[Changes in platelet adhesiveness and blood plasminogen in the course of therapy with a total extract of arterial wall by oral administration].
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Biomedical subjects
Publications and source records attributed to V Lombardi.
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In normal subjects, thallium-201, administered per rectum, is taken up mainly by the liver (heart/liver ratio in normal subjects: 0.04 to 0.12). It has been claimed that an increased heart/liver ratio is suggestive of portal-caval shunting and portal hypertension. To evaluate the possibility of using thallium-201 as a test to diagnose cirrhosis, we administered this substance per rectum to 33 patients with biochemical evidence, but no clinical symptoms, of liver disease. Laparoscopy and liver biopsy revealed chronic active hepatitis without cirrhosis in 18 patients, and chronic active hepatitis with cirrhosis in the others. The results of conventional liver function tests were similar in both groups. A significant difference, however, was found between the means of fasting serum bile acid concentrations (9.8 +/- 3.2 and 18.3 +/- 4.2 microM per liter) in chronic active hepatitis without cirrhosis and cirrhotic patients, and between the means of the heart/liver ratios 20 min after thallium-201 administration (heart/liver: 0.09 +/- 0.03 and 0.54 +/- 0.13, respectively). Unlike the serum bile acid concentration which gave some overlapping values, the thallium-201 test clearly distinguished the chronic active hepatitis without cirrhosis group from the cirrhotics. In the cirrhotic group, there was a significant correlation between the heart/liver ratio and signs of portal hypertension such as esophageal varices, increased diameter of the vena porta and hypersplenism. The thallium-201 test is therefore useful in discriminating between chronic active hepatitis with and without cirrhosis in clinically asymptomatic subjects with biochemical evidence of moderate liver function impairment. A heart/liver uptake ratio much higher than normal (above 0.30) strongly suggests the development of hepatic cirrhosis.
Changes in the functioning of the glutamatergic system in rabbit brain were studied after partial brain ischemia and reperfusion. In vitro studies were conducted relating to the release of L-[14C]glutamate from cortical brain slices, L-[14C]glutamate uptake in synaptosomes, and 45Ca uptake in synaptosomes. It was found that basal release of L-[14C]glutamate from rabbit brain cortical slices after 30 min of partial ischemia and 1 d of reperfusion was essentially without change compared to the control values. After 3 d of reperfusion, there was an increase in basal release of L-[14C]glutamate from rabbit brain cortical slices. K+ stimulated release of L-[14C]glutamate in normal Krebs-Ringer medium was essentially the same in the control group and in the experimental group after 30 min of ischemia. The K+ stimulated release of L-[14C]glutamate independent of calcium was increased to 145% after 30 min of ischemia and 1 d of reperfusion. The decreased Km value at the glutamate transporter may have contributed to this difference. Kinetic parameters of the L-[14C]glutamate uptake (Km and Vmax) in synaptosomes from rabbit brain were significantly lower after 30 min of ischemia. The authors discovered that during the reperfusion period, Vmax was almost the same as in the control group. The activity of the Na+/Ca2+ exchanger in synaptosomes of rat brain was about 70% of the control values after 30 min of ischemia and 72 h of reperfusion. According to our results, increased L-[14C]glutamate release after 30 min of ischemia appears to be the result of higher intracellular calcium concentration and possibly also of a higher uptake of glutamate.
The neurotoxic actions of MPTP and its 4-(O-tolyl) analog (2'-Me-MPTP) on two breeds of rabbits were investigated. MPTP, but not 2'-Me-MPTP, causes a reduction (about 40%) in striatal dopamine content in rabbits of the "little silver-black" breed. The dopamine content of striata of "chinchilla" rabbits was not affected by either agent.
