Incidence of stroke in the diabetic compared with the non‐diabetic population: A systematic review protocol

People with diabetes have a largely increased risk of stroke compared with people without diabetes. Exact data on incidence of stroke in people with and without diabetes are important for improvements in preventive diabetes care, avoidance of fatal outcomes and as a solid basis for health policy and the economy. However, published data are conflicting, underlining the necessity for this systematic review of population‐based studies on incidence, relative risks (RRs) and changes in stroke rates over time. The purpose of our review is to evaluate the incidence of stroke in the diabetic population and its differences with regard to sex, ethnicity, age and regions; to compare the incidence rate (IR) in the diabetic and non‐diabetic populations and to investigate time trends. We will perform a systematic literature search in MEDLINE, Embase and LILACS designed by an experienced information scientist. Two review authors will independently screen the abstracts and full texts of all references on the basis of inclusion criteria regarding types of study, types of population and the main outcome. Data extraction and assessment of risk of bias will be undertaken by two review authors working independently. We will assess IR or cumulative incidence (CumI) and RR of stroke comparing the diabetic and non‐diabetic populations. The attributable risk (AR = proportion of stroke among persons with diabetes that is attributable to diabetes) and the population attributable risk (PAR = proportion of stroke in the whole population that is attributable to diabetes) will be considered where available. In conclusion, this review will help to summarize the available evidence for incidence of stroke in the diabetic and nondiabetic population. The publication of this protocol will contribute to making the search strategy, methods, and assessment of reviews transparent and accessible for all involved professional groups.     

Pathogenesis and treatment of hepatitis e virus infection

Hepatitis E has been considered to be a travel-associated, acute, self-limiting liver disease that causes fulminant hepatic failure in specific high-risk groups only. However, hepatitis E virus (HEV) infection can also be acquired in industrialized countries-HEV genotype 3 infection is a zoonosis, with pigs and rodents serving as animal reservoirs. In recent years, cases of chronic HEV infection that were associated with progressive liver disease have been described in several cohorts of immunocompromised individuals, including recipients of organ transplants. The topic of hepatitis E is therefore re-emerging and has raised the following important questions: what is the risk for HEV infection in Western countries (eg, from eating uncooked meat)? How frequently does chronic hepatitis E develop among human immunodeficiency virus-infected patients and recipients of organ transplants? What are the treatment options? What is the current status of vaccine development? What do we know about the pathogenesis of HEV infection, and why does it have a more severe course in pregnant women? This review summarizes the current knowledge on the pathogenesis and treatment of HEV infection.     

Hepatitis delta and HIV infection

Hepatitis delta is the most severe of all chronic viral infections of the liver. Its agent, the hepatitis delta virus (HDV), is unique in many aspects. Because of similar transmission pathways, triple infection with human immunodeficiency virus (HIV), hepatitis B virus (HBV), and HDV occurs frequently in intravenous drug users. The addition of HDV to an HIV/HBV coinfection is associated with a particularly aggressive course of liver disease, frequently leading to cirrhosis, decompensation, and death. Thus, screening for antibodies against HDV should be mandatory in all HBsAg-positive/HIV-positive patients. There is no specific treatment for HDV. The only therapeutic options currently available are long-duration interferon regimens, which are effective in <30% of the patients. Additionally, long-term treatment with HBV polymerase inhibitors as part of antiretroviral treatment may lower HBsAg- and HDV-ribonucleic acid levels in some patients. Early initiation of anti-HIV therapy seems to be reasonable in patients with hepatitis delta - even though controlled studies are not available.     

Primordium of an artificial Bruch’s membrane made of nanofibers for engineering of retinal pigment epithelium cell monolayers

Transplanted retinal pigment epithelium (RPE) cells hold promise for treatment of age-related macular degeneration (AMD) and Stargardt disease (SD), but it is conceivable that the degenerated host Bruch’s membrane (BM) as a natural substrate for RPE might not optimally support transplanted cell survival with correct cellular organization. We fabricated novel ultrathin three-dimensional (3-D) nanofibrous membranes from collagen type I and poly(lactic-co-glycolic acid) (PLGA) by an advanced clinical-grade needle-free electrospinning process. The nanofibrillar 3-D networks closely mimicked the fibrillar architecture of the native inner collagenous layer of human BM. Human RPE cells grown on our nanofibrous membranes bore a striking resemblance to native human RPE. They exhibited a correctly orientated monolayer with a polygonal cell shape and abundant sheet-like microvilli on their apical surfaces. RPE cells built tight junctions and expressed RPE65 protein. Flat 2-D PLGA film and cover glass as controls delivered inferior RPE layers. Our nanofibrous membranes may imitate the natural BM to such extent that they allow for the engineering of an in vivo-like human RPE monolayer that maintains the natural biofunctional characteristics. Such ultrathin membranes may provide a promising vehicle for a functional RPE cell monolayer implantation in the subretinal space in patients with AMD or SD.