following a predation threat. Furthermore, they both showed a strong trend for longer hiding periods and shorter exploration times outside the refuge with increasing body length. Our results suggest that in sticklebacks the body length-dependence of hiding times was a result of perceived predation risks being constant with increasing body length whereas relative weight losses decreased. Thus larger fish could metabolically afford to be more cautious. In minnows, both the predation risk and metabolic expenditure decreased with increasing body length suggesting that the longer hiding times in larger fish represented a trade-off between the two factors.

The present study was designed to investigate whether the Electroacupuncture (EA) is beneficial to extenuate cerebral injuries following transient Middle Cerebral Artery Occlusion (MCAO), as well as to observe the effect of EA on expression of Basic Fibroblast Growth Factor (bFGF) -like Immunoreactivity (IR) in rat brains. The results indicate that gross neuronal damages include infarction, swelling and neuron loss, accompanied by increased bFGF-like IR expression following MCAO. In peri-infarct striatum, bFGF-like IR was mainly located in astrocytes except some neurons also showed an upregulation of the IR; in frontoparietal cortex, strong induction of bFGF-like IR was mostly seen in neurons. Both the EA applied during ischemia and reperfusion could evidently alleviate cerebral lesion extent, notably upregulate the expression of bFGF-like IR in striatum and cortex, but there was no significant difference between the effects of EA applied during ischemia and reperfusion, except EA applied during reperfusion seems to be more effective in reducing the cerebral swelling. The results implied that, in striatum, astrocytes might play an important role in the protection of neuron via the expression of bFGF; whereas in cortex, neurons may exert autoprotection through secreting bFGF themselves. One possible protective effect of EA lies in regulating the endogenous expression of bFGF.

Background—Endoscopic sphincterotomy (EST) is widely used for the removal of stones from the bile duct, but stones recur in about one fifth of patients.Aims—To investigate hepatic clearance by quantitative cholescintigraphy (QC) in patients after EST and to discern the relationship between biliary emptying and stone recurrence.Methods—One hundred and forty nine patients who had EST and clearance of the bile duct for choledocholithiasis were selected. All patients were confirmed to have complete EST by sphincter of Oddi manometry and underwent QC soon after normalisation of liver function. Regular clinical follow up was performed for each patient.Results—During a mean 36 month follow up, 22 (14.8%) patients developed recurrent stones in the bile duct. Irrespective of the status of the gall bladder, patients with recurrent stones had a slower hepatic clearance of radioisotope during QC compared with patients without stone recurrence, but only the differences in cholecystectomised patients had statistical significance. After carrying out multivariate analysis, one parameter of QC, percentage clearance of maximal count at 45 minutes, was found to be the only significant factor for stone recurrence. All recurrent stones in the common bile duct were successfully removed at endoscopy.Conclusion—Slower hepatic clearance as shown by QC is an important factor responsible for stone recurrence after sphincter ablation.

The phase recognition mechanism of nine groups of position isomers on four crown ether polysiloxanes, OV-1701 and PEG 20M has been investigsated by measuring various thermodynamic parameters. The high selectivity of crown ether polysiloxane phases is due to hydrogen bonding and the extent of fitting between the analytes and the crown ethe cavity. The effects on selectivity of cavity size, heteroatoms and substituent groups on the crown ether are discussed.

We report the long-term clinical outcome of spontaneous carotid cavernous sinus fistulae (CCF) originally supplied by branches arising from the internal carotid artery (Barrow's type B), or type-D lesion that became type B after particulate embolization. A total of 55 patients was included in this study. Their angiography revealed that cortical drainage was absent, and that the arteries supplying the fistulae originated in the dural branches of the internal carotid artery. Thirty-two patients had type-D lesions, which became type-B lesions after obliteration of the external carotid supply by endovascular treatment. The other 23 patients had type-B lesions documented by angiography, and had no embolization. The follow-up period ranged from 8 to 144.5 months. Clinical cure was achieved in 39 patients (70.9%), improvement in eight patients (14.5%), the lesion remained stable in four patients (7.3%), and was aggravated in four patients (7.3%). The number of drainage veins is the only radiographic factor that could predict the outcome. Those patients with single draining veins had a better chance of complete remission. The outcome between the group with original type D lesions after embolization and the group with original type B revealed no statistically significant difference. The time-course to complete cure was significantly shorter in the group with embolization of the external carotid supply. In the four patients whose symptoms were aggravated, embolization was performed, and the result was excellent. The clinical outcome of type-B CCF, or type D converted to type B, is good. Previous external carotid artery embolization can significantly shorten the time to complete cure. Aggressive treatment should be reserved for those who have aggravated symptoms.

The effect of the antifungal drug bifonazole on Ca2+ homeostasis in Madin Darby canine kidney (MDCK) cells was investigated. Cell suspensions were loaded with the Ca2+-sensitive dye fura-2, and the fluorescence changes were measured with a spectrofluorophotometer. At concentrations between 10-80 microM bifonazole increased cytosolic free Ca2+ levels ([Ca2+]i) in a concentration-dependent manner. The Ca2+ signals were partly inhibited by removing extracellular Ca2+. Bifonazole (40 microM) released Ca2+ from the store sensitive to 1 microM thapsigargin, an endopolasmic reticulum Ca2+ pump inhibitor. Bifonazole (40 microM) per se induced capacitative Ca2+ entry while reduced 1 microM thapsigargin-induced capacitative Ca2+ entry. Inositol 1,4,5-trisphosphate may be involved in bifonazole-induced Ca2+ release because inhibiting phospholipase C with 2 microM U73122 partly reduced the bifonazole response. Together, bifonazole increased [Ca2+]i in renal tubular cells by inducing intracellular Ca2+ release and extracellular Ca2+ influx.

