73 research outputs found

    Hepatitis B Sero-Prevalence and Risk Behaviors Among Immigrant Men in a Population-Based Household Survey in Low-Income Neighborhoods of Northern California

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    Background Despite an effective vaccine, 60,000 new HBV infections were reported in the US in 2004; 95% in adults. We evaluate HBV sero-prevalence, risk behaviors and self-reported vaccination among Latino immigrant, Asian immigrant and US born low income men in five northern California counties. Methods Population based, cross sectional survey of HBV sero-prevalence and risk behaviors in men aged 18 to 35 years. Results Among 1,512 men screened, Asian immigrants were most likely to have had prior HBV infection (15.1%) and chronic infection (3.8%) compared to US born (prior 5.1%, chronic 0.6%) and Latino immigrant men (prior 2.0%, chronic 0.3%.) Reported HBV vaccination was lowest for Latino immigrants (12%) compared to Asian immigrants and US born men (35% in both.) Latino immigrants reported less educational attainment, medical insurance coverage and access to a physician in the last six months. Discussion Healthcare providers should routinely screen Asian immigrants for HBV regardless of their self reported vaccination status. Latino immigrants may comprise an important group of under-vaccinated, at risk persons in California. HBV testing and vaccination of immigrants soon after US arrival should be encouraged

    Concurrent cisplatin, continuous infusion fluorouracil and radiotherapy followed by tailored consolidation treatment in non metastatic anal squamous cell carcinoma

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    BACKGROUND: To evaluate efficacy and feasibility of chemo-radiotherapy in patients with non-metastatic anal squamous-cell-cancer. METHODS: TNM staged anal squamous-cell cancer patients were treated with pelvic radiotherapy concomitant to continuous infusion fluorouracil plus cisplatin for at least 2 cycles. In T3-T4 or any T - N+ tumours or in "slow-responder" cases, 1-2 chemotherapy courses were subsequently administered. Tumour assessment was performed at baseline and 6-8 weeks after radiotherapy to evaluate response. RESULTS: 29 patients were enrolled: 4 males, 25 females; median age 57 years; baseline T1/T2/T3/T4 2/12/7/8; N involvement 17. Median dose pelvic radiotherapy was 59.4 Gy (range: 54-74). In 5 patients 2 chemotherapy courses, in 12 patients three and in 12 patients four courses were performed. At first evaluation, 27 CR (93.1%; 95% CI: 78% - 98%) and 2 SD were observed. Main grade (G) 3 toxic events were neutropenia (8%), diarrhoea (8%) and dermatitis (62%). Most frequent late events G3-G4 occurred in 14 patients: proctitis (5), dermatitis (4), bladder dysfunctions (2), sexual dysfunctions (9), lower extremity venous thromboses (2), dysuria (1), stenosis (1) and tenesmus (1). Five patients reported G1 leucopoenia. The rate of colostomy was 14%. After a median follow up of 42 months (range: 4-81), 20 patients are still alive without relapse and 3 died due to PD. The estimated 7-year DFS was 83.4% (C.I.: 68.3%-98.5%) and the estimated 7-year OS was 85.7% (C.I.: 70% - 100%). The 1-year and the estimated 7-year colostomy-free survivals were 85.9% (C.I.: 73.1% - 98.7%). CONCLUSIONS: Concurrent cisplatin plus fluorouracil and radiotherapy is associated with favourable local control rates and acute toxicity. Future investigations will be directed towards research into molecular biomarkers related to disease progression and resistance to chemo-radiotherapy and to the evaluation of new cytotoxic agents or targeted drugs, such as anti-epidermal growth factor receptor, concomitant to RT and to determining the role of intensity-modulated radiotherap

    Finishing the euchromatic sequence of the human genome

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    The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

    Characterization of the effect of pancreatic derived factor (PANDER) on hepatic regulation of glucose homeostasis

