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Introduction@#Cases of gastric cancer have been declining worldwide in recent years. However, gastric cancer incidence increased in the last decade in Mongolia. In Mongolia, over 80% of gastric cancer cases are diagnosed during the late stage. Several studies have revealed that serum pepsinogens (PGs) level reflects, indirectly, histological and functional characteristics of the gastric mucosa.@*Goal@#We aimed to evaluate the risk of gastric cancer and its precancerous condition based on serum PGI, PGI/II biomarkers.@*Materials and Methods@#This case-control study enrolled 114 subjects, including patients with gastric cancer (n=36), atrophic gastritis (n=40) and healthy controls (n=138). The questionnaires were obtained to determine risk factors. Serum PGI, PGII, and H. pylori IgG levels were measured by ELISA (Pepsinogen I ELISA; Pepsinogen II ELISA; H.Pylori IgG ELISA; BIOHIT Plc, Helsinki, Finland). PGI to PGII ratio was calculated. Patients were classified into the ABC(D) group according to Miki K approach. Also, we developed new scoring system based on some risk factors and serum PGI, PGI/II ratio. Logistic regressions were performed to evaluate risk and expressed by odds ratio (OR) and 95% confidence intervals (95%CI).@*Results@#Mean age of the subjects was 60±10.9 years. H.Pylori was positive in 67 subjects. The serum PGI and PGI/II ratio levels were significantly decreased in gastric cancer and atrophic gastritis groups compared to the healthy control. According to classification ABC(D), group D (OR 5.04, 95% CI 1.13-22.50) had higher proportion of atrophic gastritis cases, group C (OR 6.19, 95% CI 1.04-36.78) had higher proportion of gastric cancer cases than others. Additionally, we created a risk prediction scoring system with a score ranging from 0 to 7, based on variables age, family history of gastric cancer, prior disease history, PGI and PGI/II ratio levels. For the atrophic gastritis patients, 17 (42.5%) were classified into medium-risk category (OR 4.49, 95% CI 1.38-14.58) and 17 (42.5%) were classified into high-risk category (OR 7.69, 95% CI 2.16-27.43). Whereas, 11 (30.6%) patients with gastric cancer were classified into medium-risk category (OR 4.35, 95% CI 1.13-16.85), 21 (58.3%) were classified into high-risk category (OR 14.25, 95% CI 3.60-56.43).@*Conclusion@#The methods based on serum PGI and PGI/II may identify a high risk population of gastric cancer and atrophic gastritis.
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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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@#Gastric cancer has been and still considered one of the most common causes of cancer-related mortality and it continues to be a major public health issue. The incidence and mortality of gastric cancer in Mongolia is the highest in the world. For this reason, this paper provides the information about current status of gastric cancer in Mongolia in the first section. Morbidity and mortality of gastric cancer increased steadily during the last decade. In the second section we overview the most important factors that can accelerate the risk of gastric cancer. Evidence from case-control, cohort studies and meta-analysis have suggested that the risk of gastric cancer is related to several factors including genetics, Helicobacter pylori, other factors related to the environment and lifestyle. Risk factors could have different effects on the onset and the evolution of gastric cancer.
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@#Familial hypercholesterolemia (FH) (OMIM#143890) is the most common metabolic autosomal disorder. The prevalence of the homozygous FH has been reported as 1 in a million in the general population, compared to much more mild form heterozygous FH with prevalence of 1 in 200-500. Mutations in the low-density lipoprotein receptor (LDLR), apolipoprotein B (ApoB), proprotein convertase subtilin/kexin9 (PCSK9), and low-density lipoprotein receptor adapter protein 1 (LDLRAP1) genes have been linked to FH. These mutations result in a disorder in low-density lipoprotein cholesterol (LDL-C) catabolism, and significantly increasing the levels of LDL-C, total cholesterol in serum, leading to specific clinical signs such as tendon xanthoma, corneal arcus, cardiovascular diseases, and early death from coronary heart disease if left unattended. Therefore, there is an ardent need for early diagnosis followed by aggressive therapeutic intervention and lifestyle modification. Currently, FH can be diagnosed either clinically or genetically. There have three main clinical diagnostic criteria for FH: the US MedPed Program, the Simon Broom Register Group in the UK, and the Netherland’s criteria. The occurrence of so many different LDLR mutations and their widespread distribution throughout the gene imposes severe practical limitations on simple genetic screening. Indeed, exon by exon sequencing of LDLR and other genes in each patient is the best screening genetic methods of choice. Although the hypercholesterolemia associated with FH can be controlled with cholesterol-lowering drug therapy (statins and other), patient response can vary quite widely.
