Revealing patterns of nocturnal migration using the European weather radar network

Nocturnal avian migration flyways remain an elusive concept, as we have largely lacked methods to map their full extent. We used the network of European weather radars to investigate nocturnal bird movements at the scale of the European flyway. We mapped the main migration directions and showed the intensity of movement across part of Europe by extracting biological information from 70 weather radar stations from northern Scandinavia to Portugal, during the autumn migration season of 2016. On average, over the 20 nights and all sites, 389 birds passed per 1 km transect per hour. The night with highest migration intensity showed an average of 1621 birds km^–1 h^–1 passing the radar stations, but there was considerable geographical and temporal variation in migration intensity. The highest intensity of migration was seen in central France. The overall migration directions showed strong southwest components. Migration dynamics were strongly related to synoptic wind conditions. A wind‐related mass migration event occurred immediately after a change in wind conditions, but quickly diminished even when supporting winds continued to prevail. This first continental‐scale study using the European network of weather radars demonstrates the wealth of information available and its potential for investigating large‐scale bird movements, with consequences for ecosystem function, nutrient transfer, human and livestock health, and civil and military aviation.     

The human Werner syndrome protein stimulates repair of oxidative DNA base damage by the DNA glycosylase NEIL1

The mammalian DNA glycosylase, NEIL1, specific for repair of oxidatively damaged bases in the genome via the base excision repair pathway, is activated by reactive oxygen species and prevents toxicity due to radiation. We show here that the Werner syndrome protein (WRN), a member of the RecQ family of DNA helicases, associates with NEIL1 in the early damage-sensing step of base excision repair. WRN stimulates NEIL1 in excision of oxidative lesions from bubble DNA substrates. The binary interaction between NEIL1 and WRN (K(D) = 60 nM) involves C-terminal residues 288-349 of NEIL1 and the RecQ C-terminal (RQC) region of WRN, and is independent of the helicase activity WRN. Exposure to oxidative stress enhances the NEIL-WRN association concomitant with their strong nuclear co-localization. WRN-depleted cells accumulate some prototypical oxidized bases (e.g. 8-oxoguanine, FapyG, and FapyA) indicating a physiological function of WRN in oxidative damage repair in mammalian genomes. Interestingly, WRN deficiency does not have an additive effect on in vivo damage accumulation in NEIL1 knockdown cells suggesting that WRN participates in the same repair pathway as NEIL1.     

Does Visceral Osteopathic Treatment Accelerate Meconium Passage in Very Low Birth Weight Infants?- A Prospective Randomized Controlled Trial

Background

To determine whether the complementary approach of visceral manipulative osteopathic treatment accelerates complete meconium excretion and improves feeding tolerance in very low birth weight infants.

Methods

This study was a prospective, randomized, controlled trial in premature infants with a birth weight <1500 g and a gestational age <32 weeks who received a visceral osteopathic treatment 3 times during their first week of life or no treatment.

Results

Passage of the last meconium occurred after a median of 7.5 days (95% confidence interval: 6–9 days, n = 21) in the intervention group and after 6 days (95% confidence interval: 5-9 days, n = 20,) in the control group (p = 0.11). However, osteopathic treatment was associated with a 8 day longer time to full enteral feedings (p = 0.02), and a 34 day longer hospital stay (Median = 66 vs. 100 days i.e.; p=0.14). Osteopathic treatment was tolerated well and no adverse events were observed.

Conclusions

Visceral osteopathic treatment of the abdomen did not accelerate meconium excretion in VLBW (very low birth weight)-infants. However infants in the osteopathic group had a longer time to full enteral feedings and a longer hospital stay, which could represent adverse effects. Based on our trial results, we cannot recommend visceral osteopathic techniques in VLBW-infants.

Trial registration

Clinical trials.gov: NCT02140710     

Attenuation of cardiac hypertrophy by G‐CSF is associated with enhanced migration of bone marrow‐derived cells

Granulocyte‐colony stimulating factor (G‐CSF) has been shown to promote mobilization of bone marrow‐derived stem cells (BMCs) into the bloodstream associated with improved survival and cardiac function after myocardial infarction. Therefore, the aim of the present study was to investigate whether G‐CSF is able to attenuate cardiac remodelling in a mouse model of pressure‐induced LV hypertrophy focusing on mobilization and migration of BMCs. LV hypertrophy was induced by transverse aortic constriction (TAC) in C57BL/6J mice. Four weeks after TAC procedure. Mice were treated with G‐CSF (100 μg/kg/day; Amgen Biologicals) for 2 weeks. The number of migrated BMCs in the heart was analysed by flow cytometry. mRNA expression and protein level of different growth factors in the myocardium were investigated by RT‐PCR and ELISA. Functional analyses assessed by echocardiography and immunohistochemical analysis were performed 8 weeks after TAC procedure. G‐CSF‐treated animals revealed enhanced homing of VLA‐4⁺ and c‐kit⁺ BMCs associated with increased mRNA expression and protein level of the corresponding homing factors Vascular cell adhesion protein 1 and Stem cell factor in the hypertrophic myocardium. Functionally, G‐CSF significantly preserved LV function after TAC procedure, which was associated with a significantly reduced area of fibrosis compared to control animals. Furthermore, G‐CSF‐treated animals revealed a significant improvement of survival after TAC procedure. In summary, G‐CSF treatment preserves cardiac function and is able to diminish cardiac fibrosis after induction of LV hypertrophy associated with increased homing of VLA‐4⁺ and c‐kit⁺ BMCs and enhanced expression of their respective homing factors VCAM‐1 and SCF.     

Fine Mapping of a GWAS-Derived Obesity Candidate Region on Chromosome 16p11.2

IntroductionLarge-scale genome-wide association studies (GWASs) have identified 97 chromosomal loci associated with increased body mass index in population-based studies on adults. One of these SNPs, rs7359397, tags a large region (approx. 1MB) with high linkage disequilibrium (r²>0.7), which comprises five genes (SH2B1, APOBR, sulfotransferases: SULT1A1 and SULT1A2, TUFM). We had previously described a rare mutation in SH2B1 solely identified in extremely obese individuals but not in lean controls.MethodsThe coding regions of the genes APOBR, SULT1A1, SULT1A2, and TUFM were screened for mutations (dHPLC, SSCP, Sanger re-sequencing) in 95 extremely obese children and adolescents. Detected non-synonymous variants were genotyped (TaqMan SNP Genotyping, MALDI TOF, PCR-RFLP) in independent large study groups (up to 3,210 extremely obese/overweight cases, 485 lean controls and 615 obesity trios). In silico tools were used for the prediction of potential functional effects of detected variants.ResultsExcept for TUFM we detected non-synonymous variants in all screened genes. Two polymorphisms rs180743 (APOBR p.Pro428Ala) and rs3833080 (APOBR p.Gly369_Asp370del9) showed nominal association to (extreme) obesity (uncorrected p = 0.003 and p = 0.002, respectively). In silico analyses predicted a functional implication for rs180743 (APOBR p.Pro428Ala). Both APOBR variants are located in the repetitive region with unknown function.ConclusionVariants in APOBR contributed as strongly as variants in SH2B1 to the association with extreme obesity in the chromosomal region chr16p11.2. In silico analyses implied no functional effect of several of the detected variants. Further in vitro or in vivo analyses on the functional implications of the obesity associated variants are warranted.