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S Factor

Publications and source records attributed to S Factor.

At least 37 records · Page 2Linked to original sources
PubMed1992

Induction of tolerance to an IgG autoantibody.

Nonautoimmune mice transgenic for the heavy chain of an IgG2b anti-double-stranded-DNA antibody express the transgene in lymphoid organs and display partial allelic exclusion of this gamma 2b transgene. The spleens of these mice are characterized by marked B-cell depletion. Although there are B cells in these mice that express the transgene and recognize double-stranded DNA, they are anergic in vivo. Recovery from the state of anergy occurs in vitro after lipopolysaccharide stimulation. Thus this transgenic model demonstrates the induction of self tolerance to an IgG autoantibody.

Animals↗
PubMed1991

Effect of aging and hypertension on myosin biochemistry and gene expression in the rat heart.

The mechanisms by which the aged heart adapts to a superimposed pressure load such as hypertension have not been described. We therefore investigated biochemical and molecular genetic adaptations in the 24-month-old rat heart subjected to renovascular hypertension. Compared with 4-month-old rats, aging was associated with a 68% increase in left ventricular mass without any change in heart weight-to-body weight ratio, a 33% reduction in calcium-activated myosin ATPase activity, and a shift from a V1 to a V3 predominant myosin heavy chain (MHC) isoform distribution. A 46% reduction in alpha-MHC mRNA and a reciprocal increase in beta-MHC mRNA was seen. When hypertension was superimposed, there was a further 75% increase in ventricular mass, a 63% increase in heart weight-to-body weight ratio, and a 19% reduction in myosin ATPase. Myosin isozyme distribution was further shifted to V3, and the ratio of alpha-MHC to beta-MHC mRNA was reduced. In addition, with hypertension a significant (greater than 50%) reduction in the mRNA level of the cardiac sarcoplasmic reticular calcium-activated ATPase was seen. These data demonstrate that the aged myocardium is able to respond to a superimposed pressure load with a molecular genetic and protein synthetic pattern of hypertrophy analogous to that seen in younger animals.

Aging↗
PubMed1989

Verapamil ameliorates clinical, pathologic and biochemical manifestations of experimental chagasic cardiomyopathy in mice.

The influence of long-term verapamil administration on the consequences of Trypanosoma cruzi infection in mice was studied with regard to animal mortality, morbidity, myocardial pathologic features and myocardial beta-adrenergic adenylate cyclase activity. Verapamil administration dramatically decreased the mortality rate from 60% to 6% during the 70 day period of infection. Three clinical stages of infection were evident. In the acute stage (17 days after infection with maximal parasitemia), verapamil treatment not only decreased the incidence of myocardial disease (fibrosis and inflammation), but also protected myocardial beta-adrenergic adenylate cyclase activity. In addition, there was no increase in total body weight, which was regarded as an index of right-sided heart failure. In the subacute stage (30 to 60 days after infection), administration of verapamil continued to decrease myocardial disease and preserve beta-adrenergic adenylate cyclase activity. In addition, verapamil ameliorated the morbidity and mortality associated with this stage of infection. The chronic stage of infection was characterized by a decrease in myocardial disease and in beta-adrenergic adenylate cyclase activity. Thus, independent of the state of infection, long-term verapamil treatment enhanced beta-adrenergic adenylate cyclase activity. In addition, verapamil ameliorated the morbidity associated with infection. Although the relation among these various effects of verapamil in the setting of T. cruzi infection remains to be determined, collectively the results suggested that verapamil administration attenuated the consequences of T. cruzi infection.

Adenylyl Cyclases↗
PubMed1989

Psychogenic tremors.

We diagnosed 24 patients, 9 men and 15 women ranging in age from 15 to 78 years, with clinically established or documented psychogenic tremors. Clinical presentations were unique, with complex tremors (often resting, postural, and kinetic), unusual temporal profiles (abrupt onset with a variable course), absence of other neurologic signs, inconsistent and incongruous symptomatology, selective disability with ability to perform some functions despite severe tremors, distractibility that lessens or abolishes tremor, atypical tremorgraphic recordings with changing amplitude and frequency, unusual handwriting and drawing specimens, presence of multiple undiagnosed somatizations, unresponsiveness to all treatments, absence of documented disease by laboratory or radiographic tests, presence of psychiatric disease, spontaneous remissions, or recovery with psychotherapy. We present criteria for the diagnosis of psychogenic tremor.

Adolescent↗
PubMed1988

Effects of chronic dobutamine administration on hearts of normal and hypertensive rats.

