ObjectiveA HPLC-FLD method was developed to determine the levels of serum AAA in CRIpatients, and to studythe variationof serum AAAinCRI patientsanditsclinical significances. MethodsSerumsampleswerecollected from100healthcontrolsand 80CRI patients. According to 2002 National Kidney Foundation (NKF) staging diagnosis, CRI patients included 4 of stage 2, 12 of stage 3, 12 of stage 4, 52 of stage 5. According to pathogenesis, CRI patients were also divided into 3 groups :chronic nephritis group ( n = 32), DM group ( n = 36), hypertension group ( n = 12 ).Serums were deproteinized by equal volume of 5％ (v/v) PCA and supernate were analyzed direcdy. External standard method was used as quantitative method. The analytical column was Megres C18. 10％ acetonitrile in water was used as mobile phase. Flow rote was 1.0 ml/min. The wavelengths of fluorescence excitation and emission were changed with specific time. The levels of Tyr, Phe and Trp in CRI groups, different CKD stages and different pathogenesis were compared with healthy control groups to evaluated the sensitivity and specificity of serum AAA for CRI diagnosis. ResultsThe linear ranges of the method were 0. 550 -275.000, 3. 050 - 1220. 000 and 0. 049 -49. 000 pμmol/L for Tyr, Phe and Trp, respectively. The limit of detection (LOD) was 0.014 μmol/L for Tyr, 0.500μmol/L for Phe, and 0.005 μmol/L for Trp. The average recovery was 100. 9％, 101.3％ and 98. 5％ for Tyr, Phe and Trp, respectively. Intra-day CVwas 3. 18％ -4. 20％ ( mean was 3. 13％ )and inter-day CV was 3. 18％ -4. 20％ ( mean was 3. 58％ ). The concentration of serum AAA, Tyr and Trp and the ratio of Tyr/Phe in CRI patients were( 135.74 ±23.23 )μmol/L, (52.27 +8.25) μmol/L, (21.49 ±4.25) μmol/L and[0.87(0.68 - 1.05)]μmol/L. which were lower than that in healthy groups (t value was -14. 709, 4.452, 22. 100, U value was 266.000,respectively, P＜0. 05). The concentration of serum AAA, Tyr and Trp and the ratio of Tyr/Phe in healthy groups were ( 174. 47 ± 11.57 ) μmol/L, ( 63.53 ± 4. 68 ) μmol/L, (44. 22 ± 3. 67 ) μmol/L and[0. 97(0. 94 - 1.00)]μmoL/L. There were no statistically significant difference between the different stage of CRI. Compared with the concentration of Tyr, Phe and Trp among chronic nephritis group, DM group,hypertension group, the concentration of Tyr had no significant changes among these three kinds of diseases (P ＞ 0. 05 ). The concentration of Phe had significant changes between Chronic nephritis group and DM group, Chronic nephritis group and hypertension group ( U = 395.00, 114. 00, P ＜ 0. 05 ) ; the concentration of Trp haad significant changes between Chronic nephritis group and DM group ( U = 349.00, P ＜ 0. 05 ).The diagnostic sensitivity and specificity of serum AAA for CRI were 90％ (72/80) and 100. 0％ (100/100).ConclusionsThe method of high-performance liquid chromatography with fluorescence detection ( HPLC-FLD) is simple, rapid, sensitive and specific. Simultaneous determination of serum AAA was benefit to the diagnosis and evaluation of CRI patients.

Anti-Müllerian tube hormone(AMH), also known as Müllerian inhibitory substances, is a member of the transformation system. In males, AMH is secreted by immature Sertoli cell which promotes the degradation of male fetal Müllerian tubes,and participates in testicular development and spermatogenesis.AMH can regulate gona-dotropin-releasing hormone (GnRH), pituitary secretes follicle stimulating hormone (FSH) and luteinizing hormone (LH),testicular stromal cells secrete testosterone(T) and inhibin B causes male reproductive endocrine related diseases through HPG axis.

OBJECTIVETo reproduce an experimental model of alcoholic liver disease in rats and to investigate the preventive and treatment effects of tea polyphenols on alcoholic liver disease.

