Monoamine oxidase-B activity in alcohol withdrawal of smokers: is there any relationship with aggressiveness?

There is a considerable inconsistency in terms of the association between alcoholism and alterations in monoamine oxidase (MAO) activity. The main objectives of this study were to investigate the changes in platelet MAO-B activity throughout the alcohol withdrawal period and whether or not MAO-B activity differed between patients with high- and low-aggression tendency. We assayed platelet MAO-B levels spectrophotometrically in 22 male inpatients with alcohol dependence in their first and fourth weeks of withdrawal and in 20 healthy controls. Patients were divided into two high- and low-aggression subgroups according to scores obtained in a Brown-Goodwin Assessment for Life History of Aggression. Our data revealed that the significantly lower platelet MAO-B activity observed during the first week of alcohol withdrawal in patients, compared to controls, did not continue in the fourth week, and that there was no relationship between aggressiveness and MAO activity. These results suggest that low platelet MAO activity may be a state marker of alcohol withdrawal period or a result of high alcohol consumption rather than a trait marker of alcoholism.     

In vitro immunomodulatory activity of verbascoside from Nepeta ucrainica L

Nepeta ucrainica L. is used as a herbal tea in Kazakhistan. Phytochemical investigations of the aerial parts of the plant resulted in the isolation of verbascoside (1) and 1,5,9-epi-deoxyloganic acid (2). The structures of the compounds were elucidated by spectral (UV, IR, (1)H-NMR and (13)C-NMR) methods and HPLC analysis. The in vitro immunomodulatory activity of verbascoside was investigated by assessing neutrophil function; chemotaxis and intracellular killing activity. Verbascoside showed an increased chemotactic activity in all doses applied compared with the medium used as a negative control and had a positive effect on respiratory burst of neutrophils, but there was an opposite effect with increasing doses, pointing to a possible suppression of neutrophil intracellular killing activity.     

Gastroprotective effect of Astragaloside IV: role of prostaglandins, sulfhydryls and nitric oxide

This investigation evaluated the gastroprotective activity of Astragaloside IV, a cycloartane-type triterpene glycoside isolated from Astragalus zahlbruckneri. Gastric mucosal damage was induced in rats by intragastric ethanol (1 mL/rat). Rats treated orally with Astragaloside IV suspended in Tween 80 at 3, 10 and 30 mg kg(-1), showed 15, 37 and 52% gastroprotection, respectively. The gastroprotection observed at 30 mg kg(-1) for this compound was attenuated in rats pretreated with N(G)-nitro-L arginine methyl ester (70 mg kg(-1), i.p), a nitric oxide (NO)-synthase inhibitor, suggesting that the gastroprotective mechanism of this glycoside involves, at least in part, the participation of NO. The gastroprotective effect of Astragaloside IV was not affected by the inhibition of prostaglandin synthesis with indometacin (10 mg kg(-1), s.c.) nor by the block of endogenous sulfhydryls with N-ethylmaleimide (NEM, 10 mg kg(-1), s.c.). Carbenoxolone was used as a gastroprotective model drug and showed a dose-dependent gastroprotective effect (25, 43 and 88% of gastroprotection, at 3, 10 and 30 mg kg(-1), respectively). The partial participation of prostaglandins, sulfhydryls and NO was observed in the gastroprotective mechanism of carbenoxolone.     

Case Report: A Case of Bladder Dysfunction due to Myasthenia Gravis

Detrusor underactivity, due to myasthenia gravis (MG) is extremely rare. Only 4 cases of de novo dysfunction have been reported. We report a case of detrusor underactivity and increased post-void residual urine in a woman with MG. The patient has been managed by clean intermittent catheterization 6 times a day.     

Open surgical treatment of recurrent anterior instability of the shoulder

Recurrent anterior gleonohumeral instability is the most frequent joint instability of the body. Because of the complex stability mechanisms and diverse instability patterns of the glenohumeral joint, most cases present with more than one anatomic cause. Thus, the treatment of recurrent anterior instability of the shoulder should be designed to treat these pathologies. Although arthroscopic repair has outweighed the use of open surgical methods especially for the first dislocations, recurrent dislocations still require open repair techniques to overcome capsular laxity accompanying a Bankart lesion.     

Anatomy, biomechanics, and pathophysiology of instability of the glenohumeral joint

The stability of the shoulder is dependent on both static and dynamic anatomic restraints. In most cases, there must be insufficiency of more than one restraint for the shoulder joint to become instable. Although the role of these restraints is largely known in maintaining shoulder stability, our information on their interactions is insufficient. This article reviews the anatomy and biomechanics of the shoulder and conditions causing instability of the glenohumeral joint.     

Traumatic avulsion of knee joint

The report describes complete avulsion of knee joint en bloc, from the confines of the soft tissues of the leg but the patient was able to show full range of motion at his ankle and foot with palpable dorsalis paedis and posterior tibial vessels. Arthrodaesis was the best available management option.     

Investigation of the mechanism of nicotine induced relaxation in rabbit corpus cavernosum in vitro

In order to determine whether nicotine acts on corporal smooth muscle, the mechanism of its effect on strips of rabbit corpus cavernosum was studied in vitro. Rabbit corpus cavernosum muscle strips were mounted in an organ bath with modified Krebs-Henseleit solution and aerated with 95% O₂ and 5% CO₂. Tension was measured with isometric force transducers, and muscle relaxation was expressed as the percent decrease of precontraction induced by phenylephrine. Nicotine produced concentration dependent relaxation when preparations were precontracted by phenylephrine (10^–5 M). The maximum nicotine-induced relaxation was 60.4±4.2% of the phenylephrine contraction and was not affected by indomethacin (10^–5 M), N^w-nitro L-arginine methyl ester (3×10^–5 M), methylene blue (10^–5 M), glibenclamide (10^–5 M), clotrimazole (10^-6 M), tetraethylammonium (3×10^–4 M), or 4-aminopyridine (10^–3 M). Nicotine did not exhibit a calcium antagonizing effect. From these results, we conclude that nicotine-induced relaxation of the rabbit corpus cavernosum is not mediated by the release of nitric oxide, prostaglandins or a related substance, by the activation of potassium channels, or by the stimulation of nicotinic cholinoceptors. Further work is needed to determine the cellular mechanism(s) of the action by which nicotine acts on corporal smooth muscle.