Comparison of the cervicovaginal gram stain and rapid latex agglutination slide test for identification of group B streptococci.
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Antigens, Bacterial↗
Biomedical subjects
R B Clark
Publications and source records attributed to R B Clark.
Oxygen desaturation in women in labor.
Oxygen saturation and end-tidal CO2 tension were monitored in 15 healthy women during labor. Oxygen saturation was determined with a pulse oximeter and end-tidal CO2 with a CO2 monitor. Fetal heart rate, uterine contractions and maternal blood pressure were also monitored. End-tidal CO2 tension was followed to determine if falls in oxygen saturation during labor were related to hyperventilation. Ten of the 15 patients exhibited periods of oxygen saturation of less than 90%. End-tidal CO2 was consistently low, usually less than 30 mm Hg. Most, but not all (7 of 10), of the patients who showed desaturation had received narcotics. There were often periods of apnea and/or shallow respirations between contractions. These aberrations and hyperventilation-induced hypocarbia were probably the cause of the oxygen desaturation. No changes in fetal heart rate or low Apgar scores were noted.
Adolescent↗
Identification of a specific domain in the beta-adrenergic receptor required for phorbol ester-induced inhibition of catecholamine-stimulated adenylyl cyclase.
The molecular basis for the effects of 4 beta-phorbol 12-myristate 13-acetate (PMA) on adenylyl cyclase activation was examined using site-directed mutants of the hamster beta-adrenergic receptor (beta AR) expressed in L cells. Phorbol ester activation of protein kinase C (PKC) in L cells transfected with wild-type beta AR caused at least three discernible effects on adenylyl cyclase activity, each with an EC50 of 20 to 50 nM, (i) a 2-3-fold increase in the Kact for epinephrine stimulation, (ii) a 2-3-fold increase in the maximal level (Vmax) of hormonal stimulation, and (iii) a decrease in the Gi-mediated inhibition of forskolin stimulation. Deletion from the beta AR of amino acid residues 259-262, which removes one of the two consensus sites for phosphorylation by PKC, eliminated (greater than 90%) the PMA-induced increase in the Kact, whereas the PMA-induced increase in the Vmax and loss of Gi-mediated inhibition were not affected by the deletion. Neither deletion of the other PKC consensus site in the beta AR (residues 343-348) nor truncation of the Ser/Thr-rich C-terminal domain (residues 354-418) affected the PMA-induced changes in adenylyl cyclase. The effects of PMA on Gi-mediated inhibition and the Vmax closely mimicked the action of islet-activating protein, consistent with a direct effect of PMA-activated PKC on Gi. In contrast, the effects on the Kact appear to be receptor specific. These results demonstrate that the consensus site for phosphorylation by PKC, found in the third intracellular loop of the beta AR, is required for the PMA-induced increase in the Kact for epinephrine stimulation. Use of L cells transfected with D(259-262)beta AR allowed the characterization of the postreceptor effects of PMA without interference from receptor-level effects.
Adenylate Cyclase Toxin↗
Murine T helper cell clones secrete granulocyte-macrophage colony-stimulating factor (GmCSF) by both interleukin-2-dependent and interleukin-2-independent pathways.
Granulocyte-macrophage colony-stimulating factor (GmCSF) is a lymphokine secreted by class II major histocompatibility complex (MHC)-restricted T cells after lectin or antigen stimulation. To investigate the relationship between interleukin-2 (IL-2) and GmCSF production, we utilized long-term cultures of porcine myelin basic protein (PMBP)-specific T helper cell clones that were maintained with IL-2 in the absence of antigen or irradiated antigen-presenting cells (APC). We have found that supernatants of these T cell clones contained GmCSF activity after IL-2 stimulation. Inhibition of cell proliferation by irradiation failed to stop GmCSF production. When these clones were stimulated with PMBP and irradiated APC in the presence of anti-IL-2 receptor antibody, the T cell supernatants still contained GmCSF activity. These results indicate that (1) GmCSF production by T helper clones after IL-2 stimulation is independent of cell proliferation and (2) antigen/MHC-stimulated GmCSF production by T cell clones can occur by an IL-2-independent pathway.
Animals↗
Effects of H-7 are not exclusively mediated through protein kinase C or the cyclic nucleotide-dependent kinases.