METHODS68 male Sprague-Dawley rats were randomly divided into 3 groups: alcohol group (gastrically infused with 56% of ethanol once a day with a dose of 7 g/kg body weight for 4, 12 and 24 weeks), tea polyphenols group (gastric infusion with alcohol same as in the alcohol group and with tea polyphenols at 0.25 g/kg bw) and control group (gastric infusion with normal saline). At the end of 4, 12 and 24 weeks, blood samples were collected and then the rats were sacrificed. Liver samples were obtained for routine histological examination and the degree of hepatic steatosis and alcoholic hepatitis were examined. Blood specimens were used for evaluation of alanine transaminase (ALT) and aspartate aminotransferase (AST).

RESULTS(1) The levels of the two transaminases were elevated with the increase of the duration of ethanol feeding and the difference is significant. TP significantly mitigated the increase of ALT and AST activities induced by the alcohol. (2) Histological changes of the liver injury indicated that piecemeal or focal necrosis of hepatocytes was present in the centrilobular area. As fibrosis advanced, broader septa were formed with central-central and centra-portal bridging necrosis. In the TP infusion group, the severity of the pathological changes was significantly milder.

CONCLUSIONThe results of this study revealed that TP mitigated the development of alcoholic liver disease, and TP may be a potential drug for treatment of alcoholic liver disease.

Animals ; Flavonoids ; therapeutic use ; Liver Diseases, Alcoholic ; drug therapy ; prevention & control ; Male ; Phenols ; therapeutic use ; Phytotherapy ; Polyphenols ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Tea ; chemistry

OBJECTIVETo study the histopathological effect of hepatic arterial infusion of lipiodol on transplanted hepatoma in rats.

METHODSFourty-one rats bearing Walker-256 transplanted hepatoma were randomly divided into embolization group (n = 35, divided in 5 subgroups, with 7 rats in each) and control group (n = 6). Lipiodol (0.5 ml/kg)emulsified with 0.2 - 0.3 ml of 76% urografin (v:v = 1:1) was infused via gastroduodenal artery into hepatic artery in embolization group. Rats in the control group were given via the same route urografin only. Histopathological changes of the treated tumors were examined by light and transmission electron microscopy.

RESULTSIn the control rats treated with urografin alone, the average tumor size increased 2.8 fold on day 3, while that in the lipiodol treated rats increased 1.7 fold (P < 0.01). Compared with the control group, on day 3, 5, 10 after embolization treatment, tumor necrosis was more extensive (P < 0.01). In one of the treated rats, the tumor was completely necrotic on day 10. Inflammatory reaction was marked in the early post-embolic period, but it was replaced by fibrous tissue encapsulation. From day 1 on, in 17 of the 18 treated rats, apoptotic cells, identified by typical morphology under light and electronic microscopes, were observed, mainly in the tumor periphery.

CONCLUSIONIn addition to cellular necrosis, apoptosis may be another important mechanism leading to cell death in hepatoma treated with transarterial embolization.

Animals ; Apoptosis ; Carcinoma 256, Walker ; pathology ; therapy ; Chemoembolization, Therapeutic ; Iodized Oil ; therapeutic use ; Liver Neoplasms, Experimental ; pathology ; therapy ; Male ; Necrosis ; Neoplasm Transplantation ; Random Allocation ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo evaluate the influence of reconstructive surgery for male urethral stricture on erectile function and sexual life quality.

METHODSWe analyzed retrospectively the clinical data of 326 male patients who underwent urethroplasty for urethral stricture in our department and evaluated their erectile function and sexual life quality.

RESULTSA total of 172 groups of valid data were collected, with the mean follow-up of 28.5 months. The mean scores on IIEF-5 (P=0.002) and sexual life quality (P=0.026) were statistically significantly reduced after surgery. Erectile dysfunction was found in 88 (51.2%) of the patients after urethroplasty, as compared with 56 (32.6%) preoperatively.

CONCLUSIONThe location of urethral stricture, surgical method and urethral stricture recurrence may affect the erectile function and sexual life quality of the patient, but both can be gradually improved with the time after urethroplasty.

