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Biomedical subjects

S R Saba

Publications and source records attributed to S R Saba.

At least 19 recordsLinked to original sources
PubMed1992

Immunocytochemical localization of proANF 1-30, proANF 31-67 and atrial natriuretic factor in the kidney.

ProANF [1-30 first 30 amino acids (a.a) of the 126 a.a atrial natriuretic factor (ANF) prohormone], ProANF 31-67 (a.a 31-67) as well as atrial natriuretic factor (a.a 99-126), of the ANF prohormone localized to the sub-brush border of the pars convoluta and pars rectus of the proximal tubules of hydrated and dehydrated rat kidneys with immunoperoxidase staining. Immunofluorescent studies revealed that each of these peptides and especially ProANF 31-67 had a strong predilection for the perinuclear region in the proximal and distal tubules. ProANFs 1-30, 31-67, and 99-126 (that is, ANF) also localized with both immunoperoxidase and immunofluorescent staining to the cortical collecting ducts, glomeruli, peritubular, and interstitial blood vessels. ProANF 31-67 immunoperoxidase staining was particularly striking in the elastica of the small and large interstitial arteries. The whole prohormone being present was suggested by immunological recognition in the rat kidney of both the N-terminus and C-terminus of the ANF prohormone by radioimmunoassays. The concentration of the N-terminus in the kidney was 1.0 +/- 0.03 ng/g of kidney weight, while the C-terminus of the ANF prohormone concentration was 0.4 +/- 0.01 ng/g of kidney tissue. These findings of a sub-brush border and perinuclear location of the N-terminal and C-terminal ANF prohormone peptides suggest that the atrial natriuretic factor prohormone may be synthesized in and/or the respective peptides are captured by the proximal tubules, but also to a lesser extent by the distal tubules of the kidney.

Animals↗
PubMed1989

Spontaneous platelet aggregation in type IIB Tampa von Willebrand disease is inhibited by the 52/48-kDa fragment of normal von Willebrand factor, which contains the GPIb binding domain.

The association of Type IIB von Willebrand disease (vWD) with chronic persistent thrombocytopenia and spontaneous platelet aggregation has recently been recognized. It has been shown that IIB von Willebrand factor (vWF) can initiate platelet aggregation by binding to the platelet glycoprotein (GP) lb receptor and inducing exposure of the GpIIb/IIIa fibrinogen receptor. In this study we demonstrate the increased binding of Type IIB Tampa vWF with normal platelets when compared with nonthrombocytopenic Type IIB vWF. Studies further demonstrate that spontaneous platelet aggregation initiated by IIB Tampa vWF can be blocked by a 52/48-kDa fragment of normal vWF, which contains the binding domain.

Binding Sites↗
PubMed1989

Occupational exposure to organic solvents causing chronic tubulointerstitial nephritis.

We describe a patient with a history of ulcerative colitis and long-standing occupational exposure to organic solvents. Over a follow-up period of almost four years he had progression of tubulointerstitial damage documented by two kidney biopsies. We propose that long-term exposure to organic solvents can lead to the development of chronic tubulointerstitial nephritis. We describe experimental evidence that supports our conclusion.

Adult↗
PubMed1987

Proteinuria in hypertension.

It had been previously thought that protein excretion in hypertensive nephrosclerosis was less than 0.5 to 1.0 g/24 h. Furthermore, it was believed that proteinuria in the nephrotic range associated with hypertension was probably due to primary renal disease, malignant hypertension, renal artery stenosis, or pheochromocytoma. We report eight patients with biopsy-proven hypertensive nephropathy and heavy proteinuria in the absence of malignant hypertension or renal artery stenosis. The 24-hour protein excretion ranged from 2.7 to 4.3 g. All patients had renal insufficiency, with serum creatinine ranging from 2.0 (176.8) to 7.8 mg/dL (689.5 mumol/L). Renal function worsened in most patients during the follow-up period despite adequate control of the hypertension, and three patients had to be started on hemodialysis. Three patients died during the follow-up period. We conclude that hypertensive nephrosclerosis must be included in the differential diagnosis of marked proteinuria in patients with essential hypertension and that heavy proteinuria, along with renal insufficiency, are poor prognostic indicators in such patients.

