摘要:

A recently identified RNA virus, hepatitis G virus (HGV), has been investigated for its role in causing non-A-E hepatitis. The frequency and clinical outcome of HGV infection in children was studied. Two hundred apparently healthy children aged 6 mo to 12 y, and 90 children who had undergone open heart surgery in a prospective study for posttransfusion hepatitis were included in this study. The serum samples were tested for HGV RNA by nested reverse transcription-PCR with primers from the 5′-untranslated region. The HGV RNA viremic rate was found to be 1%(2/200) in apparently healthy children, 30% in children after open heart surgery. Among the 90 children, three were HGV-infected before the surgery. Twenty-four (28%) of the remaining 87 children tested positive for HGV RNA within 6 mo after the surgery. Sixty-five percents of these viremic children eventually became persistently infected at 1 y after surgery. No HGV RNA-positive children exhibited elevated alanine aminotransferase levels during the follow-up period. No coinfections of HGV with the hepatitis C virus or hepatitis B virus were found. Patients of younger age appeared more likely to become chronic carriers. Anti-HCV screening did not reduce the prevalence of HGV infection. In conclusion, in children with open heart surgery, the risk of transfusion-transmitted HGV infection and the chronicity rate have been found to be high. Young age is a risk factor of persistent infection.

ISSN:0031-3998    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Neutrophils in the cerebrospinal fluid (CSF) increase during the initial stage of meningitis. Some cytokines induce the accumulation of such neutrophils, and we and other investigators have revealed transient increases in the levels of granulocyte-colony stimulating factor (G-csf) and IL-8 in the CSF of patients with meningitis. To explore the coordination of other cytokines with G-csf and IL-8 in the neutrophil accumulation in the CSF, we herein investigated macrophage inflammatory protein-1α (MIP-1α), which can induce the infiltration of neutrophils. The modulation of MIP-1α levels in the CSF in children with bacterial (n= 10) and aseptic (n= 22) meningitis was examined using an ELISA. MIP-1α levels in the CSF were detectable at the stage with symptoms of meningitis: 289.9 ± 270.7 ng/L in the bacterial meningitis group and 16.1 ± 12.5 ng/L in the aseptic meningitis group. These levels decreased with the improvement of symptoms. MIP-1α was not detectable(<6 ng/L) in all of the control patients without meningitis (n= 19). The MIP-1α levels in the CSF showed a significant correlation with the CSF neutrophil counts (r= 0.750,p< 0.0001;n= 80) of meningitis, and the values of MIP-1α (log ng/L)/neutrophil counts (log/L) ratio were calculated (1.003 ± 0.576). The MIP-1α levels in the serum were significantly lower than those in the CSF (p= 0.0464). We found MIP-1α mRNA in the CSF cells by the reverse transcriptase-PCR method, and high levels of MIP-1α protein in the culture media from mononuclear cells in the CSFin vitro. In summary, The MIP-1α level increases in the CSF at the symptomatic stage of meningitis in children, and its cellular source is, in part, mononuclear cells which have infiltrated the CSF. We propose that MIP-1α, in addition to G-csf and IL-8, plays an important role in the accumulation of neutrophils in the CSF of patients with meningitis.

ISSN:0031-3998    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Spleens from 1-20-wk-old guinea pigs infectedin uterowithTreponema pallidumand age-matched controls, born to normal and heat-killed (56°C, 2 h.)T. pallidum-injected mothers, were examined for theirin vitrolymphoproliferative response to phytohemagglutinin, concanavalin A, and lipopolysaccharide. Additionally. T cell surface markers (μ-chain, pan T, CD4, and CD8) were determined in spleen, lymph node, and peripheral blood from 10-wk infected and normal pups by single and dual parameter fluorescence-activated cell sorter analysis. Compared with control animals, congenitally infected animals showed a remarkable prolonged naive-type of immune response as reflected by the higher(p< 0.01) proliferative responses to both T cell mitogens (up to 20 wk of age), and the weaker response to the B cell mitogen, significantly different (p< 0.01) at 10 wk of age. As opposed to controls, in all organs examined the level of CD8+(cytotoxic/suppressor) T cells was significantly diminished (p< 0.01); consequently, the CD4/CD8 ratio was significantly elevated (p< 0.05). The role of C4 complement component and the nature and potential role of the immature T and B lymphocyte responses in asymptomatic congenital syphilis is discussed.

