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This paper reported a rare case of hypercalcemic crisis caused by a parathyroid adenoma with hemorrhage and cystic degeneration. Preoperative imaging examination of the patient was unable to determine the histological origin of the cervical cystic lesion. Despite aggressive medical treatment and hemodialysis, hypercalcemic crisis could not be relieved. Therefore, surgical exploration and excision of the cervical lesion were performed, and final diagnosis of parathyroid adenoma with hemorrhage and cystic degeneration was confirmed by pathology. Blood calcium level and renal function returned to normal after the surgery.
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Objective:To report a rare case of renal injury secondary to Strongyloides stercoralis infection, and investigate common pathological subtypes, pathogenesis and differential diagnosis of Strongyloides stercoralis infection-associated renal injury combined with literature. Methods:The pathological features of renal biopsy were analyzed by immunofloruscence, light microscope and electronic microscope. The pathological changes of digestive tract and pathogen morphology were observed through endoscope and digestive tract biopsy. The correlation between clinical-pathological features and pathological changes of kidney and digestive tract was analized.Results:The 26-year-old male patient presented with nephrotic syndrome. The pathological changes of renal biopsy were consistent with minimal change disease with interstitial focal eosinophil infiltration. Laboratory examination showed that the patient had unexplained eosinophilia and increased IgE level. Hence the patient was treated with glucocorticoid. After 2 months of therapy, proteinuria decreased and turned to negative while the patient developed progressive headache, gastrointestinal bleeding and progressive decrease of hemoglobin. Emergency gastroscopy showed extensive congestion and erosion of the stomach and duodenum. Gastric mucosal biopsy showed a large number of slender "s" shape larvae in the mucosa. The patient also had bilateral lung infection, positive Escherichia coli in cerebrospinal fluid and purplish skin rash around the umbilicus. A serious infection of Strongyloides stercoralis was diagnosed. After antibiotics and anthelmintic treatment, gastrointestinal symptoms and headache disappeared, and no parasite was found in endoscopy. No recurrence of nephrotic syndrome was found during 2 years of follow-up. Conclusions:Strongyloides stercoralis infection might first present with nephrotic syndrome with handful hints of digestive tract combined with eosinophilia and increased IgE levels. Therefore, in epidemic areas or patients with suspicious exposure history, it is necessary to exclude Strongyloides stercoralis infection before immunosuppressive therapy to avoid fatal complications.
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Objective To detect the varicella-zoster virus (VZV) DNA load in vesicle fluid and peripheral blood,as well as plasma levels of S100β protein and neuron-specific enolase (NSE) in patients with herpes zoster before and after treatment,and to explore their correlations.Methods Vesicle fluid samples were collected before treatment,and peripheral blood samples before and after treatment from 50 inpatients with acute herpes zoster in the Department of Dermatology of the Affiliated Hospital of Southwest Medical University,and peripheral blood samplcs were also obtained from 20 heahhy controls.Real-time fluorescence-based quantitative PCR (qRT-PCR) was performed to determine the viral load in the vesicle fluid and peripheral blood samples,and enzyme-linked immunosorbent assay (ELISA) to detect the plasma levels of S100β protein and NSE.Results VZV DNA was present in all the vesicle fluid samples,as well as in peripheral blood samples from 18 patients before treatment and 5 patients after treatment,but not found in any of the healthy controls.Positive correlation was found bctween the viral load in vesicle fluid and plasma levels of S 100β protein and NSE (r =0.535,0.430,respectively,both P ＜ 0.05) in the patients with acute herpes zoster.Before treatment,patients with VZV DNA in peripheral blood showed significantly increased plasma levels of S100β protein and NSE compared with those without (both P ＜ 0.05),and the viral load in peripheral blood was positively correlated with plasma levels of S100β protein and NSE (r =0.711,0.645,respectively,both P ＜ 0.05).Conclusion VZV DNA is present in some patients with herpes zoster,and increased VZV DNA loads in the vesicle fluid and peripheral blood are related to elevated plasma levels of S100β protein and NSE before treatment.
