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Biomedical subjects

B Rossi

Publications and source records attributed to B Rossi.

At least 235 records · Page 13Linked to original sources
PubMed1977

[Muscular malformation of the wrist in an initial carpal tunnel syndrome. Clinical case].

A carpal canal syndrome in a young female subject was found at the operating table to be due to a wrist muscle abnormality. An extra muscle leaving the styloid process of the radius in the direction of the transverse ligament of the carpus, and an abnormal distal development of the muscular belly of the superficial flexor of the third finger, had led to compression on the median nerve corresponding to the carpal canal. Check on motor and sensitive conduction of the median nerve revealed nerve damage at wrist level. Removal of the extra muscle and section of the transverse ligament of the carpus resolved the painful symptomatology. Control of nervous conduction two months after operation confirmed the improvement.

Adult↗
PubMed1976

(Na+, K+)-activated adenosinetriphosphatase of axonal membranes, cooperativity and control. Steady-state analysis.

1. The ATP sites. Homotropic interactions between ATP sites have been studied in a very large range of Na+ and K+ concentrations. The ( Na+, K+)-activated ATPase displays Michaelis-Menten kinetics for ATP under standard concentration conditions of Na+ (100 mM) and K+ (10 mM). The steady-state kinetics behavior changes at very low concentrations of K+ where negative cooperativity is observed. The existence of a high affinity and a low affinity site for ATP was clearly demonstrated from the study of the ATP stimulated hydrolysis of p-nitrophenylphosphate in the presence of Na+ and K+. The ratio of apparent affinities of high and low affinity sites for ATP is 86 at pH 7.5. 2. The Na+ sites. The binding of Na+ to its specific stimulatory sites (internal sites) is characterized by positive cooperativity with a Hill coefficient n(H(Na+))=2.0. Homotropic interactions between Na+ sites are unaffected by variations of the K+ concentration. 3. The K+ sites. (a) Binding of K+ to the (external) stimulatory site of the ATPase has been analyzed by following the (Na+, K+)-ATPase activity as well as the p-nitrophenylphosphatase activity in the presence of Na+ and K+ (with or without ATP). Binding is characterized by a Hill coefficient of 1.0 and a K(0.5(K+))=0.1 to 0.8 mM. The absence of positive or negative cooperativity persists between 5 mM and 100 mM Na+. (b) The analysis of the p-nitrophenylphosphatase or of the 2, 4 dinitrophenylphosphatase activity in the presence of K+ alone indicates the existence of low affinity sites for K+ with positive homotropic interactions. The characteristics of stimulation in that case are, K(0.5)=5 mM, n(H)=1.9. The properties of this family of site(s) are the following: firstly, saturation of the low affinity site(s) by K+ prevents ATP binding to its high affinity internal site. Secondly, saturation of the low affinity sites for K+ prevents binding of Na+ to its internal sites. Thirdly, this family of sites disappears in the presence of ATP, p-nitrophenylphosphate or of both substrates, when Na+ binds to its internal sites. Na+ binding to its specific stimulatory sites provokes the formation of the high affinity type of site for K+. 4. Mg2+ stimulation of the (Na+, K+)-ATPase is characterized by a Hill coefficient n(H(Mg2+))=1.0 and a K(0.5(Mg2+))=1 mM stimulation is essentially a V effect. Heterotropic effects between binding of Mg2+ and substrate to their respective sites are small. Heterotropic interactions between the Ms2+, Na+ and K+ sites are also small. 5. The fluidity of membrane lipids also controls the (Na+, K+)-ATPase activity. Phase transitions or separations in the membrane hardly affect recognition properties of substrates, Na+, K+ and Mg2+ for their respective sites on both sides of the membrane. Only the rate of the catalytic transformation is affected.

Acetylcholinesterase↗
PubMed1976

[Familial myotonic syndrome with hyposthenia corrected with exercise (author's transl)].

In some cases of myotonic syndromes a paresis after rest has been described corrected by exercise. This syndrome is reported in two brothers. In myotonic patients repetitive stimulation of a nerve causes a transitory decrease of the muscle action potential. Probably the paresis corrected by exercise only represents the clinical evidence of the electrophysiological phenomenon mentioned above. This seems to be a common occurrence and therefore does not represent a new nosologic entity.

Adult↗
PubMedDate not supplied

Regulation of interleukin-2 production and phosphatidylserine synthesis in Jurkat T lymphocytes by K+ channel antagonists.

