Search PubMed⌕ Search

Biomedical subjects

P Hazarika

Publications and source records attributed to P Hazarika.

At least 19 recordsLinked to original sources
PubMed1992

Antibody against a cystic fibrosis transmembrane conductance regulator-derived synthetic peptide inhibits anion currents in human colonic cell line T84.

The cystic fibrosis (CF) phenotype is characterized by a regulatory defect in Cl- permeability in epithelia. A gene (250,000 base pairs) that is associated with this autosomal genetic disorder has been identified. To determine the cellular function of the recently cloned gene product, the cystic fibrosis transmembrane conductance regulator (CFTR), we have produced antibody against a synthetic peptide deduced from the CFTR cDNA sequence corresponding to positions 505-511. This site includes phenylalanine 508, the deletion of which is the most commonly expressed mutation in CF. We sought to determine whether the anti-CFTR505-511 peptide antibody could modulate the activation of the volume-sensitive, Ca(2+)-dependent, as well as the cAMP-dependent Cl- conductances present in the Cl(-)-secreting human colonic T84 cell line. Affinity-purified anti-CFTR505-511 antibody was introduced into the cytoplasm of individual T84 cells and its function studied using the whole-cell patch-clamp technique. Although cAMP-dependent Cl- current activation was inhibited in cells perfused with the anti-CFTR505-511 peptide antibody, Ca(2+)-dependent anion current activation remained unaffected. Chloride current activation, which accompanies cellular swelling, was partially attenuated in anti-CFTR505-511 antibody-loaded cells as compared with control cells perfused with either saline or irrelevant antibody. These results further support a role for CFTR in anion transport in epithelial cells and suggest its possible involvement in a number of anion transport pathways in chloride secretory epithelia.

Anions↗
PubMed1991

Annexin VI is associated with calcium-sequestering organelles.

Annexin VI is a member of a Ca(2+)-dependent, phospholipid-binding protein family. Although functions for this annexin have been proposed from in vitro studies, most remain controversial. Díaz-Muñoz et al. (J Biol Chem 265:15894, 1990) demonstrated that annexin VI modified, in a Ca(2+)-dependent manner, the gating behavior of the sarcoplasmic reticulum Ca(2+)-release channel, reconstituted into artificial bilayers, by increasing both the open probability and the mean open time. This effect was specific to the trans chamber, which represents the luminal side of the sarcoplasmic reticulum. In agreement with those findings, we show herein that annexin VI produced no effect on Ca(2+)-uptake or -release by intact heavy sarcoplasmic reticulum vesicles (analogous to the cis chamber). We also used monospecific antibodies to evaluate the subcellular localization of annexin VI by immunofluorescent microscopy. Studies in rat skeletal muscle suggest that annexin VI is present surrounding individual myofibrils. Double immunolocalization studies with cultured muscle cells (chick myotubes) using anti-annexin VI and anti-SR Ca(2+)-ATPase antibodies demonstrated superimposable staining patterns. In non-muscle tissue (normal rat kidney (NRK) cells), a punctate, perinuclear anti-annexin VI staining pattern was observed. Collectively, these data suggest that annexin VI may play a regulatory role in the Ca(2+)-release/uptake cycle in the sarcoplasmic reticulum as well as in non-muscle organelles, a key process in stimulus-response systems.

Animals↗
PubMed1991

Regulation of the sarcoplasmic reticulum Ca(2+)-release channel requires intact annexin VI.

Annexin VI has eight highly conserved repeated domains; all other annexins have four. Díaz-Muñoz et al. (J Biol Chem 265:15894, 1990) reported that annexin VI alters the gating properties of the ryanodine-sensitive Ca(2+)-release channel isolated from sarcoplasmic reticulum. The investigate the domain structure of rat annexin VI (67 kDa calcimedin) required for this channel regulation, various proteolytic digestions were performed. In each case, protease-resistant core polypeptides were produced. Annexin VI was digested with V8 protease and two core polypeptides were purified by Ca(2+)-dependent phospholipid binding followed by HPLC. The purified fragments were shown to be derived from the N- and C-terminal halves of annexin VI, and demonstrated differential immunoreactivity with monoclonal antibodies to rat annexin VI. While both core polypeptides retained their ability to bind phospholipids in a Ca(2+)-dependent manner, they did not regulate the sarcoplasmic reticulum Ca(2+)-dependent manner, they did not regulate the sarcoplasmic reticulum Ca(2+)-release channel as did intact annexin VI.

Amino Acid Sequence↗
PubMed1991

Neurogenic tumours of the parapharyngeal space in the paediatric age group.

Two cases of neurogenic tumours of parapharyngeal space in children of 7 years old are presented. Difficulties during the diagnosis, investigations and management are discussed along with a review of the available literature. CAT scan with sialography, carotid angiography during surgery, angle mandibulectomy and liberal incision to expose the great vessels for better control of bleeding are stressed to minimise the peri-operative complication and to assist in complete removal of the tumours.

Child↗
PubMed1991

Otogenic brain abscess in childhood.

