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Biomedical subjects

S Prasad

Publications and source records attributed to S Prasad.

At least 199 records · Page 11Linked to original sources
PubMed1993

Facial nerve function following cerebellopontine angle surgery: prognostic value of intraoperative thresholds.

Intraoperative stimulation of the facial nerve during surgery of the cerebellopontine angle greatly aids the surgeon in identification of the nerve. The preservation of the ability to stimulate the facial nerve, at the brain stem following tumor removal, has been shown to correlate with good postoperative facial outcome. Thresholds of facial nerve stimulation recorded in our series, using constant voltage stimulation, showed statistically significant relevance to facial nerve outcome. When the difference between thresholds before and after tumor removal was 0.2 V or less or when the threshold after tumor removal was less than or equal to 0.2 V, a good postoperative facial outcome could be expected. This paper discusses the relevance of stimulation threshold prior to tumor removal to the size of tumor.

Adult↗
PubMed1993

Right thoracotomy revisited.

From September 1991 through August 1992, 38 patients (34 female and 4 male) underwent mitral valve surgery through a limited right anterior thoracotomy. The ascending aorta was easily cannulated for arterial return in all patients. Although there was no operative mortality, 8 patients required reoperation for bleeding, usually associated with the site of chest-wall puncture for the left atrial pressure line and epicardial pacing wires, a problem that we were able to correct. Right lower lobe collapse occurred in 2 patients, but the lungs were fully expanded in all patients before hospital discharge. We believe that a return to this older surgical approach is particularly suited to young patients and provides the important advantages over median sternotomy of superior mitral valve exposure and a cosmetically acceptable scar.

Adolescent↗
PubMed1992

Bacterial components and the pathophysiology of injury to the blood-brain barrier: does cell wall add to the effects of endotoxin in gram-negative meningitis?

In animal models, the lipopolysaccharide (LPS) from Haemophilus influenzae contributes to all the signs of meningitis associated with living bacteria. However, when tested in vitro, the amount of LPS in cerebrospinal fluid (CSF) in natural disease shows much greater effects on leukocytes than on endothelial permeability. To investigate whether other bacterial components act with LPS to incite meningeal inflammation, animals were challenged intracisternally with H. influenzae lysates. Upon neutralization of endotoxin, leukocytosis was greatly attenuated, but protein accumulation in CSF persisted. Cell wall from H. influenzae induced meningeal inflammation in a pattern opposite to that of LPS. Its ability to induce blood-brain barrier permeability greatly exceeded its ability to induce leukocytosis in vivo. Thus, cell wall, by acting on endothelia, and LPS, by inducing leukocytosis, may cooperate to induce inflammation in H. influenzae meningitis. Optimal reduction of inflammation and tissue damage in meningitis may require agents directed against cell wall as well as LPS.

Animals↗
PubMed1992

Differing roles for platelet-activating factor during inflammation of the lung and subarachnoid space. The special case of Streptococcus pneumoniae.

Although well-characterized in the lung, the role of platelet-activating factor (PAF) in inflammation in the central nervous system is undefined. Using rabbit models of meningitis and pneumonia, PAF was found to induce significant blood-brain barrier permeability and brain edema at doses five times lower than those required to generate leukocyte recruitment to the subarachnoid space. Both leukocytosis and increased vascular permeability occurred in response to PAF in the lung. Antibody to the CD-18 family of leukocyte adhesion molecules inhibited leukocyte recruitment in response to PAF in the brain (greater than 80%); a similar level of inhibition in the lung required treatment with a combination of a PAF receptor antagonist (L-659,989) and anti-CD18 antibody. Treatment with L-659,989 decreased abnormal cerebrospinal fluid cytochemical values induced by intracisternal challenge with pneumococci but not Haemophilus influenzae, indicating a special role for PAF in pneumococcal disease. Antibodies directed at phosphorylcholine, a unique, shared determinant of bioactivity of PAF and pneumococcal cell wall, obviated the inflammatory potential of both agents. However, no evidence for a direct PAF-like activity of pneumococcal cell wall components was detected in vitro by bioassay using platelets or neutrophils. It is concluded that PAF can induce inflammation in the subarachnoid space. In brain, PAF effects appear to be mediated through CD-18-dependent events, while in lung, PAF effects independent of CD-18 are also evident. At both sites, PAF is of particular clinical importance during inflammation induced by pneumococci apparently due to a unique proinflammatory relationship between the pneumococcal cell wall teichoic acid and PAF.

Animals↗
PubMed1992

Double aortic arch.

In conclusion, the diagnosis of DAA should be suspected in an infant with either biphasic stridor or feeding-related respiratory distress. Radiographic studies combined with appropriate thorough endoscopic evaluation should confirm clinical suspicion. Thoracotomy with surgical division of the DAA has given excellent long-term results.

