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Introduction@#Determining stages of liver fibrosis in chronic liver disease is essential for clinical practice such as decision making on medical treatment, setting the interval of follow-up examination for its complication, screening intervals for hepatocellular carcinoma. @*Goal@#We compared non-invasive fibrosis markers among the patients with chronic hepatitis Delta. @*Materials and Methods@#Totally 70 patients with chronic hepatitis D enrolled into this study. The blood samples were examined for complete blood count, liver function test and serum M2BPGi level. Non-invasive markers such as AAR, APRI, Fib-4 scores were calculated. Those with AAR >1, APRI >0.7, FIB-4 >1.45 were considered with advanced fibrosis. All patients underwent liver stiffness measurement using FibroScan M2 probe. The cutoff values of FibroScan for advanced fibrosis were 9 kPa for patient with normal transaminase level and 11 kPa for patients with elevated transaminase. @*Results@#Advanced fibrosis was observed in 25.7%, 38.6% and 38.6% by AAR, APRI and Fib-4 score, respectively. When cut-off levels of serum M2BPGi for advanced fibrosis was 2.2 COI, 35.7% had advanced fibrosis. FibroScan tests showed 34.4% had advanced fibrosis. The AUROC of M2BPGi were 0.894 and 0.827 for predicting advanced fibrosis and liver cirrhosis. @*Conclusion@#Serum M2BPGi and FibroScan would be reliable diagnostic tool for identifying liver fibrosis in Mongolian patients with chronic hepatitis D.
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Background and Aims@#Hepatocellular carcinoma (HCC) is a common cause of cancer related death in Mongolia. Early diagnosis is the very important management to increase successful treatment and survival rate. Glypican-3 (GPC3) protein is highly expressed in hepatocellular carcinoma (HCC) tissue and in serum of HCC patients. Recent studies have been conducted and suggested as a diagnostic biomarker for detecting HCC in the early stage. Therefore, we investigated the diagnostic value of the serum GPC3 level and compared it to the alpha-fetoprotein (AFP) level as a diagnostic biomarker of HCC.@*Methods@#We enrolled a total of 90 participants and divided into 3 groups with HCC (30), with liver cirrhosis (LC/30) and healthy (30) as the control group (30). GPC3 and AFP serum (sGPC-3, sAFP) levels were measured using commercially available enzyme-linked immunosorbent assay kits. The diagnostic accuracy was analyzed using the receiver operating characteristics (ROC) curve and estimated sensitivity and specificity of each biomarker. @*Results@#sGPC3 was significantly elevated in the HCC group as compared to liver cirrhosis and healthy subjects (658±138.2 pg/ml, 378±25.5 pg/ml, 356.3±29 pg/ml) respectively. sGPC-3 sensitivity was 96.6% and specificity was 100%. The area under the ROC curve (AUC) for GPC3 was 0.999 (0.996- 1.0).</br> In comparison, the mean of AFP was significantly higher in HCC (16.9±11.7 ng/ml) than in LC (6.7±7.6 ng/ml) and in healthy subject (3.3±2.1 ng/ml) and AFP sensitivity was 43,3 %, specificity was 95 % with an AUC of 0.808 (0.696- 0.921). </br> The combination of GPC-3 with AFP achieved the highest sensitivity (97.1%) and specificity (97%).@*Conclusion@#Serum GPC3 has a higher sensitivity than AFP for the early diagnosis of HCC. Combination of two markers showed greatest diagnostic accuracy.
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@#Research of function of vitamin D on immune system has been studying since the study revealed that vitamin D receptor is expressed on the surface of the immune cells. 1,2-dihydroxyvitamin D3 [1,25(OH)2D], physiologically active form, can be generated through hydroxylation of 25-hydroxyvitamin D3 [25(OH)D], inactive form of vitamin D, in a liver, connecting with specific VDR make biological action. Vitamin D make different biological actions depends on connecting with different immunological cells. Some studies indicated that Vitamin D plays pivotal role in antibacterial innate immune responses through regulating reaction of the main cells as macrophages and dendritic cells. Moreover, calcitriol, the active form of vitamin D, is connected with VDRE, modulates the innate immune response through directly inducing expression of catelicithin and β-defensin as antimicrobial peptides, reducing secretion of IL-1b, IL-6, TNF-a, RANKL, COX-2 as proinflammatory cytokines and increasing production of IL-10, an anti-inflammatory cytokine. Vitamin D plays in proliferation and differentiation of T and B cells and regulates the activities of over 500 genes. Vitamin D differently impacts on per se stages of T cells’ proliferation. Vitamin D indirectly mitigates the differentiation from immature B cells to plasma B cells while it directly impacts on regulation of overloaded production of antibodies in plasma B cells. In conclusion, vitamin D modulates the innate- and adaptive immune response through regulation on activation of APCells, proliferation and differentiation of immune cells, secretion of some antibacterial peptides.
