672 research outputs found

    Voluntary wheel running reverses the decrease in subventricular zone neurogenesis caused by corticosterone

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    Adult neurogenesis within the dentate gyrus of the hippocampus can be increased by voluntary exercise but is suppressed under stress, such as with corticosterone (CORT). However, the effects of exercise and corticosterone on the cell proliferation of the other traditional neurogenic site, the subventricular zone (SVZ) have been reported with controversial results. In addition, the co-treatment effects of voluntary exercise and corticosterone have not been investigated. This study aims to determine whether corticosterone can suppress cell proliferation in the SVZ, and whether this can be reversed by voluntary exercise. In the present study, the effect of chronic (4 weeks) corticosterone treatment and wheel running simultaneously on the SVZ cell proliferation of adult Sprague-Dawley rats was examined. The results showed that cell proliferation indicated by bromodeoxyuridine (BrdU) was increased by voluntary wheel running whereas it was decreased by corticosterone treatment within the SVZ of the rats without running. For the rats with both corticosterone treatment and wheel running, it was found that the number of BrdU-labeled cells was approximately at the same level as the vehicle control group. Furthermore, these proliferating cells expressed doublecortin (DCX), a migrating neuroblast marker. Wheel running increased the percentage of BrdU-labeled cells expressing DCX in the SVZ whereas corticosterone treatment decreased this percentage. Thus, chronic injection of corticosterone can decrease the number of proliferating cells while wheel running can reverse the decrease in cell proliferation within the SVZ to normal levels. In addition, corticosterone can suppress the cell differentiation within the SVZ and this was alleviated by wheel running as indicated by the double-labeling of BrdU and DCX.published_or_final_versio

    Virologically confirmed population-based burden of hospitalization caused by influenza a and b among children in Hong Kong

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    Background. We sought to determine the virologically confirmed hospitalization rates associated with influenza virus infection among Hong Kong children. Methods. Patients <18 years of age who lived on Hong Kong Island (a separate island within Hong Kong) and were admitted to either of the only 2 public hospitals on the island for a febrile acute respiratory infection on 1 fixed day of the week in each hospital from October 2003 through September 2006 were prospectively recruited. These 2 hospitals together accounted for 72.5% of all general pediatric admissions in Hong Kong Island with a known population denominator. Nasopharyngeal aspirates were obtained from all recruited patients and were tested for influenza A and influenza B viruses by direct antigen detection and culture. Results. All cases of influenza A during 2003-2004 were caused by H3N2 virus, whereas 85.7% of cases during 2004-2005 were due to H3N2 virus, and 93.5% during 2005-2006 were due to H1N1 virus. During 2004-2005, infants <1 year of age had the highest rate of hospitalization for influenza A (103.8 cases per 10,000 population), whereas children 1 year of age had the highest rate of hospitalization during the other 2 seasons (95.5 and 54.6 cases per 10,000 population during 2003-2004 and 2005-2006, respectively). A protection rate of 25%, presumably attributable to maternal antibodies, was seen in infants <1 year of age who were hospitalized during 2003-2004 with infection due to an H3N2 virus that had been in circulation. The hospitalization rates for influenza B were highest among children 2-4 years of age. Conclusions. This population-based study of hospitalizations due to virologically confirmed influenza demonstrated a very high burden of disease among young children in Hong Kong. The morbidity varied with virus type, subtype, and antigenic variants. Β© 2009 by the Infectious Diseases Society of America. All rights reserved.published_or_final_versio

    Avoidance behaviors and negative psychological responses in the general population in the initial stage of the H1N1 pandemic in Hong Kong

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    <p>Abstract</p> <p>Background</p> <p>During the SARS pandemic in Hong Kong, panic and worry were prevalent in the community and the general public avoided staying in public areas. Such avoidance behaviors could greatly impact daily routines of the community and the local economy. This study examined the prevalence of the avoidance behaviors (i.e. avoiding going out, visiting crowded places and visiting hospitals) and negative psychological responses of the general population in Hong Kong at the initial stage of the H1N1 epidemic.</p> <p>Methods</p> <p>A sample of 999 respondents was recruited in a population-based survey. Using random telephone numbers, respondents completed a structured questionnaire by telephone interviews at the 'pre-community spread phase' of the H1N1 epidemic in Hong Kong.</p> <p>Results</p> <p>This study found that 76.5% of the respondents currently avoided going out or visiting crowded places or hospitals, whilst 15% felt much worried about contracting H1N1 and 6% showed signs of emotional distress. Females, older respondents, those having unconfirmed beliefs about modes of transmissions, and those feeling worried and emotionally distressed due to H1N1 outbreak were more likely than others to adopt some avoidance behaviors. Those who perceived high severity and susceptibility of getting H1N1 and doubted the adequacy of governmental preparedness were more likely than others to feel emotionally distressed.</p> <p>Conclusions</p> <p>The prevalence of avoidance behaviors was very high. Cognitions, including unconfirmed beliefs about modes of transmission, perceived severity and susceptibility were associated with some of the avoidance behaviors and emotional distress variables. Public health education should therefore provide clear messages to rectify relevant perceptions.</p

