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Biomedical subjects

S A Rubin

Publications and source records attributed to S A Rubin.

At least 19 recordsLinked to original sources
PubMed1992

Differential regulation of insulin-like growth factor I by growth hormone and thyroid hormone in the heart of juvenile hypophysectomized rats.

Recent data suggest that the heart can act as both a source and target for the actions of polypeptide growth factors. Insulin-like growth factor I (IGF-I) is a polypeptide that has both mitogenic and differentiation properties that function at the autocrine/paracrine level, and has recently been demonstrated to be expressed in the heart. This knowledge, coupled with the observation that thyroid hormone (T3) promotes relative cardiac growth compared to the proportional increases in body and heart growth evoked by growth hormone (GH), lead us to speculate whether differential induction of cardiac IGF-I may account for the specialized trophic effects of T3 on the heart. Cardiac IGF-I gene expression was studied in an in vivo model in which cardiac growth in the hypophysectomized juvenile rat was stimulated with either GH, T3 or GH + T3. Two week infusions of T3 that resulted in cardiac growth, but no gain in body weight, resulted in a 4.6-fold increase in cardiac IGF-I mRNA levels compared to hypophysectomized controls. GH infusions that resulted in similar cardiac growth, but were accompanied by proportional body growth, had no effect on cardiac IGF-I mRNA levels. These data are the first to demonstrate stimulation of cardiac IGF-I mRNA levels by T3 and further support cardiac autocrine/paracrine actions for this polypeptide growth factor.

Animals↗
PubMed1992

Pulmonary blastomycosis.

Pulmonary blastomycosis has a number of chest radiographic manifestations that may closely resemble those of tuberculosis, histoplasmosis, and other fungal diseases. Radiographic presentations of disease include airspace consolidation, nodular opacities, air bronchograms, masslike lesions, and military disease. Because the geographic distribution of blastomycosis overlaps that of histoplasmosis, distinguishing one from the other on the basis of the radiographic features may be difficult. In blastomycosis, the paucity of calcifications, lymphadenopathy, and cavitation is striking. The article reviews the clinical and radiologic features of blastomycosis and provides illustrative cases to enhance understanding of this disease.

Blastomycosis↗
PubMed1992

Thoracic histoplasmosis.

Histoplasmosis is a fungal disease that is seen throughout the world. It is the most common systemic fungal infection in North America, and it is endemic in the Mississippi, Ohio, and St Lawrence River valleys. Its radiographic and clinical spectrum ranges from a totally self-limited disease with minimal or no radiographic findings to a rapidly progressive, disseminated, and sometimes fatal disease. The article discusses the various aspects of thoracic histoplasmosis with emphasis on the radiographic findings.

Histoplasmosis↗
PubMed1992

Pulmonary zygomycosis: a radiographic and clinical spectrum.

Eight documented cases of pulmonary zygomycosis were analyzed retrospectively with regard to radiographic and clinical features. Predisposing factors were diabetes mellitus in six cases, lymphoblastic lymphoma in one case, and surgery to correct a tracheoesophageal fistula in one case. Two of the patients with diabetes had also undergone renal transplantation for diabetic nephropathy and were immunosuppressed. The more usual radiographic findings of pulmonary zygomycosis represent a spectrum that comprises a normal chest radiograph, a lung abscess, subacute or chronic pneumonia that often evolves into a lung abscess, and rapidly progressive fatal pneumonia. Awareness of the various presentations of pulmonary zygomycosis is important because early diagnosis and appropriate therapy clearly have been shown to improve the survival rate of these patients. Zygomycosis should be included in the differential diagnosis when patients with diabetes mellitus, patients with leukemia or lymphoma, or immunocompromised patients present with or develop perplexing pulmonary abnormalities.

Adolescent↗
PubMed1991

Incremental prognostic value of exercise hemodynamic variables in chronic congestive heart failure secondary to coronary artery disease or to dilated cardiomyopathy.

