Laboratory diagnosis of acute infection of hepatitis E virus (HEV) is commonly based on the detection of HEV RNA, IgM and/or rising IgG levels. However, the profile of these markers when the patients present have not been well determined. To clarify the extent of misdiagnosed sporadic hepatitis E in the initial laboratory detection, serial sera of 271 sporadic acute hepatitis cases were collected, detected and the dynamics of each acute marker during the illness course were analyzed. 91 confirmed cases of hepatitis E were identified based on the presentation of HEV RNA, IgM or at least 4 fold rising of IgG levels. 21 (23.1%) hepatitis E cases were false negative for the viral RNA and 40 (44.0%) for rising IgG, because occurrence of these markers were confined to acute phase of infection and viremia had already subsided and antibody level peaked when these patients presented. IgM was detected in 82 (90.1%) cases. It is the most prevalent of the three markers, because the antibody persisted until early convalescence. Nine cases negative for IgM were positive for rising IgG and one was also positive for the viral RNA; all of these nine cases showed high avid IgG in their acute phase sera, which indicated re-infection. In summary, it is not practicable to determine the true occurrence of sporadic hepatitis E. Nevertheless, it could be closely approximated by approach using a combination of all three acute markers.
Multiple regions in the short arm of chromosome 3 are frequently deleted in a variety of solid tumors including gallbladder carcinoma (GBC). RNA binding motif, single‑stranded interacting protein 3 (RBMS3), a tumor suppressor gene (TSG), is located in this region. However, the role of RBMS3 in GBC remains unclear. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blotting were performed to evaluate the mRNA and protein expression levels of RBMS3 in 41 fresh frozen GBC tissues and paired normal tissues. An immunohistochemical assay was performed on a tissue microarray (TMA, consisting of 125 cases GBC and 47 normal controls). Microvessel density (MVD) counts were determined using CD34 immunohistochemical staining. Moreover, univariate and multivariate analyses were performed to determine the correlations between RBMS3 expression, MVD and patient prognosis. Cellular functions including proliferation, clonogenicity and apoptosis, were assessed to further identify in vitro roles of RBMS3. It was revealed that both mRNA and protein expression levels of RBMS3 were significantly lower in GBC tissues than in normal controls. Multivariate Cox regression analyses demonstrated cytoplasmic RBMS3 expression as an independent prognostic factor correlated with GBC angiogenesis, histopathological differentiation and TNM stage. Kaplan‑Meier curves revealed that patients with lower cytoplasmic RBMS3 levels had a significantly worse OS than patients with higher cytoplasmic RBMS3 expression. Additionally, ectopic expression of RBMS3 markedly suppressed GBC cell proliferation and clonogenicity and promoted apoptosis in vitro. These findings indicated the potential of cytoplasmic RBMS3 as a tumor prognostic biomarker and a promising therapeutic target for GBC.
Pancreatitis is a common disease of the digestive system with a high mortality and complication rate. This book provides a comprehensive discussion of the anatomy and physiology of the pancreas, acute and chronic pancreatitis, and minimally invasive treatment in pancreatitis. The target audience comprises scholars and specialists in the field.
Objective
To explore the outcomes of the transplanted kidney as donor for clinical renal transplantation and summarize experience in combination with related literature.
Method
This study retrospectively analyzed the clinical documents of one case of uremia receiving renal allograft transplantation with the transplanted kidney as the donor in one case of renal transplantation after brain death in February, 2015. The donor was a 31-year-old man who received renal transplantation for uremia in November, 2014 and obtained normal renal function. Two months later, the patient was brain dead because of neurologic disorder and donated his transplanted kidney. The serum creatinine of the donor was 167 μmol/L, and the glomerular filtration rate was about 35 mL/min befor donation. The recipient was 27 years old who needed transplantation because of chronic renal function failure and uremia. Preoperation tests showed that PRA was negative, and serum creatinine was 1 353 μmol/L. After separating and dissecting the donor kidney carefully, we perfused and compensated the kidney by Lifeport Organ Perfusion and Preservation Conveyor. The warm ischemia time was about 15 min. The renal vein of the donor was anastomized with right external iliac vein of the receptor, artery with right external iliac artery, and ureter with right centrifugal ureter.
Result
The operating time was more than 3 h. Postoperatively, the recipient was given the immunosuppressive regimen as tacrolimus, mycophenolate mofetil and methylprednisolone to prevent rejection. At 1st day postoperation, the 24-h urine volume of the receptor was 5 000 mL, serum creatinine was declined gradually to a minimum of 180 μmol/L, and there was trace urine protein. The renal function of patient recovered well by now. Meanwhile, the patient was still under the follow-up.
Conclusion
It is practical that using transplanted kidney as donor kidney for re-transplantation. There were certain clinical significance for shortening the waiting time of renal transplantation in uremia patients and relieving the shortage of transplant kidney.
