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At least 667 records · Page 37Linked to original sources
PubMed1985

Changes in health conditions in the Huainan coal mine in the past three decades.

Health conditions in the Huainan Coal Mine have improved greatly since 1950. In particular, the work and living environments, the underground dust concentration, the water supply and waste disposal systems, and the nutritional value of miners' food have become much better. Thus the rates of occupational, infectious, and parasitic diseases and nutritional deficiency diseases have decreased considerably among miners. The decreases in the prevalence of anthracosilicosis and hookworm have been especially striking.

Anthracosilicosis↗
PubMed2003

[Diagnosis and treatment of biotinidase deficiency-clinical study of six patients].

OBJECTIVE: To investigate the clinical and neurodevelopmental profiles of patients with biotinidase deficiency and to determine the efficacy of current therapy with respect to outcome. METHODS: Six patients aged from 3 months to 14 years with biotinidase deficiency were confirmed by urinary organic acid analysis with gas chromatography/mass spectrometry (GC/MS) and biotinidase assay on dried blood spots. Biotin was supplemented individually (10-40 mg/d). Their clinical features, laboratory findings, and treatment regimen were reviewed. RESULTS: All the 6 patients presented with some extent of neurological abnormalities and dermatological lesions. Cases 1 - 3 had poor feeding, vomiting, seizures, mental retardation, and lethargy onset from their early infancy, with varied degree of anemia, ketosis, acidosis, and hypoglycemia. Case 2 exhibited eczema and dermatitis from his age of 7 months. Case 4 displayed motor deficit and ataxia after 6 months of age, and generalized pustular psoriasis when he was 8 months old. Cases 5 and 6 gradually showed muscle weakness and paraplegia at the age of 7 years and 5 years, respectively. Inflammatory demyelination changes of cervical cord were evident on magnetic resonance imaging in these two patients. Case 6 had progressive optic atrophy, eczema and alopecia. Remarkable elevations of urinary lactate, pyruvate, 3-OH-propionate, methylcitrate, propionylglycine, 3-OH-isovalerate, 3-methylcrontonylglycine were confirmed in cases 1, 2, 3 and 5. Slight increase of urinary lactate, pyruvate, and 3-methylcrontonylglycine was observed in cases 4 and 6. Biotinidase activities assayed on dried blood spots from all the patients were below 0.1 pmol/(min.3 mm) Biotin supplementation for all the patients, except for case 3 who was not treated, resulted in pronounced and rapid clinical and biochemical improvement. Cases 4 and 6 had residual neurological damage comprising ataxia and motor handicap of legs, due to prolonged disease course. CONCLUSIONS: Biotinidase deficiency intensively impairs nervous system and skin in the affected patients. Urinary organic acid analysis and blood biotinidase assay are crucial to the diagnosis. Early diagnosis and biotin supplementation can contribute significantly to the improvement of prognosis.

Adolescent↗
PubMed2006

[Status of vitamin A, vitamin B2, iron and an-oxidantive activity in anemic pregnant women in China].

OBJECTIVE: To investigate the status of vitamin A(VA), vitamin B2 (VB2), iron and anoxidative function in anemic and non-anemic pregnant women. METHODS: 426 anemic and 36 non-anemic pregnant women were included in the study. The survey of 24-hour's diet recall of pregnant women was made to evaluate intake of iron, VB2, folic acid, etc by the nutrition software provided by Beijing 301 hospital, iron and VA were measured by Radioimmunoassay (RIA) and by high-pressure liquid chromatography. VB2 status was detected using the assay for erythrocyte glutathione reductase (Egr; EC 1.6.4.2) activity. SOD and GSH-Px activities and MDA were determined using commercial kits. Peripheral blood erythrocyte membrane fluidity was detected by using 1,6-diphenyl-1,3,5-hexatriene as a probe, the degree of fluorescence polarization (P) at 25 degrees C of disrupted cells plasma membranes were compared for a variety of systems. RESULTS: Median intakes of protein and vitamin C met the current Chinese RNIs for pregnancy, whereas intakes of(VA) and VB2 were well below the recommendations. Intake of iron were above 90%, but the main sources of iron are vegetables. Plasma VA (1.25 micromol/L) and iron (20.57 microg/L) were lower, BGRAC (1.79) was higher than that in non-anemia group (VA 1.57 micromol/L, SF 33.16 microg/L, BGRAC 1.52). The level of plasma SOD (77.1U/ml) and the activity of GSH-Px (61.9U) were lower than those in non-anemia group (92.2U/ml, 71.6U, P < 0.05), while MDA (4.58 nmol/ml) level and erythrocyte membrane (P = 0.2622, eta = 2.7465) fluidity were higher than those non-anemia group(MDA = 3.78 nmol/ ml, P = 0.2360, eta = 2.3658). CONCLUSION: Plasam VA, VB2 and iron, antioxidantcapacity and erythrocyte membrane fluidity were decreased in the anemic pregnant women.

