The syndrome of inappropriate antidiuretic hormone secretion ( SIADH ),characterized with dilutional hyponatremia,is the most frequent pathophysiology of euvolemic hyponatremia in hospital inpatients.Conventional therapies for SIADH include fluid resriction,saline infusion,and some pharmacologic adjustments of fluid balance.For various reasons,conventional therapies show poor efficiency.Vasopressin receptor antagonist,a new class of pharmacologic agent,can directly block vasopressin-mediated receptor activation and target underlying pathophysiology of SIADH.

A reninoma is a renal juxtaglomerular cell apparatus tumor that produces excessive amounts of renin,resulting in secondary hyperaldosteronism,and associated hypertension and hypokalemia.It is a rare form of secondary hypertension and occurs mainly in young adult females.Common symptoms include headache,nocturia,polyuria,polydipsia,and fatigue.Imaging examination and selective renal vein sampling has been the traditional method of localizing the tumour.The diagnosis should be considered in all patients with hypertension and hypokalemia and no evidence of primary hyperaldosteronism and renal artery stenosis.Reninoma represents a surgically correctable cause of hypertension.

Objective To study the influence of dietary test designed by Nutritional Department of Henan Provincial People's Hospital on diabetic inpatients' dietary cognition. Methods A total of 134 diabetic inpatients were selected and tested with standard diabetic meaL Self-reporting of oil, salt, staple food, vegetables and meat intake was evaluated. Nonparametric tests were used for statistical analysis. Results There were significant differences in self-reporting of oil,salt,staple food and meat intake between pre and post test (Z= -4.642, -8.700, -2.218, -5. 528,all P<0.05) ; however,no significant change of self reporting vegetable intake was found ( Z = - 1. 385, P > 0. 05 ). Conclusion Dietary test can significantly change patients' cognition about their daily dietary intake.

Objective To investigate the TNF-? expression in hepatic tissue of Otsuka Long-Evans Tokushima Fatty(OLETF) rats(an insulin resistance model) with abnormalities of glucose-lipid metabolism and effect of metformin on TNF-? expression.Methods OLETF rats were randomly assigned to two groups(OLETF and OLETF/M).The OLETF/M group was treated with metformin [100 mg/(kg?d)],the OLETF group and age-matched LETO(nondiabetic Long-Evans Tokushima Otsuka rats) group were fed with placebo.Twenty-two weeks after treatment,we analyzed hepatic triglyceride level and measured expression of TNF-? by western-blot(protein) and quantitative RT-PCR(mRNA).Results Twenty-two weeks after treatment,the level of fasting glucose,insulin,triglyceride,free fatty acids(FFA) and hepatic triglyceride increased significantly in OLETF group as compared with LETO group.Western-blot method showed upregulated expression of TNF-? protein in OLETF group(1.57-fold vs LETO group,P

Objective To study the influence of nitric oxide synthase (NOS) inhibitor in a rat model of Parkinson’s disease. Methods Hemi-Parkinsonism rat model was established by stereotaxic 6-hydroxydopamine (6-OHDA) lesions in striatum in which nitric oxide synthase (NOS) was inhibited by L-Nitro-Arginine (L-NNA) and apomorphin-induced rotational behavior was measured. The immunohistochemical staining method was used to observe the change of striatal nNOS-positive neurons and nigral tyrosine hydroxylase(TH)-positive neurons. Results L-NNA dramatically protected 6-OHDA-injected rats against indices of severe injury to the nigrostriatal dopaminergic pathway, including decreases in numbers of TH-positive nigral neurons and rotational behavior. The nNOS-positive neurons showed no changes in numbers. Conclusions These results indicate that NO might mediate, in part, 6-OHDA-induced neurotoxicity and nNOS-positive neurons might resist the 6-OHDA neurotoxicity. NOS inhibitor may play a role in the protection of 6-OHDA neurons.