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Background @#Low triglycerides and cholesterol was associated with hepatitis C virus (HCV) infection. Chronic HCV infection is the main cause of liver injury and it may influence to serum lipid levels. We aimed to evaluate the effect of antiviral treatment on the change of lipid profiles during interferon-based anti-HCV treatment. @*Material and Methods @#Totally 863 patients who completed the interferon-based antiviral therapy in Kaohsiung Medical University Hospital were included in this present study. The lipid profile measured and assessed in the baseline of the treatment and after 6 months of completion of the treatment. @*Results @#The most of the patients (81.2%) were achieved sustained virological response (SVR) by antiviral therapy. There was no significant difference between baseline triglycerides (TG) levels in the SVR group and non SVR groups. The TG levels at 6 months after completion of the treatment was significantly elevated in SVR group (102.9±57.0 mg/dL, p=0.0001) but did not elevated in non SVR group (94.5±45.6 mg/dL, p=0.690) compared with baseline TG levels. </br> After adjusting patients by four indexes for fibrosis (FIB4) in cut-off point 3.25, serum TG levels significantly increased in low FIB4 group (103.2±57.9 mg/dL, p=0.0001) but not in high FIB4 group (98.1±49.6 mg/dL, p=0.095) after 6 months end of the treatment. Serum TG level was increased greater in patients who had low FIB4 score and patients who achieved SVR (baseline 89.1±34.8 mg/dL; 6 months after treatment 104.3±59.3 mg/dL, paired T test p=0.0001). @*Conclusion@#The eradication of HCV is the main cause of the increase of lipids after Pegylated Interferon and Ribavirin treatment. </br> However advanced fibrosis also has an effect in increase of TG after the treatment.
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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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Introduction@#When human body encounters external pathogens primary/innate immunity cells are activated by recognizing them and secondary/adaptive immunity is activated consecutively. Immune cell surface receptors, called Toll-like receptors (TLRs) recognize and bind pathogens. 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 regulatory proteins on the IFN-γ/TLR9 synergistic signaling pathway@*Materials and Methods@#This study was held in the Core Laboratory, Science Technology Center, Mongolian National University of Medical Sciences (MNUMS). In this study, murine endothelial cell (END-D) culture was used. The negative and positive regulator protein expression was detected by Western blotting. @*Result@#Result of immunoblotting assay indicated that CpG DNA enhanced IFN-γ positive regulator protein p38 phosphorylation in the endothelial cells. Treatment by TLR9 ligand CpG DNA and IFN-γ increased p38 activation in 0.5 hour and 1 hour. CpG DNA inhibited IFN-γ negative regulator SOCS1 protein expression in 4 hr and 8 hr. Therefore, TLR9 ligand CpG DNA increased IFN-γ signal transduction in the endothelial cell line.@*Conclusion@#TLR9 ligand CpG DNA has decreased IFN-γ negative regulator protein SOCS1 expression. CpG DNA has increased IFN-γ positive regulator protein p38 phosphorylation.
