PubMed Health⌕ Search

Biomedical subjects

D Gregg

Publications and source records attributed to D Gregg.

17 recordsLinked to original sources
PubMed2000

Arginine vasopressin in the treatment of 50 patients with postcardiotomy vasodilatory shock.

BACKGROUND: The barroreflex-mediated secretion of arginine vasopressin has been found to be defective in a variety of vasodilatory shock states, such as postcardiotomy shock, and administration of the hormone markedly improves vasomotor tone and blood pressure. The high incidence of vasodilatory shock in patients undergoing left ventricular assist device (LVAD) implantation makes this population an ideal model in which to assess the risks and benefits of vasopressin. METHODS: The medical records of the 102 patients receiving LVADs at Columbia-Presbyterian Medical Center from January 1995 to August 1998 were reviewed. Fifty patients were eligible for study based on a history of arginine vasopressin administration in the operating room or intensive care unit within 24 hours of implantation. RESULTS: Despite LVAD implantation and the administration of vasopressors, patients were hypotensive with a mean arterial pressure less than 60 mm Hg. The administration of vasopressin (0.09+/-0.05 U/min) increased mean arterial pressure (58+/-13 to 75+/-14 mm Hg; p<0.001) while reducing norepinephrine administration (11.7+/-13 to 7.9+/-6.0 mcg/min; p = 0.023). There was no significant change in LVAD flow. The incidence of compromised regional perfusion was not different between LVAD patients who received vasopressin as compared to hemodynamically stable LVAD patients who did not receive vasopressin. CONCLUSIONS: We have demonstrated vasopressin at low doses to be a safe and an effective vasopressor in 50 patients with postcardiotomy vasodilatory shock.

Arginine Vasopressin↗
PubMed2000

Clinical presentation and antiviral therapy for poxvirus infection in pudu (Pudu puda).

A severe poxvirus infection occurred in three pudu (Pudu puda), resulting in two fatalities. Cutaneous ulcers with mucopurulent exudate were present around the eyes and nose, at the lip margins, coronary bands, and teats. Mucosal ulcers were present in the oral cavity, esophagus, and forestomachs. In the two fatalities, a secondary disseminated fungal infection also occurred. Affected animals were leukopenic, hypocalcemic, and hyperphosphatemic and had elevated serum alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase levels. Electron microscopic examination of affected skin confirmed the presence of a poxvirus. Neutralizing antibody titers to this virus were present in the two pudu tested. One case was treated with cidofovir, 5 mg/kg i.v. q7d for four treatments. Complete recovery occurred in the treated animal. This is the second report of poxvirus infection in pudu and the first report describing clinical presentation, presence of secondary disseminated fungal infection, and successful treatment.

Animal Diseases↗
PubMed1998

Estrogen-induced rat pituitary tumor is associated with loss of retinoblastoma susceptibility gene product.

Chronic treatment of rats with the estrogens 17beta-estradiol or diethylstilbestrol (DES) induces pituitary tumors in Fischer 344 but not Brown-Norway or Sprague-Dawley rats. Functional loss of retinoblastoma susceptibility gene product (pRb), a major regulatory protein for the G1 to S transition of the cell cycle, has been shown in several tumors. Here we report a decreased level of pRb in pituitary tumors of the Fischer 344 rat as compared with resistant Sprague Dawley and Brown-Norway strains. pRb protein levels decreased 70% in Fischer 344 rats that were treated with diethylstilbestrol for 10 weeks as compared with tumor resistant control animals. Interestingly, the F1 hybrid (Fischer 344 x Norway) showed an intermediate range of pRb protein expression as compared with those of the parental strains. pRb expression levels in nonhemorrhagic F2 (F1 x F1) rats correlated with the size of the tumors. One week withdrawal of DES increased pRb levels as compared with continuously treated rats. Also, there was a decreased association of cyclin D and cyclin dependent kinase in susceptible tumors, supporting the hypothesis of a physical and possibly functional loss of pRb in the diethylstilbestrol-induced pituitary tumor. These results suggest that the difference in pRb regulation, whether it is a direct or indirect effect of estrogen, is related to tumor resistance or susceptibility in these two rat strains.

Animals↗
PubMed1998

Differential regulation by estrogens of growth and prolactin synthesis in pituitary cells suggests that only a small pool of estrogen receptors is required for growth.