Aorta, Thoracic↗
PubMed1991

Integrin-mediated localization of Bordetella pertussis within macrophages: role in pulmonary colonization.

The adherence of Bordetella pertussis to human respiratory cilia is critical to the pathogenesis of whooping cough but the significance of bacterial attachment to macrophages has not been determined. Adherence to cilia and macrophages is mediated by two large, nonfimbrial bacterial proteins, filamentous hemagglutinin (FHA), and pertussis toxin (PT). PT and FHA both recognize carbohydrates on cilia and macrophages; FHA also contains an Arg-Gly-Asp (RGD) sequence which promotes bacterial association with the macrophage integrin complement receptor 3 (CR3). We determined that virulent B. pertussis enter and survive in mammalian macrophages in vitro and that CR3 is important for this uptake process. We then determined the relative contribution of CR3 versus carbohydrate-dependent interactions to in vivo pulmonary colonization using a rabbit model. B. pertussis colonized the lung as two approximately equal populations, one extracellular population attached to ciliary and macrophage surface glycoconjugates and another population within pulmonary macrophages. Loss of the CR3 interaction, either by mutation of FHA or treatment with antibody to CR3, disrupted accumulation of viable intracellular bacteria but did not prevent lung pathology. In contrast, elimination of carbohydrate-bound bacteria, either by a competitive receptor analogue or an anti-receptor antibody, was sufficient to prevent pulmonary edema. We propose that CR3-dependent localization of B. pertussis within macrophages promotes persistence of bacteria in the lung without pulmonary injury. On the other hand, the presence of extracellular bacteria adherent to cilia and macrophages in carbohydrate-dependent interactions is associated with pulmonary pathology.

Adhesins, Bacterial↗
PubMed1991

Isolation and characterization of a full-length cDNA encoding the 55-kDa rabbit zona pellucida protein.

A full-length cDNA (rc55) encoding the major rabbit zona pellucida (ZP) glycoprotein (55 kDa) has been cloned and sequenced. A lambda gt11 expression library was constructed using poly(A)+ mRNA isolated from sexually immature rabbit ovaries which contain large numbers of developing follicles. The rc55 cDNA was identified using affinity purified polyclonal antibodies specific to ZP antigens which are shared among mammalian species. The deduced amino acid sequence of the full-length rc55 clone was matched to the NH2-terminal 25-amino acid sequence obtained for this protein. The predicted amino acid sequence consists of 540 amino acids including a putative signal peptide of 18-24 residues and six potential N-glycosylation sites. The cDNA hybridizes to a 2000-base species of mRNA from rabbit ovary which is not detected in other rabbit tissues. The message is present early in ovarian follicular development and is approximately 600-fold greater in sexually immature as compared with sexually mature rabbit ovaries. This cDNA was expressed as a cro-beta-galactosidase fusion protein using the pEX expression vector. Antibodies against native rabbit ZP, affinity-purified on the recombinant 55-kDa ZP protein, were found to recognize the native rabbit ZP glycoprotein, indicating partial conservation of native epitopes in the expressed recombinant protein.

Amino Acid Sequence↗
PubMed1991

Analysis of age-associated alteration in the synthesis of HMG nonhistone proteins of the rat liver.

HMG proteins were extracted with 5% PCA or 0.35 M NaCl from whole tissue, nuclei or chromatin of the liver of young (19 weeks) and old (118 weeks) male rats. They were resolved on acetic acid-urea polyacrylamide gel. The electrophoretic patterns of the major HMG proteins 1, 2, 14 and 17 of both ages are similar. The in vitro synthesis of HMG 1 and 2 decreases, but that of HMG 14 and 17 increases considerably in the liver of old rats. The synthesis of different HMG proteins is modulated differentially by spermine, butyrate, dexamethasone and 3-aminobenzamide in the liver of young and old rats. These findings suggest that HMG proteins contribute to alterations in the organization of chromatin and expression of genes during aging.

Aging↗
PubMed1991

Differential methylation of HMG proteins by dexamethasone in the liver of aging rats.

In vitro methylation of HMG proteins was studied in young and old rats by incubating liver slices with (methyl-14C)methionine. The level of methylation of all the four HMG proteins was relatively higher in young, as compared to old rats. Dexamethasone stimulated the methylation of HMG 2 to 12-fold, and inhibited that of other HMGs in young rats. On the other hand, it stimulated all major HMG proteins except HMG 2, which remains unchanged in old age. Such differential methylation of HMG proteins induced by dexamethasone affects the structure and function of chromatin during aging.

