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Biomedical subjects

J O Minta

Publications and source records attributed to J O Minta.

At least 37 records · Page 2Linked to original sources
PubMed1985

Inherited C8 beta subunit deficiency in a patient with recurrent meningococcal infections: in vivo functional kinetic analysis of C8.

A 16 year old with recurrent meningococcal infections is reported. Absence of haemolytic activity in both the classical and alternative pathways resulted from an absence of functional C8. Addition of functional C8 restored hemolytic activity. Antigenically deficient C8 was present in the serum and isoelectric focusing of serum confirmed the absence of the C8 beta chain. Following the infusion of fresh frozen plasma, we followed the decay in C8 functional activity as well as total haemolytic activity. C8 activity peaked at about 3 h with a half-life survival estimated to be 28 h. The kinetics of total haemolytic activity showed a slower decay with an exponential decline over 72 h and a half-life of 55 h. Fresh frozen plasma may be of value in the treatment of patients with C8 deficiency and acute Neisserial infections.

Adolescent↗
PubMed1985

Chemotactic responsiveness and random motility of polymorphonuclear leukocytes from patients with progressive systemic sclerosis.

Polymorphonuclear leukocyte (PMNL) random motility and chemotactic responsiveness and serum chemoattractant ability in 20 patients with progressive systemic sclerosis (PSS) were compared to those from 21 normal controls using a microchemotactic assembly. PSS leukocyte random motility was found to be significantly increased (p less than 0.02) compared to that in the control group. However, there were no statistically significant differences between the chemotactic migration of control and patient cells in response to C5a or zymosan activated control or patient sera. The chemotactic responsiveness of normal PMNL and the chemotactic activity of zymosan activated normal serum or C5a were not affected when treated with 10% PSS plasma. This suggests the absence of inactivators of chemotactic factors and circulating cell directed inhibitors of chemotaxis in the sera of patients with PSS.

Adult↗
PubMed1984

Migration of porcine endothelial and smooth muscle cells in response to platelet-associated factors.

A NeuroProbe multiwell microchemotaxis assembly has been used to study the migration of porcine aortic endothelial and smooth muscle cells in vitro in response to serum factors. Whole pig serum was found to be chemokinetic for endothelial cells but not smooth muscle cells. Chemokinetic activity was higher in platelet-enriched, plasma-derived serum (PDS) than in platelet-free PDS. The supernatant from washed, lysed pig platelets also showed chemokinetic activity both for endothelial and smooth muscle cells. Chromatography on Sephadex G-200 showed that the lysate contained a number of activities that act independently on the two cell types. The chemokinetic activity that we have detected appears to be distinct from the chemotactic effect of platelet-derived growth factor and platelet factor 4 on the basis of insensitivity to protamine sulfate and molecular size. The role of these platelet factors in pathological changes in vascular structure is currently under study.

Animals↗
PubMed1983

Effect on the human complement system of the major non-steroidal anti-inflammatory drugs: aspirin, indomethacin, phenylbutazone, oxyphenbutazone and sulindac.

The possibility that the major non-steroidal anti-inflammatory drugs may inhibit the complement system and thus ameliorate the acute pathological changes induced by immune complexes was investigated. Treatment of fresh human serum with indomethacin (IDM), sulindac (Su), phenylbutazone (Ph) and oxyphenbutazone (OPh) inhibited both the classical and alternative complement (C) pathway activities in a dose-dependent fashion with a 50% inhibition dose of 4.65, 1.0, 1.65 and 1.3 mg/ml respectively. Aspirin, on the other hand, had a comparatively weak anti-complementary activity. Su, Ph and OPh were shown to form complexes with C5, thereby inhibiting the interaction between C3b and C5 and the cleavage of the latter into phlogistic fragments.

Anti-Inflammatory Agents↗
PubMed1982

Neutrophil function in the immotile cilia syndrome.