PR1 cells are a prolactin (PRL)-secreting cell line derived from a pituitary lactotroph tumor found in 17beta-estradiol-treated Fischer 344 rats. We examined the effect of estrogen on cell proliferation and PRL synthesis under various culture conditions. Estrogen, at extremely low concentrations, induces cell proliferation in this cell line, whereas antiestrogen inhibits proliferation. Interestingly, the proliferation response is much more sensitive than the PRL response because 0.01 pM estradiol or diethylstilbestrol induces half-maximal growth induction [ approximately 0.1% estrogen receptor (ER) occupancy is required], whereas 0.01 nM concentration is required for half-maximal PRL induction ( approximately 50% ER occupancy is required). The proliferation response is not as sensitive to antiestrogen as the PRL response, because 10 nM concentration of the pure antiestrogen ICI 182,780 could not inhibit 1 nM estradiol- or diethylstilbestrol-induced proliferation. The same concentration of ICI 182,780 decreased PRL secretion to 1% of estradiol- or diethylstilbestrol-induced prolactin secretion suggesting a possible dichotomy of ER control of proliferation and PRL synthesis. The Kd of ER binding in these cells is about 3 x 10(-11) M. These results with the PR1 cells extend previous studies in other estrogen- regulated systems and suggest that only a small pool of ER is required for cell proliferation in contrast with the regulation of expression of specific genes. They also raise questions as to how a dimeric receptor functions when only one ligand site is occupied or when both an estrogen and an antiestrogen occupy one dimer.

Animals↗
PubMed1997

Doing it her way.

Explore the source record for details and available documents.

Attitude to Health↗
PubMed1997

Estrogens and the genetic control of tumor growth.

Biochemical and genetic studies of the estrogen-induced pituitary tumors of the F344 rat provide a new model for understanding cancer biology. Because a genetic difference in tumor susceptibly already exists in this animal model it is possible to search for the underlying mechanisms. Interestingly, thus far marked changes in expression of known or unknown oncogenes do not appear to be involved in the formation of this tumor. Similarly, known angiogenic factors have not been implicated in this model's dramatic angiogenic response to estrogen. It will be very informative to dissect out the critical genes and the products that are involved in this system and then to determine whether similar genes are involved in human, estrogen-induced cancers.

Animals↗
PubMed1996

Decreased expression of carboxypeptidase E protein is correlated to estrogen-induction of rat pituitary tumors.

Following the cleavage of peptide precursors by endopeptidases such as the proprotein convertases PC2 and PC3, carboxypeptidase E (CPE) functions to remove basic amino adds from the C-terminus of various pituitary hormones. We investigated the role of CPE in the differential sensitivity between rat strains to estrogen-induced pituitary tumors. Pituitary CPE protein levels were unchanged by diethylstilbestrol (DES) in tumor-resistant Sprague-Dawley (SD) rats. However, in tumor-susceptible Fischer 344 (F344) rats, DES decreased CPE protein levels such that by 7 and 8 weeks of treatment, CPE was barely detectable. One week withdrawal of DES caused an increase in CPE protein levels at 8 weeks. After 2 and 4 weeks of DES treatment, CPE protein levels in F344 rats decreased to 18 and 2.3% of control values, respectively, but no strain difference was observed in the protein levels of proprotein convertase 2 (PC2) or PC3. Additionally, Brown Norway (BN), F344, and F1 hybrid (BN x F344) rats were treated with DES for 10 weeks. The level of pituitary CPE protein was not affected by DES in BN rats whereas F344 rats had only 8% of the level of CPE pituitary protein of BN rats. The pituitaries of F1 rats, which had an intermediate weight response to DES, had an intermediate level of CPE protein (31% that of BN rats). Levels of CPE mRNA were not affected by DES in SD rats while in F344 rats DES tended to decrease levels of CPE mRNA after both 2 and 4 weeks of treatment, although the response was variable. It thus appears that pituitary CPE protein is differentially regulated by DES between tumor-resistant rats and F344 rats primarily at the post-transcriptional level. Furthermore, in F344 rats, levels of CPE protein are inversely correlated to increases in pituitary weight caused by DES treatment.

Animals↗
PubMed1994

Ductal carcinoma in situ of the breast: results of treatment by conservative surgery and definitive irradiation.

