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1.
Chinese Journal of Medical Genetics ; (6): 139-142, 2022.
Article in Chinese | WPRIM | ID: wpr-928376

ABSTRACT

OBJECTIVE@#To explore the characteristics of SLC25A13 gene variants in 16 infants with neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD).@*METHODS@#The infants were subjected to high-throughput DNA sequencing for coding exons and flanking regions of the target genes. Suspected variants were verified by Sanger sequencing and bioinformatic analysis.@*RESULTS@#Among the 16 NICCD cases, 15 were found to harbor pathogenic variants. Among these, IVS14-9A>G, c.1640G>A, c.762T>A, c.736delG, c.1098Tdel and c.851G>A were previously unreported.@*CONCLUSION@#Six novel SLC25A13 variants were found by high-throughput sequencing, which has enriched the spectrum of SLC25A13 gene variants and provided a basis for genetic counseling and prenatal diagnosis.


Subject(s)
Humans , Infant , Infant, Newborn , Calcium-Binding Proteins/genetics , Cholestasis, Intrahepatic/genetics , Citrullinemia/genetics , Mitochondrial Membrane Transport Proteins/genetics , Mutation , Organic Anion Transporters/genetics , Protein Deficiency
2.
Rev. invest. clín ; 73(1): 39-51, Jan.-Feb. 2021. graf
Article in English | LILACS | ID: biblio-1289743

ABSTRACT

ABSTRACT Background: Cancer gene therapy using a nonviral vector is expected to be repeatable, safe, and inexpensive, and to have long-term effectiveness. Gene therapy using the E3 and C1 (E3C1) domain of developmental endothelial locus-1 (Del1) has been shown to improve prognosis in a mouse transplanted tumor model. Objective: In this study, we examined how this treatment affects angiogenesis in mouse transplanted tumors. Materials and methods: Mouse transplanted tumors (SCCKN human squamous carcinoma cell line) were injected locally with a nonviral plasmid vector encoding E3C1 weekly. Histochemical analysis of the transplanted tumors was then performed to assess the effects of E3C1 on prognosis. Results: All mice in the control group had died or reached an endpoint within 39 days. In contrast, one of ten mice in the E3C1 group had died by day 39, and eight of ten had died or reached an endpoint by day 120 (p < 0.01). Enhanced apoptosis in tumor stroma was seen on histochemical analyses, as was inhibited tumor angiogenesis in E3C1-treated mice. In addition, western blot analysis showed decreases in active Notch and HEY1 proteins. Conclusion: These findings indicate that cancer gene therapy using a nonviral vector encoding E3C1 significantly improved life-span by inhibiting tumor angiogenesis. (REV INVEST CLIN. 2021;73(1):39-51)


Subject(s)
Animals , Rabbits , Calcium-Binding Proteins/therapeutic use , Carcinoma, Squamous Cell/blood supply , Carcinoma, Squamous Cell/therapy , Cell Adhesion Molecules/therapeutic use , Epidermal Growth Factor/therapeutic use , Discoidin Domain/genetics , Calcium-Binding Proteins/genetics , Tumor Cells, Cultured , Genetic Therapy , Cell Adhesion Molecules/genetics , Amino Acid Motifs , Epidermal Growth Factor/genetics , Mice, Nude , Neoplasm Transplantation , Neovascularization, Pathologic/therapy
3.
Rev. Assoc. Med. Bras. (1992, Impr.) ; 66(5): 680-686, 2020. tab, graf
Article in English | SES-SP, LILACS | ID: biblio-1136268

ABSTRACT

SUMMARY OBJECTIVE Pelvic organ prolapse (POP) is a very frequent situation in our population that may lead to a significant decrease in patients' quality of life. Currently, we are looking for predictive factors for the development of POPs; thus, this study seeks to evaluate whether the Fibulin 5 polymorphism (FBLN5) is associated with the occurrence of POP. METHODS This is a cohort study with postmenopausal women who were divided into groups by POP stage: POP stages 0 and I (control group) and POP stages III and IV (case group). Subsequently, analyses of genetic polymorphisms of FBLN5 were performed using the Restriction Fragment Length Polymorphism (RFLP) technique. RESULTS A total of 292 women were included in the study. Pregnancy, parity and vaginal delivery in the patients, as well as in data described in the literature, were related to the occurrence of POP in the univariate analysis. However, after binary logistic regression, home birth and age remained independent risk factors for POP. We found no association between the FBLN5 polymorphism and the occurrence of POP (p = 0.371). CONCLUSION There was no association between the FBLN5 polymorphism and the occurrence of POP in Brazilian women.