Patients with ICS have a microtubular abnormality of cilia, which is thought to contribute to frequency respiratory tract infections. Neutrophils have a cytoplasmic microtubular system that, if abnormal and malfunctioning, could also contribute to recurrent infections. Neutrophil function has been assessed in 14 patients with ICS and compared with that of controls. The ICS patients included those with the dynein defect, the radial spoke defect, and microtubular transposition. Cell migration in each patient has been examined under agarose and by Boyden chamber techniques. No significant abnormality was detected in random or directed migration of neutrophils. Six patients representing the three different types of abnormal cilia had more extensive studies of neutrophil function performed. These included assessments of bacterial phagocytosis and killing, lysosomal degranulation, and oxidative pathway activity. Phagocytosis and killing of Staphylococcus aureus 502A in vitro was normal. Hexose monophosphate pathway activity, tetrazolium dye reduction, and lysosomal degranulation by neutrophils at rest and during phagocytosis were similar to those of control neutrophils. Our findings suggest that an abnormality of neutrophil function does not play an important role in the respiratory infections of patients with ICS.

Adolescent↗
PubMed1981

Selective deficiency of the fourth component of complement in a patient with systemic lupus erythematosus (SLE): immunochemical and biological studies.

A 45-year-old female (J.B.) with clinically inactive systemic lupus erythematosus was devoid of haemolytic serum complement activity. Functional and immunoprecipitin assays showed that the complement defect was due to lack of the fourth component of complement (C4). The patient's serum and red cells were Chido-negative, Rodgers-negative. In J.B.'s serum there was marked impairment of opsonization of Staphylococcus aureus and of the formation of chemotactic activity in the presence of zymosan. The chemotactic defect was not due to the presence of inhibitory factors: the activity was increased by the addition of C4. These findings suggest that an intact classical pathway is necessary for the optimal generation of serum chemotactic factors by zymosan via the alternative pathway of the complement system.

Adolescent↗
PubMed1981

The role of sialic acid in the functional activity and the hepatic clearance of C1-INH.

The immunochemical properties, catabolic clearance, and organ distribution of highly purified radiolabeled human C1-INH were studied after treatment with glycosidases. The antigenicity and C1s inhibitory activity of C1-INH were unimpaired after removal of sialic acid residues (60%) or sialic acid and galactose residues (60 and 20%, respectively) with immobilized neuraminidase and beta-galactosidase. Treatment of C1-INH with neuraminidase was associated with increased cathodal migration of the glycoprotein. In vivo studies in the rabbit, however, showed that removal of sialic acid residues resulted in rapid blood clearance of C1-INH and enhanced localization of the asialo C1-INH in the liver. Subsequent removal of penultimate galactose residues returned the survival time in the circulation and organ distribution to near normal. Additionally, simultaneous infusion of asialo-C1-INH with asialo alpha 1-acid glycoprotein, a protein known to bind to hepatic asialoglycoprotein receptors, dramatically extended the intravascular survival time of asialo C1-INH. In agreement with the observations on other plasma glycoproteins, these results indicate that desialylation of C1-INH results in rapid clearance by hepatic asialoglycoprotein receptors.

Animals↗
PubMed1980

Immunological, structural and functional relationships between an anti-complementary protein from Crotalus atrox venom, cobra venom factor and human C3.

An anti-complementary protein which cross-reacts with antiserum to cobra venom factor (CoF) has been highly purified from Crotalus atrox venom (CAV). On an equal weight basis, the C. atrox factor (CA-F) had one-third the anti-complementary activity of CoF and similarly consumed the terminal components of complement via the alternative pathway. The subunit compositions of CoF and CAV were similar, each being composed of alpha and beta chains held together by covalent and non-covalent bonds. Agarose gel diffusion analysis using monospecific antiserum to CoF detected a reaction of partial immunological identity between CoF and CA-F and between C3 and CA-F with the CoF and C3 precipitin lines spurring over the CA-F lines. Thus CA-F probably represents a C. atrox C3 protein which is capable of activating the alternative complement pathway via the amplification loop in a manner analogous to that of C3b and CoF.

