Human leukocyte antigen (HLA) is a group of glycoproteins encoded by the major his-tocompatibility complex (MHC) that plays a pivotal role in the host's immune defense.Given that the MHC represents the most polymorphic region in the human genome, HLA typing is crucial in organ transplantation. It significantly influences graft rejection, graft-versus-host disease, and the overall patient outcome by mediating the discrimination between self and nonself. HLA typing technology began with serological methods and has evolved rapidly alongside advances in molecular technologies, progressing from DNA-based typing to next- or third-generation sequencing. These advancements have increased the accuracy of HLA typing and reduced ambiguities, leading to marked improvements in transplantation outcomes. Additionally, numerous novel HLA alleles have been identified. In this review, we explore the developmental history and future prospects of HLA typing technology, which promises to further benefit the field of transplantation.

Human leukocyte antigen (HLA) is a group of glycoproteins encoded by the major his-tocompatibility complex (MHC) that plays a pivotal role in the host's immune defense.Given that the MHC represents the most polymorphic region in the human genome, HLA typing is crucial in organ transplantation. It significantly influences graft rejection, graft-versus-host disease, and the overall patient outcome by mediating the discrimination between self and nonself. HLA typing technology began with serological methods and has evolved rapidly alongside advances in molecular technologies, progressing from DNA-based typing to next- or third-generation sequencing. These advancements have increased the accuracy of HLA typing and reduced ambiguities, leading to marked improvements in transplantation outcomes. Additionally, numerous novel HLA alleles have been identified. In this review, we explore the developmental history and future prospects of HLA typing technology, which promises to further benefit the field of transplantation.

Human leukocyte antigen (HLA) is a group of glycoproteins encoded by the major his-tocompatibility complex (MHC) that plays a pivotal role in the host's immune defense.Given that the MHC represents the most polymorphic region in the human genome, HLA typing is crucial in organ transplantation. It significantly influences graft rejection, graft-versus-host disease, and the overall patient outcome by mediating the discrimination between self and nonself. HLA typing technology began with serological methods and has evolved rapidly alongside advances in molecular technologies, progressing from DNA-based typing to next- or third-generation sequencing. These advancements have increased the accuracy of HLA typing and reduced ambiguities, leading to marked improvements in transplantation outcomes. Additionally, numerous novel HLA alleles have been identified. In this review, we explore the developmental history and future prospects of HLA typing technology, which promises to further benefit the field of transplantation.

Human leukocyte antigen (HLA) is a group of glycoproteins encoded by the major his-tocompatibility complex (MHC) that plays a pivotal role in the host's immune defense.Given that the MHC represents the most polymorphic region in the human genome, HLA typing is crucial in organ transplantation. It significantly influences graft rejection, graft-versus-host disease, and the overall patient outcome by mediating the discrimination between self and nonself. HLA typing technology began with serological methods and has evolved rapidly alongside advances in molecular technologies, progressing from DNA-based typing to next- or third-generation sequencing. These advancements have increased the accuracy of HLA typing and reduced ambiguities, leading to marked improvements in transplantation outcomes. Additionally, numerous novel HLA alleles have been identified. In this review, we explore the developmental history and future prospects of HLA typing technology, which promises to further benefit the field of transplantation.

OBJECTIVE: This study strived to evaluate the relationship between degree of pulmonary emphysema and cardiac ventricular function in chronic obstructive pulmonary disease (COPD) patients with pulmonary hypertension (PH) using electrocardiographic-gated multidetector computed tomography (CT). MATERIALS AND METHODS: Lung transplantation candidates with the diagnosis of COPD and PH were chosen for the study population, and a total of 15 patients were included. The extent of emphysema is defined as the percentage of voxels below -910 Hounsfield units in the lung windows in whole lung CT without intravenous contrast. Heart function parameters were measured by electrocardiographic-gated CT angiography. Linear regression analysis was conducted to examine the associations between percent emphysema and heart function indicators. RESULTS: Significant correlations were found between percent emphysema and right ventricular (RV) measurements, including RV end-diastolic volume (R2 = 0.340, p = 0.023), RV stroke volume (R2 = 0.406, p = 0.011), and RV cardiac output (R2 = 0.382, p = 0.014); the correlations between percent emphysema and left ventricular function indicators were not observed. CONCLUSION: The study revealed that percent emphysema is correlated with RV dysfunction among COPD patients with PH. Based on our findings, percent emphysema can be considered for use as an indicator to predict the severity of right ventricular dysfunction among COPD patients.
Adult ; Aged ; Electrocardiography ; Female ; Heart Ventricles/radiography ; Humans ; Hypertension, Pulmonary/complications/*diagnosis ; Lung/radiography ; Male ; Middle Aged ; Multidetector Computed Tomography ; Pulmonary Disease, Chronic Obstructive/complications/*radiography ; Pulmonary Emphysema/complications/*radiography ; Regression Analysis ; Ventricular Function/*physiology