The effect of oleamide, a sleep-inducing endogenous lipid in animal models, on intracellular free levels of Ca(2+) ([Ca(2+)](i)) in non-excitable and excitable cells was examined by using fura-2 as a fluorescent dye. [Ca(2+)](i) in pheochromocytoma cells, renal tubular cells, osteoblast-like cells, and bladder cancer cells were increased on stimulation of 50 microM oleamide. The response in human bladder cancer cells (T24) was the greatest and was further explored. Oleamide (10-100 microM) increased [Ca(2+)](i) in a concentration-dependent fashion with an EC(50) of 50 microM. The [Ca(2+)](i) signal comprised an initial rise and a sustained plateau and was reduced by removing extracellular Ca(2+) by 85 +/- 5%. After pre-treatment with 10-100 microM oleamide in Ca(2+)-free medium, addition of 3 mM Ca(2+) increased [Ca(2+)](i) in a manner dependent on the concentration of oleamide. The [Ca(2+)](i) increase induced by 50 microM oleamide was reduced by 100 microM La(3+) by 40%, but was not altered by 10 microM nifedipine, 10 microM verapamil, and 50 microM Ni(2+). In Ca(2+)-free medium, pre-treatment with thapsigargin (1 microM), an endoplasmic reticulum Ca(2+) pump inhibitor, abolished 50 microM oleamide-induced [Ca(2+)](i) increases; conversely, pretreatment with 50 microM oleamide reduced 1 microM thapsigargin-induced [Ca(2+)](i) increases by 50 +/- 3%. Suppression of the activity of phospholipase C with 2 microM U73122 failed to alter 50 microM oleamide-induced Ca(2+) release. Linoleamide (10-100 microM), another sleep-inducing lipid with a structure similar to that of oleamide, also induced an increase in [Ca(2+)](i). Together, it was shown that oleamide induced significant [Ca(2+)](i) increases in cells by a phospholipase C-independent release of Ca(2+) from thapsigargin-sensitive stores and by inducing Ca(2+) entry.

The role of eradication therapy is still controversial in H. pylori-related nonulcer dyspepsia (NUD). The aim of this study was to follow up the H. pylori status after eradication therapy in patients with NUD by using l3C-urea breath test (UBT).Patients with a clinical and endoscopic diagnosis of NUD were included. H. pylori infection was established by endoscopic biopsies and 13C-UBT. Patients with H. pylori infection then received a quadruple therapy with colloidal bismuth subcitrate, metronidazole, tetracycline and lansoprazole. Two months after completion of therapy, endoscopic biopsies and 13C-UBT were performed again to confirm eradication. A follow-up 13C-UBT was carried out again in one year to detect recurrence of H. pylori infection.Eighty-eight of the 148 patients (59.5%) were found to have H. pylori infection by both endoscopic biopsies and 13C-UBT. Anti-H. pylori therapy was given for 55 patients and proved successful in 33 of them two months after the end of therapy. However, recurrence was found one year later in three of these 33 cases, making a recurrence rate of 9.1% (3/33). Three of the 22 cases with unsuccessful eradication were found to have H. pylori eradication at one year by follow-up 13C-UBT. One of the 33 H. pylori-positive patients without anti-H. pylori therapy, who had negative 13C-UBT in one year follow-up, was found taking a high dose and long period of antibiotics.The recurrence rate of H. pylori infection in our study was higher than that in the Western population. Delayed eradication of H. pylori may occur after anti-H. pylori therapy. Spontaneous eradication is rare in patients not receiving anti-H. pylori eradication.

Cathepsin E is found mainly over the gastric surface and foveolar epithelial cells, and it also is found in the metaplastic pyloric glands and cancer cells. The exact function of cathepsin E in gastric mucosa remains unclear. The colonic type (type III) of intestinal metaplasia (IM) is strongly associated with intestinal-type gastric carcinoma. IM is considered to be a precancerous lesion. The aim of this study was to find out the role of cathepsin E in IM, dysplasia and cancer of stomach.Sixty nine biopsy specimens with IM and dysplasia and 33 gastrectomy specimens with gastric carcinoma were fixed, sectioned and stained with PAS-alcian blue stain, high iron-diamine alcian blue stain to classify IM and immunohistochemical stain to localize cathepsin E. Those patients with dysplastic gastric lesions received regular endoscopic follow-up.Fifteen of 69 patients with gastric dysplasia developed cancer in a median 10.5 months follow-up. Severe dysplasia developed carcinoma significantly higher than mild dysplasia (12/20 vs. 1/25, p0.001), and type III intestinal metaplasia seemed to have significantly predilection for severe dysplasia and gastric cancer. Cathepsin E was stained in intestinal metaplasia with dysplastic change in 44/69 specimens (63.8%), and carcinoma in 28/48 (58.3%) specimens, there was no significant difference between intestinal type and diffuse type carcinoma in cathepsin E staining. The positive staining for cathepsin E decreased significantly in severe dysplastic gastric mucosa.Type III IM is commonly associated with severe dysplasia and cancer; it may be a precancerous lesion. The positive staining of cathepsin E decreased with the severity of gastric dysplasia, representing dedifferentiation of the cells.

The effect of clomiphene, an ovulation-inducing agent, on cytosolic free Ca2+ levels ([Ca2+]i) in MG63 human osteosarcoma cells was explored by using fura-2 as a Ca2+ indicator. Clomiphene at concentrations between 5-75 microM increased [Ca2+]i in a concentration-dependent manner with an EC50 of 50 microM. The [Ca2+]i signal consisted of an initial rise and a sustained phase. Ca2+ removal reduced the Ca2+ signal by 40+/-10%. The [Ca2+]i increase induced by 50 microM clomiphene was inhibited by 80+/-5% by 10 microM nifedipine, but was insensitive to 50 microM La3+ or 10 microM verapamil. In Ca2+-free medium, pretreatment with 50 microM brefeldin A (to disrupt the Golgi complex Ca2+ store), 1 microM thapsigargin (to inhibit the endoplasmic reticulum Ca2+ pump), and carbonylcyanide m-chlorophenylhydrazone (CCCP; to uncouple mitochondria) inhibited 51+/-3% of 50 microM clomiphene-induced Ca2+ release; conversely, pretreatment with 50 microM clomiphene abolished the [Ca2+]i increase induced by thapsigargin, CCCP, and brefeldin A. The Ca2+ release-induced by 50 pM clomiphene was unchanged by inhibition of phospholipase C with 2 microM 1-(6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122). Collectively, the results suggest that clomiphene increased [Ca2+]i, in osteoblast-like cells, by releasing intracellular Ca2+ in a phospholipase C-independent manner and by causing nifedipine-sensitive Ca2+ influx.