We have previously shown that physical conditioning in the rat improves cardiac mechanics and biochemistry and normalizes the cardiac contractile protein abnormalities associated with renovascular hypertension. Since chronic adrenergic stimulation with dobutamine simulates some aspects of physical conditioning, this study was undertaken to investigate the effects of chronic dobutamine administration on normal and hypertensive rat hearts. Four groups of female animals were studied: controls, dobutamine-treated (2 mg/kg twice daily), renovascular hypertensives, and dobutamine-treated hypertensives. Animals were killed after 8-10 weeks and cardiac histology, myosin biochemistry, and mechanics in an isolated heart perfusion apparatus were studied. Dobutamine, unlike hypertension, was not associated with histological evidence of myocardial damage but did increase cardiac mass by 10% and calcium-activated myosin ATPase activity by 13%. Hypertension was associated with a 24% increase in mass, a 24% decrease in ATPase activity, and a shift in the myosin isoenzyme pattern from V1 to V3. The combined stimuli caused additive hypertrophy (44%) and normalized myosin biochemistry and isomyosin distribution. Dobutamine treatment was not associated with significant improvements in pump or muscle function in control or hypertensive hearts. Thus chronic dobutamine treatment, like physical conditioning, induces a physiological cardiac hypertrophy in rats that is associated with improved myosin enzymology and normalization of the contractile protein abnormalities associated with hypertension. Unlike physical conditioning, however, these biochemical alterations do not result in improved contractile function as measured in an isolated buffer-perfused heart apparatus.

Adenosine Triphosphatases↗
PubMed1988

Do heart valve bioprostheses degenerate for metabolic or mechanical reasons?

Although heart valve bioprostheses provide a normal quality of life, their durability is still of great concern. Their durability failure is defined as "degeneration," which is considered to be a consequence of metabolic factors. In this study, we demonstrate that mechanical and design factors can also be responsible for bioprosthesis failure. Large numbers of porcine and pericardial bioprostheses were tested in a fatigue-testing system in which the test conditions were proved to be reproducible and accurate by a laser Doppler anemometer. The results have allowed us to define causes of failure, previously insufficiently stressed, in each type of valve tested. There is a clear difference in factors influencing tissue disruption between porcine and pericardial valves. We have compared these in vitro results with in vivo clinical findings. The main inferences are as follows: (1) Bioprostheses rupture and fail in the same fashion in both in vitro and in vivo studies. (2) Mechanical and design factors are involved in tissue failure. (3) The in vitro/in vivo durability ratio is not 1:1. This ratio depends on the test conditions. (4) Pericardial valves fail because of damage during closure, whereas porcine valves are damaged during both opening and closing (mostly opening) because of design features. (5) Once one cusp fails and prolapses, the other cusps will fail in an accelerated fashion. (6) In vitro durability of 100 X 10(6) cycles can be considered excellent and is an achievable goal. (7) Variability is the key impediment to predicting the durability of bioprostheses. Valves can fail within 2 to 3 million cycles or can last more than 100 million cycles. Similarly, bioprostheses may require explantation within a few months or can last 10 to 13 years in patients. (8) Fatigue testing is an excellent and valuable tool to elucidate the mechanical factors responsible for this variability.

Bioprosthesis↗
PubMed1986

Central and peripheral components of cardiac failure.

Chronic heart failure results from two processes, i.e., myocardial and congestive failure. Myocardial failure is clinically silent, most often progresses slowly, and is documented by a depressed left ventricular ejection fraction. Multiple etiologic factors include systolic and diastolic overloads, myocardial necrosis and/or ischemia, and, perhaps, microvascular spasm. Myocardial failure ultimately leads to exaggerated neurohumoral compensatory mechanisms and derangements of the peripheral circulation, which are the hallmarks of congestive heart failure. At that stage of the syndrome, patients have symptoms, initially, with exercise and, later, at rest. Objective assessment of severity is afforded by determination of maximal oxygen uptake during maximal exercise testing. When congestive heart failure supervenes, the prognosis is poor. Current medical therapy is aimed at improving the derangements of the peripheral circulation, which relieves the symptoms but leaves the primary myocardial process unaffected. The goal of future therapy is to intervene at an earlier stage of the syndrome to halt or even partially reverse the myocardial failure.

Aminopyridines↗
PubMed1986

Endocarditis of a tricuspid prosthesis causing valvular stenosis and shunting through a patent foramen ovale.

A young intravenous drug user presented with Staphylococcus aureus endocarditis involving the tricuspid valve, which was replaced with a Hancock bioprosthesis. She presented again with fever and dyspnea five months later and was found to be cyanotic. Recurrent endocarditis involving the prosthesis with right-to-left shunting through a patent foramen ovale was documented by echo and confirmed at autopsy.