RESUMO OBJETIVOS O prolapso de órgãos pélvicos (POP) é uma situação muito frequente em nossa população que pode levar a uma diminuição significativa da qualidade de vida dos pacientes. Atualmente, buscam-se fatores preditivos para o desenvolvimento de POPs e, assim, este estudo correlaciona um polimorfismo de Fibulina 5 (FBLN5) com a ocorrência da doença. MÉTODOS Estudo de coorte com mulheres na pós-menopausa, divididas por grupos pelos estádios 0 e I do POP (grupo controle) e POP III e IV (grupo caso). Posteriormente, análises do polimorfismo genético de FBLN5 foram realizadas utilizando a técnica de Polimorfismo de Comprimento de Fragmentos de Restrição (RFLP). RESULTADOS Um total de 292 mulheres foi incluído no estudo. Gestação, paridade e parto vaginal, como bem descritos na literatura, foram relacionados à ocorrência de POPs na análise univariada. No entanto, após a regressão logística binária, o parto domiciliar e a idade permaneceram como fatores de risco independentes para os POPs. Não encontramos associação deste polimorfismo FBLN5 com a ocorrência de POP (p=0,371). CONCLUSÃO Não houve associação deste polimorfismo FBLN5 com a ocorrência de POPs em mulheres brasileiras.


Subject(s)
Humans , Female , Pregnancy , Quality of Life , Extracellular Matrix Proteins/genetics , Pelvic Organ Prolapse , Polymorphism, Genetic , Brazil , Calcium-Binding Proteins/genetics , Cohort Studies
4.
Braz. j. med. biol. res ; 50(11): e6177, 2017. tab, graf
Article in English | LILACS | ID: biblio-888945

ABSTRACT

The human calcium- and integrin-binding protein (CIB) family is composed of CIB1, CIB2, CIB3, and CIB4 proteins and the CIB4 gene affects fertility. Kermani sheep is one of the most important breeds of Iranian sheep breeds. The aim of this study was to analyze for the first time molecular characteristics of the CIB4 gene and protein in Kermani sheep. Different tissues were collected from the Kermani sheep and real time PCR was performed. The PCR products were sequenced, comparative analyses of the nucleotide sequences were performed, a phylogenetic tree was constructed, and different characteristics of CIB4 proteins were predicted. Real time PCR results showed that the CIB4 gene is expressed only in testis of Kermani sheep. The cDNA nucleotide sequence was identical with small tail Han sheep, cattle, goat, camel, horse, dog, mouse and human, respectively 100, 99, 99, 98, 98, 96, 96, and 96%. Hence, it can be suggested that the CIB4 gene plays a role in male fertility. Based on the phylogenetic analysis, sheep CIB4 gene has a close relationship with goat and cattle first, and then with camel and whale. Although we demonstrated that CIB4 is a testis-specific gene, expressed only in the testis and it interacts with other proteins, the mechanisms by which CIB4 expression is regulated need to be elucidated.


Subject(s)
Animals , Male , Female , Calcium-Binding Proteins/analysis , Calcium-Binding Proteins/genetics , Sheep/genetics , Amino Acid Sequence , Base Sequence , Electrophoresis/veterinary , Phylogeny , Real-Time Polymerase Chain Reaction/veterinary , Reference Values
5.
Braz. j. infect. dis ; 19(5): 498-502, tab
Article in English | LILACS | ID: lil-764505

