Use of medical necessity scales in concurrent review of psychiatric inpatient care.
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Biomedical subjects
Publications and source records attributed to L Myers.
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Myxedema coma is a rare condition associated with high mortality. The pathophysiology is complex and often involves profound hypothyroidism as well as an inciting event. The diagnosis should be suspected based on the clinical presentation, and treatment should not be delayed while awaiting confirmatory laboratory data. In critically ill patients, laboratory differentiation between severe hypothyroidism and the euthyroid-sick syndromes is difficult and may require measurement of free hormone levels. Treatment consists of correction of electrolyte abnormalities, passive rewarming, treatment of infections, respiratory and hemodynamic support, administration of stress-dose glucocorticoids, and thyroid hormone replacement. Intravenous thyroxine, between 200 and 500 micrograms as the initial dose followed by 50 to 100 micrograms/day, is recommended. Concurrent therapy with triiodothyronine can also be considered.
The Ca2(+)-independent neural cell adhesion molecule, NCAM, is expressed by both nerve and muscle cells and has been shown to mediate both nerve-nerve and nerve-muscle cell interaction. A role for NCAM in muscle-muscle cell interaction has been proposed but not demonstrated. Here we report evidence that NCAM is expressed by embryonic chick muscle cells during in vitro development and functions together with Ca2(+)-dependent adhesion molecules in mediating myoblast interaction during the formation of multinucleate cells.
The formation of multinucleate skeletal muscle cells (myotubes) is a Ca2(+)-dependent process involving the interaction and fusion of mononucleate muscle cells (myoblasts). Specific cell-cell adhesion precedes lipid bilayer union during myoblast fusion and has been shown to involve both Ca2(+)-independent (CI)2 and Ca2(+)-dependent (CD) mechanisms. In this paper we present evidence that CD myoblast adhesion involves a molecule similar or identical to two known CD adhesion glycoproteins, N-cadherin and A-CAM. These molecules were previously identified by other laboratories in brain and cardiac muscle, respectively, and are postulated to be the same molecule. Antibodies to N-cadherin and A-CAM immunoblotted a similar band with a molecular weight of approximately 125,000 in extracts of brain, heart, and pectoral muscle isolated from chick embryos and in extracts of muscle cells grown in vitro at Ca2+ concentrations that either promoted or inhibited myotube formation. In assays designed to measure the interaction of fusion-competent myoblasts in suspension, both polyclonal and monoclonal anti-N-cadherin antibodies inhibited CD myoblast aggregation, suggesting that N-cadherin mediates the CD aspect of myoblast adhesion. Anti-N-cadherin also had a partial inhibitory effect on myotube formation likely due to the effect on myoblast-myoblast adhesion. The results indicate that N-cadherin/A-CAM plays a role in myoblast recognition and adhesion during skeletal myogenesis.
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N-(5-indanylsulfonyl)-N'-(4-chlorophenyl)-urea (LY186641), a novel anticancer compound, was evaluated against six lines of rhabdomyosarcoma xenografts, each of which was established from tissue biopsies from untreated patients, and additional sublines selected as xenografts for primary resistance to vincristine, melphalan, and ifosfamide. LY186641 was given by oral gavage twice daily for 10 consecutive days or as 5-day courses repeated at 7-day intervals. At the optimal schedule, complete regressions of advanced tumors were obtained in each of the six rhabdomyosarcoma lines. There was no apparent cross-resistance in RMS lines selected for vincristine resistance or against multiple-drug-resistance KB cells in vitro. There was slight cross-resistance in xenografts selected for melphalan resistance, but not in an ifosfamide-resistant line. These results indicate that LY186641 may have significant clinical activity in the treatment of childhood rhabdomyosarcoma.
To investigate the possible role of sensory function in conditions affecting sexual function, sensory thresholds were compared between young healthy men (n = 14, means age = 29.8), aging men (n = 15, means age = 67.3), and men suffering from diabetic impotence (n = 15, means age = 45.0). Using the psychophysical method of forced choice, vibrotactile and electrical stimulation thresholds were deterlmined in two separate sessions at two body sites: the fingertip and the ventral surface of the penis, just proximal to the glans. Vibrotactile penile thresholds (VTP) were lowest for young (Y) subjects and much higher for both aging (A) and diabetic (D) subjects. Electrical stimulation of the penis (ESP) showed the same trends, although the differences only approached significance (p = 0.06). The vibrotactile finger threshold (VTF) was significantly higher for A subjects as compared with Y and D subjects, but there was no difference between the Y and D groups. Diabetic patients had significantly higher thresholds for electrical stimulation of the finger (ESF), in contrast to the VTF finding. Finger thresholds were significantly lower than penile thresholds for all groups, and the change in threshold from finger to penis was greater in both aging and diabetic than in young subjects. Age was positively correlated with thresholds for ESF, ESP, VTF, and marginally for VTP when all three groups were analyzed together. However, in general the results of threshold determinations could not be attributed merely to age. Based on a detailed questionnaire of sexuality, VTP was negatively correlated with sexual activity and both ESP and VTP were negatively correlated with erectile capacity. The data are consistent with a genital sensory role for age-related and diabetic changes in sexual function.