Adult ; Aged ; Coitus ; physiology ; psychology ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Penile Erection ; physiology ; psychology ; Quality of Life ; Reconstructive Surgical Procedures ; methods ; Retrospective Studies ; Surveys and Questionnaires ; Urethral Stricture ; physiopathology ; psychology ; surgery

BACKGROUNDThe hypothalamus plays a central role in the regulation of metabolism by sensing metabolic demands and releasing regulatory neurotransmitters. This study investigated the response of the hypothalamus to glucose ingestion in rats by blood oxygen level-dependent functional magnetic resonance imaging (BOLD-fMRI) and immunohistochemical techniques to determine the role of the hypothalamus in glyco-regulation during disturbances in carbohydrate metabolism.

METHODSThe signal intensity of the hypothalamus was monitored by fMRI for 60 minutes after oral glucose intake in 48 healthy rats (age 14 months), which included 24 normal weight rats (weighing (365 +/- 76.5) g) and 24 overweight rats (weighing (714 +/- 83.5) g). Then, 12 rats (6 normal, 6 overweight) underwent a repeat fMRI scan after consuming an equivalent amount of water without glucose on a separate day. The procedure for fMRI with water intake was the same as for glucose ingestion. fMRI data was processed using time cluster analysis and intensity averaging method. After fMRI, the expression of neuropeptide Y (NPY) and 5-hydroxytryptamine (5-HT) in the hypothalamus of all rats was determined by immunohistochemistry. Positive cells for NPY or 5-HT were counted.

RESULTSThere was a transient, but significant, decrease in fMRI signal intensity in all rats (mean (3.12 +/- 0.78)%) in the hypothalamus within 19.5 - 25.5 minutes of oral glucose ingestion. In overweight rats, the decrease in signal intensity in response to the glucose ingestion was more markedly attenuated than that observed in normal weight rats ((2.2 +/- 1.5)% vs (4.2 +/- 0.7)% inhibition, t = 2.12, P < 0.05). There was no significant response in the hypothalamus after oral water ingestion. The percentage of NPY positive cells in obese rats were slightly lower than those in control group (21% vs 23%, t = 0.71, P > 0.05); but there was no significant difference between the two groups; the percentage of 5-HT positive cells in obese rats were significantly lower than those in the control group (22% vs 31%, t = 3.25, P < 0.01).

CONCLUSIONSThere is a transient, but significant, decrease in BOLD signal intensity in the hypothalamus following glucose ingestion, which is similar to that observed in humans. The response of the hypothalamus to glucose ingestion was different in overweight and normal weight rats. The percentage of NPY positive cells in obese rats were lower than those in the control group, although this difference was not statistically significant. The percentage of 5-HT positive cells in obese rats was significantly lower than those in the control group.

Animals ; Glucose ; metabolism ; Hypothalamus ; physiology ; Immunohistochemistry ; Magnetic Resonance Imaging ; methods ; Neuropeptide Y ; analysis ; Obesity ; metabolism ; Oxygen ; blood ; Rats ; Serotonin ; analysis

AIM:To explore the influence factors of the treatment zone diameter(TZD)and its correlation with axial length growth(ALG)after Paragon CRT orthokeratology.METHODS: Retrospective clinical study. The data of 226 myopic patients(226 eyes)wearing Paragon CRT orthokeratology from April 2020 to September 2022 were collect. The correlated factors of TZD after wearing lens for 1mo, and the relationship between the overlapping treatment zone/ pupil area ratio and the ALG after wearing lens for 1a were analyzed.RESULTS: After wearing lens for 1mo, the TZD was negatively correlated with central corneal thickness(CCT)and positively correlated with the flat corneal eccentricity. After wearing lens for 1a, the ALG of the small TZD group(0.25±0.18mm)was significantly smaller than that of the large TZD group(0.34±0.24mm, P=0.002), and the ALG of the small area ratio group(0.24±0.19mm)was significantly smaller than that of the large area ratio group(0.35±0.23mm,P<0.001). Age and overlapping treatment zone area/pupil area ratio were significantly associated with the ALG in multivariate linear regression(all P<0.05).CONCLUSION: The wearers with thicker CCT and smaller flat corneal eccentricity usually had smaller TZD, and both the TZD and the overlapping treatment zone area/pupil area ratio were correlated with the ALG.

