Chloride ion is an important anion in organisms, managing various physiological events. A particular gene mu-tation leads to involved channel deifciency and to develop channelopathy. In kidney, different chloride channels distribute along certain fractions of the renal tubule, located at apical and basolateral membranes of tubular epithelial cells. Previous studies dis-covered that voltage-sensitive chloride channels in kidney are associated with Bartter syndrome and Dent’s disease. In addition, the kidney can be involved by cystic ifbrosis resulting from dysfunction of cystic ifbrosis transmembrane conductance regulator. In this review, the function and mechanism of chloride channels in maintenance of normal renal function, and the renal diseases caused by related gene defects were discussed.

Objective To investigate the role of autophagy in podocyte damage,and the intracellular mechanism of autophagy activation through passive Heymann nephritis (PHN) animal model.Methods Male Sprague-Dawley rats (n=40) were studied on day 0,2,4,7,and 21 after induction of PHN by injection of anti-Fx1A.Podocyte morphology and autophagosomes were observed by transmission electron microscopy.Podocyte numerical density was estimated by Weibel-Gomez =method.Cell apoptosis was detected by TUNEL assay and caspase-3 immunohistochemical staining.Expressions of autophagy markers and endoplasmic reticulum stress (ERS)-associated proteins were analyzed by Western blotting.Results (1) In PHN rats,immunohistochemical staining showed that C5b-9 deposited along glomerular basement membrane on day 4 to day 21.Small subepithelial electron -dense deposits and a part of foot process fusion were detected in the glomerulus of PHN rats on day 4 by transmission electron microscope,and podocyte damage was aggravated on day 21.Furthermore,compared with control,the urinary protein levels of PHN rats began to increase on day 3,and reached the top on day 21 [(50.6±6.0) mg/24 h].(2) The number of podocytes significantly decreased in PHN rats compared with control group on day 21(P ＜ 0.05).(3) In PHN rats,apoptotic podocytes were found by caspase-3 immunohistochemical staining and TUNEL assay on day 21.(4) The expression of autophagy marker LC3 Ⅱ was markedly increased on day 7 and 21,but down-regulated on day 21 compared with day 7.Moreover,accumulated autophagosomes in podocytes were detected on day 7 and 21 by transmission electron microscope.(5) The level of GRP78 was significantly increased on day 2 and 7 but reduced to baseline on day 21.At the same time,the downstream pathways (ATF6α,p-PERK and p-JNK) of unfolded protein response were also up-regulated in the early process of PHN and down-regulated later.Conclusions Autophagy is an important way to protect against immunemediated podocyte injury in membranous nephropathy.Autophagy activation is mainly related to endoplasmic reticulum stress induced by complement attack.This provides an important basis for a thorough understanding of the role of autophagy in the process of podocyte damage and the pathogenesis of membranous nephropathy.

AIM: To determine the effect of rapamycin on the progression of passive Heymann nephritis (PHN), and whether autophagy is involved in this process .METHODS:Male Sprague-Dawley rats (n=24) were ran-domly divided into 3 groups:control group , PHN group and rapamycin treatment group .The rat PHN model was induced by injection of anti-Fx1A serum through penile vein , and all rats were sacrificed on day 21.Automatic biochemical analyzer was used to detect 24 h urine protein , blood urea nitrogen and serum creatinine .Renal damage was observed through per-iodic acid-silver methenamine staining .The number of podocyte was estimated by Weibel-Gomez method .The glomerular deposition of C5b-9, the expression of caspase-3 and expression of autophagy marker LC 3 in glomeruli were examined by immunofluorescence staining , immunohistochemical staining and Western blotting , respectively.RESULTS: Rapamycin significantly reduced proteinuria in the PHN rats (P<0.05), while the renal functions in 3 groups were normal, without significant difference .Although rapamycin limited weight gain in the rats , the health of the rats during drug treatment was not affected .Rapamycin retarded glomerular basement membrane thickening in the PHN rats .Rapamycin significantly re-duced the podocyte deletion by preventing podocyte apoptosis .Rapamycin enhanced the level of autophagy of glomerular in-herent cells .CONCLUSION:In the disease process of PHN , appropriate strength of autophagy plays a protective role . Rapamycin appropriately enhances autophagy and prevents podocyte apoptosis , thus reducing nephropathy and proteinuria . This may be one of the important mechanisms of rapamycin to slow down the progress of PHN .

Firstly, this article introduced the definition of medical dispute and public remedy. Thereafter, it analyzed the causes of public remedysilence in medical disputes from four perspectives including the self-defect of public remedy, inadequacy of legal construction, lack of trust in public remedy, and the popularity of private remedy. Finally, it pointed out the countermeasures of enhanced legal construction, unimpeded public remedy and striking private remedy to solve the problem of public remedy silence in medical disputes.

