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PubMed2005

[Glutathione S-transferase M1 polymorphism and the risk on colorectal cancer: a multilevel meta regression].

OBJECTIVE: In order to investigate the relationship between Glutathione S-transferase M1 (GSTM1) status and the risk on colorectal cancer as well as to detect the related factors to this association. METHODS: A pooled analysis of multilevel Meta-regression was performed to estimate GSTM1 deficiency associated with the risks of colorectal cancer. Then subgroup Meta-regression was undertaken to evaluate the possible relationship between heterogeneity and the related characteristics. RESULTS: The overall pooled odds ratios of colorectal cancer risk associated with GSTM1 deficiency was 1.17 (95% CI: 1.08-1.26). Ethnicity, percent of GSTM1 deficiency in population had significant relationships with heterogeneity across the studies (P < 0.05). Results of subgroup Meta-regression showed that GSTM1 deficiency was significantly associated with colorectal cancer risk in ethnic subgroups of Asians, Caucasians and in low level (lower than 50%) of GSTM1 deficiency population (P < 0.05). The respective pooled ORs were 1.14, 1.25 and 1.29. CONCLUSION: GSTM1 deficiency seemed to be a risk factor for colorectal cancer, while interactions on the characteristics of ethnicity, percentage of GSTM1 deficiency in the studied population were related to this association.

Asian People↗

PubMed2006

Comparative proteomic analysis of Helicobacter pylori strains associated with iron deficiency anemia.

Helicobacter pylori is known to cause chronic gastritis, peptic ulcer, and gastric cancer, and has also been linked to iron deficiency anemia (IDA). To determine whether H. pylori clinical isolates correlate with the prevalence of H. pylori-associated IDA, we compared the proteomic profiles of H. pylori strains isolated from antral biopsy specimens of H. pylori-positive patients with or without IDA. Fifteen strains, including eight non-IDA and seven IDA strains, were cultured under iron-rich and iron-depleted conditions and then analyzed for protein expression profiles by 2-DE. The distances between two H. pylori strains were determined on the basis of similarities between their expression patterns of 189 protein spots, and a phylogenetic tree was constructed. The results revealed that the IDA strains formed a cluster separate from that of six non-IDA strains, with two non-IDA strains between the clusters. H. pylori strain 26695 was located in the non-IDA cluster. Protein spots displaying similar expression patterns were clustered, and 18 spots predominantly expressed in IDA strains were identified by MALDI-TOF analysis. These data indicate that the non-IDA and IDA strains can be distinguished by their protein expression profiles, suggesting that the polymorphism of H. pylori strains may be one of the factors determining the occurrence of H. pylori-associated IDA.

Adolescent↗

PubMed1978

Morphology of the rectinal pigment epithelium in the vitamin A deficient rat.

Ultrastructural changes in the retinal pigment epithelium (RPE) and adjacent photoreceptor cells have been followed in the Wistar rat during the course of long-term vitamin A deficiency. Of particular interest has been the discovery of unusual concentric aggregates within the photoreceptor outer segments and the inner cytoplasm of the RPE. The aggregates were present throughout the course of the retinal degeneration induced by vitamin A deficiency and could be identified in the RPE either by themselves in the apical cytoplasm or within phagolysosomes. It is postulated that the concentric aggregates result initially from abnormal formation or condensation of outer segment membranes and are then slowly degraded by lysosomal action in the RPE cytoplasm. In addition, acid phosphatase activity and typical phagosomes (shed outer segment packets) have been demonstrated in the cytoplasm of the RPE of the vitamin A deficient rats. The latter findings indicate that, at least to some extent, the normal phagocytic and lytic processes of the RPE are retained in this nutritional disorder.

Acid Phosphatase↗

PubMed2001

Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients.

