Effects of inactivated influenza virus vaccination on bronchial reactivity symptom scores and peak expiratory flow variability in patients with asthma.

Even though annual influenza vaccinations are recommended by many authorities, some doctors may be reluctant to vaccinate asthmatic patients because of the risk of inducing bronchial reactivity and exacerbating the asthma. In this study we investigated the effect of inactivated trivalent influenza vaccine on airway reactivity symptom scores and peak expiratory flow (PEF) variability in 24 patients with mild stable asthma. Baseline spirometry and methacholine challenge tests were performed on all patients. Patients were then asked to record their peak expiratory flow every morning and evening, complete daily symptom score charts (morning tightness, daytime asthma, cough, and night asthma), and note bronchodilator usage for 1 week. After baseline measurements, the patients were allocated to inactivated vaccine and placebo in a random and single-blind manner. The lung function measurements and methacholine challenge tests were repeated 1 week after vaccination and placebo administration at the same time of day. PD20 (mg/mL) methacholine doses were 3.06+/-3.0 mg/mL before vaccination, 2.96+/-3.2 mg/mL after vaccination, and 2.76+/-2.91 mg/mL after placebo administration. There were no significant changes in PD20 methacholine after influenza vaccination (p>0.05). There were also no significant changes in symptom scores, bronchodilator usage, and PEFR after vaccination (p>0.05). None of the patients experienced significant local or systemic side effects after vaccination. Immunization with inactivated influenza vaccine does not induce clinical exacerbations of asthma or airway hyperreactivity in patients with mild asthma.     

Antimicrobial activity of some isoquinoline alkaloids.

The isoquinoline alkaloids are of great importance to humanity because of their medicinal value and different structure. During the last ten years, many isoquinoline alkaloids were isolated from Fumaria and Corydalis species growing in Turkey. There have been many researches on the antimicrobial activity of extracts of higher plants, but relatively few pure compounds have been investigated.     

Radioisotopic assay of aspartate and alanine aminotransferase.

The activities of aspartate and alanine aminotransferases in biological samples were assessed through a novel and sensitive procedure, based on the conversion of [U-14C]2-ketoglutarate to L-[U-14C]glutamate. In human plasma, the generation of L-[U-14C]glutamate was proportional to the volume of plasma (20-60 microL) and to the length of incubation (30-90 min). The reaction velocity was related to the temperature with a Q10 close to 1.7 for aspartate aminotransferase and 2.0 for alanine aminotransferase. At 37 degrees C, the 95% confidence interval in healthy subjects ranged from 5.1-18.8 U/mL (mean value 11.9 U/L) for aspartate aminotransferase and from zero to 20.1 U/L (mean value 9.9 U/L) for alanine aminotransferase. The intra-assay coefficient of variation did not exceed 2.5%. The present method was also applied to homogenates prepared from rat pancreatic islets, liver, heart, parotid glands, and erythrocytes, using no more than 40 micrograms wet weight of tissue per sample, and could thus be used in small biological samples, such as those obtained by needle biopsy.     

Stimulus-secretion coupling of arginine-induced insulin release: comparison between the cationic amino acid and its methyl ester

The role currently ascribed to the accumulation of L-arginine in the pancreatic islet B-cell as a determinant of its insulinotropic action was reevaluated by comparing the uptake and the metabolic, ionic, electric, and secretory effects of the cationic amino acid with those of its more positively charged methyl ester in rat pancreatic islets. The response to L-arginine methyl ester differed from that evoked by the unesterified amino acid by a lower uptake and oxidation, lack of inhibitory action on D-glucose metabolism, more severe inhibition of the catabolism of endogenous L-glutamine, inhibition of 45Ca net uptake, decrease in both 86Rb outflow from prelabeled islets perifused at normal extracellular Ca2+ concentration and 45Ca efflux from prelabeled islets perifused in the absence of extracellular Ca2+, and delayed and lesser insulinotropic action. These findings reinforce the view that the carrier-mediated entry of L-arginine into the islet B-cells, with resulting depolarization of the plasma membrane, represents the essential mechanism for stimulation of insulin release by this cationic amino acid.     