Much progress has been made, especially in the last two decades, in laboratory aids to diagnosis and to follow the course of patients with multiple sclerosis (MS). The cerebrospinal fluid (CSF) profile indicative of MS, though not pathognomonic of MS, is present in almost every case of clinical definite MS in a chronic progressive phase (probably also true for early MS). The cardinal aspect of the profile is intra-blood-brain barrier (BBB) IgG synthesis which can be qualitatively detected by determining unique CSF oligoclonal IgG bands and quantitated by rate formula, mg/day. We believe that intra-BBB IgG synthesis is caused by a persistent antigen, most likely a virus, possibly measles. A number of issues about the profile are proposed and opportunities are presented to resolve them.
This article describes the relationship of self-assessed psychiatric skill among primary care physicians to their role in treating mental disorders. Physicians rated diagnostic skills more favorably than therapeutic skills. Factor analysis was used to identify three dimensions of physician skill: confidence in treatment of major disorders; confidence in treatment of anxiety; and diagnostic confidence. These variables were found to be associated with the reported number of patients with specific mental disorders managed by the physician.
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Human alpha lymphoblastoid interferon (Wellferon) was administered to 33 patients in a phase I study. Patients received Wellferon intramuscularly every 12 hours for 14 doses in nine dosage levels ranging from 0.75 X 10(6) units to 50.0 X 10(6) units. Toxicity tended to be dose dependent and included fever/chills, malaise, hematologic toxicity, and digestive tract toxicity. Thirty X 10(6) u q 12 h was felt to be the maximum tolerated dose. Three partial responses (renal cell carcinoma, diffuse histiocytic lymphoma, Hodgkin's disease) were achieved. Interferon rapidly (2 to 3 hours after the initial injection) reached peak serum levels which varied generally with dose and exceeded 500 u/ml at the 30 and 50 X 10(6) u dosages. Multiple doses of interferon resulted in cumulative peak levels substantially higher than first dose levels (greater than 500 u/ml at dosages greater than 3 X 10(6) u/ml and greater than 1,500 u/ml at dosages greater than or equal to 18 X 10(6) u). Interferon given at high dosages persisted up to 10 days beyond the final injection. Despite hematologic toxicity, inhibition of CFU-GM was not seen.
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The large granular lymphocyte (LGL) has been identified in normal individuals' MNC population as the NK-K cell (Ault and Weiner 1978; Timonen et al. 1981); it bears the OKM1 surface antigen (Breard et al. 1981; Fast et al. 1981) and while negative for T cell antigens OKT4 and OKT8, is a low avidity E-rosette forming cell. However, in a unfractionated nylon wool passed peripheral blood lymphocyte (NWP PBL) population, we show that not more than 50% of KN activity in normal or OND control NWP PBL and 30% NK activity in MS NWP PBL can be attributed to this cell. Nevertheless, 100% of control K cell activity and 50% of MS K cell activity can be mediated by an LGL. MS patients have normal proportions of LGLs in their NWP PBL. The proportion of LGLs in CSF of MS and OND patients is too low to account for the number of CSF K cells. While in control NWP PBLs, the LGLs are OKM1+ and mediate NK and ADCC, in MS the LGL NK effectors are probably different from LGL-K cell effectors. In MS both populations include effector cells with cell surface antigens. Thus, the OKM1+ LGL characteristics may not be used in analysis of NK and K cells in multiple sclerosis.
The effects of a stable endoperoxide analog, U-46619, were studied in five conscious chair-adapted rhesus monkeys. A dye dilution technique was used to determine simultaneously gastric fractional emptying, fluid output and ion output. A continuous infusion of either saline or U-46619 (0.2 micrograms/kg/min i.v.; 1 or 2 micrograms/kg/min s.c.) was given during a basal period and after distension of the stomach with an 80-ml water load. These studies demonstrate that U-46619 increases basal, but not postload fractinal emptying, and inhibits parietal secretion. These actions are similar to some of the effects of prostacyclin, prostaglandin E2 and prostaglandin F2 alpha on gastric emptying and secretion.
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The effects of prostacyclin (PGI2) on gastric emptying and secretion were studied in five unanesthetized chair-adapted rhesus monkeys. A dye dilution technique was used to determine simultaneously gastric fractional emptying, hydrogen ion (H+) output, fluid output, and H+ concentration of the gastric juice. A continuous intravenous infusion of either sodium carbonate buffer (control) or PGI2 (125, 175, or 250 ng/kg/min) was given during a 40-min basal period and following the intragastric administration of an 80-ml water load. During the basal period, 175 and 250 ng/kg/min significantly decreased H+ output compared to control. Only 250 ng/kg/min, however, significantly reduced basal fluid output compared to control. As a result, the H+ concentration of the gastric juice was lowered by both 175 and 250 ng/kg/min. The effects of PGI2 on H+ output, fluid output, and H+ concentration of the secreted juice after the water load were similar to those observed during the basal period. In addition to its anti-secretory action, PGI2 inhibited significantly postload, but not basal, gastric fractional emptying. Because a fall in intragastric H+ concentration is known to enhance fractional emptying, it appears that the retarding effect of PGI2 on fractional emptying is not mediated by its ability to suppress H+ output.
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