Biomedical subjects

S M Factor

Publications and source records attributed to S M Factor.

At least 37 records · Page 2Linked to original sources

PubMed1997

Pathology of the radial and internal thoracic arteries used as coronary artery bypass grafts.

BACKGROUND: This investigation compared the incidence and the degree of atherosclerosis present in radial artery (RA) and internal thoracic artery segments remaining after coronary artery bypass grafting. METHODS: One hundred seventy specimens from 102 patients were histologically analyzed, including 106 RA specimens. RESULTS: The mean degree of pathology for the RA was 0.89 on a 0 (none) to 4 (lumen completely obliterated) scale; the mean grade of pathology for the internal thoracic artery was 0.30 (p < 0.001). Presence of diabetes, aortofemoral disease, femoral-popliteal disease, age, and male gender correlated with an increase in RA pathology. Flow in the in situ RA did not correlate with the degree of pathology. CONCLUSIONS: Study of the excess RA and internal thoracic artery segments remaining after coronary artery bypass grafting demonstrated that the RA had a higher degree of atherosclerosis than the internal thoracic artery at the time of harvest. Overall severity of disease in the RA was low. The long-term performance of RA grafts will determine whether this level of atherosclerotic disease has any clinical significance.

Arteriosclerosis↗

PubMed1997

Prolonged ejection duration helps to maintain pump performance of the renal-hypertensive-diabetic rat heart: correlations between isolated papillary muscle function and ventricular performance in situ.

OBJECTIVE: The purpose of this study was to examine the degree to which mechanical alterations in left ventricular papillary muscles of renal hypertensive-diabetic rat hearts correlate with functional measurements made on the same hearts in situ. METHODS: Female Wistar rats weighing 170-200 g were made hypertensive by placing a 0.24 mm clip on the left renal artery, and made diabetic 1 week later by a single intravenous injection of streptozotocin (60 mg/kg). Approximately 3-5 months later hemodynamic measurements including left ventricular pressure and dP/dtmax, arterial pressure and aortic flow were made on control and hypertensive-diabetic hearts in situ and correlated with mechanical measurements in left ventricular papillary muscles isolated from the same hearts. Body and tissue weights and biochemical and histological measurements were made at the time of sacrifice. RESULTS: Hypertensive-diabetic rats which survived to the time of study had decreased body weights, increased left ventricular weights and increased right ventricular weight to body weight and lung weight to body weight ratios. Those rats which died before the scheduled in-situ measurements had significantly more severe hypertension, greater left ventricular hypertrophy, increased right ventricular and lung weights, and more interstitial fibrosis than either surviving hypertensive-diabetics or controls. Rates of isometric tension development (normalized) and relaxation as well as shortening and relaxation velocities were significantly depressed in papillary muscles from hypertensive-diabetic rat hearts despite unchanged developed tension and peak shortening. Time to peak tension and time to peak shortening were markedly prolonged. Mean aortic flow was maintained in the hypertensive-diabetic group despite significant depression of left ventricular dP/dtmax (normalized), peak aortic flow, peak aortic flow acceleration and heart rate. There was also significant depression of left ventricular-dP/dtmax. Ejection duration was markedly prolonged and correlated with both time to peak shortening in vitro and with stroke volume in vivo. CONCLUSIONS: Surviving hypertensive-diabetic rats were not in overt congestive heart failure; nevertheless, their hearts showed abnormal contractile performance which was qualitatively and quantitatively similar to that of left ventricular papillary muscles obtained from them. Depression of peak aortic flow, peak aortic flow acceleration and heart rate in the hypertensive-diabetic group was offset by increased ejection duration, resulting in normal mean aortic flow. The close correlation of ejection duration with time to peak shortening of the isolated papillary muscles suggests that it is a manifestation of an intrinsic change in the myocardium. To the extent that this prolongation is already maximized, further decreases in contractile speed would be expected eventually to cause depressed pump function and congestive heart failure. The possibility that this sequence of events occurred in the dying animals needs to be examined by evaluating in-vitro and in-vivo myocardial function at various stages of this disease model.