Adult↗
PubMed1984

Newer concepts in the pathophysiology of ischemic heart disease.

Thus the thrust of these studies suggests that blood flow is the overwhelming factor in determining the consequences of the imbalance of oxygen supply and demand. Moreover, the factors that determine the requirements for tissue survival in the presence of deep ischemia are not the same as those shown for the normal myocardium in figure 1. In deep ischemia, contraction ceases, and metabolism shifts from aerobic to anaerobic pathways. Survival rather than contractile function then becomes the agenda. Not only does supply tend to overshadow demand in determining extent of transmural necrosis, but the anatomical pattern of supply precisely delineates the region at risk following a coronary occlusion as well as the ultimate extent of infarction. These views are summarized in the model presented in figures 12 and 13. The anatomic distribution of the ligated artery determines the lateral limits of the ischemic region (Fig. 12) and thus the lateral extension of necrosis (Fig. 13). The extension of the necrosis across the heart wall depends largely on the status of perfusion within the ischemic region. Extension of an infarct, should it occur, has to be explained by other mechanisms. These might include: (i) vascular obstruction in adjacent vascular systems that were not involved in the first occlusion, (ii) relative ischemia in the normal tissue surrounding the ischemic tissue due to an increased wall stress at the demarcation between contracting and noncontracting tissue, or (9) interruption of vessels supplying large interdigitations of normal tissue within the originally ischemic tissue due to changes associated with the process of infarction of ischemia. Alternatively, much that is called extension of infarction may involve more of the wall transmurally without lateral extension. Additional features of the development of myocardial infarction in figures 12 and 13 include: (i) the development of collateral vessel function resulting in an increased capacity to supply the ischemic area, and (ii) a redistribution of collateral blood flow from necrotic to surviving myocardium within the ischemic area. Thus, as coronary collaterals develop, collateral blood flow becomes increasingly heterogeneous within the ischemic area. Following a coronary occlusion, blood flow is reduced more in the subendocardium, and infarction occurs. Resistance to flow in infarcting tissue increase and causes a redistribution of flow to adjacent surviving layers of myocardium that life toward the epicardium. The process continues and combined with the enlargement of collateral vessels results in a sufficient flow to the epicardial layers so that they may survive.

Animals↗
PubMed1984

Calcification of implanted xenograft pericardium. Influence of site and function.

In a series of 23 dogs, glutaraldehyde-fixed xenograft pericardium was implanted as a left atrial wall patch (Group I, 11 dogs), as a substitute for the mitral valve chordae (Group II, 12 dogs), and as an external pericardial patch (Group III, five dogs, in which one of the two former procedures was associated). All dogs of Group I survived and were put to death after 12 months. The atrial patch appeared thickened and shrunken in all, with intense fibrous reaction, calcification, and even bone formation. The structural changes were minimal in the external aspect of the patch, not in contact with the host's endocardium and blood. Eight dogs of Group II survived from 7 months to 3 years. In all, the pericardial chordae were thickened and calcified with good healing at the suture lines; that their original length was retained, however, allowed for good valve function. In the dogs of Group III the pericardial substitute appeared well preserved after 12 months, not calcified, and without noteworthy degenerative changes. Minimal or absent epicardial adhesions were noted. We conclude that (1) the tendency for xenograft pericardial tissue to calcify is strongly influenced by the site of implantation and function and by contact with host blood and endocardium; (2) heterologous pericardium may be considered suitable for closure of pericardial defects after open cardiac operations, and (3) studies on calcification of biological tissue should be carried out by long-term evaluation of such tissues inside the heart.

Animals↗
PubMed1984

Fatigue-induced failure of the Ionescu-Shiley pericardial xenograft in the mitral position. In vivo and in vitro correlation and a proposed classification.

