Hormone secretagogues increase cytosolic calcium by increasing cAMP in corticotropin-secreting cells.

Corticotropin (ACTH)-releasing factor, vasoactive intestinal peptide, and catecholamines--hormones that stimulate ACTH secretion and cAMP generation--increased cytosolic calcium in AtT-20 cells. The increase in intracellular calcium is presumably a consequence of the stimulated cAMP synthesis, since forskolin, an activator of the catalytic unit of adenylate cyclase, and the cAMP analog 8-bromoadenosine 3',5'-cyclic monophosphate (8Br-cAMP) also increased the cytosolic levels of this ion. Pretreatment with somatostatin, a neuropeptide that inhibits stimulation of the adenylate cyclase system and the secretion of ACTH blocked the increase of cytosolic calcium.

Chromosomal locations of human tissue plasminogen activator and urokinase genes.

A panel of human-mouse somatic cell hybrids and specific complementary DNA probes were used to map the human tissue plasminogen activator and urokinase genes to human chromosomes 8 and 10, respectively. This result is in contrast to a previous assignment of a plasminogen activator gene to chromosome 6. As neoplastic cells produce high levels of plasminogen activator, it is of interest that aberrations of chromosome 8 have been linked to various leukemias and lymphomas and that two human oncogenes, c-mos and c-myc, have also been mapped to chromosome 8.

Human vitreous levels of selected antistaphylococcal antibiotics.

Staphylococcus epidermidis and S. aureus are the most common causes of bacterial endophthalmitis. A study of the penetration of selected antistaphylococcal antibiotics into human vitreous was undertaken in 58 patients.

Association of the changes in cytosolic Ca2+ and iodide efflux induced by thyrotropin and by the stimulation of alpha 1-adrenergic receptors in cultured rat thyroid cells.

Thyrotropin causes a time- and concentration-dependent increase in cytosolic Ca2+ in FRTL-5 rat thyroid cells as measured by Quin2 fluorescence; the half-maximal response occurs in response to 1 X 10(-7) M thyrotropin. The effect of added thyrotropin is the same whether cells have been previously and chronically exposed to thyrotropin or whether they have been thyrotropin "starved" for several days. The thyrotropin effect on cytosolic Ca2+ has no relationship to intracellular cAMP levels with respect to dose and time course.

Case report: prosthetic valve endocarditis caused by Pseudallescheria boydii and Clostridium limosum.

This report describes a patient with a combined infection due to Pseudallescheria boydii and Clostridium limosum on a prosthetic dura mater aortic valve homograft. While this patient had C. limosum only growing in blood cultures, both organisms were isolated from the surgically resected aortic valve.

Inhibitors of the cytochrome P-450 enzymes block the secretagogue-induced release of corticotropin in mouse pituitary tumor cells.

A mouse pituitary tumor cell line (AtT-20) releases corticotropin (ACTH) in response to a number of secretagogues, including corticotropin-releasing factor (CRF), beta-adrenergic agents, N6,O2'-dibutyryladenosine 3',5'-cyclic monophosphate (Bt2 cAMP), and potassium. The stimulation of ACTH secretion induced by the secretagogues can be blocked by inhibitors of the enzymes that generate (phospholipase A2) and metabolize (lipoxygenase and epoxygenase) arachidonic acid. The phospholipase A2 blockers mepacrine and p-bromophenacylbromide inhibited the ACTH release induced by secretagogues.

Ceftriaxone. A new cephalosporin with aqueous humor levels effective against enterobacteriaceae.

One- or two-gram doses of ceftriaxone were administered intravenously to 30 patients before cataract extraction. With the 1-g dose, mean aqueous humor concentrations of 0.93 and 0.

Beta-adrenergic mechanism of insulin-induced adrenocorticotropin release from the anterior pituitary.

Intraperitoneal administration of insulin to control rats and to rats with pituitary stalk transections or with lesions of the median eminence resulted in increased plasma adrenocorticotropin (ACTH) levels. The insulin-induced stimulation of ACTH release was blocked in both the control and lesioned animals by prior treatment with either the beta-adrenergic antagonist propranolol or the glucocorticoid analog dexamethasone. The direct application of insulin to primary cultures of the anterior pituitary did not evoke ACTH release or affect the maximal ability of corticotropin-releasing factor or epinephrine to stimulate ACTH secretion.

Increase of corticotropin-releasing factor staining in rat paraventricular nucleus neurones by depletion of hypothalamic adrenaline.