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AIM:To validate the association between long noncoding (lncRNA)-H19 and microRNA-199a-5p (miR-199a-5p) through the dual-luciferase reporter gene system by construction of a luciferase reporter vector containing the gene of lncRNA-H19.METHODS:The potential complementary binding sites of lncRNA-H19 and miR-199a-5p were predicted by RegRNA 2.0.The H19 gene or its mutant ( Mut) fragment was cloned into luciferase reporter vector psi-CHECK-2.Restriction enzyme analysis and sequence analysis were used to identify whether the recombinant plasmids of the H19 and H19-Mut were successfully constructed .miR-199a-5p mimics, miR-199a-5p inhibitor, miR-199a-5p mimics neg-ative control or miR-199a-5p inhibitor negative control was co-transfected into the 293T cells with the luciferase reporters containing H19 or H19-Mut.Dual-luciferase reporter assay was performed to detect the luciferase activity in different groups in order to verify the relationship between lncRNA-H19 and miR-199a-5p.RESULTS:The results of double enzyme diges-tion and DNA sequencing showed that the sequence of luciferase reporter vector was correct .The results of dual-luciferase reporter assay indicated that the H 19 reporter gene luciferase activity significantly decreased in miR-199a-5p mimics group by 49%(P<0.01), and the H19 reporter gene luciferase activity was obviously upregulated in miR-199a-5p inhibitor group compared with miR-199a-5p mimics group ( P<0.01).However, miR-199a-5p mimics, miR-199a-5p inhibitor, miR-199a-5p mimics negative control and miR-199a-5p inhibitor negative control showed no effect at H 19-Mut reporter gene.CONCLUSION:lncRNA-H19 binds to miR-199a-5p to exert an inhibitory effect at transcriptional level .
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Objective To analyze how is the elastography of renal tissue correlated to clinical biochemical indexes and pathological changes in patients with chronic kidney disease (CKD), and toexplore the potential of renal elastography to become a new noninvasive method available for the dynamic monitoring of renal disease progression, as well as its efficacy assessment and prognosis evaluation. Methods Patients admitted to the department of nephrology of the First Affiliated Hospital of China Medical University and received renal biopsy from August 2014 to January 2015 were selected. One hundred and thirteen cases of CKD patients, 61 males and 52 females were enrolled, including 23 cases of IgA nephropathy, 39 cases of membranous nephropathy, 15 cases of minimal change nephropathy and 7 cases of focal segmental glomerulosclerosis. The Young modulus of renal cortex and medulla (YMcortex and YMmedul a) were detected by Aix Plorer type full digital color Doppler ultrasound. The correlations between the YMs and clinical biochemical indicators in blood and urine, and the difference of YMs among different pathological changes in patients with CKD were analyzed by statistics. Results The YMcortex and YMmedul a in CKD patients were higher than those in the control group (all P<0.05); and with the progression of CKD, the YMcortex and YMmedul a gradually increased. The YMcortex in CKD G5 patients was higher than that in CKD G1?3 patients (all P<0.05). The YMmedul a in CKD G3?5 patients was higher than that in CKD G1?2 patients (all P<0.05). The YMcortex was correlated with systolic pressure, serum creatinine, cystatin C, serum albumin, serum phosphorus, calcium and phosphorus product, uric acid, intact parathyroid hormone (iPTH), urinary NAG, estimate glomerular filtration rate (eGFR) and hemoglobin (all P<0.05). The YMmedul a was correlated with systolic pressure, serum creatinine, serum albumin, uric acid, iPTH, urine microalbumin (MA), urinary NAG and hemoglobin (all P<0.05). Serum cystatin C (β=0.485, P=0.018) and uric acid (β=0.418, P=0.039) were independently correlated with the YMcortex. Serum creatinine (β=0.380, P=0.019), uric acid (β=0.482, P=0.004) and smoking (β=0.337, P=0.009) were independently correlated with YMmedul a. The YMcortex and YMmedul a in different pathological types were statistically significant (P<0.001, P=0.003). The YMcortex and YMmedul a in patients with membranous nephropathy and IgA nephropathy were higher than those in the patients with minimal change nephropathy (all P<0.05). The YMmedul a in patients with focal segmental glomerulosclerosis was higher than that in the patients with minimal change nephropathy (P<0.05). The YMcortex in the patients with phases Ⅳ and Ⅴ based on the Lee grading system of IgA nephropathy was higher than that in the patients with phases Ⅱ andⅢ (P<0.05). According the Oxford classification for IgA nephropathy, the YMcortex and YMmedul a in the T1 and T2 patients were higher than those in the T0 patients (P<0.05). The YMcortex and YMmedul a showed no statistically significant differences among different stages of membranous nephropathy. Conclusions The YMcortex and YMmedul a are associated with the progress of renal insufficiency, which may become new indicators for determining CKD progression. The renal ultrasound elastography may become a new non?invasive method for early diagnosing CKD, dynamic monitoring disease progression, and assessing efficacy and prognosis.
