Biomedical subjects

D K Schmidt

Publications and source records attributed to D K Schmidt.

24 records · Page 2Linked to original sources

PubMed1985

Induction of AIDS-like disease in macaque monkeys with T-cell tropic retrovirus STLV-III.

The T-cell tropic retrovirus of macaque monkeys STLV-III has morphologic, growth, and antigenic properties indicating that it is related to HTLV-III/LAV, the etiologic agent of the acquired immune deficiency syndrome (AIDS) in humans. Four of six rhesus monkeys died within 160 days of STLV-III inoculation with a wasting syndrome, opportunistic infections, a primary retroviral encephalitis, and immunologic abnormalities including a decrease in T4+ peripheral blood lymphocytes. These data show that an immunodeficiency syndrome can be produced experimentally in a nonhuman primate by an agent from the HTLV-III/LAV group of retroviruses. The STLV-III-macaque system will thus provide a useful model for the study of antiviral agents and vaccine development for human AIDS.

Acquired Immunodeficiency Syndrome↗

PubMed1985

Retrovirus D/New England and its relation to Mason-Pfizer monkey virus.

Seventeen isolates of retrovirus D/New England have been obtained from three species of macaques at the New England Regional Primate Research Center. Seven of the isolates were obtained from macaques who subsequently died with the macaque immunodeficiency syndrome; other isolates were obtained from macaques with less severe or other forms of illness. Attempts to isolate type D retrovirus from peripheral lymphocytes of 97 apparently healthy macaques have not been successful. Cloned DNA was prepared from Hirt supernatants of cells infected with one of these isolates (D/New England 398). By restriction endonuclease analysis, cloned pD398 DNA represented full-length viral DNA with one long terminal repeat. A detailed restriction endonuclease map of pD398 was derived and compared with a map of the cloned Mason-Pfizer monkey virus genome. Forty-six percent (13 of 28) of restriction endonuclease sites were found to be conserved when these related viruses were compared. Five of the D/New England isolates, including those from three different macaque species, were examined for strain variability by restriction endonuclease typing. Comparison of over 30 restriction endonuclease sites has not distinguished any of these D/New England isolates. It thus appears that a single strain of type D retrovirus is infecting three different species of macaques in the New England colony. Markedly reduced cross-hybridization was observed between cloned pD398 and Mason-Pfizer monkey virus DNAs at high stringency; this reduced cross-hybridization was localized to the pol-env regions of the genome. Only very weak hybridization of D/New England DNA to cloned squirrel monkey type D retrovirus DNA could be detected even at low-stringency conditions. What role type D retrovirus plays in the immunodeficiency syndrome of macaques remains to be determined.

Animals↗

PubMed1984

Experimental infection of rhesus monkeys with type D retrovirus.

The naturally occurring immunodeficiency syndrome of macaque monkeys is an important animal model for the acquired immunodeficiency syndrome in humans. A new type D retrovirus, distinct from Mason-Pfizer monkey virus, has been isolated from affected animals at the New England Regional Primate Research Center. We now report the results of experimental infection of macaques with retrovirus D/New England after 13 months of study. Inoculated macaques developed lymphadenopathy without follicular hyperplasia, profound neutropenia, and a transient decrease in peripheral blood lymphocyte blastogenic responsiveness. Despite our varying the strain of virus, the manner in which the virus was grown, the size of the inoculum, and the age of the inoculated animals, infected macaques have not developed opportunistic infections or profound, prolonged loss of T cell function, key features of the macaque immunodeficiency syndrome. Therefore, experimental infection of naive macaques with D/New England has not reproduced the naturally occurring macaque immunodeficiency syndrome.

Acquired Immunodeficiency Syndrome↗

PubMed1983

Adrenergic regulation of sodium and chloride transport in the isolated cornea of rabbit and man.

Isolated corneas were mounted in Ussing-Zerahn-type chambers and short circuit current (SCC) was measured before and after application of drugs (5 X 10(-5) mol X 1(-1)) interfering with adrenergic receptors. Epinephrine increased SCC in the rabbit cornea and decreased SCC in the human cornea. alpha-Adrenergic stimulation or inhibition did not affect SCC. The increase in SCC observed after terbutaline (beta 2-agonist) was similar to the increase after isoproterenol (beta 1- and beta 2-agonist). SCC was not influenced by the beta 1-antagonist atenolol but was modified, although differently in rabbit and man, by the beta 1- and beta 2-antagonist propranolol. Thus, the catecholamine response of the rabbit and human cornea is mainly mediated by beta 2-adrenergic receptors. However, species differences were observed when testing the effect of propranolol on the transcorneal flux of 22Na and 36Cl. In the rabbit cornea the net Cl flux (directed from the aqueous to the tear side) was inhibited by propranolol, whereas net Na flux (from the tear to the aqueous side) was not influenced by the drug. In the human cornea propranolol reduced unidirectional Na flux from the aqueous to the tear side. Thus, the regulatory effect of propranolol on corneal transparency is different in man and the rabbit.

Adrenergic beta-Agonists↗

PubMed1978

Effect of honey bee venom on prostaglandin levels in mouse skin.

The effects of honey bee venom on prostaglandin (PG) E levels were studied in mouse skin under in vivo and in vitro conditions. Levels of PGE were increased 10.8-fold after 15 minutes exposure to reconstituted bee venom in vitro and 3.8-fold 35 minutes after a bee sting in vivo. Phospholipase A2 (PLA2), a major componet of bee venom, also caused a 10.9-fold increase in PGE levels in vitro and may be primarily responsible for this response of skin to bee venom.

Animals↗

PubMedDate not supplied

Evaluation of sympathetic blockade after intrathecal and epidural lidocaine in rats by laser Doppler perfusion imaging.

The widespread use of neuraxial anaesthesia increases the need for animal models to evaluate therapeutic prospects, mechanisms and risks of this technique. As a methodological prerequisite, we characterised the sympathetic blockade after different modes of neuraxial anaesthesia with regard to segments supplying the splanchnic region. Under haemodynamic monitoring, lidocaine 2% or saline were infused via intrathecal (10 microl), lumbar epidural (10 and 30 microl) or thoracic epidural (10 and 30 microl) catheters. Segmental spread of neuraxially infused local anaesthetic was assessed using methylene blue. Mean arterial blood pressure decreased more severely after neuraxial lidocaine in thoracic epidural (10 and 30 microl) compared to high-volume (30 microl anaesthesia animals. Determination of the sympathetic blockade by means of laser Doppler perfusion imaging was restricted to the paws due to a higher density of subcutaneous blood vessels as compared to the abdominal wall (mean +/- SD: 3.93 +/- 0.06 vs. 1.35 +/- 0.05/384 mm(2), p < 0.05). Only high-volume (30 microl) lumbar and thoracic epidural anaesthesia (10 and 30 microl) increased skin perfusion in both hind and front paws. This extensive sympathetic blockade was demonstrated to include splanchnic segments using thermography. Segmental spread of methylene blue did not closely correspond to laser Doppler findings and should be interpreted as minimum rather than exact epidural spread of local anaesthetic.

Anesthetics, Local↗