Biomedical subjects

P Blackshear

Publications and source records attributed to P Blackshear.

7 recordsLinked to original sources

PubMed1999

Extragonadal teratocarcinoma in chimeric mice.

Chimeric mice often are created through the genetic manipulation of the mouse embryo in the process of developing animal models of disease. These mice have variable percentages of their somatic and germ cells derived from the donor embryonic stem cells and host blastocysts. In the development of mouse models deficient in the breast cancer susceptibility gene 2 (Brca2) or the 70-kd heat shock protein (Hsp70-2), 3-4-week-old chimeras developed single or multiple masses composed of both well-differentiated and poorly differentiated tissues derived from all three germ layers. These cases of extragonadal teratocarcinoma, a rarely reported tumor, may be related to the genetic predisposition of the 129/Ola mouse strain used to generate the embryonic stem cells.

Animals↗

PubMed1998

Infectious dermatitis in a ball python (Python regius) colony.

Seven wild-caught ball pythons (Python regius), including six gravid females and one male, were obtained from Africa and were housed in a government animal facility in Research Triangle Park, North Carolina. Upon arrival, the snakes were found to be infested with ticks (Aponomma latus), which were manually removed. Four weeks following arrival, vesicular skin lesions began to appear on the snakes. Despite treatment of all affected female snakes with amikacin (5 mg/kg i.m., every 3 days) and cefotaxime (25 mg/kg i.m., every 3 days), the condition progressed and five of the female snakes died 7 wk after arrival. The remaining male and one female improved after an increase in environmental temperature, with ecdysis followed by healing. Physiologic stress, ectoparasites, and shipping may have predisposed the snakes to sepsis.

Amikacin↗

PubMed1997

Induction of early-immediate genes by tumor necrosis factor alpha contribute to liver repair following chemical-induced hepatotoxicity.

We and others have shown that tumor necrosis factor alpha (TNF-alpha) expression is increased in the livers of experimental animals following exposure to the chemical hepatotoxin, carbon tetrachloride (CCl4). Because TNF-alpha is involved in mediating inflammatory responses, its elevated expression is presumed to be associated with potentiating hepatotoxicity and/or aiding in liver repair processes. To study the role of TNF-alpha in chemical-induced hepatotoxicity, mice were administered neutralizing antibodies to TNF-alpha before administration of low, but hepatotoxic, doses of CCl4. Antibody treatment prevented CCl4-mediated increases in early-immediate gene expression associated with liver regeneration, including expression of c-jun and c-fos proto-oncogenes, as well as DNA binding of the activator protein-1 (AP-1) nuclear transcription factor. Hepatocyte proliferation following CCl4 treatment was also reduced in anti-TNF-alpha antibody-treated mice, as evidenced by a lack of proliferating cell nuclear antigen (PCNA) staining. Antibody treatment slightly delayed liver repair processes, as evidenced by extending the period in which plasma liver enzyme levels were increased and hepatocellular necrosis could be observed. Consistent with the above observations, injection of recombinant TNF-alpha into control mice induced rapid expression of c-jun and c-fos proto-oncogenes. Taken together, these results indicate that TNF-alpha positively modulates liver recovery following CCl4 exposure presumably by stimulating early-immediate genes involved in hepatic mitogenesis, a phenomenon also observed following partial hepatectomy.

Animals↗

PubMed1989

Evaluation of the yield stress of normal blood as a function of fibrinogen concentration and hematocrit.

The yield stress is a sensitive index of blood fluidity at low shear. Seven healthy adults were studied at hematocrits varying between 40 and 80% and fibrinogen concentrations from 0.0 to 0.935 g/dl. Multivariable analysis was used to determine the functional dependence of yield stress on hematocrit and fibrinogen level. The major findings from this analysis include a decreasing effect of fibrinogen at high concentrations (saturation effect), a relative insensitivity of yield stress to fibrinogen at low concentration (threshold effect), and a strong interaction between the effects of hematocrit and fibrinogen concentration on yield stress. Our results give the normal range of yield stress for a given value of fibrinogen and hematocrit and can be used to predict the effect of reductions in hematocrit or fibrinogen on the yield stress of normal blood.

Adult↗

PubMed1986

Age-related alterations in trimethoprim-sulfadiazine disposition following oral or parenteral administration in calves.

Age-related changes in the absorption and distribution patterns of trimethoprim/sulfadiazine were studied following oral or subcutaneous administration of 15 mg/kg of the drug combination in calves. Following oral administration, the time course of trimethoprim/sulfadiazine appearance and dissipation in serum, synovial fluid and urine was followed for periods up to 48 hours in calves one day, one week and six weeks of age. The profiles of drug appearance-disappearance in these body fluids were also determined after subcutaneous administration in seven week old calves. The peak serum and synovial fluid levels of trimethoprim/sulfadiazine achieved following oral administration were substantially lower with increasing maturation. In ruminating (six and seven week old) calves, subcutaneous or oral administration of the combination led to high serum levels of sulfadiazine but little or no serum trimethoprim was detected in animals at this age. The data indicate that, while therapeutic concentrations and optimum ratios of the drugs may be achieved for extended time periods in neonatal life, this dosage is unable to produce optimum serum and synovial fluid concentrations as the calves mature.

Administration, Oral↗

PubMed1985

Lifetime lead intoxication: influence on the amygdaloid kindling model of epileptogenesis.

The nature of amygdaloid kindled seizures was studied in adult rats which were intoxicated with lead starting in neonatal life. Lactating females were exposed to lead via the drinking water (0.25% lead acetate) and the litters were continued on this level of lead after weaning at 27 days of age. When compared to controls, levels of lead in the blood and brain were significantly higher in lead-exposed rats, both at the time of weaning as well as postkindling, beyond 150 days of age. Parameters relating to amygdaloid kindled seizures, including the rate of kindling, seizure latency and seizure threshold were not significantly different in lead-treated rats than in controls. However, duration of behavioral seizures and afterdischarges was significantly longer in rats exposed to lead. Our data suggest that, although lead intoxication starting in neonatal life does not appear to affect the susceptibility to development of amygdaloid kindled seizures, it may enhance seizure severity in this model of epileptogenesis.

Amygdala↗

PubMedDate not supplied

Lead intoxication and the amygdaloid kindling model of epileptogenesis in the adult rat.

The influence of lead intoxication on the seizure state produced by amygdaloid kindling was studied in rats. Exposure to 1% lead (in the form of lead acetate) in drinking water for periods up to 4 weeks led to significant increases in lead content in the blood and various brain regions. Signs of lead intoxication, including behavioral depression, loss of body weight and decreased hematocrit were produced by this treatment regime. The intensity and nature of behavioral convulsions as well as the rate of development of amygdaloid kindled seizures did not appear to be affected by lead intoxication. However, lead exposure during kindling led to significant increases in an electrographic aspect of the seizure, i.e., the afterdischarge duration. Although pair-fed controls were not utilized and therefore definitive conclusions cannot be made, our data would seem to indicate that lead intoxication has a relatively minor ability to potentiate amygdaloid kindling in adult rats.

Amygdala↗