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At least 451 records · Page 25Linked to original sources
PubMed1999

[Research on some enzyme activities in the assessment of zinc nutritional status of growing rats].

Male weaning rats were divided randomly into five groups. They were fed with diets containing zinc deficient(DZ), high zinc(HZ), normal zinc (NZ) and high zinc pair-fed with zinc deficient group(HZP) respectively. The rats in DZ and HZ groups were exchanged diets after 20 days. A part of rats in each group were killed at days 20, 50 and 70. The activities of alkaline phosphatase(ALP), 5'-nucleotidase(5'-NT) and copper-zinc-superoxidase dismutase(Cu-Zn-SOD), the zinc concentration in plasma and kidney were determined to assess the better indices for zinc nutrition. The results indicted that: The activities of ALP in DZ group at 20 d was significantly lower than that in the same group at the beginning, in the HZ group and in the HZP group, and increased significantly after the diet was changed to HZ diet after 30 days. The activities of 5'-NT in DZ group rats was decreasing with the extension of experimental period. These results indicated that the activities of ALP and 5'-NT were sensitive to zinc supplementation even though they were changed a little during zinc exhausted. The activity of ALP was decreasing with growing, and the activity of 5'-NT was increased with growing. Zinc concentration in plasma of DZ group was significantly lower than that of other groups which include DZ-HZ group at the 50th day, and it was also the lowest among groups at the end of experiment. Zinc concentration in the kidney of HZ-DZ group was significantly lower than that of HZ and DZ-HZ groups by the end of experiment. There were little changes of the activity of Cu-Zn SOD and the zinc content in kidney during the experiment period. These results indicated that the activities of both ALP and 5'-NT and plasma zinc were sensitive to zinc supplementacior and zinc deficiency.

5'-Nucleotidase↗
PubMed2003

[A novel mutation causes congenital factor V deficiency].

OBJECTIVE: To investigate the gene defect in a hereditary coagulation factor V (FV) deficiency family. METHODS: The plasma FV actigen was measured by one-stage clotting assay. The FV antigen was assayed by Biotin-Avidin enzyme linked immunosorbent assay (BA-ELISA). The full length of exon 1 to exon 25 and the 5' untranslated sequence of FV genomic DNA were analyzed by polymerase chain reaction (PCR) and direct sequencing of the amplified fragments, meanwhile the defect was identified by T/A cloning sequencing. RESULTS: The plasma coagulant activity and amount of FV of the proband were marked deficient (1% and 1.54%, respectively). DNA sequence analysis for the proband revealed a causative mutation in a heterozygous status. It was one base pair deletion in exon 4 at nucleotide 675 inherited from her mother. CONCLUSIONS: A novel mutation in the FV gene was identified in the proband with congenital FV deficiency. The mutation was 675delA in exon 4 resulting in a frameshift and a premature termination codon.

Adolescent↗
PubMed2001

[Studies on academic thoughts of Zhang Qi's Su wen shi yi (Interpretation of plain questions)].

Summing up four academic thoughts of Zhang Qi's Su wen shi yi (Interpretation of Plain Questions), it is pointed out that his academic thought included 4 points, viz. Yang is more important than yin; the relations of yin and yang, such as interdependence, opposition, restriction were elaborated; the hepatic stagnation and splenic deficiency was the main pathogenesis of diseases; and the theory of xianghuo (ministerial fire) was developed.

China↗
PubMed2005

[Effects of Eupolyphaga Sinensis Walker on erythrocyte's CR1 activity and anti-cardiolipin antibody level in rats with stagnation of blood].

AIM: To study the effect of Eupolyphaga Sinensis Walker(ESW) on red blood cell immune adherence (RCIA) and serum anticardiolipin antibody level in rat model of Yin-deficiency Huo-excess with chronic blood stasis. METHODS: The model was made by i.m. injection of dexamethasone (0.5 mg/kg) and adrenaline (0.84 mg/kg). The serum anti-cardiolipin antibodies (ACA) ACA-IgG, ACA-IgA and ACA-IgM and the plasma D-dimmer levels were measured by using enzyme-linked immunosorbent assay (ELISA). The body and organ weight of the rats were measured. RESULTS: For rats of Yin-deficiency Huo-excess, rosette rates of red blood cell C3b receptors (RBC-C3b RR) and red blood cell cancer (RBC-CaR) decreased, the serum ACA-IgG, ACA-IgA, ACA-IgM and the plasma D-dimmer levels markedly increased, body weight and the weight of spleen and thymus all decreased. ESW (5 mg/kg, 10 mg/kg) increased RBC-C3bRR and RBC-CaR, reduced serum ACA-IgG, ACA-IgA, ACA-IgM and plasma D-dimmer levels, and increased spleen weight of the rats. CONCLUSION: ESW can boost the immune function in rats of Yin-deficiency Huo-excess with chronic blood stasis.

