Disease burden caused by respiratory syncytial virus compared with influenza among adults: a retrospective cohort study from Eastern Finland in 2017-2018.

OBJECTIVES: Respiratory syncytial virus (RSV) is one of the most important causes of lower respiratory tract illnesses. In this study, we examined the number and severity of RSV infections among adult patients. The underlying diseases and background information of patients with RSV were examined and compared with the patients with influenza. DESIGN: Retrospective cohort study. SETTING: Patients receiving tertiary care services in Kuopio University Hospital (KUH) district in Eastern Finland. PARTICIPANTS: 725 patients (152 with RSV infection and 573 with influenza) treated in KUH between November 2017 and May 2018. PRIMARY AND SECONDARY OUTCOME MEASURES: Hospitalisation and mortality. RESULTS: Compared with influenza, RSV caused a more serious disease in terms of hospitalisation (84.2% vs 66.0%, p<0.001), incidence of pneumonia (37.5% vs 23.2%, p<0.001), need for antibiotics (67.1% vs 47.3%, p<0.001) and supplemental oxygen (50.7% vs 31.2%, p<0.001). The all-cause mortality during hospitalisation and 30 days after discharge was higher among the RSV-infected patients (8.6% vs 3.5%, p=0.010). Solid malignancies (23.1% vs 5.0%, p=0.042) and chronic kidney disease (30.8% vs 5.8%, p=0.011) were more common among the RSV-infected non-survivors compared with survivors. RSV was an independent risk factor for hospitalisation (adjusted OR (aOR) 2.035; 95% CI 1.17 to 3.55) and mortality (aOR 2.288; 95% CI 1.09 to 4.81) compared with influenza. CONCLUSIONS: Among all the screened patients, those with RSV infection were older and had more underlying conditions than patients with influenza. They had increased likelihood of hospitalisation and mortality when compared with influenza. Solid malignancies and chronic kidney disease seemed to be independent risk factors for death among RSV-infected patients. During RSV and influenza epidemics, it is important to test patients with respiratory symptoms for RSV and influenza to prevent the spread of the infections among elderly and chronically ill patients.

Dietary carbohydrate modification induces alterations in gene expression in abdominal subcutaneous adipose tissue in persons with the metabolic syndrome: the FUNGENUT Study.

BACKGROUND: Diets rich in whole-grain cereals and foods with a low glycemic index may protect against type 2 diabetes, but the underlying molecular mechanisms are unknown. OBJECTIVE: The main objective was to test whether 2 different carbohydrate modifications--a rye-pasta diet characterized by a low postprandial insulin response and an oat-wheat-potato diet characterized by a high postprandial insulin response--affect gene expression in subcutaneous adipose tissue (SAT) in persons with the metabolic syndrome. DESIGN: We assessed the effect of carbohydrate modification on SAT gene expression in 47 subjects [24 men and 23 women with a mean (+/-SD) age of 55 +/- 6 y] with the features of the metabolic syndrome in a parallel study design. The subjects had a mean (+/-SD) body mass index (kg/m(2)) of 32.1 +/- 3.8 and a 2-h plasma glucose concentration of 8.0 +/- 2.3 mmol/L. Adipose tissue biopsies were performed, and oral-glucose-tolerance tests and other biochemical measurements were conducted before and after the intervention. RESULTS: We detected 71 down-regulated genes in the rye-pasta group, including genes linked to insulin signaling and apoptosis. In contrast, the 12-wk oat-wheat-potato diet up-regulated 62 genes related to stress, cytokine-chemokine-mediated immunity, and the interleukin pathway. The insulinogenic index improved after the rye-pasta diet (P=0.004) but not after the oat-wheat-potato diet. Body weight was unchanged in both groups. CONCLUSIONS: Dietary carbohydrate modification with rye and pasta or oat, wheat, and potato differentially modulates the gene expression profile in abdominal subcutaneous adipose tissue, even in the absence of weight loss.

Aldose reductase gene polymorphisms and peripheral nerve function in patients with type 2 diabetes.

OBJECTIVE: We screened the human aldose reductase (ALR) gene for DNA sequence variants in type 2 diabetic and nondiabetic subjects and investigated whether the previously reported and novel polymorphisms were associated with neurophysiologic deterioration and clinical peripheral neuropathy. RESEARCH DESIGN AND METHODS: The study population included 85 Finnish type 2 diabetic and 126 nondiabetic subjects. The genetic analyses were performed using the PCR, single-strand conformation polymorphism, restriction fragment-length polymorphism, and automated laser fluorescence scanning analyses. A detailed neurologic examination and neurophysiologic analyses were performed at the time of diagnosis and at the 10-year examination. RESULTS: The genetic screening identified four polymorphisms: C-106T, C-11G, A11370G, and C19739A. The C and Z-2 alleles of the C-106T polymorphism and the previously reported (CA)(n) repeat marker were more frequent in type 2 diabetic subjects than in nondiabetic subjects. At baseline, the diabetic subjects with the T allele of the C-106T polymorphism had lower sensory response amplitude values in the peroneal (P = 0.025), sural (P = 0.007), and radial (P = 0.057) nerves and, during follow-up, a greater decrease in the conduction velocity of the motor peroneal nerve than those with the C-106C genotype. No associations were found between the polymorphisms examined and clinical polyneuropathy. CONCLUSIONS: The C-106T polymorphism of the ALR gene may contribute to an early development of neurophysiologic deterioration in type 2 diabetic patients.

A deletion in the alpha2B-adrenergic receptor gene and autonomic nervous function in central obesity.

OBJECTIVE: We investigated the impact of a three-amino acid deletion (12Glu9) polymorphism in the alpha(2B)-adrenergic receptor gene on autonomic nervous function. The short form (Glu(9)/Glu(9)) of the polymorphism has previously been associated with a reduced basal metabolic rate in obese subjects. Because autonomic nervous function participates in the regulation of energy metabolism, there could be a link between this polymorphism and autonomic nervous function. RESEARCH METHODS AND PROCEDURES: Data of a 10-year follow-up study with 126 nondiabetic control subjects and 84 type 2 diabetic patients were used to determine the effects of the 12Glu9 polymorphism on autonomic nervous function. A deep breathing test and an orthostatic test were used to investigate parasympathetic and sympathetic autonomic nervous function. In addition, cardiovascular autonomic function was studied using power spectral analysis of heart rate variability. RESULTS: No significant differences were found in the frequency of the 12Glu9 deletion polymorphism between nondiabetic and diabetic subjects. The nondiabetic men with the Glu(9)/Glu(9) genotype, especially those with abdominal obesity, had significantly lower total and low-frequency power values in the power spectral analysis when compared with other men. Furthermore, in a longitudinal analysis of 10 years, the decrease in parasympathetic function was greater in nondiabetic men with the Glu(9)/Glu(9) genotype than in the men with the Glu(9)/Glu(12) or Glu(12)/Glu(12) genotypes. DISCUSSION: The results of the present study suggest that the 12Glu9 polymorphism of the alpha(2B)-adrenergic receptor gene modulates autonomic nervous function in Finnish nondiabetic men. In the nondiabetic men with the Glu(9)/Glu(9) genotype, the general autonomic tone is depressed, and vagal activity especially becomes impaired with time. Furthermore, this association is accentuated by central obesity.