Medicine (RMH) - Research Publications
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ItemNo Preview AvailablePrevalence and risk factors for symptoms of common mental disorders in early and late pregnancy in Vietnamese women: A prospective population-based study(Elsevier, 2013-04-05)BACKGROUND: Little is known about the prevalence of and risk factors for common mental disorders (CMD) in pregnant women in low-income countries. The aim of this study was to establish the prevalence of and psychosocial risk factors for clinically significant symptoms of CMD in early and late pregnancy in women in rural Viet Nam. METHODS: A population-based sample of women was surveyed in early and late pregnancy. CMD were assessed by the Edinburgh Postnatal Depression Scale-Viet Nam Validation and psychosocial risks by study-specific structured interviews. RESULTS: In total 497/523 (97%) eligible women were recruited and 419 (84%) provided complete data. Prevalence of CMD only in early pregnancy was 22.4% (95% CI 18.4-26.4); only in late pregnancy was 10.7% (95% CI 7.8-13.7) and at both assessment waves was 17.4% (95% CI 13.8-21.1). Non-economic and economic coincidental life adversity, intimate partner violence, past pregnancy loss, and childhood abuse were positively associated with persistent antenatal CMD. Older age, having a preference for the baby's sex, and nulli- or primiparity were risk factors for CMD in early pregnancy. CONCLUSIONS: Persistent antenatal CMD are prevalent in rural areas of Viet Nam. Psychosocial risk factors play a major role in this significant public health problem.
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ItemRe-thinking the brain. new insights into early experience and brain development(Elsevier, 2013-08-18)The brain is a self-organizing system that adapts to its specific environment throughout pre- and postnatal life (Braun and Bock, 2011). Self-organization refers to the spontaneous formation of patterns and pattern change in open nonequilibrium systems. Edelman’s theory of neuronal group selection (Edelman, 1989) highlights this process. Groups of neurons are ‘selected’ or organized into groups or networks that are dynamically organized through epigenetic factors and experience. Developmental selection occurs largely before birth. Processes such as cell division, differentiation and programmed cell death and the mechanisms of neuronal migration are regulated by epigenetic factors. While genetics provides a general blueprint for neural development, the developmental processes are not precisely prespecified by genes, and produce unique patterns of neurons and neuronal groups in every brain. The result is a diverse pattern of connectivity forming primary repertoires of different neuronal groups. Structural diversity occurs through selective mechanical and chemical events regulated by cell and substrate adhesion molecules. A second process called experiential selection occurs postnatally through behavioural experience, resulting in modifications in the strength of synaptic connections, and creating diverse secondary repertoires. Finally, re-entrant signalling leads to the development of dynamic ‘maps’, an interconnected series of neuronal groups that independently receive inputs from the real world and create coherent perceptual constructs.
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ItemA Pilot Study on the use of Accelerometer Sensors for Monitoring Post Acute Stroke Patients(IEEE, 2013)The high incidence of stroke has raised a major concern among health professionals in recent years. Concerted efforts from medical and engineering communities are being exercised to tackle the problem at its early stage. In this direction, a pilot study to analyze and detect the affected arm of the stroke patient based on hand movements is presented. The premise is that the correlation of magnitude of the activities of the two arms vary significantly for stroke patients from controls. Further, the cross-correlation of right and left arms for three axes are differentiable for patients and controls. A total of 22 subjects (15 patients and 7 controls) were included in this study. An overall accuracy of 95.45% was obtained with sensitivity of 1 and specificity of 0.86 using correlation based method.
