A Comparison of the Ovulation Method With the CUE Ovulation Predictor in Determining the Fertile Period

The purpose of this study was to compare the CUE Ovulation Predictor with the ovulation method in determining the fertile period. Eleven regularly ovulating women measured their salivary and vaginal electrical resistance (ER) with the CUE, observed their cervical-vaginal mucus, and measured their urine for a luteinizing hormone (LH) surge on a daily basis. Data from 21 menstrual cycles showed no statistical difference (T= 0.33, p= 0.63) between the CUE fertile period, which ranged from 5 to 10 days (mean = 6.7 days, SD = 1.6), and the fertile period of the ovulation method, which ranged from 4 to 9 days (mean = 6.5 days, SD = 2.0). The CUE has potential as an adjunctive device in the learning and use of natural family planning methods

Direct Neutron Capture for Magic-Shell Nuclei

In neutron capture for magic--shell nuclei the direct reaction mechanism can be important and may even dominate. As an example we investigated the reaction $^{48}$Ca(n,$\gamma)^{49}$Ca for projectile energies below 250\,keV in a direct capture model using the folding procedure for optical and bound state potentials. The obtained theoretical cross sections are in agreement with the experimental data showing the dominance of the direct reaction mechanism in this case. The above method was also used to calculate the cross section for $^{50}$Ca(n,$\gamma)^{51}$Ca.Comment: REVTeX, 7 pages plus 3 uuencoded figures, the complete uuencoded postscript file is available at ftp://is1.kph.tuwien.ac.at/pub/ohu/calcium.u

Oxygen supply capacity breathes new life into critical oxygen partial pressure (Pcrit)

Author Posting. © Company of Biologists, 2021. This article is posted here by permission of Company of Biologists for personal use, not for redistribution. The definitive version was published in Journal of Experimental Biology 224(8), (2021): jeb242210, https://doi.org/10.1242/jeb.242210.The critical oxygen partial pressure (Pcrit), typically defined as the PO2 below which an animal's metabolic rate (MR) is unsustainable, is widely interpreted as a measure of hypoxia tolerance. Here, Pcrit is defined as the PO2 at which physiological oxygen supply (α0) reaches its maximum capacity (α; µmol O2 g−1 h−1 kPa−1). α is a species- and temperature-specific constant describing the oxygen dependency of the maximum metabolic rate (MMR=PO2×α) or, equivalently, the MR dependence of Pcrit (Pcrit=MR/α). We describe the α-method, in which the MR is monitored as oxygen declines and, for each measurement period, is divided by the corresponding PO2 to provide the concurrent oxygen supply (α0=MR/PO2). The highest α0 value (or, more conservatively, the mean of the three highest values) is designated as α. The same value of α is reached at Pcrit for any MR regardless of previous or subsequent metabolic activity. The MR need not be constant (regulated), standardized or exhibit a clear breakpoint at Pcrit for accurate determination of α. The α-method has several advantages over Pcrit determination and non-linear analyses, including: (1) less ambiguity and greater accuracy, (2) fewer constraints in respirometry methodology and analysis, and (3) greater predictive power and ecological and physiological insight. Across the species evaluated here, α values are correlated with MR, but not Pcrit. Rather than an index of hypoxia tolerance, Pcrit is a reflection of α, which evolves to support maximum energy demands and aerobic scope at the prevailing temperature and oxygen level.This project was supported by National Oceanic and Atmospheric Administration grants NA18NOS4780167 and NA17OAR4310081 and National Science Foundation grant OCE-1459243 to B.A.S., the Jack and Katharine Ann Lake Fellowship to A.A., the Anne and Werner Von Rosenstiel Fellowship and Garrels Memorial Endowed Fellowship to A.W.T., the Hogarth Fellowship to C.J.W., the Southern Kingfish Association Fellowship to A.L.B., and a National Science Foundation postdoctoral fellowship (DBI-1907197) to M.A.B.2022-04-3

Axonopathy in the central nervous system is the hallmark of mice with a novel intragenic null mutation of dystonin.

Dystonia musculorum is a neurodegenerative disorder caused by a mutation in the dystonin gene. It has been described in mice and humans where it is called hereditary sensory autonomic neuropathy. Mutated mice show severe movement disorders and die at the age of 3-4 weeks. This study describes the discovery and molecular, clinical, as well as pathological characterization of a new spontaneously occurring mutation in the dystonin gene in C57BL/6N mice. The mutation represents a 40-kb intragenic deletion allele of the dystonin gene on chromosome 1 with exactly defined deletion borders. It was demonstrated by Western blot, mass spectrometry, and immunohistology that mice with a homozygous mutation were entirely devoid of the dystonin protein. Pathomorphological lesions were restricted to the brain stem and spinal cord and consisted of swollen, argyrophilic axons and dilated myelin sheaths in the white matter and, less frequently, total chromatolysis of neurons in the gray matter. Axonal damage was detected by amyloid precursor protein and nonphosphorylated neurofilament immunohistology. Axonopathy in the central nervous system (CNS) represents the hallmark of this disease. Mice with the dystonin mutation also showed suppurative inflammation in the respiratory tract, presumably due to brain stem lesion-associated food aspiration, whereas skeletal muscles showed no pathomorphological changes. This study describes a novel mutation in the dystonin gene in mice leading to axonopathy in the CNS. In further studies, this model may provide new insights into the pathogenesis of neurodegenerative diseases and may elucidate the complex interactions of dystonin with various other cellular proteins especially in the CNS