Performance of hunting statistics as spatiotemporal density indices of moose (Alces alces) in Norway

Wildlife managers are often asking for reliable information of population density across larger spatial scales. In this study, we examined the spatiotemporal relationships between moose density as estimated by cohort analysis and the density indices (1) harvest density (HD; hunter kills per km2), (2) moose seen per unit effort (SPUE), seen moose density (SMD; seen moose per km2), and density of moosevehicle accidents (MVA density; e.g., traffic kills per km2) in 16 areas in Norway with 13–42 years of data. HD showed a close positive relationship with moose density both within and between regions. However, the temporal variation in HD was best explained as a delayed reflection of moose density and tended to overestimate its growth and decline. Conversely, SMD and SPUE were unable to predict the spatial variation in moose density with high precision, though both indices were relatively precise temporal reflectors of moose density. However, the SPUE tended to underestimate population growth, probably because of a decrease in searching efficiency with increasing moose density. Compared to the other indices, MVA density performed poor as an index of moose density within regions, and not at all among regions, but may, because of its independent source of data, be used to cross-check population trends suggested by other indices. Our study shows that the temporal trends in moose density can be surveyed over large areas by the use of cheap indices based on data collected by hunters and local managers, and supports the general assumption that the number of moose killed per km2 provides a precise and isometric index of the variation in moose density at the spatial scale of our study. cohort analysis; isometric index; management; monitoring; population reconstruction; precision; saturation; seen per unit effort (SPUE).Performance of hunting statistics as spatiotemporal density indices of moose (Alces alces) in NorwaypublishedVersio

Lower FEV1 in non-COPD, nonasthmatic subjects: association with smoking, annual decline in FEV1, total IgE levels, and TSLP genotypes

Few studies have investigated the significance of decreased FEV1 in non-COPD, nonasthmatic healthy subjects. We hypothesized that a lower FEV1 in these subjects is a potential marker of an increased susceptibility to obstructive lung disease such as asthma and COPD. This was a cross-sectional analysis of 1505 Japanese adults. We divided the population of healthy adults with no respiratory diseases whose FEV1/FVC ratio was ≥70% (n = 1369) into 2 groups according to their prebronchodilator FEV1 (% predicted) measurements: <80% (n = 217) and ≥80% (n = 1152). We compared clinical data – including gender, age, smoking habits, total IgE levels, and annual decline of FEV1 – between these 2 groups. In addition, as our group recently found that TSLP variants are associated with asthma and reduced lung function, we assessed whether TSLP single nucleotide polymorphisms (SNPs) were associated with baseline lung function in non-COPD, nonasthmatic healthy subjects (n = 1368). Although about half of the subjects with lower FEV1 had never smoked, smoking was the main risk factor for the decreased FEV1 in non-COPD, nonasthmatic subjects. However, the subjects with lower FEV1 had a significantly higher annual decline in FEV1 independent of smoking status. Airflow obstruction was associated with increased levels of total serum IgE (P = 0.029) and with 2 functional TSLP SNPs (corrected P = 0.027–0.058 for FEV1% predicted, corrected P = 0.015–0.033 for FEV1/FVC). This study highlights the importance of early recognition of a decreased FEV1 in healthy subjects without evident pulmonary diseases because it predicts a rapid decline in FEV1 irrespective of smoking status. Our series of studies identified TSLP variants as a potential susceptibility locus to asthma and to lower lung function in non-COPD, nonasthmatic healthy subjects, which may support the contention that genetic determinants of lung function influence susceptibility to asthma

The development of carbonate-containing apatite/collagen composite for osteoconductive apical barrier material.

The current report describes the properties of a new apical barrier material formulated from carbonate-containing apatite (CAp) and collagen. CAp particles of around 50 nm were deposited on reconstituted collagen fibers. CAp/col with about 60 wt % CAp (corresponding to apatite content of bone) was obtained after 1 day of calcification. CAp content increased up to about 80 wt % in a 15-day calcification reaction. CAp/col was composed of fine calcified collagen fibers. The crystallinity and Ca/PO(4) ratio of CAp were comparable to those of bone apatite. The mixture of CAp/col and saline reached a pH of about 9. The optimum powder-to-liquid ratio (P/L) to set into a root canal was determined to be 1.2. Furthermore, the mixture (P/L = 1.2) condensed in a root canal was liquid permeable. Thus, the CAp/col was expected as an apical barrier material with osteoconductivity.The current report describes the properties of a new apical barrier material formulated from carbonate-containing apatite (CAp) and collagen. CAp particles of around 50 nm were deposited on reconstituted collagen fibers. CAp/col with about 60 wt % CAp (corresponding to apatite content of bone) was obtained after 1 day of calcification. CAp content increased up to about 80 wt % in a 15-day calcification reaction. CAp/col was composed of fine calcified collagen fibers. The crystallinity and Ca/PO(4) ratio of CAp were comparable to those of bone apatite. The mixture of CAp/col and saline reached a pH of about 9. The optimum powder-to-liquid ratio (P/L) to set into a root canal was determined to be 1.2. Furthermore, the mixture (P/L = 1.2) condensed in a root canal was liquid permeable. Thus, the CAp/col was expected as an apical barrier material with osteoconductivity

