Geometric phase with photon statistics and squeezed light for the dispersive fiber.
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Journal Article↗
Biomedical subjects
A Banerjee
Publications and source records attributed to A Banerjee.
Genetic determination of the meso-diaminopimelate biosynthetic pathway of mycobacteria.
The increasing incidence of multiple-drug-resistant mycobacterial infections indicates that the development of new methods for treatment of mycobacterial diseases should be a high priority. meso-Diaminopimelic acid (DAP), a key component of a highly immunogenic subunit of the mycobacterial peptidoglycan layer, has been implicated as a potential virulence factor. The mycobacterial DAP biosynthetic pathway could serve as a target for design of new antimycobacterial agents as well as the construction of in vivo selection systems. We have isolated the asd, dapA, dapB, dapD, and dapE genes involved in the DAP biosynthetic pathway of Mycobacterium bovis BCG. These genes were isolated by complementation of Escherichia coli mutations with an expression library of BCG DNA. Our analysis of these genes suggests that BCG may use more than one pathway for biosynthesis of DAP. The nucleotide sequence of the BCG dapB gene was determined. The activity of the product of this gene in Escherichia coli provided evidence that the gene may encode a novel bifunctional dihydrodipicolinate reductase and DAP dehydrogenase.
Amino Acid Sequence↗
Passive digit hyperextension in the diagnosis of flexor tendon injuries.
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Adult↗
Factitious disorders presenting as acute emergencies.
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Abdomen, Acute↗
Adenosine A1-receptor mechanisms antagonize beta-adrenergic pulmonary vasodilation in hypoxia.
Hypoxic pulmonary vasoconstriction is refractory to beta-adrenergic receptor (beta-AR)-mediated pulmonary vasodilation. We hypothesized that hypoxic pulmonary arteries release adenosine (Ado) that antagonizes beta-AR-mediated pulmonary vasodilation. Using isolated rat pulmonary artery rings, we investigated 1) the effect of hypoxia and exogenous Ado on beta-AR-mediated pulmonary vasodilation, 2) the intracellular site of dysfunctional beta-AR-mediated pulmonary vasodilation in hypoxia, and 3) the Ado receptor subtype responsible for dysfunction of beta-AR-mediated pulmonary vasodilation. Hypoxia attenuated normal beta-AR-mediated pulmonary vasodilation to isoproterenol (97.5 +/- 0.8 vs. 71.5 +/- 2.3%, P < 0.01). In contrast, forskolin induced the same vasorelaxation in hypoxic pulmonary rings as controls (P = 0.09). Incubation of normoxic rings with Ado attenuated the vasorelaxation response induced by beta-AR stimulation (71.5 +/- 5.9%, P < 0.01), similar to the effect observed in hypoxia. Both nonspecific Ado receptor blockade (8-sulfophenyl-theophylline) and specific A1-receptor blockade (8-cyclopentyl-1,3-dimethylxanthine) restored the vasorelaxation response of hypoxic rings induced by beta-AR stimulation (93.3 +/- 2.3 and 92.2 +/- 2.8%, P < 0.01). The effects of hypoxia and Ado were reproduced by a specific A1 agonist (2-chloro-N6-cyclopentyladenosine), demonstrating impaired vasorelaxation induced by beta-AR stimulation in normoxia (70.6 +/- 4.5%, P < 0.01). From these data, we conclude that hypoxia antagonizes beta-AR-mediated pulmonary vasodilation via an Ado A1-receptor mechanism.
Adenosine↗
Sport-related sudden natural death in the City of Birmingham.
We undertook a prospective study of all consecutive deaths reported to the Coroner for Birmingham and Solihull in a 5 year period. We identified 52 sudden deaths associated with symptoms commencing during sport participation. We studied the characteristics of these individuals. The majority had been performing at accustomed levels of activity without symptoms for several years. The extrapolation of our findings to preventive strategies remains unclear but we wish to highlight the importance of recognizing premonitory effort-related symptoms.