Patients with end-stage renal disease undergoing regular dialysis are prone to encephalopathy, but the cause is often unclear. Dialysis patients are at risk for thiamine deficiency, which may mimic many uremic complications, including encephalopathy. To determine whether unexplained encephalopathy in regular dialysis patients is associated with thiamine deficiency, we conducted a prospective study that enrolled 30 consecutive dialysis patients with altered mental status admitted to a referred hospital during a 1-year period. A complete history, physical and neurological examinations, laboratory investigations, and computed tomographic scans or magnetic resonance imaging of the brain were obtained for each subject. In 10 of the 30 patients, diagnoses remained obscure after the initial workup. Manifestations included confusion, chorea, acute visual loss, rapidly progressive dementia, myoclonus, convulsions, and coma. Intravenous thiamine was administered to these 10 patients. All 10 patients had thiamine deficiency confirmed by a marked response to thiamine supplementation and/or a low serum thiamine concentration (35.3 +/- 6.0 nmol/L; normal, >50 nmol/L). Nine patients recovered, but one patient failed to respond because of delayed treatment. We conclude that in regular dialysis patients, unexplained encephalopathy can be mainly attributed to thiamine deficiency. This condition is fatal if unrecognized and can be successfully treated with prompt thiamine replacement.

Adult↗

PubMed1999

ERGIC-53 gene structure and mutation analysis in 19 combined factors V and VIII deficiency families.

Combined factors V and VIII deficiency is an autosomal recessive bleeding disorder associated with plasma levels of coagulation factors V and VIII approximately 5% to 30% of normal. The disease gene was recently identified as the endoplasmic reticulum-Golgi intermediate compartment protein ERGIC-53 by positional cloning, with the detection of two founder mutations in 10 Jewish families. To identify mutations in additional families, the structure of the ERGIC-53 gene was determined by genomic polymerase chain reaction (PCR) and sequence analysis of bacterial artificial chromosome clones containing the ERGIC-53 gene. Nineteen additional families were analyzed by direct sequence analysis of the entire coding region and the intron/exon junctions. Seven novel mutations were identified in 10 families, with one additional family found to harbor one of the two previously described mutations. All of the identified mutations would be predicted to result in complete absence of functional ERGIC-53 protein. In 8 of 19 families, no mutation was identified. Genotyping data indicate that at least two of these families are not linked to the ERGIC-53 locus. Taken together, these results suggest that a significant subset of combined factors V and VIII deficiency is due to mutation in one or more additional genes.

Amino Acid Substitution↗

PubMed2005

FoxP3: a genetic link between immunodeficiency and autoimmune diseases.

It has long been observed that patients with autoimmune diseases also have immune deficiency. How these two opposite extremes of immunity can be found in the same individual is largely unclear. Here we review the evidence that a FoxP3 defect may provide a critical link between autoimmunity and immune deficiency. Disruption of FoxP3 results in severe autoimmune syndromes in both human and mice. Bone marrow chimera experiments indicate that FoxP3 defects in both hematopoietic and non-hematopoietic cells are required for the development of severe autoimmune disease. FoxP3 mutation in the hematopoietic cells impairs the development of regulatory T cells (Treg). Our data demonstrate that the mutation in non-hematopoietic cells results in deficient thymopoiesis. Defective T cell production may be an underlying cause of T cell hyperproliferation, which together with Treg defects, may lead to fatal autoimmune disease in mouse and man.

Animals↗

PubMed2001

Sigmoid reconfigured vaginal construction in children.

PURPOSE: We present a modified technique of sigmoid neovaginal construction in children that protects the sigmoid pedicle from traction, allows easy adjustment of caliber and reorients the mucosal fold in a longitudinal direction. MATERIALS AND METHODS: From 1997 to 2000, 10 genetically male (46 XY) children 1 to 13 years old underwent construction of a neovagina with sigmoid, incorporating the Yang-Monti concept of intestinal reconfiguration. The diagnosis was androgen insensitivity in 7 patients, congenital adrenal hyperplasia in 2 due to 17 alpha-hydroxylase deficiency and 3 beta-hydroxysteroid dehydrogenase deficiency, respectively, and bladder exstrophy in 1 who required sex reassignment. RESULTS: Eight children had an adequate caliber neovagina after an initial period of systematic dilation. In 1 case a relevant stricture required reoperation using the same technique and the outcome was good. In another child a stricture developed in the middle of the reconfigured sigmoid segment and a regular dilation schedule is still being followed after 23 months of followup. CONCLUSIONS: The new sigmoid reconfiguration technique enables the use of smaller dimension intestinal segments and construction of a long vaginal conduit of adequate caliber. Its optimal adequacy for penetration must be assessed in the future after these patients begin sexual activity.