Key words:
Transplant kidney; Organ donation; Kidney transplantation
To study the protection of Gan by using deoxyschizandrin (Wuzhi Capsule, WC) in the renal transplantation recipients while increasing the blood concentration of tacrolimus (Tac).Seventy-three renal transplant recipients were randomly assigned to two groups, i.e., 35 in the WC group and 38 in the control group. All patients received Tac + MMF + Pred triple immunosuppressive therapy. WC was additionally given to patients in the WC group. One year was taken as one therapeutic course. Changes of the blood concentration of Tac were detected one week, 1, 3, 6, and 12 months after medication in the two groups using microparticle enzyme immune assay (MEIA). Meanwhile, the liver and kidney functions, and the blood glucose were tested.One week after the application of WC, the blood Tac concentration increased 67.2% averagely. During the 1 -12 months of WC treatment, the Tac dosage was significantly lower in the WC group than in the control group (P<0.01). There was no significant difference in the liver and renal functions, or the blood glucose levels between the two groups (P>0.05).WC could significantly increase the blood Tac concentration of renal transplant recipients, reduce their Tac dosages, with no obvious adverse reaction.
The transplantation of mesenchymal stem cells (MSCs) is considered to be a promising treatment for ischemic heart disease; however, the therapeutic effects and underlying mechanisms of action require further evaluation. Mitochondrial dysfunction is a key event in simulated ischemia/reperfusion (SI/R) injury. The purpose of the present study was to investigate the mechanism of mitochondrial transfer, which may be involved the antiapoptotic action of co-culture with MSCs. An in vitro model of simulated ischemia/reperfusion (SI/R) was used in the present study. The apoptotic indexes were significantly increased when H9c2 cardiomyocytes were induced in the SI/R group. Following co-culture with bone marrow-derived (BM)‑MSCs, H9c2 cells exhibited marked resistance against the SI/R-induced apoptotic process. Besides, mitochondrial transfer via a tunneling nanotube (TNT) like structure was detected by confocal fluorescent microscopy. In addition, following pretreated with latrunculin-A (LatA), an inhibitor of TNT formation, the BM-MSCs were not able to rescue injured H9c2 cells from apoptosis, as previously observed. In conclusion, the anti‑apoptotic ability of BM‑MSCs may be partially attributed to the recovery of mitochondrial dysfunction in SI/R, and the formation of TNTs appears to be involved in this action of mitochondrial transfer between adjacent cells.
Hand, foot, and mouth disease (HFMD) has become very common in children, with widespread occurrence across China. The aim of this study was to investigate the epidemiologic and etiologic characteristics of HFMD, including etiologic variations in Chongqing, China. An epidemiologic investigation was based on 3,472 patients who presented with HFMD manifestations and were admitted at the Children's Hospital of Chongqing Medical University between 2010 and 2013. Fecal specimens from 830 patients were analyzed by nested RT-PCR to identify the enterovirus pathogens, and the molecular characterization of HFMD was illustrated by phylogenetic tree analysis. The results of this study indicate that the peak of the HFMD epidemic in Chongqing between 2010 and 2013 occurred between April and July each year. The median age of onset was 2.24 years old, and children under the age of five accounted for 96.4% of all the HFMD cases; the male-to-female ratio was 1.89:1. Enterovirus 71 accounted for a major proportion of the isolated strains every year, including the majority (74%) of severe cases. However, the proportion of Coxsackie A (CV-A) 6 infections increased from 2.11% in 2010 to 16.36% in 2013, while the proportion of CV-A16 infections decreased from 31.23% in 2010 to 4.67% in 2013. Molecular epidemiologic study showed that all enterovirus 71 strains belonged to subgenotype C4a, whereas all CV-A16 strains belonged to genotype B1, including subgenotype B1a and subgenotype B1b.
Background: Endometrial cancer (EC) is one of the most common type of female genital malignancies. The purpose of the present study was to reveal the underlying oncogene and mechanism that played a pivotal role in postmenopausal EC patients. Methods: Weighted gene co-expression network analysis (WGCNA) was conducted using the microarray dataset and clinical data of EC patients from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases to identify significant gene modules and hub genes associated with postmenopausal status in EC patients. LASSO regression was conducted to build and validate the risk model. Finally, expression of hub gene was validated in pre- and post-menopausal EC patients in our center. Results: 1240 common genes were used to construct the WGCNA model. According to the WGCNA results, we identified a brown module with 471 genes which was significantly associated with postmenopausal status in EC patients. Furthermore, we constructed an 11-gene risk signature to predict the overall survival of EC patients. The KaplanâMeier curve and area under the ROC curve (AUC) of this model showed high accuracy in prediction. We also validate the risk model in patients in our center and it also has a high accuracy. Among the 11 genes, PKD1 was recognized as a potential biomarker in the progression of EC patients with postmenopausal status. Conclusion: Taken together, we uncovered a common PKD1-mediated mechanism underlying postmenopausal EC patientsâ progression by integrated analyses. This finding may improve targeted therapy for EC patients.
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)