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Background: As opposed to the decreasing overall rates of coronary heart disease (CHD) incidence and overall cardiovascular disease (CVD) mortality, heart failure (HF) and stroke incidence are increasing in young people, potentially due to rising rates of obesity and reduced cardiorespiratory fitness (CRF). Objectives: We investigated trends in early major CVD outcomes in a large cohort of young men. Methods: Successive cohorts of Swedish military conscripts from 1971 to 1995 (N = 1,258,432; mean age, 18.3 years) were followed, using data from the National Inpatient and Cause of Death registries. Cox proportional hazard models were used to analyse changes in 21‐year CVD event rates. Results: 21‐year CVD and all‐cause mortality and incidence of acute myocardial infarction (AMI) decreased progressively. Compared with the cohort conscripted in 1971–1975 (reference), the hazard ratios (HRs) for the last 1991–1995 cohort were 0.50 [95% confidence interval (CI) 0.42‐0.59] for CVD mortality; 0.57 (95% CI 0.54–0.60) for all‐cause mortality; and 0.63 (95% CI 0.53–0.75) for AMI. In contrast, the incidence of ischaemic stroke, intracerebral haemorrhage and HF increased with HRs of 1.43 (95% CI 1.17–1.75), 1.30 (95% CI 1.01–1.68) and 1.84 (95% CI 1.47–2.30), respectively. During the period, rates of obesity increased from 1.04% to 2.61%, whilst CRF scores decreased slightly. Adjustment for these factors influenced these secular trends only moderately. Conclusion: Secular trends of young‐onset CVD events demonstrated a marked shift from AMI and CVD mortality to HF and stroke incidence. Trends were significantly, though moderately, influenced by changing baseline BMI and CRF. [ABSTRACT FROM AUTHOR]

Abstract: Growth hormone (GH) and insulin-like growth factor I (IGF-I) increase cell genesis in several regions of the brains of GH-IGF-I-deficient hypophysectomized rats. However, it is not known to what degree GH treatment stimulates adult cell genesis in pituitary-intact rodents. We investigated the effect of peripheral administration of bovine growth hormone (bGH) on cellular proliferation in various regions of the brains of normal adult female rats. To monitor cell division, bromodeoxyuridine (BrdU) was administered daily for 5days. We studied the two areas of ongoing neurogenesis, the subventricular zone (SVZ) and the dentate gyrus (DG) of the hippocampus, as well as the corpus callosum, striatum, and the parietal and piriform cortices. After bGH treatment, the numbers of BrdU-positive cells increased 2.0- to 2.5-fold in all the brain regions, with the exception of the SVZ, in which there was no increase in the numbers of BrdU-positive cells. The present study shows for the first time that peripheral bGH administration increases the generation of new brain cells in normal adult female rats. Thus, bGH may stimulate cellular proliferation not only under GH-deficiency, but also under physiologic conditions. These findings have important implications for GH treatment strategies for patients who have normal or near-normal circulating levels of GH or IGF-I. [Copyright &y& Elsevier]

Background: The challenges of today’s society call for more knowledge about how to maintain all aspects of cognitive health, such as speed/attention, memory/learning, visuospatial ability, language, executive capacity and social cognition during the life course. Main text: Medical advances have improved treatments of numerous diseases, but the cognitive implications have not been sufficiently addressed. Disability induced by cognitive dysfunction is also a major issue in groups of patients not suffering from Alzheimer’s disease or related disorders. Recent studies indicate that several negative lifestyle factors can contribute to the development of cognitive impairment, but intervention and prevention strategies have not been implemented. Disability due to cognitive failure among the workforce has become a major challenge. Globally, the changing aging pyramid results in increased prevalence of cognitive disorders, and the diversity of cultures influences the expression, manifestation and consequences of cognitive dysfunction. Conclusions: Major tasks in the field of cognitive medicine are basic neuroscience research to uncover diverse disease mechanisms, determinations of the prevalence of cognitive dysfunction, health-economical evaluations, and intervention studies. Raising awareness for cognitive medicine as a clinical topic would also highlight the importance of specialized health care units for an integrative approach to the treatment of cognitive dysfunctions. [ABSTRACT FROM AUTHOR]

Cranial radiotherapy is common in pediatric oncology. Our purpose was to investigate if irradiation (IR) to the immature brain would increase the susceptibility to hypoxic-ischemic injury in adulthood. The left hemisphere of postnatal day 10 (P10) mice was irradiated with 8 Gy and subjected to hypoxia-ischemia (HI) on P60. Brain injury, neurogenesis and inflammation were evaluated 30 days after HI. IR alone caused significant hemispheric tissue loss, or lack of growth (2.8 +/- 0.42 mm(3), p < 0.001). Tissue loss after HI (18.2 +/- 5.8 mm(3), p < 0.05) was synergistically increased if preceded by IR (32.0 +/- 3.5 mm(3), p < 0.05). Infarct volume (5.1 +/- 1.6 mm(3)) nearly doubled if HI was preceded by IR (9.8 +/- 1.2 mm(3), p < 0.05). Pathological scoring revealed that IR aggravated hippocampal, cortical and striatal, but not thalamic, injury. Hippocampal neurogenesis decreased > 50% after IR but was unchanged by HI alone. The number of newly formed microglia was three times higher after IR + HI than after HI alone. In summary, IR to the immature brain produced long-lasting changes, including decreased hippocampal neurogenesis, subsequently rendering the adult brain more susceptible to HI, resulting in larger infarcts, increased hemispheric tissue loss and more inflammation than in non-irradiated brains.