Awareness of airflow obstruction together with antismoking advice increases success in cessation smoking

COPD is one of the leading causes of mortality and increased morbidity in developed world. In advanced disease it also imposes an important economic burden on societies. The main etiologic factor for COPD is tobacco smoking. The aim of the study was to asses if the awareness of airflow obstruction combined together with a minimal antismoking advice in middle aged smokers increases the quitting rate. Out of smokers participating in mass spirometric screening for COPD in five polish towns, we invited 734 (300 with airflow limitation and 247 with normal lung function) for a follow-up. During the second visit, at one year, spirometry was performed and smoking status was assessed. Non-smoking was validated with carbon monoxide measurements in exhaled breath. Patients who did not come for the follow-up visit were considered as smokers. Of 734 smokers invited, 543 (74%) presented for the follow-up visit. All smokers tried to modify the habit. Number of cigarettes smoked at one year was reduced by -5.5 (p < 0.001) in patients with airflow limitation and -2.2 (ns) in smokers with normal lung function. One year quit rate in smokers with airflow limitation was 11.1% vs 7.6% in smokers with normal lung function (ns). When the calculation was made for those who had the follow-up the quit rates were 15.1% vs 9.9% (p < 0.05). Cessation of smoking was correlated with lung function. Those smokers who stopped smoking permanently or tried to quit had lower FEV1 (p < 0.01) and FEV1/FVC (p < 0.05), than those who continued to smoke.     

Early detection of COPD by high risk population spirometric screening

COPD is the most frequent chronic lung disease in Poland. The disease is however under-diagnosed, especially at the early stages. The aim of the study was to assess the efficacy of spirometric screening for COPD in middle aged smokers. Informations on causes and symptoms of COPD were disseminated in mass media in 14 large cities. Subject aged over 39 and with smoking history of > 10 packyears were invited for a free spirometry in local chest clinic. However, everyone attending had the spirometry performed. Spirometry was performed according to ATS recommendations. Airway obstruction (AO) was diagnosed when FEV1/FVC < 85% of N and categorised as mild (FEV1 > 70% of N), moderate (FEV1 50-69% of N) or severe (FEV1 < 50% of N). Spirometry was accompanied by an antismoking advice. RESULTS: 12.781 subjects were screened (mean age 52 +/- 12 years, 57% males). In 8.269 subjects who complied with inclusion criteria AO was diagnosed in 29.8% (mild in 10.9%, moderate in 12% and severe in 6.9%). In smokers < 40 years of age and a history of < 10 packyears AO was found in 8.8% (mild in 6.0%, moderate in 1.8% and severe in 1.0%). CONCLUSION: Mass spirometry is an effective and easy method for early detection of COPD.     

The architecture of variant surface glycoprotein gene expression sites in Trypanosoma brucei

Trypanosoma brucei evades the immune system by switching between Variant Surface Glycoprotein (VSG) genes. The active VSG gene is transcribed in one of approximately 20 telomeric expression sites (ESs). It has been postulated that ES polymorphism plays a role in host adaptation. To gain more insight into ES architecture, we have determined the complete sequence of Bacterial Artificial Chromosomes (BACs) containing DNA from three ESs and their flanking regions. There was variation in the order and number of ES-associated genes (ESAGs). ESAGs 6 and 7, encoding transferrin receptor subunits, are the only ESAGs with functional copies in every ES that has been sequenced until now. A BAC clone containing the VO2 ES sequences comprised approximately half of a 330 kb 'intermediate' chromosome. The extensive similarity between this intermediate chromosome and the left telomere of T. brucei 927 chromosome I, suggests that this previously uncharacterised intermediate size class of chromosomes could have arisen from breakage of megabase chromosomes. Unexpected conservation of sequences, including pseudogenes, indicates that the multiple ESs could have arisen through a relatively recent amplification of a single ES.     

Developmental aspects of nevus spilus: review of the literature apropos of 7 cases

The nevus on nevus is a dischromic lesion with a double component made of a pigmented, pale-brown coloured spot, most often congenital punctuated by macular or discretely papular darker elements, with a usually later setting-up and conventionally characterized by an absence of evolutivity. A series of seven cases is reported of whom three present a very peculiar evolution: A 37 years old man is taking a medical advice for a nevus on a congenital nevus on the right buttock on which appeared later on a blue-coloured, lightly sensitive nodule which clinically calls to mind the diagnosis of a blue nevus: the surgical exeresis is refused by the patient. A little girl, born in 1972, has since her birth a nevus on nevus of her right fore-arm; in 1975 and 1976 appeared successively on this lesion three nodules evocative of Spitz melanoma (fig. 4), which are surgically removed; histologic examination confirms the clinical diagnosis (fig. 5). A woman, aged 38, presents a big nevus on congenital zosteriform nevus of the right lower limb; since 1982, one of the dark elements situated on the lower third of the leg is progressively spreading and becoming polychromic (fig. 6); the clinical suspicious of superficial spreading malignant melanoma is confirmed by the histologic examination. In the literature, the terminology aiming to call this kind of nevic pale brown spot recovered by darker macules is not quite clear, as it was already emphasized by Stewart in 1978 (27). Indeed, numerous different denomination are found in it: "nevus spilus", nevus on nevus", "spotty nevus" "speckled lentiginous nevus", "speckled nevus "spilus".(ABSTRACT TRUNCATED AT 250 WORDS)     

Pattern electroretinogram and visual evoked potential amplitudes are influenced by different stimulus field sizes and scotomata

