ABSTRACT
This study seeks to determine how panic disorder patients with anxiety and depression comorbidity differ from panic disorder patients without comorbidity at the time of presentation for treatment. One-hundred seventy-one panic disorder patients presenting for their initial assessment and treatment at the Payne Whitney Anxiety Disorders Clinic agreed to participate and completed self-report and diagnostic assessments. Sixty-seven percent of panic disorder subjects were found to have at least one comorbid anxiety or depression diagnosis. Age and gender ratio were not affected by the presence of comorbid diagnoses. Comorbidity significantly contributed to psychological distress and symptom load, overall impairment, and interpersonal impairment.
Subject(s)
Anxiety Disorders/epidemiology , Depressive Disorder, Major/epidemiology , Panic Disorder/epidemiology , Adult , Age Factors , Anxiety Disorders/diagnosis , Anxiety Disorders/psychology , Comorbidity , Depressive Disorder, Major/diagnosis , Depressive Disorder, Major/psychology , Female , Humans , Interpersonal Relations , Male , Mood Disorders/diagnosis , Mood Disorders/epidemiology , Mood Disorders/psychology , Panic Disorder/diagnosis , Panic Disorder/psychology , Psychiatric Status Rating Scales , Self-Assessment , Severity of Illness Index , Sex Factors , Surveys and QuestionnairesSubject(s)
Explosions , Mental Disorders/diagnosis , Violence/psychology , Acute Disease , Adaptation, Psychological , Adult , Anxiety Disorders/diagnosis , Anxiety Disorders/epidemiology , Anxiety Disorders/psychology , Depressive Disorder/diagnosis , Depressive Disorder/epidemiology , Depressive Disorder/psychology , Female , Follow-Up Studies , Humans , Life Change Events , Male , Mental Disorders/epidemiology , Mental Disorders/psychology , Middle Aged , Psychiatric Status Rating Scales , Stress Disorders, Post-Traumatic/diagnosis , Stress Disorders, Post-Traumatic/epidemiology , Stress Disorders, Post-Traumatic/psychology , United StatesSubject(s)
Agoraphobia/psychology , Caffeine/pharmacology , Panic Disorder/psychology , Taste Threshold/drug effects , Adult , Drug Synergism , Female , Humans , Male , Middle Aged , QuinineABSTRACT
Angiotensin II (AII) induces an initial rapid but transient rise in [Ca2+]i detected with aequorin in bovine adrenal capsule strips. The rise in [Ca2+]i begins immediately after AII addition, reaches a peak in 30 seconds, and returns to near basal values within 5 minutes. The [Ca2+]i transient is receptor-mediated and its height is dose-dependent. The increase in [Ca2+]i is largely due to the release of Ca2+ from an intracellular pool. The uncorrected peak rise in [Ca2+]i after 1 X 10(-6) M beta-[asp1]-AII stimulation is approximately 3 fold, from 110 nM to 300 nM; the peak rise, corrected for diffusion and nonsynchronous cellular response, is from 110 nM to 1.2 microM. Perifusion of aequorin-loaded strips with beta-[asp1]-AII, an aminopeptidase-resistant analog of AII, allows the simultaneous measurement of [Ca2+]i and aldosterone production rate. Levels of agonist which generate a transient rise in [Ca2+]i also produce a sustained increase in aldosterone production rate, but the two events are temporally separated: the transient rise in [Ca2+]i precedes the increase in aldosterone production rate. However, there is a strong correlation, r = 0.94, between the amplitude of the initial [Ca2+]i transient and the magnitude of the sustained increase in steroid production rate.
Subject(s)
Aldosterone/biosynthesis , Calcium/analysis , Adrenal Cortex/metabolism , Adrenal Glands/cytology , Adrenal Glands/drug effects , Adrenal Glands/physiology , Aequorin , Aldosterone/metabolism , Angiotensin II/analogs & derivatives , Angiotensin II/pharmacology , Animals , Calcium/metabolism , Calcium/pharmacology , Cattle , Luminescent Measurements , Perfusion , Time FactorsABSTRACT
The effect of atrial natriuretic peptide (ANP) on cellular calcium metabolism was evaluated in bovine adrenal glomerulosa cells stimulated by agonists that use the Ca2+-phosphoinositide messenger system. The calcium-sensitive probe aequorin was used to measure intracellular free calcium concentration, and the aldosterone secretory rate was simultaneously monitored. ANP did not block the calcium transient induced by beta-[Asp1]angiotensin II (beta-[Asp1]AII), an AII analog, but markedly reduced the stimulated rate of aldosterone secretion. Consistent with these findings, radiolabeled 45Ca efflux stimulated by AII and carbachol was not altered by the concurrent addition of ANP. These results indicate that ANP has no effect on the phosphoinositide-mediated calcium transient and the associated rise in cellular calcium efflux, suggesting that these parameters of calcium metabolism are not the locus of ANP's inhibitory action.
