Dissection of vertebral artery after cervical trauma.
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Biomedical subjects
Publications and source records attributed to J Bailey.
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We cloned and sequenced two actin promoters from Physarum, and constructed plasmids carrying these promoters upstream of a bacterial chloramphenicol acetyltransferase (cat) gene. We then tested the plasmids for their ability to express cat in Physarum amoebae. We present reliable methods for introducing plasmid DNA into Physarum amoebae by electroporation, and show that expression of the cat gene in amoebae occurs in the presence, but not the absence, of one or the other Physarum actin promoter.
Pulmonary edema is a serious complication of heart failure, but often patients with chronic heart failure resist pulmonary edema despite elevated pulmonary venous pressures. This protection might be a result of decreased pulmonary microvascular permeability. Double-isotope scintigraphy with 113mindium-labeled transferrin and 99mtechnetium-labeled erythrocytes allows noninvasive estimation of pulmonary microvascular permeability; an index of transferrin accumulation is calculated that reflects microvascular permeability. Fourteen patients with severe chronic left ventricular dysfunction were compared with a control group of 15 patients with mild coronary artery disease. In the control group the transferrin accumulation index was 0.35 (range -0.3 to 1.0) x 10(-3)/min, and in patients with heart failure the index was 0.0 (range -1.0 to 0.7) x 10(-3)/min, which was significantly lower (p less than 0.01). The reduction in the transferrin accumulation index correlated weakly with the duration of heart failure (R = -0.5, p less than 0.02). These data indicate reduced protein efflux consistent with a decrease in pulmonary microvascular permeability in patients with severe chronic heart failure. Similar changes have been observed in severe mitral stenosis and may reflect a generalized adaptation to chronic pulmonary venous hypertension.
In this case study, the views of a sample of four hospital nurses were elicited to determine underlying causes of persistent antipathy towards documentation in patients' charts. The results of this review supported a common belief that resistance to charting is influenced by extrinsic, or environmental factors, such as inflexibility of charting systems and insufficient allocation of time. In addition, intrinsic factors or cognitive and psychosocial factors, not emphasized in earlier studies, such as lack of confidence about written expression, a tendency to succumb to group norms governing charting and difficulty in articulating the nature of nursing practice, surfaced as impediments to documentation. This review suggests that a broader study approach is required; one that addresses intrinsic, as well as extrinsic, factors.
To investigate preliminary reports that benzodiazepine-induced sedation may be reversed by thyrotropin-releasing hormone (TRH), we examined the effect of TRH or saline placebo on two variables which are sensitive to benzodiazepine agonists: changes in sedation and saccadic eye movements. Lorazepam 10 micrograms/kg i.v. increased self-ratings of sedation and reduced self-ratings of alertness and these changes were almost completely reversed by TRH. In contrast the slowing of saccadic eye movements by lorazepam was not reversed by TRH. The effects of TRH do not appear to be due to a direct antagonism at the benzodiazepine receptor, since flumazenil reverses changes in both variables. Moreover ligand binding studies reveal that TRH has very low affinity at this receptor. These clinical data provide the first demonstration that it is possible to distinguish between the effects of benzodiazepines on saccadic eye movements and psychological self-ratings.
A system for evaluating the activity of antiviral agents against Rauscher murine leukemia virus (R-MuLV) has been developed using an enzyme linked immunosorbent assay technique. The activity of various antiviral compounds demonstrated in this assay system has been compared to their activity in the UV-XC plaque reduction assay, which has been used historically for evaluating anti-R-MuLV compounds. The assay is based upon detection of R-MuLV encoded p30 protein production in virus infected murine cells. The assay reagents are readily available and the assay system is amenable to automated data collection systems. Cytotoxicity evaluations are conducted in parallel to the Rauscher MuLV ELISA assay in order to assess drug-induced reductions in cell viability. Cytotoxicity evaluations are important to interpretation of the ELISA results since reductions in cell viability reduce viral protein production which would indicate an antiviral drug effect. This system is less sensitive than the classical UV-XC plaque reduction assay; however, it does offer an alternative to the time-consuming and labor-intensive plaque assay.
The development of an amoeba into a plasmodium involves extensive changes in cellular organisation and gene expression. The genetic basis of a number of recessive mutations that block plasmodium development has been elucidated. The stage at which development becomes abnormal has been determined for all the mutants, as has the terminal phenotype. In order to investigate the changes in gene expression that accompany plasmodium development, a cDNA library has been made using RNA isolated from cell populations in which development was occurring.