Animals↗
PubMed2001

Stress incontinence observed with real time sonography and dynamic fastscan magnetic resonance imaging--insights into pathophysiology.

Our concepts of pathophysiology of stress urinary continence have been greatly shaped by developments in radiographic imaging. Simple radiographs with and without contrast initially revealed the importance of urethral descent in pathogenesis. More recently, magnetic resonance imaging (MRI) and real time ultrasonography are showing soft tissue detail within both a global pelvic and a local urethral context. Careful examination of these studies can extend our concepts of pathophysiology and lead us beyond existing paradigms. We propose a unified theory of stress incontinence based on our dynamic fastscan MRI and real time ultrasonograms of stress incontinence, incorporating known details of pelvic anatomy, sphincteric location and function. The hypothesis introduces the concept of a continence threshold at which the urethra is subjected simultaneously to both shearing and explusive forces. If these forces are sufficient to overcome urethral coaptation at threshold, leakage results. The model proposes an anatomical sequence of changes through which the incontinent urethra cycles between periods of rest and increased abdominal pressure, and suggests a way in which repeated episodes of prolpase and urethral traction by shearing forces exerted by the vagina on the urethra may contribute to the development of intrinsic sphincteric deficiency.

Computer Systems↗
PubMed1996

Genetic Dissection of the Relative Roles of Auxin and Gibberellin in the Regulation of Stem Elongation in Intact Light-Grown Peas.

Exogenous gibberellin (GA) and auxin (indoleacetic acid [IAA]) strongly stimulated stem elongation in dwarf GA1-deficient le mutants of light-grown pea (Pisum sativum L.): IAA elicited a sharp increase in growth rate after 20 min followed by a slow decline; the GA response had a longer lag (3 h) and growth increased gradually with time. These responses were additive. The effect of GA was mainly in internodes less than 25% expanded, whereas that of IAA was in the older, elongating internodes. IAA stimulated growth by cell extension; GA stimulated growth by an increase in cell length and cell number. Dwarf lkb GA-response-mutant plants elongated poorly in response to GA (accounted for by an increase in cell number) but were very responsive to IAA. GA produced a substantial elongation in lkb plants only in the presence of IAA. Because lkb plants contain low levels of IAA, growth suppression in dwarf lkb mutants seems to be due to a deficiency in endogenous auxin. GA may enhance the auxin induction of cell elongation but cannot promote elongation in the absence of auxin. The effect of GA may, in part, be mediated by auxin. Auxin and GA control separate processes that together contribute to stem elongation. A deficiency in either leads to a dwarfed phenotype.

Journal Article↗
PubMed1992

Abnormalities of ion-exchange proteins of the red cell membrane in iron deficiency anemia.

The influences of iron deficiency on erythrocyte spanning membrane proteins, band 3 protein and Na(+)-K(+)-ATPase, were studied in the growing rats with iron deficient anemia. The main findings were (1) reduction of band 3 and increment of band 4.1 protein. (2) diminished rate constant of pyruvate-chloride exchange (Kp:Cl.h-1) of the erythrocytes and (3) significant decrease of Na(+)-K(+)-ATPase activity only at the early stage of iron exhaustion. In addition, there was a significant negative correlation between Kp:Cl.h-1 and Na(+)-K(+)-ATPase activity both in iron deficient rats and in the controls. It is suggested that the composition and function of the erythrocyte spanning-membrane proteins for ion exchange could be affected by iron deficiency.

Anemia, Hypochromic↗
PubMed1995

Studies on human dietary requirements and safe range of dietary intakes of selenium in China and their application in the prevention of related endemic diseases.

The human dietary selenium requirement in China has been estimated by various methods. The minimum dietary selenium requirement for the prevention of Keshan disease (KD) was found to be around 17 micrograms/d. On the other hand, an intake of 40 micrograms/d is required to maintain the plasma glutathione peroxidase (GPx) activity at plateau. Hence 40 micrograms/d is considered as the adequate dietary selenium requirement. Studies conducted in a chronic selenosis area indicate that the toxic dietary selenium intake (adverse effect level), which would maintain the characteristic fingernail changes, was approximately 1600 micrograms/d. The mean value of dietary selenium intakes, which enabled the five patients to recover from fingernail lesions, was found to be 819 +/- 126 micrograms/d. At a 95% confidence limit, the lower limit is around 600 micrograms/d. Therefore, 600 and 400 micrograms/d were suggested as the individual daily maximum safe selenium intake and the safe dietary selenium intake, respectively. The results were used in the prevention of Se-related endemic KD and Kashin-Beck disease (KBD).

Cardiomyopathy, Dilated↗
PubMed1991

Cellular immune responses in pigs fed a vitamin E- and selenium-deficient diet.

