[Application of urethral pressure profilometry in artificial urinary sphincter implantation].

Objective: To investigate the changes of maximum urethral pressure (MUP) and maximum urethral closure pressure (MUCP) after artificial urethral sphincter (AUS) implantation and their prognostic value. Methods: The clinical data of patients who had undergone AUS implantation in multiple medical centers between March and July 2019 were retrospectively analyzed. Data of urethral pressure profilometry, pad usage, related scores and complications related to surgery were collected and compared. The primary endpoint was social continence (defined as 0-1 pad/d) 1 month after activation of the pump. Results: A total of five male patients were included in this study. Two underwent transurethral resection of the prostate for benign prostatic hyperplasia, two underwent radical prostatectomy for prostate cancer, and one underwent urethral reunion, urethral stricture dilatation and cystostomy due to trauma from traffic accident. All patients had different degrees of urinary incontinence. The results of preoperative urethral profilometry test showed that the MUP of five patients were 52, 53, 88, 32, and 66 cmH(2)O(1 cmH(2)O=0.098 kPa), respectively, and the MUCP were 17, 52, 62, 27, and 40 cmH(2)O, respectively. AUS implantation was performed. The intraoperative urethral pressure profilometry showed that the MUP were 53, 113, 50, 77, and 89 cmH(2)O in the inactivated state, and the MUCP were 50, 97, 31, 71, and 51 cmH(2)O, respectively. In the activated state, the MUP were 112, 174, 193, 121, and 120 cmH(2)O, and the MUCP were 109, 160, 175, 114, and 92 cmH(2)O, respectively. All patients met the social continence (0-1 pad/d) criterion. No complications were reported during the follow-up. Conclusions: The relationship between the range of intraoperative urethral pressure and the effect of urinary control can be gained by measuring the specific values of MUP and MUCP during AUS implantation and the post-operative effects, which provides as a data basis for standardizing AUS implantation.

[Discussion on the curative effect and mechanisms of berberine in rats with non-alcoholic fatty liver].

Objective: To observe the curative effects of berberine in rats with high-fat diet induced non-alcoholic fatty liver and to further explore its possible mechanism. Methods: Twenty-six Sprague-Dawley rats (120-160 g) were randomly divided into 3 groups: control group (n = 8), model group (n = 10) and treatment group (n = 8). Rats in the control group were fed with regular diet, and the model group and the treatment group were fed a high-fat diet. At the 12th week, two rats in the in the model group were sacrificed to verify whether model was successful established. Subsequently, treatment group rats were given a gavage of berberine at a dose of 150 mg·kg(-1)·d(-1) for 4 weeks, and the control and the model group rats were given the same dose of normal saline. Rats were sacrificed at week 16th. HE staining was used to observe the changes in the intestinal mucosa of rats. Sudan black B staining was used to observe the fatty changes in liver. Immunohistochemical staining was used to observe the expression level of occludin protein in the intestinal epithelium. A real-time 16S rDNA PCR method was used to measure the number of escherichia coli, bacteroides and faecalibacterium prausnitzii in the feces of rats. Results: Model group had a higher serum levels of endotoxin (0.288 ± 0.045) and tumor necrosis factor (TNF)-α (1.07 ± 0.11) than the control group (0.192 ± 0.049, 0.94 ± 0.07) (P < 0.05). Berberine intervention had significantly reduced endotoxin (0.213 ± 0.025) and TNF-α level (0.93 ± 0.07) (P < 0.05). The expression level of occludin protein was significantly lower in the intestinal mucosa of model group than that of control group (0.166 ± 0.014), and berberine had promoted the expression of occludin protein in intestinal mucosa (0.055 ± 0.009), but the difference was not statistically significant (P > 0.05). At the same time, compared with the model group (7.29 ± 0.47), the number of bacteroidetes in the control group (9.49 ± 0.59) was decreased, while the number of bacteroidetes in the treatment group was increased (9.77 ± 0.87). The number of escherichia coli (6.92 ± 0.77) and faecalibacterium prausnitzii (8.70 ± 0.62) in the model group were increased than control group (5.42 ± 0.63, 9.49 ± 0.59), while the number of escherichia coli (6.34 ± 0.71) and faecalibacterium prausnitzii (9.77 ± 0.87) (P < 0.05) was reduced with the intervention of berberine. Conclusion: Berberine could effectively protect the intestinal barrier function in rats with NAFLD and the possible mechanism of action behind it may be the regulation of intestinal flora.

