Dynamic cerebral autoregulation after intracerebral hemorrhage: A case-control study

<p>Abstract</p> <p>Background</p> <p>Dynamic cerebral autoregulation after intracerebral hemorrhage (ICH) remains poorly understood. We performed a case-control study to compare dynamic autoregulation between ICH patients and healthy controls.</p> <p>Methods</p> <p>Twenty-one patients (66 ± 15 years) with early (< 72 hours) lobar or basal ganglia ICH were prospectively studied and compared to twenty-three age-matched controls (65 ± 9 years). Continuous measures of mean flow velocity (MFV) in the middle cerebral artery and mean arterial blood pressure (MAP) were obtained over 5 min. Cerebrovascular resistance index (CVR_i) was calculated as the ratio of MAP to MFV. Dynamic cerebral autoregulation was assessed using transfer function analysis of spontaneous MAP and MFV oscillations in the low (0.03-0.15 Hz) and high (0.15-0.5 Hz) frequency ranges.</p> <p>Results</p> <p>The ICH group demonstrated higher CVR_icompared to controls (ipsilateral: 1.91 ± 1.01 mmHg·s·cm^-1, <it>p </it>= 0.04; contralateral: 2.01 ± 1.24 mmHg·s·cm^-1, <it>p </it>= 0.04; vs. control: 1.42 ± 0.45 mmHg·s·cm^-1). The ICH group had higher gains than controls in the low (ipsilateral: 1.33 ± 0.58%/mmHg, <it>p </it>= 0.0005; contralateral: 1.47 ± 0.98%/mmHg, <it>p </it>= 0.004; vs. control: 0.82 ± 0.30%/mmHg) and high (ipsilateral: 2.11 ± 1.31%/mmHg, <it>p </it>< 0.0001; contralateral: 2.14 ± 1.49%/mmHg, <it>p </it>< 0.0001; vs. control: 0.66 ± 0.26%/mmHg) frequency ranges. The ICH group also had higher coherence in the contralateral hemisphere than the control (ICH contralateral: 0.53 ± 0.38, <it>p </it>= 0.02; vs. control: 0.38 ± 0.15) in the high frequency range.</p> <p>Conclusions</p> <p>Patients with ICH had higher gains in a wide range of frequency ranges compared to controls. These findings suggest that dynamic cerebral autoregulation may be less effective in the early days after ICH. Further study is needed to determine the relationship between hematoma size and severity of autoregulation impairment.</p

Drive counts as a method of estimating ungulate density in forests: mission impossible?

Although drive counts are frequently used to estimate the size of deer populations in forests, little is known about how counting methods or the density and social organization of the deer species concerned influence the accuracy of the estimates obtained, and hence their suitability for informing management decisions. As these issues cannot readily be examined for real populations, we conducted a series of ‘virtual experiments’ in a computer simulation model to evaluate the effects of block size, proportion of forest counted, deer density, social aggregation and spatial auto-correlation on the accuracy of drive counts. Simulated populations of red and roe deer were generated on the basis of drive count data obtained from Polish commercial forests. For both deer species, count accuracy increased with increasing density, and decreased as the degree of aggregation, either demographic or spatial, within the population increased. However, the effect of density on accuracy was substantially greater than the effect of aggregation. Although improvements in accuracy could be made by reducing the size of counting blocks for low-density, aggregated populations, these were limited. Increasing the proportion of the forest counted led to greater improvements in accuracy, but the gains were limited compared with the increase in effort required. If it is necessary to estimate the deer population with a high degree of accuracy (e.g. within 10% of the true value), drive counts are likely to be inadequate whatever the deer density. However, if a lower level of accuracy (within 20% or more) is acceptable, our study suggests that at higher deer densities (more than ca. five to seven deer/100 ha) drive counts can provide reliable information on population size

Continuing versus stopping prestroke antihypertensive therapy in acute intracerebral hemorrhage: a subgroup analysis of the efficacy of nitric oxide in stroke trial

Background and purpose: More than 50% of patients with acute intracerebral haemorrhage (ICH) are taking antihypertensive drugs before ictus. Although antihypertensive therapy should be given long term for secondary prevention, whether to continue or stop such treatment during the acute phase of ICH remains unclear, a question that was addressed in the Efficacy of Nitric Oxide in Stroke (ENOS) trial. Methods: ENOS was an international multicenter, prospective, randomized, blinded endpoint trial. Among 629 patients with ICH and systolic blood pressure between 140 and 220 mmHg, 246 patients who were taking antihypertensive drugs were assigned to continue (n = 119) or to stop (n = 127) taking drugs temporarily for 7 days. The primary outcome was the modified Rankin Score at 90 days. Secondary outcomes included death, length of stay in hospital, discharge destination, activities of daily living, mood, cognition, and quality of life. Results: Blood pressure level (baseline 171/92 mmHg) fell in both groups but was significantly lower at 7 days in those patients assigned to continue antihypertensive drugs (difference 9.4/3.5 mmHg, P < .01). At 90 days, the primary outcome did not differ between the groups; the adjusted common odds ratio (OR) for worse outcome with continue versus stop drugs was .92 (95% confidence interval, .45- 1.89; P = .83). There was no difference between the treatment groups for any secondary outcome measure, or rates of death or serious adverse events. Conclusions: Among patients with acute ICH, immediate continuation of antihypertensive drugs during the first week did not reduce death or major disability in comparison to stopping treatment temporarily