Spontaneous remission in children with IgA nephropathy

Abstract Background Some patients with IgA nephropathy (IgAN) achieve spontaneous remission even when not receiving medication. However, details on such remissions remain unknown. The aim of our study was to clarify this information in the clinical setting of childhood IgAN with minor glomerular abnormalities or focal mesangial proliferation (MGA/FMP). Methods This study was a retrospective analysis of 96 children with MGA/FMP who did not receive medication from among the 555 patients with newly diagnosed childhood IgAN treated between January 1972 and December 2000. The Kaplan-Meier method and Cox proportional hazard model were used for the analysis. Results Of the 96 pediatric patients who did not receive medication, 57 (59.4 %) achieved spontaneous remission. The cumulative spontaneous remission rates among these patients were 57.5 and 77.4 % at 5 and 10 years, respectively, from onset. The mean time from onset to remission was 5.9±0.4 years. Clinical and histological findings were similar between the remission and non-remission groups. Of the 57 patients with spontaneous remissions, ten (17.5 %) also developed a recurrence of urinary abnormalities. The cumulative recurrence-free rates were 79.9 and 67.9 % at 5 and 10 years, respectively, after remission. Conclusions The spontaneous remission rate in childhood IgAN with MGA/FMP was higher than expected. Our results suggest that physicians should consider the potential for spontaneous remission and refrain from very aggressive treatment in IgAN patients with MGA/FMP

Genetic association of the functional CDHR3 genotype with early-onset adult asthma in Japanese populations

BackgroundRecent studies have demonstrated that a coding SNP (rs6967330, Cys529→Tyr) in cadherin-related family member 3 (CDHR3), which was previously associated with wheezing illness and hospitalizations in infancy, could support efficient human rhinovirus C (RV-C) entry and replication. Here, we sought to examine the genetic contribution of this variant to the development of adult asthma.MethodsWe performed a candidate gene case–control association study of 2 independent Japanese populations (a total of 3366 adults). The odds ratios (ORs) for association of the A allele at rs6967330 with adult asthma were calculated according to age at onset of asthma. In addition, the effect of the CDHR3 genotype on the development of specific asthma phenotypes was examined.ResultsThe A allele was associated with asthma (OR = 1.56; Mantel–Haenszel p = 0.0040) when the analysis was limited to patients with early-onset adult asthma. In addition, when the analysis was limited to atopic individuals, a stronger association of the CDHR3 variant with early-onset asthma was found, and interaction of the CDHR3 genotype with atopy was demonstrated. Finally, a significant association of this variant was specifically found with a phenotype of asthma characterized by atopy, early-onset, and lower lung function.ConclusionsOur study supports the concept that the CDHR3 variant is an important susceptibility factor for severe adult asthma in individuals who develop the disease in early life. The interaction between the CDHR3 variant and atopy indicates that genetic predisposition to early respiratory viral infection is combined with atopy in promoting asthma

Improved renal survival in Japanese children with IgA nephropathy

Since the beginning of the 1990s, Japanese medical practitioners have extensively prescribed angiotensin-converting enzyme (ACE) inhibitors for children with mild IgA nephropathy (IgA-N) and steriods for those with severe IgA-N. We have performed a retrospective cohort study to clarify whether the long-term outcome has improved in Japanese children with IgA-N. Renal survival was defined as the time from onset to end-stage renal disease (ESRD). We divided the study period into two time periods based on the occurrence of the initial renal biopsy:1976–1989 and 1990–2004. Actuarial survivals were calculated by Kaplan–Meier method, and comparisons were made with the logrank test. The Cox proportional hazard model was used for multivariate analysis. Between 1976 and 2004, 500 children were diagnosed as having IgA-N in our hospitals. The actuarial renal survival from the time of apparent disease onset was 96.4% at 10 years, 84.5% at 15 years and 73.9% at 20 years. Renal survival in the 1990–2004 period was significantly better than that in 1976–1989 (p = 0.008), and a marked improvement in renal survival in patients with severe IgA-N was also observed (p = 0.0003). Multivariate analysis indicated that diagnosis year was a significant factor for ESRD-free survival independently of baseline characteristics. The results of this study show that there has been an improvement in terms of renal survival in Japanese children with IgA-N

Total transferrin in cerebrospinal fluid is a novel biomarker for spontaneous intracranial hypotension

Spontaneous intracranial hypotension (SIH) is caused by cerebrospinal fluid (CSF) leakage. Patients with SIH experience postural headaches, nausea, etc., due to CSF hypovolemia. Imaging studies and clinical examinations, such as radioisotope (RI) scintigraphy, are useful for diagnosing SIH. However, 20-30% of patients do not show typical morphology and clinical test results. We previously reported that CSF contains transferrin (Tf) isoforms:"brain-type" Tf derived from the choroid plexus and "serum-type" Tf derived from blood. We showed that both isoforms increased in the CSF of patients with SIH by Western blotting. In the present study, we demonstrate that conventional ELISA for quantifying total Tf is useful for diagnosing SIH more accurately than Western blotting. In addition, SIH with chronic subdural hematoma (CSDH) was also accurately diagnosed. Total Tf in the CSF can serve as a useful biomarker for diagnosing SIH with or without CSDH

Role of Lung Function Genes in the Development of Asthma

Although our previous GWAS failed to identify SNPs associated with pulmonary function at the level of genomewide significance, it did show that the heritability for FEV1/FVC was 41.6% in a Japanese population, suggesting that the heritability of pulmonary function traits can be explained by the additive effects of multiple common SNPs. In addition, our previous study indicated that pulmonary function genes identified in previous GWASs in non-Japanese populations accounted for 4.3% to 12.0% of the entire estimated heritability of FEV1/FVC in a Japanese population. Therefore, given that many loci with individual weak effects may contribute to asthma risk, in this study, we created a quantitative score of genetic load based on 16 SNPs implicated in lower lung function in both Japanese and non-Japanese populations. This genetic risk score (GRS) for lower FEV1/FVC was consistently associated with the onset of asthma (P = 9.6 × 10−4) in 2 independent Japanese populations as well as with the onset of COPD (P = 0.042). Clustering of asthma patients based on GRS levels indicated that an increased GRS may be responsible for the development of a particular phenotype of asthma characterized by early onset, atopy, and severer airflow obstruction