In order to investigate the effect of 7-nitroindazole (7-NI) on penicillin-induced epilepsy and the relationship between NO and anti-epileptic effect of electro-acupuncture, computerized physiological polygraph and NO-sensitive electrode with potentiostat were respectively used to record the total power spectrum (TPS) of EEG and the concentration of NO in rat hippocampus pretreated with electro-acupuncture or 7-NI for 30 min before penicillin. The results showed that the TPS of EEG and concentration of NO in hippocampus increased greatly after the epilepsy induction. Treatment with electroacupuncture inhibited the TPS of EEG sharply (P0.01). The latency and threshold of epilepsy induction were decreased by 7-NI, but paroxysm abated and the TPS was inhibited (P0.05) as compared with the control group. Both pretreatments with 7-NI and electroacupuncture decreased the NO concentration (P0.01). The above results suggest that the propagation of penicillin-induced seizures is facilitated by nNOS, but with some increase in the latency and threshold of induction. Electroacupunture may inhibit seizure through decreasing nNOS transcription in hippocampus.

The effect of fendiline, an anti-anginal drug, on cytosolic free Ca2+ levels ([Ca2+]i) in A10 smooth muscle cells was explored by using fura-2 as a Ca2+ indicator. Fendiline at concentrations between 10-50 microM increased [Ca2+]i in a concentration-dependent manner with an EC50 of 20 microM. External Ca2+ removal reduced the Ca2+ signal by 75%. Addition of 3 mM Ca2+ increased [Ca2+]i in cells pretreated with fendiline in Ca2+-free medium. The 50 microM fendiline-induced [Ca2+]i increase in Ca2+-containing medium was inhibited by 10 microM of La3+, nifedipine, or verapamil. In Ca2+-free medium, pretreatment with 1 microM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor) to deplete the endoplasmic reticulum Ca2+ store partly inhibited 50 microM fendiline-induced Ca2+ release; whereas pretreatment with 50 microM fendiline abolished 1 microM thapsigargin-induced Ca2+ release. Inhibition of phospholipase C activity with 2 microM U73122 did not alter 50 microM fendiline-induced Ca2+ release. Incubation with 50 microM fendiline for 10-30 min decreased cell viability by 10-20%. Together, the findings indicate that in smooth muscle cells fendiline induced [Ca2+]i increases. Fendiline acted by activating Ca2+ influx via L-type Ca2+ channels, and by releasing internal Ca2+ in a phospholipase C-independent manner. Prolonged exposure of cells to fendiline induced cell death.

The effect of histamine on intracellular free Ca2+ levels ([Ca2+](i)) in MG63 human osteosarcoma cells was explored using fura-2 as a Ca2+ dye. Histamine increased ([Ca2+](i)) in a concentration-dependent fashion with an EC(50) value of 0.5 microM. Extracellular Ca2+ removal inhibited the ([Ca2+](i)) signals. Histamine failed to increase ([Ca2+](i)) in Ca2+-free medium after cells were pretreated with thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor). Addition of Ca2+ induced concentration-dependent ([Ca2+](i)) increases after preincubation with histamine in Ca2+-free medium. Histamine-induced intracellular Ca2+ release was abolished by inhibiting phospholipase C with 1-(6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122). The ([Ca2+](i)) increase induced by histamine in Ca2+ medium was abolished by cimetidine, but was not altered by pyrilamine, nifedipine, verapamil, and La(3+). Together, this study shows that histamine increased in ([Ca2+](i)) in osteosarcoma cells by stimulating H2 histamine receptors. The Ca2+ signal was caused by Ca2+ release from the endoplasmic reticulum in a phospholipase C-dependent manner. The Ca2+ release was accompanied by Ca(2+) influx.

Using a nitric oxide (NO)-sensitive platinum microelectrode (SNM) modified with chitosan nickel (II) complex and Nafion (Nafion-CTS (Ni)-Pt), we observed the effect of nitric oxide synthase (NOS) inhibitor 7-nitro-indazole (7-NI) and N omega-nitro-L-arginine (L-NNA) on penicillin-treated hippocampal slices by simultaneously recording the stimulus-evoked field potentials and nitric oxide release from CA1 pyramidal neurons. Our results show: (1) The linear relationship range and detection limit of SNM were 4.5 x 10(-4)-1.0 x 10(-8) mol/L and 5.0 x 10(-8) mol/L respectively. (2) Penicillin (PEN) could elevate NO release, the number and amplitude of stimulus-evoked field potentials spike (SEPS) in concentration-dependent manner; (3) Both 7-NI and L-NNA depressed NO release and partly reversed the effect of penicillin. The above findings suggest that convulsant provoking effect of NO could be inhibited by NOS inhibitors. The NO-sensitive electrode may provide an useful tool for continuous detection of NO in biological tissues.

The time course of alteration in neuronal nitric oxide synthase (nNOS) and the influence of glutamate receptor antagonists on immunoreactivity of nNOS were investigated immunohistochemically in rat hippocampus during penicillin-induced epilepsy. It was found that nNOS-like immunoreactivity in hippocampus increased at 4 h after initiation of seizure and reached a peak at 24 h. When MK-801 (6 micrograms) and DNQX (4 micrograms) were injected respectively into hippocampus 20 min before administration of penicillin, seizure was reduced in strength. Meanwhile, the nNOS-like immunoreactivity in hippocampus was decreased, compared with the group which were administered penicillin alone. These results suggest that the increase of nitric oxide may be related to the injury of neurons during and after epilepsy; the changes' of nNOS may be related to the activity of NMDA and non-NMDA receptors. Neuron protective effect of MK-801 and DNQX may be in part mediated by nNOS.