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Background@#De-novo donor and non-donor specific antibodies could be detrimental to the kidney allograft. Kidney transplantation has being performed in Mongolia since 2006. However there is currently no published data available on post-transplant de-novo antibodies and long-term graft survival. Our aim was to determine immunosuppressive drug through level, its combination, de-novo HLA antibodies and its influence on graft survival in different immunosuppressive protocols. @*Methods@#We analyzed data from 56 adult first kidney transplant recipients at our hospital from August 2006 to May 2013. We determined the level of tacrolimus, cyclosporine A, and the presence of pre and post-transplant anti-HLA antibodies.@*Results@#Post-transplant follow up period was 1-8 years. Mean recipient age on transplantation was 33.9±9.1 years. Male 45 (80.4%). Cadaver donor kidney was 5 (8.9%). Mean donor age on transplantation was 39.98±11.13 years. Rejection occurrence was 12(21.4%). Tacrolimus and cyclosporine A through levels were 3-12.8ng/ml and 65- 324ng/ml respectively. Anti-HLA class I antibodies were detected in 17.9% of pretransplantation (n=10) and in 23.2% of post-transplantation (n=13) cases respectively (p=0.607). On the other hand, anti-HLA class II antibodies were detected in 5.4% of pretransplantation (n=3) and in 33.9% of post-transplantation (n=19) cases (p=0,001). We determined anti-HLA class II antibody specificity. Anti-DQ, DR, DP antibodies were 25% ( n=14), 14.3% ( n=8) and 7.1% ( n=4) respectively on all 56 cases. Two (3.6%) patients’ samples were positive on three loci of HLA class II. Six patient samples (10.7%) were positive on two loci. Nine (64.3%) of anti-DQ positive patients have rejected their grafts and begun hemodialysis treatment. All 9 graft rejected recipients were anti-HLA DQ positive and had taken cyclosporine mono-therapy for the first year after transplantation.@*Conclusion@#The presence of de-novo anti-HLA class II antibodies, especially de-novo anti-DQ were significantly increased on cyclosporine mono-therapy group following transplantation and negatively affected kidney graft survival. The blood through level of cyclosporine was very variable. The graft survival was better in standard triple regimen. Therefore, it is essential to monitor immunosuppressive drug combinations with drug blood level and anti-DSA antibodies as well as to manage antibody removal therapies such as therapeutic plasma exchange, intravenous immunoglobulin and Rituximab therapy on time. HLA –DQ-DP antigen determination is important for the kidney transplantation.
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Background@#However kidney transplantation has being performed in Mongolia since 2006, because of pre-transplant sensitization, ABO incompatibility, hepatitis B and C virus activation many patients are taken kidney transplantation in abroad. The transplantation centers use own immunosuppressive regimens.@*Objective@#Our aim was to assess the immunosuppressive regimens efficacy and toxicity in kidney transplant Mongolian recipients.@*Methods@#We analyzed data from 96 adult kidney transplant recipients who had taken kidney transplantation in different transplant centers from August 2006 through January 2014. There were 3 kinds of regimens Group I Simulect induction with standard triple /FK506/CyA+MMF/AZA+steroid/, Group II Campath-1H induction with CNI monotherapy and Group III Campath-1H induction with standard triple /FK506/CyA+MMF/AZA+steroid/. We retrospectively collected the post-transplant first two years serum creatinine. The study was performed in 2014. The questionnaire was taken and blood samples collected for determination of tacrolimus through level and for other laboratory tests. The primary end point was the first two years serum creatinine, the secondary end points included rejection episodes, blood through level of tacrolimus and some laboratory findings. @*Results@#The post-transplant first two years serum creatinine levels were significantly different in 3 groups. Group III showed similar results compared to Group I. There was not enough data of biopsy proven acute rejection episodes however group II said more rejections occurred. However participants said that rejection occurred in 15 (15.6%) biopsy was done only 3 (3.1%) cases. Blood through level of tacrolimus was significantly different in three groups. Some laboratory findings showed different between three groups. @*Conclusions@#A regimen of Campath-1H induction with CNI monotherapy (Group II) may be advantageous for short-term renal function and cost effective but there were more rejection complications and increased creatinine. The regimen of Campath-1H induction 11 with standard triple (Group III) may be advantageous for long-term renal function, allograft survival, but there should consider about infection complications and polycythemia. Simulect induction with standard triple could be best choice but transplantations were performed in experienced centers. The study enrolled few cases and cases which were performed at the beginning of transplant program so many things could influence on the result. The study was compared beginner transplant center with experienced centers. Longitudinal cohort study needed in the future.