Background Familial hyperaldosteronism type Ⅱ(FH-Ⅱ) is characterized by autosomal dominant inheritance and hyperaldosteronism.Linkage analysis demonstrated chromosome 7q22 most likely harbor the genetic defect.Objective To identify the disease locus in a Chinese pedigree with FH-Ⅱ using genetic linkage analysis.Methods Haplotypes of the FH-Ⅱ pedigree were analyzed using four microsatellite markers(D7S531,D7S2521,D7S511,D7S481) at 7p22 to determine the critical region,and multipoint logarithm of odds(LOD) scores were calculated to assess linkage with FH-Ⅱ.Results Several members(affected members) in the family had hypertension,hypokalemia,hyperaldosteronism,low renin activity.Hypertension and hypokalemia was improved by spironolactone test.Dexamethasone suppression test was performed but without clinical or hyperaldosteronism improvement in three affected members,confirmed FH-Ⅱ family pedigree.The same haplotypes D7S531(ac,n=24)-D7S2521(ac,n=11)-D7S511(ca,n=21)-D7S481(ac,n=16) were shared by all known affected members and one suspicious member,but also by one unaffected member of the family,making it unlikely that this region contains the causative gene mutation.In this FH-Ⅱ family,the LOD scores of the four markers were

Lymphocytic hypophysitis(LH) is a rare but increasingly recognized autoimmune endocrine condition that causes partial or total hypopituitarism and is often associated with peripartum young women.We here report a 28-year-old patient who had a spontaneous and uneventful pregnancy following LH that had been treated with transspenoidal surgery and followed by anti-inflammatory agent.The woman failed to lactate and developed frontal headaches 3 months after normal delivery of her first child 3 years ago.Lab test showed the reduced concentrations of thyroxine,estradial and cortisol,suggesting hypopituitarism.Magnetic resonance imaging of the brain with contrast was performed and showed a uniformly enhancing pituitary mass with elevated optic chiasm.She underwent transsphenoidal surgery and histological examination of the resected specimen was consistent with lymphocytic hypophysitis.Anti-inflamation was started with prednisolone 40 mg per day because of a recurrence of headache that had completely recovered after surgery and regularly withdrawn to a long term maintenance dose of 10 mg per day.Physiological thyroxine replacement therapy was maintained.Her menstruation was restored without sex hormone replacement after 3 months.Three years after surgery,she got pregnant spontaneously and had normal breastfeeding after delivery.LH did not recur during this peripartum.

Adults-onset nesidioblastosis,as a differential diagnosis of organic hyperinsulinemic hypoglycemia,is very rare and has been recognised as "noninsulinoma pancreatogenous hypoglycaemia syndrome(NIPHS)".Here we described an extremely rare case of NIPHS in an eldly type 2 diabetes mellitus with insulin therapy.A 84-year old male was diagnosed as type 2 diabetes six years ago and switched from an oral hypoglycemic drug to pro-mixed insulin treatment 3 years ago.According to medical records,he had good-glucose control over few hypoglycemia.He was admitted to hospital due to frequent fasting hypoglycaemic episodes and comas despite withdrawal of any anti-diabetes drugs and continous infusion of homogenate meal at night.Lab test showed low fasting glucose level and inappropriate high insulin/C-peptide level,and anti-insulin antibody was negative.A characteristic of hyperinsulinemic hypoglycemia with high C-peptide level was consistent with the possible diagnosis of insulinoma,but localizing studies including computed tomography of the abdomen and somatostatin receptor scintigraphy were negative.Surgical exploration by the palpation and intraoperative ultrasonography failed to detect any mass in the pancreas and 70% distal pancreatectomy was performed.Histological examination of the resected pancrease revealed an increased number and size of islets consistent with nesidioblastosis.After transient decline,his serum insulin travelled back to the level before pancreaectomy,but recurrent fasting hypoglycemia was mild and controlled by regular night eating postpancreaectomy.Abstract:SUMM ARY Adults-onset nesid ioblastosis,as a d ifferential d iagnosis of organic hyperinsulinem ic hypo-glycem ia,is very rare and has been recognised as"noninsulinoma pancreatogenous hypoglycaem ia syn-drome(NIPHS)".Here we described an extremely rare case ofNIPHS in an eldly type 2 d iabetesmelli-tus with insulin therapy.A 84-year old male was d iagnosed as type 2 d iabetes six years ago and switched from an oral hypoglycem ic drug to pro-m ixed insulin treatment 3 years ago.Accord ing tomed ical records,he had good-glucose control over few hypoglycem ia.He was adm itted to hospital due to frequent fasting hypoglycaem ic episodes and comas despite withdrawal of any anti-d iabetes drugs and continous infusion of homogenate meal at night.Lab test showed low fasting glucose level and inappropriate high insulin /C-peptide level,and anti-insulin antibody was negative.A characteristic of hyperinsulinem ic hypoglycem ia with high C-peptide level was consistentwith the possible d iagnosis of insulinoma,but localizing stud ies includ ing computed tomography of the abdomen and somatostatin receptor scintigraphy were negative.Surgical exploration by the palpation and intraoperative ultrasonography failed to detect any mass in the pancreas and 70% d istal pancreatectomy was performed.H istological exam ination of the resected pancre-ase revealed an increased number and size of islets consistent with nesid ioblastosis.After transient de-cline,his serum insulin travelled back to the level before pancreaectomy,but recurrent fasting hypoglyce-m ia was m ild and controlled by regular night eating postpancreaectomy.