Four patients had signs of primary bioprosthetic dysfunction within the fourth postoperative year after mitral valve replacement with an Ionescu-Shiley pericardial xenograft; they represent approximately 9% of patients with Ionescu-Shiley pericardial xenograft mitral valves followed up for more than 3 years at our institution. Pathological investigation showed severe incompetence of all explanted valves due to cusp tears and lacerations. Histologic study of the pericardial tissue disclosed mild to moderate collagen degeneration, without infection or calcification. Neoendothelial formation on the Dacron cloth of the sewing ring was either absent or minimal. The high incidence of valvular incompetence prompted us to try to establish a correlation between the in vivo and in vitro modes of failure of the Ionescu-Shiley pericardial xenograft. For this purpose, 10 unimplanted Ionescu-Shiley pericardial xenograft valves were tested in a fatigue test system. Severe fatigue-induced lesions occurred in this group after an average of 29.09 +/- 17.26 X 10(6) cycles; initial failure could be recognized in six of them after an average of 16.94 +/- 20.12 X 10(6) cycles. Valves tested in the fatigue test system showed tears and lacerations similar to those noted in the Ionescu-Shiley pericardial xenografts obtained from the four patients (which were assumed to have functioned for more than 100 X 10(6) cycles in each case). Correlation between results of the fatigue testing and our clinical experience enabled us to recognize four types of tears which may occur in the Ionescu-Shiley pericardial xenograft. The results of this investigation showed the following: (1) Primary tissue failure of the Ionescu-Shiley pericardial xenograft may occur suddenly. (2) A classification of tears occurring in Ionescu-Shiley pericardial xenograft valves is useful since the clinical presentation of patients may differ according to type and location of the lesion. (3) In the manufacture of pericardial valves, particular care must be observed in selection of the tissue and in the frame design. (4) Improvement of the quality control is one of the clues to enhance durability of the Ionescu-Shiley pericardial xenograft.

Aged↗
PubMed1983

Reproducible replacement of elongated or ruptured mitral valve chordae.

Anatomical rules that make it possible to accurately replace mitral anterior cusp chordae tendineae with tanned xenograft pericardium are defined. Anterior and posterior cusp chordae were replaced with xenograft and autologous pericardium in 11 patients who had ruptured or elongated chordae. The xenograft occasionally became calcified; however, because it did not become elongated or shortened, competence was maintained for up to 3 years. Insufficiency was corrected, and the correction maintained for up to 4 months. Degenerative disease proved easier to treat than rheumatic disease. Two-dimensional echocardiography was a valuable aid in both preoperative planning and postoperative evaluation.

Adult↗
PubMed1983

Xanthogranuloma of the dura in systemic Weber-Christian disease.

A 51-year-old woman who had systemic Weber-Christian disease (WCD) displayed multiple xanthomatous lesions and a large xanthogranuloma of the tentorium cerebelli with signs of brainstem and cerebellar compression. Three other cases of dural xanthomatous lesions associated with systemic WCD have been reported. These dural and leptomeningeal xanthomatous lesions in WCD, a nonsuppurative inflammatory condition, are similar to those of Hand-Schüller-Christian disease, a quasi-neoplastic process.

Dura Mater↗
PubMed1979

Right atrial myxoma: unusual clinical presentation and atypical glandular histology.

A 57-year-old black female presented with a 1-month of right-sided congestive heart failure and clinical evidence of pulmonic and tricuspid valvular stenosis and insufficiency. The echocardiographic examination and ventriculography demonstrated a large right atrial tumor interfering with the function of both right-sided valves. The patient underwent successful surgical resection of the tumor. Histologically, the tumor had cellular areas typical of myxoma, as well as glandular areas, a feature which has been described very rarely in this lesion. Electron microscopy of the glandular zones, which has never been reported previously, shown cells having essential homology with the usual myxoma elements. The atypical histopathology of this lesion supports the theory that atrial myxomas are true neoplasms, and are not derived from unusually organized mural thrombi.

Collagen↗
PubMed1978

Progressive occlusive thrombarteriopathy: a case report.

A case of occlusive arterial disease of obscure nature and etiology is reported. The most puzzling aspect of this case was an apparent lack of correlation between the acute, progressive clinical course of the disease, especially in its final stages and the absence of any corresponding acute changes on microscopic examination of the affected vessels. Furthermore the combination of clinical features and pathologic findings--particularly the thrombotic involvement of the heart and the thoracic aorta by a process starting in the small and medium size vessels of the lower extremities--is not consistent with any of the recognized syndromes leading to a thrombotic occlusion of the arterial system. We conclude that the case represents an obscure syndrome of progressive occlusive thrombarteriopathy, perhaps related to a cumulative effect of heavy smoking, alcoholism, and drug addiction. It is possible that increased coagulability of the blood contributed to the thrombotic process but was not recognized by means of the hematologic studies performed.

Adult↗
PubMed1976

Primary cardiac neurilemoma.

A rare case of primary cardiac neurilemoma arising in the right atrium is reported. The patient was a 55-year-old woman who was treated for 20 years with drug and radiation therapy for a metastatic ovarian carcinoma. The cardiac tumor was an incidental finding at autopsy. Both light and electron microscopic examination of the tumor confirmed the Schwann cell origin of the neoplasm. Review of the literature reveals only one other unequivocal report of a primary cardiac neurilemoma.

Autopsy↗