Adolescent↗
Adult respiratory distress syndrome caused by superior mesenteric artery syndrome.
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Adult↗
Theodore Howard Somervell OBE FRCS: surgeon, missionary, mountaineer, painter, musician.
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History, 20th Century↗
Bradykinin receptor blockade does not affect oxygen-mediated pulmonary vasodilation in fetal lambs.
Both oxygenation and rhythmic stretching of the lungs are factors known to be responsible for pulmonary vasodilation at birth. Based on our previous studies, we proposed that the pulmonary vasodilation caused by oxygen could be mediated, at least in part, through bradykinin release. To test this hypothesis, we evaluated the cardiovascular responses to in utero ventilation during infusion of a B2-subtype bradykinin receptor antagonist (BKA), [N-adamantaneacetyl-D-Arg0,Hyp3,Thi5,8,D-Phe7]bradykinin, at 15-20 micrograms.kg-1.min-1 in eight near-term fetal lambs and during drug vehicle infusion in five control fetal lambs. Prostacyclin synthesis was inhibited by meclofenamate infusion (1.5 mg.kg-1.h-1). Surgical placement of vascular catheters, a flow transducer around the left pulmonary artery, and a tracheostomy tube and formalin infiltration of the ductus arteriosus to maintain its patency in the presence of meclofenamate were performed 72 h before the study. Hemodynamic variables and pulmonary blood flow were measured and pulmonary vascular resistance was calculated before and after in utero ventilation with 100% oxygen. Despite complete blockade by BKA of the pulmonary vasodilation produced by exogenous bradykinin, ventilation with oxygen significantly increased pulmonary blood flow by 676% over baseline state (157.8 +/- 66 to 1224 +/- 265 mL.min-1.100 g-1, p < 0.01) and decreased the pulmonary vascular resistance by 89% from baseline state (0.44 +/- 0.16 to 0.048 +/- 0.01 torr.mL-1.min.100 g, p < 0.01). Such responses to ventilation with oxygen were comparable to those noted in the control animals, in whom bradykinin receptors had not been blocked.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylcholine↗
Enzymic preparation of (3R-cis)-3-(acetyloxy)-4-phenyl-2-azetidinone: a taxol side-chain synthon.
A key chiral intermediate [(3R-cis)-3-(acetyloxy)-4-phenyl-2-azetidinone (2)] for the semi-synthesis of paclitaxel (taxol; 5), an anti-cancer compound, was prepared by an enzymic process. The stereoselective enzymic hydrolysis of cis-3-(acetyloxy)-4-phenyl-2-azetidinone (1) to the corresponding (S)-(-)-alcohol (3) was carried out using various lipases. Lipase PS-30 (Pseudomonas cepacia) and BMS (Bristol-Myers Squibb) lipase (Pseudomonas sp. SC13856) catalysed hydrolysis of the undesired enantiomer of racemic compound 1, producing the (S)-(-)-alcohol (3) and the desired (R)-(+)-acetate (2). Reaction yields of > 96% and optical purities of > 99.5% were obtained. For a very efficient enzyme source (BMS lipase), a lipase fermentation using Pseudomonas sp. SC13856 was developed. In a fed-batch process using soybean oil, the fermentation resulted in 1500 units of extracellular lipase activity/ml. Crude BMS lipase (1.7 kg, containing 140,000 units/g) was recovered from the filtrate by ethanol precipitation. BMS lipase and commercially available lipase PS-30 were independently immobilized on Accurel polypropylene. These immobilized lipases were re-used (ten cycles) without loss of enzyme activity, productivity or optical purity of the product. The enzymic reaction process was scaled up to 75 and 150 litres using immobilized BMS lipase and lipase PS-30 respectively. From the reaction mixture, compound 2 was isolated in 88-90 mol% yield and 99.5% optical purity. A purity of 99.9 (area %) was demonstrated by g.c. for isolated compound 2.
Antineoplastic Agents↗
[Morphological abnormalities of the pituitary stalk of unknown cause in 4 cases of diabetes insipidus in children].