ISSN:0031-3998    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Group B streptococci (GBS) are one of the major causes of invasive neonatal infection. The pathogenesis of early onset disease is a multistep process. Adhesion of GBS to eucaryotic cells is considered to be an important step for the establishment of infection. Subsequent to adhesion, GBS invade cells and give rise to septicemia and meningitis. To investigate passage of GBS across epithelial cell linings we examined the interaction between bacteria and Madin-Darby canine kidney (MDCK) cells. When grown on permeable support, these cells form a polarized epithelial monolayer with an apical-to-basolateral orientation, which more reflects thein vivosituation compared with conventionally cultured cells. Our results show that GBS are translocated in vacuoles from the apical to the basolateral surface of MDCK cells in a temperature-dependent process. The passage of GBS through the cells is selective with only small numbers of bacteria penetrating in the basolateral-to-apical direction. Transcytosis of GBS starts before decrease in transepithelial resistance of the monolayer. These data suggest a mechanism for traversal of GBS over intact chorioamniotic membranes and from alveoli into the circulation of the fetus.

ISSN:0031-3998    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

We have investigated the impact of chronic restriction of placental function on circulating catecholamine concentrations and responses to the indirectly acting, sympathomimetic amine, tyramine, in the fetal sheep in late gestation. In 10 ewes, endometrial caruncles or placental placentation sites were removed before conception (placental restriction (PR) group). Fetal sheep in the PR group were hypoxemic throughout late gestation and growth-restricted(3.02 ± 0.35 kg) when compared with control fetal sheep (4.30 ± 0.29 kg;n= 8) at 140 d of gestation. Fetal plasma concentrations of noradrenaline and adrenaline were higher (p< 0.05) in the PR(7.06 ± 3.17 pmol/mL and 2.89 ± 2.01 pmol/mL, respectively) than in the control group (3.55 ± 0.54 pmol/mL and 1.30 ± 0.48 pmol/mL, respectively) throughout late gestation. Plasma noradrenaline, but not adrenaline concentrations, increased significantly between 110 and 140 d of gestation in both the PR and control group, and there was a significant inverse relationship between plasma noradrenaline and arterial Po2in the PR and control groups (plasma noradrenaline = 12.34 - 0.40 Po2). In the PR group, plasma noradrenaline increased (p< 0.05) after tyramine infusion from 4.51 ± 1.28 pmol/mL to a peak of 19.40 ± 3.56 pmol/mL. In the control group, noradrenaline increased from 2.08 ± 0.30 pmol/mL to a peak of 12.23 ± 1.67 pmol/mL after tyramine infusion. There was no difference, however, in the maximal proportional changes in plasma noradrenaline concentrations in the PR (319 ± 55%) and control(449 ± 100%) groups after tyramine. We conclude that the most likely source of the increased plasma catecholamines in the PR group is enhanced catecholamine synthesis and secretion from developing sympathetic neurons.

ISSN:0031-3998    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Thyroid status was characterized in very preterm infants (gestational age≤32 wk;n= 61) from birth through d 14, and in infants who died within 16 d after delivery (n= 10), where it was also correlated with metabolism of iodothyronines in peripheral tissues (brain, liver, kidney, skeletal muscle, and adipose tissue). At 3 d of life, mean plasma levels of thyroxine, triiodothyronine, and TSH started to decrease, being lower in the critically ill compared with healthy premature neonates. Activities of the three iodothyronine deiodinases enzymes (type I, II, and III, respectively) were detected in all postmortem tissue samples, except for absence of the type II activity in kidney. All activities were the highest in liver and differed in other tissues. Lack of correlation between the type I activity in liver(and kidney), and plasma levels of thyroid hormones suggested that the thyroid was the primary source of circulating triiodothyronine. On the other hand, namely in brain, correlations between activity of the deiodinases and plasma hormone levels were found which suggested a complex control by thyroid hormones of their own metabolism. High activity of type III in liver, adipose tissue, and skeletal muscle demonstrated a role of these tissues in thyroid hormones degradation. Results support the view that peripheral tissues of very preterm infants are engaged in local generation of triiodothyronine, and inactivation of thyroid hormones, but do not represent a major source of circulating triiodothyronine.

ISSN:0031-3998    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

The nutritional requirements of preterm infants for the long chain polyunsaturated essential fatty acids, arachidonic acid (AA) and docosahexaenoic acid (DHA), have not been clearly defined. The present study evaluated preterm infants of less than 2.3 kg birth weight fed a commercial formula (Preemie SMA®) devoid of AA and DHA and compared this control group with similar infant groups fed one of three formulas containing a range of 0.32 to 1.1% AA and 0.24 to 0.76% DHA. An analogous group of infants fed their mothers' breast milk and a breast milk fortifier (when indicated) was also studied. Erythrocyte membrane phospholipids were isolated from blood samples collected at 12 d of age and after a further 4 wk of feeding. Infants fed the formula without AA and DHA showed a reduction in AA level in erythrocyte phosphatidylcholine, and a reduced level of DHA in phosphatidylethanolamine in comparison with infants fed breast milk or infant formula containing AA and DHA. Supplementing infant formula with increasing levels of AA and DHA produced a clear dose response in the levels of AA and DHA found in erythrocyte membrane phospholipids. From comparison of membrane phospholipid fatty acid composition it appears that a formula level of 0.32-1.1% AA and 0.24-0.76% DHA provides sufficient levels of these fatty acids to achieve a similar fatty acid composition to that of infants fed human milk for most of the lipid fractions examined.

