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1.
QJM ; 112(1): 11-16, 2019 Jan 01.
Article in English | MEDLINE | ID: mdl-30295857

ABSTRACT

BACKGROUND: There were recurrent upsurges in demand for public hospital services in Hong Kong. An understanding of the contribution of some possible factors for the rise in health care burden would help to inform hospital management strategies. AIM: To evaluate the utilization patterns of hospitalizations in medical wards among public acute hospitals in Hong Kong during surge periods. DESIGN: Retrospective study. METHODS: By extracting the information in press releases between 2014 and 2018, descriptive statistics about medical ward occupancy situation during six surge periods were generated. A time series model was constructed to estimate the occupancy rate at each hospital and assess its relationship with the intensity of seasonal influenza activity, extreme weather, day of week and long holidays. RESULTS: There was a significant increase in the number of admissions to medical wards in all six surge periods. A significant variation in occupancy rate between weekdays and geographic regions was observed. The occupancy rate in 10, out of 15, hospitals was significantly associated with the influenza activity, while there was limited effect of weather on the occupancy rate. A significant holiday effect was observed during Christmas and Chinese New Year, resulting in a lower bed occupancy rate. CONCLUSIONS: A differential burden in public hospitals during surge periods was reported. Contingency bed and staff management shall be tailored to individual hospitals, given their differences in the determinants for inpatient bed occupancy.


Subject(s)
Bed Occupancy/statistics & numerical data , Hospitals, Public/statistics & numerical data , Inpatients/statistics & numerical data , Seasons , Bed Occupancy/trends , Geography , Health Services Needs and Demand , Holidays , Hong Kong , Humans , Influenza, Human/epidemiology , Regression Analysis , Retrospective Studies
2.
Neurobiol Dis ; 113: 11-22, 2018 05.
Article in English | MEDLINE | ID: mdl-29367010

ABSTRACT

Fragile X Syndrome (FXS) is the most common inherited cause of intellectual disability, and is the leading known single-gene cause of autism spectrum disorder. FXS patients display varied behavioural deficits that include mild to severe cognitive impairments in addition to mood disorders. Currently there is no cure for this condition, however minocycline is becoming commonly prescribed as a treatment for FXS patients. Minocycline has been reported to alleviate social behavioural deficits, and improve verbal functioning in patients with FXS; however, its mode of action is not well understood. Previously we have shown that FXS results in learning impairments that involve deficits in N-methyl-d-aspartate (NMDA) receptor-dependent synaptic plasticity in the hippocampal dentate gyrus (DG). Here we tested whether chronic treatment with minocycline can improve these deficits by enhancing NMDA receptor-dependent functional and structural plasticity in the DG. Minocycline treatment resulted in a significant enhancement in NMDA receptor function in the dentate granule cells. This was accompanied by an increase in PSD-95 and GluN2A and GluN2B subunits in hippocampal synaptoneurosome fractions. Minocycline treatment also enhanced dentate granule cell dendritic length and branching. In addition, our results show that chronic minocycline treatment can rescue performance in novel object recognition in FXS mice. These findings indicate that minocycline treatment has both structural and functional benefits for hippocampal cells, which may partly contribute to the pro-cognitive effects minocycline appears to have for treating FXS.


Subject(s)
Fragile X Mental Retardation Protein/physiology , Hippocampus/physiology , Memory/physiology , Minocycline/administration & dosage , Neurons/physiology , Receptors, N-Methyl-D-Aspartate/physiology , Animals , Drug Administration Schedule , Excitatory Postsynaptic Potentials/drug effects , Excitatory Postsynaptic Potentials/physiology , Hippocampus/drug effects , Hippocampus/pathology , Male , Memory/drug effects , Mice , Mice, Inbred C57BL , Mice, Knockout , Neurons/drug effects , Neurons/pathology , Organ Culture Techniques , Treatment Outcome
3.
Neurobiol Dis ; 96: 261-270, 2016 Dec.
Article in English | MEDLINE | ID: mdl-27659109

ABSTRACT

Fragile-X syndrome (FXS) is caused by the transcriptional repression of the Fmr1 gene resulting in loss of the Fragile-X mental retardation protein (FMRP). This leads to cognitive impairment in both male and female patients, however few studies have focused on the impact of FXS in females. Significant cognitive impairment has been reported in approximately 35% of women who exhibit a heterozygous Fmr1 gene mutation, however to date there is a paucity of information regarding the mechanistic underpinnings of these deficits. We, and others, have recently reported that there is significant impairment in N-methyl-d-aspartate receptor (NMDAR)-dependent long-term potentiation (LTP) and long-term depression (LTD) in the hippocampal dentate gyrus (DG) of male Fmr1 knock out mice. Here we examined if female mice displaying a heterozygous loss of the Fmr1 gene (Fmr1+/-) would exhibit similar impairments in DG-dependent spatial memory processing and NMDAR hypofunction. We found that Female Fmr1+/- mice did not show impaired metabotropic glutamate receptor (mGluR)-LTD in the CA1 region, and could perform well on a temporal ordering task that is thought to involve this brain region. In contrast, female Fmr1+/- mice showed impairments in a pattern separation task thought to involve the DG, and also displayed a significant impairment in both NMDAR-dependent LTD and LTP in this region. The LTP impairment could be rescued by administering the NMDAR co-agonist, glycine. Our data suggests that NMDAR hypofunction in the DG may partly contribute to learning and memory impairment in female Fmr1+/- mice. Targeting NMDAR-dependent mechanisms may offer hope as a new therapeutic approach for treating female FXS patients with learning and memory impairments.