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Introduction@#Valproic acid (VPA) has been used in the treatment of seizures and bipolar disorders. In the present study, we examined how VPA affected PI3K-Akt pathway in response to LPS by using mouse RAW 264.7 macrophage cells.@*Material and methods@#Mouse RAW 264.7 macrophage-like cells cultured and the cell viability checked by MTT and TUNEL assay. In addition, protein expression and protein interaction were detected by immune blotting and immune precipitation, respectively. TLR4 expression on cell surface studied by FACS analysis.@*Results@#The MTT and TUNEL assays demonstrated no significant difference between VPA at 2 mM treated and untreated control cells. VPA attenuated LPS-induced phosphorylation of phosphatidylinositol 3-kinase (PI3K) and Akt, but not nuclear factor (NF)-κB and mitogen activated protein kinases (MAPKs). There was no significant difference in the TLR4 expression on the cell surface between cells treated with or without VPA. VPA inhibited LPS-induced PI3K/Akt signal transduction in a dose dependent manner.@*Conclusion@#VPA at 2mM exhibits nontoxic effect in the RAW 264.7 cells. VPA down regulates LPS-induced phosphorylation of Akt via inhibition of PI3K activation.
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Background@#Kidney transplantation has being performed in Mongolia since 2006. However there is currently no published data available on long-term graft and patient survival. @*Objective@#Our aim was to assess the long-term graft and patient survival rate correlation with HLA-A-B-DR matching.@*Methods@#We retrospectively analyzed data from 70 adult kidney transplants performed at our hospital from August 2006 through January 2014. The data was retrospectively collected from patient files, including characteristics of the recipient and donor, post transplant features and HLA-A-B-DR DNA based typing results. The Kaplan-Meier method was used to analyze graft and patient survival. @*Results@#The mean patient follow-up period after kidney transplantation was 39,6±25.9 months, and the mean kidney graft follow-up period was 36.6±23.7 months for 70 cases. Overall graft and patient survivals were 52 (74.3%) and 60 (85.7%) respectively in 70 cases. Five-year graft and patient survivals were 23 (67.6%) and 29 (85.3%) respectively in 34 cases. The group with four to six mismatched were found to have a significantly lower 3 and 5-year graft and patient survival (71%; 35%); (80%; 40%) compared to 0 to 1 mismatched group (100%) (p=.030; p=.015). Furthermore we analyzed the association of HLA matching, immunosuppressive therapy and long-term graft survival. We selected CNI mono-therapy group for long-term survival analysis and observed a similar pattern. In mono-therapy group, the group with four to six mismatched were found to have a significantly lower 3 and 5-year graft and patient survival (75%; 30%); (65%; 30%) compared to 0 to 1 mismatched group (100%) (p=.037; p=.001). @*Conclusion@#The results showed that graft and patient survival rates were lower compared with results from established centers. Statistically highly significant effect of HLA matching on kidney graft and patient survival rates was found in our analysis. Five years after transplantation the graft survival rate of first adult kidney transplant with 4-6MM was 65-70% lower than that of grafts with 0-1MM. Longitudinal cohort study needed in the future to exhibit an improved transplantation outcome.