To determine the prognostic value of hemodynamic variables at rest and during exercise, 49 patients with chronic congestive heart failure undergoing hemodynamic evaluation at rest and during symptom-limited exercise were followed for 1 year. One-year mortality rate was 33%. On univariate analysis, nonsurvivors differed significantly from survivors in pulmonary arterial wedge pressure at rest (22 +/- 10 vs 15 +/- 10 mm Hg; p = 0.01) and during exercise (32 +/- 9 vs 24 +/- 9 mm Hg; p = 0.003), stroke work index at rest (19 +/- 6 vs 25 +/- 9 g-m/m2; p = 0.03) and during exercise (20 +/- 7 vs 32 +/- 14 g-m/m2; p = 0.001) and exercise-induced increment in stroke work index (0.5 +/- 0.4 vs 7 +/- 8 g-m/m2; p = 0.004), but not with respect to left ventricular ejection fraction, exercise duration, peak oxygen consumption or peak left ventricular hydraulic power. Patients with a peak exercise stroke work index less than 20 g-m/m2 had a 66% mortality rate compared with a mortality rate of 13% in patients with a peak exercise stroke work index greater than 20 g-m/m2 (p = 0.0001). Multiple logistic regression analysis identified pulmonary arterial wedge pressure at rest and peak exercise stroke work index as the only independent predictors of mortality. A receiver-operating characteristic curve analysis revealed that peak exercise stroke work index provided significant incremental prognostic information over the resting hemodynamic variables.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1991

Pet-associated lung diseases.

With the development of new diagnostic techniques, several diseases have emerged in recent years as zoonotic or potentially zoonotic. Even so, most pet-associated illnesses are infrequent, and therefore, health care providers may not be familiar with their manifestations or with the appropriate preventive measures. This article reviews the epidemiology, diagnosis, therapy and prevention of lung disorders acquired from dogs and cats.

Animals↗
PubMed1991

Interventional procedures used for diagnosing and treating lung cancer.

In recent years interventional radiology has played an increasingly important role in the diagnosis and treatment of lung cancer. Useful interventional procedures include biopsy techniques, direct infusion of chemotherapeutic agents into neoplasms, and a number of palliative procedures. The article reviews the indications, contraindications, techniques, and complications of these procedures with emphasis on some of the newer procedures.

Antineoplastic Agents↗
PubMed1991

Borna disease: association with a maturation defect in the cellular immune response.

Borna disease virus (BDV) is a negative-strand RNA virus which produces persistent infection in a variety of experimental animals. In the rat, the presence or absence of clinical signs of Borna disease, a characteristic, biphasic neurobehavioral illness, depends on host-related factors. A window of opportunity exists after birth wherein inoculation with BDV produces a persistently infected rat without signs of Borna disease or encephalitis (persistent, tolerant infection-newborn [PTI-NB] rat). Although immunopathological destruction of the nervous system does not occur in the PTI-NB rat, significant alterations in the development of the nervous system were noted, including site-specific lysis of neurons. Unlike the case with other pharmacologically produced, persistent, tolerant BDV infections, adoptive transfer of spleen cells from BDV-infected rats did not produce disease in the PTI-NB rats. PTI-NB rats developed Borna disease after being connected by parabiosis to rats with Borna disease. Bone marrow transplantation experiments revealed that bone marrow cells from PTI-NB rats produced Borna disease in lethally irradiated, BDV-infected recipient rats. Bone marrow from PTI-NB rats contained a complement of inflammatory cells capable of inducing Borna disease. Thus, the loss of BDV-specific cellular immunity appeared to occur after the release of cells from the bone marrow.

Animals↗
PubMed1991

Respiratory and circulatory analysis of CO2 output during exercise in chronic heart failure.