Adult↗
PubMed1987

Hypocomplementemic vasculitis and renal involvement.

Hypocomplementic urticarial vasculitis is a disorder that not only affects the skin, but other organs as well. We are describing a patient with this rare disorder and serious renal involvement that was treated with immunosuppressive therapy with good response and stabilization of the renal function. We emphasize the fact that renal involvement can occur with this disease and that the renal involvement is of the immune-mediate type and cannot be considered as benign as thought in the past.

Complement C3↗
PubMed1986

Antiheparin activity in human endothelial cells.

Human endothelial cells possess antiheparin activity that neutralizes the anticoagulant action of heparin as measured by different tests of the clotting system. The antiheparin activity appears to be associated with an acid-soluble basic protein present in the particulate fraction of the endothelial cell cytoplasm. This finding might have some relevance in the maintenance of hemostasis. Furthermore, it might also have a pharmacological role in terms of resistance to exogenously infused heparin in patients with thromboembolic disorders.

Chemical Fractionation↗
PubMed1986

Hypernephroma associated with multiple endocrine neoplasia type I: a case report.

We report a case of multiple endocrine neoplasia type I and hypernephroma. Parathyroid hyperplasia, adrenocortical hyperplasia, a nodular goiter, multiple lipomas, a chromophobe adenoma of the pituitary and hypernephroma had all been diagnosed previously. All but the last are features consistent with the diagnosis of multiple endocrine neoplasia type I (Wermer's syndrome). The association of multiple endocrine neoplasia type I and hypernephroma may represent a new manifestation of this pleiotropic syndrome.

Aged↗
PubMed1986

Coagulation and immunology.

One of the most vital functions of the vertebrates is to maintain hemostasis through coagulation and fibrinolysis. This is achieved by the interaction of vascular walls with blood components such as cells and proteins (coagulation factors, immunoglobulins, and complement). Deficiency of coagulation factors results in bleeding disorders. The immune system, in response to foreign proteins or defective self proteins, produces antibodies triggering an Ag-Ab interaction with the related host of different reactions including abnormal coagulation leading to hemorrhagic diathesis.

Antigen-Antibody Complex↗
PubMed1985

Heparin-mediated neutralization of platelet antiaggregatory activity of prostacyclin (PGI2): studies on mechanism.

Prostacyclin (PGI2) is a well-known potent inhibitor of platelet aggregation. Its role has been implicated in physiological and pathological states of hemostasis. Heparin blocks the prostacyclin-mediated antiaggregatory activity on platelets. Prior treatment of heparin with heparinase as well as with protamine destroyed heparin's ability to neutralize PGI2. Studies on the mechanism of heparin blocking of PGI2 activity suggested that heparin interacted directly with PGI2, as shown by the loss of PGI2 mobility on thin layer chromatography concomitant with the loss of PGI2-mediated inhibition of platelet aggregation. PGI2 in this combination with heparin, nevertheless, retained its time-dependent ability to be hydrolyzed to 6-keto-PGF1 alpha. Findings of these studies may have implications in thrombosis and hemostasis, particularly in heparin-mediated abnormalities of circulating platelets.

Chromatography, Thin Layer↗
PubMed1985

Ankylosing spondylitis and glomerulonephritis. Study of a case.

Ankylosing spondylitis is a seronegative spondyloartropathy associated with IgA glomerulonephritis. We described a case not associated with IgA immunoglobulin deposition in the glomerulus, but with C3 complement deposition. At the same time circulating immune complexed of the IgG type were found. The possible association of glomerulonephritis and seronegative spondyloartropathies are discussed.

Complement C3↗
PubMed1985

Type IIB Tampa: a variant of von Willebrand disease with chronic thrombocytopenia, circulating platelet aggregates, and spontaneous platelet aggregation.

