Effect of corticosteroids on post-intubation tracheal stenosis.

A 57 year old patient presented with progressive tracheal stenosis two months after intubation. An intraluminal polypoid lesion was found at the site of the cuff of the endotracheal tube. It disappeared within five days of treatment with inhaled beclomethasone.

Increased membrane-bound calcium in platelets of hypertensive patients.

The fluorescent indicator chlortetracycline was used to estimate membrane-bound calcium in mild, untreated hypertensive patients (n = 39) and normotensive controls (n = 42). All participants were black. After incubation with chlortetracycline, platelet-rich plasma was centrifuged into a pellet and fluorescence was measured with a microspectrofluorometer.

Eicosapentaenoic acid and docosahexaenoic acid are antagonists at the thromboxane A2/prostaglandin H2 receptor in human platelets.

The present study investigated the mechanism by which eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) inhibit platelet activation induced by thromboxane A2. DHA was found to be more potent than EPA in blocking platelet aggregation induced by the stable thromboxane A2 mimetic, U46619. Furthermore, this inhibition by DHA or EPA was competitive.

Correlation of severity of panic disorder and neuroanatomical changes on magnetic resonance imaging.

Thirty consecutive lactate-sensitive panic disorder patients were studied with magnetic resonance imaging (MRI) to investigate the relationship between temporal lobe abnormalities and panic disorder. Neuroanatomical abnormalities, most involving the right temporal lobe, were found in 43% of patients, compared with 10% of the control subjects. Patients with temporal lobe abnormalities were significantly younger at the onset of panic disorder and had more panic attacks compared with patients with normal MRI scans (p less than .

The radiological report: what is useful for the referring physician?

To assess what constitutes a useful radiological report for referring physicians, we sent a questionnaire to 200 doctors (general practitioners, internists, and surgeons). Questions testing style, length of the report, and several points of content, including mention of clinical correlation, negative findings, and sequence of further investigations, were included. The principal qualities useful to the clinician were clarity, brevity, and clinical correlation.

Modulation of Ca2+ fluxes in isolated platelet vesicles: effects of cAMP-dependent protein kinase and protein kinase inhibitor on Ca2+ sequestration and release.

In the present study, we investigated the role of cAMP-dependent protein kinase in the process of Ca2+ uptake and release from platelet-derived membrane vesicles enriched in the dense tubular system. It was found that these membrane vesicles contain endogenous cAMP-dependent protein kinase and that stimulation of protein kinase by cAMP resulted in the phosphorylation of a single protein band (22 kDa). Addition of cAMP-dependent protein kinase produced effects on vesicle Ca2+ accumulation which were dependent on the Ca2+ concentration in the incubation medium.

Hemodynamic changes in portal circulation after portosystemic shunts: use of duplex sonography in 43 patients.

Forty-five patients with 46 surgical portosystemic shunts were examined by duplex Doppler sonography, and the results were compared with those of esophageal endoscopy, angiography, surgery, and clinical follow-up. Thirty-eight shunts were patent, and in 33 of these, the shunt was directly visualized and flow was observed with Doppler sonography. Eight shunts were obstructed.

[Neurobiology in panic states].

Research in panic disorder (PD) has highlighted a low biological threshold (lactate infusion). Also, several studies have shown neurophysiological changes with PD patients: increased brain perfusion (Stewart), parahypocampal hyper-perfusion (Reiman) and we reported an increased incidence of epileptiform abnormalities. In order to assess neuroanatomical changes we carried out a study with magnetic resonance imaging (MRI) of P.

Preparation and biological evaluation of a potential photoaffinity label for the prostaglandin H2/thromboxane A2 receptor.

Two aromatic azides (24 and 26) were prepared as potential photoaffinity probes for the PGH2/TXA2 receptor. The compounds are based on the well-characterized PGH2/TXA2 receptor antagonist 13-azaprostanoic acid, with the terminus of its lower side chain replaced with phenoxy (24) or benzyl (26) azide functionality. The two compounds were shown to irreversibly inhibit platelet function after photolysis and resuspension.

A photoaffinity label for the thromboxane A2/prostaglandin H2 receptor in human blood platelets.

A photoactive iodoarylazide derivative (I-APA-PhN3) of the competitive thromboxane A2/prostaglandin H2 (TXA2/PGH2) antagonist 13-azaprostanoic acid is evaluated. Upon photoactivation, the compound was found to inhibit specifically and irreversibly human platelet aggregation induced by the TXA2/PGH2 mimetic U46619. In receptor-binding studies using [3H]U46619, I-APA-PhN3 exhibited an IC50 of 300 nM for inhibition of U46619 binding.

Effect of single-dose aspirin on TXA2 and PGI2 cyclooxygenases in vivo.

The present study investigated the sensitivities of the thromboxane A2 (TXA2) cyclooxygenase and the prostacyclin (PGI2) cyclooxygenase to aspirin using an in vivo animal model. In this model, arachidonic acid (AA) was administered to mice via cardiac puncture, and plasma levels of thromboxane B2 (TXB2) and 6-keto prostaglandin F1 alpha (6-keto PGF1 alpha) were determined. Infusion of AA (5, 10, 25 and 50 mg/kg) resulted in a dose-dependent increase in both TXB2 and 6-keto PGF1 alpha.

The V-shaped artifact of the gallbladder wall.

Among 20,000 patients who had undergone abdominal or gallbladder sonographic examinations, 36 had a short V-shaped artifact originating from an hyperechoic focus in the gallbladder wall. Associated symptoms were varied and nonspecific. The 10 gallbladders excised because of associated cholelithiasis showed a thickened wall, and seven patients had diverticulosis of the wall with impacted stones.

Ascites: ultrasound guidance or blind paracentesis?

The classic site for paracentesis in generalized ascites is in the left lower quadrant of the abdomen at a position equivalent to McBurney's point. Its use has an average success rate of 58%, depending on the amount of liquid. To assess the efficacy of paracentesis at this site and to establish the ideal site for blind puncture, we studied 27 consecutive patients with ascites detected by abdominal ultrasonography.

Characterization of U46619 binding in unactivated, intact human platelets and determination of binding site affinities of four TXA2/PGH2 receptor antagonists (13-APA, BM 13.177, ONO 3708 and SQ 29,548).

The binding of U46619 and the inhibition of this binding by four TXA2/PGH2 receptor antagonists (13-APA, BM 13.177, ONO 3708 and SQ 29,548) were studied in unactivated, intact human platelets. Washed platelets were equilibrated with [3H]-U46619 (5 nM) and the time course of binding determined.

Sonography of the hypertrophied column of Bertin.

A prospective sonographic analysis of kidneys in 136 adults without clinical or radiologic evidence of renal disease revealed 22 cases of large columns of Bertin. Most were located in the middle third of the kidney, more frequently on the left side. They were bilateral in 18%.

Ascites as a cause of hyperechogenic kidneys.

In 40 patients with ascites, hyperechogenicity of the kidneys was directly proportional to the amount of fluid interposed between the clinically normal kidney and the transducer. The beam-enhancing phenomenon of ascites on renal parenchymal echogenicity should be distinguished from renal disease causing the increase in parenchymal echoes.

Thromboxane A2/prostaglandin H2 mobilizes calcium in human blood platelets.

The present study investigated the mechanism by which thromboxane A2/prostaglandin H2 (TXA2/PGH2) stimulates platelet activation. Previous studies in isolated platelet vesicles have suggested that TXA2/PGH2 functions to release calcium from intraplatelet stores. On this basis, we investigated whether TXA2/PGH2 causes mobilization of calcium in intact platelets.