Prevalence, incidence and associated factors for HBV infection among male and female prisoners in Central Brazil: A multicenter study.

BACKGROUND: Prison populations are at high risk for hepatitis B virus (HBV) infection. The aim of this study was to assess the prevalence, incidence, HBV associated factors and circulating genotypes/subtypes. METHODS: A total of 3,368 prisoners from 12 closed prisons were randomly recruited for a cross-sectional study. In addition, a cohort study was conducted 12 months later and included 1,656 individuals. Participants underwent an interview and blood collection for the detection of HBV serological markers and HBV-DNA phylogenetic analysis. RESULTS: HBV exposure (anti-HBc+) was 9.8% (95% CI: 8.8-10.8); 11.2% were female and 9.6% were male. HBsAg+ was 0.6%. Only 31.4% of the participants had HBV vaccination-like profile (anti-HBs+ alone; 30.4% male vs. 36.8% female; p=0.004). Most individuals were susceptible to HBV (60.2% female vs. 52.2% male, p=0.001). HBV isolates were classified as genotypes A (45.4%), D (27.3%) and F (27.3%). In males, HBV exposure was associated with increased age. Male prisoners had more evidence of HCV/HBV co-infection (10.7%) than females (3.4%) and the frequency of Treponema pallidum infection among prisoners who had been exposed to HBV was higher in female prisoners when compared with male (39.7% vs. 19.1%). The incidence of HBV was 0.18/100 person-years (95% CI: 0.12%-0.25%). CONCLUSIONS: Our results indicate a high prevalence of HBV exposure in prisoners. Despite the low incidence of this infection, the occurrence of new cases indicates the need to implement preventive measures.

Genome-wide expression profiling of mid-gestation placenta and embryo using a 15,000 mouse developmental cDNA microarray.

cDNA microarray technology has been increasingly used to monitor global gene expression patterns in various tissues and cell types. However, applications to mammalian development have been hampered by the lack of appropriate cDNA collections, particularly for early developmental stages. To overcome this problem, a PCR-based cDNA library construction method was used to derive 52,374 expressed sequence tags from pre- and peri-implantation embryos, embryonic day (E) 12.5 female gonad/mesonephros, and newborn ovary. From these cDNA collections, a microarray representing 15,264 unique genes (78% novel and 22% known) was assembled. In initial applications, the divergence of placental and embryonic gene expression profiles was assessed. At stage E12.5 of development, based on triplicate experiments, 720 genes (6.5%) displayed statistically significant differences in expression between placenta and embryo. Among 289 more highly expressed in placenta, 61 placenta-specific genes encoded, for example, a novel prolactin-like protein. The number of genes highly expressed (and frequently specific) for placenta has thereby been increased 5-fold over the total previously reported, illustrating the potential of the microarrays for tissue-specific gene discovery and analysis of mammalian developmental programs.

Spatio-temporal expression of Xenopus vasa homolog, XVLG1, in oocytes and embryos: the presence of XVLG1 RNA in somatic cells as well as germline cells.

The expression of Xenopus vasa homolog or XVLG1 was examined in oocytes and embryos by whole-mount in situ hybridization and reverse transcription polymerase chain reaction (RT-PCR). To confirm the results in embryos, both methods were also applied to explants of germ plasm-bearing cells (GPBC) from 32-cell embryos and to those of partial embryos deprived of GPBC. By hybridization, XVLG1 ribonucleic acid (RNA) was shown to be present throughout the cytoplasm in oocytes at stages I-III, except for the mitochondrial cloud. It was barely recognizable in a portion of germline cells of embryos at specific stages, notwithstanding that XVLG1 protein was present in those cells almost throughout their life-span. A weak signal for the RNA was detectable in some of the presumptive primordial germ cells (pPGC, descendants of GPBC from the gastrula stage onward) from the late gastrula (stage 12) to the hatching tadpole stage (stage 33/34), and in some of the PGC at stages 49-50. The results for pPGC were confirmed by the hybridization of explants of GPBC at equivalent stages in control embryos. In contrast, XVLG1 RNA was detected in certain somatic cells of embryos until stage 46. These observations were supported in part by the results of RT-PCR for embryos and explants. The possible role of the product of XVLG1 was reconsidered given its presence in both germline and somatic cells.