To investigate the distribution and expression changes of basic fibroblast growth factor (bFGF)-like immunoreactivity (IR) in focal cerebral ischemic rat brain.The expression of bFGF was observed by fluoro-immunohistochemistry. The focal cerebral ischemic injury was carried out using middle cerebral artery occlusion (MCAO) model.Confocal images demonstrated that both the striatum and the frontoparietal cortex showed increases of bFGF-like IR after 2-h MCAO and 24-h reperfusion. In striatum, the increase patterns of bFGF-like IR were different according to the ischemic extent. In the core of infarct and its surrounding region (with more IR induction), bFGF-like IR was mainly located in astrocytes. In region adjacent to infarct (with most IR induction, the grey ratio of bFGF-like IR increased from sham-98% +/- 10% to ischemia-125% +/- 6%), some neurons also showed an upregulation of bFGF-like IR. In frontoparietal cortex, strong induction of bFGF-like IR was mostly seen in neurons (The grey ratio of bFGF-like IR increased from sham-104% +/- 11% to ischemia-132% +/- 28%), although it was observed in astrocytes as well.The expression of bFGF increased after focal cerebral ischemia in rats, suggesting that: in striatum, astrocytes may play an important role in the protection of neurons via the overexpression of bFGF; whereas in cortex, neurons probably exert an autoprotection through expressing bFGF themselves.

In this study, the fluorescent dye Fluo-3 (AM) was applied to rat hippocampus by microinjection, to label neurons in situ. A large number of CA1 pyramidal cells could be labeled by a single injection. With this improvement of labeling and the use of the confocal laser scanning microscope (Leica Lasetechnik GmbH), changes of calcium fluorescence intensity in CA1 pyramidal cells of rat hippocampal slices on the models of mimic epilepsy (induced by penicillin or glutamate) or hypoglycemia/hypoxia were studied in vitro. The results showed that in magnesium free artificial CSF, the intracellular calcium level of the CA1 pyramidal cells increased following application of glutamate or penicillin. Similar phenomenon was also observed on the in vitro model to hypoglycemia/hypoxia.

The effect of histamine on intracellular free Ca2+ levels ([Ca2+]i) in HA22/VGH human hepatoma cells were evaluated using fura-2 as a fluorescent Ca2+ dye. Histamine (0.2-5 microM) increased [Ca2+]i in a concentration-dependent manner with an EC50 value of about 1 microM. The [Ca2+]i response comprised an initial rise, a slow decay, and a sustained phase. Extracellular Ca2+ removal inhibited 50% of the [Ca2+]i signal. In Ca2+-free medium, after cells were treated with 1 microM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor), 5 microM histamine failed to increase [Ca2+]i. After pretreatment with 5 microM histamine in Ca2+-free medium for 4 min, addition of 3 mM Ca2+ induced a [Ca2+]i increase of a magnitude 7-fold greater than control. Histamine (5 microM)-induced intracellular Ca2+ release was abolished by inhibiting phospholipase C with 2 microM 1-(6-((17beta-3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione (U73122), and by 5 microM pyrilamine but was not altered by 50 microM cimetidine. Together, this study shows that histamine induced [Ca2+]i increases in human hepatoma cells by stimulating H1, but not H2, histamine receptors. The [Ca2+]i signal was caused by Ca2+ release from thapsigargin-sensitive endoplasmic reticulum in an inositol 1,4,5-trisphosphate-dependent manner, accompanied by Ca2+ entry.

Although the eradication of Helicobacter pylori infection benefits patients with gastric or duodenal ulcers, the value of eradicating the infection in the patients with functional dyspepsia (FD) remains controversial.To determine whether eradicating H. pylori can prevent the subsequent development of ulcers or relieve the symptoms of functional dyspepsia patients.In a double-blind, placebo-controlled trial, 161 patients infected with H. pylori who had functional dyspepsia were randomly assigned to 7 days of treatment with a lansoprazole-based triple therapy or placebo and then followed for 1 year. The main outcome measures were the development of peptic ulcers and the resolution of symptoms.H. pylori was eradicated in 63 out of 81 patients (78%) in the treatment group and none of the 80 patients (0%) in the placebo group. During the follow-up period, two patients in the treatment group and six patients in the placebo group developed peptic ulcers at repeat endoscopy (2.5% vs. 7.5%; 95% CI: -12 to 2). The reduction in ulcer rates was statistically significant in the 'ulcer-like' sub-group (0% vs. 16.7%; 95% CI: -32 to -2), but not in the 'dysmotility-like' and 'unclassifiable' sub-groups. Regarding symptom response, the resolution rates of symptoms were similar between the treatment and placebo groups (58.0% vs. 55.0%, 95% CI: -12 to 18). Additionally, no significant differences existed in the symptom responses between the treatment and control arms in each of the dyspepsia sub-groups.Eradicating H. pylori can prevent the subsequent development of peptic ulcers in the patients with 'ulcer-like' functional dyspepsia. However, this approach does not significantly reduce the symptoms of functional dyspepsia patients.

A novel type of amorphous silicon (a-Si) thin-film transistor (TFT) in which a depletion gate is added to the top of the second nitride layer of a conventional a-Si TFT has been fabricated. In this transistor, switching is done by the depletion gate instead of the accumulation gate as in conventional a-Si TFTs. The pinch-off voltage and ON-OFF current ratio of the transistor can be changed by the accumulation gate bias. The transistor exhibits high ON-OFF current ratio, low contact resistance, and low gate-source capacitance. >

Gallstones are a common problem in Taiwan and surgical removal remains the essential treatment. Successful dissolution of the stones with chemical solutions and then removal by endoscopic or percutaneous methods have previously been reported. We designed this study to find the ideal agent for dissolving gallstones.Twelve chemical solutions with dimethylsulfoxide (DMSO), methyl tert-butyl ether (MTBE) and ethylenediamine tetra-acetic acid (EDTA) in different mixtures were tested to investigate their ability to dissolve gallstones in vitro. The dissolution of stones was performed at 37 degrees C and each procedure was repeated five to seven times.The solvent containing DMSO/MTBE (1/1) had a higher dissolving capacity for cholesterol stones, with solubility reaching 96.8% after 6 hours. The solution containing DMSO/MTBE (7/3) had the maximal solubility for calcium bilirubinate stones, with solubility reaching 22.9% after 6 hours. Also, we found that the intact stones of calcium bilirubinate became fragmented after treatment with the DMSO/MTBE solution without stirring.The DMSO, MTBE and EDTA agents that we used effectively dissolved gallstones, especially cholesterol stones, in vitro. Further in vivo studies are necessary to confirm the efficacy and safety of these solvents before clinical application.