AIM:In podocytes , autophagy occurs at a high basal level and dysregulated autophagy is associa -ted with a variety of podocytopathies .This paper is to investigate the role of autophagy in sublytic C 5b-9-induced podocyte injury.METHODS: Sublytic complement C5b-9 stimulation was used as an in vitro model.Autophagosomes were con-firmed using monodansylcadaverine (MDC) staining.Immunoblotting was used to measure the change of autophagy-related markers.Cellular morphological changes were observed by Wright-Giemsa staining.Immunofluorescence staining and con-focal microscopy were used to detect the expression and distribution of nephrin .The cell viability was assessed by methylth-iazol tetrazolium (MTT) assay.The cell apoptosis was assessed by Annexin V-fluorescein isothiocyanate/PI staining.RE-SULTS:For ensuring sublytic complement injury , the maximal amounts of anti-podocyte antiserum and 160 ×-diluted nor-mal human serum were used without inducing cell lysis (defined as >5%LDH release).Sublytic C5b-9 promoted autoph-agy of podocytes in vitro.The proautophagic effect of sublytic C 5b-9 manifested in the form of accumulated MDC-labeled vesicles and enhanced the expression of LC 3-Ⅱ.Autophagy inhibitor 3-methyladenosine (3-MA) promoted sublytic C5b-9-induced podocyte morphological abnormalities .Compared with the sublytic C5b-9-injured podocytes, 3-MA exposure further decreased the expression of nephrin .3-MA enhanced sublytic C5b-9-induced podocyte apoptosis .CONCLUSION: Sub-lytic C5b-9 attack induces autophagy , which may play a protective role against complement-mediated podocyte injury .

ObjectiveTo study the role of L-arginine/nitric oxide (NO) pathway in the antidepressant effects of ketamine.MethodsForty two male Wistar rats (200-250 g) were equally randomized into 7 groups ( n =6 ):control group ( C group ),L-Arginine ( a precursor of NO ) group ( LA group),L-NAME ( an non-selectivity inhibitor of NO synthase) group ( LN group),ketamine 3 mg/kg group ( K3 group),ketamine 10 mg/kg group (K10 group),L-Arginine + ketamine 10 mg/kg group(LAK10 group),L-NAME + ketamine 3 mg/kg group (LNK3 group).The forced swimming test (FST) of 15 min (pre-test session) was used to establish a rat depression model,then twenty-four hours later FST (test session) was carried out of 6 min and the immobility time in last 5 min was recorded. All the groups were pretreated with saline 1.0 ml,L-arginine 750 mg/kg or L-NAME 30 mg/kg 90 min before FST.Saline 1.0 ml,ketamine 3.0 mg/kg or ketamine 10.0 mg/kg were injected 60 min before FST.The content of hippocampal NO was detected immediately after ethology measurement.ResultsCompared with C group (immobility time:( 139.0 ± 27.6)s),the immobility time decreased significantly (( 85.5 ± 34.2),(91.3 ±31.6)s) in K10 group and LNK3 group (P＜0.05),K3 group,LA group,LAK10 group and LN group had no significant difference (P＞0.05) ;compared with C group ( (0.61 ±0.21 ) μmol/gProt),the content of NO increased in LA group ( ( 1.09 ±0.39) μmol/gProt) and decreased in K10 group and LNK3 group significantly( (0.28 ± 0.12),(0.31 ± 0.14 ) μmol/gProt) (P ＜ 0.05 ),K3 group,LAK10 group and LN group had no significant difference (P ＞ 0.05).ConclusionThe antidepressant effects of ketamine are related to the suppression of L-arginine/nitric oxide pathway.

Objective To explore the relationship among social support, postpartum depression and quality of life of puerperal women. Methods A total of 348 puerperal women were investigated with Postnatal Social Support Questionnaire,Edinburgh Postnatal Depression Scale (EPDS) and WHO Quality of Life-BREF (WHOQOL-BREF). Results Pearson correlation analysis showed that there was a significant positive correlation between social support and the quality of life (r=0.483, P < 0.01), and a significant negative correlation to postpartum depression (r=-0.243, P < 0.01),and a significant negative correlation between postpartum depression and quality of life (r=-0.408, P<0.01). Intermediary effect of postpartum depression was tested. Conclusions A good social support system is benefit to improve depression scores for EPDS, and promote the life quality in puerperal women.

