["For Aesculapius and the health of my fellow-soldiers": updated synthesis of Roman military medicine].
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History, Ancient↗
Biomedical subjects
L Rossi
Publications and source records attributed to L Rossi.
Serum bile-acids in liver cirrhosis: prognostic significance evidenced by a multivariate statistical model.
In order to evaluate the prognostic value of serum bile acids (SBA) in liver cirrhosis, we compared SBA levels with a theoretical expected survival length (ESL), computed on the ground of a previously proposed and validated multivariate statistical model. We demonstrated a strict correlation between SBA levels and ESL in subjects with liver cirrhosis by means of both standard linear correlation analysis and Logrank test. Our results account for a high predictive significance of SBA levels in liver cirrhosis, even in long term prognosis.
Adult↗
[Diagnosis of total block in the bundle of His with rhythm of idioventricular substitution].
His bundle (HB) recording does not allow the recognition of third degree intrahisian block in patients with complete atrio-ventricular block (AVB) associated with idioventricular rhythm, due to the absence of pacemaker activation in the distal HB region. We have observed fixed retrograde distal HB activation in the standard HB recording of a patient with complete AVB and ventricular rhythm at a rate of 28/min. Retrograde distal HB activation (h'r) did not disappear during apical right ventricular pacing, in association with the complete absence of retrograde nodal conduction: concealed retroconduction into the proximal HB did not allow the recording of anterograde hisian deflection when the interval between h'r deflection and the subsequent sinus atriogram was shorter than 200 msec. Distal HB bipolar pacing using low energy stimulus resulted in 1:1 ventricular response and normal QRS duration in the absence of nodal retroconduction, thus proving the localization of bidirectional block within the HB. The unmasking of retrograde V-h' conduction during idioventricular rhythm was likely related to phase 4 retrograde delay in the branch ipsilateral to the site of the emergency ventricular focus and to the subsequent trans-septal activation of the other side of His-Purkinje system. Referring to arrhythmic problems after DDD pace-marker implantation the localization of complete AV blocks and retrograde conduction patterns are discussed.
Aged↗
[Anisoinotropism of myocardial cells: elementary histological picture of early ischemic dys-asynergy].
Twelve autoptic hearts from victims of cardiogenic shock, within a few hours from infarction, were studied at light microscope. At the site of early ischemia, a discrepancy in contraction of myocardiocytic units along single fibers (otherwise normal) has been observed. It configurated as an asynergic contracture (with Z lines impinging upon A bands), side by side with relaxed elements (with evident I bands); frequent dehiscence of intercalated disks ensues, due to imbalanced mechanic strain. These morphologic features, only rarely seen in 20 control hearts, are consistent with pertinent knowledge in pathophysiology, and can be defined "anisoinotropism" of myocardial fibers. They seem to be the microscopic substrate for the contractile dys-asynergy, which is credited in modern clinical diagnostics among the earliest signs of cardiac ischemia. The discal injury may also imply an impairment in intercellular conductivity, with an arrhythmogenic potential (reentry). Anisoinotropism presents as the forerunner of the well known "contraction band degeneration-necrosis", by progressive coagulative denaturation of the contractile proteins, up to conglutination and cancellation of sarcomere structures. The changes described herein can be taken into consideration in histopathology of heart's acute ischemia, before the occurrence of patent pictures of initial infarction.
Adult↗
Quinone toxicity in hepatocytes without oxidative stress.
The toxicity of quinones is believed to be mediated via redox cycling involving formation of semiquinone radicals which autoxidize to form active oxygen species. However, when the cytotoxicity of benzoquinones was compared using freshly isolated rat hepatocytes, benzoquinones which did not mediate oxidative stress were highly toxic. Thus, the benzoquinone analogs in decreasing order of cytotoxicity were 2-CH3-, 2-Br-, unsubstituted, 2,6-(CH3)2-, 2,5-(CH3)2-, and 2,3,5-(CH3)3-benzoquinone. Cellular thiols were rapidly depleted and glutathione (GSH) was converted to a quinone conjugate without oxidation to glutathione disulfide. No increase in cyanide-resistant respiration was observed and benzoquinone-induced cytotoxicity was not enhanced by inactivation of catalase or glutathione reductase. In contrast, duroquinone [2,3,5,6-(CH3)4-benzoquinone], which stimulated cyanide-resistant respiration and GSH oxidation, was only cytotoxic when catalase or glutathione reductase was inactivated. These results suggest that alkylation and/or oxidative stress may be important mechanisms in the cytotoxicity of benzoquinone derivatives.
Alkylating Agents↗
Familial arrhythmogenic right ventricular disease.
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Adolescent↗
[Hypokalemic syndrome due to a pseudo-aldosteronism secondary to the endoconjunctival administration of a mineraloactive steroid].
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Female↗
Trisomy 12 in B cells of patients with B-cell chronic lymphocytic leukemia.
