[Mortality in a cohort of alcoholics from Arezzo in 1979-1997]. / La mortalità in una coorte di alcolisti di Arezzo nel periodo 1979-1997.

This study evaluates the risk of mortality in a cohort of Italian alcoholics resident in a rural area characterised by traditional drinking habits. Individual vital status of the 1,037 patients enrolled at the Centro Alcologico in Arezzo during the 1979-1997 period has been traced. Causes of death (ICD-IX) have been retrieved from the Regional Mortality Register. Standardised mortality ratios (SMR) have been computed according to gender and 5-year age group mortality rates of the general population resident in Tuscany during the same period. This cohort is representative of the traditional rural alcoholism of the Tuscany region based on wine consumption. Among the 9,190 person-years followed-up, 333 deaths have occurred, corresponding to approximately 2.6 fold the expected number of deaths (SMR males: 2.6; females: 2.4). In both genders, significantly high SMRs for liver cirrhosis, oesophagus and liver cancer are reported, while SMRs of cancers at all sites, oral and respiratory cancers, injuries as a whole, road and traffic accidents, and suicides are significantly elevated only among males. No relevant variation between expected and observed deaths for pancreatic diseases, colon cancer, female breast cancer, and, despite a large proportion of heavy smokers, for cardiovascular diseases (hypertension, cerebrovascular diseases, coronary heart diseases) has been recorded. This research confirms the high mortality among a cohort of Italian alcoholics. However, causes of death related with violence and trauma are proportionally less represented, in accordance with the social pattern of Mediterranean alcoholism. The absence of cardiovascular mortality risk in a wine-based cohort of alcoholics is an unexpected finding that requires to be further examined. Finally, to prevent smoking related deaths, alcohol addiction services should begin to introduce smoking cessation practices among treatment protocols.

Iliac vein reconstructions to treat acute and chronic venous occlusive disease.

PURPOSE: The treatment of permanent and benign iliac vein occlusion responsible for acute vein thrombosis or chronic symptoms remains controversial. Different methods of reconstruction using a reinforced expanded polytetrafluoroethylene bypass graft associated with an arteriovenous fistula and their intermediate-term results are analyzed. METHODS: Eight consecutive patients (six men, two women; mean age, 45.6 years; range, 29 to 70 years) were treated over a period of 38 months for iliac vein obstruction. Three short bypass procedures between the left iliac vein and the right common iliac vein with temporary arteriovenous fistulas were carried out after an iliofemoral (and caval in two cases) venous thrombectomy, which revealed May-Thurner syndrome (n = 1) and a compression of the left common iliac vein by the left hypogastric artery (n = 2). Five long bypass procedures (one femorofemoral, two left common femoral-vena caval, one right superficial femoral-common iliac, and one bifemorocaval) with a definitive arteriovenous fistula were performed for long chronic venous occlusion in four cases (responsible for venous claudication [n = 3], recurrent ulcers [n = 1] and after iatrogenic ligature of the left external iliac vein during total cystectomy with double ureterostomy in one case. RESULTS: There was no evidence of pulmonary embolism, and no deaths were recorded in the perioperative period. Two patients had an early bypass thrombectomy, but one returned with a further graft occlusion. Seven grafts remained patent after a mean follow-up of 19.5 months (range, 10 to 45 months). One successful thrombectomy was necessary during the twenty-third postoperative month. CONCLUSIONS: Reconstruction of iliac veins in case of permanent compression, mostly discovered after venous thrombectomy, or for selected patients with symptomatic benign iliac vein occlusion, is safe and provides good intermediate-term results.

Modulation of left and right ventricular beta-adrenergic receptors from spontaneously hypertensive rats with left ventricular hypertrophy and failure.

Inotropic responsiveness to beta-adrenergic stimulation is generally found to be depressed in cardiac hypertrophy and failure. To investigate whether inotropic responsiveness is associated with alterations in beta-adrenergic receptors in spontaneously hypertensive rats (SHR), we studied left ventricular myocardial contractile responses to isoproterenol and beta-adrenergic receptor density and affinity in age-matched rats (18 to 24 months), including SHR without heart failure, SHR with evidence of heart failure, and normotensive control Wistar-Kyoto rats (WKY). In the baseline state, papillary muscles from failing SHR demonstrated decreased isometric tension development and a reduction in maximal rate of tension development relative to normotensive WKY and compensated SHR. Compared with WKY, beta-adrenergic receptor density of the left ventricle was unchanged in nonfailing SHR and increased in failing SHR (P < .05 versus WKY and nonfailing SHR), and beta-adrenergic receptor affinity did not differ among groups. In the right ventricle, beta-adrenergic receptor density was decreased in failing SHR relative to WKY and nonfailing SHR, and beta-adrenergic receptor affinity was not different among groups. Muscle preparations did not exhibit a positive inotropic response to 10(-8) to 10(-5) mol/L isoproterenol or 6.3 mumol/L forskolin in either failing or nonfailing SHR, whereas a positive inotropic response to both drugs was observed in the normotensive WKY. The lusitropic response to isoproterenol and forskolin was intact and similar in both SHR groups and WKY. The findings suggest that in the SHR model of heart failure, impaired intrinsic left ventricular myocardial function and depressed inotropic responsiveness to beta-adrenergic stimulation are not associated with downregulation of the beta-adrenergic receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

Q beta replicase: mapping the functional domains of an RNA-dependent RNA polymerase.

We have localized a functional region of the RNA bacteriophage Q beta replicase following an extensive mutational analysis. Using the method of oligonucleotide linker-insertion mutagenesis, we specifically introduced mutations into a cloned DNA copy of the Q beta replicase gene so that the resulting replicase products would putatively contain small amino acid insertions. In a selective phenotypic assay, we screened mutant replicases for RNA-directed replication activity in vivo. Analysis of 37 different mutant clones indicated that Q beta replicase can accept amino acid substitutions and insertions at several sites at the amino and carboxy termini without abolishing functional activity in vivo or in vitro. However, disruption within the internal amino acid sequence resulted almost exclusively in nonfunctional enzyme. The results suggest that the central region of the replicase protein contains a rigid amino acid composition that is required for replicase function, whereas the amino and carboxy termini are much more receptive to small amino acid insertions and substitutions. These experiments should further enable us to analyze the coding function of the Q beta replicase gene independently of other phage RNA functions contained within this nucleotide region.

[Cardiac rhythm in the newborn infant. A contribution to the definition of normality]. / Il ritmo cardiaco nel neonato. Un contributo alla definizione di normalità.

The definition of normal cardiac rhythm in newborn is still uncertain. Authors studied thirty healthy newborns by standard and dynamic ECG; results were compared and discussed.

Muscle carnitine palmityltransferase deficiency and myoglobinuria.

Muscle carnitine palmityltransferase activity, measured by three different methods, was very low (0 to 20 percent of controls) in a patient with a familial syndrome of recurrent myoglobinuria. Long-chain fatty acyl CoA synthetase activity was normal; acetylcarnitine transferase activity was decreased by 40 percent, and carnitine content was 1.7 times higher than the mean control value. Utilization of palmitate by isolated mitochondria was more impaired than utilization of palmitylcarnitine, suggesting a more severe defect of carnitine palmityltransferase I than transferase II. Thus, myoglobinuria may be due to a genetic defect of lipid metabolism in skeletal muscle.