Hereditary hemorrhagic telangiectasia, commonly known as Osler-Weber-Rendu disease, is a systemic autosomal dominant inherited disorder, that occurs in Caucasian populations. We report the case of a 56-year-old housewife who was admitted to the gastrointestinal and cardiovascular ward because she had suffered from recurrent gastrointestinal bleeding and heart failure from 1994 to 1997. Panendoscopy showed vascular ectasia scattered over the tongue, larynx, esophagus, and posterior wall of the gastric body. Colonoscopy showed clusters of telangiectasia over the cecum and ascending colon. Arteriovenous malformations (AVMs) were found in the liver and lungs on computerized tomography. Recurrent gastrointestinal bleeding was controlled by estrogen treatment during the follow-up period. In July 1997, the patient was readmitted to our cardiovascular section due to aggravated dyspnea, orthopnea and bilateral lower leg edema. Cardiac catheterization showed a large fistula from the left pulmonary artery to the left atrium and left ventricle, pulmonary arterial pressure of 37/13 mmHg and cardiac output of 9.61/minute. Other studies excluded the possibility of sepsis, and high-output cardiac failure was suspected. The patient was discharged in a stable condition and scheduled for AVM embolization management. Unfortunately, she died of a suspected heart attack at home two weeks following discharge.

Chronic Helicobacter pylori infection leads to the development of mucosa-associated lymphoid tissue (MALT), gland atrophy, intestinal metaplasia, and in certain individuals, gastric lymphoma and adenocarcinoma. We conducted a prospective study to determine the effect of H pylori eradication on the development of MALT, gland atrophy and intestinal metaplasia.From July 1995 to October 1996, 63 consecutive patients with H pylori-associated peptic ulcer disease were enrolled in a bacterial eradication trial. The grade of MALT and the degree of gastritis of the antrum were assessed using Wotherspoon's scale and the Sydney system before treatment, and at eight weeks and one year after H pylori eradication therapy.During the study period, 43 patients received complete follow-up. In the patient group with eradication failure (n = 22), MALT score was significantly decreased at the end of the eighth week (p0.05) but returned to the initial level by one year of follow-up. There were no changes in the scores for inflammation, neutrophil activity, gland atrophy or intestinal metaplasia at the end of the eighth week and at one year following H pylori eradication therapy. In contrast, there was a marked reduction in the MALT, inflammation, and activity scores at eight weeks (p0.01,0.05 and0.05, respectively) and one year after treatment (p0.05,0.001 and0.001, respectively) in the patient group with successful eradication (n = 21). However, no significant changes in gland atrophy and intestinal metaplasia were observed during the follow-up period.Eradication of H pylori leads to regression of MALT in the stomach, but the degrees of gland atrophy and intestinal metaplasia remain unchanged, even after one-year of follow-up.

This study investigates the cell proliferation and the expression of p53 protein in Helicobacter pylori (H. pylori)-associated gastritis and assesses the effect of bacterial eradication on these epithelial factors.Seventy-nine patients with H. pylori-associated gastritis were randomized into the control group (n = 38) and anti-H. pylori group (n = 41). Each patient received endoscopic examinations with gastric biopsy before and 8 weeks after the treatment. The specimens from gastric antrum were immunostained for monoclonal antibodies against the proliferating cell nuclear antigen (PCNA) and p53 protein.In the control group, the total labeling index (L.I.) of PCNA and the positive index (P.I.) of p53 in the whole foveolar epithelium were unchanged after treatment. In the anti-H. pylori group, 35 of 41 cases (85.3%) achieved eradication of H. pylori. Amongst the H. pylori-eradicated cases, the total L.I. of PCNA in the whole foveolar epithelium did not meaningfully alter after H. pylori elimination (p0.05). However, a significant reduction of L.I. was observed in the middle compartments of the gastric pits (before vs. after treatment: 14.0 vs. 7.3, p0.05). With regard to the p53 expression, the P.I.s were significantly decreased in the whole foveolar epithelium (before vs. after treatment: 0.57 vs. 0.17, p0.05) and in each compartment of the gastric pits (before vs. after treatment: [upper compartment]: 0.34 vs. 0.15, p0.05; [middle compartment]: 0.67 vs. 0.23, p0.05; [lower compartment]: 0.71 vs. 0.20, p0.05) after eradication of H. pylori.Bacterial eradication reverses the hyperproliferating status of the foveolar epithelium in patients with H. pylori gastritis and leads to a decrease in p53 accumulation in the epithelial cells.

Endoscopic sphincterotomy and basket extraction are currently used to remove bile duct stones, with a duct clearance rate of 85% to 90%. A biliary endoprosthesis (stent) is an alternative method to treat difficult cases, especially high-risk surgical patients. The aim of this study was to investigate the long-term effect of biliary endoprostheses in patients with irretrievable common bile duct stones.From December, 1990, to November, 1998, 546 patients were referred to the Veterans General Hospital-Kaohsiung for endoscopic removal of common bile duct stones. Of them, 12 received long-term biliary endoprosthesis because endoscopic removal or surgery was not suitable. Large-caliber stents (10 French) were inserted into 12 patients (5 women and 7 men, mean age, 78.4 years) and they were followed up with regular clinical visits. Quantitative cholescintigraphy was performed in four patients to evaluate biliary emptying after liver function returned to normal.No early complications from stent insertion occurred and a satisfactory resolution of jaundice, pain and fever were noted in all patients. One patient had repeated cholangitis due to stent occlusion and five died from unrelated causes. The median effective period of stent placement was 11 months (range, 1-38 months). Quantitative cholescintigraphy revealed delayed biliary drainage in four patients despite an absence of symptoms after their liver function returned to normal.Large-caliber stents are a safe and effective treatment for long-term palliation in high-risk patients with retained common bile duct stones.

