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Biomedical subjects

K Meier

Publications and source records attributed to K Meier.

43 records · Page 3Linked to original sources
PubMedDate not supplied

cAMP- and diacylglycerol-mediated pathways elevate cytosolic free calcium concentration via dihydropyridine-sensitive, omega-conotoxin-insensitive calcium channels in normal rat anterior pituitary cells.

The effect of 8-bromocyclic AMP (8-Br-cAMP) and phorbol 12-myristate 13-acetate (PMA), a protein kinase C activator, on cytosolic free calcium concentration ([Ca2+]i) in normal rat anterior pituitary cells was examined. [Ca2+]i was monitored directly by the fluorescent indicator fura-2. 8-Br-cAMP as well as PMA elevated [Ca2+]i in a concentration-dependent manner. Forskolin (10 mumol/l), which activates adenylate cyclase, and 1-oleoyl-2-acetyl-glycerol (10 mumol/l), another activator of protein kinase C, also increased [Ca2+]i. Both the 8-Br-cAMP (2 mmol/l)- and the PMA (100 nmol/l)-induced increase in [Ca2+]i was dependent on the presence of extracellular calcium and could be inhibited by the calcium channel blockers Mg2+ and nifedipine, but not by omega-conotoxin (100 nmol/l). The half-maximally inhibitory concentrations of Mg2+ and nifedipine were about 12 mmol/l and 160 nmol/l, respectively, for the [Ca2+]i response to 8-Br-cAMP (2 mmol/l), and were about 6 mmol/l and 400 nmol/l, respectively, for the PMA (100 nmol/l)-induced increase in [Ca2+]i. The sodium channel blocker tetrodotoxin (5 mumol/l) or PMA (100 nmol/l) on [Ca2+]i. After pretreatment for 3 min with PMA (100 nmol/l), the subsequent K+ (100 mmol/l)- or arachidonic acid (3 mumol/l)-induced increase in [Ca2+]i was decreased by about 50%. By contrast, pretreatment (3 min) with 8-Br-cAMP (2-10 mmol/l) markedly enhanced the subsequent [Ca2+]i response to K+ (100 mmol/l), and left the effect of arachidonic acid (3 mumol/l) on [Ca2+]i unimpaired.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Bromo Cyclic Adenosine Monophosphate↗
PubMedDate not supplied

Recovery of erythrocyte Li+/Na+ countertransport and choline transport from lithium therapy.

Li+/Na+ countertransport, choline transport, and intracellular Li+ and choline were measured in the RBC of a manic-depressive subject as a function of time after termination of Li+ therapy. Countertransport recovered from its inhibition by Li+ in 10 days. This recovery involved a decrease in the Michaelis-Menten parameter Km, without change in Vmax. RBC choline decreased, and choline influx rose, much more slowly back towards pre-Li+ values over the course of two months. Thus, choline transport was still inhibited long after Li+ levels in RBC and plasma had become undetectable. Measurements on age-separated RBC fractions showed that recovery of choline transport was mainly in the young-cell fraction. Hence inhibition of choline transport by Li+ may be irreversible at the level of the individual RBC.

Bipolar Disorder↗
PubMedDate not supplied

[Askin tumor. Rare neurogenic tumor with metastasis to mouth, jaw and face regions].

One case of a malignant peripheral neuroectodermal tumor of the thoracopulmonary region (Askin-Tumor) is reported. The tumor represents a distinct pathologic entity of neuroectodermal origin. The patient developed a metastasis in the upper jaw and in a lumbar vertebra. Morphologic and immunocytochemical findings of this extremely rare tumor were described and differential diagnosis from other soft-tissue round-cell sarcomas, such as Ewing's sarcoma and neuroblastoma are discussed. Problems associated with the clinical behavior and treatment are outlined. The prognosis in most cases of Askin-tumor is poor. The recommended therapy is radical resection, irradiation and combination chemotherapy containing anthracyclines and a high dose of alkylating agents.

Diagnosis, Differential↗