Modification of phospholipid metabolism during T cell activation has been repeatedly reported. Recently, we have shown that phytohaemagglutinin, CD3 and CD2 mAbs, which are potent in vitro activators of helper T lymphocytes, markedly inhibit phosphatidylserine synthesis concomitantly as they induce the secretion of IL-2. In this paper, we show evidence that in T lymphocytes K+ channels, which have been shown to participate in the cell activation process, are also reciprocally related to phosphatidylserine synthesis. In fact, in resting T cells the drugs affecting the activity of K+ channels, such as quinine and 4-aminopyridine, induce a rise of phosphatidylserine synthesis. In activated cells, quinine and 4-amidopyridine also caused a rise in phosphatidylserine synthesis which paralleled a decreased production of IL-2, strongly suggesting that these two events are correlated in a reciprocal manner. More precisely, phosphatidylserine synthesis was stimulated by drugs which have been reported to inhibit potassium channels in lymphocytes, e.g. quinine, 4-aminopyridine, tetraethylammonium. These data suggest that the decreased PS synthesis observed during T cell activation intervenes in the cascade of events leading to IL-2 secretion. The decrease in the biosynthesis of this phospholipid seems to be dependent on the activity of K+ channels.

4-Aminopyridine↗
PubMedDate not supplied

The insulin receptor kinase.

The insulin receptor appears as a tetrameric glycoprotein consisting of two Mr 130,000 subunits (alpha), and two Mr 95,000 subunits (beta) in a disulfide-linked complex. Insulin bound to its specific cell surface receptors in its target cells leads to a complex array of molecular events resulting in insulin effects. It is now generally believed that protein phosphorylation-dephosphorylation reactions represent an important mechanism by which a variety of extracellular stimuli regulate cellular functions. Insulin mediates such reactions, but it is not known whether these are the biochemical link between the binding of insulin to its receptor and its final cellular effects. In search of initial post-binding events which might play a role in insulin action, we looked for phosphorylation of insulin receptors. We show that the insulin receptor displays two functional domains, an insulin binding alpha-subunit, and an insulin responsive protein kinase contained in the beta-subunit. We envisage the insulin receptor as an integrated system for transmembrane signal transmission in which hormone binding to the alpha-subunit leads to activation of the beta-subunit via conformational changes.

Adenosine Triphosphate↗
PubMedDate not supplied

Alpha-fetoprotein gene expression in early and full-term human trophoblast.

Alpha-fetoprotein (AFP) is a major serum glycoprotein synthesized during fetal life mainly by the yolk sac and the fetal liver. At term, it reaches high concentrations in the maternal intervillous blood, which is in direct contact with the placental trophoblastic microvillous membrane, and this suggests the placental origin of the AFP at the fetal-maternal interface. We used several experimental approaches to investigate the expression of AFP gene and fetal protein production in early gestation and term placentas. RT-PCR and immunological studies clearly identified AFP messenger RNA and AFP protein in the placental villi from first trimester of pregnancy. The AFP gene was also expressed in highly purified cytotrophoblasts from early placentas, and enzymo-immunoassay showed that AFP protein was synthesized and secreted by early cytotrophoblasts. AFP was also detected in the cytoplasm of these cells by immuno-cytochemistry. However, none of these methods detected any expression of the AFP gene in full-term placental villi or in cultured trophoblasts. These findings demonstrate that both AFP mRNA and protein are present in trophoblastic cells early in pregnancy. The absence of AFP gene expression in term placental villi also suggests, that the AFP at the fetal-maternal interface is attributable to a notable transplacental passage of AFP from fetal blood in late pregnancy.

Adult↗
PubMedDate not supplied

Treatment of secondary hyperparathyroidism with low dose intermittent calcitriol in hemodialysis patients. Imaging and cost analysis.

Calcitriol therapy is effective in the treatment of secondary hyperparathyroidism both during intravenous and oral administration, but there are doubts about the length of therapy and the duration of results. There are conflicting reports about results in size and activity of enlarged glands studied by ultrasound and double-tracer-subtraction-scintigraphy (DTSS). In 12 patients, 1 microgram of calcitriol was administered three times a week, intravenously and orally in alternate modes, for 46 weeks (therapy period) and orally for 46 weeks (follow-up period). During therapy, parathyroid hormone levels decreased in all patients, and in eight decreased by about 50% and were maintained at low levels during follow-up in five patients. Nine enlarged glands were detected by ultrasonography at the start of the study, and four hotspots were detected by DTSS; ultrasonography and DTSS were repeated at the end of the therapy and at the end of the follow-up: ultrasonography did not yield any significant variation in size, while one hot spot disappeared on DTSS. Basing their judgment on the lower cost of oral rather than intravenous administration, and on the good results of oral therapy, the authors stress the advisability of taking into account clinical and financial considerations before choosing the route of administration.

Administration, Oral↗
PubMedDate not supplied

Screening of human bladder carcinomas for the presence of Ha-ras codon 12 mutation.