Homonuclear 1H 2D NMR spectroscopy (COSY experiments at 400 and 600 MHz) were used to study the rat brain in vivo and the rabbit spinal cord and sciatic nerve in vitro. The following metabolites were identified: lactate, alanine, threonine, GABA, glutamine/glutamate, N-acetyl aspartate, aspartate, taurine, inositol derivatives, choline derivatives, and glucose. The sciatic nerve spectra showed characteristic COSY graphs of saturated and unsaturated fatty acids, and linoleic and linolenic type structures were identified.
Steinert's myotonic dystrophy (DM) is a genetic autosomal dominant disease and the most frequent muscular dystrophy in adulthood. Although causative mutation is recognized as a CTG trinucleotide expansion on 19q13.3, pathogenic mechanisms of multisystem involvement of DM are still under debate. It has been suggested that mitochondrial abnormalities can occur in this disease and deficiency of coenzyme Q 10 (CoQ10) has been considered one possible cause for this. The aim of this investigation was to evaluate, in 35 DM patients, CoQ10 blood levels and relate them to the degree of CTG expansion as well as to the amount of lactate production in exercising muscle as indicator of mitochondrial dysfunction. CoQ10 concentrations appeared significantly reduced with respect to normal controls: 0.85 +/- 0.25 vs. 1.58 +/- 0.28 microg/ml (p < 0.05). Mean values of blood lactate were significantly higher in DM patients than controls (p < 0.05) both in resting conditions (2.9 +/- 0.55 vs. 1.44 +/- 1.11 mmol/L) and at the exercise peak (6.77 +/- 1.79 vs. 4.90 +/- 0.59 mmol/L), while exercise lactate threshold was anticipated (30-50% vs. 60-70% of the predicted normal maximal power output, p < 0.05). Statistical analysis showed that serum CoQ10 levels were significantly (p < 0.05) inversely correlated with both CTG expansion degree and lactate values at exercise lactate threshold level. Our data indicates the occurrence of reduced CoQ10 levels in DM, possibly related to disease pathogenic mechanisms associated with abnormal CTG trinucleotide amplification.
The present study analyzes the results obtained by the AA with the different types of surgery adopted in the treatment of the complicated diverticulosis of the colon, highlighting, on the basis of data available in literature, the possible treatments in the different clinical settings. A retrospective study analyzing type of complication, the surgical technique adopted, Hinchey stage, mortality and morbidity rates and average hospital stay correlated with the kind of intervention has been carried out on 83 surgical interventions performed between 1984 and 1988. The results show that 43 R.A.P. (R.A.P. = primitive anastomosis resection) (32 cases at the I-II stage and 11 cases at the III-IV stage), 27 Hartmann (11 at the I-II and 16 at the III-IV), 9 colostomies (2 at the I-II and 7 at the III-IV), 2 esteriorizations and 2 simple drains have been carried out on a total of 44 intestinal perforations, 16 recurrent diverticulitis, 13 intestinal occlusions, 2 fistulae, 5 abscesses and 3 hemorrhages. The total mortality rate amounts to 10.6%; the morbidity rate of the R.A.P. interventions to 14.4 (I-II stage-related morbidity = 15.6%, III-IV stage = 63.6%), Hartmann's to 9.6% and that of the colostomies to 3.6%. Furthermore, in this work, we have considered the cases of riconversation after Hartmann interventions (9 cases): in the second operations the mortality and morbility rate amounts to 0 and the hospital stay to 9 days. The AA analyze on the surgical technique adopted in the different cases and the of choice criteria. According to the data obtained and to current literature, it results that the primitive anastomosis resection represents the first choice intervention at the I-II stage, although, in selected cases, it can be carried out also at the III-IV stage. Hartmann surgery confirms its effectiveness while simple colostomy is no longer accepted in literature.