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Background@#In the era of science and technology /development, it have been using a laboratory animals to confirm theory and evidences of biology, medical and veterenary sciences. The value of laboratory animals sciences are still a very important. Because, the studies of laboratory animals are used for instead of human being and biosafety evaluation, and so on.@*Goal@#To describe the current sitution analysis of general usage of laboratory animals in the Mongolian institutes, universities and biotechnological factories. @*Materials and Method@#In this study, we used a questionnaire that is covering belongs to the quantity counting numbers of laboratory animals, information of colonies and breeding, euthanizing methods, infectious disease in the laboratory animals, experimental types, special food and bedding. @*Results@#Each year were used more than 10000 animal of 9 species. Mouse, rat, rabbit and guine pig are commonly used in laboratory experiments in Mongolia. Laboratory animals imported from Russia and China, mainly. These animals uses to study toxicity and virulences, lethal dose of newly revealed substances, drug testing and diagnosis. We have conducted some comparison of laboratory animal used with the same situation of other countries. @*Conclusions@#</br> 1. Study results are indicating that the usage of laboratory animals on biological studies among the Mongolian scientists is too low as compaired to other countries. </br>2. It has no standarzided technical, legal provisions technical legal documents such as SOPs and other douments, but also specialized HRs. </br>3. Therefore, it has been raised following requirements which are to expand national- and international cooperation, to be a official member in the international association of laboratory animal sciences, to share experiences and reports between the specialists in the Asian- and international level.
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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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Introduction: Leading cause of mortality was cardiovascular disease alone last two decade and occurs5500-6000 deaths annually in Mongolia. Familial hypercholesterolemia is the most common inheritedmetabolic disorders and is characterized by severely elevated LDL-cholesterol levels. The prevalenceof the heterozygous state has been estimated at 1 in 200 to 1 in 500 and of the homozygous state from1 in 160,000 to 1 in 1,000, 000.Goal: To identify Heterozygous Familial hypercholesterolemia among the patients with cardiovasculardisease and study clinical features.Materials and Methods: After view medical examination patients with coronary heart disease andcerebral vascular disease, we selected 183 patients among 26 family who possible to have HeterozygousFamilial hypercholesterolemia. We analyzed family history, clinical examination and lipid parameters.And identifi ed Heterozygous Familial hypercholesterolemia by diagnostic criteria of Netherlands.Results: The mean age for males was 42.3±14, for females was 45.8±15 and gender distribution was42.6% (78) male, 57.4% (105) female. Hypertension occurred in 80.9% (148). BMI was increasedwith age in both sexes (P<0.001). The frequency of tendon xanthoma was 26.8% (49) and cornealarcus was 36.6% (67). The level of total cholesterol and LDL-C were signifi cantly elevated in patients.Identity Heterozygous Familial hypercholesterolemia by criteria of Netherlands was certain-36.1%,probable-42.6%, possible-18.6%, unlikely FH-2.7%.Conclusion: Identifi cation of these individuals at an early age and an aggressive treatment of all knownrisk factors are important for reduce mortality of cardiovascular disease. The Netherland’s criteria issuitable for diagnosing Familial hypercholesterolemia in the Mongolian population, although it does notdiagnose the condition at the genetic level.
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BACKGROUND:Congenital heart defects (CHD) turn out to be the leading cause of infant mortality in their first yearafter infectious diseases. Per 1,000 infants, born with CHD, about 19-75 failed to survive. It revealsthe fact that CHD is a major cause of childhood mortality in worldwide. Beyond the progress ofmedicine and surgery, the cause of CHD is not fully defined. The majority of studies reveal that CHDis triggered by many factors, such as the genetic and environmental factors.Based on the evidences of the sequence of the human genome and advances in moleculartechnology, genetic factors play a major role. Per 100 newborninfants, they’re found one child, bornwith a CHD is concerned as a highly frequent incident for birth anomaly. Only 0.5% of these congenitaldefects enable to be inherited in accordance with Mendel’s genetic laws, which is associated withthe change and mutation of a single gene. Many found that most congenital anomalies dependupon mutation or change in multiple genes and other relevant factors. As a result of the progressivedevelopment