Trisomy 12 is the most frequently reported chromosome abnormality in patients with B-cell chronic lymphocytic leukemia, but only normal karyotypes are found in one third of patients with that disorder. Moreover, samples from patients with trisomy 12 also have many normal metaphases. To identify immunologically the cells in which both the trisomy 12 and the normal karyotypes occur, we studied two patients with B-cell chronic lymphocytic leukemia--one whose neoplastic cells demonstrated lambda light-chain clonality and one whose cells had kappa light-chain clonality. We used a recently developed cytogenetic method that allows simultaneous analysis of cell morphology, immunologic phenotype, and karyotype in the same mitotic cell. In cultures of blood cells stimulated with pokeweed mitogen and tetradecanoylphorbol acetate, all the mitotic cells with either the lambda or the kappa immunoglobulin had trisomy 12, whereas all the cells that lacked these light chains or that had T-cell markers (OKT8 or OKT4) had normal karyotypes. These results show that trisomy 12 in B-cell chronic lymphocytic leukemia occurs in the neoplastic B cells, but not in the T cells, and they thus provide an explanation for the common finding of mitoses with normal karyotypes in patients with B-cell chronic lymphocytic leukemia.
B-Lymphocytes↗
[Isolation and purification of soluble antigens from the bovine retina].
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Animals↗
Anticentromere antibody in localized scleroderma.
Using metaphase chromosome spreads as substrate for indirect immunofluorescence technic, we observed anticentromere antibody in three of twenty-five patients affected with various clinical forms of localized scleroderma. Anticentromere antibody is generally considered a serologic marker of the CREST syndrome, a more benign subset of systemic sclerosis. However, none of the three anticentromere antibody-positive patients with localized scleroderma had Raynaud's phenomenon, acrosclerosis, or any signs or symptoms of systemic disease; on physical and laboratory examination, they showed only typical cutaneous features of localized scleroderma: two showed linear scleroderma, and one showed localized morphea. A 2-year 8-month follow-up of two patients did not disclose any clinical evidence of systemic sclerosis. The occurrence of anticentromere antibody in patients with localized scleroderma seems to offer supportive evidence that a relationship exists between localized scleroderma and systemic sclerosis.
Adolescent↗
Status epilepticus due to abrupt diazepam withdrawal: a case report.
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Adult↗
Cardiac amyloidosis involving the conduction system and the aortocoronary neuroreceptors. Clinicopathologic correlates.
In a patient with cardiac primary amyloidosis with conduction disturbances and dynamic cardiocirculatory disorders, the specialized system of the heart and the hitherto neglected cardiac nerve plexus and annexed aortocoronary glomera were studied histologically. Amyloid deposition in the conduction system and in the nerves and neuroreceptors seemed to correlate with the dysrhythmic manifestations, and, respectively, with some undue responses to vasodilator therapy. The possible hazards deriving from involvement of the aortocoronary glomera in patients with amyloidosis have been pointed out accordingly.
Amyloidosis↗
Effects of oxidative stress caused by hyperoxia and diquat. A study in isolated hepatocytes.
The effects of oxidative stress caused by hyperoxia or administration of the redox active compound diquat were studied in isolated hepatocytes, and the relative contribution of lipid peroxidation, glutathione (GSH) depletion, and NADPH oxidation to the cytotoxicity of active oxygen species was investigated. The redox cycling of diquat occurred primarily in the microsomal fraction since diquat was found not to penetrate into the mitochondria. Depletion of intracellular GSH by pretreatment of the animals with diethyl maleate promoted lipid peroxidation and sensitized the cells to oxidative stress. Diquat toxicity was also greatly enhanced when glutathione reductase was inhibited by pretreatment of the cells with 1,3-bis(2-chloroethyl)-1-nitrosourea. Despite extensive lipid peroxidation, loss of cell viability was not observed, with either hyperoxia or diquat, until the GSH level had fallen below approximately 6 nmol/10(6) cells. The iron chelator desferrioxamine provided complete protection against both diquat-induced lipid peroxidation and loss of cell viability. In contrast, the antioxidant alpha-tocopherol inhibited lipid peroxidation but provided only partial protection from toxicity. The hydroxyl radical scavenger alpha-keto-gamma-methiol butyric acid, finally, also provided partial protection against diquat toxicity but had no effect on lipid peroxidation. The results indicate that there is a critical GSH level above which cell death due to oxidative stress is not observed. As long as the glutathione peroxidase - glutathione reductase system is unaffected, even relatively low amounts of GSH can protect the cells by supporting glutathione peroxidase-mediated metabolism of H2O2 and lipid hydroperoxides.
Animals↗
[Arrhythmia in patients with a DDD bicameral pacemaker].
