Experience with a transfusion recipient education program about hepatitis C

Shortly after test kits for antibodies to the hepatitis C virus (HCV) were licensed in May of 1990, our medical community undertook a public education program encouraging previous transfusion recipients to see their physicians about the wisdom of being tested for anti-HCV. In response, 1034 samples were received for testing. All samples repeatably reactive (RR) with anti-HCV enzyme-linked immunoassay (EIA) were tested further with a research recombinant immunoblot assay (RIBA). Overall, 76 of the 1034 (7.4%) recipient samples were RR and 64 of these (84.2%) were reactive with RIBA. Recipients transfused prior to surrogate testing (alanine aminotransferase [ALT] and anti-hepatitis B core [anti-HBc]) in 1986 showed a 8.6 percent reactivity with RIBA and those transfused after surrogate testing showed a 4.8 percent reactivity, a 44 percent reduction. Of the 57 recipient samples reactive with RIBA and suitable for assay, 11 (19.3%) had an elevated ALT. Among 76 randomly selected blood donors with RR EIAs studied for comparison with recipients, 20 (26.3%) were reactive with RIBA, 9 of which had an abnormal surrogate test that would have disqualified them. ALT concentrations were abnormal in 6 (30%) of the donors who were reactive on RIBA. We conclude that an education program that encourages previous transfusion recipients to seek medical advice about anti-HCV testing is practical from the standpoint of the blood center. We believe more widespread implementation of similar programs should be considered.(ABSTRACT TRUNCATED AT 250 WORDS)     

Murine lymphoid procoagulant activity induced by bacterial lipopolysaccharide and immune complexes is a monocyte prothrombinase

Murine lymphoid cells respond rapidly to bacterial lipopolysaccharide or antigen-antibody complexes to initiate or accelerate the blood coagulation pathways. The monocyte or macrophage has been identified as the cellular source, although lymphocyte collaboration is required for the rapid induction of the procoagulant response. This procoagulant activity is identified in the present study as a direct prothrombin activator, i.e., a prothrombinase. Studies with plasmas deficient in single coagulation factors demonstrate that the induced murine procoagulant activity effector molecule does not require factors XII, VIII, VII, X, or V, but does require prothrombin to transform fibrinogen to fibrin. This enzyme(s) produces limited proteolysis of prothrombin to yield thrombin or thrombinlike products that are functionally capable of converting fibrinogen to fibrin. The prothrombinase is undetectable in freshly isolated Murine lymphoid cells respond rapidly to bacterial lipopolysaccharide or antigen-antibody complexes to initiate or accelerate the blood coagulation pathways. The monocyte or macrophage has been identified as the cellular source, although lymphocyte collaboration is required for the rapid induction of the procoagulant response. This procoagulant activity is identified in the present study as a direct prothrombin activator, i.e., a prothrombinase. Studies with plasmas deficient in single coagulation factors demonstrate that the induced murine procoagulant activity effector molecule does not require factors XII, VIII, VII, X, or V, but does require prothrombin to transform fibrinogen to fibrin. This enzyme(s) produces limited proteolysis of prothrombin to yield thrombin or thrombinlike products that are functionally capable of converting fibrinogen to fibrin. The prothrombinase is undetectable in freshly isolated     

Genome-wide association study with 1000 genomes imputation identifies signals for nine sex hormone-related phenotypes

Genetic factors contribute strongly to sex hormone levels, yet knowledge of the regulatory mechanisms remains incomplete. Genome-wide association studies (GWAS) have identified only a small number of loci associated with sex hormone levels, with several reproductive hormones yet to be assessed. The aim of the study was to identify novel genetic variants contributing to the regulation of sex hormones. We performed GWAS using genotypes imputed from the 1000 Genomes reference panel. The study used genotype and phenotype data from a UK twin register. We included 2913 individuals (up to 294 males) from the Twins UK study, excluding individuals receiving hormone treatment. Phenotypes were standardised for age, sex, BMI, stage of menstrual cycle and menopausal status. We tested 7 879 351 autosomal SNPs for association with levels of dehydroepiandrosterone sulphate (DHEAS), oestradiol, free androgen index (FAI), follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin, progesterone, sex hormone-binding globulin and testosterone. Eight independent genetic variants reached genome-wide significance (P<5 × 10⁻⁸), with minor allele frequencies of 1.3–23.9%. Novel signals included variants for progesterone (P=7.68 × 10⁻¹²), oestradiol (P=1.63 × 10⁻⁸) and FAI (P=1.50 × 10⁻⁸). A genetic variant near the FSHB gene was identified which influenced both FSH (P=1.74 × 10⁻⁸) and LH (P=3.94 × 10⁻⁹) levels. A separate locus on chromosome 7 was associated with both DHEAS (P=1.82 × 10⁻¹⁴) and progesterone (P=6.09 × 10⁻¹⁴). This study highlights loci that are relevant to reproductive function and suggests overlap in the genetic basis of hormone regulation.     