Animals↗

PubMed1997

Review and hypothesis: the eosinophil and peripartum heart disease (myocarditis and coronary artery dissection)--coincidence or pathogenetic significance?

OBJECTIVES: To examine a possible relationship between peripartum heart disease (myocarditis and spontaneous coronary dissection) and the presence of eosinophils. BACKGROUND: Eosinophils have been shown to have potential collagenolytic and cytotoxic activity. Eosinophils may play a role in postpartum uterine involution. The presence of eosinophils in spontaneous coronary dissection and myocarditis in the postpartum period raises the possibility of a role for eosinophils in these diseases. METHODS: We reviewed the files of one of us (S.M.F.) for cases of peripartum myocarditis and spontaneous coronary dissection and assessed the frequency of eosinophilic inflammation. Seventeen postpartum myocarditis and/or cardiomyopathy cases were found and two spontaneous coronary dissections. Fifteen sex- and age-matched controls on non-postpartum myocarditis and borderline myocarditis were evaluated and eosinophil counts per unit area compared. Also, a Medline search of all previously published cases of spontaneous coronary dissection was performed back to 1966. RESULTS: Of the 16 heart biopsies and one autopsy in the peripartum period, 10 were shown to contain easily identified eosinophils (6 myocarditis, 1 borderline, 3 cardiomyopathy). When presence of eosinophils was compared with the control group, a statistically significant difference was obtained (P = 0.036). The two new spontaneous coronary dissection cases had eosinophils along the dissection plane; the literature search produced 13 of 24 autopsied peripartum spontaneous coronary dissections with eosinophils for a total of 15 of 26 with our cases. CONCLUSIONS: An association exists between eosinophils and peripartum cardiac disease (myocarditis and spontaneous coronary dissection). The role of eosinophils in labor, uterine involution and collagenolysis and the possible relation to cardiac disease are discussed.

Aortic Dissection↗

PubMed1997

Distribution of endothelin immunoreactivity in human kidney correlates with antemortem acute renal failure: a possible postmortem immunohistochemical test.

The role of endothelin in the normal kidney function, as well as in disease states, has been studied in animal models. In addition, it was shown previously that endothelial, mesangial, and epithelial components of the nephron produce endothelins, in particular ET-1. We performed immunohistochemistry for ET-1 reactivity on 31 autopsy and four surgically removed kidneys. Eighteen cases had clinical diagnoses of acute renal failure (ARF) In the remaining 17 cases with normal or unchanged renal function before death or surgery, ET-1 immunoreactivity was present in tubular epithelium, with the most intense staining in the medullary collecting tubules. In 13 of 18 cases of ARF, tubular staining was either replaced or accompanied by interstitial reactivity in the inner and outer medulla, corresponding to the location of the vasa recta and interlobular arteries identified by factor VIII immunostaining. Controlled autolysis performed on normal kidney over 72 hours postmortem produced tubular epithelial degradation with reduced epithelial cell endothelin reactivity, but not an interstitial pattern. In situ hybridization for ET mRNA localized expression to tubular and collecting duct epithelium in both normal and acute renal failure cases. The change in the localization of ET-1 immunoreactivity from tubular epithelium to the interstitium in these ARF cases does not appear to be the result of increased vascular endothelial production of endothelin. This altered immunoreactivity pattern for ET-1 may be a marker of antemortem tubular damage and can be used as an adjunct in the autopsy diagnosis of ARF.

Acute Kidney Injury↗

PubMed1997

GLUT4 heterozygous knockout mice develop muscle insulin resistance and diabetes.