Objective To explore the effect of amifostine combined with low-dose cyclosporine in treatment of refractory immune thrombocytopenia effect and related mechanisms.Methods 60 cases of refractory immune thrombocytopenia patients using parallel randomized controlled groups, divided into three groups, 20 cases in each group, amifostine group were treated with amifostine, cyclosporine group were treated with cyclosporine, amifostine+CSA group received amifostine+cyclosporine A treatment.The platelet count, platelet membrane glycoprotein antibody, lymphocyte subsets and bone marrow megakaryocyte count were observed and compared.Results After different treatment of three, six months, the level of platelet count of patients in three groups were compared with the group before treatment were significantly increased, and the treatment of platelet count level of amifostine group and cyclosporine group were significantly lower than that of amifostine +CSA group, the difference was statistically significant (P<0.05), there was no significant difference between amifostine group and cyclosporine group.The total efficacy of amifostine+CSA group was significantly higher than the other two groups, the difference was statistically significant ( P<0.05 ) , there was no significant difference between amifostine group and cyclosporine group.After the treatment, the platelet membrane glycoprotein GPIIb/IIIa antibody levels in three groups were significantly increased, and ring the detection level of amifostine+CSA group after treatment was significantly higher than the other two groups, the difference was statistically significant (P<0.05), there was no significant difference between amifostine group and cyclosporine group.After treatment, the three groups of CD4 +, CD4 +/CD25 +and CD4 +/CD8 +levels were significantly increased, CD8 +decreased significantly, the difference was statistically significant (P<0.05).And the level of change after treatment with amifostine +cyclosporine group was significantly higher than that of the other two groups, the difference was statistically significant (P<0.05), there was no significant difference between amifostine group and cyclosporine group.After treatment, the number of bone marrow megakaryocytes in the three groups was significantly lower than that before treatment , the level of count after treatment with amifostine +cyclosporine was significantly lower than that of the other two groups, the difference was statistically significant (P<0.05).there was no significant difference between amifostine group and cyclosporine group.The adverse reactions of amifostine group and amifostine+CSA group were significantly lower than that in cyclosporine group, the difference was statistically significant (P<0.05).there was no significant difference between amifostine group and amifostine+CSA group.Conclusion Amifostine combined with low dose of cyclosporine in treatment of refractory immune thrombocytopenia can play a synergistic effect, improve the therapeutic effect, and effectively reduce the dosage and adverse reactions.

Objective:To explore whether esketamine (ESK) can inhibit the proliferation and induce apoptosis of breast cancer cells, and explore the mechanism.Methods:CCK-8 assay was used to detect the inhibitory effect of ESK on the proliferation of breast cancer cells. Annexin V/PI staining was used to detect the morphological changes of cells; Apoptosis and reactive oxygen species were detected by flow cytometry. Western blot was used to detect apoptosis and pathway expression.Results:CCK-8 experiment results proved that ESK could inhibit the proliferation of breast cancer cells in a time-dependent manner. The survival rate of MDA-MB-468 cells treated with ESK at 20 μM was (35.47±2.61) %, which was statistically different from that treated with vinorelbine at the same concentration ( P<0.05). The IC50 value of ESK on MDA-MB-468 cells was (14.54±2.12) μM. After treatment with ESK, the mitochondrial membrane potential was significantly reduced. In the protein level, the expression of Cytochrome C, Bax and Caspase-3 was up-regulated, and the expression of Bcl-2 was down regulated, which induced the mitochondrial dependent apoptosis of MDA-MB-468 cells. ESK could up regulate the level of reactive oxygen species in MDA-MB-468 cells and regulate the expression of PI3K/AKT signaling pathway. Conclusions:ESK can inhibit the proliferation and migration of breast cancer cells and induce them to play a mitochondrial dependent apoptosis. Its mechanism is achieved by up regulating the level of ROS in breast cancer cells, thereby regulating the PI3K/AKT signaling pathway, which provides a theoretical basis for the development and utilization of Aln.