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Background@#The effect of lipopolysaccharide (LPS) on valproic acid (VPA)-induced cell death was examined by using mouse RAW 264.7 macrophage cells. @*Materials and methods, results@#LPS inhibited the activation of caspase 3 and poly (ADP-ribose) polymerase (PARP) and prevented VPA-induced apoptosis. LPS inhibited VPA-induced p53 activation and pifithrin-α as a p53 inhibitor as well as LPS prevented VPA-induced apoptosis. LPS abolished the increase of Bax/Bcl-2 ratio, which is a critical indicator of p53-mediated mitochondrial damage, in response to VPA. The nuclear factor (NF)-κB inhibitors, Bay 11-7082 and parthenolide, abolished the preventive action of LPS on VPA-induced apoptosis. A series of toll-like receptor (TLR) ligands, Pam3CSK4, poly I:C, and CpG DNA as well as LPS prevented VPA-induced apoptosis. @*Conclusion@#Taken together, LPS was suggested to prevent VPA-induced apoptosis via activation of anti-apoptotic NF-κB and inhibition of pro-apoptotic p53 activation.
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Background@#Stroke is a leading cause of death and disability, especially in low-income and middle-income countries and it impacts a tremendous medical, emotional and fiscal burden on society. Due to advances in Western healthcare, the prevalence of stroke since 1970 has decreased by 42%, whereas it has more than doubled in low-income to middle-income countries. </br> Stroke is a heterogeneous, multifactorial disease regulated by modifiable and nonmodifiable risk factors. Approximately 80% of stroke events could be prevented by making simple lifestyle modifications. In fact, nationwide characterization of well-known stroke factors in all social backgrounds is essential, however; populations can differ significantly not only in their socio-behavioral, legal, and geographical conditions, but also from other, historically understudied. Therefore, it is crucial to determine characterization of risk factors for ischemic stroke among Mongolian population.@*Objective@#To determine etiology and risk factors for ischemic stroke among Mongolian population@*Material and methods@#Our study was conducted by case-control study design. Cases were patients with acute first stroke; controls were matched with cases, recruited in a 1.2:1 ratio, for age and sex. The case series study was conducted in Stroke center of Third State Central hospital from January 2017 to December 2017. Structured questionnaires were administered and physical examinations were done in the same manner in cases and controls. Self-reported history of hypertension and diabetes mellitus or blood pressure of 140/90 mm Hg and blood sugar 6.4 mmol/L or higher was used to hypertension and diabetes mellitus, respectively. Smoking status was defined as never, former, or current smoker. Alcohol use was categorized into never or former, low intake, moderate intake, and high or episodic heavy intake. Atrial fibrillation was based on previous history, review of baseline electrocardiograph results (for cases and controls). Odds ratios (OR) and logistic regression were calculated, with 95% confidence intervals. @*Results@#In total, 173 patients with ischemic stroke and 146 controls were included. The patients’ age ranged from 17 to 92, the mean age was 61.2. Ischemic stroke more frequent in man than women by 27.4%. Previous history of hypertension or blood pressure of 140/90 mm Hg or higher (OR 2.40, 95% CI 1.48-3.88), diabetes mellitus (OR 3.08, 95% CI 1.44-6.57), hyperlipidemia (OR 5.09, 95% CI 2.64-9.82) atrial fibrillation (OR 8.70, 95% CI 2.01-37.64 ), current smoking (OR 2.07, 95% CI 1.26-3.40), alcohol consumption (OR 4.75, 95% CI 2.58-8.73) were all significantly associated with ischemic stroke. The mean age was lower in patients with stroke of other determined etiology. The frequency of hypertension was higher in patients with lacunar infarct than other subtypes. Smoking was high frequent in patients with large artery atherosclerosis.@*Conclusion@#6 potentially modifiable risk factors were collectively associated with ischemic stroke and were different among ischemic stroke subtypes. The odds ratios of these risk factors are higher than other countries’ study.
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Introduction@#When human body encounters external pathogens primary/innate immunity cells are activated by recognizing them and secondary/adaptive immunity is activated consecutively. In our previous study, we revealed that there is a synergistic action between TLR9 and IFN-γ signaling in the endothelial cells. @*Purpose@#To determine the role of negative and positive regulator proteins on the IFN-γ/TLR9 signaling pathway. @*Methods@#In this study, murine endothelial cell (END-D) culture was used. END-D cells pre-treated with TLR9 ligand CpG DNA and then stimulated with IFN-γ. The negative (SHP-2, SOCS1, PIAS1) and positive (p38) regulator protein expression was detected by Western blotting. @*Results and Conclusion@#Treatment by TLR9 ligand CpG DNA and IFN-γ increased positive regulator p38 phosphorylation in 0.5 hour. CpG DNA inhibited IFN-γ negative regulator PIAS1 protein expression in 6 hour and SOCS1 and SHP-2 expression could not affect in 4 hour.