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    The liver is a critical organ for regulating blood glucose levels. During fasting, it produces glucose to supply fuel for tissues that utilize glucose exclusively for energy, and after ingestion of a meal, it clears and stores a significant portion of the ingested glucose in the form of glycogen. These hepatic processes are mediated by the actions of two pancreas-derived hormones, insulin and glucagon, the two main regulators of glucose homeostasis. However, the hepatic signaling pathways activated by these key hormones can be modulated by the presence of other circulating factors, including cytokines. Of potential interest is Pancreatic Derived factor, a novel cytokine-like molecule secreted from the endocrine pancreas but whose its biological function is currently unknown. Here we examine how PANDER regulates glucose homeostasis with a focus on hepatic glucose metabolism and we discuss the potential implications of its effect in promoting metabolic disease states. Employing adenoviral gene delivery, we demonstrate that PANDER overexpression induces elevated fasting glucose, insulin and corticosterone levels in mice. Additionally, PANDER overexpressing mice displayed impaired glucose tolerance but had no defects in glucose-stimulated insulin secretion or peripheral insulin sensitivity. Concomitantly, fasted, hyperglycemic PANDER overexpressers had elevated transcription of hepatic gluconeogenic enzymes, PEPCK and G6Pase. Next we examined the means by which PANDER promotes fasting hyperglycemia and found that treatment of primary hepatocytes with PANDER adenovirus elevated gluconeogenic gene expression and increased glucose output. Furthermore, PANDER increased levels of intracellular cAMP and serine-133 phosphorylated cAMP response element-binding protein (CREB) upon stimulation with adenylate cyclase and glucagon receptor agonists respectively, but no impairment in insulin signaling or action was observed. Further investigation into the association between PANDER and fasting hyperglycemia revealed that loss of PANDER protected mice on a HFD from developing severe fasting hyperglycemia. Collectively, these findings have identified a biological role for PANDER in hepatic glucose regulation. PANDER serves as a novel factor that acts counterregulatory to insulin to induce gluconeogenic gene expression and glucose output by amplifying hepatic cAMP and CREB signaling

    Characterization of the effect of pancreatic derived factor (PANDER) on hepatic regulation of glucose homeostasis

    No full text
    The liver is a critical organ for regulating blood glucose levels. During fasting, it produces glucose to supply fuel for tissues that utilize glucose exclusively for energy, and after ingestion of a meal, it clears and stores a significant portion of the ingested glucose in the form of glycogen. These hepatic processes are mediated by the actions of two pancreas-derived hormones, insulin and glucagon, the two main regulators of glucose homeostasis. However, the hepatic signaling pathways activated by these key hormones can be modulated by the presence of other circulating factors, including cytokines. Of potential interest is Pancreatic Derived factor, a novel cytokine-like molecule secreted from the endocrine pancreas but whose its biological function is currently unknown. Here we examine how PANDER regulates glucose homeostasis with a focus on hepatic glucose metabolism and we discuss the potential implications of its effect in promoting metabolic disease states. Employing adenoviral gene delivery, we demonstrate that PANDER overexpression induces elevated fasting glucose, insulin and corticosterone levels in mice. Additionally, PANDER overexpressing mice displayed impaired glucose tolerance but had no defects in glucose-stimulated insulin secretion or peripheral insulin sensitivity. Concomitantly, fasted, hyperglycemic PANDER overexpressers had elevated transcription of hepatic gluconeogenic enzymes, PEPCK and G6Pase. Next we examined the means by which PANDER promotes fasting hyperglycemia and found that treatment of primary hepatocytes with PANDER adenovirus elevated gluconeogenic gene expression and increased glucose output. Furthermore, PANDER increased levels of intracellular cAMP and serine-133 phosphorylated cAMP response element-binding protein (CREB) upon stimulation with adenylate cyclase and glucagon receptor agonists respectively, but no impairment in insulin signaling or action was observed. Further investigation into the association between PANDER and fasting hyperglycemia revealed that loss of PANDER protected mice on a HFD from developing severe fasting hyperglycemia. Collectively, these findings have identified a biological role for PANDER in hepatic glucose regulation. PANDER serves as a novel factor that acts counterregulatory to insulin to induce gluconeogenic gene expression and glucose output by amplifying hepatic cAMP and CREB signaling
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