Colostrum source and passive immunity transfer in dairy bull calves

Colostrum is essential for good neonate health; however, it is not known whether different calves absorb the nutrients from colostrum equally well. In this study, the absorption of protein, IgG, and γ-glutamyl transferase was compared in newborn dairy bull calves for 1 wk after feeding colostrum from different sources. Thirty-five Holstein-Friesian bull calves were randomly allocated into 3 groups and fed colostrum within 4 h after birth. Group A calves (n = 12) were bottle fed colostrum from their own dam for 3 d. Colostrum from these group A cows was also used as foster cow colostrum for the group B calves (n = 12), such that each group A and B calf pair received identical colostrum from each milking of the respective group A dam (10% of birth weight per day). The group C calves (n = 11) were fed 1 bottle (2 L) of pooled colostrum and transition milk (referred to as pooled colostrum), as was the standard practice on the dairy farm. The pooled colostrum was collected from the other dairy cows on the farm 0 to 4 d postpartum and stored at 4°C for less than 12 h. Blood was sampled from calves before the first feeding and at 1, 2, 3, and 7 d after birth. Levels of total solids, total protein, and IgG were higher in the dam colostrum than in the pooled colostrum. At birth, there were no differences between the calf groups for any measurements, and all calves had very low IgG levels. After receiving colostrum, the glucose, plasma γ-glutamyl transferase, serum total protein, and IgG concentrations increased significantly in all calves. There were no differences in any blood measurements at any time point between the pairs of group A and group B calves that received colostrum from the same cow except for the IgG concentration 2 d after birth. However, the group A calves had a higher total serum protein level and IgG concentration than the group C calves for all the time points after the first feeding. The group B calves had a higher IgG concentration than the group C calves on d 1, 2, and 7 after birth. Compared with groups A and B, there was no difference in the proportion of calves in group C that failed to have passive immunity transferred adequately based on the IgG threshold (<10 g/L). Thus, the calves receiving identical colostrum from the same cow had the same levels of IgG, and even the pooled colostrum provided sufficient transfer of IgG as the calves were fed within 4 h after birth.     

Skeletal Muscle Health and Cognitive Function: A Narrative Review

Sarcopenia is the loss of skeletal muscle mass and function with advancing age. It involves both complex genetic and modifiable risk factors, such as lack of exercise, malnutrition and reduced neurological drive. Cognitive decline refers to diminished or impaired mental and/or intellectual functioning. Contracting skeletal muscle is a major source of neurotrophic factors, including brain-derived neurotrophic factor, which regulate synapses in the brain. Furthermore, skeletal muscle activity has important immune and redox effects that modify brain function and reduce muscle catabolism. The identification of common risk factors and underlying mechanisms for sarcopenia and cognition may allow the development of targeted interventions that slow or reverse sarcopenia and also certain forms of cognitive decline. However, the links between cognition and skeletal muscle have not been elucidated fully. This review provides a critical appraisal of the literature on the relationship between skeletal muscle health and cognition. The literature suggests that sarcopenia and cognitive decline share pathophysiological pathways. Ageing plays a role in both skeletal muscle deterioration and cognitive decline. Furthermore, lifestyle risk factors, such as physical inactivity, poor diet and smoking, are common to both disorders, so their potential role in the muscle–brain relationship warrants investigation.     

Chromophore-Free Sealing and Repair of Soft Tissues Using Mid-Infrared Light-Activated Biosealants

Poor strength, infection, leakage, long procedure times, and inflammation limit the efficacy of common tissue sealing devices in surgeries and trauma. Light-activated sealing is attractive for tissue sealing and repair, and can be facilitated by the generation of local heat following absorption of nonionizing laser energy by chromophores. Here, the inherent ability of biomaterials is exploited to absorb nonionizing, mid-infrared (midIR) light in order to engender rapid photothermal sealing and repair of soft tissue wounds. In this approach, the biomaterial simultaneously acts as a photothermal convertor as well as a biosealant, which dispenses the need for exogeneous light-absorbing nanoparticles or dyes. Biomechanical recovery, mathematical modeling, histopathology analyses, tissue strain mapping using digital imaging correlation, and visualization of the biosealant-tissue interface using hyperspectral imaging indicate superior performance of midIR sealing in live mice compared to conventional sutures and glue. The midIR-biosealant approach demonstrates rapid sealing of soft tissues, improves cosmesis, lowers potential for scarring, obviates safety concerns because of the nonionizing light used, and allows adoption of a wide diversity of biomaterials. Taken together, the studies demonstrate a novel advance both in biomaterials for surgical sealing along with the use of nonionizing midIR light, with high potential for clinical translation.     