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Previous work has documented an acceleration of proteolysis and branched-chain amino acid oxidation when muscles from rats with chronic metabolic acidosis were incubated in vitro. The present study examines the impact of chronic metabolic acidosis on whole body amino acid turnover and oxidation in chronically catheterized awake male Sprague-Dawley rats using stochastic modeling and a primed continuous infusion of L-[1-14C] leucine. Whole body protein turnover was accelerated by acidosis as reflected in a 70% increase in proteolysis and a 55% increase in protein synthesis. Amino acid oxidation was increased 145% in rats with chronic metabolic acidosis relative to control rats receiving diets identical in protein and calories based on a reciprocal pool model and plasma alpha-ketoisocaproate specific radioactivity. These changes were accompanied by a 104% increase in liver branched-chain ketoacid dehydrogenase (BCKAD) activity in rats with acidosis, similar to previously documented increases in skeletal muscle BCKAD activity caused by acidosis. In contrast, kidney BCKAD activity was decreased 38% by acidosis, illustrating the tissue-specificity of the changes that were present. We conclude that chronic metabolic acidosis accelerates whole body protein turnover and affects the reincorporation of amino acid into body proteins by accelerating amino acid oxidation.
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Fibrin gel (FG) has recently been shown to be bactericidal in the management of contaminated hepatic injury; antibiotic loading of fibrin gel (AFG) may augment this effect. We evaluated the antimicrobial properties of FG and AFG in a rat model of contaminated splenic injury. Fibrin gel was made from centrifuged plasma of separate donor rats and bovine thrombin. Antibiotic fibrin gel was similarly produced following intravenous injection of 70 mg/kg ticarcillin. Male Holtzman rats (250-300 g) were anesthetized and a laparotomy done. The abdomen was contaminated with 1 x 10(7) Bacteroides fragilis and the spleen transected in the midportion. Treatment consisted of splenorrhaphy (S) (n = 7), FG application (n = 7), or AFG (n = 7). The animals were autopsied at 1 week to evaluate abscess formation and abdominal adhesions (grade I = none, grade II = mild, grade III = severe). Antibiotic/fibrin gel significantly decreased abscess formation following splenic injury when compared with S (2 of 7 vs. 7 of 7; p less than 0.05 by ANOVA) without an increase in adhesions. Fibrin gel also decreased abscess formation but not significantly (4 of 7 vs. 7 of 7). Histologic analysis confirmed the beneficial effect of FG and AFG on wound healing. The bactericidal effect of FG is improved by antibiotic loading in contaminated intraabdominal injury.
In Physarum, microscopic uninucleate amoebae develop into macroscopic multinucleate plasmodia. In the mutant strain, RA614, plasmodium development is blocked. RA614 carries a recessive mutation (npfL1) in a gene that functions in sexual as well as apogamic development. In npfL+ apogamic development, binucleate cells arise from uninucleate cells by mitosis without cytokinesis at the end of an extended cell cycle. In npfL1 cultures, apogamic development became abnormal at the end of the extended cell cycle. The cells developed a characteristic rounded, vacuolated appearance, nuclear fusion and vigorous cytoplasmic motion occurred, and the cells eventually died. Nuclei were not visible by phase-contrast microscopy in most of the abnormally developing cells, but fluorescence microscopy after DAPI staining revealed intensely staining, condensed nuclei without nucleoli. Studies of tubulin organization during npfL1 development indicated a high frequency of abnormal mitotic spindles and, in some interphase cells, abnormally thick microtubules. Some of these features were observed at low frequency in the parental npfL+ strain and may represent a pathway of cell death, resembling apoptosis, that may be triggered in more than one way. Nuclear fusion occurred during interphase and mitosis in npfL1 cells, and multipolar spindles were also observed. None of these features were observed in npfL+ cells, suggesting that a specific effect of the npfL1 mutation may be an incomplete alteration of nuclear structure from the amoebal to the plasmodial state.
The Tell Me a Story (TEMAS) Test is a thematic apperception technique composed of 23 chromatic pictures, depicting either minority or nonminority characters interacting in primarily urban and familial settings, and is scored for perceptual and cognitive style, affective state, and personality functioning. Previous research has supported the reliability and validity of the ethnic minority version of the TEMAS test for Hispanic and Black children and adolescents. In this study, we investigated the validity of the nonminority version by discriminating public school (n = 49) and outpatient (n = 36) samples of White examinees from inner city, low to lower middle socioeconomic status, largely female-headed households. Results indicate that TEMAS profiles significantly discriminated between the normal functioning and clinical groups (p < .001), with 86% classification accuracy. The results, which provide some support for the general clinical utility of the TEMAS technique, are discussed in terms of the need to develop and validate unbiased projective techniques for both ethnic minority and nonminority children.