BACKGROUND: Magnetic resonance imaging (MRI) is the best technique for studying hypothalamic and hypophyseal structures. CASE REPORTS: Four children aged 2 years 5 months to 8 years with idiopathic diabetes insipidus were studied. Their condition had been identified for 2-6 years. All the patients had undergone complete clinical, neurological and endocrinological investigations during the search for the cause of their diabetes insipidus. A CT scan was performed in one patient and MRI in all four; the investigations were repeated each 6 months for 4 years. RESULTS: The first examination showed complete lack of antidiuretic hormone (four patients) and growth hormone deficiency (two patients). An enlarged pituitary stalk was seen in three patients, one patient had a small anterior pituitary, and three patients gave no posterior pituitary hypersignal. Follow-up showed that three patients completely lacked of growth hormone. One was thyrotropin deficient, three had persistent enlarged pituitary stalks, three had sub-normal anterior pituitaries and all four patients produced no post-pituitary hypersignal. None of the patients developed signs of histiocytosis or germinoma. CONCLUSION: The finding of abnormal pituitary stalks by MRI raises the possibility that the apparently idiopathic diabetes insipidus is due to some type of infiltrating disease of the hypothalamus and pituitary.
Child↗
Disparate signal transduction in neutrophil CD18 adhesion receptor expression versus superoxide generation.
BACKGROUND: We have previously shown that platelet-activating factor (PAF) primes polymorphonuclear neutrophils (PMNs) for superoxide generation and, concurrently, increases CD11/CD18 receptor expression; both events appear central to the pathogenesis of postinjury multiple organ failure. Recently, the counterinflammatory role of the neuroendocrine response to trauma has been emphasized, and, specifically, beta-adrenergic stimulation has been found to inhibit PMN activation. METHODS: Normal human PMNs were primed with PAF (10(-9) mol/L for 5 minutes) or pretreated with beta-receptor stimulation (isoproterenol, 10(-7) mol/L) or adenylate cyclase (AC) activation (forskoklin, 10(-7) mol/L) for 5 minutes and then primed with PAF. Superoxide generation in response to N-formyl-methionyl-leucyl-phenylalanine (10(-6) mol/L) was measured by superoxide dismutase inhibitable reduction of cytochrome C and CD18 expression determined by flow cytometry. RESULTS: PAF primed PMNs for superoxide generation (229.5 +/- 42.3 nmol/10(6) cells/min versus 18.7 +/- 6.5), whereas pretreatment with beta-adrenoreceptor stimulation (112.9 +/- 20.6) or AC activation (115.3 +/- 12.6) dramatically attenuated this process (p < 0.0001). PAF also enhanced CD18 expression (6.1 +/- 1.1 mean fluorescence intensity versus 10.3 +/- 2.3), but beta-adrenoreceptor stimulation (10.1 +/- 2.1) and AC activation (9.7 +/- 1.9) had no discernible effect. CONCLUSIONS: PAF priming of PMNs for superoxide generation was inhibited by the beta-adrenergic signal transduction pathway, but CD18 expression was not regulated via this pathway.
Adult↗
Nerve growth factor induces sensitivity to botulinum neurotoxin type A in norepinephrine-secreting PC12 cells.
Inhibition of Ca(2+)-activated norepinephrine secretion by the botulinum neurotoxin (NT) serotypes A and E was examined in permeabilized PC12 cells. The dichain type E NT reduced with dithiothreitol (DTT) completely inhibited secretion whereas the dichain type A NT reduced with DTT exhibited incomplete inhibitory activity. In contrast, Ca(2+)-activated secretion in PC12 cells treated with nerve growth factor (NGF) was completely inhibited by reduced type A NT. The NGF-treated PC12 cells retained a sensitivity to the type E NT similar to that of untreated PC12 cells. These results indicate that the intracellular mechanisms of inhibition of the types E and A NTs are distinct. NGF appears to either induce the expression of a component selectively required for type A NT sensitivity, or otherwise modifies the secretory apparatus to acquire type A NT sensitivity.
