[show abstract][hide abstract] ABSTRACT: BACKGROUND: Ethnic minority groups have higher prevalence of cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). We assessed general practitioners' (GPs') performance with respect to the pharmacological prevention of CVD in patients with T2DM from different ethnic backgrounds in Oslo. METHODS: Of 1653 T2DM patients cared for by 49 GPs in 2005, 380 had a diagnosis of CVD. Ethnicity was categorized as Norwegian, South Asian and other. Risk factor levels, medication use, achievement of treatment targets (HbA1c <= 7.5%, systolic blood pressure (SBP) <= 140 mmHg, total cholesterol/HDL-cholesterol < 4) and therapeutic intensity (number of drugs targeting each risk factor) were recorded. Chi-square, Wald tests and multiple linear regression analyses were used. RESULTS: Of the 1273 patients receiving primary prevention, 1.5% had their Hb1Ac, 4.8% SBP and 12.7% lipids levels above treatment thresholds without relevant prescriptions. Among patients on pharmacological therapy, 66% reached the HbA1c, 62% SBP and 62% lipid target. Proportions not achieving the HbA1c target were 26% in Norwegians, 38% in South Asians and 29% in others (p = 0.008). Proportions not achieving the SBP target were 42% in Norwegians, 22% in South Asians and 25% in others (p <= 0.001). Of those not achieving the HbA1c and SBP targets, 43% and 35% respectively, used only one agent.In secondary prevention, 0.8% of the patients had their HbA1c, 0.5% SBP and 7.4% lipid levels above treatment thresholds without relevant prescriptions. Among patients on pharmacological therapy, 65% reached the HbA1c, 64% SBP and 66% lipid target. Proportions not achieving the HbA1c target were 26% in Norwegians, 47% in South Asians and 40% in others (p = 0.03). Proportions not achieving the SBP target were 36% in Norwegians, 22% in South Asians and 56% in others (p = 0.050). Of those not achieving HbA1c and SBP targets, 49% and 21% respectively, were on mono-therapy. CONCLUSIONS: Norwegian GPs comply reasonably well with guidelines for pharmacological prevention of CVD in T2DM patients across ethnic groups. However, lipid-lowering therapy was generally underused, and the achievement of treatment targets for HbA1c in ethnic minorities and for BP in Norwegians could be improved.
BMC Health Services Research 05/2013; 13(1):182. · 1.77 Impact Factor
[show abstract][hide abstract] ABSTRACT: Influenza virus infection results in host cell death and major tissue damage. Specific components of the apoptotic pathway, a signaling cascade that ultimately leads to cell death, are implicated in promoting influenza virus replication. BAD is a cell death regulator that constitutes a critical control point in the intrinsic apoptosis pathway, which occurs through the dysregulation of mitochondrial outer membrane permeabilization and the subsequent activation of downstream apoptogenic factors. Here we report a novel pro-viral role for the pro-apoptotic protein BAD in influenza virus replication. We show that influenza virus-induced cytopathology and cell death are considerably inhibited in BAD knockdown cells and that both virus replication and viral protein production are dramatically reduced, which suggests that virus-induced apoptosis is BAD-dependent. Our data showed that influenza viruses induced phosphorylation of BAD at residues S112 and S136 in a temporal manner. Viral infection also induced BAD cleavage, late in the viral lifecycle, to a truncated form that is reportedly a more potent inducer of apoptosis. We further demonstrate that knockdown of BAD resulted in reduced cytochrome c release and suppression of the intrinsic apoptotic pathway during influenza virus replication, as seen by an inhibition of caspases-3, caspase-7 and PARP cleavage. Our data indicate that influenza viruses carefully modulate the activation of the apoptotic pathway that is dependent on the regulatory function of BAD, and failure of apoptosis activation resulted in unproductive viral replication.
[show abstract][hide abstract] ABSTRACT: The population in Norway has become multi-ethnic due to migration from Asia and Africa over the recent decades. The aim of the present study was to explore differences in the self-reported prevalence of cardiovascular disease (CVD) and associated risk factors by diabetes status in five ethnic minority groups compared to ethnic Norwegians.
Pooled data from three population-based cross-sectional studies conducted in Oslo between 2000 and 2002 was used. Of 54,473 invited individuals 24,749 (45.4%) participated. The participants self-reported health status, underwent a clinical examination and blood samples were drawn. A total of 17,854 individuals aged 30 to 61 years born in Norway, Sri-Lanka, Pakistan, Iran, Vietnam or Turkey were included in the study. Chi-square tests, one-way ANOVAs, ANCOVAs, multiple and logistic regression were used.
Age- and gender-standardized prevalence of self-reported CVD varied between 5.8% and 8.2% for the ethnic minority groups, compared to 2.9% among ethnic Norwegians (p < 0.001). Prevalence of self-reported diabetes varied from 3.0% to 15.0% for the ethnic minority groups versus 1.8% for ethnic Norwegians (p < 0.001). Among individuals without diabetes, the CVD prevalence was 6.0% versus 2.6% for ethnic minorities and Norwegians, respectively (p < 0.001). Corresponding CVD prevalence rates among individuals with diabetes were 15.3% vs. 12.6% (p = 0.364). For individuals without diabetes, the odds ratio (OR) for CVD in the ethnic minority groups remained significantly higher (range 1.5-2.6) than ethnic Norwegians (p < 0.05), after adjustment for age, gender, education, employment, and body height, except for Turkish individuals. Regardless of diabetes status, obesity and physical inactivity were prevalent in the majority of ethnic minority groups, whereas systolic- and diastolic- blood pressures were higher in Norwegians. In nearly all ethnic groups, individuals with diabetes had higher triglycerides, waist-to-hip ratio (WHR), and body mass index compared to individuals without diabetes. Age, diabetes, hypertension, hypercholesterolemia, and WHR were significant predictors of CVD in both ethnic Norwegians and ethnic minorities, but significant ethnic differences were found for age, diabetes, and hypercholesterolemia.
