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Background: The investigation of prevalence trends of metabolic cardiovascular risk factors is important for appropriate planning of future health programs aiming to prevent cardiovascular morbidity and mortality. In a previous study, we demonstrated an increase in the prevalence of type 2 diabetes (T2D) between 2000 and 2010 in Northeast Germany. The purpose of this study is to investigate prevalence trends of T2D treatment, dyslipidemia and hepatic steatosis in Northeast Germany., Methods: The baseline examinations of the first Study of Health in Pomerania (SHIP) project were carried out from 1997 to 2001 (SHIP-START-0, 4308 subjects). A second, independent random sample of the same region was enrolled between 2008 and 2012 (SHIP-TREND-0, 4420 subjects). All data were standardized with post-stratification weighting derived from the adult population of the German federal state of Mecklenburg-West Pomerania., Results: The prevalence of metformin intake increased from 2.1% to 4.1% and insulin use from 2.0% to 2.8%. While the prevalence of statin intake increased from 6.8% to 12.2%, the prevalence of dyslipidemia decreased slightly from 49.0% in SHIP-START-0 to 45.5% in SHIP-TREND-0. The prevalence of hepatic steatosis increased from 29.7% to 37.3%. This increase was most prominently observed in women and younger age groups., Conclusions: T2D, dyslipidemia and hepatic steatosis are common and increasing health problems among adults in Northeast Germany. Reassuring healthy diet and controlling obesity may result in prevention of above-mentioned health problems., (© The Author(s) 2024. Published by Oxford University Press on behalf of Faculty of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: The fractalkine/CX 3 C chemokine receptor 1 (CX 3 CR1) pathway has been identified to play an essential role in the chemotaxis of microglia, leukocyte trafficking and microglia/macrophage recruitment. It has also been shown to be important in the regulation of the inflammatory response in the early phase after experimental stroke. The present study was performed to investigate if CX 3 CR1 deficiency affects microglia during the first 14 days with consequences for tissue damage after experimental stroke., Results: CX3CR1 deficiency significantly increased the number of intersections of GFP positive microglia in the proximal peri-infarct area at 2, 7 and 14 days following tMCAO compared to heterozygous and wildtype littermates. In addition, the length of microglial branches increased until day 7 in CX 3 CR1 knockout mice while the presence of a functional CX3CR1 allele resulted in a gradual reduction of their length following tMCAO. After stroke, wildtype, heterozygous and CX3CR1 deficient mice did not show differences in the composite neuroscore and assessment of infarct volumes from CX3CR1 wildtype, heterozygous and deficient mice revealed no differences between the genotypes 7 and 14 days after stroke., Conclusion: Results demonstrate that CX3CR1 deficiency affects the morphology of GFP positive microglia located in the proximal peri-infarct region during the first 14 days after tMCAO. Our data also indicate that CX3CR1 deficiency does not affect definite infarct volumes. Modulation of the CX3CR1 pathway may have implication for microglia function contributing to mechanisms of tissue reorganization in the post-ischemic brain.

Background: One important aspect in combatting resistance to antibiotics is to increase the awareness and knowledge by epidemiological studies. We therefore conducted a German-wide point-prevalence survey for multidrug resistant bacterial organisms (MDROs) and Clostridium difficile (CD) to assess the epidemiology and structure quality of infection control in German hospitals., Method: 1550 hospitals were asked to participate and to report surveillance data on the prevalence of Methicillin-resistant and Vancomycin resistant Staphylococcus aureus (MRSA, VRSA/GRSA), Vancomycin resistant Enterococcus faecalis/faecium (VRE), multiresistant strains of Escherichia coli (EC), Klebsiella spp. (KS), Enterobacter spp. (ES), Acinetobacter spp. (AB) and Pseudomonas spp. (PS). as well as CD infections., Results: Surveys from 73,983 patients from 329 hospitals were eligible for analysis. MRSA was the most often reported pathogen (prevalence: 1.64 % [CI95: 1.46-1.82]), followed by 3 multidrug resistant EC (3MRGN-EC) (0.75 % [CI95: 0.60-0.89]), CD (0.74 % [CI95: 0.60-0.88]), VRE (0.25 % [CI95: 0.13-0.37]) und 3MRGN-KS (0.22 % [CI95: [0.15-0.29]). The majority of hospitals met the German recommendations for staffing with infection control personnel., Conclusion: The continuing increase in participating hospitals in this third survey in a row indicates a growing awareness to MDROs and our pragmatic approach. Our results confirm that MRSA, 3MRGN-EC, VRE and 3MRGN-KS remain the most prevalent MDROs in German hospitals.

Autoimmune type 1 diabetes (T1D) in humans and NOD mice results from interactions between multiple susceptibility genes (termed Idd) located within and outside the MHC. Despite sharing ∼88% of their genome with NOD mice, including the H2(g7) MHC haplotype and other important Idd genes, the closely related nonobese resistant (NOR) strain fails to develop T1D because of resistance alleles in residual genomic regions derived from C57BLKS mice mapping to chromosomes (Chr.) 1, 2, and 4. We previously produced a NOD background strain with a greatly decreased incidence of T1D as the result of a NOR-derived 44.31-Mb congenic region on distal Chr. 4 containing disease-resistance alleles that decrease the pathogenic activity of autoreactive B and CD4 T cells. In this study, a series of subcongenic strains for the NOR-derived Chr. 4 region was used to significantly refine genetic loci regulating diabetogenic B and CD4 T cell activity. Analyses of these subcongenic strains revealed the presence of at least two NOR-origin T1D resistance genes within this region. A 6.22-Mb region between rs13477999 and D4Mit32, not previously known to contain a locus affecting T1D susceptibility and now designated Idd25, was found to contain the main NOR gene(s) dampening diabetogenic B cell activity, with Ephb2 and/or Padi2 being strong candidates as the causal variants. Penetrance of this Idd25 effect was influenced by genes in surrounding regions controlling B cell responsiveness and anergy induction. Conversely, the gene(s) controlling pathogenic CD4 T cell activity was mapped to a more proximal 24.26-Mb region between the rs3674285 and D4Mit203 markers.