BACKGROUND: The output of carbon dioxide (VCO2) is controlled by both hemodynamics and ventilation. To understand VCO2 in patients who have chronic heart failure (CHF), we studied 14 patients who had New York Heart Association functional class III failure by measurements of hemodynamics, ventilation, and arterial and venous blood gases at rest and at 50 W of cycle ergometry exercise. METHODS AND RESULTS: Fick principle analysis of VCO2 showed that because of a limited increase in cardiac output, CHF patients widened their venoarterial CO2 content difference from 4.9 +/- 3.5 ml/dl at rest to 11.1 +/- 4.0 ml/dl with exercise (p less than 0.05). This increase in CO2 content difference was achieved with no change in venous CO2 content (from 54.3 +/- 3.3 ml/dl at rest to 54.5 +/- 4.8 ml/dl at exercise, p = NS); however, there was a decrease of arterial CO2 content (from 49.4 +/- 3.7 ml/dl at rest to 43.4 +/- 2.3 ml/dl with exercise, p less than 0.05). Modeling of the CO2 tension-content relation showed that there would have been a small, nonproportional increase of venous CO2 content as venous CO2 tension increased from 43.2 +/- 1.8 mm Hg at rest to 55.3 +/- 4.2 mm Hg during exercise (p less than 0.05); however, the development of metabolic acidosis during exercise entirely blunted the increase of CO2 content. In contrast, both the shape of the tension-content relation and the acidosis of exercise further influenced the decrease of arterial CO2 content as arterial CO2 tension decreased from 37.0 +/- 2.9 mm Hg at rest to 32.0 +/- 3.4 mm Hg during exercise (p less than 0.05) as a result of excess ventilation. CONCLUSIONS: In CHF patients during exercise, the circulatory limitations imposed by a low cardiac output on VCO2 are compensated by a widened venoarterial CO2 content difference. The content difference is not widened through an increase of venous CO2 content but rather by a decrease of arterial CO2 content caused by arterial hypocapnia and metabolic acidosis.

Biological Transport↗
PubMed1991

Lung cancer: past, present, and future.

The epidemiology of lung cancer in industrialized nations during the 20th century is a fascinating phenomenon. It is predicted that 161,000 new cases of lung cancer will be diagnosed in the United States in 1991. Lung cancer will cause 143,000 deaths in the United States in 1991, and it has surpassed breast cancer as the leading cause of cancer-related deaths in women. The 5-year survival for patients with lung cancer has not changed significantly over the past several decades and is approximately 13%. The current attack on lung cancer is aimed at earlier detection, better understanding of its biology, or effective therapy, and prevention, the last of which is the key to controlling this disease. Medical historians of the future will surely be both amused by and disappointed in our efforts of the past five decades. Despite our knowledge of the most important causative factor in the development of lung cancer, our efforts to control this deadly epidemic have been paltry at best.

Disease Outbreaks↗
PubMed1990

Cardiac physiology, biochemistry and morphology in response to excess growth hormone in the rat.

The cardiac effects of excess growth hormone (GH) were studied in the intact adult rat and in tissues prepared from the rat. Female Wistar-Furth rats were inoculated with a clonal cell line of pituitary cells which secrete GH. Five weeks later, heart weight had increased 37% compared to control (P less than 0.01) due to concomitant increases in left and right ventricular weight. Hemodynamic measurements in the anesthetized rat showed that GH stimulated rats had a decrease in blood pressure and heart rate and a small increase of left ventricular end-diastolic pressure (P less than 0.05). Measurement of left ventricular contractility and relaxation, and response to beta-adrenergic stimulation were decreased in GH compared to control (P less than 0.05). Contractile protein biochemistry showed an 18% reduction in Ca2(+)-myosin ATPase activity of the left ventricle (P less than 0.05) and non-denaturing pyrophosphate gels of purified myosin demonstrated a significant shift of isoforms from the exclusive V1 pattern to both V1 and V3 isomyosins in both ventricles (P less than 0.05). In contrast to the physiological and protein biochemistry adaptations, left ventricular morphology by light microscopy and ultrastructure by electron microscopy were normal in the GH stimulated heart. There were no significant changes in myofibril fraction, in the myofibril to mitochondria ratio or in the capillary numerical density of the hypertrophied left ventricle (P = N.S.). This study demonstrates that under prolonged and extreme stimulation by GH, the heart undergoes considerable growth/hypertrophy. Although cardiac morphology remains normal during this growth, there are alterations of the isomyosins such that ATPase activity is diminished and ventricular function is decreased.