Although the genetic component in the etiology of rheumatoid arthritis (RA) has been consistently suggested, many novel genetic loci remain to uncover. To identify RA risk loci, we performed a genome-wide association study (GWAS) with 100 RA cases and 600 controls using Affymetrix SNP array 5.0. The candidate risk locus (APOM gene) was re-sequenced to discover novel promoter and coding variants in a group of the subjects. Replication was performed with the independent case-control set comprising of 578 RAs and 711 controls. Through GWAS, we identified a novel SNP associated with RA at the APOM gene in the MHC class III region on 6p21.33 (rs805297, odds ratio (OR) = 2.28, P = 5.20 x 10(-7)). Three more polymorphisms were identified at the promoter region of the APOM by the re-sequencing. For the replication, we genotyped the four SNP loci in the independent case-control set. The association of rs805297 identified by GWAS was successfully replicated (OR = 1.40, P = 6.65 x 10(-5)). The association became more significant in the combined analysis of discovery and replication sets (OR = 1.56, P = 2.73 +/- 10(-10)). The individuals with the rs805297 risk allele (A) at the promoter region showed a significantly lower level of APOM expression compared with those with the protective allele (C) homozygote. In the logistic regressions by the phenotype status, the homozygote risk genotype (A/A) consistently showed higher ORs than the heterozygote one (A/C) for the phenotype-positive RAs. These results indicate that APOM promoter polymorphisms are significantly associated with the susceptibility to RA.
Apolipoproteins/*genetics ; Arthritis, Rheumatoid/*genetics ; Case-Control Studies ; DNA/genetics ; Female ; *Genetic Predisposition to Disease ; Genome-Wide Association Study ; Genotype ; Heterozygote ; Homozygote ; Humans ; Lipocalins/*genetics ; Luciferases/metabolism ; Male ; Middle Aged ; Polymorphism, Single Nucleotide/*genetics ; Promoter Regions, Genetic/*genetics ; Real-Time Polymerase Chain Reaction ; Risk Factors

True malignant mixed tumor (carcinosarcoma) of the salivary gland is an extremely rare tumor. By definition, it is a heterologous neoplasm that's composed of both malignant epithelial and mesenchymal components. We report here on a case of an 83 year old female patient with a parotid gland mass. Histologic examination showed a biphasic pattern of growth with both a poorly differentiated epithelial component and a sarcomatous spindle cell background. The immunohistochemical and ultrastructural findings support the diagnosis of a small cell neuroendocrine epithelial tumor and an undifferentiated malignant mesenchymal features. The histologic and ultrastructural features along with the immunohistochemical findings are presented. We also review the literature and we discuss the different opinions on the exact histogenesis of the true malignant mixed tumor of the salivary gland. To the best of our knowledge, this histological pattern has not been previously reported in the English medical literature.
Female ; Humans

We established an in vitro experimental system using the following procedure. We first introduced tritium-labeled norepinephrine ([3H]-NE) into PC12 cells. The [3H]-NE incorporated-PC12 cells were stimulated by a high concentration (60 mM) of K+ buffer during 12 minutes. Then, we collected 100 microliter supernatant and counted the amount of [3H]-NE release from PC12 cells with a scintillation counter. After screening fungal, Streptomyces spp. or bacterial product using this experimental sytem, we obtained FS390 from Streptomyces spp. which inhibited [3H]-NE release from PC12 cells. FS390 also inhibits the release of ATP as a neurotransmitter of PC12 cells and rat cortical neurons. The inhibitory effect was seen even when the PC12 cells were treated with low K+ buffer containing ionomycin (1 micrometer) as an ionopore. This result suggests that the inhibitory action of FS390 on neurotransmitter release appeared after the influx of Ca2+.
Adenosine Triphosphate ; Animals ; Exocytosis ; Ionomycin ; Mass Screening* ; Neurons ; Neurotransmitter Agents* ; Norepinephrine ; PC12 Cells* ; Rats ; Scintillation Counting ; Streptomyces