Preferential alteration of oxidative relative to total glycolysis in pancreatic islets of two rat models of inherited or acquired Type 2 (non-insulin-dependent) diabetes mellitus

Summary In islets from both adult rats injected with streptozotocin during the neonatal period and spontaneously diabetic rats obtained by repeated selective breedings (GK rats), the ratio between d-[3, 4-¹⁴C]glucose oxidation and d-[5-³H]glucose conversion to ³HOH was 25% lower than in islets from control rats, indicating an impaired contribution of oxidative to total glycolysis. No primary defect in the Krebs cycle was found in the islets of diabetic rats, as judged from the ratio between either d-[2-¹⁴C]glucose or d-[6-¹⁴C]glucose and d-[3, 4-¹⁴C]glucose oxidation. Therefore, we propose that a preferential alteration of oxidative glycolysis in the pancreatic beta cell may contribute to the impairment of glucose-induced insulin release not only in a cytotoxic but also in a spontaneous model of non-insulin-dependent diabetes mellitus.     

Is the glucose-induced phosphate flush in pancreatic islets attributable to gating of volume-sensitive anion channels?

d-Glucose and other nutrient insulin secretagogues have long been known to induce a transient increase in inorganic phosphate release from pancreatic islets, a phenomenon currently referred to as a “phosphate flush”. The objective of this study was to explore the possible participation of volume-sensitive anion channels in such a process. Rat pancreatic islets were preincubated for 60 min in the presence of [³²P]orthophosphate and then perifused for 90 min to measure ³²P fractional outflow rate and insulin secretion. From minutes 46 to 70 inclusive either the concentration of d-glucose was increased from 1.1 to 8.3 mmol L⁻¹ or the extracellular osmolarity was decreased by reducing the NaCl concentration by 50 mmol L⁻¹. The increase in d-glucose concentration induced a typical phosphate flush and biphasic stimulation of insulin release. Extracellular hypoosmolarity caused a monophasic increase in both effluent radioactivity and␣insulin output. The inhibitor of volume-sensitive anion␣channels 5-nitro-2-(3-phenylpropylamino)benzoate (0.1 mmol L⁻¹) inhibited both stimulation of insulin release and phosphate flush induced by either the increase in d-glucose concentration or extracellular hypoosmolarity. It is proposed that gating of volume-sensitive anion channels accounts for the occurrence of the phosphate flush and subsequent stimulation of insulin secretion in response to either an increase in d-glucose concentration or a decrease in extracellular osmolarity.     

Peripheral ameloblastoma: a case report

Peripheral ameloblastoma, a rare and unusual variant of odontogenic tumour, comprises about 1% of all ameloblastomas. The extraosseous location is the peculiar feature of this type of tumour, which is otherwise similar to the classical ameloblastoma. An additional case of this infrequent tumour is described on the lingual alveolar mucosa of the right mandibular premolar region in a 60-year-old man. Clinical evidence, microscopic findings, CT imaging and recurrence for this tumour are discussed.     

The effect of carbamazepine treatment on serum leptin levels

Patients with epilepsy may manifest metabolic adverse effects throughout the course of their management with antiepileptic drugs. Leptin is a hormone that plays a major role in the regulation of feeding and energy expenditure. Leptin has been expected to form a link to weight gain in epilepsy with the use of some antiepileptic drugs. The aim of this study is to evaluate the effect of carbamazepine on body weight and serum leptin levels.This study was conducted in Izmir Tepecik Training and Research Hospital, Neurology Department. 56 epileptic patients who were on continuous carbamazepine monotherapy for at least 6 months before the study and 42 control subjects were included. Serum leptin and insulin levels were measured.Body mass index, leptin and insulin were not significantly elevated in carbamazepine group compared to control subjects (p > 0.05).Our study demonstrated that carbamazepine therapy does not affect significantly body mass index, leptin and insulin. Data regarding the effect of carbamazepine on serum leptin level is limited but the results of these recent studies are correlated with ours. It can be concluded that carbamazepine is a relatively low risky antiepileptic drug in terms of obesity and metabolic syndrome but further studies are needed.