    Physicians Infrequently Adhere to Hepatitis Vaccination Guidelines for Chronic Liver Disease

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    Background and Goals:Hepatitis A (HAV) and hepatitis B (HBV) vaccination in patients with chronic liver disease is an accepted standard of care. We determined HAV and HBV vaccination rates in a tertiary care referral hepatology clinic and the impact of electronic health record (EHR)-based reminders on adherence to vaccination guidelines.Methods:We reviewed the records of 705 patients with chronic liver disease referred to our liver clinic in 2008 with at least two follow-up visits during the subsequent year. Demographics, referral source, etiology, and hepatitis serology were recorded. We determined whether eligible patients were offered vaccination and whether patients received vaccination. Barriers to vaccination were determined by a follow-up telephone interview.Results:HAV and HBV serologic testing prior to referral and at the liver clinic were performed in 14.5% and 17.7%; and 76.7% and 74% patients, respectively. Hepatologists recommended vaccination for HAV in 63% and for HBV in 59.7% of eligible patients. Patient demographics or disease etiology did not influence recommendation rates. Significant variability was observed in vaccination recommendation amongst individual providers (30-98.6%), which did not correlate with the number of patients seen by each physician. Vaccination recommendation rates were not different for Medicare patients with hepatitis C infection for whom a vaccination reminder was automatically generated by the EHR. Most patients who failed to get vaccination after recommendation offered no specific reason for noncompliance; insurance was a barrier in a minority.Conclusions:Hepatitis vaccination rates were suboptimal even in an academic, sub-speciality setting, with wide-variability in provider adherence to vaccination guidelines. Β© 2013 Thudi et al

    Hippocampal Neurogenesis and Dendritic Plasticity Support Running-Improved Spatial Learning and Depression-Like Behaviour in Stressed Rats

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    Exercise promotes hippocampal neurogenesis and dendritic plasticity while stress shows the opposite effects, suggesting a possible mechanism for exercise to counteract stress. Changes in hippocampal neurogenesis and dendritic modification occur simultaneously in rats with stress or exercise; however, it is unclear whether neurogenesis or dendritic remodeling has a greater impact on mediating the effect of exercise on stress since they have been separately examined. Here we examined hippocampal cell proliferation in runners treated with different doses (low: 30 mg/kg; moderate: 40 mg/kg; high: 50 mg/kg) of corticosterone (CORT) for 14 days. Water maze task and forced swim tests were applied to assess hippocampal-dependent learning and depression-like behaviour respectively the day after the treatment. Repeated CORT treatment resulted in a graded increase in depression-like behaviour and impaired spatial learning that is associated with decreased hippocampal cell proliferation and BDNF levels. Running reversed these effects in rats treated with low or moderate, but not high doses of CORT. Using 40 mg/kg CORT-treated rats, we further studied the role of neurogenesis and dendritic remodeling in mediating the effects of exercise on stress. Co-labelling with BrdU (thymidine analog) /doublecortin (immature neuronal marker) showed that running increased neuronal differentiation in vehicle- and CORT-treated rats. Running also increased dendritic length and spine density in CA3 pyramidal neurons in 40 mg/kg CORT-treated rats. Ablation of neurogenesis with Ara-c infusion diminished the effect of running on restoring spatial learning and decreasing depression-like behaviour in 40 mg/kg CORT-treated animals in spite of dendritic and spine enhancement. but not normal runners with enhanced dendritic length. The results indicate that both restored hippocampal neurogenesis and dendritic remodelling within the hippocampus are essential for running to counteract stress

    Isolated sixth cranial nerve palsy as the presenting symptom of a rapidly expanding ACTH positive pituitary adenoma: a case report

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    <p>Abstract</p> <p>Background</p> <p>Pituitary adenoma may present with neuro-ophthalmic manifestations and, typically, rapid tumor expansion is the result of apoplexy. Herein, we present the first case of an isolated sixth cranial nerve palsy as initial feature of a rapidly expanding ACTH positive silent tumor without apoplexy.</p> <p>Case Presentation</p> <p>A 44 year old female with a history of sarcoidosis presented with an isolated sixth cranial nerve palsy as the initial clinical feature of a rapidly expanding ACTH positive silent pituitary adenoma. The patient underwent emergent transsphenoidal hypophysectomy for this rapidly progressive tumor and subsequently regained complete vision and ocular motility. Despite tumor extension into the cavernous sinus, the other cranial nerves were spared during the initial presentation.</p> <p>Conclusions</p> <p>This case illustrates the need to consider a rapidly growing pituitary tumor as a possibility when presented with a rapidly progressive ophthalmoplegia.</p

