摘要:

Serum luteinizing hormone (LH) concentration after exposure to gonadotropin-releasing hormone (GnRH) indicates that an instantaneous increase occurs in the rate of release of LH directly from the anterior pituitary, as measured dynamically during superfusion in vitro. On the other hand, estra-diol-17β (E2) alone shows no such instantaneous effect on LH release rate (at least for the first four hours), in either physiologic or pharmacologic concentrations. At the same time, brief (ten to 30 minute) exposure of isolated anterior pituitary plasma membranes to physiologic concentrations of E2significantly alters the binding of a fully biologically active125[-GnRH to its plasma membrane receptor protein. In order to characterize the effect of E2on GnRH binding further, we preincubated dispersed bovine anterior pituitary cells for six hours in the presence or absence of physiologic concentrations of E2(10−10M). Following preincubation in the presence of E2, the cell suspension was incubated for 30 minutes with physiologic concentrations (5 x 10−11– 5 x 10−10M) of a fully biologically active125[-GnRH. The treatment, at least, doubled the number of biologically important high affinity GnRH binding sites (Kd's= 7.5 x-10−11– 4.5 x 10−10M), and changed the binding capacity of some of the binding sites up to three fold, which altered the cooperativity of GnRH-receptor interaction. Thus, the interaction of E2with GnRH at the level of GnRH receptor is mandatory for the short-term pituitary effect of E2on LH release in vitro and in vivo. At least, during the initial exposure of anterior pituitary cells, GnRH and E2function more as a controller and modulator, respectively.

ISSN:0002-9629    

出版商:OVID    

年代:1985

数据来源: OVID

ISSN:0002-9629    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The occurrence of otosclerosis and hyperlipidemia in four generations of a single family is described. The lipid abnormality fulfilled the characteristics of combined familial hyperlipidemia. Whereas a genetic linkage between combined hyperlipidemia and otosclerosis is feasible, our study indicates that both conditions are inherited through autosomal but unlinked genes.

ISSN:0002-9629    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

A patient whose initial hematologic evaluation suggested the diagnosis of a microangiopathic hemolytic anemia (MAHA) was further evaluated and found to have erythroleukemia (DiGuglielmo's syndrome). This prompted us to review retrospectively the peripheral blood morphology of 12 patients with erythroleukemia. Anisocytosis, poikilocytosis, macrocytosis, and nucleated red cells have been described in patients with erythroleukemia; however, changes characteristic of a microangiopathic hemolytic process (schistocytes) have not been previously described. Our patients with erythroleukemia had prominent helmet and fragmented red cells, as well as ellip-tocytosis. Six of our 12 patients with erythroleukemia did not have blasts on their peripheral smear, and platelets were decreased (platelet count ranged from 2 to 92 x 103/μl), resulting in changes similar to patients with MAHA due to thrombotic thrombocytopenic purpura (TTP), traumatic RBC lysis, and disseminated intravascular coagulation. Our data indicate the RBC changes characteristic of MAHA are commonly seen in erythroleukemia, and that as many as half of these patients may not have white cell changes suggestive of leukemia on the peripheral smear. Patients presenting with microangiopathic hemolytic anemia require a bone marrow examination to confirm or exclude a myelodysplastic syndrome.

ISSN:0002-9629    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

The problem of a possible interaction between amiodarone and digoxin is still unsettled. We have recently treated two patients with digoxin intoxication who had received amiodarone for eight and 36 months respectively. Both developed extreme bradycardia requiring temporary pacemakers. The presence of hypothyroidism was confirmed in both cases by laboratory data. Judging by present knowledge concerning the interaction between amiodarone, thyroid function, and digoxin, it is suggested that digoxin intoxication was not the result of its direct interaction with amiodarone. The possibility that amiodarone-induced hypothyroidism precipitated digoxin intoxication seems to be more plausible. Prevention of digitalis toxicity in amiodarone-treated patients would therefore require monitoring of thyroid function every three to six months. Frequent monitoring of digitalis blood levels is also indicated in patients with amiodarone associated hypothyroidism. Early detection of hypothyroidism and digitalis intoxication is necessary in view of the severity of the course of the disease.

ISSN:0002-9629    

出版商:OVID    

年代:1985

数据来源: OVID

ISSN:0002-9629    

出版商:OVID    

年代:1985

数据来源: OVID

摘要:

Mastocytosis represents a spectrum of clinical disorders that results from an aberrant proliferation of tissue mast cells. This disease process may be confined to the skin (cutaneous mastocytosis) or may involve multiple organs (systemic mastocytosis). Parameters that are useful in differentiating cutaneous from systemic disorders include patient age, symptom complex, and clinical signs. A wide range of clinical symptoms may be encountered in patients with mastocytosis which result from the release of pharmacologically potent mast cell mediators. Distinct cutaneous patterns resulting from skin mast cell infiltrates can be helpful in identifying patients with systemic involvement. The diagnosis of mastocytosis is confirmed by demonstrating increased tissue mast cells in involved organs.The overall prognosis for patients with proliferative mast cell disease is relatively good, although a small percentage are at risk for developing a fatal neoplastic disorder (malignant mastocytosis). Treatment of mastocytosis is directed at both inhibiting mast cell degranulation and blocking the potential systemic effects of released secretory products. Future therapeutic advances depend upon an improved understanding of the basic mechanisms involved in mast cell mediator release and the forces that govern mast cell growth and development.

ISSN:0002-9629    

出版商:OVID    

年代:1985

数据来源: OVID