Aims We quantified the concurring dynamics affecting total and hippocampal brain volume and cognitive function in patients with chronic heart failure (HF) over a period of three years. Methods and results A total of 148 patients with mild stable HF entered this monocentric prospective cohort study: mean age 64.5 (10.8) years; 16.2% female; 77% in New York Heart Association functional classes I–II; 128 and 105 patients attended follow-up visits after 1 and 3 years, respectively. The assessment included cardiological, neurological, psychological work-up, and brain magnetic resonance imaging. Total and regional brain volumes were quantified using an operator-independent fully automated approach and reported normalized to the mean estimated intracranial volume. At baseline, the mean hippocampal volume was ∼13% lower than expected. However, the 3-year progressive hippocampal volume loss was small: −62 mm3 [95% confidence interval (CI) −81 to −42, P < 0.0001). This corresponded to a relative change of −1.8% (95% CI −2.3 to −1.2), which was similar in magnitude as observed with physiological aging. Moreover, the load of white matter hypointensities increased within the limits of normal aging. Cognitive function during the 3-year observation period remained stable, with ‘intensity of attention’ as the only domain declining (LSmean −1.82 points, 95% CI −3.05 to −0.58, P = 0.004). After 3 years, performance in all domains of cognition remained associated with hippocampal volume (r ≥ 0.29). Conclusion In patients with predominantly mild HF, the markedly reduced hippocampal volume observed at baseline was associated with impaired cognitive function, but no accelerated deterioration in cognition and brain atrophy became evident over a mid-term period of three years.
Diseases caused by Rhizoctonia solani lead to significant reductions in peanut yields and quality throughout the world. A subset of accessions from the peanut germ plasm core collection plus the commercial cultivars Florunner, Southern Runner, Georgia Browne, and Georgia Green were evaluated for resistance to limb and seedling hypocotyl infections caused by R. solani. Georgia Green and core accessions 95 (PI 497351), 197 (PI 331326), 208 (PI 274193), 244 (PI 343361), 246 (PI 343398), and 524 (PI 288178) had levels of resistance comparable to Georgia Browne, the only commercial cultivar reported to have partial resistance to Rhizoctonia limb rot. Eleven core accessions, representing the full range of disease expression, and the commercial cultivars were evaluated in growth chambers to quantify their susceptibility to seedling hypocotyl infections and to determine if evaluating seedlings could serve as a primary screening method to identify potential sources of limb rot resistance. The most resistant core accessions to seedling hypocotyl infections were 234 (PI 159664) and 366 (PI 268968), and the most resistant commercial cultivar was Georgia Green. There was not a significant correlation between resistance to limb rot in the field and the severity of hypocotyl infections in growth chambers, indicating that resistance to hypocotyl infections is not a good indicator of resistance to Rhizoctonia limb rot.
The fungicide sensitivity of more than 450 isolates of Sclerotium rolfsii from 11 different peanut fields in Georgia was determined based on percent inhibition of mycelial growth on agar amended with tebuconazole, flutolanil, or PCNB. The 11 locations represented a wide geographic distribution and variety of exposure histories to tebuconazole, flutolanil, and PCNB. Most of the populations sampled were significantly more sensitive than the populations that had the longest exposure to the fungicides. Of the three fungicides tested, tebuconazole and flutolanil demonstrated the strongest positive correlation in 1994 and 1995. The differences in sensitivity among locations suggest that fungicide sensitivity among S. rolfsii populations varies across Georgia. The location with the longest exposure history had the lowest sensitivity to all three fungicides.
Background In acute ischemic stroke, cessation of blood flow causes immediate tissue necrosis within the center of the ischemic brain region accompanied by functional failure in the surrounding brain tissue designated the penumbra. The penumbra can be salvaged by timely thrombolysis/thrombectomy, the only available acute stroke treatment to date, but is progressively destroyed by the expansion of infarction. The underlying mechanisms of progressive infarction are not fully understood. Methods To address mechanisms, mice underwent filament occlusion of the middle cerebral artery (MCAO) for up to 4 h. Infarct development was compared between mice treated with antigen-binding fragments (Fab) against the platelet surface molecules GPIb (p0p/B Fab) or rat immunoglobulin G (IgG) Fab as control treatment. Moreover, Rag1−/− mice lacking T-cells underwent the same procedures. Infarct volumes as well as the local inflammatory response were determined during vessel occlusion. Results We show that blocking of the platelet adhesion receptor, glycoprotein (GP) Ibα in mice, delays cerebral infarct progression already during occlusion and thus before recanalization/reperfusion. This therapeutic effect was accompanied by decreased T-cell infiltration, particularly at the infarct border zone, which during occlusion is supplied by collateral blood flow. Accordingly, mice lacking T-cells were likewise protected from infarct progression under occlusion. Conclusions Progressive brain infarction can be delayed by blocking detrimental lymphocyte/platelet responses already during occlusion paving the way for ultra-early treatment strategies in hyper-acute stroke before recanalization.
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