    Expression of Telomerase and Telomere Length Are Unaffected by either Age or Limb Regeneration in Danio rerio

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    BACKGROUND:The zebrafish is an increasingly popular model for studying many aspects of biology. Recently, ztert, the zebrafish homolog of the mammalian telomerase gene has been cloned and sequenced. In contrast to humans, it has been shown that the zebrafish maintains telomerase activity for much of its adult life and has remarkable regenerative capacity. To date, there has been no longitudinal study to assess whether this retention of telomerase activity equates to the retention of chromosome telomere length through adulthood. METHODOLOGY/PRINCIPAL FINDINGS:We have systematically analyzed individual organs of zebrafish with regard to both telomere length and telomerase activity at various time points in its adult life. Heart, gills, kidney, spleen, liver, and intestine were evaluated at 3 months, 6 months, 9 months, and 2 years of age by Southern blot analysis. We found that telomeres do not appreciably shorten throughout the lifespan of the zebrafish in any organ. In addition, there was little difference in telomere lengths between organs. Even when cells were under the highest pressure to divide after fin-clipping experiments, telomere length was unaffected. All aged (2 year old) tissues examined also expressed active amounts of telomerase activity as assessed by TRAP assay. CONCLUSIONS/SIGNIFICANCE:In contrast to several other species including humans, the retention of lifelong telomerase and telomeres, as we have reported here, would be necessary in the zebrafish to maintain its tremendous regenerative capacity. The ongoing study of the zebrafish's ability to maintain telomerase activity may be helpful in unraveling the complexity involved in the maintenance (or lack thereof) of telomeres in other species such the mouse or human

    Gap Junctions and Epileptic Seizures – Two Sides of the Same Coin?

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    Electrical synapses (gap junctions) play a pivotal role in the synchronization of neuronal ensembles which also makes them likely agonists of pathological brain activity. Although large body of experimental data and theoretical considerations indicate that coupling neurons by electrical synapses promotes synchronous activity (and thus is potentially epileptogenic), some recent evidence questions the hypothesis of gap junctions being among purely epileptogenic factors. In particular, an expression of inter-neuronal gap junctions is often found to be higher after the experimentally induced seizures than before. Here we used a computational modeling approach to address the role of neuronal gap junctions in shaping the stability of a network to perturbations that are often associated with the onset of epileptic seizures. We show that under some circumstances, the addition of gap junctions can increase the dynamical stability of a network and thus suppress the collective electrical activity associated with seizures. This implies that the experimentally observed post-seizure additions of gap junctions could serve to prevent further escalations, suggesting furthermore that they are a consequence of an adaptive response of the neuronal network to the pathological activity. However, if the seizures are strong and persistent, our model predicts the existence of a critical tipping point after which additional gap junctions no longer suppress but strongly facilitate the escalation of epileptic seizures. Our results thus reveal a complex role of electrical coupling in relation to epileptiform events. Which dynamic scenario (seizure suppression or seizure escalation) is ultimately adopted by the network depends critically on the strength and duration of seizures, in turn emphasizing the importance of temporal and causal aspects when linking gap junctions with epilepsy

    The Flagellum of Pseudomonas aeruginosa Is Required for Resistance to Clearance by Surfactant Protein A

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    Surfactant protein A (SP-A) is an important lung innate immune protein that kills microbial pathogens by opsonization and membrane permeabilization. We investigated the basis of SP-A-mediated pulmonary clearance of Pseudomonas aeruginosa using genetically-engineered SP-A mice and a library of signature-tagged P. aeruginosa mutants. A mutant with an insertion into flgE, the gene that encodes flagellar hook protein, was preferentially cleared by the SP-A(+/+) mice, but survived in the SP-A(-/-) mice. Opsonization by SP-A did not play a role in flgE clearance. However, exposure to SP-A directly permeabilized and killed the flgE mutant, but not the wild-type parental strain. P. aeruginosa strains with mutation in other flagellar genes, as well as mucoid, nonmotile isolates from cystic fibrosis patients, were also permeabilized by SP-A. Provision of the wild-type fliC gene restored the resistance to SP-A-mediated membrane permeabilization in the fliC-deficient bacteria. In addition, non-mucoid, motile revertants of CF isolates reacquired resistance to SP-A-mediated membrane permeability. Resistance to SP-A was dependent on the presence of an intact flagellar structure, and independent of flagellar-dependent motility. We provide evidence that flagellar-deficient mutants harbor inadequate amounts of LPS required to resist membrane permeabilization by SP-A and cellular lysis by detergent targeting bacterial outer membranes. Thus, the flagellum of P. aeruginosa plays an indirect but important role resisting SP-A-mediated clearance and membrane permeabilization
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