3,640 research outputs found

    R.J. Sommers

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    The single-spaced paragraph on the “About the Author” page of R.J. Sommers’ latest novel says she lives in a one-story house on the edge of a city. It says she is renowned for writing relatable characters and compelling relationships. It says nothing about her own friends. Gazing from a photo at the top of the page, R.J. Sommers appears to point a camera toward her readers..

    Dietary manipulation of Bos indicus x heifers during gestation affects the reproductive development of their heifer calves

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    The effect of nutrition during the first and second trimesters of pregnancy in composite beef heifers on reproductive parameters of their female calves was determined in the present study. At artificial insemination, heifers were assigned to one of four treatment groups (i.e. HH, HL, LowH and LL) depending on the level of crude protein intake (H = high; L = low) for first and second trimesters of pregnancy. Gonadotrophin concentrations and ovarian parameters were measured in their female calves at 5 and 23 months of age. Crude protein intake was positively associated with dam plasma urea (P < 0.001). The density of healthy follicles in heifers at the time of death was negatively correlated with dam plasma urea at Day 179 (P = 0.009). Heifers from LowH dams had a smaller-sized prepubertal largest ovarian follicle (P = 0.03) and lower densities of primordial and primary follicles (P = 0.02) and healthy antral follicles (P = 0.009) when they were killed. There was a positive correlation between plasma FSH concentrations at 5 and 23 months of age (P = 0.02), as well as between the sizes of the largest ovarian follicles at 6 and 23 months of age (P = 0.01). In conclusion, the reproductive development of heifers may be affected by prenatal nutrition during early and mid-gestation.T.M. Sullivan, G.C. Micke, R.M. Greer, H.F. Irving-Rodgers, R.J. Rodgers and V.E.A. Perr

    Pancreatic islet basement membrane loss and remodeling after mouse islet isolation and transplantation: impact for allograft rejection

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    The isolation of islets by collagenase digestion can cause damage and impact the efficiency of islet engraftment and function. In this study, we assessed the basement membranes (BMs) of mouse pancreatic islets as a molecular biomarker for islet integrity, damage after isolation, and islet repair in vitro as well as in the absence or presence of an immune response after transplantation. Immunofluorescence staining of BM matrix proteins and the endothelial cell marker platelet endothelial cell adhesion molecule-1 (PECAM-1) was performed on pancreatic islets in situ, isolated islets, islets cultured for 4 days, and islet grafts at 3-10 days posttransplantation. Flow cytometry was used to investigate the expression of BM matrix proteins in isolated islet β-cells. The islet BM, consisting of collagen type IV and components of Engelbreth-Holm-Swarm (EHS) tumor laminin 111, laminin α2, nidogen-2, and perlecan in pancreatic islets in situ, was completely lost during islet isolation. It was not reestablished during culture for 4 days. Peri- and intraislet BM restoration was identified after islet isotransplantation and coincided with the migration pattern of PECAM-1+vascular endothelial cells (VECs). After islet allotransplantation, the restoration of VEC-derived peri-islet BMs was initiated but did not lead to the formation of the intraislet vasculature. Instead, an abnormally enlarged peri-islet vasculature developed, coinciding with islet allograft rejection. The islet BM is a sensitive biomarker of islet damage resulting from enzymatic isolation and of islet repair after transplantation. After transplantation, remodeling of both peri- and intraislet BMs restores β-cell-matrix attachment, a recognized requirement for β-cell survival, for isografts but not for allografts. Preventing isolation-induced islet BM damage would be expected to preserve the intrinsic barrier function of islet BMs, thereby influencing both the effector mechanisms required for allograft rejection and the antirejection strategies needed for allograft survival.H. F. Irving-Rodgers, F. J. Choong, K. Hummitzsch, C. R. Parish, R. J. Rodgers and C. J. Simeonovi