GLUT4, the insulin-responsive glucose transporter, plays an important role in postprandial glucose disposal. Altered GLUT4 activity is suggested to be one of the factors responsible for decreased glucose uptake in muscle and adipose tissue in obesity and diabetes. To assess the effect of GLUT4 expression on whole-body glucose homeostasis, we disrupted the murine GLUT4 gene by homologous recombination. Male mice heterozygous for the mutation (GLUT4 +/-) exhibited a decrease in GLUT4 expression in adipose tissue and skeletal muscle. This decrease in GLUT4 expression did not result in obesity but led to increased serum glucose and insulin, reduced muscle glucose uptake, hypertension, and diabetic histopathologies in the heart and liver similar to those of humans with non-insulin-dependent diabetes mellitus (NIDDM). The male GLUT4 +/- mice represent a good model for studying the development of NIDDM without the complications associated with obesity.

Animals↗

PubMed1997

Correlation of histopathologic and bacteriologic changes with cytokine expression in an experimental murine model of bacteremic Staphylococcus aureus infection.

Staphylococcus aureus infections are often life threatening. Relatively little is known about the host response to these infections, in particular, the role played by cytokines. We established a mouse model of bacteremic S. aureus infection to correlate bacteriologic findings and pathologic changes with cytokine gene expression. Bacterial density in blood and tissue was highest at 1 h and minimal by 48 h. Despite the rapid clearance of bacteria, pathologic abnormalities and inflammatory cytokines were detected after clearance of the bacteria. The number of infiltrating inflammatory cells, as well as the size of inflammatory foci, increased with time. Interstitial accumulation of inflammatory cells and tissue damage, such as microabscesses, edema, and necrosis progressed following clearance of bacteria from the tissues. Levels of tumor necrosis factor and interleukin-1 protein in serum were detectable at 1 h and peaked at 4 h. Interleukin-6 protein expression showed different kinetics, with low levels detected at 1 h and increasing levels at 72 h postinfection. Tumor necrosis factor and the interleukins were expressed in inflammatory and noninflammatory cells in lung, liver, and heart tissues. Leukocytes in the infected tissues were highly reactive with antibodies to the three cytokines, suggesting that activated leukocytes are a major source of inflammatory cytokines after staphylococcal infection. Expression of interleukin-1 and interleukin-6 in tissue-specific cells and endothelial cells was also detected in infected tissues, indicating that cells other than leukocytes contribute to the elevated cytokine levels in this model. Once initiated, expression of inflammatory cytokines contributes to the pathogenesis of S. aureus disease.

Animals↗

PubMed1996

Myocardial alterations in diabetes and hypertension.

Diabetes mellitus is a complex group of diseases that has hyperglycemia as a common metabolic abnormality. Although it is well-known that diabetic patients are susceptible to the effects of large vessel atherosclerosis with specific cardiac and cerebral complications, the association of diabetes mellitus with cardiac dysfunction caused by cardiomyopathy in the absence of significant coronary artery disease has been recognized for many years. However, the pathogenesis of diabetic cardiomyopathy remains unknown and has been somewhat controversial. Specifically, whether diabetes mellitus with its metabolic effects is sufficient to account for cardiomyopathy remains to be proven. This paper reviews the evidence for and against a metabolic etiology. In addition, we review the clinical and experimental evidence that supports the view that diabetes mellitus acts together with hypertension to produce structural damage in the heart that manifests as ventricular dysfunction and ultimately congestive heart failure. The concomitant effects of the metabolic derangements of diabetes and the vascular abnormalities associated with hypertension may lead to microvascular-induced tissue injury. Findings supporting this hypothesis are presented, along with observations suggesting that treatment with vasodilating calcium channel blockers or angiotensin converting enzyme inhibitors may be beneficial in regard to tissue pathology and mortality in experimental models. Recent clinical studies also support a role for the microcirculation in diabetics. Finally, it is suggested that if the microcirculation is pathogenetically involved in diabetic cardiomyopathy, then agents that improve microcirculatory flow along with tight control of hypertension may be as beneficial in the treatment or prevention of diabetic cardiomyopathy as strict metabolic control of hyperglycemia.

Cardiomyopathies↗

PubMed1996

Autopsy patterns of disease among subgroups of an inner-city Bronx AIDS population.