Involvement of the protein of Xenopus vasa homolog (Xenopus vasa-like gene 1, XVLG1) in the differentiation of primordial germ cells.

In order to understand the role of the protein of Xenopus vasa homolog (Xenopus vasa-like gene 1, XVLG1) in germ line cells, an attempt was made to perturb the function of the protein with the anti-vasa antibody 2L-13. The 2L-13 or the control antibody was microinjected with a lineage tracer (FITC-dextran-lysine, FDL) into single vegetal blastomeres containing the germ plasm of Xenopus 32-cell embryos, the descendants of which were destined to differentiate into a small number of primordial germ cells (PGC) and a large number of somatic cells, mostly of endodermal tissues at the tadpole stage. No significant effect of the injection of the antibodies on FDL-labeled, presumptive PGC (pPGC) was observed in embryos until stage 37/38. However, FDL-labeled PGC were not observed in almost all the 2L-13 antibody-injected tadpoles, although a similar number of labeled somatic cells were always present. As 2L-13 antibody specifically reacts with XVLG1 protein in the embryos by immunoblotting, the present results suggest that the antibody perturbed the function of XVLG1 protein in the pPGC, resulting in failure of PGC differentiation at the tadpole stage.

The cause of the decreased number of primordial germ cells in albino Xenopus resides not in the micro-environment but in the presumptive PGC.

The number of primordial germ cells (PGC) in albino tadpoles of Xenopus is significantly decreased as compared with that of the wild-type. Whether the decreased number of PGC is caused by the presumptive PGC (pPGC) themselves or the micro-environment surrounding those cells in the albino, or both was investigated in the present study. [3H]thymidine-labeled pPGC of wild-type and albino were implanted into unlabeled, host neurulae of wild-type or albino and wild-type, respectively. Labeled PGC in the genital ridges of experimental tadpoles were examined by autoradiography. There were no significant differences in the proportion of tadpoles with labeled PGC and in the average number of those PGC between the albino and wild-type tadpoles, into which wild-type pPGC had been implanted. The proportion in wild-type tadpoles with albino pPGC was much lower than that in wild-type tadpoles with wild-type pPGC. These results suggest that the pPGC of the albino and not the micro-environment are responsible for the decreased number of PGC.

In vitro effects of beta-carotene and vitamin A on peripartum bovine peripheral blood mononuclear cell proliferation.

The effects of beta-carotene, retinol, and retinoic acid on function of mononuclear cells during the peripartum period was assessed in vitro. Blood was collected from 14 Holstein cows on wk -4, -1, 0, 1, and 4 postpartum, and mononuclear cells were obtained by gradient centrifugation. Mononuclear cell proliferation induced by concanavalin A was measured in the presence of beta-carotene, retinol (1 x 10(-9) and 1 x 10(-8) M), and retinoic acid (1 x 10(-10) and 1 x 10(-9) M). Retinol and beta-carotene had no effect on spontaneous cell proliferation, whereas retinoic acid was suppressive. However, 1 x 10(-9) M beta-carotene enhanced concanavalin A-induced proliferation at wk -1, whereas 1 x 10(-8) M beta-carotene was suppressive at wk -4. Retinoic acid suppressed concanavalin A-induced proliferation at wk 0, but retinol had no effect. These results suggest a mechanism by which beta-carotene affords the mammary gland protection against infection immediately prepartum.

Beta-carotene and vitamin A effects on bovine phagocyte function in vitro during the peripartum period.