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Aim To study the effects of prenatal hy-poxia on the risk of fatty liver disease to search the drug targets .Methods Intrauterine hypoxia rats model was established .The bodies and livers of fetal rats of 21 days, and adult offspring rats of 5 months with and without anoxic treatment were all weighed .The liver index was calculated and the concentrations of renin-angiotensin system components in circulation system and livers of offspring rats were measured .Results The weight of the bodies , livers and index of liver weight to body weight ( liver index ) were significantly decreased in the PH group compared with the normal group.These differences disappeared in adulthood . However, the liver index of adult offsprings in the PH group after hypoxia stress for 7 days was significantly increased compared with that of adult offsprings in nor-mal group.There were no significant differences in the concentrations of AngⅠ, AngⅡ and ACE in plasma and livers between the two groups of fetal rats and the two groups of adult offspring rats separately .The con-centrations of AngⅡ in the livers of adult rats in PH group were significantly higher than those in normal group.The concentrations of AngⅠ in livers and the concentrations of AngⅡ in plasma and livers in the group treated with hypoxia stress for 7 days were signif-icantly higher than those without hypoxia stress .The concentrations of ACE in livers and the concentrations of AngⅡ in plasma and livers in PH adult offsprings were significantly higher than those of normal adult off-springs .Conclusion PH can induce the increase of RAS content in the livers of fetus and adult rats , RAS is more likely to be activated after hypoxia stimulation in the following adulthood .PH is a potential mecha-nism that mediates offspring susceptibility of fatty liver .
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BACKGROUND:Previous studies have demonstrated that the electrophysiological stability and ventricular fibril ation threshold after myocardial infarction in rats are significantly improved in the mid-term of cardiac stem cel transplantation, but relative regulatory mechanism and pathway remain unclear. OBJECTIVE:To explore the relative molecular regulatory mechanism of cardiac stem cel s improving the electrophysiological stability and ventricular fibril ation threshold after myocardial infarction in rats. METHODS:Myocardial infarction was induced in 20 Sprague-Dawley rats by ligation of the left anterior descending coronary, which were then randomized into two groups (n=10 per group) and were subjected to the injection of cardiac stem cel s labeled with PKH26 in phosphate buffer solution (cardiac stem cel group) or the same amount of phosphate buffer solution (PBS) alone (PBS group) into the local infarct zone at 2 weeks after modeling, respectively. Six weeks later, relevant signaling molecules involved in the ANGII/AT1R/TGF-β1/SMAD/Cx43 pathway were al examined in myocardial tissues of the left ventricle and harvested blood samples. RESULTS AND CONCLUSION:Compared with the PBS group, expressions of connexin 43 in different zones of the left ventricle were significantly increased in the cardiac stem cel group (P<0.01);there was a significant reduction of the angiotensin II level in plasma and different regions of the left ventricular (P<0.05;P<0.01). Furthermore, in the cardiac stem cel group, expressions of angiotensin II type I receptor, transforming growth factor-β1, SMAD2 and SMAD3 were significantly decreased (P<0.01). Whereas SMAD7 was significantly elevated (P<0.05) in different areas of the left ventricle compared with the phosphate buffer solution group. These findings suggest that the cardiac stem cel transplantation can improve the electrophysiological stability and ventricular fibril ation threshold after myocardial infarction by enhancing the expression of connexin 43 via ANGII/AT1R/TGF-beta1/SMAD/CX43 signaling pathway.