Brain abscesses are quite rare complications of middle ear infections. Although temporal lobe abscesses are more common than cerebellar abscesses, the converse was found to be true in our series of 10 cases. Eight cases of cerebellar abscess and 2 cases of temporal lobe abscess in the paediatric age group were reported including 4 cases of latent brain abscesses which manifested themselves after mastoidectomy for middle ear infection. Brain abscess is by far the most serious of otogenic complications.

Adolescent↗
PubMed1990

Modulation of Ca2+ release channel activity from sarcoplasmic reticulum by annexin VI (67-kDa calcimedin).

The effect of annexin VI (67-kDa calcimedin) on the activity of the Ca2+ release channel was studied using heavy sarcoplasmic reticulum membranes reconstituted into planar bilayers. Annexin VI, in a range of 5-40 nM, modified the gating behavior of the Ca2+ release channel by increasing the probability of opening by 2.7-fold and the mean open time by 82-fold relative to controls. Annexin VI caused no change in the slope conductance of the channel. The modulatory effect of annexin VI on the activity of Ca2+ release channels was Ca2+ dependent, and the annexin VI-modified channel was sensitive to both ruthenium red and ryanodine. The effect of annexin VI was observed when this protein was added specifically to the trans chamber, which corresponds to the luminal side of sarcoplasmic reticulum as determined by the ATP activation of the channel. In addition, differential extraction studies demonstrated that some annexin VI is localized within the lumen of the isolated heavy sarcoplasmic reticulum vesicles prepared by several different procedures. Annexin VI did not modify, from either the cis or trans chambers, the activity of K+ or Cl- channels from sarcoplasmic reticulum or the dihydropyridine sensitive Ca2+ channel from transverse tubules. In addition, the 38-kDa core proteolytic fragments of annexin VI had no effect on the Ca2+ release channel activity. Annexin VI is therefore a candidate for a physiological modulator of the Ca2+ release channel and as such, may play an important role in the excitation-contraction coupling.

Animals↗
PubMed1990

Infantile hemangiopericytoma of nasal cavity.

Hemangiopericytoma is an uncommon vascular tumour. Of the 26 intranasal hemangiopericytomas reported in the English literature only two paediatric cases have been noted. A benign course is more common in the nose and paranasal sinuses. A pre-operative diagnosis being not possible, definitive treatment cannot be preplanned. Wide surgical excision by a lateral rhinotomy approach is still the treatment of choice. The appropriate investigations and treatment line followed are described. A lifelong followup is mandatory.

Female↗
PubMed1990

Elongated styloid process: an overview.

Stylalgia is a condition that causes a dull, nagging pain in the oropharynx, often referred to the ear and the mastoid region. The clinical diagnosis is certain if the elongated styloid process is palpated through the tonsillar area. Radiological investigations, such as orthopantomograms, give information about the medial angulation. The treatment of choice is surgical shortening of the process. Trans-tonsillar fossa excision is a simple technique and does not involve greater morbidity than a routine tonsillectomy.

Adult↗
PubMed1989

Differential tissue expression of three 35-kDa annexin calcium-dependent phospholipid-binding proteins.

We have purified three 35-kDa calcium- and phospholipid-binding proteins from rat liver. These three calcimedins bind to phosphatidylserine in a calcium-dependent manner and have been termed 35 alpha, 35 beta, and 35 gamma based on their relative charge as determined by isoelectric focusing. Purification of the three 35-kDa calcimedins is achieved by phenyl-Sepharose, ion exchange, and gel filtration chromatography. Antibody was produced against the annexin consensus peptide, Lys-Ala-Met-Lys-Gly-Leu-Gly-Thr-Asp-Glu, which was derived from the sequence of several Ca2+/phospholipid-binding proteins including calpactin, lipocortin, endonexin II, 67-kDa calelectrin, lymphocyte 68-kDa protein, and protein II. Recognition of each 35-kDa calcimedin by anticonsensus sequence antibody places them in this protein family. Antibodies against each 35-kDa calcimedin were raised and purified by antigen-affinity chromatography. Each antibody is monospecific for the respective 35-kDa calcimedin. Immunological cross-reactivity defines 35 alpha, 35 beta, and 35 gamma as lipocortins III, IV, and V, respectively. Surveys by immunoblot analysis using these monospecific antibodies demonstrate a markedly different tissue expression pattern for each 35-kDa calcimedin. Furthermore, the levels of 35 alpha, 35 beta, and 35 gamma are differentially regulated in maturing rat ovary and uterus. Each calcimedin has been localized by indirect immunofluorescence within specific cell types. These results support the concept that mediation of the intracellular calcium signal can occur via multiple pathways through several related yet independent mediator proteins.