Aging↗
PubMed1991

Preliminary results of left heart bypass in pigs using a heparin-coated centrifugal pump.

To assess the feasibility of left ventricular assist without systemic heparinization, we used a commercially available (Sarns 3M) centrifugal pump with tubing set and cannulas, all internally precoated for the purpose of this study with heparin, to bypass the left ventricle in 12 pigs for periods of either 1 or 3 hours. There was no significant activation of clotting and there was no sign of generalized embolization. However, on postmortem studies, 5 kidneys out of 22 examined showed signs of minimal thromboembolism. This experiment shows that artificial left ventricular assist, free of systemic heparinization but using heparin precoating, is feasible and safe, at least for a short period of time.

Animals↗
PubMed1991

Possible roles for TGF beta 1 in the gastrulating chick embryo.

We have examined the immunocytochemical distribution of TGF beta 1 (transforming growth factor beta 1) in the gastrulating chick embryo, and have correlated the results with the ability of this factor to promote in vitro changes in the phenotype of mesoderm and epiblast cells. The findings, together with the demonstration that exogenous TGF beta 1 is also able to modulate extracellular matrix deposition by these cells in culture, are consistent with a role for this factor in the formation and morphogenesis of the early mesoderm. Immunofluorescence analysis, using an antibody to the amino-terminal fragment of TGF beta 1, indicates that this factor is located in, or between, cells of the medial epiblast, Hensen's node and primitive streak. At Hensen's node, cells of the hypoblast were also strongly labelled. Ingressed mesoderm cells, lateral to the streak, show considerably stronger and more diffuse labelling than the overlying epiblast cells. Although the fluorescent labelling appears to be associated with the extracellular matrix surrounding the mesoderm cells, it is not bound to hyaluronic acid, which is the preponderant molecule in the matrix at this time in development. When added exogenously to cultures of mesoderm cells growing with epithelial characteristics on fibronectin, TGF beta 1 effects an epithelial-mesenchymal transformation within 24 h. The reverse transformation is effected in mesoderm cells grown on laminin, while the epiblast cell phenotype is not affected by this treatment regardless of the substratum. TGF beta 1 is also able to down-regulate the deposition of fibronectin by mesoderm cells grown on fibronectin and of epiblast cells grown on laminin, but up-regulate fibronectin deposition by mesoderm on laminin. Similar substratum-dependent changes are seen in laminin deposition, which is down-regulated in mesoderm on laminin and up-regulated in epiblast on laminin. No effect on laminin deposition is seen in either cell type grown on fibronectin. Expression of the fibronectin receptor is also down-regulated by TGF beta 1 in mesoderm cells grown on fibronectin, and this may explain the decreased deposition of fibronectin associated with these cells under these conditions. We suggest that these results are consistent with a reinforcing role for TGF beta 1 in the transformation that results in the emergence of mesoderm cells at gastrulation. This factor may also be involved in the maintenance of the fibroblastic phenotype of the mesoderm cells after their ingression, by effects on the expression of receptors for extracellular matrix and on the deposition of matrix by these cells during their early morphogenesis.

Animals↗
PubMed1991

Odontoma of the middle ear cleft.

Odontoma of the middle ear cleft is an unusual cause of conductive hearing loss. We report two cases and discuss the developmental mechanism by which this anomaly may occur. The differential diagnosis of calcified masses in the middle ear is also discussed.

Adult↗
PubMed1990

ADP-ribosylation of HMG proteins and its modulation by different effectors in the liver of aging rats.

The in vitro ADP-ribosylation of high mobility group (HMG) non-histone proteins and its modulation by spermine, butyrate, dexamethasone and 3-aminobenzamide were studied in the liver of young (14 weeks) and old (113 weeks) male rats. ADP-ribosylation of HMG 1 was similar in both ages, whereas that of HMG 2 and 14 decreased but HMG 17 increased in the old. HMG 1 was ADP-ribosylated to a greater extent in young but to a lower level in the old by different effectors except spermine which showed no influence in old age. ADP-ribosylation of HMG 2 was stimulated by spermine, butyrate and dexamethasone in old but only by spermine in young rats. Other effectors decreased the ADP-ribosylation of HMG 2 in young. The ADP-ribosylation of HMG 14 was stimulated by spermine in the old but that of HMG 17 was reduced by butyrate in young and by spermine in the old. Dexamethasone decreased the ADP-ribosylation of both HMG 14 and 17 in young, whereas this showed no change in old age. Aminobenzamide inhibited ADP-ribosylation of only HMG 2 in young but all HMGs except HMG 2 in the old. Such alteration in the ADP-ribosylation of HMG proteins may affect various cellular and nuclear functions of rat liver during aging.

Adenosine Diphosphate Ribose↗