Culturing murine T cell tumor lines in the presence of the protein kinase inhibitor H-7 for 4 days led to their dependence on H-7 for maximal constitutive proliferation. Withdrawal of H-7 from H-7-conditioned cells led to inhibition of proliferation and cell death. The mechanism underlying this H-7 dependence does not appear to be related to clonal selection or to effects on protein kinase C or the cyclic nucleotide-dependent kinases. This suggests that all the effects of the widely used H-7 may not be completely understood, and that H-7 may be useful in the dissection of the complex patterns of growth regulation in T cell malignancies.
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
Group A streptococcal peritonitis in a patient undergoing continuous ambulatory peritoneal dialysis.
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Female↗
Citing the differential diagnosis.
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Blindness↗
Cell-free heterologous desensitization of adenylyl cyclase in S49 lymphoma cell membranes mediated by cAMP-dependent protein kinase.
We have examined the cell-free heterologous desensitization of adenylyl cyclase in plasma membrane preparations from S49 wild-type (WT) and kin- cells (which lack cAMP-dependent protein kinase) incubated with purified catalytic subunit of cAMP-dependent protein kinase (cA.PKc). cA.PKc caused a rapid (t1/2 = 40 s) decrease in the hormone responsiveness of adenylyl cyclase in the WT membrane preparations that mimicked the intact cell heterologous desensitization; that is, there was an increase in the Kact for both epinephrine and prostaglandin E1 (PGE1) stimulations of adenylyl cyclase induced at the receptor level because neither forskolin- nor NaF-stimulated activity was affected. The desensitization was independent of agonist occupancy of the receptor, and the effects were blocked both by the active fragment (amino acids 5-22) of the specific inhibitor of cA.PK and by p[NH]ppA. cA.PKc treatment of kin- membranes resulted in a heterologous desensitization that resembled the effects of WT adenylyl cyclase, with the exception that forskolin-stimulated activity was also reproducibly decreased by 24%. cA.PKc had no effect on WT membranes isolated from cells that had previously undergone maximal heterologous desensitization during treatment with 10 microM forskolin. In contrast, cA.PKc-induced heterologous desensitization of kin- membranes was additive with the epinephrine-induced homologous desensitization of intact cells. Cell-free desensitizations were reversed by incubation of membranes with cA.PKc and ADP, conditions that drive the kinase reaction backward. The similarities of our cell-free cA.PKc-mediated heterologous desensitization of adenylyl cyclase with the intact cell desensitization support our hypothesis that heterologous desensitization of the WT lymphoma cells is mediated by cA.PK via a mechanism independent of homologous desensitization.
Adenosine Diphosphate↗
In vitro sensitivity of Candida (Torulopsis) glabrata to clotrimazole.
Vulvovaginitis caused by Candida (Torulopsis) glabrata is often refractory to intravaginal imidazole therapy. Clotrimazole achieves its fungistatic activity for Candida albicans and C. glabrata by inhibiting different steps in intermediary cell metabolism. For C. glabrata, alkylation precedes dimethylation. The possibility that this altered sequence might account for the relative therapeutic nonresponsiveness was studied by determining comparative minimal inhibitory concentrations (MICs) of clotrimazole. In vitro analyses of ten strains of C. glabrata and 30 control strains of C. albicans performed using both agar and broth dilution tests revealed that four-fold lower MICs were consistently demonstrable with C. glabrata, irrespective of inoculum size. The data suggest that clinical difficulties encountered in the therapy of torulopsis vulvovaginitis probably represent the inability of intravaginal medication to eradicate urethral/urinary bladder colonization and subsequent reinfection rather than true therapeutic failures.
Candida↗
Listeria monocytogenes peritonitis in a patient on continuous ambulatory peritoneal dialysis.
We report a case of peritonitis in a patient on continuous ambulatory peritoneal dialysis caused by Listeria monocytogenes. The patient was taking oral corticosteroids for underlying systemic lupus symptoms, and had classic signs and symptoms of peritonitis. There was initial clinical deterioration while in vitro data indicating that the organism was sensitive to vancomycin with a minimum inhibitory concentration of 0.5 micrograms/ml. The patient rapidly responded to intravenous ampicillin. We believe this to be the second reported case of L. monocytogenes peritonitis in a CAPD patient.
Adult↗
Identification of a specific site required for rapid heterologous desensitization of the beta-adrenergic receptor by cAMP-dependent protein kinase.