[Effects of selenium supplement on atherogenesis of ApoE-knockout mice fed high fat diet].

OBJECTIVE: To investigate the effects of selenium supplement on atherogenesis and endothelial function in ApoE-knockout mice fed high fat diet. METHODS: ApoE-knockout mice fed with selenium-deficient and high fat diet were randomly allocated into 3 groups based on random number table including control group (not supplied with sodium selenite, n=10), low dosage selenium supplement group (supplied water with 0.1 mg/L sodium selenite, n=10) and high dosage selenium supplement group (supplied water with 0.2 mg/L sodium selenite, n=10). After 15 weeks, the following values were measured: the concentrations of selenium in heart and liver, the levels of serum lipid, the parameters of antioxidant function including activities of superoxide dismutase(SOD) and glutathion peroxidase (GSH-Px) and malondialdehyde (MDA) level in serum, the parameters of endothelial function including serum nitric oxide (NO), endothelin 1(ET-1), and vascular endothelial growth factor (VEGF) levels, and ET-1 and VEGF levels in aorta roots. The atherosclerotic lesions in aorta roots were analyzed with oil red O staining. RESULTS: (1) The selenium concentrations in heart and liver were significantly higher in high dosage and low dosage selenium supplement groups compared to control group (both P<0.05). (2) The levels of triglyceride, total cholesterol, low density lipoprotein cholesterol, very low density lipoprotein cholesterol and high-density lipoprotein cholesterol were similar among groups (all P>0.05). (3) The activity levels of serum SOD were significantly higher in low dosage ((113.8±12.5)U/ml) and high dosage selenium supplement group ((152.3±11.3)U/ml) compared to control group ((90.7±10.7)U/ml, all P<0.05). The activity levels of serum GSH-Px were significantly higher in low dosage ((53.9±7.2)U/ml) and high dosage ((69.6±8.7)U/ml) selenium supplement groups than that of control group ((36.4±5.6)U/ml, all P<0.05). The serum MDA levels in low dosage ((4.73±1.05)nmol/ml) and high dosage ((4.13±1.21)nmol/ml) selenium supplement groups were significantly lower than that of control group ((5.97±1.08)nmol/ml, all P<0.05). (4) The serum NO concentrations in low dosage ((61.5±12.8)µmol/L) and high dosage ((79.0±14.6)µmol/L)selenium supplement groups were significantly higher than that of control group((42.7±9.1)µmol/L, all P<0.05). The concentrations of serum ET-1 in low dosage ((52.8±6.3)ng/L)and high dosage ((46.3±4.7)ng/L)selenium supplement groups were significantly lower than that of control group((72.2±6.3)ng/L, P<0.05). The concentrations of serum VEGF in low dosage ((97.4±16.5)ng/L)and high dosage ((83.5±22.0)ng/L)selenium supplement groups were significantly lower than that of control group((125.8±18.6)ng/L, P<0.05). The expression levels of ET-1 and VEGF in aorta roots among low dosage and high dosage selenium supplement groups were significantly lower compared to control group (all P<0.05). (5) The plaque area of aorta roots in low dosage ((0.95±0.19)×10(5) µm(2))and high dosage selenium supplement ((0.75±0.15)×10(5) µm(2)) groups were significantly smaller than that of control group((1.13±0.23)×10(5) µm(2)), and the plaque area in high dosage selenium supplement group was significantly smaller than in low dosage selenium supplement group (P<0.05). CONCLUSION: Supplement of selenium can attenuate atherogenesis in ApoE-knockout mice fed high fat diet, which is possibly mediated via reducing lipid peroxidation and improving endothelial functions.

Quinoid radio-toxin (QRT) induced metabolic changes in mice: an ex vivo and in vivo EPR investigation.