Animals↗
PubMed1980

Inhibition of vitamin D2-induced arteriosclerosis in rats by depletion of complement with cobra venom factor.

Widespread calcerous deposits developed in the aorta, heart and kidneys of rats fed for 4 days with purina chow and high doses of vitamin D2 (200,000 IU/kg body wt/day). Decomplementation of rats with highly purified cobra venom factor (CoF) prior to vitamin D2 feeding, almost completely prevented calcium deposition in the aorta and arteritis. The mortality rate in the CoF-treated vitamin D2-fed rats was much lower than in untreated rats. These findings suggest that the complement system may be recruited in the pathogenesis of vitamin D2-induced arteriosclerosis.

Animals↗
PubMed1979

Purification and characterization of a single chain precursor C3-protein (pro-C3) from normal human plasma.

Fresh human plasma was treated with proteinase inhibitors and passed through an immunoadsorbent column of Sepharose anti-C3 globulin. The insolubilized C3 was eluted with 5 M guanidine and, after extensive dialysis, was reduced with 0.2 M 2-mercaptoethanol and electrophoresed on SDS-polyacrylamide gels. The bulk of the eluted C3 dissociated into two major protein bands, m.w. 125,000 and 75,000 corresponding to the alpha- and beta-chains of C3. In addition, a nonreducible single polypeptide chain (SPC) with a m.w. value of 197,000 +/- 2,000 similar to the apparent m.w. of unreduced C3 was consistently present. SPC has been purified by elution from SDS (SPC) and found to remain a single polypeptide chain upon re-electrophoresis on SDS gels in the presence of 0.2 M 2-mercaptoethanol. The purified SPC reacted with antisera to denatured C3, C3alpha, and C3beta chains. Additionally, antisera to SPC, also reacted with denatured C3, C3alpha-, and C3beta-chains, revealed a reaction identity between SPC and C3, and detected partial identity between SPC and C3alpha- as well as C3beta-chains. This suggested that SPC and C3 are antigenically related. The amino acid compositions and tryptic peptide maps of SPC and C3 were similar. Based on these findings, it is suggested that SPC must represent a single-chain precursor C3 (pro-C3) in plasma that escaped post-synthetic proteolytic cleavage into a two-subunit chain C3 molecule.

Amino Acids↗
PubMed1979

Anticomplementary activity of cornea, vitreous and chorioretina in rabbits.

We wished to determine if inhibitors of the complement system are present in different rabbit ocular tissues. Soluble extracts of cornea, vitreous humor and chorioretina in different dilutions were incubated with normal human serum (as source of complement). The ability of the latter to lyse sheep erythrocytes sensitized with antisheep rabbit hemolysin was assessed. The cornea did not show any inhibition of complement. The vitreous humor exhibited very low inhibitory activity. The extracts of the uveo-retinal tissue contained heat-labile and heat-stable factors capable of cleaving C3 and factor B.

Animals↗
PubMed1979

C3 deposition in cholesterol-induced atherosclerosis in rabbits: a possible etiologic role for complement in atherogenesis.

Hypercholesterolemia was induced in rabbits by feeding Purina Chow supplemented with cholesterol (5 g/kg body weight/day). The serum cholesterol levels of these rabbits increased progressively and after 3 to 5 months were 4 to 9-fold greater than those of the control animals. Decrease in total hemolytic complement was not apparent during the feeding regimen. Morphologic examination of aortae of these hypercholesterolemic rabbits showed typical atherosclerotic intimal plaques. Immunofluorescent microscopy with fluorescein (F)-labeled anti-rabbit C3 showed deposition of C3 in the intimal and inner medial layers as early as 3 months on high cholesterol diet. C3 deposits were also observed in the renal glomeruli and in the walls of coronary arteries. However, fluorescent studies failed to demonstrate the presence of IgG, IgM, and C4 at these sites. Tissues from control animals fed normal diets were negative for immunoglobulins, C3, and C4. These results suggest that the complement system may be implicated in the pathogenesis of cholesterol-induced atherosclerosis in rabbits.

Animals↗