EFFECT OF SUBCLINICAL LEAD INTOXICATION ON LARYNGEAL CANCER

SUMMARY In this study we investigated the possible relationship of laryngeal cancer and subclinical lead intoxication, using the depression of aminolevulinic acid dehydratase (ALAD) activity in blood as indicator. Twenty-six patients with laryngeal cancer and 53 normal controls met the criteria to enter the study. Blood ALAD activity values in the patients with laryngeal cancer ranged from 27.1 to 75.3 U/l with a mean of 50.79 U/l. The respective values in the control group ranged from 36.2 to 98 U/l with a mean of 59.76 U/l. There was a statistically significant difference between the two means (0.001 <p<0.01), whereas blood lead concentrations in all patients were within normal limits. These findings support the hypothesis that low level lead intoxication (subclinical blood lead levels), from cars, industries and products, may contribute to the risk of laryngeal cancer. Further investigation is needed to clarify the exact relationship between lead and cancer of the larynx.     

Prevalence of antibody to Trypanosoma cruzi among blood donors in Los Angeles, California

Transfusion-associated Chagas' disease is a serious public health problem in Central and South America. With the recent influx of immigrants from Chagas' disease-endemic areas, concern about the risk of disease from blood transfusion has increased in the United States. To assess the prevalence of Trypanosoma cruzi infection in one area, 1024 consecutive blood donations from 988 voluntary blood donors at a medical center in Los Angeles County were screened serologically. The median age of donors screened was 32.5 years; 53.4 percent were male, and 38.4 percent were born in Chagas' disease-endemic countries. All donor sera were tested by complement fixation (CF) and indirect immunofluorescence (IIF) tests. A radioimmunoprecipitation assay (RIPA) was also done on all sera from CF- or IIF-reactive donors and an equal number of sera from nonreactive donors. A second serum specimen was obtained, and interviews were completed for 18 (67%) of 27 donors with an initial CF titer greater than or equal to 8 or an IIF titer greater than or equal to 64. The overall seroreactivity (by CF and IIF) was 1.1 percent (11/988). One donor (0.1%) had antibody specific to the 72- and 90-kDa antigens of T. cruzi on RIPA. Seven recipients of blood components from the seroreactive donors were located and were seronegative at 3 to 6 months. Seroreactive donors were 3.6 times more likely to have been born or to have resided in Mexico or Central America, 8.7 times more likely to have donated blood in the past, and 11.8 times more likely to have a history of malaria prophylaxis or treatment.     

Storage of human platelet concentrates in an artificial medium without dextrose

It was shown previously that human blood platelets stored in an artificial medium (PCD) for up to 5 days remain functional in vitro and have normal survival and recovery in vivo. This report demonstrates that the medium can be simplified further by the removal of dextrose, leaving for study a medium consisting simply of balanced salts and citrate anticoagulant (PC). Some dextrose, 3.2 mM, was present in the fresh PC platelet concentrates due to plasma carryover in the production of platelet concentrates, but this dextrose concentration was considerably less than the 22.6 to 25.5 mM present in platelet concentrates in PCD or plasma. Platelet count, pH, PCO2, and PO2, as well as platelet aggregation and release responses to stimulation, in vitro, were as well preserved in the PCD or PC media as in the plasma controls. In the PC medium, platelets consumed 2.5 mM dextrose over 5 days and left 0.7 mM dextrose. The same consumption of dextrose was noted in PCD platelet concentrates, while platelets in plasma metabolized twice as much dextrose and formed twice as much lactate. Thus, the rate of glycolysis in platelet concentrates was independent of the dextrose concentration in the medium, and the platelet functions were well preserved.     

护士对院内卒中识别和救治流程的知晓率及教学需求调查分析

目的     调查护士对院内卒中识别和救治的知晓率和教学需求,为针对性地制订培训内容和计划提供借鉴,以提高培训质量。     

Large numbers of primitive stem cells are active simultaneously in aggregated embryo chimeric mice

The possibility has been repeatedly raised that erythropoiesis results from clonal succession--the differentiation of one or a very small number of the most primitive stem cells that are sequentially activated to proliferate forming clones of differentiated cells and then eventually decline, to be replaced by new stem cell clones. We studied this possibility in chimeric mice made by combining embryos from two different strains so that they would have two distinct stem cell populations, each of which produces a different hemoglobin type (d and s). These were compared with F1 hybrids in which every stem cell produces both types. We measured the percentage of type d in seven to ten serial samples of circulating reticulocytes taken at three- to seven-day intervals and found that the variability in percent of this hemoglobin was only slightly higher in the chimeric mice than in F1 controls; SD ranged from 2.7% to 5.5% in the chimeric mice and from 3.4% to 3.9% in the controls. Using the binomial formula, the numbers of new clones formed during the reticulocyte life span, approximately three days, ranged from 33 to 118 in the individual chimeric mice. However, these numbers are underestimates because estimated numbers of clones depend inversely on variabilities, and the calculations did not exclude the contribution of experimental error to the overall variability. Total percentages of type d hemoglobin were also measured in seven to nine successive serial samples at 60- to 136-day intervals. These gave mean values similar to measures of newly synthesized hemoglobin in the same mice, but SD were larger, ranging from 5.3% to 8.4%. This reflects experimental error, both because of excess day-to- day variability found in this type of measurement and because there could not be fewer primitive stem cells activated to form clones of erythrocytes during the 45-day erythrocyte life span than during the three-day life span of reticulocytes. Since most and maybe all of the variation between successive samples in the same chimeric mouse appear to result from experimental error, many or even all of the primitive stem cells may simultaneously contribute to erythropoiesis.     