To explore the role of poly (ADP-ribose) polymerase (PARP) in focal cerebral ischemia with reperfusion injury.Male Wistar rats underwent 3.5-h of temporary middle cerebral artery occlusion by intraluminal suture. Infarction volume was showed with 2,3,5-triphenyltetrazolium chloride (TTC) staining and quantitated by image analysis system, neurologic scores were determined with a 0-5 grading scale.3-Aminobenzamide (3-AB) 10 mg.kg-1 or nicotinamide (Nic) at 20 mg.kg-1 showed potent neuroprotective effects within 0-6 h, neurologic deficits were attenuated. With the increasing dose of PARP inhibitors, beneficial effects were compromised, particularly, administration of Nic 60 mg.kg-1 at the onset of reperfusion drastically accelerated brain damage. Phytomenadione, a selective inhibitor of mono (ADP-ribosyl) transferase, had little effect on infarction volume.Transient incomplete inhibition of PARP provides a neuroprotective effects against cerebral ischemia-reperfusion injury, with a relatively wide therapeutic window, whereas severe inhibition of this enzyme, especially in reperfusion phase, is detrimental.

No stones are retrieved from the bile duct in 10-20% of patients with suspected common bile duct (CBD) stones after endoscopic sphincterotomy (EST). The clinical outcome in these patients remains unclear. This study followed patients from whom no stones were retrieved, to discover their clinical outcome.From October, 1990, to October, 1996, 401 patients with suspected CBD stones received EST for stone removal. Only patients from whom no stones were retrieved from the bile duct were included in this study. All enrolled patients were regularly interviewed and received liver function tests. Sonography, computerized tomography, endoscopic retrograde cholangiopancreatography (ERCP), and/or intrapapillary biopsy were performed as indicated.Forty-two patients were included in this study. The indications for EST included 34 cases with filling defects in the common bile duct on ERCP and eight cases with suspected impacted stones as seen by imaging studies. After a mean follow-up period of 28.6 months (range, 1-61 months), six patients developed biliary stones, four had carcinoma of the ampulla of Vater, one was found to have intrabiliary growth of hepatocellular carcinoma, and there was no pathologic change in 31 cases. Of the six patients with formation of biliary stones, two had an intact gallbladder and four had received previous cholecystectomy. Of the four patients with ampullary tumors, three were diagnosed by intrapapillary biopsy soon after EST, and one was diagnosed nine months later.Biliary problems were found in 26% of patients soon after EST, although no stones were retrieved from the bile duct. Regular follow-up is warranted.

The present study investigated the role of nitric oxide (NO) in epileptogenesis and whether this role correlated with ionotropic glutamate receptor (IGR). Using a self-constructed NO-sensitive microelectrode (SNM), we observed the effect of nitric oxide synthase (NOS) inhibitors, NMDA and non-NMDA selective antagonists on penicillin(PEN)-treated hippocampal slices by simultaneously recording evoked field potentials and nitric oxide release from CA1 pyramidal neurons. 7-nitroindazole (7-NI),Nomega-nitro-L-arginine (L-NNA) and DL-2-amino-phospho-novaleric acid (APV), but not 6,7-dinitroquinoxaline-2,3 (1h,4h)-dione(DNQX), depressed NO release and partly reversed PEN's epileptogenetic effect, while APV + 7-NI + L-NNA did not display a further inhibitory effect. These findings suggest both NOS inhibitor and NMDA antagonist involve as anticonvulsant factors in epileptogenesis, providing direct evidence for NO release in response to NMDA receptor activation. The anticonvulsant effect of NMDA antagonist may ascribe to its action on NO release.

Angiogenesis occurs in response to tissue damage, and is of vital importance for tumor growth and metastasis. Basic fibroblast growth factor (bFGF), a well-known angiogenic factor, has been suggested to be a useful diagnostic marker in certain hypervascular tumors. However, the relevance of its detection has not been well evaluated in patients with hepatocellular carcinoma (HCC) and benign chronic liver diseases. In the current study, immunoassay of bFGF was performed on serum samples from 39 patients with HCC, 21 with liver cirrhosis, 22 with chronic hepatitis and 40 normal subjects. The serum bFGF level was significantly increased in patients with liver cirrhosis and HCC when compared with those with chronic hepatitis or normal subjects (all p-values0.001). However, no difference was observed between the groups with liver cirrhosis and HCC (p0.05). If we set 9.6 pg/ml (mean + 3 standard deviations of bFGF in the control group) as the upper limit of normal serum level of bFGF, elevated bFGF concentrations were noted in 9.1%, 42.9% and 51.3% of patients with chronic hepatitis, liver cirrhosis and HCC respectively. In non-cancer patients, the coexistence of acute illness (p = 0.000) was an independent factor related to the elevation of serum bFGF. On the other hand, a multivariate analysis demonstrated that both advanced stage of cancer (p = 0.026) and coexistence of acute illness (p = 0.000) influence the serum level of bFGF in patients with HCC. We conclude that serum bFGF levels are significantly higher in patients with HCC and are positively correlated with advanced tumor stage. Nevertheless, elevation of serum bFGF may also be observed in a significant number of patients with liver cirrhosis. Therefore, measurement of serum bFGF alone cannot be satisfactory as a tumor marker for diagnosis of HCC. In addition, it is important to point out that coexistence of acute illness may be a crucial confounding factor in the diagnosis or monitoring of any cancer by the estimation of serum bFGF.