Ethnic differences in the prevalence of CVD were prominent for individuals without diabetes. Primary CVD prevention including identification of undiagnosed diabetes should be prioritized for ethnic minorities without known diabetes.
BMC Public Health 07/2011; 11:554. · 2.08 Impact Factor
[show abstract][hide abstract] ABSTRACT: In recent decades immigration to Norway from Asia, Africa and Eastern Europe has increased rapidly. The aim of this study was to assess the quality of care for type 2 diabetes mellitus (T2DM) patients from these ethnic minority groups compared with the care received by Norwegians.
In 2006, electronic medical record data were screened at 11 practices (49 GPs; 58857 patients). 1653 T2DM patients cared for in general practice were identified. Ethnicity was defined as self-reported country of birth. Chi-squared tests, one-way ANOVAs, multiple regression, linear mixed effect models and generalized linear mixed models were used.
Diabetes was diagnosed at a younger age in patients from the ethnic minority groups (South Asians (SA): mean age 44.9 years, Middle East/North Africa (MENA): 47.2 years, East Asians (EA): 52.0 years, others: 49.0 years) compared with Norwegians (59.7 years, p < 0.001). HbA1c, systolic blood pressure (SBP) and s-cholesterol were measured in >85% of patients in all groups with minor differences between minority groups and Norwegians. A greater proportion of the minority groups were prescribed hypoglycaemic medications compared with Norwegians (>or=79% vs. 72%, p < 0.001). After adjusting for age, gender, diabetes duration, practice and physician unit, HbA1c (geometric mean) for Norwegians was 6.9% compared to 7.3-7.5% in the minority groups (p < 0.05). The proportion with poor glycaemic control (HbA1c > 9%) was higher in minority groups (SA: 19.6%, MENA: 18.9% vs. Norwegians: 5.6%, p < 0.001. No significant ethnic differences were found in the proportions reaching the combined target: HbA1c <or= 7.5%, SBP <or= 140 mmHg, diastolic blood pressure (DBP) <or= 85 mmHg and total s-cholesterol <or=5.0 mmol/L (Norwegians: 25.5%, SA: 24.9%, MENA: 26.9%, EA: 26.1%, others:17.5%).
Mean age at the time of diagnosis of T2DM was 8-15 years younger in minority groups compared with Norwegians. Recording of important processes of care measures is high in all groups. Only one in four of most patient groups achieved all four treatment targets and prescribing habits may be sub-optimal. Patients from minority groups have worse glycaemic control than Norwegians which implies that it might be necessary to improve the guidelines to meet the needs of specific ethnic groups.
BMC Health Services Research 01/2010; 10:145. · 1.77 Impact Factor
[show abstract][hide abstract] ABSTRACT: Avian reoviruses (ARV) are less well understood than their mammalian counterparts. ARV are ubiquitous in commercial poultry and frequently isolated from acutely infected chickens. We previously described isolation of ARV temperature-sensitive (ts) mutants after nitrosoguanidine mutagenesis of wild-type ARV138, their assignment to 7 recombination groups (A-G), and genetic mapping of mutants in groups A-D to specific gene segments. For this study, wild-type serotype ARV176 was crossed with ts mutants tsE158 (Group E), tsF206 (Group F), or tsG247 (Group G) and reassortant progenies analyzed. Reassortant temperature-sensitivities were determined by efficiency of plating at permissive and non-permissive temperatures. Mapping results indicated tsE158, tsF206, and tsG247 mapped to the L1, S4, and L3 genes, respectively, which encode the lambdaA core shell, sigmaNS non-structural, and lambdaC core spike proteins, respectively. Specific amino acid substitutions in each mutant were determined and locations of structural protein alterations were placed within the 3-dimensional structure of homologous mammalian reovirus proteins. Mapping recombination groups E-G marks completion of gene assignments for all seven ts mutant groups previously generated.
[show abstract][hide abstract] ABSTRACT: We recently generated a new set of avian orthoreovirus (ARV) temperature-sensitive (ts) mutants after chemical mutagenesis of wild-type strain ARV138 and described mutants in the A recombination group. Here, each prototype ts mutant from ARV recombination groups B, C, and D was crossed with wild-type ARV strain 176 to generate reassortant clones that were used to map the ts lesions in the respective mutants. Reassortant clones were identified by comparison of segment mobility to parental markers in polyacrylamide gels. An efficiency of plating (EOP) value, which measures the capacity of a virus clone to grow under non-permissive conditions, was used to assign reassortant clones to either a ts group or non-ts group. Analysis of EOP values and parental origin of genome segments in the reassortant clones revealed that the group B lesion in tsB31 was located on the M2 genome segment; the group C lesion in tsC37 was on the S3 genome segment; and the group D lesion in tsD46 was on the L2 genome segment. The assignments of tsB31 and tsC37 were further confirmed by sequence analysis and amino acid substitutions in the corresponding muB and sigmaB proteins localized within the recently determined homologous mammalian reovirus mu1/sigma3 heterohexameric crystal structure.