Perinate

Abstract: We investigated if prostaglandins might regulate the increased choroidal endothelial (e) nitric oxide synthase (NOS) expression in the perinate. Prostaglandins, eNOS mRNA, immunoreactive protein an...

Abstract: While non-infectious causes are more commonly diagnosed in cases of bovine perinatal mortality (PM), the proportion caused by infections is highly variable between studies (~5-35%); the reasons for this variation, and possible underestimation, are discussed The most important pathogen-specific infectious causes of PM are bacteria (in particular, Bacillus licheniformis and Leptospira spp), viruses (in particular BVDv) and a parasite (Neospora caninum) However, co-infection may occur in a small proportion of cases and in many cases no single pathogen is detected but gross or microscopic lesions of an inflammatory response are identified Diagnosis is complicated by the criteria required to establish exposure, infection and causation Additionally, pathogens can be classified as primary or secondary though such differentiation can be arbitrary The majority of infectious cases of PM are due to in utero infections but postnatal infections (0-2 days) can also cause PM Diagnosis of infectious PM is based on a systematic investigation of the herd health history and dam and cohort sampling and examination of the perinate and its placenta Gross and histopathologic examinations and maternal/herd and perinate serology form the basis of current infectious PM investigations

Abstract: Despite increasingly frequent and longer lasting hypoxic episodes during progressive labor, the neonate is alert and vigorous at birth. We investigated whether high levels of PGs during the perinat...

Abstract: The perinate is particularly risk-prone to chemical species which have the potential of inducing neuronal apoptosis or necrosis and thereby adversely altering development of the brain, to produce life-long functional and behavioral deficits. This paper is an overview for many substances of abuse, but the purview is much more broadened by the realization that even elevated levels of estrogens and corticosteroids in the pregnant mother can act as neuroteratogens, by passing via the placenta and altering neural development or inducing apoptosis in the perinate. Finally, therapeutic risks of anesthetics are highlighted, as these too induce neuronal apoptosis in the neonate by either blocking N-methyl-D-aspartate receptors or by acting as gamma-aminobutyric acid agonists. By understanding the mechanisms involved it may ultimately be possible to interrupt the mechanistic scheme and thereby prevent neuroteratological processes.