ABSTRACT

ABSTRACTThe serine-aspartate repeat proteins (Sdr) are members of a family of surface proteins and contribute to the pathogenicity of Staphylococcus aureus. Among 288 S. aureus isolates including 158 and 130 associated with skin and soft tissue infections and bloodstream infection, respectively; 275 (95.5%) were positive for at least one of threesdr genes tested. The positivity rates for sdrC, sdrD, and sdrE among S. aureusisolates were 87.8% (253/288), 63.9% (184/288), and 68.1% (196/288), respectively. 224 (77.8%) of 288 isolates were concomitantly positive for two or three sdr genes. There was an association between carriage ofsdrE and methicillin-resistant S. aureus(MRSA) isolates, while the carriage rates of sdrC andsdrD in MRSA isolates were similar to those in methicillin-sensitive S. aureus (MSSA) isolates. The prevalence of co-existence of sdrC and sdrE among MRSA isolates was significantly higher than that among MSSA isolates (p < 0.05). All ST1, ST5, ST7, and ST25 isolates were positive for sdrD. While all ST121 and ST398 isolates were negative for sdrD. All ST59 and ST88 isolates were positive forsdrE. All ST1 isolates were concomitantly positive forsdrC and sdrD. Concomitant carriage ofsdrC, sdrD, and sdrE was found among all ST5, 75.0% (9/12) of ST1, 69.2% (9/13) of ST6, 78.6% (11/14) of ST25, and 90.9% (20/22) of ST88 isolates. sdrD was linked to CC5, CC7 and CC88 isolates, especially CC88 isolates. There was a strong association between the presence of sdrE and CC59, CC88, and CC5 isolates. A significant correlation between concomitant carriage of sdrC, sdrD, and sdrE and CC88 isolates was found.sdrC-positive, sdrD-positive andsdrE-negative gene profile was significantly associated with CC7 clone. There was an association between sdrC-positive,sdrD-negative, and sdrE-positive gene profile and CC59 isolates. A correlation between sdrC-positive,sdrD-negative, and sdrE-negative gene profile and CC121 clone was found. More CC59 isolates carriedsdrC-negative, sdrD-negative, andsdrE-positive gene profile relative to other four CCs isolates. All ST1 and ST5, 95.2% (20/21) of ST188 and 95.2% (20/21) of ST630 isolates were positive for sdrC. Taken together, our investigation indicated that different S. aureus lineages were associated with specific patterns of carriage of sdr genes.


Subject(s)
Humans , Bacterial Proteins/genetics , Calcium-Binding Proteins/genetics , Carrier Proteins/genetics , Methicillin-Resistant Staphylococcus aureus/genetics , Staphylococcal Infections/microbiology , Multilocus Sequence Typing , Methicillin-Resistant Staphylococcus aureus/isolation & purification
6.
Arq. bras. cardiol ; 100(3): 229-237, mar. 2013. ilus, tab
Article in Portuguese | LILACS | ID: lil-670863

ABSTRACT

FUNDAMENTO: Vários autores mostraram que a deterioração da função cardíaca associa-se com o grau e a duração da obesidade. Os padrões de expressão gênica após longos períodos de obesidade precisam ser estabelecidos. OBJETIVO: Este estudo testou a hipótese de que a exposição prolongada à obesidade leva à redução nos níveis de RNAm de proteínas envolvidas na homeostase do Ca2+ miocárdico. Além disso, este estudo avaliou se uma diminuição no hormônio tireoidiano causava redução na expressão de RNAm. MÉTODOS: Ratos Wistar machos de 30 dias de idade foram distribuídos em dois grupos: controle (C) e obeso (Ob). O grupo C recebeu uma dieta padrão e o grupo Ob recebeu dietas hiperlipídicas por 15, 30 e 45 semanas. A obesidade foi definida pelo índice de adiposidade. A expressão gênica foi avaliada por PCR em tempo real quantitativa. RESULTADOS: O índice de adiposidade foi maior no grupo Ob do que no C em todas as etapas. Enquanto a obesidade nas semanas 15 e 45 determinou uma redução no RNAm de Ca2+-ATPase do retículo sarcoplasmático (SERCA2a), trocador Na+/Ca2+ (NCX) e calsequestrina (CSQ), observou-se aumento da expressão do RNAm de canal de Ca2+ do tipo L, receptor de rianodina, SERCA2a, fosfolamban (PLB), NCX e CSQ após a semana 30, em comparação ao grupo C. Não houve associação significativa entre os níveis de T3 e a expressão de RNAm. CONCLUSÕES: Nossos dados indicam que a obesidade por curtos ou longos períodos de tempo pode promover alteração na expressão gênica de proteínas reguladoras da homeostase do Ca2+ sem influência do hormônio tireoidiano.


