Biomedical subjects

K Hendricks

Publications and source records attributed to K Hendricks.

22 records · Page 2Linked to original sources

PubMed1985

Quantitation of herpes simplex virus in rabbit corneal epithelium.

The authors have developed an objective method for quantitation of herpes simplex virus in the corneal epithelium of rabbits. At appropriate times postinfection, full-thickness rabbit corneas were removed by trephination and subjected to one cycle of freezing and thawing. The corneal epithelium was then disrupted by sonication. The amount of infectious virus recovered from sonicated specimens was determined by an in vitro plaque assay, providing a measure of the quantity of virus present during the acute stage of herpetic keratitis. Using this technique, the authors found that the mean virus titer was reduced from 1.5 X 10(5) plaque forming units (pfu) per cornea in control rabbits to less than 200 pfu per cornea in rabbits treated topically for 2 days with 1% trifluridine. In contrast, instillation of 1% prednisolone acetate resulted in the persistence of higher levels of virus (275 pfu) than those observed in control rabbits (3 pfu) 4 days after the cessation of therapy.

Animals↗

PubMed1985

The in vitro photosensitivity of systemic lupus erythematosus skin fibroblasts.

To investigate the role of DNA damage in the pathogenesis of systemic lupus erythematosus (SLE), we studied the ability of skin fibroblasts derived from SLE patients to recover from ultraviolet (UV) light radiation of varying wavelengths. Four of five SLE cell strains were more sensitive to UV-C (254 nm), sun lamp, and UV-A (320 to 400 nm) light than were normal cells. SLE cellular recovery was most sensitive to broad spectrum, long wavelength light. This hypersensitivity did not appear to result from the UV light activation of a clastogenic factor. Experiments which examined the DNA repair capacity of irradiated cells indicated that SLE fibroblasts may be able to excise certain DNA lesions as well as normal cells. The mechanisms responsible for the hypersensitivity of SLE cells remain under investigation.

Adolescent↗

PubMed1983

alpha 1-acid glycoprotein involvement in high affinity binding of tricyclic antidepressants to human plasma.

The binding of the tricyclic antidepressants imipramine (IMI) and desmethylimipramine (DMI) to human plasma and individual proteins was studied by equilibrium dialysis. Both drugs bound extensively to plasma, albumin, and alpha 1-acid glycoprotein, while there was very little binding to the gamma-globulin fraction. The binding of both IMI and DMI to alpha 1-acid glycoprotein was high affinity (association constant K, 9.2 X 10(4)/M and 4.7 X 10(4)/M respectively) and low capacity (number of binding sites, n = 1 for both IMI and DMI), whereas the binding to albumin was low affinity (K for IMI, 2.3 X 10(2)/M and for DMI, 3 X 10(2)/M) and high capacity (n = 7). The binding of IMI to a mixture of human serum albumin and alpha 1-acid glycoprotein revealed two sets of binding sites; a high affinity binding site corresponding to alpha 1-acid glycoprotein and a low affinity binding site corresponding to albumin. The binding affinity and/or number of binding sites for IMI binding to albumin decreased with increasing albumin concentrations. The free fraction in plasma of nineteen normal, male controls was significantly correlated with the concentration of alpha 1-acid glycoprotein (r = 0.601, P less than 0.01), although there was no correlation with albumin or free fatty acid concentrations in plasma.

Antidepressive Agents, Tricyclic↗

PubMedDate not supplied

Lack of serologic evidence for an association between Cache Valley Virus infection and anencephaly and other neural tube defects in Texas.

We tested the hypothesis that Cache Valley Virus (CVV), an endemic North American bunyavirus, may be involved in the pathogenesis of human neural tube defects. This investigation followed a 1990 and 1991 south Texas outbreak of neural tube defects with a high prevalence of anencephaly and the demonstration in 1987 that in utero infection by CVV was the cause of outbreaks of central nervous system and musculoskeletal defects in North American ruminants. Sera from 74 women who gave birth to infants with neural tube defects in south Texas from 1993 through early 1995 were tested for CVV neutralizing antibody. All tested sera did not neutralize CVV. These data suggest that CVV is not involved in the induction of human neural tube defects during nonepidemic periods but do not preclude CVV involvement during epidemics. Other endemic bunyaviruses may still be involved in the pathogenesis of neural tube defects or other congenital central nervous system or musculoskeletal malformations.

Anencephaly↗