The molecular basis for heterologous desensitization of the beta-adrenergic receptor (beta AR) was investigated by site-directed mutagenesis of the beta AR protein. Rapid heterologous desensitization of agonist-stimulated adenylyl cyclase activity was observed when L cells expressing the wild-type beta AR were incubated with 50 nM epinephrine. This desensitization response could be mimicked in a cell-free system by incubation with cAMP-dependent protein kinase (cA.PK). Deletion of amino acid residues 259-262 from the beta AR, removing one of the two consensus sequences in the receptor for phosphorylation by cA.PK, abolished the ability of the receptor to undergo rapid heterologous desensitization. In contrast, deletion of the other cA.PK consensus sequence (residues 343-348) or truncation of the Ser/Thr-rich C-terminal tail of the beta AR (deletion of residues 354-418) did not affect this heterologous desensitization process. These results suggest that the action of cA.PK on amino acid residue(s) contained within the sequence 259-262 of the beta AR is required for rapid heterologous desensitization of the receptor in response to agonists.
Adenylyl Cyclases↗
Pseudallescheria boydii brain abscess: association with near-drowning and efficacy of high-dose, prolonged miconazole therapy in patients with multiple abscesses.
Brain abscess caused by Pseudallescheria boydii is a highly lethal infection, usually seen in immunosuppressed patients. Five patients with P. boydii brain abscesses are described. Four of these patients acquired their infection after near-drowning; 1 patient developed an abscess after penetrating head trauma. Two patients survived their infections, which included involvement of other body sites (lung, eye, bone) as well as multiple undrained brain abscesses, after prolonged courses of high-dose parenteral miconazole (80-90 mg/kg/d). Progressive increases in miconazole dosage during the treatment periods were required to produce serum levels above the minimum inhibitory concentrations of the fungal isolates.
Adult↗
Co-infection with Legionella pneumophila and Pneumocystis carinii in a patient with chronic lymphocytic leukemia.
A patient with chronic lymphocytic leukemia was found to have pneumonitis caused by a simultaneous Pneumocystis carinii and Legionella pneumophila infection. Although both microorganisms frequently cause pulmonary infections in immunocompromised patients, co-infection has not been reported. This patient responded to antimicrobial therapy, but superinfection with Candida albicans led to his death. As there are numerous infective and noninfective causes of pneumonia in such patients, this case illustrates that the identification of a single etiologic agent does not obviate the search for other potential causes.
Aged↗
Subtypes of helper cells. Non-inflammatory type 1 helper T cells.
Class II MHC-restricted T cells recently have been characterized as being either type 1 (Th1) or type 2 (Th2) based on their ability to both secrete different lymphokines and perform different functions. Characterization of these subtypes to date have indicated that Th1 cells secrete IL-2, IFN-gamma, lymphotoxin, and IL-3, whereas Th2 cells secrete IL-4, IL-5, and IL-3. Functionally, Th1 cells mediated cytotoxicity and delayed-type hypersensitivity, and have been termed "inflammatory cells," whereas Th2 cells mediate helper function for Ig secretion and have been termed, "regulatory cells." We now present evidence that not all Th1 clones are inflammatory and capable of mediating cutaneous delayed-type hypersensitivity. We have generated a number of myelin basic protein-specific Th1 clones that do not mediate swelling when injected together with myelin basic protein directly into the footpads of syngeneic mice. These results suggest that Th1 cells can be further subdivided based on their ability to mediate delayed-type hypersensitivity, and that the Th1/Th2 characterization of Th cells may be insufficient to adequately characterize all functional subtypes of class II MHC-restricted T cells.
Animals↗
Identification of the glucose transporter in mammalian cell membranes with a 125I-forskolin photoaffinity label.
The glucose transporter has been identified in a variety of mammalian cell membranes using a photoactivatable carrier-free radioiodinated derivative of forskolin, 3-[125I]iodo-4-azidophenethylamido-7-O-succinyldeacetylforskoli n ([125I]IAPS-forskolin) at 1-3 nM. The membranes that were photolabelled with [125I]IAPS-forskolin were human placental membranes, rat cortical and cerebellar synaptic membranes, rat cardiac sarcolemmal membranes, rat adipocyte plasma membranes, smooth-muscle membranes, and S49 wild-type (WT) lymphoma-cell membranes. The glucose transporter in plasma membranes prepared from the insulin-responsive rat cardiac sarcolemmal cells, rat adipocytes and smooth-muscle cells were determined to be approx. 45 kDa by SDS/polyacrylamide-gel electrophoresis (PAGE). Photolysis of human placental membranes, rat cortical and cerebellar synaptic membranes, and WT lymphoma membranes with [125I]-IAPS-forskolin, followed by SDS/PAGE, indicated specific derivatization of a broad band (43-55 kDa) in placental membranes and a narrower band (approx. 45 kDa) in synaptic membranes and WT lymphoma membranes. Digestion of the [125I]IAPS-forskolin-labelled placental and WT lymphoma membranes with endo-beta-galactosidase showed a reduction in the apparent molecular mass of the radiolabelled band to approx. 40 kDa. The membranes that were photolabelled with [125I]IAPS-forskolin and trypsin-treated produced a radiolabelled proteolytic fragment with an apparent molecular mass of 18 kDa. [125I]IAPS-forskolin is a highly effective probe for identifying low levels of glucose transporters in mammalian tissues.