BACKGROUND: Several authors have shown that deterioration of cardiac function is associated with the degree and duration of obesity. It is necessary to establish the gene expression patterns after prolonged periods of obesity. OBJECTIVE: This study tested the hypothesis that increased duration of exposure to obesity leads to a reduction in the mRNA levels of proteins involved in regulation of myocardial Ca2+ homeostasis. In addition, this study verified whether the decrease in mRNA expression was caused by a reduction in thyroid hormone. METHODS: Thirty-day-old male Wistar rats were distributed in two groups: control (C) and obese (Ob). The C group was fed a standard diet and the Ob was fed with high-fat diets for 15, 30 and 45 weeks. Obesity was defined by adiposity index. The gene expression was assessed by quantitative real-time PCR. RESULTS: The adiposity index was higher in the Ob compared to the C after all periods. While obesity at 15 and 45 weeks resulted in a reduction in mRNA of sarcoplasmic reticulum Ca2+- ATPase (SERCA2a), Na+/Ca2+ exchanger (NCX), and calsequestrin (CSQ), L-type Ca2+ channels, ryanodine receptor, SERCA2a, phospholamban (PLB), NCX, and CSQ expression were increased compared to the C after 30 weeks. There was no significant association between T3 levels and mRNA expression. CONCLUSIONS: Our data indicate that obesity over the short and long periods of time may promote alteration in gene expression of Ca2+ homeostasis regulatory proteins without influence by thyroid hormone.


Subject(s)
Animals , Male , Rats , Calcium-Binding Proteins/genetics , Calcium/metabolism , Gene Expression/genetics , Homeostasis/genetics , Myocardium/metabolism , Obesity/complications , Thyroid Hormones/metabolism , Analysis of Variance , Disease Models, Animal , Obesity/chemically induced , Obesity/metabolism , Random Allocation , Rats, Wistar , RNA, Messenger/genetics , Time Factors
7.
Experimental & Molecular Medicine ; : e65-2013.
Article in English | WPRIM | ID: wpr-152459

ABSTRACT

Vascular smooth muscle cells (VSMCs) undergo phenotypic changes in response to vascular injury such as angioplasty. Protein kinase G (PKG) has an important role in the process of VSMC phenotype switching. In this study, we examined whether rosiglitazone, a peroxisome proliferator-activated receptor (PPAR)-gamma agonist, could modulate VSMC phenotype through the PKG pathway to reduce neointimal hyperplasia after angioplasty. In vitro experiments showed that rosiglitazone inhibited the phenotype change of VSMCs from a contractile to a synthetic form. The platelet-derived growth factor (PDGF)-induced reduction of PKG level was reversed by rosiglitazone treatment, resulting in increased PKG activity. This increased activity of PKG resulted in phosphorylation of vasodilator-stimulated phosphoprotein at serine 239, leading to inhibited proliferation of VSMCs. Interestingly, rosiglitazone did not change the level of nitric oxide (NO) or cyclic guanosine monophosphate (cGMP), which are upstream of PKG, suggesting that rosiglitazone influences PKG itself. Chromatin immunoprecipitation assays for the PKG promoter showed that the activation of PKG by rosiglitazone was mediated by the increased binding of Sp1 on the promoter region of PKG. In vivo experiments showed that rosiglitazone significantly inhibited neointimal formation after balloon injury. Immunohistochemistry staining for calponin and thrombospondin showed that this effect of rosiglitazone was mediated by modulating VSMC phenotype. Our findings demonstrate that rosiglitazone is a potent modulator of VSMC phenotype, which is regulated by PKG. This activation of PKG by rosiglitazone results in reduced neointimal hyperplasia after angioplasty. These results provide important mechanistic insight into the cardiovascular-protective effect of PPARgamma.