The effects of dietary restriction of vitamin E (Vit E) and selenium (Se) on lymphocyte proliferation, natural killer (NK) cell activity, antibody-dependent cell-mediated cytotoxicity (ADCC), and on burst respiratory response of stimulated granulocytes as measured by chemiluminescence (CL) were studied in pigs. Six male weanling pigs were maintained for 25 d on a torula yeast-based diet containing no measurable amount of alpha-tocopherol and less than .02 mg of Se per kilogram of feed. Six others received the same basal diet supplemented with 33 IU of DL-alpha-tocopheryl acetate and .2 mg of Se per kilogram of feed. All pigs were inoculated with Salmonella typhisuis on d 21 of the feeding period and killed on d 25. Tests to measure cellular immune functions were performed on cells isolated from blood samples taken on d 21 and 25. After 21 d of feeding, lymphocyte blastogenesis responses to phytohemagglutinin, concanavalin A, and pokeweed mitogen in pigs fed the Vit E- and Se-deficient diet were normal compared with the response in pigs fed the supplemented diet. Moreover, the cytotoxic activity of NK cells, the ADCC response, and the CL response of granulocytes were not affected. After 25 d, a marked suppression of lymphocyte response to mitogens occurred in pigs fed the Vit E- and Se-deficient diet when the cells were cultured in the presence of autologous serum. When fetal bovine serum replaced autologous serum in the cultures, no suppression was observed. No effect on NK activity and ADCC was observed, whereas the CL peak response of granulocytes tended to be higher in pigs fed the deficient diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Differential expression of carbonic anhydrase isoenzymes in various types of anemia.

BACKGROUND: The aim of the present study was to determine the concentrations of cytosolic carbonic anhydrase (CA) isoenzymes in erythrocytes of patients with aplastic, autoimmune hemolytic, iron deficiency or beta-thalassemia anemia. METHODS: Western blotting and CA esterase activity analysis were used to analyze cytosolic erythrocyte CA isoenzymes in 118 subjects with various types of anemia and 35 healthy controls. RESULTS: Total CA activity and CAII concentration of anemia patients were significantly higher than that of the control subjects while CAI concentration was significantly lower in patients of autoimmune hemolytic anemia (P<0.01). Compared with controls, CAIII concentration was lower in iron deficiency anemia (P<0.01), but higher in beta-thalassemia anemia (P<0.001). CONCLUSIONS: Carbonic anhydrase isoenzymes may contribute differently to various types of anemia. CAI may be an indicator to differentiate autoimmune hemolytic anemia from other types of anemia. CAII provides the CA activity necessary for maintaining ion transport in erythrocytes while CAIII may play an agent against oxidative damage in iron deficiency and beta-thalassemia anemia.

Anemia↗
PubMed1992

Glucose-6-phosphate dehydrogenase deficiency--report of 4 cases.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common hereditary enzyme disorder and more than 200 million people have a deficiency in this enzyme. It is a globally important cause of neonatal jaundice and causes life-threatening hemolytic crisis in childhood. At later ages, certain drugs such as antimalarials, and fava beans cause hemolysis among G6PD deficiency patients. The frequency and severity is influenced by genetic and cultural factors. It is common in Mediterranean, African, and some East Asian populations but rare in Korea. Four cases of G6PD deficiency which were first noticed in Korea are investigated with their clinical features.

Child↗
PubMed2003

Partial response to biotin therapy in a patient with holocarboxylase synthetase deficiency: clinical, biochemical, and molecular genetic aspects.

We report the clinical course and biochemical findings of a 10-year-old, mentally retarded girl with late-onset holocarboxylase synthetase (HCS, gene symbol HLCS) deficiency and only partial response to biotin. On treatment, even with an unusually high dose of 200mg/day, activities of the biotin-dependent mitochondrial carboxylases in lymphocytes remained below 50% of the mean control values. Not only urinary 3-hydroxyisovaleric acid excretion has been persistently elevated, but also plasma and, with even higher concentrations, cerebrospinal fluid 3-hydroxyisovaleric acid have not normalized. The unusual and insufficient response of this patient to biotin treatment can be explained by the effect of the combination of the common HLCS allele IVS10 +5 g>a on one chromosome and a truncating mutation on the other. This case illustrates mechanisms involved in the genotype-phenotype correlation that unequivocally exists in HCS deficiency.

Age of Onset↗
PubMed2006

Diagnosis of alpha-1-antitrypsin deficiency: An algorithm of quantification, genotyping, and phenotyping.