Dual chamber pacemakers, with coordinate atrial and ventricular sensing and stimulation (DDD), even if allowing "physiological" pacing, exhibited new and complicated arrhythmic manifestations, whose real frequency is still unascertained. In 65 patients (mean age 68 +/- 12 years), implanted with a DDD multiprogrammable device (15 pts. Medtronic Versatrax 7000 A, 50 pts. Pacesetter AFP 283), we carried out a 24 hours Holter monitoring while pacemaker was programmed with standard parameters. In a subset of 15 patients Holter monitoring was performed before and after pacemaker implantation. We evidenced: a) atrial sensing and/or pacing malfunction in 3 patients (4.5%); b) pacer-unrelated arrhythmias in 49 patients (75%): atrial extra beats 35 patients (54%), ventricular extra beats 23 patients (35%), non-sustained ventricular tachycardias 10 patients (15%), atrial tachyarrhythmias 8 patients (12%); c) supraventricular arrhythmias with PM-mediated high rate ventricular pacing in 12 patients (18%); d) PM induced and sustained endless loop tachycardias in 31 patients (47%); e) arrhythmias depending on over-sensing in 11 patients (17%): myopotential interferences 9 patients (14%), cross-talk ventricular pacing inhibition 2 patients (3%). The prevalence of ventricular arrhythmias was not different before and after the pacemaker implantation. The prevalence of atrial extrasystoles (53% versus 40%) and atrial tachyarrhythmias (26% versus 6%) decreased after the pacemaker implantation. Aimed reprogramming with progressive extension of atrial refractory period (from 250 to 400 msec and DDX) achieved disappearance of PM-endless loop tachycardias in 95%. Use of multi-programmability lowered the incidence and symptoms of most PM-related arrhythmias. Drug therapy was of choice in clinical arrhythmias unrelated to pacer.
Amiodarone↗
[Myocardial mechanical injury in acute ischemia: a pathophysiologic and histopathologic review].
The recognition of histopathologic substrates of myocardial contractile damage in human acute ischemia is still very poor, notwithstanding the impressive advances in the inherent clinical diagnostic technology and concepts. The first and foremost inotropic abnormality ensuing ischemia, easily taken for atonic in origin, actually consists of a pathologic contracture of the injured myocardium, depending upon abrupt fall of ATP, and defective extrusion calcium pump with persistence of actomyosin rigor-complexes. In sustained ischemia, further membrane damage exposes the myocell to massive calcium intrusion, with eventual precipitation of it and cell death (reperfusion stone-heart). In case of transient, "hit and run" ischemia, the "stunned" myocardium undergoes prolonged contractile abnormalities. In keeping with fundamentals in pathophysiology of contraction, ischemic myofibrils in human hyperacute infarct, showed spare I bands, accounting for contracture and followed by loss of the regular cross-striation register; then, groups of adjacent sarcomeres were seen to join into true "contraction" bands, with Z lines impinging upon A bands and obliterating the I bands. Coagulative denaturation of contractile proteins follows, presenting as irregular, amorphous degeneration stripes astride irreversibly damaged myocells. As such, these cells can be passively overstretched by the nearby functioning muscle. In turn, the fixed waviness of viable, acutely ischemic myocardium was thought to configure, histologically, the loss of ATP-dependent "plasticity" of myofilaments, in a state of contracture. The "relaxant effect" of inotropic-chronotropic-positive catecholamines, favoring diastole, has been also pointed out. The present microscopic findings are cogent to clinicopathologic problems of coronary ischemia-reperfusion, and sudden death from cardiogenic shock.
Adenosine Triphosphate↗
Grading scores and survivorship functions in liver cirrhosis: a comparative statistical analysis of various predictive models.
In a group of followed-up liver cirrhotics we evaluated the reliability of prognostic estimates predicted on the basis of a previously described multivariate statistical model (MSM). In the same subjects we also compared theoretical survival estimates obtained by fitting some other liver cirrhosis grading scores (Child-Turcotte's, McCormick's and Orrego's) to prognostic purposes. No statistical difference between actual and MSM-estimated survivorship functions was found (employing a life-table method with Logrank test), thus confirming the prognostic reliability of this multivariate classification model. Such a global and prognosis-correlated index may be recommendable both for comparing different groups of patients, and for assessing treatment effectiveness. Or results also substantially confirm the other investigated classificative methods such as reliable liver cirrhosis severity indexes, although their use for prognostic purposes seems to be less suitable.
Actuarial Analysis↗
[Specific extranodal sinoatrial muscle cells in the crista terminalis. Cyto-morphometric study and anatomoclinical considerations].
To assess the occurrence, location and structure of specialized pacemaker slender cells, beyond the conventional anatomic boundaries of the sinoatrial node, cyto-morphometric evaluations were made in specimens from 10 human hearts. The morphometric analysis showed significant histocytological peculiarities of extranodal slender cells, which presented 60% to 70% smaller than those of the ordinary atrial muscle; their preferential location was at a mean distance of 12 to 14 mm from the posterior tip of the sinoatrial node, beneath the crista terminalis. These morphologic data were taken into consideration with regard to electrophysiologic recording of shifts in pacemaking, within and around the sinoatrial node. It was also remarked that the presence and action of extranodal specialized cells along the crista terminalis are consistent with clinical and pathologic evidence obtained from human cases of sick sinus syndrome, as well as from animal experiments at sinoatrial node damage.
Adult↗