Subject(s)
Animals , Rats , Aorta/injuries , Calcium-Binding Proteins/genetics , Cell Proliferation , Cyclic GMP/metabolism , Cyclic GMP-Dependent Protein Kinases/genetics , Hyperplasia/metabolism , Microfilament Proteins/genetics , Muscle, Smooth, Vascular/metabolism , Myocytes, Smooth Muscle/drug effects , Nitric Oxide/metabolism , PPAR gamma/agonists , Promoter Regions, Genetic , Rats, Sprague-Dawley , Sp1 Transcription Factor/metabolism , Thiazolidinediones/pharmacology , Thrombospondins/genetics , Tunica Intima/metabolism , Vascular System Injuries/metabolism
8.
Braz. j. med. biol. res ; 41(7): 615-620, July 2008. ilus, tab, graf
Article in English | LILACS | ID: lil-489520

ABSTRACT

Obesity is a complex multifactorial disorder that is often associated with cardiovascular diseases. Research on experimental models has suggested that cardiac dysfunction in obesity might be related to alterations in myocardial intracellular calcium (Ca2+) handling. However, information about the expression of Ca2+-related genes that lead to this abnormality is scarce. We evaluated the effects of obesity induced by a high-fat diet in the expression of Ca2+-related genes, focusing the L-type Ca2+ channel (Cacna1c), sarcolemmal Na+/Ca2+ exchanger (NCX), sarcoplasmic reticulum Ca2+ ATPase (SERCA2a), ryanodine receptor (RyR2), and phospholamban (PLB) mRNA in rat myocardium. Male 30-day-old Wistar rats were fed a standard (control) or high-fat diet (obese) for 15 weeks. Obesity was defined as increased percent of body fat in carcass. The mRNA expression of Ca2+-related genes in the left ventricle was measured by RT-PCR. Compared with control rats, the obese rats had increased percent of body fat, area under the curve for glucose, and leptin and insulin plasma concentrations. Obesity also caused an increase in the levels of SERCA2a, RyR2 and PLB mRNA (P < 0.05) but did not modify the mRNA levels of Cacna1c and NCX. These findings show that obesity induced by high-fat diet causes cardiac upregulation of Ca2+ transport_related genes in the sarcoplasmic reticulum.


Subject(s)
Animals , Male , Rats , Calcium Channels/genetics , Calcium-Binding Proteins/genetics , Calcium-Transporting ATPases/genetics , Myocardium/metabolism , Obesity/metabolism , Sarcoplasmic Reticulum Calcium-Transporting ATPases/genetics , Sodium-Calcium Exchanger/genetics , Calcium Channels/metabolism , Calcium-Binding Proteins/metabolism , Calcium-Transporting ATPases/metabolism , Homeostasis , Myocardium/chemistry , Obesity/genetics , Rats, Wistar , Reverse Transcriptase Polymerase Chain Reaction , RNA, Messenger , Sarcolemma/chemistry , Sarcolemma/metabolism , Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism , Sodium-Calcium Exchanger/metabolism , Up-Regulation
9.
J Biosci ; 2007 Mar; 32(2): 251-60
Article in English | IMSEAR | ID: sea-110868

ABSTRACT

Entamoeba histolytica contains a novel calcium-binding protein like calmodulin,which was discovered earlier,and we have reported the presence of its homologue(s)and a dependent protein kinase in plants.To understand the functions of these in plants,a cDNA encoding a calcium-binding protein isolated from Entamoeba histolytica (EhCaBP)was cloned into vector pBI121 in antisense orientation and transgenic tobacco plants were raised.These plants showed variation in several phenotypic characters,of which two distinct features,more greenness and leaf thickness,were inherited in subsequent generations.The increase in the level of total chlorophyll in different plants ranged from 60% to 70%.There was no major change in chloroplast structure and in the protein level of D1,D2,LHCP and RuBP carboxylase.These morphological changes were not seen in antisense calmodulin transgenic tobacco plants,nor was the calmodulin level altered in EhCaBP antisense plants.