8-Methoxy-4-[(2-isopropylphenyl)amino]-3-quinolinecarboxylate ethyl ester (AHR-9294) inhibited acid secretion stimulated by histamine, pentagastrin or carbachol in rats, and by histamine or feeding in dogs. AHR-9294 was about half as potent as omeprazole and exhibited a shorter duration of action. Based on its inhibition of acid secretion induced by different secretagogues and its lack of effect on histamine-stimulated adenylate cyclase activity, AHR-9294 does not appear to operate at the histamine receptor or adenylate cyclase. Rather, studies on enriched oxyntic microsomal preparations showed AHR-9294 to be an effective inhibitor of the H+ pump enzyme, H,K-ATPase, suggesting this might be the site of antisecretory activity. Kinetic studies revealed that inhibition of both K(+)-activated ATPase and p-nitrophenylphosphatase by AHR-9294 was purely competitive with K+ and its congeners, indicating that AHR-9294 and its analogs belong to the class of compounds known as "K+)-site" inhibitors. On the other hand, inhibition by AHR-9294 was noncompetitive with both ATP and p-nitrophenylphosphatase on their respective rates of hydrolysis (i.e., both Vmax and the apparent Km were reduced, but Vmax/Km was unchanged). Studies on partial reactions of the H,K-ATPase showed that the rate of ATP/ADP exchange was unaffected by AHR-9294 and the steady-state level of phosphoenzyme was only partially reduced (thus ATP/enzyme interaction was not affected); however, the rate of K(+)-catalyzed dephosphorylation of phosphoenzyme was markedly decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
Previous work documented an acceleration of proteolysis and branched-chain amino acid oxidation when muscles from rats with chronic metabolic acidosis were incubated in vitro. The present study examines the impact of chronic metabolic acidosis on whole body amino acid turnover and oxidation in chronically catheterized, awake, male Sprague-Dawley rats using stochastic modeling and a primed continuous infusion of L[1-14C] leucine. Whole body protein turnover was accelerated by acidosis as reflected in a 70% increase in proteolysis and a 55% increase in protein synthesis. Amino acid oxidation was increased by 145% in rats with acidosis relative to control rats receiving diets identical in protein and calories based on a reciprocal pool model and plasma alpha-ketoisocaproate specific radioactivity. These changes were accompanied by a 104% increase in liver branched-chain ketoacid dehydrogenase (BCKAD) activity in rats with acidosis, similar to previously documented increases in skeletal muscle BCKAD activity caused by acidosis. In contrast, kidney BCKAD activity was decreased by 38%, illustrating the tissue specificity of the changes that were present. We conclude that chronic metabolic acidosis accelerates whole body protein turnover and reduces the efficiency of protein utilization by accelerating amino acid oxidation. These changes may require an intact glucocorticoid axis.
BACKGROUND: Pulmonary compromise with altered surfactant metabolism is frequently noted during sepsis; triiodothyronine is necessary for normal surfactant synthesis. We evaluated the role of physiologic replacement of triiodothyronine during sepsis-induced hypothyroidism on surfactant synthesis and lung structural integrity. METHODS: Male Sprague Dawley rats (average weight, 330 gm) underwent sham laparotomy or cecal ligation and puncture; treatment was administered to rats that underwent cecal ligation and puncture by Alzet osmotic pump consisting of triiodothyronine (3 ng/hr) or saline control. The rats were killed 24 hours after serum triiodothyronine determination by radioimmunoassay (normal, 60 to 160 ng/dl). Surfactant was obtained by saline lavage. Lipid content was determined by Folch extraction; phospholipid content was verified by chromatography. Blinded histologic analysis of lung confluence and alveolar sparing was done in separate subgroups. Results are +/- SE. RESULTS: Control rats with sepsis were hypothyroid at 24 hours; rats given triiodothyronine were euthyroid (rats that underwent sham laparotomy, 67.7 +/- 4.9 ng/dl; control rats, 37.6 +/- 5.7 ng/dl; and triiodothyronine, 85.7 +/- 19 ng/dl; p less than 0.05 compared with triiodothyronine by analysis of variance). Surfactant production was significantly improved by triiodothyronine compared with control (60.7 +/- 22.6 mg vs 23.2 +/- 11.3 mg; p less than 0.05 by analysis of variance). Lung histologic integrity was maintained by triiodothyronine treatment during sepsis. CONCLUSIONS: Triiodothyronine supplementation may be beneficial in septic-induced pulmonary dysfunction.
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