Adult↗
PubMed2002

Therapeutic effects of NaFeEDTA-fortified soy sauce in anaemic children in China.

The therapeutic effects of NaFeEDTA-fortified soy sauce on anaemic students were investigated. Three hundred and four iron-deficient anaemic school children (11-17 years) were randomly assigned to three treatment groups: control group (consuming non-fortified soy sauce), low-NaFeEDTA group (consuming fortified soy sauce, providing 5 mg Fe/day) and high-NaFeEDTA group (consuming fortified soy sauce, providing 20 mg Fe/day). Blood haemoglobin (Hb) levels were determined before and after 1 month, 2 months and 3 months of intervention. In addition, serum iron (SI), serum ferritin (SF), free erythrocytic porphyrin (FEP), total iron binding capability (TIBC) and transferritin (TF) were measured before and after consumption of soy sauce for 3 months. The results obtained herein show that the parameters measured were not changed remarkably within the 3-month intervention in the control group (P < 0.05). However, increased Hb, SI, SF and TF levels and decreased TIBC and FEP levels were observed in both the high-NaFeEDTA group (P <0.01) and the low-NaFeEDTA group (P < 0.05). The effectiveness of iron intervention in the low-NaFeEDTA group and high-NaFeEDTA group had no statistical significance after 3 months. It was concluded that nutritional intervention for anaemic students using NaFeEDTA-fortified soy sauce could play a positive role in the improvement of iron status and control of anaemia.

Adolescent↗
PubMed2003

Heart xenograft survival with chimeric pig donors and modest immune suppression.

OBJECTIVE: To assess the use of donor pigs with cellular chimerism for prevention of acute rejection with modest immune suppression. The clinical use of pig organ xenografts is currently precluded by severe acute rejection, which resists standard immune suppression. SUMMARY BACKGROUND DATA: For long-term survival of pig organ xenografts, immune suppression significantly greater than used with allografts would currently be necessary, leaving the recipient immune deficient and at increased risk for infections. Induction of immune tolerance and tissue accommodation could enhance xenograft survival but would lead to complications and frequent graft failure. Induction of cellular chimerism within the donor pigs, however, could accomplish these goals before transplantation, significantly reducing the risk. METHODS: Marrow cells from sheep were infused into fetal pigs. Heart xenografts from chimeric or nonchimeric pigs were transplanted heterotopically into recipient sheep, simultaneous with infusion of splenocytes. Posttransplant suppression consisted of cyclosporine and tapered corticosteroids, comparable with allotransplants. RESULTS: All of the control grafts (n = 12) were rejected by acute vascular rejection in 4 to 8 days. In contrast, only one episode of vascular rejection was observed in the experimental group (n = 13). Four experimental recipients had an episode of moderate diffuse cellular rejection (grade 3) and one had moderate focal cellular rejection (grade 2). Each episode responded to pulse steroids. Seven grafts showed no significant rejection. There was little evidence of immune deficiency, infection, or toxicity. CONCLUSIONS: Acute vascular rejection was prevented in a large animal model without the need for severe immune suppression.

Acute Disease↗
PubMed1993

Vitamin E requirement of rats fed on a diet containing grains from the endemic region of Keshan disease.

Keshan disease (KD) is an endemic cardiomyopathy occurring in China. Combined selenium and vitamin E (VE) deficiency might be involved in the development of KD. It was shown in this paper that addition of 20 and 100 mg/kg DL-alpha-tocopherol tended to decrease malondialdehyde (MDA) content of myocardium in the rats receiving the low selenium (0.013 ppm) grains from the endemic region of KD, but not to a statistically significant extent. And addition of 200 mg/kg DL-alpha-tocopherol significantly decreased the myocardial MDA content, which suggested that VE requirement of the rats receiving KD endemic grains was 200 mg/kg DL-alpha-tocopherol. However, the MDA content in the myocardium of rats receiving KD grains added with 100 mg/kg DL-alpha-tocopherol was significantly decreased when selenium (0.1 ppm) was supplemented, which suggested that VE requirement of these rats was decreased to 100 mg/kg DL-alpha-tocopherol in the presence of selenium. The ability of VE in counteracting free radicals in myocardium of rats appeared greater than that of selenium.