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ItemEndovascular stenting for atherosclerotic subclavian artery stenosis in patients with other craniocervical artery stenosis(SPRINGER, 2013-01)Atherosclerotic subclavian artery stenosis (SAS) accompanied with other craniocervical artery stenosis (OCAS) is not uncommon in practice. We sought to investigate the safety and efficacy of endovascular stenting for SAS in patients with OCAS. Between January 2004 and February 2012, 71 consecutive atherosclerotic SAS patients who underwent primary stenting in our medical center were included. The enrolled patients were divided into combined-SAS group (n = 51) and solitary-SAS group (n = 20) depending on the presence or absence of OCAS. Data of demographics, procedure, and the followed-up were retrieved and analyzed. The technical success rate was 95.8%; the clinical success rate was 90.1%. There was no catheter-related major stroke or death. The immediate outcomes had no statistical difference between groups. During a mean of 27 ± 20 months (range 2-88 months) followed-up, 7 (10.3%) restenosis and 12 (17.6%) clinical events were identified. The primary patency rate was 95.3, 84.9 and 84.9% at 12, 24 months, and final followed-up respectively, which had no statistical difference between groups (odds ratio (OR), 2.60; 95% confidence interval (CI), 0.54-12.53; P = 0.232). The overall clinical event-free survival rate was 93.5, 86.2 and 54.6%, respectively, where the result of combined-SAS group was inferior to that of the solitary-SAS group (OR, 3.34; 95% CI, 1.02-11.00; P = 0.047). Endovascular stenting was safe and feasible for atherosclerotic SAS in patients with OCAS, although the combined OCAS may have a significant influence on the long-term outcome. Further studies are warrant to investigate the effects of revascularization for multiple craniocervical artery stenoses on the cerebral hemodynamics and long-term outcomes.
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ItemFactors associated with long-term functional outcomes, psychological sequelae and quality of life in persons after primary brain tumour(SPRINGER, 2013-02)To examine factors impacting long-term functional outcomes and psychological sequelae in persons with primary brain tumours (BT) in an Australian community cohort. Participants (n = 106) following definitive treatment for BT in the community were reviewed in rehabilitation clinics to assess impact on participants' current activity and restriction in participation, using validated questionnaires: Functional Independence Measure (FIM), Perceived Impact Problem Profile (PIPP), Depression Anxiety Stress Scale, Cancer Rehabilitation Evaluation System-Short Form and Cancer Survivor Unmet Needs Measure. Mean age of the participants was 51 years (range 21-77 years), majority were female (56 %) with median time since BT diagnosis 2.1 years and a third (39 %) had high grade tumours. Majority showed good functional recovery (median motor FIM score 75). Over half reported pain (56 %), of which 42 % had headaches. Other impairments included: ataxia (44 %), seizures (43 %); paresis (37 %), cognitive dysfunction (36 %) and visual impairment (35 %). About 20 % reported high levels of depression, compared with only 13 % in an Australian normative sample. Two-third (60 %) participants reported highest impact on the PIPP subscales for psychological wellbeing (scores of >3 on 6-point scale) and participation (45 %). Factors significantly associated with poorer current level of functioning and wellbeing included: younger participants (≤40 years), recent diagnoses, aggressive tumour types and presence of pain. No significant differences in scale scores were found across various treatments (surgery, chemotherapy or radiotherapy) on outcomes used. Rehabilitation for BT survivors is challenging and requires long-term management of psychological sequelae impacting activity and participation. More research into participatory limitation is needed to guide treating clinicians.