Subject(s)
Animals , Blotting, Northern , Blotting, Southern , Blotting, Western , Calcium-Binding Proteins/genetics , Chlorophyll/biosynthesis , Cytokinins/metabolism , DNA, Antisense/metabolism , Entamoeba histolytica/genetics , Enzyme-Linked Immunosorbent Assay , Genetic Vectors/genetics , Microscopy, Electron, Transmission , Phenotype , Plant Leaves/metabolism , Plants, Genetically Modified/genetics , Polyamines/metabolism , Nicotiana/anatomy & histology
10.
Braz. j. med. biol. res ; 40(1): 27-31, Jan. 2007. graf, tab
Article in English | LILACS | ID: lil-439677

ABSTRACT

We have shown that myocardial dysfunction induced by food restriction is related to calcium handling. Although cardiac function is depressed in food-restricted animals, there is limited information about the molecular mechanisms that lead to this abnormality. The present study evaluated the effects of food restriction on calcium cycling, focusing on sarcoplasmic Ca2+-ATPase (SERCA2), phospholamban (PLB), and ryanodine channel (RYR2) mRNA expressions in rat myocardium. Male Wistar-Kyoto rats, 60 days old, were submitted to ad libitum feeding (control rats) or 50 percent diet restriction for 90 days. The levels of left ventricle SERCA2, PLB, and RYR2 were measured using semi-quantitative RT-PCR. Body and ventricular weights were reduced in 50 percent food-restricted animals. RYR2 mRNA was significantly decreased in the left ventricle of the food-restricted group (control = 5.92 ± 0.48 vs food-restricted group = 4.84 ± 0.33, P < 0.01). The levels of SERCA2 and PLB mRNA were similar between groups (control = 8.38 ± 0.44 vs food-restricted group = 7.96 ± 0.45, and control = 1.52 ± 0.06 vs food-restricted group = 1.53 ± 0.10, respectively). Down-regulation of RYR2 mRNA expressions suggests that chronic food restriction promotes abnormalities in sarcoplasmic reticulum Ca2+ release.


Subject(s)
Animals , Male , Rats , Calcium-Binding Proteins/metabolism , Down-Regulation/physiology , Food Deprivation/physiology , Ryanodine Receptor Calcium Release Channel/metabolism , Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism , Calcium-Binding Proteins/genetics , Down-Regulation/genetics , Rats, Inbred WKY , Reverse Transcriptase Polymerase Chain Reaction , RNA, Messenger/genetics , Ryanodine Receptor Calcium Release Channel/genetics , Sarcoplasmic Reticulum Calcium-Transporting ATPases/genetics
11.
Experimental & Molecular Medicine ; : 492-496, 2005.
Article in English | WPRIM | ID: wpr-207070

ABSTRACT

Calmegin is a testis-specific molecular chaperon playing a key role in spermatogenesis. However, the transcriptional regulatory mechanisms for calmegin expression are entirely unknown. Herein, we revealed that calmegin is transcriptionally regulated by histone deacetylase (HDAC) and CpG methyltransferase. The cDNA microarray analysis of the human fibrosarcoma cells treated with trichostatin A (TSA) showed an increased level of calmegin mRNA. The induction of calmegin mRNA by TSA was added by the treatment with 5-aza-2'-deoxycytidine (5'Aza- dC), implying that epigenetic alterations are involved in the transcriptional repression of the gene. Moreover, chromatin immunoprecipitation assay using an anti-acetyl-histone H3 antibody exhibited that the proximal region (-152~-31) of the calmegin promoter is responsible for HDAC-mediated transcriptional repression of the gene. These results demonstrate that calmegin expression is regulated by HDAC and CpG methyltransferase in a coordinative way.


Subject(s)
Animals , Humans , Male , Mice , Calcium-Binding Proteins/genetics , Cell Line, Tumor , Gene Expression Regulation , Histone Deacetylases/metabolism , Methyltransferases/metabolism , Molecular Chaperones/genetics , Organ Specificity , Promoter Regions, Genetic/genetics , Testis/metabolism , Transcription, Genetic
12.
Experimental & Molecular Medicine ; : 193-203, 2004.
Article in English | WPRIM | ID: wpr-217502

ABSTRACT

A growing body of evidence, including studies using genetically engineered mouse models, has shown that Ca2+ cycling and Ca2+ -dependent signaling pathways play a pivotal role in cardiac hypertrophy and heart failure. In addition, recent studies identified that mutations of the genes encoding sarcoplasmic reticulum (SR) proteins cause human cardiomyopathies and lethal ventricular arrhythmias. The regulation of Ca2+ homeostasis via the SR proteins may have potential therapeutic value for heart diseases such as cardiomyopathy, heart failure and arrhythmias.


