Chamindrani Mendis-Handagama

The University of Tennessee Medical Center at Knoxville, Knoxville, Tennessee, United States

Are you Chamindrani Mendis-Handagama?

Claim your profile

Publications (4)12.33 Total impact

  • Michael H Sims · Chamindrani Mendis-Handagama · Robert N Moore
    [Show abstract] [Hide abstract]
    ABSTRACT: Teaching faculty in the University of Tennessee College of Veterinary Medicine assist students in their professional education by providing a new way of viewing microscopic slides digitally. Faculty who teach classes in which glass slides are used participate in a program called Virtual Microscopy. Glass slides are digitized using a state-of-the-art integrated system, and a personal computer functions as the "microscope." Additionally, distribution of the interactive images is enhanced because they are available to students online. The digital slide offers equivalent quality and resolution to the original glass slide viewed on a microscope and has several additional advantages over microscopes. Students can choose to examine the entire slide at any of several objectives; they are able to access the slides (called WebSlides) from the college's server, using either Internet Explorer or a special browser developed by Bacus Laboratories, Inc.,(a) called the WebSlide browser, which lets the student simultaneously view a low-objective image and one or two high-objective images of the same slide. The student can "move the slide" by clicking and dragging the image to a new location. Easy archiving, annotation of images, and Web conferencing are additional features of the system.
    No preview · Article · Feb 2007 · Journal of Veterinary Medical Education
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Androgens and the androgen receptor (AR) play important roles in the testes. Previously we have shown that male total AR knockout (T-AR-/y) mice revealed incomplete germ cell development and lowered serum testosterone levels, which resulted in azoospermia and infertility. However, the consequences of AR loss in particular types of testicular cells remain unclear. Using a Cre-loxP conditional knockout strategy, we generated a tissue-selective knockout mouse with the AR gene deleted in testis peritubular myoid cells (PM-AR-/y). Phenotype analyses showed that PM-AR-/y mice were indistinguishable from WT AR (AR+/y) mice with the exception of smaller testes size. PM-AR-/y mice have serum testosterone concentrations comparable with AR+/y mice. PM-AR-/y mice have oligozoospermia in the epididymis; however, fertility was normal. Although normal germ cell distribution ratio was found, total germ cell number decreased in PM-AR-/y mice. Further mechanistic studies demonstrated that PM-AR-/y mice have defects in the expression of Sertoli cells' functional marker genes such as tranferrin, epidermal fatty acid-binding protein, androgen-binding protein, and other junction genes including occludin, testin, nectin, zyxin, vinculin, laminingamma3, gelsolin, connection43, and N-cadherin. Furthermore, there were defects in peritubular myoid cell contractility-related genes such as endothelin-1, endothelin receptor A and B, adrenomedullin, adrenomedullin receptor, and vasopressin receptor 1a. Together, our PM-AR-/y mice provide in vivo evidence for the requirement of functional AR in peritubular myoid cells to maintain normal Sertoli cells function and peritubular myoid cell contractility, thus ensuring normal spermatogenesis and sperm output.
    Full-text · Article · Dec 2006 · Proceedings of the National Academy of Sciences
  • C Mendis-Handagama · S Ariyaratne
    [Show abstract] [Hide abstract]
    ABSTRACT: Hypothyroidism arrests the differentiation of adult Leydig cells (ALC) in the neonatal rat testis, and transient neonatal hypothyroidism produces a two-fold increase in the ALC numbers in the adult rat testis. We investigated 1) whether prolonged hypothyroidism beyond the neonatal period could continue to arrest the differentiation of the ALC, and 2) to understand how a two-fold increase in the number of ALC is produced in adult rats subjected to transient neonatal hypothyroidism. Three groups of Sprague Dawley rats were used; control, PTU-water group (transiently hypothyroid; added 0.1% propyl thiouracil/PTU to drinking water of lactating mothers at parturition until weaning of pups at day 21, pups were fed regular water thereafter), and PTU group (prolonged hypothyroid; mothers were fed 0.1% PTU in drinking water from parturition until pups were sacrificed at days 28 and 40 (pups had access to solid food after 21 days). Findings showed that PTU treatment continued to arrest ALC differentiation. Withdrawal of the PTU treatment at 21 days resulted in ALC differentiation by two-fold in number in PTU-water rats. Findings on luteinizing hormone (LH)-stimulated androgen secretory capacity per testis in vitro agreed with the morphological data. These results confirmed that 1) thyroid hormone is crucial to the onset of ALC differentiation in the postnatal rat testis, 2) increased numbers of mesenchymal cells present in the hypothyroid testes differentiate into ALC upon withdrawal of the PTU treatment to produce a two-fold number of ALC in adult rats subjected to transient neonatal hypothyroidism (i.e., PTU-water treatment), and 3) numbers of ALC and mesenchymal cells increase with age at a rate of 2:1 during the process of ALC differentiation in testes of control and PTU-water rats.
    No preview · Article · Sep 2004 · Archives of Andrology
  • S Ariyaratne · I Kim · N Mills · I Mason · C Mendis-Handagama
    [Show abstract] [Hide abstract]
    ABSTRACT: In ethane dimethane sulfonate (EDS)-treated adult Sprague Dawley rats, Leydig cells (LC) were not present up to 14 days but seen at 21 days. They increased in number thereafter and reached the values of age-matching controls (i.e., 150-day-old untreated) at day 60. Mesenchymal cell number per testis also increased and reached a peak at day 21, and remained at a higher (p<.05) value than the controls at days 28-60. LC were smaller at day 21, but were larger at days 28-60 (compared to untreated 90- and 150-day-old rats) and secreted more testosterone at day 60 compared to both control groups. Testes of treated rats had greater numbers of macrophages (except at day 28) and they were smaller than those in untreated rats and 60-day EDS rats. Immunolabeling studies on 3beta-HSD, 11beta-HSD1, and LH receptor activity and androgen data agreed with morphological findings. The relationship between mesenchymal and LC numbers during LC differentiation following EDS treatment is reminiscent of this process in prepubertal testis. The presence of increased numbers of macrophages in treated testes agreed with the role of macrophages on LC differentiation. The absence of aging signs in LC of 60-day treated rats who were 150 days of age can be attributed at least in part to their newly differentiated status in older rats (i.e., equivalent to pubertal LC and not to aged LC). Larger LC observed in EDS rats at days 28-60 and their increased testosterone secretory capacity at day 60 (compared to controls) are attributed to elevated plasma LH levels and locally produced factors in EDS rats.
    No preview · Article · Jul 2003 · Archives of Andrology