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Introduction@#Toll like receptors (TLRs) are a class of proteins that key role in the innate immune system. The SOCS1 and SHP2 proteins are negative-feed loop inhibitors of signaling of JAK/STAT and TLRs pathways.@*Purpose@#To determine negative regulator protein activation which is activated through TLR7 ligand/IFN-γ signal transduction in endothelial cells. @*Methods@#We used mouse aortic linear endothelial cell (END-D); protein expressio was detected by western blotting @*Results@#We analyzed a time dependent stimulation effects of negative regulator proteins stimulated by TLR7 ligand/IFN-γ in endothelial cell cultures. Imiquimod of 10 μg/ml treatment of 1 hr was followed by 100 ng/ml IFN-γ stimulation for 1-8hr to analysis of negative regulator SOCS1 and SHP2 protein expression. </br> In untreated cells, there was low activations of negative regulator SOCS1 and SHP2 proteins. IFN-γ stimulation alone had increased SOCS1 and SHP2 protein expressions, also imiquimod treatment highly <i>elevated</i> SOCS1 and SHP2 expressions. However imiquimod and IFN-γ doubled treatment have decreased activation of negative regulator SOCS1 and SHP2 proteins. These findings suggest SOCS1 and SHP2 proteins are inhibitors in the TLR7 ligand/IFN-γ signaling. @*Conclusion@#Negative regulators, SOCS1 and SHP2 strongly suppressed activations of TLR7 ligand/IFN-γ signaling
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@#BACKGROUND: Toll like receptors (TLRs) are a class of proteins that key role in the innate immune system. TLR7 is expressed on monocytes, macrophages and dendritic cells, T cell, B cell and eosinophiles. TLR7, originally identified as recognizing imidaquinoline, loxibrine, broprimine and ssRNA, ssRNA viruses such as vesicular stomatitis virus, influenza A virus and human immunodefiency virus. It is known that virus ssRNA affects signaling molecule of IFN-y. Objective: To determine gene and protein activation of IFN-y signal transduction by TLR7 ligand in the endothelial cells. MATERIAL: In study we used mouse aortic linear endothelial cell which is cultured (END-D) in 5% heat- inactivated fetal calf serum (FCS), medium (DMEM) containing antibiotic mix(penicillin G, streptomycin, amphotericin B) at 37°C (5% CO2). Endothelial cells treated with synthetic IFN-γ and imiquimodligands, then the NO (nitric oxide) concentration in the supernatant is determined by Griess reagent. Endothelial cells are cultured in 6 well cell culture plate and in each well 2*104cells are expected to be grown for 24 hours of culture. Then, the cells are treated with synthetic IFN-γ and имиквимод ligand for 6 hours and the NO signaling gene activation iNOS mRNA expression which is induced by IFN-γ is determined by RT-qPCR. Endothelial cells are cultured in 12 well cell culture plate and in each well 2*104 cells are expected to be grown for 18 hours of culture. Then, the cells are treated with synthetic IFN-γ and imiquimodligands for 24 hours and the NO signaling protein iNOS expression which is induced by IFN-γ is determined by western blotting. The experiment was conducted as representation mean of at least three test results. The difference between statistical probabilities is determined by the “Students” t test. The p<0.01 value is assumed to be statistically different. RESULTS: TLR7 ligand imiquimodaugmented interferon gamma induced nitric oxide production TLR7 ligand imiquimodincreased interferon gamma induced iNOS mRNA gene expression. TLR7 ilgand imiquimodup-regulated interferon gamma induced iNOS protein expression. CONCLUSIONS: TLR7 ligand imiquimod augments IFN-γ signaling in the endothelial cells. This synergistic effect has revealed in the levels of gene and protein expression.