The effects of in vitro supplementation of beta-carotene, retinol, and retinoic acid on phagocyte function during the peripartum period were assessed. Blood was collected at wk -4, -1, 0 (calving), 1, and 4; mammary secretions were collected at wk -1, 0, 1, and 4 from 14 Holstein cows for the isolation of phagocytic cells. Blood polymorphonuclear leukocytes and mammary macrophages and polymorphonuclear leukocytes (phagocytic cells) were assayed for phagocytic and intracellular kill abilities of Staphylococcus aureus in the presence of beta-carotene and retinol at 10(-8) and 10(-7) M and retinoic acid at 10(-9) and 10(-8) M. Phagocytosis by blood or milk phagocytic cells was not influenced by beta-carotene. However, beta-carotene enhanced kill by blood and milk phagocytic cells during certain prepartum and post-partum periods. In contrast to beta-carotene, retinol and retinoic acid either had no effect or suppressed phagocytosis and kill. These results are interpreted to suggest a mechanism by which beta-carotene affords the mammary gland protection against infection, i.e., through enhanced intracellular kill by phagocytes.

Effect of dietary vitamin A and beta-carotene on polymorphonuclear leukocyte and lymphocyte function in dairy cows during the early dry period.

Vitamin A and beta-carotene improved mammary health in dairy cows around dry off. To define possible mechanisms, cows were fed 1) 53,000 IU vitamin A, 2) 213,000 IU vitamin A, or 3) 53,000 IU vitamin A plus 400 mg beta-carotene/cow per d (n = 10/treatment) from 6 wk before to 2 wk after dry off. Blood polymorphonuclear neutrophil function (phagocytosis, kill, and chemotaxis) and lymphocyte proliferation were measured at wk -6, 0 (dry off), and 2. Concentrations of vitamin A in serum did not differ across vitamin treatments. beta-Carotene in serum was elevated in cows fed beta-carotene. Treatment did not influence phagocytosis or kill. Kill ability increased after dry off in all treatment groups, but phagocytosis tended to decrease after dry off in cows fed vitamin A only. Lymphocyte blastogenesis stimulated by concanavalin A on wk 2 for cows fed 53,000 IU vitamin A but did not vary in the other two groups. Lipopolysaccharide-stimulated blastogenesis peaked at wk 0 and then decreased to pretreatment values by wk 2 in cows fed 213,000 IU vitamin A. These data indicate lymphocyte function is influenced by vitamin A supplementation and that beta-carotene supplementation seems to exert a stabilizing effect on neutrophil and lymphocyte function during the period around dry off.

Bovine vitamin A and beta-carotene intake and lactational status. 2. Responsiveness of mitogen-stimulated peripheral blood lymphocytes to vitamin A and beta-carotene challenge in vitro.

The interaction of dietary vitamin A and beta-carotene with lactational status on the in vitro proliferation of mitogen-induced peripheral blood lymphocytes was studied. Cows were fed (IU/cow per d) 1) 53,000 IU vitamin A, 2) 213,000 IU vitamin A, or 3) 53,000 IU vitamin A plus 400 mg beta-carotene from 6 wk before to 2 wk after dry off. Lymphocytes were incubated with retinol, retinoic acid, or beta-carotene. Concanavalin A-induced blastogenesis was inhibited by 10(-6) M retinol and 10(-8) M retinoic acid in cows fed 53,000 IU vitamin A before dry off. In contrast, 10(-7) M retinol and 10(-7) M retinoic acid stimulated Concanavalin A-induced blastogenesis for cows fed vitamin A plus beta-carotene before dry off. After dry off, retinol and retinoic acid did not affect Concanavalin A-induced blastogenesis in all treatment groups. In vitro, 10(-5) M beta-carotene inhibited Concanavalin A-induced blastogenesis before and after dry off in all treatment groups. Blastogenesis in the absence of mitogen stimulation or induced by lipopolysaccharide was inhibited by all vitamins before and after dry off in all treatment groups. These data indicate that vitamin A and beta-carotene supplementation interact with lactational status to influence the responsiveness of bovine blood lymphocytes to vitamin challenge in vitro.