The Bronx, New York, has a large, inner-city, AIDS population which contains a greater proportion of women and intravenous drug users and a lower percentage of homosexuals than the U.S. AIDS population overall. Because this population is reflective of the evolving trends in the national AIDS population, our objective was to gain an understanding of patterns of infections, malignancies, and cause of death among these individuals. All autopsies (252) performed on patients with AIDS at two hospitals affiliated with a major academic center in the Bronx between 1982 and 1995 were reviewed. Cytomegalovirus (CMV) as an infection or as a cause of death (COD) occurred more commonly among patients who had been infected with HIV through sexual relations (p = 0.0002 and p = 0.0011, respectively). Bacterial pneumonia was the most common source of pulmonary infection, although Pneumocystis carinii pneumonia was more often a cause of death. A higher frequency of aspergillus infection in female subjects was also noted (p = 0.010). These and other observations may have ramifications for treatment and prevention in analogous AIDS inner-city populations.

Acquired Immunodeficiency Syndrome↗

PubMed1996

Compromised microcirculation in acute murine Trypanosoma cruzi infection.

Microvascular compromise has been 1 of many factors implicated in the etiology of the cardiomyopathy associated with Chagas' disease. To further assess the effect of Trypanosoma cruzi infection on the microcirculation, we examined the cremaster microvascular model in CD-1 male mice infected with the Brazil strain at 20-25 days postinfection. There was a significant decrease in red cell velocity (Vrbc) in first and third-order arterioles and venules, which was reversed by verapamil treatment. Video recordings revealed a marked inflammatory response that was confirmed by transmission electron microscopy. A marked inflammatory response was not seen in verapamil-treated infected mice. Segmental vasospasm and dilatation was evident in the microvascular bed of infected mice. This was not seen in control or verapamil-treated mice. This model provides a readily accessible method to observe directly the effects of T. cruzi infection on the microcirculatory flow in vivo. In addition, it confirms and extends our previous observations regarding T. cruzi-associated microvascular spasm and underscores a role for verapamil, a calcium-channel blocker, in the amelioration of the Chagas' disease.

Acute Disease↗

PubMed1996

Mice expressing mutant myosin heavy chains are a model for familial hypertrophic cardiomyopathy.

BACKGROUND: Familial hypertrophic cardiomyopathy (HCM) is an autosomal dominant disease characterized by ventricular hypertrophy, myocellular disarray, arrhythmias, and sudden death. Mutations in several contractile proteins, including cardiac myosin heavy chains, have been described in families with this disease, leading to the hypothesis that HCM is a disease of the sarcomere. MATERIALS AND METHODS: A mutation in the myosin heavy chain (Myh) predicted to interfere strongly with myosin's binding to actin was designed and used to create an animal model for HCM. Five independent lines of transgenic mice were produced with cardiac-specific expression of the mutant Myh. RESULTS: Although the mutant Myh represents a small proportion (1-12%) of the heart's myosin, the mice exhibit the cardiac histopathology seen in HCM patients. Histopathology is absent from the atria and primarily restricted to the left ventricle. The line exhibiting the highest level of mutant Myh expression demonstrates ventricular hypertrophy by 12 weeks of age, but the further course of the disease is strongly affected by the sex of the animal. Hypertrophy increases with age in female animals while the hearts of male show severe dilation by 8 months of age, in the absence of increased mass. CONCLUSIONS: The low levels of the transgene protein in the presence of the phenotypic features of HCM suggest that the mutant protein acts as a dominant negative. In addition, the distinct phenotypes developed by aging male or female transgenic mice suggest that extragenic factors strongly influence the development of the disease phenotype.

Animals↗

PubMed1996

Comparison of changing autopsy trends in the Bronx population with acquired immunodeficiency syndrome.