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ItemAssociations Between Fibrocytes and Postcontrast Myocardial T1 Times in Hypertrophic Cardiomyopathy(WILEY, 2013-10)BACKGROUND: Fibrocytes are bone marrow-derived mesenchymal progenitors that have been linked to various fibrotic disorders. This study was undertaken to investigate whether fibrocytes are increased in diffuse myocardial fibrosis in humans. METHODS AND RESULTS: Thirty-seven patients with hypertrophic cardiomyopathy (HCM) and 20 healthy controls were recruited. Cardiac magnetic resonance imaging with postcontrast T1 mapping was performed to non-invasively quantify diffuse myocardial fibrosis and these patients were classified into 2 groups (T1 < 470 ms or T1 ≥ 470 ms, as likely or unlikely to have diffuse fibrosis, respectively). Circulating fibrocytes (CD45+/CD34+/collagen I+) were measured by flow cytometry. Peripheral blood mononuclear cells (PBMCs) were cultured for 13 days and fibrocytes were quantitated by flow cytometry (CD45+/collagen I+) and real-time PCR (gene expression of matrix proteins). Plasma cytokines/chemokines mediating fibrocyte trafficking and differentiation were measured by multiplex assays. Circulating fibrocytes were decreased in HCM patients compared to controls. The proportion of fibrocytes derived from PBMCs was increased in patients with diffuse fibrosis compared with those without or controls (31.1 ± 4.1% versus 18.9 ± 3.9% and 10.9 ± 2.0%, P < 0.05 and P < 0.001, respectively), and the proportion of fibrocytes was inversely correlated with T1 time (r = -0.37, P = 0.03). Plasma levels of stromal cell-derived factor-1 were elevated in patients with diffuse fibrosis compared with those without or controls (5131 ± 271 pg/mL versus 3893 ± 356 pg/mL and 4172 ± 185 pg/mL, respectively, both P < 0.05). CONCLUSIONS: HCM patients with diffuse fibrosis as assessed by postcontrast T1 mapping have elevated plasma SDF and an enhanced ability of PBMCs to differentiate into fibrocytes, suggesting that fibrocytes may contribute to the pathogenesis of myocardial fibrosis.
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ItemUrocortin protects chondrocytes from NO-induced apoptosis: a future therapy for osteoarthritis?(Springer Science and Business Media LLC, 2013-07-11)Osteoarthritis (OA) is characterized by a loss of joint mobility and pain resulting from progressive destruction and loss of articular cartilage secondary to chondrocyte death and/ or senescence. Certain stimuli including nitric oxide (NO) and the pro-inflammatory cytokine tumor necrosis factor α (TNF-α have been implicated in this chondrocyte death and the subsequent accelerated damage to cartilage. In this study, we demonstrate that a corticotrophin releasing factor (CRF) family peptide, urocortin (Ucn), is produced by a human chondrocyte cell line, C-20/A4, and acts both as an endogenous survival signal and as a cytoprotective agent reducing the induction of apoptosis by NO but not TNF-α when added exogenously. Furthermore, treatment with the NO donor S-nitroso-N-acetyl-D-L-penicillamine upregulates chondrocyte Ucn expression, whereas treatment with TNF-α does not. The chondroprotective effects of Ucn are abolished by both specific ligand depletion (with an anti-Ucn antibody) and by CRF receptor blockade with the pan-CRFR antagonist α-helical CRH(9-41). CRFR expression was confirmed by reverse transcription-PCR with subsequent amplicon sequence analysis and demonstrates that C-20/A4 cells express both CRFR1 and CRFR2, specifically CRFR1α and CRFR2β. Protein expression of these receptors was confirmed by western blotting. The presence of both Ucn and its receptors in these cells, coupled with the induction of Ucn by NO, suggests the existence of an endogenous autocrine/paracrine chondroprotective mechanism against stimuli inducing chondrocyte apoptosis via the intrinsic/mitochondrial pathway.