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@#BACKGROUND Bovine colostrums is the milk secreted by cows during the first few days after parturition. It contains many essential nutrients and bioactive components, including growth factors, immunoglobulins, lactoperoxidase, lactoferrin and cytokines ets. Lactoferrin has been reported for its multifunctional properties such as antifungal, antibacterial, antiviral antioxidant and anticancer activities. The aims of this study focused on the isolation and purification of lactoferrin from Mongolian bovine colostrums. Lactoferrin purified using HiTrap DEAE an ion exchange chromatography. Lactoferrin purification efficiency was about 60.5%. The single band of purified lactoferrin has been observed in SDS-PAGE electrophoresis. METHODS Bovine colostrum was collected at a cow farm in the Darkhan province of Mongolia. At first the cream was separated by centrifugation (10000 xg 20 min at 4oC). In order to separate the whey, the samples were precipitated with 1mol/l to pH 4.6 and centrifuged at 10000 g 20 min again. The samples of whey were stored at -18oC to the analysis. Lactoferrin was purified by HiTrap DEAE an ion exchange chromatography using 0.005 M phosphate buffer (pH 7.7) and linear gradient NaCl from 0.25M, 0.5M, 1M. During chromatography, protein in the eluents was monitored by ultraviolet absorbation at 280 nm with the instrument. Purity test done by using polyacrylamide gel electrophoresis under denaturated condition (SDS-PAGE) method by Laemmli (1970). For HPLC determination of the lactoferrin by Shimadzu Nexera X2 HPLC system with UV/ VIS detector were used. Detection was carried out at the wavelength 280 nm. Separation was performed on a chromatographic column Protein R C18 ,2.2 x 150 mm, 5 μm particle size. Linear gradient and flow rate 0.2 ml/min were used. Mobile phase a consisted of water / acetonitrile/ trifluoroacetic acid ( 95:5:0.1). The column temperature was set at 40oC and injection volume was 10 μl. Data were collected and evaluated by software Lab Solution. An external standard method for quantification analytes was used. RESULTS Purified lactoferrin in the present study had a good concentration and purification efficiency was about 60.5 %. Protein fraction from 1M NaCl gradient delivers sharp and clean peak to HPLC chromatogram that fits intensity and retention time of standard bovine lactoferrin. Ammount of lactoferrin in bovine colostrums was 0.6 mg/ml and it`s molecular weight 80 kDa as a standard sample. The retention time of lactoferrin fraction which is purified by SDS-PAGE gel electrophoresis. The peak of fraction same compared to the standard lactoferrin 5.8 minutes by HPLC analysis. CONCLUSION Ion exchange chromatography shows reliable and easy isolation of lactoferrin from Mongol bovine colostrum.
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Introduction@#The aim of this research project is to elucidate the crosstalk of innate and adaptive immune reactions against the DNA containing bacteria.@*@#This study held in the Core laboratory, Science Technology Center, Mongolian National University of Medical Sciences (MNUMS). Murine aortal endothelial cells, END-D cultured and the cell viability checked by MTT assay. In addition, the NO production, protein and gene expression studied by Griess Reagent assay, R.T-PCR and immunoblotting, respectively. @*Results@#0.1µM, 1µM and 10µM of TLR9 ligand exhibited no cytotoxic action against the cells by MTT assay. IFN-ү alone induced NO production in END-D cells. In the other hand, TLR9 ligand at 0.1µM, 1µM and 10µM up-regulated IFN-ү induced NO production in dose dependent manner. RTPCR results exhibit that TLR9 ligand up regulates iNOS mRNA. Immunoblotting analysis showed the enhanced iNOS protein expression and phosphorylation of STAT1 in cells pre-treated with TLR9 ligand.@*Discussion@#We have demonstrated CpG DNA, TLR9 ligand, up-regulates IFN-ү induced NO via enhanced IFN-ү signaling. The result of Western Blotting and RT-PCR support the up-regulation of NO. CpG DNA can be used as agent against virus and bacteria. Further research need to be conducted. @*Conclusion@#TLR9 ligand, CpG DNA up-regulates IFN-ү induced NO production in time and dose dependent manner. TLR9 ligand augments the expression of iNOS mRNA and STAT1 phosphorylation in response to IFN-ү.