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BACKGROUND:Piglitazone, aperoxisome proliferator-activated receptor γ(PPAR-γ) agonist, has been demonstrated topromote survivalandcardiac differentiation ofexogenous bone marrow mesenchymal stem celsto improvecardiacfunction.In this study, we attempted to investigate whether pioglitazone couldinduce cardiac differentiation of endogenous bone marrow mesenchymal stem celsandimprove cardiacfunction, andmeanwhile, probed into the relevant mechanisms. OBJECTIVE:To compare the therapeutic efficacy ofpioglitazone combined with bone marrow mesenchymal stem cel transplantation, pioglitazone alone and phosphate buffer solution(PBS)and to investigatetherelevant mechanisms. METHODS:ThirtySprague-Dawley ratswith myocardial infarctioninducedby ligation of the left anterior descending coronary artery were randomized intocombined group (combination of bone marrow mesenchymal stem cels and pioglitazone), pioglitazone group andPBSgroup. Two weeks later, PKH26-labeled bone marrow mesenchymal stem cels inPBSorPBSalone wereinjected into the local infarct zone in the combinedgroup andthe other twogroups, respectively. Pioglitazone (3 mg/kg/d) was given by the oral gavage in the combinedand pioglitazone groups forcontinuous2weeks after cels transplantation. At 2weeks after treatment, cardiac functions were evaluated. In addition, expressions of PPAR-γ, connexin 43 and relative factors in transforming growth factor-β1/SMAD signaling pathway were examined in different areas of the left ventricle from each harvested heart. RESULTS AND CONCLUSION:There were no differences in the baseline parameters of cardiac function between the two groups.Twoweeksafter treatment, left ventricular end-diastolic diameter, left ventricular end-systolic diameter and left ventricular ejection fraction were significantlyimprovedin the combined groupcompared with the other two groups; the expression of PPAR-γ was significantly increased in different zones of the left ventriclein the combined andpioglitazone groups.In the combined group, there was a significantlyhigher expression of connexin 43, and the levels of transforming growth factor-β1, SMAD2 and SMAD3 were obviously attenuated in the infarctand marginal zones.However, no differences were found in the abovedeterminants between the pioglitazone andPBSgroups. To conclude, pioglitazone cannot induce the differentiation andproliferation of endogenous bone marrow mesenchymal stem cels, but pioglitazone combined with exogenous bone marrow mesenchymal stem cels can improve cardiac function post myocardial infarction.In this process,PPAR-γmight promote the connexin 43 expression inexogenous bone marrow mesenchymal stem celsviathe blockade oftransforming growth factor-β1/SMAD signaling pathway.