To study the effect of dextromethorphan (DM) in focal cerebral ischemia.The c-fos protein was detected immunohistochemically in the brain of rats after focal cerebral ischemia (induced by placing a nylon thread in the lumen of the internal carotid artery) with and without treatment with DM.Focal cerebral ischemia induced c-fos protein expression outside the core territory of the middle cerebral artery (MCA) and neuronal damage in the core territory of the MCA. There was an evident expression of c-fos protein in the ipsilateral regions outside the MCA territory (e.g. cingulate cortices, piriform cortices and entorhinal cortices), and in the contralateral regions of hippocampus after 4-h reperfusion following 1-h MCA occlusion. But morphological results showed severe edema and neuronal damage in the core territory and the ipsilateral hippocampus. DM blocked both the c-fos protein induction and neuronal damage in all regions.DM reduced c-fos protein expression and blocked the neuronal damage after focal cerebral ischemia.

Dysfunction of the sphincter of Oddi (SOD) is one of the causes of postcholecystectomy syndrome and biliary pain. Endoscopic sphincterotomy (EST) is recommended in some patients refractory to conservative treatment. This study was designed to evaluate the efficacy of, and complications from EST in patients with SOD.Between 1990 and 1993, 24 patients clinically diagnosed as having papillary stenosis were treated by endoscopic sphincterotomy. All patients had dilated common bile duct (CBD) in addition to 1) elevation of transaminases and alkaline phosphatase (n = 13); 2) elevation of transaminases and serum amylase (n = 4); 3) normal liver enzymes but delayed biliary emptying on quantitative hepatobiliary scintigraphy (QHS) (n = 7). No CBD stones, organic obstruction or other disorders were found in these patients.EST was successfully performed in 24 patients. One patient had minor hemorrhage and one patient developed pancreatitis after EST. Twenty-two of the 24 patients (91.7%) were symptomatically improved before discharge. Twenty-one patients were regularly followed over a median period of 18 months (range 5-36) after EST. Two patients with symptom had recurrence at five and eight month follow up because of restenosis of papilla; another two patients with recurrent biliary symptoms, but the sphincter of Oddi remained wide open. Seventeen of 21 regularly followed patients were symptom free after the median 18-month follow up.EST is an effective and safe modality for treatment of sphincter of Oddi dysfunction.

Variceal bleeding is a major life-threatening complication of cirrhosis of the liver. Transjugular intrahepatic portosystemic shunts (TIPS) have been accepted as an effective method for portal decompression. Experiences here with the use of TIPS for control of gastroesophageal variceal bleeding is presented.Sixteen TIPS procedures were performed for 15 patients who suffered from intractable gastroesophageal variceal bleeding. Nine cases (60%) were hepatitis-related cirrhosis of liver, four (27%) were alcoholic liver cirrhosis and two were cryptogenic in origin. Liver function tests revealed four patients were Child-Pugh's classification A, five were B and six, C. Twelve cases had received failed endoscopic management of varices; and one patient had recurrent variceal bleeding after devascularization. TIPS procedure was performed electively in nine cases and, as an emergency in six cases.Fifteen of the 16 TIPS procedures attempted were successfully performed. The technically successful rate was 94% (15/16), but two cases with successful TIPS procedure expired at the end of the procedure from hypovolemic shock and acute respiratory distress, respectively; thus the completely successful rate was 81% (13/16), The initial bleeding control rate was 83% (5/6) for the six patients with active bleeding. Portal venous pressure was significantly decreased from 30.8 +/- 5.8 mmHg before TIPS to 21.7 +/- 6.0 mmHg after the procedure (P0.01) and the porto-systemic pressure gradient also significantly decreased from 23.0 +/- 3.6 mmHg to 11.9 +/- 2.7 mmHg after TIPS (P0.01). Recurrent variceal bleeding was noted in four patients (33%) and that was managed by percutaneous transluminal angioplasty (PTA) of shunt, placement of additional stent, second TIPS procedure and a devascularization operation. Hepatic encephalopathy was noted in three patients (25%) after TIPS.TIPS is an effective method to control variceal bleeding caused by portal hypertension, especially when endoscopic or surgical management has failed or is contraindicated.

We report a previously undescribed ultrastructural calcification of glomerular immune complex depositions in a patient with lupus nephritis. Such processes give rise to a distinctive ultrastructural calcified microspheriol in electron-dense immune deposits, and were associated with hypercalcemia and nephrocalcinosis. The cause of hypercalcemia in this patient was uncertain, but related to a granulomatous inflammation and abscess of the breast. Whereas ultrastructural microcalcification was associated with hypercalcemia, its distribution in the segmental glomerular lesions suggests that an inflammatory process was contributory. The clinical follow-up indicates that the microcalcifications of immune complexes have not affected the outcome of nephritis and renal function.

Recurrent common bile duct (CBD) stones after cholecystectomy are a common biliary tract disease. The role of biliary emptying in the formation of these stones is not yet well defined.Cholescintigraphy was used to evaluate the biliary motility in 50 cholecystectomized patients with recurrent CBD stones after endoscopic sphincterotomy (EST) with stone extraction. Complete clearance of the CBD stones was confirmed in all patients by endoscopic retrograde cholangiopancreatography. Absence of sphincter of Oddi (SO) pressure after EST was determined by means of biliary manometry, and 99mTc-diisopropyl iminodiacetic acid (DISIDA) cholescintigraphy was performed four to six weeks after recovery from sphincterotomy.Complete clearance of the radioisotopes from the bile duct within 1, and more than 1 hour, was observed in 3 (6%) and 47 (94%) of the patients, respectively. When a cutoff value of 2 hours indicating abnormal biliary motility was employed, 31 out of the 50 patients (62%) had delayed biliary emptying. In comparing the clinical parameters between the two groups, patients with delayed biliary emptying time demonstrated an increase in CBD size greater than those of the normals (11.7 +/- 0.5 vs 9.2 +/- 0.4 mm, p0.05), while the presence of juxtapapillary diverticula and length of time for recurrence of CBD stones after cholecystectomy were not significant. Follow-up study showed that repeated recurrence rate of CBD stones appeared to be higher in the patients associated with delayed (12.9%) rather than normal (5.3%) biliary emptying.These results suggested that, in the absence of a functioning SO, abnormal biliary motility in cholecystectomized patients is one of the clinical factors involved in the pathogenesis of recurrent CBD stones.

