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The objective was to determine associations between behavior during head-lock restraint and reproductive performance in dairy heifers. Behavior of 817 Holstein heifers from four farms was evaluated at feeding (Days 0 and 7) while restrained in a self-locking stanchion. All heifers were assigned a body condition score (BCS; 1, emaciated to 5, obese) on Day 0. Heifers were timed-inseminated on a maximum of three occasions to determine impact of behavior for first service pregnancy per AI (FS-P/AI) and cumulative P/AI (C-P/AI). Ovulation was synchronized with an Ovsynch synchronization protocol for first service and thereafter either Ovsynch and/or prostaglandin F 2α -based protocols. More heifers displayed calm escape behavior (P < 0.05) compared with mild or aggressive escape behaviors (45.2, 28.2 and 26.6%, respectively). Adjusting for BCS (P < 0.05), FS-P/AI was greater (P < 0.05) for calm heifers compared with aggressive escape behavior, 58.0% (214/369) vs 48.2% (105/218), with FS-P/AI of heifers with mild aggressive behavior [53.5% (123/230)] intermediate and did not differ from other means. Adjusting for BCS (P < 0.0001), C-P/AI was greater (P < 0.0001) for heifers with calm compared with mild or aggressive escape behaviors [84.8% (313/369), 71.3% (164/230) and 64.7% (141/218), respectively]. Serum cortisol concentrations were not different among behavior categories, but serum substance P concentrations were greater (P < 0.05) in aggressive heifers compared with mild or calm heifers, 97.1 ± 4.9, 58.4 ± 2.9 and 52.3 ± 2.6 ng/mL, respectively. In conclusion, Holstein heifers with aggressive escape behavior during head-lock restraint had significantly reduced reproductive performance., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Major depressive disorder has been associated with activation of inflammatory processes as well as with reductions in innate, adaptive and non-specific immune responses. The objective of this study was to evaluate the association between major depression and a disease-relevant immunologic response, namely varicella-zoster virus (VZV)-specific immunity, in elderly adults. A cross-sectional cohort study was conducted in 104 elderly community dwelling adults ≥ 60years of age who were enrolled in the depression substudy of the shingles prevention study, a double blind, placebo-controlled vaccine efficacy trial. Fifty-two subjects had a current major depressive disorder, and 52 age- and sex-matched controls had no history of depression or any mental illness. VZV-specific cell-mediated immunity (VZV-CMI) was measured by VZV responder cell frequency (VZV-RCF) and interferon-γ enzyme-linked immunospot (ELISPOT) assays, and antibody to VZV was measured by an enzyme-linked immunosorbent assay against affinity-purified VZV glycoproteins (gpELISA). VZV-CMI, measured by VZV-RCF, was significantly lower in the depressed group than in the controls (p<0.001), and VZV-RCF was inversely correlated with the severity of depressive symptoms in the depressed patients. In addition, an age-related reduction in VZV-RCF was observed in the depressed patients, but not in the controls. Furthermore, there was a trend for depressive symptom severity to be associated with lower ELISPOT counts. Finally, VZV-RCF was higher in depressed patients treated with antidepressant medications as compared to untreated depressed patients. Since lower levels of VZV-RCF appear to explain the increased risk and severity of herpes zoster observed in older adults, these findings suggest that, in addition to increasing age, depression may increase the risk and severity of herpes zoster., (Copyright © 2011 Elsevier Inc. All rights reserved.)

The neurotoxic actions of homocysteine on central nervous system neurons have been well established, yet its effects on the neurons of the peripheral nervous system remain largely unknown. We analysed the consequences of homocysteine exposure for the in vitro survival of embryonic and postnatal murine trigeminal sensory neurons from E14 to P1, and also quantified the effects of homocysteine exposure on neurite outgrowth. We discovered that homocysteine was toxic to these neurons when they were grown with NGF, or, in the case of P1 trigeminal neurons, with CNTF. Cell death induced by homocysteine was blocked using caspase inhibitors indicating that this cell loss was apoptotic. In addition, we demonstrated that homocysteine toxicity was mediated through the actions of the NMDA receptor, nitric oxide and peroxynitrite. We found that homocysteine had no effect on neurite outgrowth. Taken together our data show that homocysteine induces apoptosis in trigeminal sensory neurons via a nitric oxide-dependent mechanism. These data represent the first demonstration that homocysteine is toxic to a population of cranial sensory neurons and elucidate key components of the signalling pathway engaged to bring this about. These findings are of importance to our understanding of homocysteine's influence on neurodevelopment and on peripheral neuropathies.

Plasma pyruvate kinase (PK) and creatine kinase (CK) were measured in healthy subjects engaging in (a) mild exercise, 30 min on an exercise cycle maintaining a pulse rate of 150/min, (b) moderate exercise, squeezing a ball until exhaustion with a sphygmomanometer cuff inflated above systolic pressure around the arm (max. 2 min) and (c) severe exercise, completing a marathon race. Mild exercise resulted in no change in enzyme levels over 24 h. Moderate exercise produced a small increase in PK but no change in CK. PK activity rose from 35.3 +/- 10 U/l pre-exercise to 41.3 +/- 13 U/l 15 min post-exercise (n = 8, p less than 0.025). Severe exercise (completing a marathon race) resulted in a 3-fold increase in PK from 26 (4-87) U/l pre-race to 69 (21-156) U/l immediately post-race, and also, as expected, an increase in CK from 60 (15-164) U/l to 257 (72-1535) U/l (results are means and ranges, n = 69, p less than 0.001 for both enzymes). Runners showed parallel increases in PK and CK (p less than 0.05 by Spearman rank correlation). The mean post-race activity of CK-MB was less than 5% of total CK but 18 runners had values greater than 6% (mean 4.8, range 1-18). We conclude that PK, like CK, is increased following exercise due to liberation of muscle enzyme. However, only severe exercise is likely to lead to a substantial increase in plasma PK activity and therefore prejudice its clinical usefulness as a diagnostic test.

This study was undertaken to test the hypothesis that a compensatory response of the heart to a chronic and continuous, metabolic and heart rate overload was an increase in the calcium sequestering activity of the myocardial sarcoplasmic reticulum. Calcium sequestering activity was estimated by determination of the calcium-dependent ATPase (Ca2+-ATPase) activity of isolated microsomes. Chronic rate overload was modelled by comparing: dysthyroid and control rats; control swine and swine with implanted cardiac pacemakers set at 180 beats/min; and different species of mammals with widely different heart rates. The myocardial sarcoplasmic reticulum Ca2+-ATPase pump activity was significantly increased by 39% for hyperthyroid rats compared to control rats and by 87% for control rats compared to thyroidectomized rats; by 63% for paced swine compared to control swine; and by 43% for rats compared to guinea pigs, by 140% for guinea pigs compared to dogs and by 120% for dogs compared to cows. These data indicate that calcium sequestering activity of myocardial sarcoplasmic reticulum increases in equivalent proportion to the chronotropic demand and that heart rate is a hemodynamic correlate of the sarcoplasmic reticulum Ca2+-ATPase activity.