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AIM:To analyze the alterations of angiotensin Ⅱ (Ang Ⅱ), connexin 43 (Cx43), angiotenisinⅡreceptor type 1 (AT1) and signaling molecules in the TGF-β1/Smad pathway in different regions of the left ventricular heart tissue for exploring whether Ang Ⅱregulates Cx43 expression via the TGF-β1/Smad signaling pathway in myocardial infarction ( MI) rats.METHODS:MI was induced in 20 male Sprague-Dawley rats by the left anterior descending coronary artery ligation.The rats were then randomized into 2 groups.In the losartan group, 20 mg· kg-1· d-1 of losartan were ad-ministered for 2 weeks.Heart functions were assessed after surgery and 2 weeks later again following the above treatments . All the rats were sacrificed and relevant molecules , including Ang Ⅱ, AT1, and Cx43 were determined thereafter in diffe-rent areas of the left ventricle .TGF-β1 and its downstream signaling molecules , including Smad 2, Smad 3 and Smad 7, were also detected .RESULTS:In losartan group , both left ventricular internal dimension diastole ( LVIDd) and left ven-tricular internal dimension systole (LVIDs) were smaller, with diminished interventricular septal thickness (IVSd) and left ventricular posterior wall depth ( LVPWd ) and distinct improvement of left ventricular ejection fraction ( LVEF ) ( P<0.05 ) .Losartan therapy exhibited a reduction of Ang Ⅱin the infarct zone and the border zone in the cardiac tissues .AT1 was obviously attenuated in the infarct zone with an enhanced expression of Cx 43, which was also elevated in the border zone and none infarct zone .TGF-β1, Smad 2 and Smad 3 were decreased in different zones of the left ventricle , while Smad 7, in contrary to the above factors , presented a converse alteration .CONCLUSION:The activation of Ang Ⅱpro-vokes downregulation of Cx 43 through TGF-β1/Smad signaling pathway in MI rats .
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BACKGROUND:Our previous work has demonstrated that bone marrow mesenchymal stem cels (BMSCs) transplantation can improve the heart function of rats with myocardial infarction. However, the overal efficacy is not satisfactory. OBJECTIVE: To adopt pioglitazone as a peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist combined with BMSCs transplantation therapy, thereby further improving cardiac function of rats with myocardial infarction as wel as investigating the relevant mechanisms. METHODS:Twenty Sprague-Dawley rats with myocardial infarction were induced by the left anterior descending coronary artery ligation. The animals were randomized into two groups: BMSCs and BMSCs+pioglitazone. Two weeks later, al the animals received the injection of BMSCs labeled with PKH26 in PBS into the local infarct zone, and then pioglitazone (3 mg/kg/d) was given by the oral gavage for 2 weeks in the BMSCs+pioglitazone group after the cel transplantation. After 2 weeks of cel transplantation, cardiac functions were evaluated by echocardiography. The expressions of PPAR-γ, Connexin 43 and molecules in TGF-β1/SMAD signaling pathway were examined in different areas of the left ventricle from each harvested heart using immunofluorescent staining, western blot assay and qRT-PCR. RESULTS AND CONCLUSION:There were no differences in the baseline parameters of cardiac function between the two groups. At 2 weeks after cel transplantation, the left ventricular internal diameter at end-diastole, left ventricular internal diameter at end-systole and left ventricular ejection fraction were significantly improved in the BMSCs+ pioglitazone group; the expressions of PPAR-γ and Connexin 43 were distinctly increased in different zones of the left ventricle; the levels of TGF-β1, SMAD2 and SMAD3 were obviously attenuated in the infarct zone and border zone. The above-mentioned findings suggest that pioglitazone, a PPAR-γ agonist, can enhance BMSCs potential in improvingthe heart function after myocardial infarction, and PPAR-γ may elevate the expression of Connexin 43via the blockade of the TGF-β1/SMAD signaling pathway in the procedure.
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Objective To study the expression of HIF-1αand and its correlation with gastric cancer recurrence, and to identify its prog-nosis evaluation in gastric cancer recurrence. Methods 80 patients with gastric cancer recurrence after radical surgery were selected as the observation group, and 50 patients without gastric cancer recurrence 5 or more than 5 years after surgery were selected as the control group. The immunohistochemical situation and expression of VEGF of the two groups were compared, and the correlation of HIF-1αand VEGF and gastric cancer recurrence were analyzed. Results The positive expression rate of HIF-1αand VEGF were 77. 50% and 73. 75% respectively in the observation group, which were significantly higher than 12. 00% and 10. 00% in the control group. Univariate analysis showed that the related indices such as degree of differentiation, depth of invasion, lymph node metastasis, vascular invasion, and TNM clinical stage were associated with VEGF expression and positive expression of HIF-1α. The Spearman correlation analysis showed that HIF-1α and VEGF was positively correlated (r=0. 458,P=0. 000). 1-year survival rate of HIF-1α-positive group was 45. 16%, and the average survival time was (8. 62 ± 2. 32) months, which was significantly lower than 77. 77% and (18. 96 ± 3. 14) months respectively in the negative group. Cox risk model analysis showed that HIF-1αand VEGF expression were high risk factors for gastric cancer recurrence. Conclusion HIF-1αand VEGF expression have a very colse correlation with gastric cancer recurrence, and it can be used as evaluation of gastric cancer recurrence and prognosis.