OBJECTIVE: The aim of this study was to investigate the gene expression profiles using GeneFishingTM kit in human placentae and their membranes delivered at preterm caused by preterm labor. METHODS: Specimens were obtained from placenta, chorion, and amnion delivered at preterm and term, respectively. Total RNAs were isolated from each specimen. Thereafter, the profiles of expression genes between preterm and term specimens were compared using a new and accurate reverse transcription-polymerase chain reaction (RT-PCR) that involves annealing control primers (ACPs) to identify the genes expressed differentially and screened by basic local alignment search tool (BLAST) search. RESULTS: Using 20 ACPs, 13 differentially expressed genes (DEGs) were identified and sequenced. 7 of them were expressed up-regulation, while 6 were expressed down-regulation in preterm deliveries. A BLAST searches revealed that 11 were known genes and 2 were unknown genes. Among known genes, up-regulated genes were insulin-like growth factor II associated protein, vigilin, acyl-Coenzyme A dehydrogenase, tissue inhibitor of metalloproteinase 1 (TIMP1), ribosomal protein S26 (RPS26), follistatin-like 1 (FSTL1) and down-regulated genes were two mitochondrial DNAs, ribosomal protein S28 (RPS28), transglutaminase 2 (TGM2), heparin sulfate proteoglycan (HSPG, perlecan). CONCLUSION: This study shows that the ACP system is a good method for the identification of preterm-related genes. Furthermore, this study suggests that further analysis of the differentially expressed genes in preterm we have identified should provide insights into the molecular basis of preterm delivery caused by preterm labor.
Acyl-CoA Dehydrogenase ; Amnion ; Chorion ; DNA, Mitochondrial ; Down-Regulation ; Female ; Heparin ; Humans* ; Insulin-Like Growth Factor II ; Membranes* ; Obstetric Labor, Premature ; Placenta* ; Pregnancy ; Proteoglycans ; Ribosomal Proteins ; RNA ; Tissue Inhibitor of Metalloproteinase-1 ; Transcriptome ; Up-Regulation

Crohn 's disease is characterized by a chronic relapsing inflammation of the bowel in which pro-inflammatory cytokines play an important role. Rebamipide is an anti-gastric ulcer drug with anti-inflammatory properties in vivo and in vitro. The effects of rebamipide on Crohn 's disease have not been carefully evaluated. This study investigated the potential of rebamipide to protect Crohn 's disease using a murine model of colitis induced by trinitrobenzene sulfonic acid (TNBS). Rebamipide dramatically improved histopathological symptom involving myeloperoxidase (MPO)activation and increase of microscopic damage score in TNBS induced colitis. Rebamipide suppressed IL-8 secretion, ICAM-1 induction and nuclear factor-kappaB (NF-kappaB) activation by TNF-alpha and induced heme oxygenase-1(HO-1)in HT-29 cells. HO-1 inducer cobalt protoporphyrin IX (CoPPIX)suppressed NF-kappaB activation by TNF-alpha in HT-29 cells like rebamipide, and mimicked the protective effects of rebamipide on TNBS induced colitis. This suggests that rebamipide exerts anti-inflammatory effects by down-regulating NF-kappaB activity via inducting HO-1 expression. In conclusion, this study suggests that rebamipide represents a potential therapeutic agent and HO-1 is an important therapeutic target for the treatment of Crohn's disease.
Cobalt ; Colitis ; Colon* ; Crohn Disease ; Cytokines ; Down-Regulation* ; Heme Oxygenase (Decyclizing)* ; Heme* ; HT29 Cells ; Humans ; Inflammation ; Intercellular Adhesion Molecule-1 ; Interleukin-8 ; NF-kappa B* ; Peroxidase ; Tumor Necrosis Factor-alpha ; Ulcer