Objective To determine the effect of rapamycin on sublytic C5b-9-induced podocyte adhesion damage,and whether autophagy is involved in this progression.Methods Sublytic complement C5b-9 stimulation was used in vitro.Autophagosomes were viewed using electron microscopy.Western blotting was used to measure the change of autophagy-related markers.Attachment assay was used to assess the adhesion of podocyte.Confocal microscopy was used to explore the expression patterns of cytoskeletal protein F-actin.Flow cytometry was used to measure the level of adhesion-associated protein integrin α3.Results (1) For ensuring sublytic complement injury,the maximal amounts of anti-podocyte antiserum and 160×-diluted normal human serum were used without inducing cell lysis (defined as ＞ 5％ LDH release).(2) Sublytic C5b-9 promoted autophagy in podocyte in vitro.The proautophagic effect of sublytic C5b-9 manifested in the form of accumulated autophagosomes and enhanced expression of LC3-lⅡ.(3) Inhibition of autophagy by 3-methyadenine enhanced the effect of sublytic C5b-9-induced podocyte injury,including serious cytoskeleton damage and markedly reduced adhesion of podocyte.(4) Rapamycin treatment significantly improved the above lesions.(5) Rapamycin enhanced autophagy induced by sublytic C5b-9 in podocyte.Conclusions In summary,rapamycin can improve sublytic CSb-9-induced podocyte adhesion damage by appropriate autophagy activation.These findings provide important information for the development of appropriate protocols for the application of mTOR (mammalian target of rapamycin) inhibitors in podocytopathy.

Objective To investigate the safety and efficacy of ultrasound ablation in treatment of uterine fibroids. Methods Ninety-nine patients with 117 leiomyomas in total treated by Haifu JC focused ultrasound tumor therapeutic system were enrolled in prospective and non-randomized clinical trial in First Affiliated Hospital of Chongqing Medical University and Academy of Military Medical Sciences. Ultrasound ablation was performed guided by real-time ultrasonography under conscious sedation for single session. All patients were followed up at 6 months after treatment. On the day of treatment and after 1 month, patients were given by magnetic resonance imaging(MRI) exam to evaluate the effect of fibroids ablation. At 3 and 6months after treatment, the ratio of ablated area and volume reduction of fibroids more than 50% were evaluated by MRI exam again. The symptoms improvements were evaluated by uterine fibroid symptom (UFS) and complications were analyzed by guideline of society of international radiation (SIR). Results The average ablated area ratio of the target fibroid was (76 ± 24)%. The average reduction in fibroid volume determined by MRI at 3 and 6 months after treatment was (45 ± 21)% and (59 ± 26)%. Which were significantly decreased than those before treatment (P < 0. 05). At 6 months after treatment, 84. 6% (99/117) of patients showed more than 50% volume reduction, the rate of improved symptom score was 92%(66/72). All patients could resume normal daily activities at 2 hours after treatment. The adverse reactions of SIR C - D included delayed hospitalization, repeat treatment and increased level of nursing. E - F included permanent sequelae and death. In this study, no adverse reactions of C - F were recorded. Common complications (SIR A- B, only observation or simple management without sequelae) were 35% (35/99).Four cases with adverse reactions B of SIR were found, including 2 cases with skin burning of degree Ⅱ and 2 cases with febrile, they were administered by symptomatic therapy and changing dressing The other adverse reaction A of SIR included sorness of buttock, vaginal discharge, dysuria and painful urination, they were only suggested by follow-up. Conclusion It was efficacy and safe that ultrasound ablation as a single strategy were used in treatment of uterine fibroids.

Objective To improve clinically the recognition of fungal infection associated with hemophagocytic lymphohistiocytosis (HLH) in children. Methods Clinical data of 3 children with fungal infection complicated with HLH in our hospital was retrospectively analyzed. Results All the 3 cases complained of recurrent fever, 2 cases with cough and one case with vomiting. Hepatosplenomagaly and lymphadenectasis were found in the medical examination. The time of diagnosis of fungal infection through etiological examination was 5 days after admission. It was further diagnosed as hemophagocytic lymphohistiocytosis after failure of effective antifungal therapy. Routine blood test showed the counts of leukocytes were increased in early stage, while the number of platelets and hemoglobin decreased in different degrees. The recovery is not satisfactory using antifungal therapy alone, and 2 of them are gradually aggravated and treated with mechanical ventilation. On the basis of antifungal therapy, 2 cases were treated under HLH-2004 regimen, 1 received dexamethasone treatment. All the 3 cases received intravenous immune globulin, and showed improvement. Conclusions Fungal infection complicated with HLH in childhood is rare. The effect of simple antifungal therapy on the progression is limited. However, increasing immunosuppressive therapy based on effective antifungal therapy can improve the prognosis.