PURPOSE: To determine local control, survivorship, and cosmesis in women with ductal carcinoma in situ treated by conservative surgery and radiation therapy. METHODS AND MATERIALS: We retrospectively analyzed the results of treatment in 56 women with in situ carcinoma of the breast, treated between 1976 and 1990 by conservative surgery and irradiation. Two women had bilateral tumors, for a total of 58 breasts at risk. All patients underwent gross excision of the tumor followed by radiation to the entire breast and a sequential boost to the tumor bed. Eight of the 21 evaluable tumors (38%) had inadequate pathologic margins at the time of excision. Routine re-excision was not performed. The median dose to the whole breast and primary tumor site was 5000 cGy and 6940 cGy, respectively. Median follow-up was 61 months (range 27-191 months). RESULTS: Five patients (9%) failed in the breast for an 8-year actuarial local failure rate of 11%. Median time to failure was 34 months. All five patients with local recurrence underwent mastectomy and are alive, without evidence of disease at a mean of 40 months post mastectomy. The 8-year actuarial absolute and cause specific survivals were 89% and 100%, respectively. Cosmetic results were excellent or totally acceptable in 90% of patients. CONCLUSION: Patients with ductal carcinoma in situ treated by excision and irradiation achieved acceptable local control and excellent survival and cosmetic results. Because of the long time course associated with local failure, diligent and protracted follow-up is mandatory.

Adult↗
PubMed1986

In vitro and in vivo association of African swine fever virus with swine erythrocytes.

The association of African swine fever virus (ASFV) with swine erythrocytes in vivo, in high titers, was verified by inoculating 30 pigs with 17 ASFV isolates and assaying their plasma and washed erythrocyte fractions for residual virus. Viral antigens were specifically localized on the surface of in vitro and in vivo swine erythrocytes, using the fluorescent antibody technique and 3 monoclonal antibodies specific for ASFV. The same monoclonal antibodies immunoprecipitated virus-specific polypeptides of molecular weights 13 kd and 73 kd from ASFV-infected Vero cells. Erythrocytes from viremic swine infected with Lisbon-60, Dominican Republic, Badajoz-M98, or Cameroon isolates of ASFV were studied by transmission electron microscopy. Virus was found in membrane depressions at the surface of erythrocytes. These surface depressions resembled stages of smooth surfaced pits. Erythrocytes from viremic pigs were fragile osmotically.

African Swine Fever↗
PubMed1983

The role of human growth hormone in the regulation of cholesterol and bile acid metabolism.

Cholesterol and bile acid metabolism was studied in 16 children with human GH (hGH) deficiency (11 with isolated hGH deficiency and 5 with multiple trophic hormone deficiency) before and after 6 months of hGH therapy. We measured plasma lipid concentrations, biliary lipid composition, and cholesterol saturation indices; calculated the bile acid pool size measured by the isotopic dilution technique using the stable isotope chenodeoxycholic-[11,12-d2] acid; and measured cholesterol and bile acid synthetic rates by sterol balance techniques. In all 16 patients, plasmas lipid concentrations were unchanged after hGH therapy; total plasma cholesterol was 182 +/- 10 (+/-SEM) mg/dl before and 179 +/- 9 mg/dl after treatment, high density lipoprotein-cholesterol was 47 +/- 2 mg/dl before and 49 +/- 3 mg/dl after treatment, low density lipoprotein-cholesterol was 112 +/- 10 mg/dl before and 111 +/- 8 mg/dl after therapy, and triglyceride was 113 +/- 13 mg/dl before and 107 +/- 10 mg/dl after hGH therapy. Biliary lipid composition and cholesterol saturation in 10 patients were similar to those in controls and unchanged with hGH therapy. Cholesterol synthesis (n = 14) was unchanged (7.6 +/- 1.4 vs. 9.6 +/- 1.2 mg/kg X day); however, bile acid synthesis (n = 15) increased from 3.1 +/- 0.4 to 4.3 +/- 0.6 mg/kg X day (P less than 0.025) after therapy. The chenodeoxycholate pool size (n = 8) was significantly reduced (P less than 0.025) before hGH treatment (416 +/- 64 mg/m2) compared to that in controls (617 +/- 45 mg/m2) and increased to 620 +/- 72 mg/m2 after hGH therapy (P less than 0.05). Chenodeoxycholate pool size expansion during hGH therapy was, at least in part, caused by an increase in hepatic bile acid synthesis. These findings suggest that hGH may indirectly modulate cholesterol metabolism through regulation of hepatic cholesterol 7 alpha-hydroxylase activity, the rate-limiting enzyme of bile acid synthesis.

Adolescent↗
PubMed1968

Renal trauma.

Explore the source record for details and available documents.

Humans↗