Dynamic creep and pre-conditioning of the Achilles tendon in-vivo

Warm-up exercises are often advocated prior to strenuous exercise, but the warm-up duration and effect on muscle–tendon behavior are not well defined. The gastrocnemius–Achilles tendon complexes of 18 subjects were studied to quantify the dynamic creep response of the Achilles tendon in-vivo and the warm-up dose required for the Achilles tendon to achieve steady-state behavior. A custom testing chamber was used to determine each subject's maximum voluntary contraction (MVC) during an isometric ankle plantar flexion effort. The subject's right knee and ankle were immobilized for one hour. Subjects then performed over seven minutes of cyclic isometric ankle plantar flexion efforts equal to 25–35% of their MVC at a frequency of 0.75 Hz. Ankle plantar flexion effort and images from dual ultrasound probes located over the gastrocnemius muscle–Achilles tendon and the calcaneus–Achilles tendon junction were acquired for eight seconds at the start of each sequential minute of the activity. Ultrasound images were analyzed to quantify the average relative Achilles tendon strain at 25% MVC force (ε_25%MVC) for each minute. The ε_25%MVC increased from 0.3% at the start of activity to 3.3% after seven minutes, giving a total dynamic creep of ~3.0%. The ε_25%MVC increased by more than 0.56% per minute for the first five minutes and increased by less than 0.13% per minute thereafter. Therefore, following a period of inactivity, a low intensity warm-up lasting at least six minutes or producing 270 loading cycles is required for an Achilles tendon to reach a relatively steady-state behavior.     

Bovicin HC5 inhibits wasteful amino acid degradation by mixed ruminal bacteria in vitro

Streptococcus bovis HC5 produces a broad spectrum lantibiotic (bovicin HC5) that inhibits pure cultures of hyper ammonia-producing bacteria (HAB). Experiments were preformed to see if: (1) S. bovis HC5 cells could inhibit the deamination of amino acids by mixed ruminal bacteria taken directly from a cow, (2) semi-purified bovicin was as effective as S. bovis HC5 cells, and 3) semi-purified and the feed additive monensin were affecting the same types of ammonia-producing ruminal bacteria. Because purified and semi-purified bovicin HC5 was as effective as S. bovis HC5 cells, it appeared that bovicin HC5 was penetrating the cell membranes of HAB before it could be degraded by peptidases and proteinases. Mixed ruminal bacteria that were successively transferred and enriched nine times with trypticase did not become significantly more resistant to either bovicin HC5 (50 AU mL⁻¹) or monensin (5 μM), and amplified rDNA restriction analysis indicated that bovicin HC5 and monensin appeared to be selecting against the same types of bacteria.     

Modelling Associations between Public Understanding,Engagement and Forest Conditions in the Inland Northwest,USA

Opinions about public lands and the actions of private non-industrial forest owners in the western United States play important roles in forested landscape management as both public and private forests face increasing risks from large wildfires, pests and disease. This work presents the responses from two surveys, a random-sample telephone survey of more than 1500 residents and a mail survey targeting owners of parcels with 10 or more acres of forest. These surveys were conducted in three counties (Wallowa, Union, and Baker) in northeast Oregon, USA. We analyze these survey data using structural equation models in order to assess how individual characteristics and understanding of forest management issues affect perceptions about forest conditions and risks associated with declining forest health on public lands. We test whether forest understanding is informed by background, beliefs, and experiences, and whether as an intervening variable it is associated with views about forest conditions on publicly managed forests. Individual background characteristics such as age, gender and county of residence have significant direct or indirect effects on our measurement of understanding. Controlling for background factors, we found that forest owners with higher self-assessed understanding, and more education about forest management, tend to hold more pessimistic views about forest conditions. Based on our results we argue that self-assessed understanding, interest in learning, and willingness to engage in extension activities together have leverage to affect perceptions about the risks posed by declining forest conditions on public lands, influence land owner actions, and affect support for public policies. These results also have broader implications for management of forested landscapes on public and private lands amidst changing demographics in rural communities across the Inland Northwest where migration may significantly alter the composition of forest owner goals, understanding, and support for various management actions.     

Exceptional Antibodies Produced by Successive Immunizations

Antibodies stand between us and pathogens. Viruses mutate quickly to avoid detection, and antibodies mutate at similar rates to hunt them down. This death spiral is fueled by specialized proteins and error-prone polymerases that change DNA sequences. Here, we explore how B lymphocytes stay in the race by expressing activation-induced deaminase, which unleashes a tsunami of mutations in the immunoglobulin loci. This produces random DNA substitutions, followed by selection for the highest affinity antibodies. We may be able to manipulate the process to produce better antibodies by expanding the repertoire of specific B cells through successive vaccinations.     

Dephospho‐CoA kinase,a nuclear‐encoded apicoplast protein,remains active and essential after Plasmodium falciparum apicoplast disruption

Malaria parasites contain an essential organelle called the apicoplast that houses metabolic pathways for fatty acid, heme, isoprenoid, and iron–sulfur cluster synthesis. Surprisingly, malaria parasites can survive without the apicoplast as long as the isoprenoid precursor isopentenyl pyrophosphate (IPP) is supplemented in the growth medium, making it appear that isoprenoid synthesis is the only essential function of the organelle in blood‐stage parasites. In the work described here, we localized an enzyme responsible for coenzyme A synthesis, DPCK, to the apicoplast, but we were unable to delete DPCK, even in the presence of IPP. However, once the endogenous DPCK was complemented with the E. coli DPCK (EcDPCK), we were successful in deleting it. We were then able to show that DPCK activity is required for parasite survival through knockdown of the complemented EcDPCK. Additionally, we showed that DPCK enzyme activity remains functional and essential within the vesicles present after apicoplast disruption. These results demonstrate that while the apicoplast of blood‐stage P. falciparum parasites can be disrupted, the resulting vesicles remain biochemically active and are capable of fulfilling essential functions.     

Mutations in CSPP1 Cause Primary Cilia Abnormalities and Joubert Syndrome with or without Jeune Asphyxiating Thoracic Dystrophy

Joubert syndrome (JBTS) is a recessive ciliopathy in which a subset of affected individuals also have the skeletal dysplasia Jeune asphyxiating thoracic dystrophy (JATD). Here, we have identified biallelic truncating CSPP1 (centrosome and spindle pole associated protein 1) mutations in 19 JBTS-affected individuals, four of whom also have features of JATD. CSPP1 mutations explain ∼5% of JBTS in our cohort, and despite truncating mutations in all affected individuals, the range of phenotypic severity is broad. Morpholino knockdown of cspp1 in zebrafish caused phenotypes reported in other zebrafish models of JBTS (curved body shape, pronephric cysts, and cerebellar abnormalities) and reduced ciliary localization of Arl13b, further supporting loss of CSPP1 function as a cause of JBTS. Fibroblasts from affected individuals with CSPP1 mutations showed reduced numbers of primary cilia and/or short primary cilia, as well as reduced axonemal localization of ciliary proteins ARL13B and adenylyl cyclase III. In summary, CSPP1 mutations are a major cause of the Joubert-Jeune phenotype in humans; however, the mechanism by which these mutations lead to both JBTS and JATD remains unknown.