Amino Acid Sequence↗
PubMed1988

Immunoreactive alpha transforming growth factor activity in effusions from cancer patients as a marker of tumor burden and patient prognosis.

alpha Transforming growth factors (alpha-TGFs) are polypeptides that stimulate anchorage-independent growth of various nontransformed cells in vitro and are believed to be involved in autocrine stimulation of tumor cells. alpha-TGF activity is secreted by a variety of human cancers leading to the possibility that it may serve as a tumor marker. alpha-TGF activity was measured in 130 effusions from patients with various types of cancer with a radioimmunoassay using sheep antibodies against the C-terminal 17 amino acids of linear rat alpha-TGF. Forty-two % of the effusions contained immunoreactive alpha transforming growth factor (Ir-alpha-TGF) activity, including 13 of 34 (38%) breast cancer, 12 of 24 (50%) lung cancer, and 13 of 31 (42%) ovarian cancer specimens. Concentrations ranged from 1.56 to 50 ng/ml. Only 3 of 17 control effusions from noncancer patients had low levels of activity, all less than 2 ng/ml. The presence of Ir-alpha-TGF activity correlated with patients' performance status (PS) and tumor burden. It was present in 18 of 67 (27%) effusions of patients with PS less than or equal to 2 and in 23 of 33 (70%) with PS 3 or 4 (P less than 0.0001). Only 2 of 43 (4%) patients with one site of metastatic disease had detectable Ir-alpha-TGF (mean, 0.23 ng/ml); 18 of 37 (48%) with two sites (mean, 5.22 ng/ml, P less than 0.0001); and 33 of 34 (97%) with greater than two sites (mean, 5.93 ng/ml, P = 0.002). It was present in a larger percentage of effusions from breast cancer patients with estrogen- and progesterone receptor-negative tumors. Univariate analysis revealed that detectable Ir-alpha-TGF activity, PS 3 or 4, and the number of sites of disease correlated with a shorter survival. Only Ir-alpha-TGF and PS 3 or 4 retained significance in a multivariate analysis. In conclusion, Ir-alpha-TGF is frequently detectable in effusions from cancer patients, it correlates with other known adverse prognostic factors, and its presence predicts for a poor survival. Further studies of alpha-TGF activity in more readily accessible body fluids such as serum or urine are warranted.

Ascitic Fluid↗
PubMed1988

Determination of transforming growth factor activity in effusions from cancer patients.

Transforming growth factors (TGF) are polypeptides that stimulate anchorage-independent growth of various nontransformed cells in vitro. Transforming growth factors have been found in tumor extracts and in the urine of cancer patients. The specific questions of our study were whether TGF activity can be detected in malignant effusions, how different assays for TGF correlate with each other, and how assays for TGF correlate with soft agar tumor colony formation as measured by the human tumor cloning assay (HTCA). The TGF activity was measured by a normal rat kidney transformation assay (NRKA), a 125I-EGF radioreceptor assay (RRA), and a radioimmunoassay (RIA) for TGF-alpha. Cells from effusions were cytologically examined and plated in the HTCA. A total of 104 effusions from cancer patients and 17 effusions from non-cancer patients was tested. Transforming growth factor activity was detected in some specimens. Only the TGF-alpha RIA and the HTCA showed significant differences between cancer and noncancer patients. Immunoreactive TGF-alpha was measurable in some cases by RIA even when cytologic testing failed to detect malignant cells. Spearman correlations between assays indicated that RIA results correlate significantly with all other assays. It is concluded that TGF-alpha activity might be important for in vitro colony formation of human tumor cells.

Ascitic Fluid↗
PubMed1988

Epitope mapping of alpha-transforming growth factor: evidence of an immunodominant region.

Antisera were produced in rabbits and sheep against both full-length synthetic rat alpha-transforming growth factor and peptides corresponding to the carboxy-terminal 17 amino acids. These antisera were used to develop a peptide based radioimmunoassay of alpha-TGF. All antisera reacted only with a restricted region of the alpha-TGF corresponding to the 8 residues (43-50) at the carboxy-terminus: (formula; see text) A series of synthetic peptides representing deletions or substitutions of amino acids in this carboxy-terminal region were tested for competition with 125I-alpha-TGF. All changes in the above peptide sequence resulted in a marked reduction in competition. All of the polyclonal antisera demonstrated similar specificity whether they were produced against the 50 amino acid, full-length alpha-TGF, against shorter 17 amino acid and 8 amino acid carboxy-terminal sequences.

Amino Acid Sequence↗
PubMed1988

Familial Treacher-Collins syndrome.

The major congenital malformations of the first and second branchial arch derivatives such as mandibulofacial dysostosis have a genetic basis. Treacher-Collins syndrome is transmitted as an autosomal dominant trait, although many cases occur as spontaneous mutations. The characteristics are hypoplasia of the malar, mandibular and maxillary bones, antimongoloid slanting of the palpebral fissures and a receding chin. The aural findings include malpositioning or maldevelopment of the pinna or external auditory meatus, an atretic bony plate instead of tympanic membrane, or ossicular malformations. Five members of a Hindu family affected by Treacher-Collins syndrome spanning three generations are examined in detail, with special reference to their hearing.

Humans↗
PubMed1988

Lingual thyroid.

Explore the source record for details and available documents.

Adolescent↗