Animals↗
PubMed1990

Chronic therapy for congestive heart failure with benazepril HCl, a new angiotensin converting enzyme inhibitor.

Benazepril HCl is an orally effective angiotensin converting enzyme (ACE) inhibitor previously shown to have significant acute hemodynamic benefits in patients with congestive heart failure. In this study, 21 patients with New York Heart Association Class III or IV congestive heart failure were treated with 2 to 15 mg of benazepril HCl as a single daily oral dose for 28 days to determine the clinical and hemodynamic value of chronic therapy. Each patient underwent clinical evaluation during the 28-day period, as well as invasive hemodynamic studies on the first two and last two days of the trial. Plasma ACE activity and aldosterone levels fell significantly and renin levels rose after therapy. Benazepril HCl produced significant (p less than 0.01) reductions in arterial pressure and systemic vascular resistance, with corresponding increases in cardiac output and decreases in pulmonary artery wedge pressure. Responses after 28 days of therapy were equivalent to those after the initial doses. Clinical effects included reduced rest, exertional and paroxysmal nocturnal dyspnea, as well as reduced peripheral edema. Only one patient developed symptomatic orthostatic hypotension. Thus, benazepril HCl, given once daily, is an effective and well tolerated oral agent for the chronic treatment of advanced congestive heart failure.

Aged↗
PubMed1990

Thoracic complications of tuberculosis.

Tuberculosis is a disease that has plagued humankind for centuries. In spite of excellent antituberculous chemotherapy, a number of important complications of tuberculosis are still commonly seen. Some of these are caused by the disease, and others are the sequelae of therapy. Thus some are seen immediately, and others occur months or even years after the onset of disease. These complications may involve the lungs, mediastinum, pleura, chest wall, or any combination of these structures. This article reviews the pathophysiology, diagnosis, and treatment of the many complications of thoracic tuberculosis.

Humans↗
PubMed1990

Point mutations of ras oncogenes are an early event in thyroid tumorigenesis.

Identifying the nature of the genetic mutations in thyroid neoplasms and their prevalence in the various tumor phenotypes is critical to understanding their pathogenesis. Mutational activation of ras oncogenes in human tumors occurs predominantly through point mutations in two functional regions of the molecules, codons 12, 13 (GTP-binding domain) or codon 61 (GTPase domain). We examined the prevalence of point mutations in codons 12, 13, and 61 of the oncogenes K-ras, N-ras, and H-ras in benign and malignant human thyroid tumors by hybridization of PCR-amplified tumor DNA with synthetic oligodeoxynucleotide probes. None of the eight normal thyroid tissues harbored point mutations. Four of nineteen nodules from multinodular goiters (21%), 6/24 microfollicular adenomas (25%), 3/14 papillary carcinomas (21%), and 0/3 follicular carcinomas contained ras point mutations. The predominant mutation was a valine for glycine substitution in codon 12 of H-ras. None of the multinodular goiter tumors known to be polyclonal (and thus due to hyperplasia) had point mutations, whereas one of the two monoclonal adenomas arising in nodular glands contained in H-ras codon 12 valine substitution, which was confirmed by sequencing the tumor DNA. These data show that ras activation is about equally prevalent in benign and malignant thyroid neoplasms, and thus may be an early event in the tumorigenic process.

Adenocarcinoma↗
PubMed1990

Effect of chemical sympathectomy on cardiac hypertrophy and hemodynamics following myocardial infarction in the rat.

