COVID-19 prevalence and mortality in longer-term care facilities

European Journal of Epidemiology - This essay considers the factors that have contributed to very high COVID-19 mortality in longer-term care facilities (LTCFs). We compare the demographic...     

Aortic root abscess--echocardiographic image

Autopsy findings point to a high prevalence of perivalvular abscesses in patients with infective endocarditis. Diagnosis of this complication, which may have therapeutical implications, is difficult. The authors present echocardiographic image obtained in a patient with bacterial endocarditis in whom an aortic root abscess was subsequently found at operation.     

Anti-VEGF agents confer survival advantages to tumor-bearing mice by improving cancer-associated systemic syndrome

The underlying mechanism by which anti-VEGF agents prolong cancer patient survival is poorly understood. We show that in a mouse tumor model, VEGF systemically impairs functions of multiple organs including those in the hematopoietic and endocrine systems, leading to early death. Anti-VEGF antibody, bevacizumab, and anti-VEGF receptor 2 (VEGFR-2), but not anti-VEGFR-1, reversed VEGF-induced cancer-associated systemic syndrome (CASS) and prevented death in tumor-bearing mice. Surprisingly, VEGFR2 blockage improved survival by rescuing mice from CASS without significantly compromising tumor growth, suggesting that “off-tumor” VEGF targets are more sensitive than the tumor vasculature to anti-VEGF drugs. Similarly, VEGF-induced CASS occurred in a spontaneous breast cancer mouse model overexpressing neu. Clinically, VEGF expression and CASS severity positively correlated in various human cancers. These findings define novel therapeutic targets of anti-VEGF agents and provide mechanistic insights into the action of this new class of clinically available anti-VEGF cancer drugs.     

Prestroke Mobility and Dementia as Predictors of Stroke Outcomes in Patients Over 65 Years of Age: A Cohort Study From The Swedish Dementia and Stroke Registries

Objectives

To explore the association between prestroke mobility dependency and dementia on functioning and mortality outcomes after stroke in patients>65 years of age.

Use of cardiopulmonary bypass decreases leukocyte count and activation of the complement system]

Platelet damage, complement activation and neutropenia during extracorporeal circulation are the result of blood contact with artificial surfaces, mainly in the oxygenator. To evaluate the biocompatibility of the ++auto-oxygenation technique of cardiopulmonary bypass (CPB) 2 techniques of extracorporeal circulation were compared in 40 patients undergoing elective coronary bypass surgery. Patients were studied in 2 groups, 20 patients in each: I (++auto-oxygenation --patients lungs used in CPB) and II (conventional technique of CPB with bubble oxygenator). Several blood samples were taken before, during and after perfusion to estimate pulmonary leukocytes sequestration in all patients and additionally complement C3a and C5a anaphylatoxins + were measured (radioimmunoassays) in 6 patients of each group. During cardiopulmonary bypass the decline in leukocyte number was observed in both groups, but leukocyte count was higher in group I then II, due to the transpulmonary leukocyte sequestration which was higher in group II. The difference between leukocytes count in group II was 1.46 +/- 0.5 x 10(3)/mm3 vs only 0.34 +/- 0.2 x 10(3)/mm3 in group I, p less than 0.001. In postoperative period an increase in circulating white blood cells was observed in both groups when compared to pre-bypass time, but the difference between groups was non significant. The level of C3a increased in group I from 244 +/- 46 ng/ml to 418 +/- 34 ng/ml, in group II from 268 +/- 46 ng/ml to 521 +/- 65 ng/ml, p less than 0.001, but in group I the levels were significantly lower, p less than 0.001. The current study confirms that cardiopulmonary bypass results in significant leukocyte and complement activation and supports the theoreticaly better biocompatibility of CPB with lung over oxygenator.     

Sex and gender differences in Alzheimer’s disease: current challenges and implications for clinical practice

Alzheimer’s disease (AD) is characterized by high heterogeneity in disease manifestation, progression and risk factors. High phenotypic variability is currently regarded as one of the largest hurdles in early diagnosis and in the design of clinical trials; there is therefore great interest in identifying factors driving variability that can be used for patient stratification. In addition to genetic and lifestyle factors, the individual’s sex and gender are emerging as crucial drivers of phenotypic variability. Evidence exists on sex and gender differences in the rate of cognitive deterioration and brain atrophy, and in the effect of risk factors as well as in the patterns of diagnostic biomarkers. Such evidence might be of high relevance and requires attention in clinical practice and clinical trials. However, sex and gender differences are currently seldom appreciated; importantly, consideration of sex and gender differences is not currently a focus in the design and analysis of clinical trials for AD. The objective of this position paper is (i) to provide an overview of known sex and gender differences that might have implications for clinical practice, (ii) to identify the most important knowledge gaps in the field (with a special regard to clinical trials) and (iii) to provide conclusions for future studies. This scientific statement is endorsed by the European Academy of Neurology.     

The −22c/t polymorphism in presenilin 1 gene is not connected with late-onset and early-onset familial Alzheimer’s disease in Poland

Summary. The –22c/t polymorphism in the promoter of the presenilin 1 gene is associated with increased risk for Alzheimers disease (AD) in some populations. It was shown that –22c allele is connected with two-fold decrease in promoter activity. We studied the impact of the polymorphism in groups of Polish late-onset and early-onset AD patients. Our results suggest that –22c/t polymorphism is not connected with AD in Polish population. The –22t allele showed a high degree of linkage disequilibrium with –2797 insertion of 13bp. An additional –2923g/t polymorphism is also not connected with –22c/t and is not a risk factor for AD.