Change in albuminuria as a surrogate endpoint for progression of kidney disease: a meta-analysis of treatment effects in randomised clinical trials

Background Change in albuminuria has strong biological plausibility as a surrogate endpoint for progression of chronic kidney disease, but empirical evidence to support its validity is lacking. We aimed to determine the association between treatment effects on early changes in albuminuria and treatment effects on clinical endpoints and surrograte endpoints, to inform the use of albuminuria as a surrogate endpoint in future randomised controlled trials. Methods In this meta-analysis, we searched PubMed for publications in English from Jan 1, 1946, to Dec 15, 2016, using search terms including “chronic kidney disease”, “chronic renal insufficiency”, “albuminuria”, “proteinuria”, and “randomized controlled trial”; key inclusion criteria were quantifiable measurements of albuminuria or proteinuria at baseline and within 12 months of follow-up and information on the incidence of end-stage kidney disease. We requested use of individual patient data from the authors of eligible studies. For all studies that the authors agreed to participate and that had sufficient data, we estimated treatment effects on 6-month change in albuminuria and the composite clinical endpoint of treated end-stage kidney disease, estimated glomerular filtration rate of less than 15 mL/min per 1·73 m2, or doubling of serum creatinine. We used a Bayesian mixed-effects meta-regression analysis to relate the treatment effects on albuminuria to those on the clinical endpoint across studies and developed a prediction model for the treatment effect on the clinical endpoint on the basis of the treatment effect on albuminuria. Findings We identified 41 eligible treatment comparisons from randomised trials (referred to as studies) that provided sufficient patient-level data on 29 979 participants (21 206 [71%] with diabetes). Over a median follow-up of 3·4 years (IQR 2·3–4·2), 3935 (13%) participants reached the composite clinical endpoint. Across all studies, with a meta-regression slope of 0·89 (95% Bayesian credible interval [BCI] 0·13–1·70), each 30% decrease in geometric mean albuminuria by the treatment relative to the control was associated with an average 27% lower hazard for the clinical endpoint (95% BCI 5–45%; median R2 0·47, 95% BCI 0·02–0·96). The association strengthened after restricting analyses to patients with baseline albuminuria of more than 30 mg/g (ie, 3·4 mg/mmol; R2 0·72, 0·05–0·99]). For future trials, the model predicts that treatments that decrease the geometric mean albuminuria to 0·7 (ie, 30% decrease in albuminuria) relative to the control will provide an average hazard ratio (HR) for the clinical endpoint of 0·68, and 95% of sufficiently large studies would have HRs between 0·47 and 0·95. Interpretation Our results support a role for change in albuminuria as a surrogate endpoint for the progression of chronic kidney disease, particularly in patients with high baseline albuminuria; for patients with low baseline levels of albuminuria this association is less certain

DNA-Sequence Variation Among Schistosoma mekongi Populations and Related Taxa; Phylogeography and the Current Distribution of Asian Schistosomiasis

Schistosomiasis is a disease caused by parasitic worms of the genus Schistosoma. In the lower Mekong river, schistosomiasis in humans is called Mekong schistosomiasis and is caused by Schistosoma mekongi. In the past, Mekong schistosomiasis was known only from the lower Mekong river. Here DNA-sequence variation is used to study the relationships and history of populations of S. mekongi. Populations from other rivers are compared and shown to be S. mekongi, thus confirming that this species is not restricted to only a small section of one river. The dates of divergence among populations are also estimated. Prior to this study it was assumed that S. mekongi originated in Yunnan, China, migrated southwards across Laos and into Cambodia, later becoming extinct in Laos (due to conditions unsuitable for transmission). In contrast, the dates estimated here indicate that S. mekongi entered Cambodia from Vietnam, 2.5–1 Ma. The pattern of genetic variation fits better with a more recent, and ongoing, northwards migration from Cambodia into Laos. The implications are that Mekong schistosomiasis is more widespread than once thought and that the human population at risk is up to 10 times greater than originally estimated. There is also an increased possibility of the spread of Mekong schistosomiasis across Laos