Influence of Sward Height, Concentrate Supplementation and Season on Grazing Activity of Beef Cows

The influence of sward height, concentrate supplementation and season on daily pattern of forage consumption of lactating beef cows grazing cool season pastures was determined. Cows (n=24; BW=535±10.8 kg) were randomly assigned to eight plots maintained at sward heights (SH) of either 4-8 cm or 8-12 cm and fed three levels of concentrate supplement: none = 0 kg/day, low = 3.12 kg/day or high = 6.24 kg/day. Cows on lower SH had greater (P \u3c .08) forage dry matter intake and spent an additional 1.2 hours/day (P \u3c .01) grazing compared to the higher SH. Cows on lower SH consumed 7.7 kg/day of forage dry matter and grazed 9.4 hours/day whereas those on higher SH consumed 7.1 kg/day and grazed 8.2 hours/day. Cows on lower SH grazed 0.7 hours/day (P \u3c .06) and 0.4 hours/day (P \u3c .08) longer at 06:00-10:00 hour and 11:00-13:00 hour, respectively, compared to the higher SH. Grazing efficiency (kg of forage consumed/hour of grazing) decreased (P \u3c .01) as season progressed. Season influenced duration of grazing activity (P \u3c .01). Cows grazed 0.5 hours longer (P \u3c .01) at 06:00-10:00 hour late in summer (August) compared to spring (May) and mid summer (June/July). Cows grazed 0.3 hours longer (P \u3c .08) at 11:00-13:00 hour during spring compared to late summer

Sward Height; Visual Estimate Compared with Plate Meter Height

Sward height (SH) is widely used in pasture research and farm practice to evaluate pasture conditions. Visual estimates can take less time than actual measurements. This study compared visually estimated SH, of continuously grazed cool-season permanent pasture with plate meter height. Weekly estimates, by five people, were made on 12, 0.75 to 1 ha fields, grazed at two intensities. Paired data (visual estimate and plate meter height) were subjected to variance and covariance analyses and prediction equations were developed. Average visual height accounted for 86% of the variability in plate meter height. Inclusion of other sources of variability in the model (treatment, date and interactions) accounted for only a further 8% of the variability in plate meter height. On the basis of the strong linear relationships found between visual and plate meter heights, a procedure combining both methods is proposed that would reduce by 25% the time required to make weekly SH measurements of 12, 0.75 to 1 ha fields

Increased prevalence of the pfdhfr/phdhps quintuple mutant and rapid emergence of pfdhps resistance mutations at codons 581 and 613 in Kisumu, Kenya

<p>Abstract</p> <p>Background</p> <p>Anti-malarial drug resistance in Kenya prompted two drug policy changes within a decade: sulphadoxine-pyrimethamine (SP) replaced chloroquine (CQ) as the first-line anti-malarial in 1998 and artemether-lumefantrine (AL) replaced SP in 2004. Two cross-sectional studies were conducted to monitor changes in the prevalence of molecular markers of drug resistance over the period in which SP was used as the first-line anti-malarial. The baseline study was carried out from 1999-2000, shortly after implementation of SP, and the follow-up study occurred from 2003-2005, during the transition to AL.</p> <p>Materials and methods</p> <p>Blood was collected from malaria smear-positive, symptomatic patients presenting to outpatient centers in Kisumu, Kenya, during the baseline and follow-up studies. Isolates were genotyped at codons associated with SP and CQ resistance. <it>In vitro </it>IC₅₀values for antifolates and quinolones were determined for isolates from the follow-up study.</p> <p>Results</p> <p>The prevalence of isolates containing the <it>pfdhfr </it>N51I/C59R/S108N/<it>pfdhps </it>A437G/K540E quintuple mutant associated with SP-resistance rose from 21% in the baseline study to 53% in the follow-up study (p < 0.001). Isolates containing the <it>pfdhfr </it>I164L mutation were absent from both studies. The <it>pfdhps </it>mutations A581G and A613S/T were absent from the baseline study but were present in 85% and 61%, respectively, of isolates from the follow-up study. At follow-up, parasites with mutations at five <it>pfdhps </it>codons, 436, 437, 540, 581, and 613, accounted for 39% of isolates. The CQ resistance-associated mutations <it>pfcrt </it>K76T and <it>pfmdr1 </it>N86Y rose from 82% to 97% (p = 0.001) and 44% to 76% (p < 0.001), respectively, from baseline to follow-up.</p> <p>Conclusions</p> <p>During the period in which SP was the first-line anti-malarial in Kenya, highly SP-resistant parasites emerged, including isolates harboring <it>pfdhps </it>mutations not previously observed there. SP continues to be widely used in Kenya; however, given the highly resistant genotypes observed in this study, its use as a first-line anti-malarial should be discouraged, particularly for populations without acquired immunity to malaria. The increase in the <it>pfcrt </it>K76T prevalence, despite efforts to reduce CQ use, suggests that either these efforts are not adequate to alleviate CQ pressure in Kisumu, or that drug pressure is derived from another source, such as the second-line anti-malarial amodiaquine.</p