BACKGROUND: Laboratory testing in suspected alpha-1-antitrypsin (A1AT) deficiency involves analysis of A1AT concentrations and identification of specific alleles by genotyping or phenotyping. The purpose of this study was to define and evaluate a strategy that provides reliable laboratory evaluation of A1AT deficiency. METHODS: Samples from 512 individuals referred for A1AT phenotype analysis were analyzed by quantification, phenotype, and genotype. A1AT concentrations were measured by nephelometry. Phenotype analysis was performed by isoelectric focusing electrophoresis. The genotype assay detected the S and Z deficiency alleles by a melting curve analysis. RESULTS: Of the 512 samples analyzed, 2% of the phenotype and genotype results were discordant. Among these 10 discordant results, 7 were attributed to phenotyping errors. On the basis of these data we formulated an algorithm, according to which we analyzed samples by genotyping and quantification assays, with a reflex to phenotyping when the genotype and quantification results were not concordant. Retrospective analyses demonstrated that 4% of samples submitted for genotype and quantitative analysis were reflexed to phenotyping. Of the reflexed samples, phenotyping confirmed the genotype result in 85% of cases. In the remaining 15%, phenotyping provided further information, including identifying rare deficiency alleles and suggesting the presence of a null allele, and allowed for a more definitive interpretation of the genotype result. CONCLUSIONS: The combination of genotyping and quantification, with a reflex to phenotyping, is the optimal strategy for the laboratory evaluation of A1AT deficiency.

Algorithms↗
PubMed2006

MRI analysis of in vivo meniscal and tibiofemoral kinematics in ACL-deficient and normal knees.

The objectives of this study were to analyze simultaneously meniscal and tibiofemoral kinematics in healthy volunteers and anterior cruciate ligament (ACL)-deficient patients under axial load-bearing conditions using magnetic resonance imaging (MRI). Ten healthy volunteers and eight ACL-deficient patients were examined with a high-field, closed MRI system. For each group, both knees were imaged at full extension and partial flexion ( approximately 45 degrees ) with a 125N compressive load applied to the foot. Anteroposterior and medial/lateral femoral and meniscal translations were analyzed following three-dimensional, landmark-matching registration. Interobserver and intraobserver reproducibilities were less than 0.8 mm for femoral translation for image processing and data analysis. The position of the femur relative to the tibia in the ACL-deficient knee was 2.6 mm posterior to that of the contralateral, normal knee at extension. During flexion from 0 degrees to 45 degrees , the femur in ACL-deficient knees translated 4.3 mm anteriorly, whereas no significant translation occurred in uninjured knees. The contact area centroid on the tibia in ACL-deficient knees at extension was posterior to that of uninjured knees. Consequently, significantly less posterior translation of the contact centroid occurred in the medial tibial condyle in ACL-deficient knees during flexion. Meniscal translation, however, was nearly the same in both groups. Axial load-bearing MRI is a noninvasive and reproducible method for evaluating tibiofemoral and meniscal kinematics. The results demonstrated that ACL deficiency led to significant changes in bone kinematics, but negligible changes in the movement of the menisci. These results help explain the increased risk of meniscal tears and osteoarthritis in chronic ACL deficient knees.

Adult↗
PubMed2003

Relationship between complement components C4A and C4B diversities and two TNFA promoter polymorphisms in two healthy Caucasian populations.

The RP-C4-CYP21-TNX (RCCX) modules and the tumor necrosis factor (TNF) gene cluster are probably the most polymorphic genomic regions in the human central major histocompatibility complex (MHC). Using definitive methods for genotypic and phenotypic analyses of complement components C4A and C4B, determination of the RCCX length variants, and SSP-PCR/RFLP analyses of TNFA promoter polymorphisms at positions -308 and -238, we studied the complex relationships between the C4 and TNFA polymorphisms in two normal Caucasian populations. The patterns of the RCCX modular structures and the allelic frequency of -308A TNFA (TNF2) were similar between the Budapest (n = 125) and the Ohio (n = 80) Caucasians. However, the frequency of the -238A allele was significantly higher in the Ohio (11.3%) than in the Budapest (1.6%) study population (p < 0.0001). Marked features were found in the RCCX length variants in the TNF2 carriers and noncarriers. Strong associations were found between the C4AQ0 B1 haplotype from the monomodular short (mono-S) RCCX structure and the TNF2 allele, and between the C4A6 B1 haplotype from the bimodular long-short (LS) structure of the RCCX and the TNFA -238A allele. However, 36%-46% of the TNF2 carriers did not associate with a mono-S in both study cohorts, and 57.1% of the TNFA -238A carriers in Ohio did not associate with C4A6, which has a defective complement C5 convertase activity. The carriers of TNF2 allele had significantly lower C4A serum concentration (0.17 +/- 0.08 g/l) than noncarriers (0.23 +/- 0.09 g/l) (p < 0.001). The lowest C4A serum levels were found in TNF2 carriers with mono-S structures (0.14 +/- 0.06 g/l). In essence, our results demonstrated the heterogeneities of the TNFA promoter polymorphisms, and the linkage disequilibrium of TNFA -308A and -238A alleles with complement C4A deficiency and impaired C4A protein function, respectively.

Blotting, Southern↗