Animals↗
PubMed1997

Two newly identified mutations (Thr233Ile and Leu152Met) in partially adenosine deaminase-deficient (ADA-) individuals that result in differing biochemical and metabolic phenotypes.

Deficiency of adenosine deaminase (ADA-) results in autosomal recessive immunodeficiency disease of varying severity. Partial ADA- [ADA deficiency in erythrocytes (RBCs) but substantial ADA in non-RBCs] has also been identified, primarily by population screening of healthy adults in Africa and newborns in New York State. Normal immune function and/or minimal elevations of toxic metabolites in childhood suggested that partial ADA deficiency was benign and therefore that six mutations identified in partially ADA-deficient newborns and expressing 8-80% of normal ADA in non-RBCs were not pathogenic. However, the lowest activity mutation (Arg211Cys) has now been reported in patients with adult-onset immunodeficiency. We have now molecularly and biochemically studied two additional individuals whom we found to represent opposite ends of the spectrum of partial ADA deficiency as to biochemical abnormalities and age of ascertainment. Homozygosity for a newly identified Leu152Met mutation expressing considerably less activity than the pathogenic Arg211Cys mutation was found in a currently healthy 10-year-old Afghanistani child (ascertained at birth). He had the highest accumulation of the metabolite dATP among 13 partially ADA-deficient patients studied, but considerably lower than in those with immunodeficiency. Homozygosity for a newly identified Thr233Ile mutation expressing somewhat greater ADA activity than Arg211Cys was found in a healthy young adult Kung individual, associated with very low metabolite concentrations. Biochemical findings and a family history suggestive of immunodeficiency in prior offspring support the idea that the Leu152Met mutation could result in disease in homozygous individuals challenged by severe environmental insult or in heterozygosity with a null mutation. The pathogenicity of the Thr233Ile mutation, as well as a previously described Ala215Thr mutation with relatively lower activity is less likely but will only be determined by long-term observation of individuals carrying these mutations. Although, in contrast to other partial mutations, neither of these two mutations are at CpG hot spots, the frequency of CpG mutations remains high for partial mutations but is also similarly high in ADA- immunodeficient patients (5/8 vs 12/21).

Adenosine↗
PubMed2004

Effects of the CRF1 antagonist SSR125543A on aggressive behaviors in hamsters.

Corticotropin-releasing factor (CRF) and its receptor subtypes have been implicated in endocrine and behavioral responsivity to stress and emotion, including fear, anxiety, and aggression. SSR125543A is a new nonpeptide selective antagonist at the CRF1 receptor that has been shown to produce an anxiolytic-like effect in a number of animal models of anxiety. The present study investigated effects of an oral dose of 10, or 30 mg/kg of SSR125543A on aggressive behaviors of resident male Syrian hamsters toward male intruders. The high dose (30 mg/kg) of the CRF1 receptor antagonist produced a higher latency to bite and lower lateral attack frequencies and chase durations, indicating a reduction in aggression toward intruders in resident hamsters. The same dose of SSR125543A also enhanced frequency and duration of olfactory investigation, indicating that neither avoidance of the opponent nor deficiency in social activity is responsible for the reduction in aggression seen in these animals.

Aggression↗
PubMed1980

Holocarboxylase synthetase deficiency: a biotin-responsive organic acidemia.

The clinical and biochemical features of an infant affected by holocarboxylase synthetase deficiency are presented. The patient was the sibling of the deceased child in whose cultured skin fibroblasts the precise enzymatic disorder was first determined. This fact permitted administration of specific therapy in the form of oral biotin, resulting in immediate improvement from impending respiratory failure and shock. The clinical response to biotin was accompanied by recovery of the biochemical mechanisms known to be biotin-dependent, as manifested by disappearance of intermediates in urine and blood. The variability of biotin responsiveness and the diversity of clinical presentation in the patients originally thought to have a deficiency of beta methylcrotonylCoA carboxylase, a biotin-dependent enzyme, raises the question of a separate, specific apocarboxylase defect.