Adolescent↗

PubMed2005

[Study on pathological rhythm of traditional Chinese medicine about circadian distribution of premature ventricular contractions in 240 patients with viral myocarditis].

OBJECTIVE: To explore the circadian distribution of premature ventricular contractions (PVCs) in patients with viral myocarditis (VM) according to the theory of chronomedicine in traditional Chinese medicine (TCM) in order to find out the scientific evidence for a reasonable administration time. METHODS: Two hundred and forty patients with VM were enrolled and electrocardiograms were examined for all by Holter monitor. The circadian distribution of PVCs was evaluated according to the theory of chronomedicine of TCM about time periods corresponding to five zang viscera. RESULTS: PVCs mostly happened in periods of 3:00-5:00, 5:00-7:00, 7:00-9:00 and 9:00-11:00, in which 5:00-7:00 was the most serious time. Less PVCs happened in periods of 17:00-19:00, 19:00-21:00 and 21:00-23:00. The frequency of PVCs in midnight also increased with aging. The time periods of the frequency peak of PVCs in patients with different syndromes were also different. In patients with syndrome of pathogenic heat invading heart (PHIH), the PVCs mostly appeared in midday. In patients with syndrome of flaring of fire due to yin-deficiency (FFYD), the PVCs were most serious in daytime and aggravated at noon. And in patients with syndrome of insufficiency of heart-qi and yang (IHQY), the PVCs mostly happened in early morning or midnight. CONCLUSION: There was a manifest regulation of the pathological circadian rhythm of PVCs in patients with VM. The circadian distributions of PVCs were variable in patients with different syndromes. Therefore the theory of chronomedicine of TCM may be used to guide the treatment based on syndrome differentiation.

Adolescent↗

PubMed2006

Infectious pathogens in pediatric patients with primary immunodeficiencies.

BACKGROUND AND PURPOSE: Primary immunodeficiency diseases (PIDs) are rare disorders. Unusual infections often guide the initial investigation for immunodeficiency. METHODS: In order to ascertain the organisms that lead to a predisposition for PIDs, we reviewed the charts of 92 children diagnosed with PIDs at the National Taiwan University Hospital between March 1984 and March 2004. RESULTS: Pneumonia was diagnosed in 92%, 81%, and 76.5% of patients with antibody, combined, and cellular deficiencies, respectively. Other major illnesses were similar in the 3 groups and included bronchiolitis, acute gastroenteritis, otitis media, and bacteremia. Skin abscess, pneumonia, and lymphadenitis (54.5%, 45%, and 27% of cases, respectively) were the most common infections in patients with phagocyte defects. Organisms were speciated in only 44.8% of infection episodes. Most viral infections were diagnosed by traditional and time-consuming viral culture. Prophylactic antibiotics were prescribed to 9 out of the 92 patients with PIDs. CONCLUSIONS: Early recognition of PIDs requires that practitioners be aware of the infection characteristics, and subsequent reliable and rapid molecular diagnosis are needed in such immunocompromised patients.

Causality↗

PubMed2001

Identification of three novel 6-pyruvoyl-tetrahydropterin synthase gene mutations (226C>T, IVS3+1G>A, 116-119delTGTT) in Chinese hyperphenylalaninemia caused by tetrahydrobiopterin synthesis deficiency.