The effects of sympathectomy on cardiac structure and function were studied in an animal model of myocardial infarction. Ninety-six rats were double randomized to control or infarction disease state and to placebo or chemical sympathectomy (guanethidine, 30 mg/kg daily, intraperitoneal). Five weeks after anterior infarction, there was hypertrophy in placebo-treated animals in myocardial fibers remote from the infarct (9.8 +/- 1.8 microns in infarction vs 8.1 +/- 1.0 microns in control, p less than 0.05). However, myocardial hypertrophy was not present in guanethidine-treated animals (8.6 + 1.6 microns in infarction vs 8.0 + 0.6 microns in control, p = N.S.). Guanethidine treatment caused significant reductions in systolic arterial blood pressure and indices of left ventricular contractility and relaxation (p less than 0.05), but these effects were not different between infarct and control treatments (p = N.S.). Although both effects of guanethidine treatment (sympathectomy and hemodynamic) were correlated with myocardial fiber diameter by univariate analysis, only sympathectomy was significant by stepwise regression analysis (p less than 0.05). Therefore, the cardiac sympathetic nerves have important effects on the development of hypertrophy after myocardial infarction, and sympathectomy alters this process in the rat model.

Analysis of Variance↗
PubMed1989

A multicenter study of the safety and efficacy of benazepril hydrochloride, a long-acting angiotensin-converting enzyme inhibitor, in patients with chronic congestive heart failure.

Benazepril hydrochloride is a nonsulfhydryl, long-acting angiotensin-converting enzyme inhibitor that is orally effective. This study was designed to determine the acute hemodynamic effects of this agent in patients with chronic congestive heart failure. Twenty-six patients with New York Heart Association class III or IV congestive heart failure and left ventricular ejection fractions less than 35%, cardiac indexes less than 2.1 L/min/m2, and pulmonary artery wedge pressures greater than 12 mm Hg were given 2 or 5 mg benazepril hydrochloride. All does produced significant (p less than 0.05) increases in cardiac output (26.7% to 31.6% above control) and heart rate (5.4% to 11.2% above control) and decreases in systemic (27.1% to 32.0% below control) and pulmonary (34.8% to 55.5% below control) vascular resistances, mean pulmonary (25.3% to 30.3% below control) and systemic (13.4% to 18.5% below control) arterial pressures, and pulmonary artery wedge pressure (46.9% to 51.1% below control). Twenty-four hours after an initial dose, systemic vascular resistance and pulmonary artery wedge pressures remained below control levels. Angiotensin-converting enzyme activity fell by 67.8% +/- 6.4%, with a 15.8% +/- 7.6% decline in aldosterone levels. Thus benazepril hydrochloride is an effective angiotensin-converting enzyme inhibitor that produces hemodynamic effects that persist for 24 hours after a single oral dose.

Adult↗
PubMed1989

Identification of growth hormone at the myocardial cell surface.

Growth hormone immunoreactivity has been demonstrated in a variety of normal human tissues, and ectopic production has been documented in a number of malignant tumors. However, myocardium has not previously been reported to contain growth hormone. Monkey anti-rat growth hormone antiserum was used in a sensitive immunoperoxidase staining method to histologically localize growth hormone in myocardium obtained from normal rats and rats harboring growth hormone-secreting tumors. Immunoreactive growth hormone was localized to the myocardial cell surface and was not seen in vascular endothelial cells of small arteries, veins, or capillaries. No intracellular staining of myocytes was evident. Specific staining was abolished by neutralization with purified growth hormone. Specific staining was abolished by neutralization with purified growth hormone. Myocardial cells did not stain with anti-triiodothyronine or anti-thyroxine immune serum. The cell surface staining is consistent with the binding of growth hormone to the myocardial cell surface, as it is unlikely that the myocardium synthesizes growth hormone polypeptide. These findings suggest that growth hormone may have a direct growth promoting or metabolic effect on cardiac tissue.

Animals↗