Substernal goitre is a clinical condition in which the masin bulk of the enlarged gland is firmly located in the chest. The incidence of this pathology ranges in literature from 1.7% and 30%. This study examines 230 cases of substernal goitre out of a total 5.362 operations performed from 1965 to 2000, for thyroid gland pathologies (4.36%). According to their experience the Authors propose a classification based on the anatomical location of the goitre: right, left, anterior and posterior goitre are therefore identified. The surgical procedures performed include 136 subtotal thyroidectomies (59.1%), 59 emithyroidectomies (25.7%) and 23 total thyroidectomies (10%). In 12 cases the operation was confined to removal of the mediastinal mass (5.2%). The cervical approach was the only surgical access route used in all the patients, regardless of the different anatomical variants. Appreciable venous stasis, due to the mediastinal mechanical obstruction exerted by the goitre, was always evident at the operation. In order to limit the risk of bleeding during operation, careful hemostasis of the major vascular pedicles must be performed. Any attempt to legate the smallest vessel, should be avoided since it is a difficult, useless and time-consuming procedure. Minor bleeds promptly stop as soon as the pathological mass is removed. Ligation of the vascular pedicles can be easily achieved; in this way, the goitre is freed from its anatomical connections and the surgeon can safely manage the substernal portion of the mass. The mortality reported in this study was 0.43% (one patient died 30 days postoperatively due to respiratory complications), whereas the morbidity rate was 2.6%.
Constitutive genomics are probably determinant for the onset of dementia in conjunction with cerebrovascular and environmental factors. Furthermore, pharmacogenomic studies predict that the therapeutic response in Alzheimer's disease (AD) is genotype-specific, and that the expression of genes involved in the regulation of drug metabolism can influence efficacy and safety issues in pharmacotherapy. AD and dementia with a vascular component (DVC = VD + MXD) are the most prevalent forms of dementia. These clinical entities share many similarities, but they differ in major phenotypic and genotypic profiles, as revealed by structural and functional genomics studies. Comparative phenotypic studies have identified significant differences in 25% of more than 100 parametric variables, including anthropometry, cardiovascular function, aortic atherosclerosis, brain atrophy, blood pressure, blood biochemistry, hematology, thyroid function, folic acid and vitamin B(12) levels, brain hemodynamics and lymphocyte markers. The phenotypic profile of patients with DVC differs from that of AD patients in the following: (a) anthropometric values, (b) cardiovascular function, (c) blood pressure, (d) lipid metabolism, (e) uric acid levels, (f) peripheral calcium levels, (g) liver function (GOT, GPT, GGT), (h) alkaline phosphatase, (i) lactate dehydrogenase, (j) red and white blood cells, (k) regional brain atrophy (left temporal region, inter-hippocampal distance) and (l) brain blood flow velocity. Functional genomics studies incorporating APOE-related changes in biological markers extended the difference between AD and DVC up to 57%. Structural genomics studies with AD-related genes, including APP, MAPT, APOE, PS1, PS2, A2M, ACE, AGT, cFOS and PRNP genes, demonstrate different genetic profiles in AD and DVC, with an absolute genetic variation rate ranging from 30 to 80%, depending upon genes and genetic clusters. Single gene analysis identifies relative genetic variations ranging from 0 to 5%. The relative polymorphic variation in genetic clusters integrated by 2, 3 or 4 genes associated with AD ranges from 1 to 3%. The main phenotypic differences between AD and DVC are genotype-dependent, especially in AD, probably indicating that different genomic factors are essential for the expression of dementia symptoms that might be accelerated or induced by environmental and/or cerebrovascular factors.
According to the OMS classification of the epithelial benign neoplasm of the liver, the adenomas represent the most important group. In literature an increase of their incidence in the last years is reported especially in the female sex, in relationship to the diffusion of the use of hormonal contraceptives. The biliar cistoadenoma (BCA) represents a not frequent neoplasm of the liver that has origin on the inside of the liver, and less frequently from the extrahepatic biliar system. The surgical interest is underlined by the potentiality of the malignant evolution of the lesion and by its high tendency to the relapse. The real difficulty is represented by differential diagnosis from the other cystic lesions of the liver and by the need of its radical excision and therefore of real hepatectomy.
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