Subject(s)
Animals , Humans , Animals, Genetically Modified , Arrhythmias, Cardiac/genetics , Calcium/metabolism , Calcium Channels/genetics , Calcium-Binding Proteins/genetics , Cardiac Output, Low/genetics , Cardiomyopathies/genetics , Heart Diseases/etiology , Mutation/genetics , Sarcoplasmic Reticulum/metabolism
13.
Indian J Exp Biol ; 2002 Jul; 40(7): 780-4
Article in English | IMSEAR | ID: sea-60080

ABSTRACT

Androgen deprivation is associated with decline in intestinal calcium absorption. The effect of androgen on CaR and VDR intestinal mucosa has not yet been studied. Calcium homeostasis, a real bone mineral density (aBMD, dual energy X-ray absorptiometry) and expression of CaR and VDR mRNA in duodenal mucosa of orchidectomized (ORX) and sham operated (Sham) adult Sprague Dawley rats at 4 week have been studied. There was no significant difference in serum calcium, alkaline phosphatase, calcidiol and calcitriol levels between both the groups. Serum testosterone (T) (ng/dl) and inorganic phosphorous (iP) (mg/dl) levels were significantly lower in ORX rats. As compared to sham rats, ORX rats had significant decline in in-vitro aBMD at proximal, middle and distal tibia, proximal, mid and distal femur and femoral neck (P < 0.05). Northern blot analysis revealed no significant alteration in the CaR and VDR mRNA expression in duodenal mucosa in ORX rats. CaR and VDR mRNA expression in duodenal mucosa is therefore, not affected by physiological concentrations of testosterone in rats.


Subject(s)
Androgens/deficiency , Animals , Blotting, Northern , Calcium-Binding Proteins/genetics , Duodenum/metabolism , Intestinal Mucosa/metabolism , Male , Orchiectomy , RNA, Messenger/metabolism , Rats , Rats, Sprague-Dawley , Receptors, Calcitriol/genetics
14.
Southeast Asian J Trop Med Public Health ; 2002 Jun; 33(2): 365-72
Article in English | IMSEAR | ID: sea-34565

ABSTRACT

Fibrocalculous pancreatopathy is a form of diabetes, associated with tropical chronic calcific pancreatitis, in which islet beta-cell loss and pancreatic stone formation are found. It is likely to be a multifactorial disease with both genetic and environmental components. Regenerating (reg) gene encodes protein that has been involved in pancreatic lithogenesis and the regeneration of islet cells and therefore the abnormality of reg genes could be associated with fibrocalculous pancreatopathy. In this study, regla and reg1beta mRNAs were isolated from peripheral blood lymphocytes obtained from 16 patients with fibrocalculous pancreatopathy, 42 patients with type 1 diabetes, 37 patients with type 2 diabetes, and 22 normal controls. mRNAs were amplified by reverse-transcription polymerase chain reaction (RT-PCR) and analysed by a single strand conformation polymorphism (SSCP) technique. The reg1alpha and reg1beta mRNAs were isolated, indicating the ectopic expression of these genes in peripheral blood lymphocytes; however, variation among mobility patterns was not observed in the SSCP analysis of the RT-PCR products. The results indicated that there was no abnormality of the regla and reg1beta mRNAs obtained from the study groups.


Subject(s)
Calcium-Binding Proteins/genetics , DNA Restriction Enzymes/metabolism , Electrophoresis, Agar Gel , Humans , Lithostathine , Nerve Tissue Proteins , Pancreatic Diseases/genetics , Polymerase Chain Reaction , Polymorphism, Single-Stranded Conformational , RNA, Messenger/genetics , Thailand
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