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BACKGROUND:Our previous work demonstrated that cardiac stem cel s (CSCs) transplantation could significantly improve the electrophysiological stability and ventricular fibril ation threshold in rats with myocardial infarction. OBJECTIVE:To compare the influence of CSCs and bone marrow mesenchymal stem cel s (BMSCs) transplantation on the electrophysiological stability and ventricular fibril ation threshold in rats with myocardial infarction in the short term. METHODS:Thirty male healthy Sprague-Dawley rats were selected to make myocardial infarction models induced by the left anterior descending coronary artery ligation. Then, animals were randomly divided into three groups, CSCs group, BMSCs group and the PBS group, with 10 rats in each group. Two weeks after modeling, animals were respectively given the injection of 5×106 CSCs labeled with PKH26 in 0.1 mL PBS, 5×106 BMSCs labeled with PKH26 in 0.1 mL PBS or 0.1 mL PBS alone into the infracted anterior ventricular free wal . Two weeks after intervention, the electrophysiological characteristics and ventricular fibril ation threshold were measured respectively at the infarct zone, the infarct marginal zone and the non-infarct zone. Labeled CSCs and BMSCs were detected, and the expression of connexin-43 was examined in 5 μm cryostat sections from the infarct marginal zone of each heart. RESULTS AND CONCLUSION:Compared with the BMSCs group and PBS group, significant differences were revealed in the correct unipolar electrograms activation recovery time dispersion (ARTcd), electrical stimulation-induced malignant ventricular arrhythmias and ventricular fibril ation threshold at the infarct zone, the infarct marginal zone and the non-infarct zone in the CSCs group (P<0.05). Obvious differences were discovered in the ARTcd, electrical stimulation-induced malignant ventricular arrhythmias and ventricular fibril ation threshold on the non-infarct area in the BMSCs group in contrast to the PBS group. Labeled CSCs or BMSCs were identified at the infarct marginal zone and expressed connexin-43. Connexin-43 was abundantly expressed in the CSCs group whereas it was rarely expressed in the BMSCs group, and even not expressed in the PBS group. These findings suggest that CSCs are superior to BMSCs in modulating the electrophysiological stability and the ventricular fibril ation threshold in the short term after transplantation, which is closely correlated with the expression of connexin-43.
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Aim Toexaminethecombinedeffectsof 5-ALA and metformin on diabetes mellitus induced by streptozotocin( STZ) in mice, and to discuss the mech-anisminitially.Methods Thediabeticmiceinduced by intraperitoneal injection of STZ were treated with 5-ALA and/or metformin for 30 days. Physical signs, fasting blood glucose ( FBG ) , fasting plasma insulin ( FIns) , plasma leptin ( Lep) , glucose tolerance, and histological changes of liver and pancreas were as-sessed. Insulin resistance was evaluated by the homeo-stasismodelassessment(HOMA).Results There were more significant effects when 5-ALA combined with metformin than only using metformin on lowering FBG, FIns and Lep. And 5-ALA combined with met-formin could improve glucose tolerance and the insulin sensitivity. Microscopic analysis demonstrated that sig-nificant changes in pancreatic islet and characteristic feature of the vacuolization phenotype in liver was ob-served on diabetic mice, and use of 5-ALA could in-hibit shrinking pancreatic islet number and hepatic morphological changes, especially in combination with metformin.Conclusions Asynergisticeffectof5-ALA and metformin is observed. Combined therapy of 5-ALA and metformin can decrease FBG and improve glucose tolerance, insulin sensitivity and islet ? cells function and morphology.