scMRI Reveals Large-Scale Brain Network Abnormalities in Autism

Autism is a complex neurological condition characterized by childhood onset of dysfunction in multiple cognitive domains including socio-emotional function, speech and language, and processing of internally versus externally directed stimuli. Although gross brain anatomic differences in autism are well established, recent studies investigating regional differences in brain structure and function have yielded divergent and seemingly contradictory results. How regional abnormalities relate to the autistic phenotype remains unclear. We hypothesized that autism exhibits distinct perturbations in network-level brain architecture, and that cognitive dysfunction may be reflected by abnormal network structure. Network-level anatomic abnormalities in autism have not been previously described. We used structural covariance MRI to investigate network-level differences in gray matter structure within two large-scale networks strongly implicated in autism, the salience network and the default mode network, in autistic subjects and age-, gender-, and IQ-matched controls. We report specific perturbations in brain network architecture in the salience and default-mode networks consistent with clinical manifestations of autism. Extent and distribution of the salience network, involved in social-emotional regulation of environmental stimuli, is restricted in autism. In contrast, posterior elements of the default mode network have increased spatial distribution, suggesting a ‘posteriorization’ of this network. These findings are consistent with a network-based model of autism, and suggest a unifying interpretation of previous work. Moreover, we provide evidence of specific abnormalities in brain network architecture underlying autism that are quantifiable using standard clinical MRI

Evaluation of the inion and asterion as neurosurgical landmarks for dural venous sinuses: osteological study on a sample of South African skull specimens

BACKGROUND : Sub-Saharan neurosurgeons most likely need to perform invasive procedures without the latest imaging and navigation technology in the operating room. Therefore, these surgeons need to utilize other methods such as superficial surface landmarks for neuro-navigation. Bony landmarks, including the inion and asterion, are commonly used during invasive procedures to pinpoint the location of the confluence of sinuses and transverse-sigmoid sinus junction, respectively. The purpose of this study was to investigate whether the inion and asterion can be used as superficial landmarks for the confluence of sinuses and the transverse-sigmoid sinus junction, respectively, in a South African population. METHODS : Fifty South African human skulls were used (25 male, 25 female). The micro-focus X-ray radiography and tomography facility (MIXRAD) at Necsa scanned and created three-dimensional virtual images of the skull specimens. Reference points were then inserted on the images and the relation between bony landmarks and venous sinuses was documented. RESULTS : The inion was directly related to the confluence of sinuses in 4% of the sample, whereas the asterion was directly related to the transverse-sigmoid sinus junction in 28% of the cases, on both the right and left sides. CONCLUSIONS : This study confirmed that neither the inion, nor the asterion, are directly related the confluence of sinuses and transverse-sigmoid sinus junction, respectively. These bony landmarks are more likely to be located either inferior, or not related at all, to the investigated dural venous sinuses.https://www.minervamedica.it/en/journals/neurosurgical-sciences2022-04-01hj2022Anatom

The Amidase Domain of Lipoamidase Specifically Inactivates Lipoylated Proteins In Vivo

BACKGROUND:In the 1950s, Reed and coworkers discovered an enzyme activity in Streptococcus faecalis (Enterococcus faecalis) extracts that inactivated the Escherichia. coli and E. faecalis pyruvate dehydrogenase complexes through cleavage of the lipoamide bond. The enzyme that caused this lipoamidase activity remained unidentified until Jiang and Cronan discovered the gene encoding lipoamidase (Lpa) through the screening of an expression library. Subsequent cloning and characterization of the recombinant enzyme revealed that lipoamidase is an 80 kDa protein composed of an amidase domain containing a classic Ser-Ser-Lys catalytic triad and a carboxy-terminal domain of unknown function. Here, we show that the amidase domain can be used as an in vivo probe which specifically inactivates lipoylated enzymes. METHODOLOGY/PRINCIPAL FINDINGS:We evaluated whether Lpa could function as an inducible probe of alpha-ketoacid dehydrogenase inactivation using E. coli as a model system. Lpa expression resulted in cleavage of lipoic acid from the three lipoylated proteins expressed in E. coli, but did not result in cleavage of biotin from the sole biotinylated protein, the biotin carboxyl carrier protein. When expressed in lipoylation deficient E. coli, Lpa is not toxic, indicating that Lpa does not interfere with any other critical metabolic pathways. When truncated to the amidase domain, Lpa retained lipoamidase activity without acquiring biotinidase activity, indicating that the carboxy-terminal domain is not essential for substrate recognition or function. Substitution of any of the three catalytic triad amino acids with alanine produced inactive Lpa proteins. CONCLUSIONS/SIGNIFICANCE:The enzyme lipoamidase is active against a broad range of lipoylated proteins in vivo, but does not affect the growth of lipoylation deficient E. coli. Lpa can be truncated to 60% of its original size with only a partial loss of activity, resulting in a smaller probe that can be used to study the effects of alpha-ketoacid dehydrogenase inactivation in vivo

Model prediction vs. reality--testing the predictions of a European eel (Anguilla anguilla) stock dynamics model against the in situ observation of silver eel escapement in compliance with the European eel regulation