of molecular biology in the past 20 years discovered a range of genes involved in fetusformation, development, growth and control of processes. In our country case, corrective surgeryfor CHD dominates among all cardiovascular surgery in Mongolia. Particularly, for all incidents donesome corrective surgery of congenital heart defects, atrial septal defect operation occupies 42.44%,in other word it is a substantial part of the CHDoperation (D.Tsegeenjav, 2009). Molecular geneticsstudy of infant born with heart defects and simultaneous anomaly of other organ system researchstill has not been done for Mongolian population. In many cases the diagnosis of CHD is delayeduntil their adulthood, which is a research gap to address without further delay and the finding mustbe applied in practice in the near future.GOAL:The aim of the research is to conduct a molecular genetic study of children, born with CHD andcombined abnormalities of other organs and systems, identify gene lesion, location and characteristicsof mutations, pathogenetic mechanism of congenital defects and anomalies among the Mongolianpopulation.RESULT:For this study, there are 118 patients, with congenital heart disease, received surgical treatmentin the cardiovascular department of III central state hospital named P.N. Shastin, involved afterconfirmed diagnosis through objective and instrumental investigations (ECG, Fluoroscopy, EchoKG).The 118 healthy family members of patients sampled as a control group. According to the diagnosisof patients with congenital heart defect, such as atrial septal defects-95 (81.2% ± 3.6), ventricularseptal defects-17 (14.5% ± 3.3), patent ductusarteriosus- 2 (1.7± 0 .0%) have combined severedefects - 4 (3.3% ± 1.0). Out of 118 patients with congenital heart defects, 32.2% (38 patients)was male, whereas women accounted for 67.8% (80 patients) with average age of 22, 3 ± 12.9(minimum 1.0 year, maximum 51 year). These comprised 42.4% in 1-17 years old (average age10 ± 5.27) and 57.6% in 18-51 years old (average age 31 ± 9.54). The 33.9% ± 4.4 (40 patients) of operated patients responded the questionnaire that they have a hereditary heart defect. Shortnessof breath, heart pain, and recurrent pneumonia were the main complaints of patients with CHDthat significantly authentic to statistical probability. From the taken 118 blood samples, 95 werediagnosed ASD, in 7 diagnosed VSD, in 2 diagnosed PDA, in 4 diagnosed combined defects. Forthe 95 samples, we decided to examine the ASD associated GATA4, TBX5gene. It draws attentionto the fact that 81.2% of all congenital heart defects found only ASD. To examine the ASD genes inthe sample, the following changes have occurred. The study found 8 variants of mutations formingASD. It includes on exon 1 Gly 93 Ala (c.278G> C), on exon 1 P163S (c.487C>T).CONCLUSIONS:1. Patients with ASD alone occupy 81,2% of all heart defects in our study.2. For the samples of ASD, the study found 8 different mutations of GATA4.3. In the sample of blood not found TBX5 gene mutation.4. In the samples, one patient with dextrocardiasitusinvertus was combined with congenital heartdefects found E359Xfs (c.1075delG) deletion variation on exon3.
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Background and Purpose Liver disease that caused by iron metabolism failure is called Hemochromatosis (clinically “Bronze diabetes”, “Over spotted liver cirrhosis”). The two types of hemochromatosis are primary and secondary. Primary hemochromatosis is caused by a defect in the genes that control how much iron the human body absorb from food. Secondary hemochromatosis usually is the result of another disease or condition that causes iron overload. According to the study there is a real need to study the clinical reveals of hemachromatosis in Mongolian patients. The purpose of the study to determine the hemachromatosis in patients with liver cirrhosis and cancer.Methods and Materials: The study involved 68 patients with diagnosis Liver cirrhosis and HCC (1st stage) who were hospitalized in Clinic of Gastroenterology of Shastin clinical hospital and “Shagdarsuren” Hepatic hospital from April to July, 2011. All patients were increased blood iron and iron compounded proteins (ferritin, transferrin). DNA analyze have made in Molecular Biological Laboratory of Institute of Biology, Mongolia. Sequencing assay has made in Molecular Biological Laboratory of Humboldt University, Germany.Results. The patient’s age was 25-86, the mid aging – 55.42±1.7. The allele frequencies of the C282Y, H63D, and S65C mutation (which in chromosome 6) were 16/136, 11.7% (heterozygous 7, homozygous 2), 9/136, 6.6% (heterozygous 0, homozygous 9), 3/136, 2.2% (heterozygous 0, homozygous 3), equally 28/136, 20.5% (heterozygous 7, homozygous 14). Conclusions. In conclusion, the occurrence of the C282Y, H63D, and S65C mutation within HFE in this studied cohort of hereditary hemochromatosis. Therefore, these data incline that other factors than the HFE gene may play a role in determining hereditary hemochromatosis in Mongolians.