Subject(s)
Dentate Gyrus/pathology , Fragile X Mental Retardation Protein/metabolism , Fragile X Syndrome/pathology , Neuronal Plasticity/genetics , Receptors, N-Methyl-D-Aspartate/metabolism , Animals , Disease Models, Animal , Estrous Cycle/drug effects , Estrous Cycle/genetics , Female , Fragile X Mental Retardation Protein/genetics , Fragile X Syndrome/drug therapy , Fragile X Syndrome/genetics , Genotype , Glycine/therapeutic use , Hindlimb Suspension , Male , Memory/drug effects , Memory/physiology , Mice , Mice, Inbred C57BL , Mice, Transgenic , Neuronal Plasticity/drug effects , Neuronal Plasticity/physiology , Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors , Spatial Behavior/drug effects , Spatial Behavior/physiology , Swimming/psychology , Valine/analogs & derivatives , Valine/pharmacology , Valine/therapeutic use
4.
Neuroscience ; 222: 289-301, 2012 Oct 11.
Article in English | MEDLINE | ID: mdl-22813995

ABSTRACT

Previous studies have shown that a 2-week treatment with 40 mg/kg corticosterone (CORT) in rats suppresses hippocampal neurogenesis and decreases hippocampal brain-derived neurotrophic factor (BDNF) levels and impairs spatial learning, all of which could be counteracted by voluntary wheel running. BDNF and insulin-like growth factor (IGF-1) have been suggested to mediate physical exercise-enhanced hippocampal neurogenesis and cognition. Here we examined whether such running-elicited benefits were accompanied by corresponding changes of peripheral BDNF and IGF-1 levels in a rat model of stress. We examined the effects of acute (5 days) and chronic (4 weeks) treatment with CORT and/or wheel running on (1) hippocampal cell proliferation, (2) spatial learning and memory and (3) plasma levels of BDNF and IGF-1. Acute CORT treatment improved spatial learning without altered cell proliferation compared to vehicle treatment. Acute CORT-treated non-runners showed an increased trend in plasma BDNF levels together with a significant increase in hippocampal BDNF levels. Acute running showed no effect on cognition, cell proliferation and peripheral BDNF and IGF-1 levels. Conversely, chronic CORT treatment in non-runners significantly impaired spatial learning and suppressed cell proliferation in association with a decreased trend in plasma BDNF level and a significant increase in hippocampal BDNF levels. Running counteracted cognitive deficit and restored hippocampal cell proliferation following chronic CORT treatment; but without corresponding changes in plasma BDNF and IGF-1 levels. The results suggest that the beneficial effects of acute stress on cognitive improvement may be mediated by BDNF-enhanced synaptic plasticity that is hippocampal cell proliferation-independent, whereas chronic stress may impair cognition by decreasing hippocampal cell proliferation and BDNF levels. Furthermore, the results indicate a trend in changes of plasma BDNF levels associated with a significant alteration in hippocampal levels, suggesting that treatment with running/CORT for 4 weeks may induce a change in central levels of hippocampal BDNF level, which may not lead to a significant change in peripheral levels.


Subject(s)
Cell Proliferation , Hippocampus/cytology , Learning/physiology , Memory/physiology , Nerve Growth Factors/blood , Running/psychology , Stress, Psychological/psychology , Animals , Body Weight/physiology , Brain-Derived Neurotrophic Factor/metabolism , Bromodeoxyuridine , Cell Differentiation/physiology , Fluorescent Antibody Technique , Hydrocortisone/metabolism , Immunohistochemistry , Insulin-Like Growth Factor I/metabolism , Male , Maze Learning/physiology , Organ Size/physiology , Physical Conditioning, Animal/physiology , Rats , Rats, Sprague-Dawley , Stress, Psychological/blood , Taste/drug effects , Taste/physiology
5.
J Hosp Infect ; 77(3): 252-6, 2011 Mar.
Article in English | MEDLINE | ID: mdl-21236516

ABSTRACT

N95 respirators are recommended by the World Health Organization (WHO) and the Centers for Disease Control and Prevention (CDC) to prevent the inhalation of droplets which may transmit respiratory pathogens. The reliability of N95 respirators in preventing transmission depends on their fit to the wearer. Quantitative fit testing (QNFT) is the gold standard used to determine this fit objectively. The manufacturers of the respirators also recommend performing a self-reported user-seal-check to detect for leakage. This study aims to investigate the capability of the user-seal-check in determining the fit of N95 respirators by investigating the sensitivity and specificity of the user-seal-check compared with QNFT. A prospective and cross-sectional research design was used. A total of 204 local Chinese undergraduate nursing students were recruited to test two commonly used respirator models (3M 1860S and 3M 1862). The results of the user-seal-check were compared with the results of the gold standard QNFT using the Condensation Nucleus Counter Fit Tester System. The sensitivity and specificity of the user-seal-check results obtained with the respirators were calculated. The results indicated low sensitivity, accuracy and predictive value of the user-seal-check in determining the fit of the N95 respirators. The user-seal-check was not found to be reliable as a substitute for QNFT. The results also suggested that the user-seal-check may be unreliable for detecting gross leakage. We recommend that QNFT is used to determine the fit of N95 respirators.


Subject(s)
Equipment Design , Equipment Failure Analysis/methods , Respiratory Protective Devices/standards , Adolescent , Cross-Sectional Studies , Equipment Failure , Equipment Failure Analysis/instrumentation , Face/anatomy & histology , Female , Humans , Male , Prospective Studies , Sensitivity and Specificity , Students, Nursing , Young Adult
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