Animals↗
The bacterially expressed yeast CDC34 gene product can undergo autoubiquitination to form a multiubiquitin chain-linked protein.
The CDC34 gene of Saccharomyces cerevisiae encodes a 295-residue ubiquitin-conjugating enzyme (E2). The function of this ubiquitin-conjugating activity remains to be defined as its in vivo substrates are presently unknown. The bacterially expressed and purified Cdc34 protein is shown here to catalyze its own ubiquitination via an intramolecular transfer of its thiol ester-linked ubiquitin to a lysine. In this process, multiple ubiquitin groups are added to Cdc34, and these ubiquitin groups were shown to be arranged predominantly in the form of a single Lys48-specific multiubiquitin chain. Analysis of the hydroxylamine-dependent cleavage of ubiquitin-Cdc34 conjugates at the single Asn-Gly sequence in Cdc34 placed the major ubiquitin linkage site within the C-terminal 215-295 residues of Cdc34. The 4 Lys residues (Lys273, Lys277, Lys293, and Lys294) in this region of CDC34 were substituted by arginine either singly or in combination to produce a set of Cdc34 mutants. Analysis of these Cdc34 mutants for autoubiquitination revealed that the multiubiquitin chain can be formed on any one of these 4 lysines although most Cdc34 conjugates contain a single multiubiquitin chain. Since the presence of a Lys48-specific multiubiquitin chain in protein conjugates is known to target acceptor proteins for degradation in the ubiquitin-mediated proteolytic pathway, the present result raises the possibility that one function of the ubiquitin-conjugating activity in CDC34 may be used to target its own degradation.
Anaphase-Promoting Complex-Cyclosome↗
Cardiac preconditioning. Induction of endogenous tolerance to ischemia-reperfusion injury.
Cardiac preconditioning is a phenomenon by which a brief exposure to ischemia renders the heart more tolerant of a subsequent sustained ischemic insult. Understanding the mechanism involved may allow pharmacologic access to this protective state before cardiopulmonary bypass surgery and transplantation. We discuss herein the preconditioning phenomenon, the potential mechanisms involved, and the therapeutic implications of cardiac preconditioning.
Adenosine↗
Protecting myocardial creatine kinase activity during reperfusion improves bioenergetics and contractile function.
The exact mechanisms underlying reperfusion (RP) injury are unclear but are thought to involve toxic oxygen metabolites such as H2O2. The purpose of our study was to determine whether increasing endogenous catalase (CAT) stores would protect creatine kinase (CK) activity and improve bioenergetics and mechanical function during RP. Rats (n = 6/group) were pretreated with myristic acid (MA) or nothing 6 to 12 hr prior to cardiectomy. Hearts were Langendorff perfused and developed pressure (DP) was monitored during 25 min of 37 degrees C ischemia and 10 or 40 min of RP. CK activity was determined at baseline, end ischemia, and 40 min RP. CAT activity and H2O2 production was assayed at baseline, end ischemia, and 10 min RP. 31P NMR spectra were continuously acquired to determine ATP and phosphocreatine (PCr) concentrations. MA-pretreated hearts demonstrated elevated CAT stores (121 +/- 4%, P < 0.05). No H2O2 was produced during ischemia, and both groups generated significant but equal amounts of H2O2 at RP 10 (P < 0.001 vs preischemia (PI), P = NS between groups). By RP 40, MA-pretreated hearts recovered more DP than did control hearts (75 +/- 5% of PI vs 35 +/- 4% of PI, P < 0.001) and retained more CK activity as well (66 +/- 4% vs 52 +/- 2%, P < .05). PCr/ATP ratios of control hearts were abnormally elevated above baseline and that of MA hearts during RP (2.4 +/- 0.1 vs 1.85 +/- 0.08, P < 0.05 at RP 40).(ABSTRACT TRUNCATED AT 250 WORDS)
Adenosine Triphosphate↗