Bovine vitamin A and beta-carotene intake and lactational status. 1. Responsiveness of peripheral blood polymorphonuclear leukocytes to vitamin A and beta-carotene challenge in vitro.

Dietary vitamin A and beta-carotene were assessed on their interaction with lactational status to influence neutrophil function in vitro. Cows were fed 1) 53,000 IU or 2) 213,000 IU vitamin A, or 3) 53,000 IU vitamin A plus 400 mg beta-carotene/cow per d from 6 wk before to 2 wk after dry off. Blood neutrophils were isolated the day of dry off and 2 wk after dry off and incubated with retinol, retinoic acid, or beta-carotene. Phagocytosis and kill of Staphylococcus aureus were measured. Across all treatments, kill was higher after dry off than before dry off. Phagocytosis tended to be lower after dry off than before in cows fed vitamin A only. In vitro, 10(-6) M beta-carotene stimulated phagocytosis after dry off and kill before dry off in cows fed vitamin A only. In general, retinol and retinoic acid suppressed phagocytosis but did not affect kill. Neutrophils from cows fed high amounts of vitamin A were more susceptible to in vitro suppression than those from cows fed adequate amounts of vitamin A. Therefore, vitamin A and beta-carotene supplementation interacts with lactational status to influence the responsiveness of bovine neutrophils to vitamin challenge in vitro.

In vitro growth inhibition of mastitis causing bacteria by phenolics and metal chelators.

Antimicrobial activities of three phenolic compounds and four metal chelators were tested at 0, 250, 500, and 1000 ppm in vitro against four major mastitis-causing bacteria, Streptococcus agalactiae, Staphylococcus aureus, Klebsiella pneumoniae, and Escherichia coli. Overall, butylated hydroxyanisole and tert-butylhydroquinone showed the greatest antimicrobial activity. These phenolics were bactericidal at 250 to 500 ppm against all four bacteria tested. The butylated hydroxytoluene was bactericidal against the gram-positive bacteria but was ineffective against the coliforms. At 250 ppm, disodium ethylenediaminetetraacetic acid was bactericidal against the gram-positive bacteria but much less effective against the gram-negatives. However, diethylenetriaminepentaacetic acid was more growth inhibitory than ethylenediaminetetraacetic acid against the gram-negative bacteria and especially against Escherichia coli. All other compounds were generally much less effective or ineffective against all four microorganisms. Therefore, butylated hydroxyanisole, butylated hydroxytoluene, tert-butylhydroquinone, ethylenediaminetetraacetic acid, and diethylenetriaminepentaacetic acid may have practical implications in the prevention or treatment of bovine mastitis.

Arginine infusion stimulates prolactin, growth hormone, insulin, and subsequent lactation in pregnant dairy cows.

L-Arginine or saline was administered intravenously by rapid infusion into 16 late-pregnant Holstein cows to study changes of prolactin, growth hormone, insulin, total protein, urea nitrogen, and subsequent lactation. Arginine was infused daily at .1 g/kg body weight starting about 7 days prior to predicted calving until calving. Blood was sampled via a jugular cannula at 0700, 0715, 0730 (infusion immediately followed 0730 h sample), 0745, 0815, 0845, 1100, 1300, 1500, 1700, and 1900 h. Arginine infusion evoked dramatic but transient increase of concentrations of blood serum prolactin, growth hormone, and insulin. Urea nitrogen also was elevated in blood serum but not total protein. The secretory response of prolactin, growth hormone, and insulin to daily arginine infusion during the entire prepartum period was not diminished. Milk production for the first 22 wk of lactation tended to be higher (by about 10%) for cows infused with arginine as compared to cows infused with saline. Therefore, repeated arginine infusion in late-pregnant cows dramatically increased prolactin, growth hormone, and insulin and tended to increase subsequent milk yield.