Demographic,clinical and microbiological characteristics of maternity patients: A Canadian clinical cohort study

OBJECTIVE:

To determine the demographic, clinical and microbiological characteristics of a representative Canadian obstetrical population.

DESIGN:

A one-year cohort study of all maternity patients who were followed to delivery, using detailed patient questionnaires containing more than 60 demographic and clinical variables, and three microbiological evaluations during gestation - first trimester, 26 to 30 weeks, and labour and delivery. Outcome measurements included birth weight and gestational age.

SETTING:

Labour and delivery suites of all office obstetrical practices affiliated with a single hospital.

POPULATION STUDIED:

A consecutive sample of pregnant women in the study practices during one year were eligible for enrolment; 2237 consecutive patients were approached for consent, 2047 enrolled and 1811 completed the study through delivery.

RESULTS:

The average patient was white, married and 29 years of age. Slightly more than half of the patients had postsecondary education, but 10% fell below the national poverty line for income. Frequency of factors linked to adverse pregnancy outcomes included cigarette smoking (19%), alcohol ingestion (18%), previously having had a premature infant (7%), and maternal diabetes (2%). Overall prevalence of genital microbes variously implicated in prematurity was 37% for ureaplasma, 11% for group B streptococcus and 4% for Mycoplasma hominis. Prevalence of bacterial vaginosis was 14%. The median gestational age for the cohort was 39 weeks, with 7% of infants born less than 37 weeks'' gestation. Mean birth weight was 3415 g.

CONCLUSIONS:

The present clinical cohort represents demographic and medical characteristics of the Canadian obstetrical population. The birth outcomes are consistent with national data. This database provides valuable information about a general obstetrical population that is managed by a universal health care system.Key Words: Genital tract infections, Prematurity, Risk factorsPremature birth (PB), defined as occurring at less than 37 weeks'' gestation, is the leading cause of perinatal mortality and morbidity in the industrialized world (1,2). Despite this recognition and advances in perinatal care, the prevalence of PB in the developed world has increased in recent years (3-6). The medical and economic impact of PB is appreciated specifically in the perinatal and/or neonatal periods, but also continues throughout life. Many factors, including socioeconomic, reproductive and medical conditions have been implicated in the etiology of PB (5,7). Infections have been increasingly recognized as important risk factors for PB (8-11). In some cases, such as with bacterial vaginosis, the stage of gestation during which infection occurs appears to be important in pregnancy outcome (12,13). However, results from several studies have been inconsistent and confounding risk factors have often not been assessed (10,14,15). Antibiotic treatment trials designed to eradicate infections to decrease the incidence of PB have yielded inconsistent results (14,16-21). The majority of studies on PB, carefully conducted and sometimes including large numbers of patients, have involved high risk obstetrical populations, and the results may not necessarily be extrapolated to general populations (1). The purpose of the present study was to evaluate a general obstetrical cohort population and to ultimately assess genital infections at various stages of pregnancy, including labour, in conjunction with other potential risk factors related to PB or low birth weight (less than 2500 g).     

Synergistic effects of butyrate on platelet responses to arachidonate, A23187, PGE1, and forskolin

With eukaryotic cells, butyrate is known to induce a series of morphological and biochemical changes that mimic cellular differentiation. With platelets, we have found that butyrate (10 mmol/L) caused an approximately threefold increase in sensitivity to calcium ionophore A23187 and arachidonate. Maximum aggregation was observed at agonist concentrations of 3 mumol/L and 170 mumol/L, respectively, as compared with required concentrations of 10 mumol/L and 400 mumol/L in the absence of butyrate. Similar effects were seen with isobutyric acid, and about one-half the effect was shown with valerate and caproate, but lower homologues showed no synergistic effect. No ultrastructural changes were observed in platelets incubated with butyrate, and the aggregation effects were reversible and returned to normal on removal of butyrate. Membrane fluidity was unchanged by butyrate as measured by changes in the fluorescence depolarization of diphenylhexatriene. Butyrate caused a 60% to 70% increase in the uptake of 3H-arachidonate. Butyrate also potentiated the inhibition of platelet function by prostaglandin E1 and forskolin and uptake of 3H- forskolin was increased approximately 20%. In contrast, platelet response to other agonists (ADP, epinephrine, collagen, thrombin, and platelet-activating factor) was essentially unaffected by butyrate. These results suggest that butyrate may increase the uptake of certain hydophobic agonists and antagonists by platelets. Similar mechanisms for uptake of endogenous effectors may explain the response of eukaryotic cells to butyrate in culture.