Type IIB von Willebrand disease is characterized by enhanced ristocetin-induced platelet aggregation and absence of large von Willebrand factor multimers from plasma. An alteration of the von Willebrand factor molecule resulting in increased reactivity with platelets appears to be the basis for these abnormalities. We have now identified a new variant of type IIB von Willebrand disease in a family in which the four affected members also have chronic thrombocytopenia, in vivo platelet aggregate formation, and spontaneous platelet aggregation in vitro. In spite of repeatedly prolonged bleeding times and persistent thrombocytopenia, their bleeding diathesis is only moderate.

Adult↗
PubMed1984

Ultrastructural and immunohistochemical studies of bronchiolo-alveolar carcinoma.

A detailed ultrastructural study was made of seven cases of bronchiolo-alveolar carcinoma, and the findings were correlated with histochemical and immunohistochemical data. By electron microscopic examination all seven tumors displayed glandular differentiation, manifested by the presence of microvilli and intercellular junctions, with or without mucin production. Variable proportions of tumor cells retained ultrastructural characteristics of alveolar type II cells and Clara cells. In addition, some tumor cells revealed desmosomes and tonofilaments consistent with squamous differentiation. Immunohistochemical evaluation was carried out using a peroxidase-antiperoxidase technique and specific antibodies against surfactant high molecular weight glycoproteins, keratin proteins, IgA + secretory piece, carcinoembryonic antigen (CEA), human chorionic gonadotropin (HCG), and alpha-fetoprotein (AFP). Four tumors with type II cell-like differentiation stained with anti-surfactant glycoprotein sera. All seven tumors stained focally with anti-keratin and IgA + anti-secretory piece antibodies, and diffusely with CEA. These tumors failed to stain with antisera against HCG and AFP. It is concluded that bronciolo-alveolar carcinomas are primarily composed of cells with alveolar and bronchiolar cell differentiation. Adequate criteria were established for ultrastructural identification of tumor cells with differentiation to type II alveolar cell or Clara cell. Moreover, the findings of this study indicate that the surfactant glycoprotein marker, when present in a given tumor either diffusely or focally, is diagnostic of bronchiolo-alveolar carcinoma.

Adenocarcinoma↗
PubMed1984

Endotoxin-mediated inhibition of human platelet aggregation.

A variety of endotoxins, when added to human platelet-rich plasma (PRP) or to suspensions of washed platelets (WP), demonstrated an inhibitory effect on platelet aggregation induced by various aggregating agents. Endotoxin blocked the release of 14C serotonin from platelets but had no influence on cyclic AMP production. Endotoxin did not interfere with thromboxane generation by platelets. However, endotoxin-treated platelets failed to respond to added thromboxane. The inhibitory effect of endotoxin on platelet aggregation was more pronounced in the presence of ionophore A23187 as compared to other aggregating agents and was effectively reversed by calcium but not by magnesium, another divalent cation. Furthermore, endotoxin failed to inhibit the ristocetin-induced agglutination of formaldehyde-fixed platelets; a non-calcium dependent phenomenon. These findings appear to suggest that endotoxin-mediated inhibitory activity of platelet aggregation is related to the interference in the role of calcium. The antiaggregatory activity of endotoxin appears to be due to a direct and rapid action on platelets and not due to a non-specific binding, as the effect was not abolished by washing the endotoxin-incubated platelets. Endotoxin-mediated alteration of platelet function may contribute to bleeding diathesis in septecemic and endotoxemic patients.

Blood Platelets↗
PubMed1984

Effect of heparin on platelet aggregation.