Contradictory results were obtained from previous studies aiming at defining the frequency of Ha-ras codon 12 mutations in bladder tumors. Differences in the sensitivities of the methods used could account for this discrepancy. In this study, we reevaluated the frequency of Ha-ras codon 12 mutations in a series of 87 human bladder tumors using a combination of two different methods. The first was derived from the protocol of Ooi et al and consisted in a one-step allele-specific polymerase chain reaction using mismatched primers in two separate PCR. This method is very rapid and highly sensitive, detecting the presence of minor populations (less than 10%) of mutant alleles. The second strategy consisted in screening all tumors using natural restriction fragment length polymorphism (RFLP) analysis. The two methods were in complete concordance and enabled us to show that only one out of 87 primary bladder carcinomas (1%) exhibited the mutation, in accordance with previous studies. These results strongly suggest that, even if minor cell populations overexpress codon 12 Ha-ras mutation, the analysis of this mutation cannot be used to screen potentially invasive transitional cell tumors of the bladder.

Base Sequence↗
PubMedDate not supplied

[T-cell interferon-gamma, tumor necrosis factor-alpha and interleukin-6 receptor binding in patients with multiple sclerosis. Effects of interferon-beta-1b treatment].

INTRODUCTION: Multiple sclerosis (MS) is a T-cell-mediated demyelinating disease of the central nervous system (CNS), in which the cytokine network may be deranged. Interferon (IFN)-gamma, interleukin (IL)-6, and tumor necrosis factor (TNF)-alpha are cytokines with several effects on the neuroimmune system. Specific IFN-gamma, IL-6, and TNF-alpha receptors have been found on human lymphocytes and other cell types. PATIENTS AND METHODS: We assayed IFN-gamma, TNF-alpha, and IL-6 binding on peripheral blood T cells from MS patients, as compared with healthy subjects. T cells from MS patients have significantly less IFN-gamma receptors, and more TNF-alpha and IL-6 receptors than those from controls. Such receptors are of the same type in patients and healthy subjects. By comparing MS patients' subgroups with each other, significant differences in mean Bmax values have been found between patients in a stable phase and those in relapse, and between stable patients and those in an evolutive phase. As far as IL-6 binding is concerned, significant differences in mean Bmax values were observed only between patients in stable phase and those in relapse. RESULTS: T lymphocytes from untreated MS patients, which had significantly smaller amounts of IFN-gamma receptors than those from controls, and more TNF-alpha and IL-6 receptors than controls showed a significant increase in IFN-gamma binding, and a significant decrease in TNF-alpha and IL-6 binding after a 3-month IFN-beta 1b treatment. T-cell IFN-gamma Bmax values were even higher, and those of TNF-alpha and IL-6 were lower after 6 months. CONCLUSION: We discuss these results in terms of MS immunopathophysiology, since activated T cells have decreased IFN-gamma, and increased TNF-alpha and IL-6 receptor amounts.

Adjuvants, Immunologic↗
PubMedDate not supplied

Rock steady nurse.

Explore the source record for details and available documents.

Community Health Nursing↗
PubMedDate not supplied

Calcium-dependent regulation of phosphatidylserine synthesis in control and activated Jurkat T cells.

Activation of Jurkat T cells with phytohemagglutinin (PHA), CD3 or CD2 monoclonal antibodies (mAbs) results in a marked inhibition of phosphatidylserine (PS) synthesis. Activation of Jurkat T cells with PHA in a Ca(2+)-free medium resulted in an arrest of PS synthesis which was not reversed by the addition of Ca2+. The use of BAPTA to chelate Ca2+ ions released from intracellular stores prevented PHA-induced inhibition of PS synthesis. In addition, it was found that during activation, in the presence of BAPTA, a net Ca2+ influx paralleled an increase in PS synthesis, demonstrating that Ca2+ uptake caused an enhanced PS synthesis rather than an inhibition. The use of a CD2 mAb, D66, able to mobilize exclusively Ca2+ from intracellular stores, resulted in 51% inhibition of PS synthesis. N-Ethylmaleimide (NEM), which inhibits both the release of Ca2+ from internal stores and the influx of Ca2+, totally prevents the inhibition of PS synthesis induced by PHA, anti-CD3 or anti-CD2 mAbs. The presence, in the incubation medium, of either NDGA, TPCK or TPA, three drugs able to markedly inhibit Ca2+ influx without modifying the release of Ca2+ from internal stores, did not modify the inhibition of PS synthesis induced by PHA. Moreover all the drugs known to interact with calmodulin were also found to prevent the PHA-induced inhibition of this phospholipid. Taken together, these results show that the inhibition of PS synthesis induced by T cell activators is regulated by both calmodulin and Ca2+ ions recruited from intracellular compartments.