The opportunistic infections, malignancies, and causes of death related to acquired immunodeficiency syndrome (AIDS) are changing, perhaps as a result of improved treatment, prophylaxis, and education. With its high percentage of persons who acquired the human immunodeficiency virus from intravenous drug (IVD) use, the population of patients with AIDS in the Bronx is potentially unique. All of the 257 consecutive adult human immunodeficiency virus and/or AIDS cases from two Bronx teaching hospitals from 1982 through 1995 were collected. The reports were reviewed for patient demographics, opportunistic infections, malignancies, and causes of death. One hundred thirteen cases from 1982 through 1988 were compared with 144 cases from 1989 through 1995, separated by the institution of antiretroviral therapy and Pneumocystis carinii (PCP) prophylaxis in the latter period. Male homosexuality as a risk factor significantly decreased from 24.8% of the cases in our study from the 1982/88 period to 12.5% during the 1989/95 period (P = 0.014), but IVD use cases showed no change. Cases of AIDS in heterosexual patients increased from 23.9 to 36.1% (P = 0.041) but did not achieve statistical significance unless the unknown risk category (a population shown to be infected predominantly through heterosexual transmission) was included. The prevalence of PCP at autopsy as an opportunistic infection decreased from 37.2 to 25% (P = 0.04), and its prevalence as a cause of death decreased from 31.9 to 13.9% (P = 0.007). This decrease was seen in the homosexual and heterosexual populations but not in the population of IVD users. The homosexual population, as opposed to the population of IVD users, may have taken greater advantage of PCP treatment and prevention. As a result, bronchopneumonia, not PCP, is now the leading cause of death among the patients with AIDS in this study. These findings have important implications for therapy and prophylaxis to control the spread of AIDS and its related infections, particularly in an inner city population troubled by drug use and poverty.

AIDS-Related Opportunistic Infections↗

PubMed1995

A second generation transgenic mouse model expressing both hemoglobin S (HbS) and HbS-Antilles results in increased phenotypic severity.

We report on a second generation of transgenic mice produced by crossing a transgenic mouse line expressing high levels of human alpha and beta S chains (alpha H beta S [beta MDD]) with a line expressing human alpha and beta S-Antilles (beta SAnt). We hypothesized that mice expressing both hemoglobins (Hbs) would have a more severe phenotype because the reduced oxygen affinity and solubility of the beta S-Antilles might enhance the rate and extent of polymer formation. We obtained mice that expressed both beta S and beta S-Antilles. The doubly transgenic mice that are heterozygous for deletion of mouse beta Major (beta MD) occurred with reduced frequency and those that are homozygous for deletion of mouse beta Major (beta MDD) occurred at a much reduced frequency and suffered early mortality. Human alpha was 58% of all alpha globin for all animals, whereas beta S and beta S-Antilles were 34% and 28% of all beta globins for beta MD mice and 42% and 36% for beta MDD mice. Hematocrit, Hb, and mean corpuscular Hb were normal for all transgenic mice, but reticulocyte levels were higher for the doubly transgenic mice versus alpha H beta S [beta MDD] mice older than 30 days (10.0% +/- 1.0% v 4.3% +/- 0.4%; P < .001, mean +/- SE, n = 20 and n = 10, respectively) and control mice (3.9% +/- 0.4%). Reticulocytosis was more severe in mice less than 30 days old ( > 20% for alpha H beta S beta S-Ant[beta MDD] mice). The median mean corpuscular hemoglobin concentration of doubly transgenic mice was higher than that of alpha H beta S[beta MDD] mice with a variable number of very dense cells. Delay times for polymerization of Hb in red blood cells from alpha H beta S beta S-Ant[beta MDD] mice were shorter than those of alpha H beta S[beta MDD] mice, and there were fewer cells with delay times greater than 100 seconds. Urine-concentrating ability in control mice under ambient conditions is 2,846 +/- 294 mOsm and was reduced 30% to 1,958 +/- 240 mOsm, P < 4 x 10(-8) in all mice expressing both transgenes. We conclude that doubly transgenic mice have a more severe phenotype than either of the two parental lines. These mice may be suitable for validating therapeutic intervention in sickle cell disease.