In response to stress, adrenocorticotropic hormone (ACTH) is released by corticotrophs in the anterior pituitary under the control of several central and peripheral factors including corticotropin-releasing factor (CRF), which was recently isolated from the brain and sequenced. Immunocytochemical studies have shown that most of the CRF-containing cell bodies that project to the median eminence are present in the hypothalamic paraventricular nucleus (PVN). A dense PNMT(phenylethanolamine-N-methyltransferase)-containing fibre network was also observed in the same region--PNMT is the final enzyme in the biosynthesis of adrenaline and has been demonstrated in the brain.

Multiple primaries among gynecologic malignancies.

Seventy-eight synchronous or metachronous tumors among 2362 patients followed by the Downstate Gynecologic Tumor Registry are reviewed. Significant synchronous tumor pairs include cervix (invasive and in situ)-ovary, cervix (in situ)-uterus, cervix (in situ)-kidney, endometrium-ovary, endometrium-rectosigmoid, and ovary-breast. Significant metachronous pairs include cervix (invasive and in situ combined)-lung, cervix (invasive and in situ combined)-upper alimentary tract, and cervix (invasive)-rectosigmoid.

Ceftazidime concentrations in human aqueous humor.

Two grams of ceftazidime was given to 25 patients before cataract surgery. Mean aqueous humor concentrations of 2.8, 3.

Stress hormones: their interaction and regulation.

Stress stimulates several adaptive hormonal responses. Prominent among these responses are the secretion of catecholamines from the adrenal medulla, corticosteroids from the adrenal cortex, and adrenocorticotropin from the anterior pituitary. A number of complex interactions are involved in the regulation of these hormones.

Chrysosporium, a new causative agent in osteomyelitis. A case report.

A 24-year-old black man presented with a two-month history of swelling of the right ankle. Roentgenograms were initially read as negative. One month later the patient returned with increased pain and swelling, and roentgenograms demonstrated a large lucency involving the distal tibia.

Cefonicid concentrations in human aqueous humor.

One-gram doses of cefonicid sodium were given intravenously to patients prior to cataract surgery. Although serum levels were high, cefonicid levels in aqueous humor were low: mean peak concentrations of 0.25 and 0.

Direct stimulation of beta 2-adrenergic receptors in rat anterior pituitary induces the release of adrenocorticotropin in vivo.

Previous work in our laboratory has shown that stimulation of beta 2-adrenergic receptors on mouse anterior pituitary tumor cells causes the secretion of immunoreactive adrenocorticotropin (ACTH). The present study was designed to test the hypothesis that catecholamines can cause the release of ACTH in vivo by the direct stimulation of beta 2-adrenergic receptors in the rat anterior pituitary. Systemic administration of a beta-adrenergic receptor agonist (-)-isoproterenol resulted in an increase in plasma ACTH levels in intact animals and in rats with transected pituitary stalks.

Prolonged somatostatin pretreatment desensitizes somatostatin's inhibition of receptor-mediated release of adrenocorticotropin hormone and sensitizes adenylate cyclase.

Addition of somatostatin-14 (SRIF) inhibits corticotropin releasing factor (CRF) and forskolin-stimulated cyclic AMP formation and ACTH release from tumor cells of the mouse anterior pituitary (AtT-20/D16-16). After long-term pretreatment of these cells with SRIF, the ability of SRIF to inhibit CRF and forskolin-stimulated cyclic AMP accumulation or ACTH secretion is markedly reduced. SRIF pretreatment also increases the formation of cyclic AMP in response to forskolin.

Severe, reversible neutropenia during high-dose mebendazole therapy for echinococcosis.

Two patients receiving oral high-dose mebendazole therapy for echinococcosis were found to have severe, reversible neutropenia, apparently due to marrow suppression; platelets and RBCs were also reversibly suppressed in one. High blood levels of mebendazole (239 ng/mL) in one patient may have resulted in the neutropenia and several toxic side effects, as well as a striking shrinkage of the patient's pulmonary and liver cysts. Neutropenia with high-dose mebendazole therapy may occur in up to 5% of patients and may be much more common than previously recognized.

Bradykinin stimulates phospholipid methylation, calcium influx, prostaglandin formation, and cAMP accumulation in human fibroblasts.

The biochemical events that lead to bradykinin stimulation of cAMP accumulation in human fibroblasts were examined. Treatment of human fibroblasts with bradykinin increases phospholipid methylation, Ca2+ influx, arachidonic acid release, prostaglandin formation, and cAMP content. The dose-response curves of bradykinin for the increase in the above changes were similar.