Amino Acid Metabolism, Inborn Errors↗
PubMed2004

Co-accumulation of vascular endothelial growth factor with beta-amyloid in the brain of patients with Alzheimer's disease.

Alzheimer's disease (AD) is accompanied by the progressive deposition of beta-amyloid (Abeta) in both senile plaques and cerebral blood vessels, loss of central neurons, and vessel damage. Cerebral hypoperfusion is one of the major clinical features in AD and likely plays a critical role in its pathogenesis. In addition to its major roles in angiogenesis, vascular endothelial growth factor (VEGF) has neurotrophic and neuroprotective effects. VEGF is an ischemia-inducible factor and increased expression of VEGF often occurs in AD. Although the presence of VEGF immunoreactivity in the AD brain has been described previously, the direct interaction of VEGF with Abeta has not been established. Here, we show that VEGF is co-localized with Abeta plaques in the brains of patients with AD. In vitro experiments show that VEGF binds to Abeta with high affinity (K(D) approximate to 50 pM). VEGF is co-aggregated with Abeta without any apparent effect on the rate of aggregation, strongly binds to pre-aggregated Abeta, and is very slowly released from the co-aggregated complex. Continuous deposition of VEGF in the amyloid plaques most likely results in deficiency of available VEGF under hypoperfusion and, thus, may contribute to neurodegeneration and vascular dysfunction in the progression of AD.

Aged↗
PubMed2002

In-vitro forming of calcium phosphate layer on sol-gel hydroxyapatite-coated metal substrates.

In-vitro deposition of calcium phosphate layer (CPL) on metallic substrate requires special surface preparation in order to provide an interfacial bond. In this work 316 stainless steel surface is modified through deposition of a thin film ( approximately 0.5 microm) of sol-gel hydroxyapatite (SG-HA). This well-bonded film acts as an intermediary and nucleation surface of the CPL film. The SG-HA films were annealed at 375 degrees C (samples coded 375-ACS) and 400 degrees C (400-ACS) to achieve different crystallinity of the films, and thus to affect and study the CPL nucleation process. The CPL growth was investigated in terms of deposition kinetics and microstructural development. A deposition rate of dense CPL of about 0.43 microm/day was achieved on the crystallized film of 400-ACS, and 0.22 microm/day of porous CPL on amorphous 375-ACS. A compositional variation of Ca/P ratio across the CPL film thickness (400-ACS) was observed. Lower Ca/P ratio of 1.2 was detected near the substrate-CPL interface and about 1.5 near the solution-CPL interface. Infrared analysis showed the CPL to be of apatitic calcium-deficient structure. Kinetic model explaining the advancement of the CPL upon the in-vitro immersion is proposed.

Journal Article↗
PubMed2025

Cockayne syndrome mice reflect human kidney disease and are defective in de novo NAD biosynthesis.

Cockayne Syndrome (CS) is a premature aging disorder caused by mutations in the CSA and CSB genes involved in DNA metabolism and other cellular processes. CS patients display many features including premature aging, neurodegeneration, and kidney abnormalities. Nicotinamide dinucleotide (NAD+) deprivation has been observed in CS patient-derived cells. NAD+ has essential roles in regulating cellular health, stress responses, and renal homeostasis. While kidney dysfunction is a common feature in CS patients, its molecular pathogenesis is not understood. Here, we report that severe kidney pathology is present in CS A and B mice. We find that the NAD+ biosynthetic pathways are impaired in kidneys from these mice. Using human renal tubular epithelial cells, we show that CSA/B downregulation causes persistent activation of the ATF3 transcription factor on the quinolinate phosphoribosyl transferase gene locus, a rate-limiting enzyme in de novo NAD+ biosynthesis in the kidney, causing impaired transcription and deficient NAD+ homeostasis.

Animals↗
PubMed1978

Genetic mapping of the 21-hydroxylase-deficiency gene within the HLA linkage group.

To document further the proposed genetic linkage between congenital adrenal hyperplasia due to 21-hydroxylase deficiency and HLA, 34 unrelated families from New York and Zurich, with a total of 48 patients, 48 siblings and their parents, were studied. All patients were HLA genotypically different from the healthy sibs; when two or more children were affected in the same sibship they were always HLA-B identical. The gene for 21-hydroxylase deficiency was separated by genetic recombination from the HLA-A locus and from the locus for glyoxalase I-polymorphism. No HLA-A, HLA-B or HLA-C antigen was selectively increased among the 34 unrelated patients. Lod-score analysis for HLA-B:21-hydroxylase deficiency gave a peak for theta approximately 0.00 at 5.20 for females and 4.30 for males, giving a total peak lod score of 9.5 at theta approximately 0.00 when male and female lod scores were combined. Close genetic linkage between HLA-B and 21-hydroxylase deficiency was thus established.