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Background:Kidney transplantation has being performed in Mongolia since 2006. However there is currently no published data available on long-term graft and patient survival.Objective:Our aim was to assess the long-term graft and patient survival rate correlation with HLA-A-B-DR matching. Material and Methods:We retrospectively analyzed data from 70 adult kidney transplants performed at our hospital from August 2006 through January 2014. The data was retrospectively collected from patient fles, including characteristics of the recipient and donor, post transplant features and HLA-A-B-DR DNA based typing results. The KaplanMeier method was used to analyze graft and patient survival.Results:The mean patient follow-up period after kidney transplantation was 39,6±25.9 months, and the mean kidney graft follow-up period was 36.6±23.7 months for 70 cases. Overall graft and patient survivals were 52 (74.3%) and 60 (85.7%) respectively in 70 cases. Five-year graft and patient survivals were 23 (67.6%) and 29 (85.3%) respectively in 34 cases. The group with four to six mismatched were found to have a signifcantly lower 3 and 5-year graft and patient survival (71%; 35%); (80%; 40%) compared to 0 to 1 mismatched group (100%) (p=.030; p=.015). Furthermore we analyzed the association of HLA matching, immunosuppressive therapy and long-term graft survival. We selected CNI mono-therapy group for long-term survival analysis and observed a similar pattern. In mono-therapy group, the group with four to six mismatched were found to have a significantly lower 3 and 5-year graft and patient survival (75%; 30%); (65%; 30%) compared to 0 to 1 mismatched group (100%) (p=.037; p=.001).Conclusion:The results showed that graft and patient survival rates were lower compared with results from established centers. Statistically highly signifcant effect of HLA matching on kidney graft and patient survival rates was found in our analysis. Five years after transplantation the graft survival rate of frst adult kidney transplant with 4-6MM was 65-70% lower than that of grafts with 0-1MM. Longitudinal cohort study needed in the future to exhibit an improved transplantation outcome.
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Background:However kidney transplantation has being performed in Mongolia since 2006, because of pre-transplant ensitization, ABO incompatibility, hepatitis B and C virus activation many patients are taken kidney transplantation in abroad. The transplantation centers use own immunosuppressive regimens.Objective:Our aim was to assess the immunosuppressive regimens efficacy and toxicity in kidney transplant Mongolian recipients.Material and Methods:We analyzed data from 96 adult kidney transplant recipients who had taken kidney transplantation in different transplant centers from August 2006 through January 2014. There were 3 kinds of regimens Group I Simulect induction with standard triple /FK506/CyA+MMF/AZA+steroid/, Group II Campath-1H induction with CNI monotherapy and Group III Campath-1H induction with standard triple /FK506/CyA+MMF/AZA+steroid/. We retrospectively collected the post-transplant first two year serum creatinine. The study was performed in 2014. The questionnaire was taken and blood samples collected for determination of tacrolimus through level and for other laboratory tests. The primary end point was the first two years serum creatinine, the secondary end points included rejection episodes, blood through level of tacrolimus and some laboratory findings.Results:The post-transplant first two years serum creatinine levels were significantly different in 3 groups. Group III showed similar results compared to Group I. There was not enough data of biopsy proven acute rejection episodes however group II said more rejections occurred. However participants said that rejection occurred in 15 (15.6%) biopsy was done only 3 (3.1%) cases. Blood through level of tacrolimus was significantly different in three groups. Some laboratory findings showed different between three groups.Conclusion:A regimen of Campath-1H induction with CNI monotherapy (Group II) may be advantageous for short-term renal function and cost effective but there were more rejection complications and increased creatinine. The regimen of Campath-1H induction with standard triple (Group III) may be advantageous for long-term renal function, allograft survival, but there should consider about infection complications and polycythemia. Simulect induction with standard triple could be best choice but transplantations were performed in experienced centers. The study enrolled few cases and cases which were performed at the beginning of transplant program so many things could influence on the result. The study was compared beginner transplant center with experienced centers. Longitudinal cohort study needed in the future.
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BACKGROUND: Bladder cancer is a cancer of significant morbidity and mortality in the worldwide. It is the second most common urological cancer in Mongolia. It is important to understand the risk factors of bladder cancer.We evaluated the association of smoking, alcohol intake, body mass index and other potential risk factors with bladder cancer incidence in Mongolians.MATERIALS AND METHODS: We analyzed data from a case-control study (116 histologically confirmed bladder cancer cases and 300 cancer-free healthy, age, gender-matched controls). All participants signed the consent form andfilled out the structured questionnaire including cigarette smoking, BMI, chronic urinary disease andalcohol drinking etc. Using logistic regression we estimated the covariate-adjusted odds ratio (OR) and95% confidence interval (CI) of the associations.RESULTS: Mean age of the patients with bladder cancer was 56±10.5 years and 79.3% male and 20.7% female.Cigarette smoking, history of urinary tract diseases and body mass index were associated with an increased risk of bladder cancer OR 6, 48 (95% CI 1, 61-1, 70), OR 80 (95% CI 1, 48-1, 93) and OR=9.8 (95% CI 2.32-2.91) respectively but not alcohol drinking OR 0, 26 (95% CI 1, 56-1, 66).CONCLUSIONS: The results suggest that cigarette smoking, history of urinary tract diseases and body mass indexincreased risk of bladder cancer in Mongolian patients.