Affinity Labels↗
Activation of cAMP-dependent protein kinase is required for heterologous desensitization of adenylyl cyclase in S49 wild-type lymphoma cells.
We report here that, contrary to previously reported findings, treatment of S49 wild-type (WT) lymphoma cells with 0-50 nM epinephrine resulted in a heterologous desensitization of adenylyl cyclase (EC 4.6.1.1)--that is, epinephrine and prostaglandin E1 (PGE1) stimulations of adenylyl cyclase were reduced. Observation of this heterologous desensitization required the assay of adenylyl cyclase with submillimolar concentrations of Mg2+ and low concentrations of epinephrine. Also, whereas previously there had been no evidence for any role of cAMP-dependent protein kinase in the desensitization of the WT beta-adrenergic receptor, our data comparing the characteristics of the desensitization in WT, kin-, and cyc- lymphoma cells [where kin- and cyc- refer to variants of S49 WT cells lacking cAMP-dependent protein kinase activity (kin-) and the alpha subunit of the stimulatory guanine nucleotide-binding regulatory protein (cyc-)] now suggest that cAMP-dependent protein kinase mediates the heterologous desensitization of adenylyl cyclase. Specifically, we found that only the WT cells exhibited epinephrine-induced heterologous desensitization. The kin- and cyc- cells exhibited only homologous desensitization, and much higher concentrations of epinephrine were required to elicit the homologous desensitization in the variants relative to the heterologous desensitization of the WT. Treatment of WT and cyc- cells with dibutyryl cAMP or treatment of WT with forskolin or PGE1 caused the heterologous desensitization of adenylyl cyclase, indicating that neither receptor occupancy nor activation of adenylyl cyclase was necessary for the heterologous desensitization.
Adenylyl Cyclases↗
Selective block of calcium current by lanthanum in single bullfrog atrial cells.
A single suction microelectrode voltage-clamp technique was used to study the actions of lanthanum ions (La3+) on ionic currents in single cells isolated from bullfrog right atrium. La3+, added as LaCl3, blocked the "slow" inward Ca2+ current (ICa) in a dose-dependent fashion; 10(-5) M produced complete inhibition. This effect was best fitted by a dose-response curve that was calculated assuming 1:1 binding of La3+ to a site having a dissociation constant of 7.5 x 10(-7) M. La3+ block was reversed (to 90% of control ICa) following washout and, in the presence of 10(-5) M La3+, was antagonized by raising the Ca2+ concentration from 2.5 to 7.5 mM (ICa recovered to 56% of the control). However, the latter effect took approximately 1 h to develop. Concentrations of La3+ that reduced ICa by 12-67%, 0.1-1.5 x 10(-6) M, had no measurable effect upon the voltage dependence of steady state ICa inactivation, which suggest that at these concentrations there are no significant surface-charge effects of La3+ on this gating mechanism. Three additional findings indicate that doses of La3+ that blocked ICa failed to produce nonspecific effects: (a) 10(-5) M La3+ had no measurable effect on the time-independent inwardly rectifying current, IK1; (b) the same concentration had no effect on the kinetics, amplitude, or voltage dependence of a time- and voltage-dependent K+ current, IK; and (c) 10(-4) M La3+ did not alter the size of the tetrodotoxin-sensitive inward Na+ current, INa, or the voltage dependence of its steady state inactivation. Higher concentrations (0.5-1.0 mM) reduced both IK1 and IK, and shifted the steady state activation curve for IK toward more positive potentials, presumably by reducing the external surface potential. Our results suggest that at a concentration of less than or equal to 10(-5) M, La3+ inhibits ICa selectively by direct blockade of Ca channels rather than by altering the external surface potential. At higher concentrations, La3+ exhibits nonspecific effects, including neutralization of negative external surface charge and inhibition of other time- and voltage-dependent ionic currents.
Action Potentials↗