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ItemComparisons between intragastric and small intestinal delivery of enteral nutrition in the critically ill: a systematic review and meta-analysis(BMC, 2013)INTRODUCTION: The largest cohort of critically ill patients evaluating intragastric and small intestinal delivery of nutrients was recently reported. This systematic review included recent data to compare the effects of small bowel and intragastric delivery of enteral nutrients in adult critically ill patients. METHODS: This is a systematic review of all randomised controlled studies published between 1990 and March 2013 that reported the effects of the route of enteral feeding in the critically ill on clinically important outcomes. RESULTS: Data from 15 level-2 studies were included. Small bowel feeding was associated with a reduced risk of pneumonia (Relative Risk, RR, small intestinal vs. intragastric: 0.75 (95% confidence interval 0.60 to 0.93); P=0.01; I2=11%). The point estimate was similar when only studies using microbiological data were included. Duration of ventilation (weighted mean difference: -0.36 days (-2.02 to 1.30); P=0.65; I2=42%), length of ICU stay (WMD: 0.49 days, (-1.36 to 2.33); P=0.60; I2=81%) and mortality (RR 1.01 (0.83 to 1.24); P=0.92; I2=0%) were unaffected by the route of feeding. While data were limited, and there was substantial statistical heterogeneity, there was significantly improved nutrient intake via the small intestinal route (% goal rate received: 11% (5 to 16%); P=0.0004; I2=88%). CONCLUSIONS: Use of small intestinal feeding may improve nutritional intake and reduce the incidence of ICU-acquired pneumonia. In unselected critically ill patients other clinically important outcomes were unaffected by the site of the feeding tube.
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ItemFuture Directions for Intra-Arterial Therapy for Acute Ischaemic Stroke: Is There Life after Three Negative Randomized Controlled Studies?(KARGER, 2013)BACKGROUND: The three randomised controlled trials, Interventional Management of Stroke III (IMS3), Mechanical Retrieval and Revascularization of Stroke Clots Using Embolectomy (MR RESCUE) and Synthesis Expanasion: A Randomized Controlled Trial on Intra-Arterial Versus Intravenous Thrombolysis in Acute Ischaemic Stroke (SYNTHESIS EXP) showed no significant difference in clinical outcomes comparing intra-arterial (IA) therapy with intravenous thrombolysis. This article will explore the reasons for failure to show superiority of IA therapy. SUMMARY: There are many reasons for the disappointing results of the three randomised controlled trials. Opposing views on IA therapy exist. Critics argue that only a small percentage of patients will be eligible for IA therapy and that it will never be cost-effective. Additionally, current trials have failed to address superior recanalization rates of new generation devices and lack of patient selection by advanced imaging. Time-to-treatment is longer in these randomised controlled trials and stroke outcomes were worse than anticipated. The current randomised controlled trials also took long periods to complete. There is emerging evidence that general anesthetic negatively influences outcome. Next generation trials will attempt to address these issues. Key Messages: There are disparate explanations for the disappointing results from the three IA therapy randomized controlled studies. Poor recanalisation rates with first generation endovascular devices, lack of advanced neuroimaging to aid in patient selection, lack of data surrounding the use of general anaesthesia, and prolonged time-to-treatment are potential contributors to negative results. The new generation of trials has the potential of addressing these pressing issues.
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ItemNo Preview AvailableFine-Mapping the Genetic Association of the Major Histocompatibility Complex in Multiple Sclerosis: HLA and Non-HLA Effects(PUBLIC LIBRARY SCIENCE, 2013-11)The major histocompatibility complex (MHC) region is strongly associated with multiple sclerosis (MS) susceptibility. HLA-DRB1*15:01 has the strongest effect, and several other alleles have been reported at different levels of validation. Using SNP data from genome-wide studies, we imputed and tested classical alleles and amino acid polymorphisms in 8 classical human leukocyte antigen (HLA) genes in 5,091 cases and 9,595 controls. We identified 11 statistically independent effects overall: 6 HLA-DRB1 and one DPB1 alleles in class II, one HLA-A and two B alleles in class I, and one signal in a region spanning from MICB to LST1. This genomic segment does not contain any HLA class I or II genes and provides robust evidence for the involvement of a non-HLA risk allele within the MHC. Interestingly, this region contains the TNF gene, the cognate ligand of the well-validated TNFRSF1A MS susceptibility gene. The classical HLA effects can be explained to some extent by polymorphic amino acid positions in the peptide-binding grooves. This study dissects the independent effects in the MHC, a critical region for MS susceptibility that harbors multiple risk alleles.