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Autosomal dominant PKD (ADPKD) is the most common monogenic genetic disease, and affects one in 500–1000 humans. Approximately half of all affected patients develop end-stage renal disease in the fifth to sixth decade of life. In a majority of cases (80-85%), the gene involved is PKD1, which is located on chromosome 16 (16q13.3) and encodes polycystin-1, a large receptor-like integral membrane protein that contains several extracellular mo-tifs indicative of cell-cell and cell-matrix interaction. In the remaining (10-15%) cases, the disease is milder and is caused by mutational changes in another gene (PKD2), which is located at chromosome 4 (4q21-23) and encodes polycystin-2, a transmembrane protein, which acts as a nonspecific calcium-permeable channel. ADPKD is gener¬ally a late-onset multisystem disorder characterized by bilateral renal cysts; cysts in other organs including the liver, seminal vesicles, pancreas, and arachnoid membrane; vascular abnormalities including intracranial aneurysms, dilatation of the aortic root, and dissection of the thoracic aorta; mitral valve prolapse; and abdominal wall hernias. Renal manifestations include hypertension, renal pain, and renal insufficiency. PKD1 and PKD2 gene mutations result in similar extra-renal manifestations, including PLD and intracranial aneurysms. Autosomal recessive polycystic kidney disease (ARPKD) is an important cause of childhood renal- and liver-related morbidity and mortality with variable disease expression. While most cases manifest peri-/neonatally with a high mortality rate in the first month of life, others survive to adulthood. ARPKD is caused by mutations in the Polycystic Kidney and Hepatic Disease 1 (PKHD1) gene on chromosome 6p12. PKHD1 is an exceptionally large gene (470 kb) with a longest open reading frame transcript of 67 exons predicted to encode a 4,074-amino acid (aa) (447 kDa) multidomain integral membrane protein (fibrocystin/polyductin) of unknown function.
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Hemochromatosis is a common inherited disorder of iron metabolism in which an inappropriate increase in intestinal iron absorption results in deposition of excessive amounts of iron in parenchymal cells with eventual tissue damage and impaired organ function. The human HFE gene was identified as the most common form of hemochromatosis in 1996. A homozygous G A mutation resulting in a cysteine to tyrosine substitution at position 282 (C282Y) is the most common mutation. It is identified in 85–90% of patients with hereditary hemochromatosis in populations of northern European descent. A second relatively common HFE mutation (H63D) results in a substitution of histidine to aspartic acid at codon 63. Homozygosity for H63D is not associated with clinically significant iron overload. Some compound heterozygotes (e.g., one copy each of C282Y and H63D) have moderately increased body iron stores but develop clinical disease only with cofactors such as heavy alcohol intake or hepatic steatosis. Thus, HFE-associated hemochromatosis is inherited as an autosomal recessive trait; heterozygotes have no, or minimal, increase in iron stores. However, this slight increase in hepatic iron can act as a cofactor that modifies the expression of other diseases such as porphyria cutanea tarda (PCT) and nonalcoholic steatohepatitis. Mutations in other genes involved in iron metabolism are responsible for non-HFE-associated hemochromatosis, including juvenile hemochromatosis, which affects persons in the second and third decade of life. Mutations in the genes encoding hepcidin, transferrin receptor 2 (TfR2), and hemojuvelin result in clinicopathologic features indistinguishable from HFE-associated hemochromatosis. However, mutations in ferroportin, responsible for the efflux of iron from enterocytes and most other cell types, result in iron loading of reticuloendothelial cells and macrophages, as well as parenchymal cells.
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According to estimations there are corresponds approximately 380000 carriers of HCV in Mongolia, this is approximately 15,4% of the population. Standard therapy of the HCV infection is the donation of PEG-Interferonalfa plus Ribavirin. The therapy successes dependents on the viral genotype. Diagnostic and therapy of the HCV are very expensive and complicated. But accurate diagnosis and therapy are always our main goal in order to clarify to elucidate. Therefore, I would like to propose the foundation of a specialized laboratory in Ulaanbaatar with the help of the German government and develop health programs for the education of the population. German clinics are prepared to support this project of the HCV.