Crystallography of fracture facets in a near-alpha titanium alloy

A faceted initiation site is observed in Ti-6242 alloy for both the cyclic and static-loading test conditions. In this experimental study, the crystallographic orientation of the facets has been determined using the electron backscattered diffraction (EBSD) technique in conjunction with the quantitative tilt fractography in a scanning electron microscope (SEM). Quantitative tilt fractography analysis has been used to determine the spatial orientation of fracture facets. The results indicate that the normal-fatigue (no-dwell) fracture facets are oriented at ∼5 deg with respect to the basal plane; the dwell-fatigue fracture facets are oriented at ∼10 to 15 deg with respect to the basal plane and the static-loading fracture facets are oriented at ∼20 deg with respect to the basal plane. These crystallographic orientation determinations of the fracture facets at the crack-initiation site can be used to obtain an idea about the type of loading that produced them.     

Viral dynamics of primary viremia and antiretroviral therapy in simian immunodeficiency virus infection

Mathematical modeling of viral replication dynamics, based on sequential measurements of levels of virion-associated RNA in plasma during antiretroviral treatment, has led to fundamental new insights into human immunodeficiency virus type 1 pathogenesis. We took advantage of the simian immunodeficiency virus (SIV)-infected macaque model to perform detailed measurements and mathematical modeling during primary infection and during treatment of established infection with the antiretroviral drug (R)-9-(2-phosphonylmethoxypropyl)adenine (PMPA). The calculated clearance half-life for productively infected cells during resolution of the peak viremia of primary infection was on the order of 1 day, with slightly shorter clearance half-lives calculated during PMPA treatment. Viral reproduction rates upon discontinuation of PMPA treatment after 2 weeks were approximately twofold greater than those obtained just prior to initiation of treatment in the same animals, likely reflecting accumulation of susceptible target cells during treatment. The basic reproductive ratio (R0) for the spread of SIV infection in vivo, which represents the number of productively infected cells derived from each productively infected cell at the beginning of infection, was also estimated. This parameter quantifies the extent to which antiviral therapy or vaccination must limit the initial spread of virus to prevent establishment of chronic disseminated infection. The results thus provide an important guide for efforts to develop vaccines against SIV and, by extension, human immunodeficiency virus.     

Sucralfate attenuates gastric mucosal lesions and increased vascular permeability induced by ischaemia and reperfusion in rats

Recent evidence suggests that oxygen-derived free radicals are involved in mediating gastric microvascular and parenchymal cell injuries induced by ischaemia and reperfusion. Therefore, the effect of the locally acting anti-ulcer drug, sucralfate, was studied on ischaemia and reperfusion (e.g. induced gastric lesions, intraluminal bleeding, changes in vascular permeability and non-protein sulfhydryl levels in the rat stomach). Allopurinol was used as a known standard antioxidant drug. Rats were subjected to 30 min of gastric ischaemia in the presence of 100 mmol/L hydrochloric acid and reperfusion periods of 15, 30 or 60 min duration. The gastric lesions were assessed microscopically under an inverted microscope. The vascular permeability was quantified by measuring the extravasated Evans blue in the stomach. There were significantly greater numbers of gastric lesions, intraluminal bleeding and leakage of Evans blue during all reperfusion periods as compared with those of ischaemia, with maximum effects occurring at 60 min following reperfusion. Pretreatment with sucralfate (31.25-250 mg/kg, p.o.) or allopurinol (12.5-50 mg/kg, i.p.) 30 min before the procedure, dose-dependently reduced the gastric lesions, intraluminal bleeding, and decreased the vascular permeability induced by ischaemia and reperfusion. Furthermore, sucralfate dose-dependently reverses the ischaemia and reperfusion-induced depletion of mucosal non-protein sulfhydryl levels and inhibited the superoxide radical production in both cell-free xanthine-xanthine oxidase and in the stimulated polymorphonuclear cellular systems. These results suggest that the protection produced by sucralfate against gastric injury may be due to its antioxidant effects.     

Modeling ion implantation of HgCdTe

Ion implantation of boron is used to create n on p photodiodes in vacancy-doped mercury cadmium telluride (MC.T). The junction is formed by Hg interstitials from the implant damage region diffusing into the MC.T and annihilating Hg vacancies. The resultant doping profile is n⁺/n^-/p, where the n⁺ region is near the surface and roughly coincides with the implant damage, the n^- region is where Hg vacancies have been annihilated revealing a residual grown-in donor, and the p region remains doped by Hg vacancy double acceptors. We have recently developed a new process modeling tool for simulating junction formation in MC.T by ion implantation. The interstitial source in the damage region is represented by stored interstitials whose distribution depends on the implant dose. These interstitials are released into the bulk at a constant, user defined rate. Once released, they diffuse away from the damage region and annihilate any Hg vacancies they encounter. In this paper, we present results of simulations using this tool and show how it can be used to quantitatively analyze the effects of variations in processing conditions, including implant dose, annealing temperature, and doping background.