Antibodies, Monoclonal↗
PubMedDate not supplied

[Fatigue at various muscular lengths in myotonic dystrophy].

In myotonic dystrophy alteration in membrane excitability characterizes, in addition to the dystrophic process, modifications of contractile function detectable after fatigue. To verify in which extent sarcolemmal activation or contractility mechanisms are involved in fatigue, some electrophysiological and dynamometer parameters have been studied in tibialis anterior of 5 myotonic dystrophy patients. Evaluation has been performed basally and after protocol consisting of intermittent isometric voluntary contractions lasting 15', at two different muscle lengths, optimal and short. Administration at several recovery times of 20 and 50 Hz tetanizing sequences shows how processes distal to membrane excitability are mainly responsible for fatigue at optimal length, while relative potentiation of excitability preserves the muscle from excessive force loss at short length.

Adult↗
PubMedDate not supplied

[Mechanisms of muscular fatigue].

According to Merton (1954), Bigland-Ritchie (1978), Edwards (1981) and De Luca (1984), two groups of mechanisms, central and peripheral, may be distinguished in physiopathology of fatigue process. Central mechanisms are related to subjective phenomena, like fatigue sensation or motivation, and to objective aspects as spatial and temporal motoneurones recruitment.

Electroencephalography↗
PubMedDate not supplied

[Mitochondrial oculopharyngeal myopathy: description of a case].

We describe a 55 years old man affected by eyelid ptosis, mild ophthalmoplegia externa and severe dysphagia owing to pharyngoesophageal dyskinesia. Skeletal and eyelid constrictor muscles EMG showed myogenic alterations. Muscle histological findings of ragged red fibers and oxidative histochemical alterations, together with ultrastructural investigation clue for mitochondrial myopathy diagnosis. This, considering the unusual clinical aspects of the case, confirms as mitochondrial disease can widely vary in their phenotypical expression.

Blepharoptosis↗
PubMedDate not supplied

[Changes in muscular excitability and contractility caused by fatigue in Steinert's disease].

To study effects of fatigue on muscle excitability and contractility in myotonic dystrophy (MyD), we evaluated, by ulnar nerve supramaximal stimulation, both single shock and 40 Hz tetanus, M wave and force parameters from adductor pollicis. In 8 MyD patients and in 6 controls amplitude of M wave, electromechanical delay, single twitch and tetanus tension, contraction and half-relaxation times were recorded in basal condition and at different times after 75 sec. of maximal voluntary contraction. Reduction of force related to fatigue was per cent lesser in MyD compared to controls. Electro-mechanical delay, basally longer in MyD, showed after fatigue 15% increment compared to 47% in controls. Half-relaxation time increased in both groups, but in MyD recovery was faster. Peculiar alterations of excitation-contraction coupling and contractility occurring in MyD can explain the observed modifications of fatigue phenomena in this disease.

Adult↗
PubMedDate not supplied

Breakdown of a phosphatidylcholine pool arising from the metabolic conversion of phosphatidylethanolamine as a novel source of diacylglycerol in activated T cells.

Activation of Jurkat T cells with either phytohemagglutinin (PHA), CD3 or CD2 monoclonal antibodies (mAbs) induces the production of diacylglycerol (DAG) from two different sources. Activation of the phosphatidylinositide cycle in activated T cells is a well-known source of the second messengers DAG and inositol triphosphate (IP3). The present report demonstrates that a particular pool of phosphatidylcholine (PC) arising from the sequential methylation of phosphatidyl-ethanolamine (PE) is probably a second source of DAG. The occurrence of two distinct sources of DAG in activated T cells is supported by the fact that DAG production was not accompanied by a decrease of phosphatidylinositol mono- and bisphosphate (PIP/PIP2) pools as measured after [3H]glycerol labeling whereas [3H]arachidonic acid PIP/PIP2 pools decrease in parallel with DAG production. The presence of a second generating pathway for DAG was demonstrated by measuring phospholipid synthesis and degradation in cells labeled with [3H]choline, [3H]ethanolamine or [3H]serine. In Jurkat cells, PHA decreased the incorporation of [3H]ethanolamine and [3H]serine but not [3H]choline into PC suggesting that the PC pool arising from the methylation of PE was utilized during activation whereas the PC pool synthesized through the CDP choline pathway was not. In [3H]ethanolamine-prelabeled cells, but not in [3H]choline-prelabeled cells, PHA, CD3 and CD2 induced the breakdown of PC. The PC breakdown was accompanied by a release of [3H]choline and the production of DAG and phosphatidic acid (PA). The breakdown of PC described in the present report strongly suggests that PC participates in T lymphocyte activation through the production of DAG.

Calcimycin↗