Endoscopic nasobiliary drainage (ENBD) is a safe and effective modality which has been well documented for obstructive jaundice. However, factors predicting success rate of ENBD remain inconclusively. This study analyses those factors and discusses the outcome of patients with obstructive jaundice.One hundred and sixteen patients (male 99, female 17; mean age 68.2 years) with obstructive jaundice received ENBD after endoscopic retrograde cholangiogram (ERC) by Olympus JF-lT20 endoscope and 7F Wilson-Cook nasobiliary catheter from Sep. 1990 to Oct. 1993. Bile output (QD), serum bilirubin (BIW), liver biochemistry (QW), bile culture (next day), blood culture (if BT38.5 degrees C) were checked until definite treatment or death. Adequate drainage was defined as a daily output of bile more than 200cc, a gradual drop in serum bilirubin and no signs of cholangitis. Factors such as causes of jaundice, obstruction level, serum bilirubin, albumin, juxtapapillary diverticulum (JPD), bacteremia, fever before ERCP and ascites were analyzed.The success rate was 86.2% (100/116) in ERC and 78% (78/100) in ENBD. Adequate biliary drainage was 82.1% (64/78), and serum bilirubin was reduced from 14.3 +/- 8.5 mg% to 7.5 +/- 5.6 mg% within one week. In patients with non-cancerous causes, higher success rate and adequate drainage rate were obtained compared with those with cancerous causes (94.3% vs. 69.2%, p0.01 and 88.6% vs. 50.8%, p0.01, respectively). In all patients, a higher success rate was achieved at the obstruction level at the common bile duct (CBD) compared with periampullary and hilar levels (90.7% vs 69.2%, p0.05 and 90.7% vs 28.6%, p0.001, respectively). In patients with cancer as a cause, higher success rate was achieved at CBD level than at hilar level (85% vs 28.6%, p0.05). Those patients with cancer and serum bilirubin above 15 mg/dl had a higher failure rate in ENBD. Success rate of ENBD was not related to the presence of JPD, bacteremia or fever before ERCP and serum albumin level.Factors decreasing the success rates of ENBD were underlying cancerous causes, obstruction level at hilum or periampullary region and serum bilirubin level more than 15 mg%.

We conducted a prospective, randomized trial comparing sclerotherapy and ligation in 120 patients with acute bleeding of esophageal varices. All the patients were cirrhotic, 59 received sclerotherapy, and 61 received ligation. Treatment was repeated regularly until the varices were obliterated. The mean follow-up period was 295 +/- 120 days and 310 +/- 105 days for the sclerotherapy and ligation groups, respectively. The control of active bleeding was 12/15 (80%) in the sclerotherapy group and 18/19 (94%) in the ligation group (P = .23). The numbers of treatment sessions required to achieve variceal obliteration were 6.5 +/- 1.2 in the sclerotherapy group and 3.8 +/- 0.4 in the ligation group (P.001). Recurrent bleeding from the gastrointestinal tract was 51% in the sclerotherapy group compared with 33% in the ligation group (P.05). Recurrent bleeding from esophageal varices was 36% in the sclerotherapy group and 11% in the ligation group (P.01). However, bleeding from ectopic varices and congestive gastropathy was less common in the sclerotherapy group (7%) than in the ligation group (18%) (P = .05). Significant complications were encountered in 19% of the sclerotherapy group and in 3.3% of the ligation group (P.01). Comparison of Kaplan-Meier estimates of time to death of both groups showed a significantly lower mortality in the ligation group (P = .011). Both sclerotherapy and ligation can effectively arrest active bleeding from esophageal varices. However, ligation is more effective than sclerotherapy in decreasing the risk of rebleeding from esophageal varices with fewer complications. Ligation can also achieve obliteration of esophageal varices more rapidly than sclerotherapy.(ABSTRACT TRUNCATED AT 250 WORDS)

To study the neuroprotective effects of dextromethorphan against transient cerebral ischemia/reperfusion injury.Transient cerebral ischemia/reperfusion injury in gerbils was produced by temporarily clamping the common carotid arteries (CCA) for 10 min.Intrahippocampal (ih) injection of 2.0 microL dextromethorphan (DM, 100 mumol.L-1) 5 min before ischemia quickened the recovery of EEG changes, the total power spectra of EEG, and the power of dominant frequency following reperfusion. The total power of EEG was increased to 92 +/- 30 (P0.01) at 240 min following reperfusion. DM substantially reduced the severe ischemic neuronal damage (SIND) after 10 min of cerebral ischemia and 24 h of reperfusion.DM has neuroprotective effects against transient cerebral ischemia and reperfusion injury in gerbils.

Fifty-two patients with Forrest Ia or Ib bleeding ulcers were randomized to receive endoscopic injection therapy with either 1:10,000 epinephrine in water (Group I) or distilled water (Group II). Twenty-five out of 27 patients in group I, versus 22 out of 25 patients in group II, achieved initial hemostasis after endoscopic injection therapy (p > 0.05). Five patients who did not respond to local injection had bleeding controlled by heater probe thermocoagulation or surgical intervention. Three patients in each group developed rebleeding after initial hemostasis. Four of these patients had bleeding controlled by surgical intervention, while the other two died of underlying diseases. No change in systemic blood pressure, but a significant drop in the pulse rate were noted in both groups after injection therapy. Patients with shock at admission or ulcer size greater than 2 cm had a significantly higher rebleeding rate after initial hemostasis than patients with normal blood pressure and ulcers under 2 cm (p < 0.05). No serious complications were observed after injection therapy, and no significant difference in the amounts of solution required for successful hemostasis was noted between the two groups. We conclude that a local tamponade with distilled water is as effective and safe as diluted epinephrine solution for endoscopic injection therapy.