Anemia, Sickle Cell↗

PubMed1995

WW6: an embryonic stem cell line with an inert genetic marker that can be traced in chimeras.

Mutant mice produced by gene targeting in embryonic stem (ES) cells often have a complex or embryonic lethal phenotype. In these cases, it would be helpful to identify tissues and cell types first affected in mutant embryos by following the contribution to chimeras of ES cells homozygous for the mutant allele. Although a number of strategies for following ES cell development in vivo have been reported, each has limitations that preclude its general application. In this paper, we describe ES cell lines that can be tracked to every nucleated cell type in chimeras at all developmental stages. These lines were derived from blastocysts of mice that carry an 11-Mb beta-globin transgene on chromosome 3. The transgene is readily detected by DNA in situ hybridization, providing an inert, nuclear-localized marker whose presence is not affected by transcriptional or translational controls. The "WW" series of ES lines possess the essential features of previously described ES lines, including giving rise to a preponderance of male chimeras, all of which have to date exhibited germ-line transmission. In addition, clones selected for single or double targeting events form strong chimeras, demonstrating the feasibility of using WW6 cells to identify phenotypes associated with the creation of a null mutant.

Alleles↗

PubMed1995

Overexpression of NGF within the heart of transgenic mice causes hyperinnervation, cardiac enlargement, and hyperplasia of ectopic cells.

Nerve growth factor (NGF) supports the survival of developing sympathetic and a subpopulation of sensory neurons. In the adult it participates in maintenance of the neurotransmitter phenotype of responsive neurons. The amount of NGF synthesized by a given target tissue determines its final innervation density; those developing neurons that fail to receive sufficient NGF undergo apoptosis. In order to examine the ramifications of this principle in the context of a specific target organ, a transgenic mouse model was developed in which NGF expression was increased in developing and adult cardiac tissue by placing a NGF minigene under the transcriptional control of the cardiac-specific alpha-myosin heavy chain promoter. Transgenic mice developed cardiac enlargement secondary to both an increase in myocardial mass and the presence of an abundant ectopic cell population. Immunohistochemical analyses with the neural marker S-100 revealed staining of a subpopulation of ectopic cells, suggesting their derivation from the neural crest. Whereas immunostaining for the neuronal-specific protein neuron-specific enolase demonstrated labeling of another subpopulation of ectopic cells within the heart. Measurements of cardiac tissue catecholamine levels revealed a marked elevation in transgenic mice, consistent with sympathetic hyperinnervation. Analysis of mediastinal sympathetic ganglia revealed increases in both the size and the number of neurons. In this model, increased expression of NGF produced hyperinnervation of the heart, pathological cardiac growth, and the recruitment and/or expansion of an ectopic, neural crest-derived cell type.

Animals↗

PubMed1995

A murine model for hypertrophic cardiomyopathy.

A leading cause of sudden death among young athletes is the autosomal dominant genetic heart disease, familial hypertrophic cardiomyopathy (FHC). Mutations in several contractile proteins, including cardiac myosin heavy chains, have been described in families with FHC, leading to the hypothesis that FHC is a disease of the sarcomere (17). To create an animal model for this disease, five lines of transgenic mice have been produced that express a mutant myosin heavy chain in their hearts. The hearts of these mice exhibit the histopathological features seen in patients and demonstrate enlarged left ventricles. Our analysis suggests that the mutant protein acts as a dominant negative, since it constitutes only 5-10% of the total myosin in the heart. In addition, while the transgene is expressed in all chambers of the heart, only the left ventricle demonstrates pathology and enlargement, suggesting that several prominent features of the disease represent secondary responses influenced by other factors, such as hemodynamics.

Animals↗

PubMed1994

Hippocampal sclerosis: a common pathological feature of dementia in very old (> or = 80 years of age) humans.