Subject(s)
Aldosterone/metabolism , Angiotensin II/pharmacology , Atrial Natriuretic Factor/pharmacology , Calcium/metabolism , Aequorin/metabolism , Animals , Carbachol/pharmacology , CattleABSTRACT
We previously showed that formyl peptide chemotactic receptors (FPCR) of human phagocytic cells contain at least two asparagine-linked oligosaccharide chains located at the distal end of the receptor. The requirement of these N-linked oligosaccharide chains for expression and function of FPCR was investigated in HL-60 cells induced to differentiate by N6,O2-dibutyryladenosine 3',5'-monophosphate (Bt2cAMP) in the presence or absence of 5 micrograms/ml tunicamycin. Tunicamycin did not prevent the changes in morphology associated with Bt2cAMP-induced differentiation of HL-60 cells. Autoradiographic analysis after SDS-PAGE of FPCR affinity labeled with N-formyl-Nle-Leu-Phe-Nle-[125I]iodo-Tyr-Lys (formyl 125I-hexapeptide) and ethylene glycol bis(succinimidyl succinate) demonstrated that greater than 95% of FPCR expressed by tunicamycin-treated cells completely lacked N-linked oligosaccharide (Mr 32,000), and no fully glycosylated FPCR (Mr 62,000 to 85,000) was detectable. Scatchard analysis of formyl 125I-hexapeptide binding indicated the presence of two classes of binding sites for both control and tunicamycin-treated cells (control cells, 82,000 +/- 32,000 sites/cell with Kd 10.0 +/- 4.3 nM and 520,000 +/- 40,000 sites/cell with Kd 250 +/- 80 nM; tunicamycin-treated cells, 11,000 +/- 5000 sites/cell with Kd 3.0 +/- 1.9 nM and 470,000 +/- 70,000 sites/cell with Kd of 500 +/- 140 nM). Both control and tunicamycin-treated cells augmented superoxide anion release, exhibited a migratory response, and showed a transient rise in intracellular free Ca2+ upon stimulation with N-formyl-Nle-Leu-Phe. However, the responses of the tunicamycin-treated cells were less than that of the control cells. The present studies demonstrate that N-glycosylation of FPCR is not essential for cell surface expression or for several FPCR-mediated cell responses.
Subject(s)
Glucosamine/analogs & derivatives , Leukemia, Myeloid, Acute/metabolism , N-Formylmethionine Leucyl-Phenylalanine/metabolism , Receptors, Immunologic/drug effects , Tunicamycin/pharmacology , Calcium/metabolism , Carbohydrate Conformation , Cell Differentiation , Cell Division , Cell Line , Chemotaxis , Humans , Leukemia, Myeloid, Acute/pathology , N-Formylmethionine Leucyl-Phenylalanine/pharmacology , Radioligand Assay , Receptors, Formyl Peptide , Receptors, Immunologic/analysis , Receptors, Immunologic/physiology , Superoxides/metabolismABSTRACT
Binding of murine monoclonal antibody PMN7C3 to human neutrophils results in a large rapid, dose dependent transient increase in intracellular free calcium as measured by QUIN-2 fluorescence. Unlike other calcium mobilizing agents PMN7C3 does not induce any increase in respiratory burst activity over basal level. The PMN7C3 effect requires multivalent binding. Chelation of extracellular calcium does not significantly decrease the fluorescence transient generated by exposure to PMN7C3. Lowering of basal levels of intracellular free calcium concentration by maintaining QUIN-2-loaded PMN in calcium free medium eliminates the fluorescence transient. The observations demonstrate that a cell surface receptor mediated intracellular free calcium transient may be generated without any associated respiratory burst activation.