A direct monitoring of European silver eel (Anguilla anguilla, L) escapement from rivers and estuaries has been proven to be challenging, and a Europe-wide documentation of escaping silver eel numbers therefore hardly seems realistic. To reinforce management decisions, policy-makers are thus widely reliant on the accuracy of escapement models. A 3-year programme of silver eel escapement monitoring was undertaken to compile model input data and revise an eel population model (German Eel Model II; GEM II) already used in the decision-making process of management authorities. By compiling necessary input data and analysing vital system-specific population characteristics, it was possible to compare the documented silver eel escapement with the modelled potential silver eel escapement. Resulting model predictions were close to actually monitored escapement numbers, which were distinctly lower than reference escapement values for the same freshwater system given in the implementation report of the German Eel Management Plans. Applying different commercial and recreational catch scenarios revealed the sensitivity of the model. The results show the potential of the GEM II and highlight the importance of high-quality input data to use model predictions as the basis for management measures

What is a biosecurity measure? A definition proposal for animal production and linked processing operations

While biosecurity, a central component of the One Health concept, is clearly defined, a harmonized definition of the term ´biosecurity measure´ (BSM) is missing. In turn, particularly at the farm and policy level, this leads to misunderstandings, low acceptance, poor implementation, and thus suboptimal biosecurity along the food animal production chain. Moreover, different views on BSMs affects making comparisons both at the policy level as well as in the scientific community. Therefore, as part of the One Health EJP BIOPIGEE project, a work group i) collected and discussed relevant inclusion and exclusion criteria for measures to be considered in the context of biosecurity and ii) conducted a systematic literature review for potentially existing definitions for the term BSM. This exercise confirmed the lack of a definition of BSM, underlining the importance of the topic. In the pool of articles considered relevant to defining the term BSM, specific research themes were identified. Based on these outcomes, we propose a definition of the term BSM: “A biosecurity measure (BSM) – is the implementation of a segregation, hygiene, or management procedure (excluding medically effective feed additives and preventive/curative treatment of animals) that specifically aims at reducing the probability of the introduction, establishment, survival, or spread of any potential pathogen to, within, or from a farm, operation or geographical area.” The definition provides a basis for policymakers to identify factual BSMs, highlights the point of implementation and supports to achieve the necessary quality standards of biosecurity in food animal production. It also enables clear, harmonized, cross-sectoral communication of best biosecurity practices to and from relevant stakeholders and thus contribute to improving biosecurity and thereby strengthen the One Health approach

Copper binding to the Alzheimer’s disease amyloid precursor protein

Alzheimer’s disease is the fourth biggest killer in developed countries. Amyloid precursor protein (APP) plays a central role in the development of the disease, through the generation of a peptide called Aβ by proteolysis of the precursor protein. APP can function as a metalloprotein and modulate copper transport via its extracellular copper binding domain (CuBD). Copper binding to this domain has been shown to reduce Aβ levels and hence a molecular understanding of the interaction between metal and protein could lead to the development of novel therapeutics to treat the disease. We have recently determined the three-dimensional structures of apo and copper bound forms of CuBD. The structures provide a mechanism by which CuBD could readily transfer copper ions to other proteins. Importantly, the lack of significant conformational changes to CuBD on copper binding suggests a model in which copper binding affects the dimerisation state of APP leading to reduction in Aβ production. We thus predict that disruption of APP dimers may be a novel therapeutic approach to treat Alzheimer’s disease

Atypical development of white matter microstructure of the corpus callosum in males with autism: a longitudinal investigation

Background: The corpus callosum is the largest white matter structure in the brain, and it is the most consistently reported to be atypical in diffusion tensor imaging studies of autism spectrum disorder. In individuals with typical development, the corpus callosum is known to undergo a protracted development from childhood through young adulthood. However, no study has longitudinally examined the developmental trajectory of corpus callosum in autism past early childhood. Methods: The present study used a cohort sequential design over 9 years to examine age-related changes of the corpus callosum in 100 males with autism and 56 age-matched males with typical development from early childhood (when autism can first be reliably diagnosed) to mid-adulthood (after development of the corpus callosum has been completed) (3 to 41 years of age). Results: The group with autism demonstrated a different developmental trajectory of white matter microstructure in the anterior corpus callosum’s (genu and body) fractional anisotropy, which suggests atypical brain maturation in these regions in autism. When analyses were broken down by age group, atypical developmental trajectories were present only in the youngest participants (10 years of age and younger). Significant main effects for group were found in terms of decreased fractional anisotropy across all three subregions of the corpus callosum (genu, body, and splenium) and increased mean diffusivity, radial diffusivity, and axial diffusivity in the posterior corpus callosum. Conclusions: These longitudinal results suggest atypical early childhood development of the corpus callosum microstructure in autism that transitions into sustained group differences in adolescence and adulthood. This pattern of results provides longitudinal evidence consistent with a growing number of published studies and hypotheses regarding abnormal brain connectivity across the life span in autism. Electronic supplementary material The online version of this article (doi:10.1186/s13229-015-0001-8) contains supplementary material, which is available to authorized users