Radio-toxins are toxic metabolites produced by ionizing irradiation and have toxic effects similar to those caused by direct irradiation. We have investigated the effect of a quinoid radio-toxin (QRT) obtained from gamma-irradiated potato tuber on various organs in mice using ex vivo and in vivo EPR spectroscopy. Results indicate a decrease in the activity of ribonucleotide reductase enzyme in spleen of mice treated with 0.2mg QRT. A dose of 2mg QRT was fatal to mice within 45-60 min of treatment. Nitrosyl hemoglobin complexes alpha-(Fe(2+)-NO)alpha-(Fe(2+))beta-(Fe(2+))(2) were detected from spleen, blood, liver, kidney, heart, and lung tissue samples of mice treated with lethal doses of QRT. A significant decrease of pO(2) in liver and brain was observed after administration of QRT at the lethal dose. The time of the appearance of the nitrosyl hemoglobin complex and its intensity varied with the dose of QRT and the type of tissue. These results indicate that the effect of the QRT is more prominent in spleen and to a lesser extent in liver and blood. The QRT action at the lethal doses resulted in an increased hypoxia over time with disruption of compensatory adaptive response. The results indicate similar outcome of QRT as observed with gamma-irradiation.

[Identification of medicinal plant Xanthium L. produced in China].

OBJECTIVE: To gain a clear idea on the resources and pharmacognostic identification of medicinal plant Xanthium in China. METHOD: Identification of botanical origin, analysis of fruit shapes and properties, microscopic characteristics, TLC and UV. RESULT: Identification criteria have been worked out for Xanthium and its confused species. CONCLUSION: The resources of medicinal plant Xanthium may be appropriately expanded.

Effect of a spider toxin (JSTX) on excitatory postsynaptic current at neuromuscular synapse of spiny lobster.

1. We studied the blocking properties of a spider (Nephila clavata) toxin (JSTX) purified from venom on the spiny lobster neuromuscular junction. 2. When a small amount of JSTX was applied to the neuromuscular junction, the excitatory postsynaptic potential (EPSP) was partially suppressed. The amplitude of EPSPs remained at a steady level for several hours during the washing of the preparation, showing that the action of JSTX is irreversible. 3. We recorded the excitatory postsynaptic current (EPSC) from synaptic site using a macro-patch electrode. The amplitude of EPSC increased linearly with hyperpolarization of the membrane potential in the presence and absence of JSTX. 4. The decay phase time constant of EPSC and spontaneous EPSC was decreased by hyperpolarizing the membrane potential both in the absence and in the presence of JSTX. The relationship between the decay time constant and the membrane potential was not modified by JSTX. 5. It is suggested that JSTX irreversibly blocks EPSC by acting on the site that is apart from the ionic channel of the glutamate receptor molecule.

Spider toxin (JSTX) on the glutamate synapse.

A new neurotoxin (JSTX) was separated from spider (Nephila clavata, Joro spider) venom. JSTX irreversibly suppressed the excitatory postsynaptic potential (EPSP) and the glutamate potential in the lobster neuromuscular junction with high degree of specificity. The threshold concentration for suppressing EPSPs corresponds to a small fraction of the toxin in a venom gland, roughly estimated as low as 10(-10) M/l. 10(-10) M/l. In the giant synapse of squid stellate ganglion JSTX suppressed EPSPs without affecting the antidromic response. Glutamate-induced membrane depolarization was blocked by JSTX. In mammalian brain slice preparation, JSTX suppressed the orthodromic spike response but failed to affect on the antidromic spike in the hippocampal pyramidal neuron of CA1 and CA3 region. The above results strongly support the view that the squid giant synapse and synapses in the hippocampal pyramidal neuron are mediated by glutamate.

Vitamin B1 in the treatment of leprosy. 1- Vitamin B1 excretion in urine

1- Among thirty-one patients selected from a leprosarium the urinary excretion of vitamin B1 was found to be either nil or far below normal. 2- Following the oral administration of moderately large doses of vitamin B1 the urinary excretion rapidly increased, the response being similar to that observed in normal individuals. 3- The urinary excretion of vitamin B1 among lepers after parenteral administration was similar to that following oral administration. 4- Vitamin B1 excretion during treatment with that substance was apparently not influenced by factors such as fever, parenteral administration of chaulmoogra preparations or iodides, the duration of the disease, or the type of the lesions.