The pattern electroretinogram and the visual evoked potential were recorded simultaneously with various stimulus fields and artificial scotomata of increasing sizes. In contrast to an earlier study, a smaller check size (20) and two stimulus field sizes (20° × 20° and 10° × 10°) for the scotomata were used. With a concentric decreasing stimulus field, a reduction of both the pattern electroretinogram and visual evoked potential was found. Both showed a simultaneous reduction of amplitudes, but, compared with the amplitude in the full field, the reduction was more extensive for the pattern electroretinogram at each test field size. This implies a greater contribution to the pattern electroretinogram from more eccentric retinal parts. An artificial central scotoma of increasing size in the 20° × 20° field had less influence on the pattern electroretinogram than on the visual evoked potential. The percentage amplitude loss of the visual evoked potential was more pronounced. The visual evoked potential was eventually abolished by a scotoma size from 10° × 10° upward, while the pattern electroretinogram was still registrable. When scotomata of similar size were introduced in a smaller (10° × 10°) field, percentage pattern electroretinogram and visual evoked potential amplitude losses were less separated than in a larger (20° × 20°) test field.     

Sympathoinhibition by rilmenidine in conscious rabbits: involvement of α2-adrenoceptors

Summary Cardiovascular and sympathetic nervous system effects of the mixed ₂-adrenoceptor and imidazoline receptor agonist rilmenidine were studied in conscious rabbits chronically instrumented for the recording of the firing rate of renal sympathetic fibers. Separate experiments were carried out on pithed rabbits with electrically stimulated (2 Hz) sympathetic outflow. Drugs were administered intravenously in a cumulative manner.In conscious rabbits, rilmenidine 0.1, 0.3 and 1.0 mg kg^–1 dose-dependently lowered blood pressure, renal sympathetic nerve activity, heart rate and the plasma concentration of noradrenaline and adrenaline. The effect on blood pressure and plasma catecholamines was maximal after 0.3 mg kg^–1 whereas heart rate and renal sympathetic nerve activity decreased further after rilmenidine 1.0 mg kg^–1. Yohimbine 0.1 and 0.5 mg kg^–1, when injected subsequently, attenuated and at the higher dose abolished all effects of rilmenidine. The effects of rilmenidine were also antagonized by the ₂-adrenoceptor antagonist 2-(2,3-dihydro-2-methoxy-1,4-benzodioxin-2-yl)-4,5-dihydro-1H-imidazole HCl (RX821002; 0.1 and 0.5 mg kg^–1). Yohimbine 0.1 and 0.5 mg kg^–1 did not attenuate or attenuated only slightly the decrease of heart rate and renal sympathetic nerve activity produced by infusion of vasopressin. In pithed rabbits with electrically-stimulated sympathetic outflow, yohimbine 0.1 submaximally and yohimbine 0.5 mg kg^–1 maximally increased the plasma noradrenaline concentration.The experiments show by direct measurement of sympathetic nerve firing and plasma catecholamines that rilmenidine causes sympathoinhibition in conscious rabbits, presumably through central sites of action. The antagonism by yohimbine, at doses which are selective for ₂-adrenoceptors (vs. imidazoline receptors), demonstrates the involvement of ₂-adrenoceptors in the sympatho-inhibition.Correspondence to: B. Szabo at the above address     

Inhibition of uptake1 by (+)-oxaprotiline reveals a differential central regulation of noradrenaline and adrenaline release

Summary Inhibition of uptake, in the central nervous system leads to a decrease of sympathetic outflow to many tissues; central a2-adrenoceptors are involved in this decrease. The aim of the present study was to compare the effects of the selective uptake, inhibitor (+)-oxaprotiline on the plasma kinetics of noradrenaline and adrenaline in anaesthetized and in conscious rabbits. [³H]Noradrenaline and [^3H]adrenaline were infused iv. The arterial plasma concentrations of endogenous and radiolabelled noradrenaline and adrenaline were measured, and the clearance from and spillover into the plasma of noradrenaline and adrenaline were calculated.Results obtained in conscious and anaesthetized rabbits were similar. (+)-Oxaprotiline 0.2, 0.6 and 1.8 mg kg^–1 iv. dose-dependently reduced the clearance of [³H]noradrenaline from the plasma. The clearance of [³H]adrenaline was reduced less. The spillover of endogenous noradrenaline was decreased by up to 35%. In contrast, the spillover of adrenaline tended to be enhanced. Prazosin 0.1 and 1 mg kg^–1 was injected iv. in a second part of each experiment. It lowered the blood pressure and caused a marked increase in noradrenaline spillover but no increase or even a decrease in adrenaline spillover.The results are compatible with the following hypothesis. The sympathetic outflow from the central nervous system is subject to a twofold a-adrenoceptor-mediated modulation: -adrenoceptor-mediated inhibition and ₁-adrenoceptor-mediated excitation. In the control of the sympathetic outflow to many extra-adrenal tissues, the ₂-adrenergic inhibition prevails. Uptake₁ inhibitors depress sympathetic outflow to such tissues by enhancing the ₂-adrenergic inhibition. In the regulation of the sympathetic outflow to the adrenal medulla, in contrast, ₂-adrenergic inhibition and ₁-adrenergic excitation have a similar impact. Uptake, inhibitors, hence, cause little change in adrenaline release: the two opposing influences cancel out. Prazosin produces an increase in noradrenaline but not adrenaline release because the loss of the central ₁ sympathoexcitation attenuates at best slightly the baroreflex to most extra-adrenal tissues but dampens markedly the baroreflex to the adrenal medulla. Correspondence to B. Szabo at the above address