The enzyme 6-Pyruvoyl-tetrahydropterin synthase (PTS) deficiency is the major cause of BH(4)-deficient HPA. The frequency of BH(4)-deficient HPA was estimated to be around 30% among Chinese HPA population in Taiwan, which is much higher than that in Caucasian population (1.5-2% of HPA). Approximately 86% of Chinese BH(4)-deficient HPA was found to be caused by PTS-deficiency. Seven mutations - namely R25G, N52S, V56M, V70D, P87S, D96N, and T106M - had been identified in Chinese PTS-deficient patients previously. In this study, five additional mutations in the PTS gene, namely 200C>T (T67M), 226C>T (L76F), IVS3+1G>A (K54X), 116-119delTGTT (K38X) and 169-171delGTG (V57del), were identified by PCR and DNA sequencing in Chinese PTS-deficient patients. The 116-119delTGTT introduces a frameshift stop after lysine of codon 38 (K38X). The G-to-A transition at the consensus sequence of splicing donor site of exon 3 (IVS3+1G>A) resulted in exon 3 skipping of the PTS transcript and caused a frameshift stop after lysine of codon 54 (K54X). The T67M and V57del mutations have been found in Caucasian PTS deficient patients, while the L76F, IVS3+1G>A, and K38X mutations are novel. None of 100 normal alleles screened was found to have the L76F substitution, which indicated that the L76F substitution is a mutation causing PTS deficiency. Hum Mutat 18:83, 2001.

Alleles↗

PubMed2006

A negative regulatory role for auxin in sulphate deficiency response in Arabidopsis thaliana.

Sulphate is a major macronutrient required for the synthesis of the sulphur (S)-containing amino acid cysteine and thus is critical for cellular metabolism, growth and development and response to various abiotic and biotic stresses. A recent genome-wide expression study suggested that several auxin-inducible genes were up-regulated by S deficiency in Arabidopsis. Here, we examined the relationship between auxin signaling and S deficiency. Investigation of DR5::GUS expression patterns indicates that auxin accumulation and/or response is suppressed by S deficiency. Consistently, S deficiency resulted in the suppression of lateral root development, but the axr1-3 mutant was insensitive to this response. Furthermore, the activation of the promoter for the putative thioglucosidase gene (At2g44460) by S deficiency was suppressed by auxin, cytokinin and abscisic acid (ABA). Interestingly, the activation of At2g44460 by S deficiency is regulated by the availability of carbon and nitrogen nutrients in a tissue-specific manner. These results demonstrate that auxin plays a negative role in signaling to S deficiency. Given that activation of the genes encoding the sulphate transporter SULTR1;2 and 5'-adenylylsulphate reductase APR2 are suppressed by cytokinin only, we hypothesize that while cytokinin may play an important role in general S deficiency response, auxin might be only involved in a subset of S deficiency responses such as the release of thiol groups from the S storage sources.

Arabidopsis↗

PubMed2003

Molecular cloning and expression of a smooth muscle-specific gene SM22alpha in zebrafish.

SM22alpha is a kind of 22-kDa protein which is exclusively expressed in smooth muscle containing tissues of the vertebrates. Here we report molecular cloning of a novel zebrafish SM22alpha gene. The full length of zebrafish SM22alpha cDNA is 1296bp and it encodes a polypeptide of 201 amino acids which shares 69.2%, 69.7%, 69.2%, 67.2%, and 61.2% overall identity with human, mouse, rat, chicken, and bovine SM22alpha, respectively. Characterization of zebrafish SM22alpha genomic sequence reveals that it spans 7.7kb and contains five exons and four introns. The expression pattern of SM22alpha in zebrafish embryonic development is studied by whole-mount in situ hybridization. Strong expression is observed in vascular, gut, swim bladder, branchial arches, and fin epidermis. Furthermore, we carry out gene knock-down by antisense morpholino oligonucleotide, which results in disappearance of yolk extension, caudal fin aberrance, and deficiency of circulation system in zebrafish embryo. Cross-section of SM22alpha-deficient embryo suggests that SM22alpha may play roles in smooth muscle cell morphology transform.

Amino Acid Sequence↗

PubMed2004

Fenofibrate prevents obesity and hypertriglyceridemia in low-density lipoprotein receptor-null mice.