Adrenocortical Hyperfunction↗
PubMed1998

Effects of repletion with zinc and other micronutrients on neuropsychologic performance and growth of Chinese children.

The knowledge that zinc is essential for growth and neuropsychologic performance and a report of zinc-responsive stunting in Chinese children prompted this project. This article summarizes findings from a 10-wk, double-blind, controlled trial of zinc repletion in 740 urban, 6-9-y-old first graders from low-income families in Chongqing, Qingdao, and Shanghai, People's Republic of China. Treatments were 20 mg Zn alone (Z), 20 mg Zn with micronutrients (ZM), and micronutrients alone (M). The M mixture was based on National Research Council guidelines. Nutrients that might interfere with zinc retention were excluded or given in lower amounts. Main outcomes were changes in neuropsychologic performance and knee height. Hemoglobin, serum ferritin, plasma and hair zinc, and whole blood and hair lead were also measured. Anemia was not common, and serum ferritin concentrations were usually within the range of normal. Mean baseline plasma zinc concentrations were marginal in children from Chongqing and Qingdao and normal in children from Shanghai. After treatment with ZM or M plasma zinc increased. Hair zinc tended to decrease after all treatments. Mean baseline whole blood lead concentrations were slightly below the limit considered excessive for children by the US Centers for Disease Control and Prevention. Neuropsychologic performance and growth were most improved after treatment with ZM. These findings were consistent with the presence of zinc and other micronutrient deficiencies.

Brain↗
PubMed1991

Betaine deficiency in maize : complementation tests and metabolic basis.

Maize (Zea mays L.) is a betaine-accumulating species, but certain maize genotypes lack betaine almost completely; a single recessive gene has been implicated as the cause of this deficiency (D Rhodes, PJ Rich [1988] Plant Physiol 88: 102-108). This study was undertaken to determine whether betaine deficiency in diverse maize germplasm is conditioned by the same genetic locus, and to define the biochemical lesion(s) involved. Complementation tests indicated that all 13 deficient genotypes tested shared a common locus. One maize population (P77) was found to be segregating for betaine deficiency, and true breeding individuals were used to produce related lines with and without betaine. Leaf tissue of both betaine-positive and betaine-deficient lines readily converted supplied betaine aldehyde to betaine, but only the betaine-containing line was able to oxidize supplied choline to betaine. This locates the lesion in betaine-deficient plants at the choline --> betaine aldehyde step of betaine synthesis. Consistent with this location, betaine-deficient plants were shown to have no detectable endogenous pool of betaine aldehyde.

Journal Article↗
PubMed2006

Mouse model of inducible nephrogenic diabetes insipidus produced by floxed aquaporin-2 gene deletion.

Transgenic mouse models of defective urinary concentrating ability produced by deletion of various membrane transport or receptor proteins, including aquaporin-2 (AQP2), are associated with neonatal mortality from polyuria. Here, we report an inducible mouse model of AQP2 gene deletion with severe polyuria in adult mice. LoxP sequences were inserted into introns 1 and 2 in the mouse AQP2 gene by homologous recombination in embryonic stem cells. Mating of germ-line AQP2-loxP mice with tamoxifen-inducible Cre-expressing mice produced offspring with inducible homozygous Cre-AQP2-loxP, which had a normal phenotype. Tamoxifen injections over 10 days resulted in AQP2 gene excision, with undetectable full-length AQP2 transcript in kidney and a >95% reduction in immunoreactive AQP2 protein. Urine osmolality decreased from approximately 2,000 to <500 mosmol/kgH(2)O after 4-5 days, with urine output increasing from 2 to 25 ml/day. Urine osmolality did not increase after water deprivation. Interestingly, AQP3 protein expression in the collecting duct was increased by about fivefold after AQP2 gene excision. Mild renal damage was seen after 6 wk of polyuria, with collecting duct dilatation, yet normal creatinine clearance and serum chemistries. These results establish the first adult model of nephrogenic diabetes insipidus (NDI) caused by AQP2 deficiency, with daily urine output comparable to body weight, although remarkable preservation of renal function compared with non-inducible NDI models.

Animals↗