The effect of heparin on platelet aggregation was systematically examined on platelets in plasma (PRP), as well as on gel-filtered, washed, and formaldehyde-fixed platelets. Results indicate that, although heparin causes a mild potentiation of platelet aggregation in the PRP systems, a significant inhibitory activity is observed when heparin is added to isolated platelets. This inhibitory activity appears to be specific and not related to the impurities in the heparin preparations, as heparinase, as well as protamine, effectively neutralizes the heparin-mediated inhibitory activity on platelet aggregation. Although heparin-mediated inhibitory activity can be demonstrated in the presence of a number of different agonists (ADP, arachidonic acid, thrombin, Ionophore A23187, epinephrine, and ristocetin), the most pronounced inhibition is seen in the presence of ristocetin. Further studies show that heparin enhances thromboxane generation in isolated platelets. Platelets pretreated with heparin, however, fail to respond to preformed thromboxane. These findings suggest that, in addition to the potentiation of thromboxane production in platelets, heparin may also attribute some change(s) to the platelet(s)/platelet membrane, which interferes with their ability to respond to the agonists of platelet aggregation. This antiaggregatory activity of heparin was found to be inhibited by a factor(s) present in plasma but not in serum.

Blood Coagulation↗
PubMed1984

Hemolytic uremic syndrome after Campylobacter-induced diarrhea in an adult.

Campylobacter fetus subspecies jejuni is a recognized pathogen of the gastrointestinal (GI) tract resulting in a spectrum of illness from mild gastroenteritis to severe colitis with bloody diarrhea. Campylobacter is also being recognized as capable of producing systemic illness. Furthermore, antibody response, hypocomplementemia, and bacteremia with enterotoxic organisms have been described. Many of the clinical features, both local (le, in the GI tract) and systemic, parallel those of Shigella. Since the hemolytic uremic syndrome (HUS) may be produced by the effect of endotoxins or the immunocomplex on vascular endothelium in susceptible patients, it is expected that this syndrome may follow Campylobacter enteritis as it does Shigella enteritis. We, therefore, believe Campylobacter jejuni enteritis should be considered as one of the causative agents capable of inducing the HUS.

Age Factors↗
PubMed1983

Carcinomas of the lung: an ultrastructural and immunocytochemical study.

Fifty-two primary carcinomas of the lung were studied by electron microscopy and by an immunoperoxidase method, using an anti-human keratin antiserum. The results were compared with light microscopic observations. One-third of the carcinomas of the lung showed ultrastructural evidence of both glandular and squamous differentiation. The group of small cell carcinomas was found to be particularly heterogenous ultrastructurally with only three out of eight tumors showing neurosecretory-type granules. Indirect immunoperoxidase staining revealed presence of a keratin-type protein in the vast majority of carcinomas, including foci of small cell carcinomas. Our studies emphasize the heterogeneity and frequent intermixing of the four major categories of lung carcinomas: squamous cell carcinomas, adenocarcinomas, small cell carcinomas, and large cell carcinomas. It is suggested that all these tumors might be derived from pluripotential "reserve" bronchial or bronchioalveolar cells. The segregation of small cell carcinomas from other groups continues to be justified on pragmatic grounds because these carcinomas constitute a group of predominantly small fast-replicating cells amenable to chemotherapy.

Adenocarcinoma↗
PubMed1982

In vitro cytotoxicity of human endothelial cells in polymyalgia rheumatica and giant cell arteritis.

We studied sera from 20 patients with polymyalgia rheumatica (PMR)/giant cell arteritis (GCA), 15 patients with systemic lupus erythematosus (SLE), 15 patients with the CREST syndrome (calcinosis, Raynaud's phenomenon, esophageal dysfunction, sclerodactyly, and telangietasia) and 33 age and sex matched controls for cytotoxicity against human endothelial cells using a 51Cr release assay. We observed increased levels of endothelial cytotoxic activity in the PMR/GCA sera compared with controls (P less than 0.001). This cytotoxicity was predominantly found in the GCA group, where 7 out of 10 patients (70%) demonstrated significant cytotoxicity. Sequential studies showed that the cytotoxic activity returned to normal when the disease was under control. Although 7 SLE and 3 CREST sera had significant cytotoxic activity, as a group they did not differ from controls (P less than 0.05). Pre-incubation with soybean trypsin inhibitor suppressed the cytotoxic activity in the positive sera suggesting the cytotoxicity is mediated via a protease mechanism. Our results demonstrate the presence of a cytotoxic factor in the serum of patients with PMR/GCA which may play an important role in the pathogenesis of the vascular lesions observed in these disorders.

Aged↗