Our previous study demonstrated that fenofibrate improves both lipid metabolism and obesity, in part through hepatic peroxisome proliferator-activated receptor alpha (PPARalpha) activation, in female ovariectomized, but not in sham-operated, low-density lipoprotein receptor-null (LDLR-null) mice. The aim of this study was to determine whether fenofibrate prevents obesity and hypertriglyceridemia in male LDLR-null mice. Mice fed a high-fat diet for 8 weeks exhibited increases in body and white adipose tissue (WAT) weights and developed severe hypertriglyceridemia compared with mice fed a low-fat control diet. However, these effects were effectively prevented by fenofibrate. Mice given a fenofibrate-supplemented high-fat diet showed significantly reduced body weight, WAT weight, and serum triglycerides versus high-fat diet-fed animals. Triton WR1339 study showed that fenofibrate-induced reduction in circulating triglycerides was due to the decreased secretion of triglycerides from the liver. Moreover, the administration of fenofibrate not only resulted in liver hypertrophy and reduction in hepatic lipid accumulation, but also regulated the transcriptional expression of PPARalpha target genes, such as hepatic acyl-coenzyme A (CoA) oxidase and apolipoprotein C-III (apoC-III). Therefore, our results suggest that alterations in hepatic PPARalpha action by fenofibrate seem to suppress diet-induced obesity and severe hypertriglyceridemia caused by LDLR deficiency in male mice.

Acyl-CoA Oxidase↗

PubMed2006

Arginase induction by sodium phenylbutyrate in mouse tissues and human cell lines.

Hyperargininemia is a urea cycle disorder caused by mutations in the gene for arginase I (AI) resulting in elevated blood arginine and ammonia levels. Sodium phenylacetate and a precursor, sodium phenylbutyrate (NaPB) have been used to lower ammonia, conjugating glutamine to produce phenylacetylglutamine which is excreted in urine. The elevated arginine levels induce the second arginase (AII) in patient kidney and kidney tissue culture. It has been shown that NaPB increases expression of some target genes and we tested its effect on arginase induction. Eight 9-week old male mice fed on chow containing 7.5 g NaPB/kg rodent chow and drank water with 10 g NaPB/L, and four control mice had a normal diet. After one week all mice were sacrificed. The arginase specific activities for control and NaPB mice, respectively, were 38.2 and 59.4 U/mg in liver, 0.33 and 0.42 U/mg in kidney, and 0.29 and 1.19 U/mg in brain. Immunoprecipitation of arginase in each tissue with AI and AII antibodies showed the activity induced by NaPB is mostly AI. AII may also be induced in kidney. AI accounts for the fourfold increased activity in brain. In some cell lines, NaPB increased arginase activity up to fivefold depending on dose (1-5 mM) and exposure time (2-5 days); control and NaPB activities, respectively, are: erythroleukemia, HEL, 0.06 and 0.31 U/mg, and K562, 0.46 and 1.74 U/mg; embryonic kidney, HEK293, 1.98 and 3.58 U/mg; breast adenocarcinoma, MDA-MB-468, 1.11 and 4.06 U/mg; and prostate adenocarcinoma, PC-3, 0.55 and 3.20 U/mg. In MDA-MB-468 and HEK most, but not all, of the induced activity is AI. These studies suggest that NaPB may induce AI when used to treat urea cycle disorders. It is relatively less useful in AI deficiency, although it could have some effect in those patients with missense mutations.

Animals↗

PubMed1994

Quantitative measurements of dietary and [1-14C]linoleate metabolism in pregnant rats: specific influence of moderate zinc depletion independent of food intake.