In a neuropathological study of 81 brains of prospectively studied subjects of 80 years of age or older at the time of death, 13 cases (16%), including 4 men and 9 women, had hippocampal sclerosis (HpScl) affecting the vulnerable region of the hippocampus. In demented subjects of 80 years of age or older, the frequency of HpScl was even higher, 26%. Cases with HpScl had significantly fewer hippocampal senile plaques (SP) and neurofibrillary tangles (NFT) and parahippocampal NFT than cases without HpScl, but did not differ significantly in any of the other measured pathological parameters. Enzyme-linked analysis of synaptic protein immunoreactivity in a subset of 33 cases demonstrated significant decreases in the hippocampus, but not in frontal, temporal, parietal or parahippocampal cortices. All but 1 of the cases with HpScl had Blessed information, memory and concentration scores (BIMC) of 8 or more, and all were considered to be demented. In some patients memory disturbance was disproportionate to deficits in other cognitive areas. All but 4 of the cases with HpScl had many non-neuritic, amyloid plaques in the neocortex meeting NIA criteria for Alzheimer's disease (AD); however, given the advanced age of the subjects, amyloid plaques were considered to represent age-related cerebral amyloid deposition ("pathological aging") in most cases. Only 3 cases had both many SP and NFT in multiple cortical regions consistent with AD. Another case had brain stem and cortical Lewy bodies consistent with diffuse Lewy body disease (DLBD). A few ballooned neurons were present in the limbic cortices in 3 cases, including one case of dementia with argyrophilic grains (DAG) in limbic and orbital frontal and temporal cortices. The 8 cases without AD, DLBD or DAG included 4 cases in which no other obvious cause of dementia was detected and 4 cases in which HpScl was accompanied by either multiple cerebral infarcts or leukoencephalopathy, or both, that could have contributed to dementia. Patients with HpScl had risk factors, clinical signs and post-mortem pathological findings of cardiovascular disease, but due to the high prevalence of these conditions in very old humans, no significant correlation with HpScl was detected. This study demonstrates that HpScl is a common post-mortem finding in demented, but not normal, elderly subjects. It may contribute to. or be a marker for, the increased risk of dementia in subjects with documented cardiovascular disease or a history of myocardial infarction.

Aged↗

PubMed1994

Use of neurosurgical techniques for removal of a cardiac tumor.

A 6-week-old male infant with a capillary hemangioma of the right atrioventricular groove adjacent to the right coronary artery and conduction system underwent successful resection with the aid of microneurosurgical instrumentation. The technical challenge was thought to be analogous to that encountered by microneurosurgeons in their dissection of brain tumors.

Heart Neoplasms↗

PubMed1994

Immunocytochemical studies of atherosclerotic lesions of cerebral berry aneurysms.

Immunocytochemical analysis of human saccular aneurysms, commonly referred to as berry aneurysms, was performed on formalin-fixed, paraffin-embedded sections using monoclonal antibodies with single and double staining methods. Atherosclerotic lesions were detected in all aneurysms, which ranged in size from 2 mm to 3 cm in diameter. Changes consistent with the earliest stages of atherogenesis, so-called "fatty streaks," were not detected. In the smallest aneurysms, atherosclerotic lesions were characterized by diffuse intimal thickening composed predominantly of proliferating smooth muscle cells (SMC) with a small number of macrophages and lymphocytes. Large aneurysms had advanced atherosclerotic lesions with cellular infiltrates composed mostly of macrophages, more mature looking SMC and a greater number of lymphocytes. Major histocompatibility complex (MHC) class II expression was detected predominantly in macrophages in all aneurysms. Some SMC in advanced atherosclerotic lesions, but not in diffuse intimal thickening, had MHC class II immunoreactivity. A significant number of lymphocytes and NK cells were found at the site of aneurysmal rupture. The progression of atherosclerosis within the aneurysmal sac correlated positively with aneurysmal growth, and we speculate may have contributed to aneurysmal rupture. Some evidence also suggested a possible role of atherosclerosis in the formation of berry aneurysms.

Adult↗