OBJECTIVE: To study the clinical features and recurrence factors of myelin oligodendrocyte glycoprotein (MOG) antibody disease in children and the effect of recurrence prevention regimens. METHODS: A retrospective analysis was performed on the medical data of 41 children with MOG antibody disease who were hospitalized in the Department of Pediatric Neurology, Xiangya Hospital of Central South University, from December 2014 to September 2020. According to the presence or absence of recurrence, they were divided into a monophasic course group ( RESULTS: For these 41 children, acute disseminated encephalomyelitis was the most common initial manifestation and was observed in 23 children (56%). Of the 41 children, 22 (54%) experienced recurrence, with 57 recurrence events in total, among which optic neuritis was the most common event (17/57, 30%). The proportion of children in the recurrence group who were treated with corticosteroids for less than 3 months in the acute phase was higher than that in the monophasic course group (64% CONCLUSIONS More than half of the children with MOG antibody disease may experience recurrence. Most children with recurrence are treated with corticosteroids for less than 3 months in the acute phase. Rituximab and azathioprine may reduce the risk of recurrence.
Autoantibodies ; Child ; Humans ; Myelin-Oligodendrocyte Glycoprotein ; Optic Neuritis ; Recurrence ; Retrospective Studies

Objective To explore the mechanism of the intestinal barrier damage caused by Blastocystis hominis infections in rats. Methods Thirty SD rats were randomly divided into the control group, and the 1-, 3-, 6- and 9-week-infection groups, of 6 rats in each group. Rats in each infection group were orally infected with B. hominis trophozoites at a density of 2 × 10⁸ parasites per rat, and the control group was given an equal volume of phosphate buffered saline solution. The 7-hour urine samples were collected 1, 3, 6 and 9 weeks post-infection for the measurement of the intestinal permeability. Then, rats were sacrificed using the cervical dislocation method, and the cecum specimens were collected for the detection of the intestinal epithelial cell permeability. The expression of tight junction-related Occludin and Claudin - 1 genes and apoptosis-related Bcl - 2 and Bax genes was quantified in cecum epithelial cells using the real-time fluorescent quantitative PCR (qPCR) assay, and cell apoptosis was detected in the rat cecum using the TdT-mediated dUTP nick-end labeling (TUNEL) assay. Results The median urinary lactolose to mannitol ratios were 0.29, 0.72, 0.44, 0.46 and 0.38 in the control group, and the 1-, 3-, 6- and 9-week-infection groups, respectively, and the difference was statistically significant (H = 12.09, P < 0.05). B. hominis invasion and epithelial injury were observed in intestinal epithelial cells of rats infected with B. hominis, and transmission electron microscopy displayed the destruction of tight junctions between intestinal epithelial cells. The relative expression of Occludin, Claudin-1, Bcl-2 and Bax genes was 1.04, 0.62, 0.71, 0.68 and 0.96; 1.03, 0.61, 0.63, 0.76 and 0.86; 1.08, 0.70, 0.75, 0.74 and 1.03; and 1.00, 1.57, 1.33, 1.35 and 1.10 in the control group and the 1-, 3-, 6- and 9-week-infection groups, respectively, and all differences were statistically significant (F = 2.86, 2.85, 3.37 and 4.45, all P values < 0.05). The median number of positive staining cells were 1.00, 13.00, 9.00, 3.50 and 1.00 in rat cecum specimens in the control group, and the 1-, 3-, 6- and 9-week-infection groups, respectively, and the difference was statistically significant (H = 22.95, P < 0.01). Conclusion B. hominis infection may cause an increase in the rat intestinal permeability through triggering the apoptosis of intestinal epithelial cells to destroy the tight junction between intestinal epithelial cells, thereby destroying the intestinal barrier function.