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Mongolian blue spots are birthmarks that are present at birth and their most common location issacrococcygeal or lumbar area. There are macular and round, oval or irregular in shape. Lesionsmay be single or multiple. They usually spontaneously regress and disappear during childhood.The prevalence of Mongolian blue spots varies among different ethnic groups according to theoverall depth of pigmentation. Mongolian blue spots are common among Asian, East Indian, andAfrican races, but rare among Caucasian and other races. Mongolian blue spot is a congenital,developmental condition exclusively involving the skin. Mongolian blue spot results from entrapmentof melanocytes in the dermis during their migration from the neural crest into the epidermis. Thismigration is regulated by exogenous peptide growth factors that work by the activation of tyrosinekinase receptors. It is postulated that accumulated metabolites such as GM1and heparin sulfatebind to this tyrosine kinase receptor and lead to severe neurologic manifestations and aberrantneural crest migration.
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The purpose of the present study was to elucidate genealogical and clinical features of hereditary neuropathy in the several kindreds of Gobi-Altai province.Materials and Methods: In the present study, we investigated five kindreds originated from Bayan-Uul sum, Gobi-Altai province on the basis of previous surveys. Each participant was enrolled for genealogical and neurological examinations according to specific questionnaire. We also collected biological samples for further genetic study. Genomic DNA was isolated from biological samples, and quantitative analysis of DNA was determined by spectrophotometer and Picogreen assays.Results: Twenty members from five kindreds were investigated. Genealogical analysis revealed that there is a linkage between two kindreds within the families enrolled into study, whereas no association was revealed among the other pedigrees. As a phenotype of the hereditary neuropathy, the clinical features were inherited in every generation, and the inheritance was not dependent on the gender. In neurological examination, age of hereditary neuropathy onset was detected as follows. The clinical features appeared in the first decade of life in 4 patients, in the second decade of life in 5 patients, and for the other members the disease started in the age of over 20 years. Common clinical features of hereditary neuropathy were characterized by hypomimic- and mask shape face, muscular atrophy of upper and lower limbs, and pes cavus. Interestingly five female patients had similar gynecological problems. Conclusions:1. The hereditary neuropathy exists in the kindreds of Bayan-Uul sum, Gobi-Altai province and the type of inheritance could be categorized as autosomal dominant.2. Onset of hereditary neuropathy disease was started mostly in the second decade of life. Common clinical features of hereditary neuropathy were characterized by hypomimic- and mask shape face, muscular atrophy of upper and lower limbs, and pes cavus. Apart from general clinical features, the specific complications related to metabolic disorders and pregnancy was detected.
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Charcot-Marie-Tooth disease (CMT) is a clinically and genetically heterogenous group of disorders. Useful classifi cation is still clinical and electrophysiological classifi cation that divides CMT into CMT type 1 - demyelinating form and CMT type 2 - axonal form. An intermediate type is also increasingly being determined. Inheritance can be autosomal dominant, X-linked and autosomal recessive (AR). In this review, we will focus on the clinical and/or electrophysiological findings and molecular genetics of ARCMT1 (CMT4). Ten genes, GDAP1, MTMR2, MTMR13, SH3TC2, NDRG1, EGR2, PRX, CTDP1, FGD4 and SAC3 have been identifi ed in the CMT4A, CMT4B1, CMT4B2, CMT4C, CMT4D, CMT4E, CMT4F, CCFDN, CMT4H and CMT4J types, respectively. In addition, susceptibility locus on chromosome 10q23 has been found for CMT4G disease. Molecular genetics of demyelinating ARCMT are large disabilities of proteins in Schwann cells and their functions (transcriptional factor, protein transport, protein sorting, intra/extra cellular compartments, signal transduction, cell division, and cell differentiation). It has been rising necessary requirements to defi ne clinical and genetic subtypes of the ARCMT1, prevent from disease, give reproductive and genetic counselling, and develop methods for reducing and clear disease risk factor.