    Remodeling of extracellular matrix at ovulation of the bovine ovarian follicle

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    The definitive version may be found at www.wiley.comUsing immunohistochemistry and RNA analyses we examined the fate of components of a newly identified matrix that develops between granulosa cells (focimatrix, abbreviated from focal intraepithelial matrix) and of the follicular basal lamina in ovulating bovine ovarian follicles. Pre- and postovulatory follicles were generated by treatment with estradiol (Day 1), progesterone (Days 1-10), and prostaglandin analogue (Day 9) with either no further treatment (Group 1, n = 6) and or with 25 mg porcine LH (Day 11, Group 2, n = 8 or Day 10, Group 3, n = 8) and ovariectomy on Day 12 (12-14 hr post LH in Group 2, 38-40.5 hr in Group 3). In the time frame examined no loss of follicular basal lamina laminin chains beta2 and gamma1 or nidogen 1 was observed. In the follicular basal lamina collagen type IV alpha1 and perlecan were present prior to ovulation; after ovulation collagen type IV alpha1 was discontinuously distributed and perlecan was absent. Versican in the theca interna adjacent to the follicular basal lamina in preovulatory follicles was not observed post ovulation, however, the granulosa cells then showed strong cytoplasmic staining for versican. Expression of versican isoforms V0, V1, and V3 was detected at all stages. Focimatrix was observed in preovulatory follicles. It contained collagen type IV alpha1, laminins beta2 and gamma1, nidogen 1 and perlecan and underwent changes in composition similar to that of the follicular basal lamina. In conclusion focimatrix and the follicular basal lamina are degraded at ovulation. Individual components are lost at different times.H.F. Irving-Rodgers, K.D. Catanzariti, W.J. Aspden, M.J. D'Occhio, R.J. Rodger

    Genetic relationships between early menopause and the behaviour of theca interna during follicular atresia

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    Genetic variants are known to contribute to about 50% of the heritability of the age of menopause and recent studies suggest that genes associated with genome maintenance are involved. The idea that increased rates of follicular atresia could lead to depletion of the primoridial follicle reserve and early menopause has also been canvassed, but there is no direct evidence of this. In studies of the transcriptomics of follicular atresia, it was found that in the theca interna, the largest group of genes are in fact down-regulated and associated with 'cell cycle and DNA replication', in contrast with the up-regulation of apoptosis-associated genes which occurs in granulosa cells. Many of the genes down-regulated in the theca interna are the same as or related to the genes in loci associated with early menopause. From these findings, we suggest that early menopause could be due to increased rates of follicular atresia initiated from the theca interna.Raymond J. Rodgers and Joop S.E. Lave

    Accuracy and errors about the human ovary; the good, bad and the ugly

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    This collection is dedicated to the memory of Professor Ken McNatty and Professor Rex Scaramuzzi, both of whom made outstanding contributions to the understanding of reproductive, and particularly ovarian, biology. In fact, the impetus for this commentary began when the authors questioned why some textbooks continued to print an earlier theory of ovarian development by Haward Sawyer and Ken McNatty (Sawyer et al. 2002), when important additional findings were published in 2013 (Hummitzsch et al. 2013). The authors question why textbooks, websites and YouTube videos continue to present misinformation about the ovary with statements and illustrations that are patently inaccurate or incorrect. We are aware that medical and science textbook publishers may take no responsibility for the accuracy of content by printing a disclaimer to this effect. Webpages and YouTube videos, in the main, exist with no such caveat. Do authors of textbooks accept responsibility to publish up-to-date factual material and avoid demonstrably incorrect information? In some cases, apparently not. Here we will show examples from the ovarian biology that we encounter regularly, that authors often do not check nor update content for the multiple book editions published over decades. If original sources are not consulted by authors, where are they getting their information? Erroneous statements and dogma continue to be represented in scientific literature as established facts. Textbooks, in particular, are supposed to be reliable sources of information. Unfortunately, too many mislead students and scholars and promulgate misinformation. If the contributions of Professor Ken McNatty, Professor Rex Scaramuzzi and others are to be truly valuable, then knowledge amplified by textbooks and the web must at least be accurate.Raymond J. Rodgers and Jeffrey B. Ker

    Morphometric and gene expression analyses of stromal expansion during development of the bovine fetal ovary

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    During ovarian development stroma from the mesonephros penetrates and expands into the ovarian primordium and thus appears to be involved, at least physically, in the formation of ovigerous cords, follicles and surface epithelium. Cortical stromal development during gestation in bovine fetal ovaries (n = 27) was characterised by immunohistochemistry and by mRNA analyses. Stroma was identified by immunostaining of stromal matrix collagen type I and proliferating cells were identified by Ki67 expression. The cortical and medullar volume expanded across gestation, with the rate of cortical expansion slowing over time. During gestation, the proportion of stroma in the cortex and total volume in the cortex significantly increased (P  0.05). The expression levels of 12 genes out of 18 examined, including osteoglycin (OGN) and lumican (LUM), were significantly increased later in development (P < 0.05) and the expression of many genes was positively correlated with other genes and with gestational age. Thus, the rate of cortical stromal expansion peaked in early gestation due to cell proliferation, whilst late in development expression of extracellular matrix genes increased.M.D. Hartanti, A K. Hummitzsch, H.F. Irving-Rodgers, W.M. Bonner, K.J. Copping, R.A. Anderson, I.C. McMillen, V.E.A. Perry and R.J. Rodger
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