ISSN:0031-3998    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

The dietary bioequivalence during the brain growth spurt ofα-linolenic (LNA) and docosahexaenoic acids (DHA) as substrates for brain and retinaln-3 fatty acid accretion is reported for the fetal baboons, whose mothers consumed a long chain polyunsaturate-free diet with an-6/n-3 ratio of 10:1. Pregnant baboons received i.v. doses of U-13C-labeled fatty acids (LNA or DHA), plasma was collected from mother and fetus, and fetal brain (occipital cortex), retina, and liver were analyzed at various times post-dose. Fetal brain DHA plateaued 15-35 d post-dose with 1.6% of the preformed [U-13C-]DHA dose recovered in the brain. In contrast, LNA-derived DHA accretion also plateaued but was 20-fold lower. Liver and retinal results were of the same order of magnitude, but showed evidence of peaks and decline. Conversion products ton-3 long chain polyunsaturate were observed in the maternal circulation at 1 h after administration, as was transfer of both fatty acids to the fetus. From these measurements we estimate that a dietary level of about 0.45% of energy as LNA is sufficient to meet the requirements of the growing fetal brain, whereas 0.03% of energy as DHA would suffice. These data are the first direct measurements of the bioequivalence of DHA and LNA in developing primates and imply thatn-3 fatty acid requirements for the developing fetal brain can be met by attainable dietary LNA for diets low in long chain polyunsaturates.

ISSN:0031-3998    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Mucosal damage is commonly observed in food-sensitive enteropathy in infants, and the generation of leukotrienes is involved in the pathogenesis of this enteropathy. Because supplementingn-3 fatty acids is known to modify the production of leukotrienes, we investigated whether a change of dietary fatty acid composition affects leukotriene synthesis and food hypersensitivity reactions in the intestine by using a mouse model of food-sensitive enteropathy. The model was prepared by feeding ovalbumin to BALB/c mice after intraperitoneal injection of cyclophosphamide. Diets were prepared from soybean oil (control), perilla oil, lard, corn oil, and 0.125 volume of corn oil (low fat diet) and given to mice for 4 wk. Villous heights, crypt depths, leukotriene B4and C4production in the intestine were measured. Crypt hyperplasia and villous atrophy were severer in the corn oil-fed group than those of control group, whereas mucosal damage in the perilla oil and low fat diet groups was minimal. In the corn oil-fed group, red blood cell membrane levels ofn-3 fatty acids were lower than the control, and the synthesis of leukotrienes was highest among all groups. In the perilla oil and low fat diet groups,n-6 fatty acids were lower than those of control group and leukotriene production was significantly suppressed. These results indicate that reducing cell membrane levels ofn-6 fatty acids by feeding lessn-6 fatty acids or supplementingn-3 fatty acids, is important to suppress leukotriene biosynthesis for prevention from mucosal damage in food-sensitive enteropathy.

ISSN:0031-3998    

出版商:OVID    

年代:1997

数据来源: OVID

摘要:

Biotinidase deficiency is an autosomal recessively inherited disorder that results in the inability to recycle the vitamin biotin. The disorder can cause neurologic and cutaneous abnormalities that can be treated effectively with pharmacologic doses of biotin. We identified 21 mutations that cause profound biotinidase deficiency in 37 symptomatic children (30 different probands and 7 siblings), as well as provide relevant biochemical and clinical information for each child. The two most common mutations (G98:d7i3 and R538C) were found in 31 of 60 alleles (52%), whereas the remainder of the alleles are accounted for by the 19 other unique mutations. Serum samples were available from 18 children, of these 11 had no detectable cross-reacting material (CRM) to antibody prepared against normal human serum biotinidase, three had reduced quantities of CRM and four had normal quantities of CRM in serum. All of these mutations result in complete absence of biotinyl-transferase activity in serum. Two polymorphisms were also identified in normal individuals. It is apparent that a child who inherits any of these mutations, either in the homozygous state or in combination, can develop the clinical features of the disorder if untreated. There are, however, no clear genotype/phenotype correlations that would allow for the prediction of the type, severity, or age of onset of symptoms.

ISSN:0031-3998    

出版商:OVID    

年代:1997

数据来源: OVID