Our objective was to investigate whether the effects of moderate zinc deficiency on metabolism of linoleate during pregnancy could be distinguished from the effects of low food intake. Rats were force-fed an isoenergetic zinc-deficient (3.2 mg/kg) or control (26.4 mg/kg) semiliquid diet during the second half of pregnancy. Fatty acid quantity and composition in both maternal and fetal organs were analyzed at term. Recovery of 14C in lipid- and water-soluble metabolites from orally injected [1-(14)C]linoleate was also studied. After 10 days of gavaging identical amounts of the diet, zinc-deficient rats had lower serum zinc and lower uterus and placenta weights than controls, but body weights were similar. At term, zinc-deficient rats had a fatty acid composition in organs and carcass similar to that of the controls, but the zinc-deficient fetuses had lower long-chain n-6 and n-3 polyunsaturates in brain, liver, and carcasses. Lipids extracted from most organs of zinc-deficient rats contained lower 14C levels, but 14C was raised in the maternal carcass lipids and in water-soluble metabolites. We conclude that zinc deficiency during pregnancy increases oxidation of linoleate and decreases synthesis or transport of polyunsaturates to the fetuses and that these effects are independent of depressed food intake, i.e., they are specific to zinc depletion. Thus, zinc deficiency has distinct effects on fatty acid metabolism, which are readily observed using 14C tracer methods.

Animals↗

PubMed2002

Natural killer cell deficiency associated with Hodgkin's lymphoma: a case report.

Natural killer (NK) cells are large granular lymphocytes that play important roles in immunity against viral infection. NK cell deficiency is associated with recurrent episodes of severe herpes group virus reactivation. Few cases of NK cell deficiency have been reported. Here, we report the case of a Taiwanese girl who had suffered from severe atopic dermatitis since infancy, and recurrent episodes of herpes virus reactivation since the age of 3 years old. NK cell deficiency was diagnosed based on the finding of persistently low NK cell counts in peripheral blood. Hodgkin's lymphoma developed when she was 6 years old. The present case suggests that NK cell deficiency may be an important risk factor in the development of Hodgkin's lymphoma.

Child↗

PubMed2003

[Prevalence of postpartum thyroiditis in three different iodine intake areas].

OBJECTIVE: To investigate the prevalence of postpartum thyroiditis (PPT) in three different iodine intake areas, to explore the relationship between iodine intake and PPT. METHODS: Panshan, Zhangwu and Huanghua are three different iodine intake areas. The median urinary iodine concentration were 103 micro g/L, 374 micro g/L and 614 micro g/L, respectively. One hundred and nineteen lactational women were investigated during the first year postpartum. Thyroid stimulating hormone (TSH), free thyroxine (FT(4)), free triiodothyronine (FT(3)), thyroid peroxidase antibody (TPOAb) and thyroglobulin antibody (TGAb) were determined with immulite method, and UI was determined by As-Ce(4+) catalytic spectrophotometry method. RESULTS: The prevalence of PPT is 11.8%, 10.1% of subclinical PPT, whereas 1.7% of clinical PPT. There was statistically significant difference in the frequency of PPT in three areas (Panshan 5.6%, Zhangwu 23.1% and Huanghua 6.8%, P < 0.05), but no difference in the frequency of thyroid autoimmune antibody (TAA). 50% of positive TAA women developed into PPT. CONCLUSION: Higher prevalence of subclinical PPT was found in the area with moderate iodine deficiency after iodine supplementation, suggesting a possible role of iodine supplementation in PPT.

Autoantibodies↗

PubMed1975

Healthy blood donors with selective absence of immunoglobulin A: prevention of anaphylactic transfusion reactions caused by antibodies to IgA.

Gel diffusion analysis of sera from 73,569 healthy volunteer blood donors revealed apparent lack of IgA in 113 (1:650) samples, all with normal levels of IgG and IgM. Of these, 30 sera had low levels of IgA, while the remaining 83 had no IgA detectable by a more sensitive hemagglutination inhibition assay. The frequency of absent IgA (algA) was 1:886. High-titer anti-IgA was detected in the sera of 13 algA donors; only two had any known history of parenteral injection of IgA. Passive transfusion of high-titer anti-IgA in the units of blood elicited no clinical reaction in the recipients. Precipitating antibodies to ruminant IgM were present in 14 of the 83 donors. The incidence of hepatitis B surface antigen (HB-sAg), anti-HB-sAG, and antinuclear antibodies was the same in IgA-deficient and control sera. The algA donors form a unique resource for blood components for the clinical management of patients with anapylactic reactions caused by anti-IgA.

Anaphylaxis↗