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Biomedical subjects

D Patel

Publications and source records attributed to D Patel.

At least 127 records · Page 7Linked to original sources
PubMed1994

Metabolic bone disease in black teenagers with genu valgum or varum without radiologic rickets: a bone histomorphometric study.

Calcium deficiency in black (African) children can cause rickets and osteomalacia with severe limb deformities. It is not known whether black teenagers with genu valgum or varum but without radiologic rickets suffer from a related disorder. To examine this question we studied 26 such patients by iliac crest bone biopsy and serum and urine biochemistry: 12 patients (46%) had osteopenia with normal or low bone turnover, 5 (19%) mildly increased bone turnover, 4 (15%) histologic hyperparathyroidism, 2 (8%) preosteomalacia, and 3 (12%) osteomalacia (with features of hyperparathyroidism). Radiographs did not reflect the severity of the bone disease. Serum calcium levels correlated inversely with eroded mineralized surface (p < 0.001), osteoid surface (p < 0.01), osteoid thickness (p < 0.001), mineralization lag time (p < 0.001), and 1,25-(OH)2 vitamin D (p < 0.005), and 1,25-(OH)2 vitamin D correlated positively with osteoid surface (p < 0.05), osteoid thickness (p < 0.05), osteoid volume (p < 0.01), eroded surface (p < 0.05), and eroded mineralized surface (p < 0.0005). Tubular reabsorption of phosphate and 25-OH vitamin D levels were normal, and 1,25-(OH)2 vitamin D levels were normal to high. This suggests that calcium deficiency may have caused the increase in bone turnover and the mineralization defects. The most severe osteomalacia was found in males aged 16-19 years. We cannot explain the cause of the osteopenia. We conclude that all patients had bone disease.

Adolescent↗
PubMed1994

Interrelationship of prolactin and its receptor in carcinoma of colon and rectum: a preliminary report.

The prolactin receptors (PRLR) were correlated with circulating prolactin and various clinicopathologic parameters to investigate its prognostic value in patients with colorectal cancer. The prolactin (by radioimmunoassay) and its receptors (by radioligand method) were estimated in a total of 71 male patients with colorectal cancer enrolled at the Gujarat Cancer and Research Institute, Ahmedabad. The patients were followed for a period of 3 years. We have observed that 51% colorectal tumors were PRLR+. Significant correlation was not observed between presence/absence of PRLR and clinicopathologic variables. Dukes' D patients were lost to follow-up after 2-3 months; therefore, the results of prognostic significance were analysed only in patients with Dukes' A, B, and C (N = 64). Statistically significant difference in overall survival was not observed when the patients were subgrouped according to the presence/absence of PRLR and according to the cutoff level (i.e., 2%). PRLR+ hyperprolactinemic (Prolactin > 20.0 ng/ml plasma) patients had better overall survival than that of patients with PRLR- hyperprolactinemia, although the difference was statistically nonsignificant. However, PRLR- hyperprolactinemia patients had a more unfavourable prognosis than that of their counterparts. A similar trend was observed in patients with Dukes' B and C disease. Our preliminary study suggests an unequivocal finding, that PRLR- with concomitant hyperprolactinemia probably characterises a subgroup of patients with aggressive colorectal cancer.

Adult↗
PubMed1994

Selective inhibition of [D-Ala2, Glu4]deltorphin antinociception by supraspinal, but not spinal, administration of an antisense oligodeoxynucleotide to an opioid delta receptor.

Evidence in vivo has suggested the existence of subtypes of the delta opioid receptor (DOR), which have been termed delta 1 and delta 2. These proposed DOR subtypes are thought to be activated by [D-Pen2, D-Pen5]enkephalin (DPDPE, delta 1) and [D-Ala2, Glu4]deltorphin (delta 2). Recent work in which an antisense oligodeoxynucleotide (oligo) to a cloned DOR was administered by the intrathecal (i.th.) route has demonstrated a reduction in the antinociceptive actions of both i.th. DPDPE and [D-Ala2, Glu4]deltorphin, but not of [D-Ala2, NMPhe4, Gly-ol]enkephalin (DAMGO, mu agonist) in mice. The present investigation has extended these observations by administering the same DOR antisense oligo sequence by the intracerebroventricular (i.c.v.) route and evaluating the antinociceptive actions of i.c.v. agonists selective for delta, mu and kappa receptors. I.th. treatment with DOR antisense oligo, but not mismatch oligo, significantly inhibited the antinociceptive actions of both i.th. DPDPE and [D-Ala2, Glu4]deltorphin but not of i.th. DAMGO or U69,593 (kappa agonist), confirming previous data. In contrast, i.c.v. DOR antisense oligo, but not mismatch oligo, selectively inhibited the antinociceptive response to i.c.v. [D-Ala2, Glu4]deltorphin without altering the antinociceptive actions of i.c.v. DPDPE, DAMGO or U69,593. The data suggest that the cloned DOR corresponds to that pharmacologically classified as delta 2 and further, suggest that this delta receptor subtype may play a major role in eliciting spinal delta-mediated antinociception.

Analgesics↗
PubMed1994

Comparison of the effect of heparin and aspirin versus aspirin alone on transient myocardial ischemia and in-hospital prognosis in patients with unstable angina.

OBJECTIVES: This study compared the effects of heparin and aspirin versus aspirin alone on transient myocardial ischemia and in-hospital prognosis in patients with unstable angina. BACKGROUND: Transient myocardial ischemia occurring in patients with unstable angina is associated with an adverse prognosis. Heparin and aspirin are two drugs used frequently in the treatment of this condition, but the effect of combination therapy versus aspirin alone on transient myocardial ischemia is unknown. METHODS: Two hundred eighty-five consecutive patients with unstable angina were randomized to receive either intravenous heparin plus oral aspirin (150 mg once daily) (Group H + A) or aspirin alone (Group A). Patients also received a beta-adrenergic blocking agent, diltiazem and intravenous nitrates. ST segment monitoring was performed for the 1st 48 h of treatment. Patients were followed up for the duration of their in-hospital stay. RESULTS: One hundred fifty-four patients (30 women, mean [+/- SEM] age 58.3 +/- 0.8 years) received heparin and aspirin (Group H + A), and 131 patients (26 women, mean age 60.6 +/- 0.8 years) received aspirin only (Group A). ST segment monitoring (11,622 h) yielded 244 episodes of transient myocardial ischemia of a total duration of 7,819 min. There were no significant differences between the two treatment arms in the number of patients with transient myocardial ischemia (27 [18%] in Group H + A vs. 31 [24%] in Group A), number of episodes (96 in Group H + A vs. 148 in Group A) or total duration of transient myocardial ischemia (2,911 min in Group H + A vs. 4,908 min in Group A). The incidence of in-hospital myocardial infarction or death was significantly higher in patients with transient myocardial ischemia (53% vs. 22%, p < 0.0001). Five of the six deaths occurred in patients with transient myocardial ischemia. Event-free survival from myocardial infarction or death was similar in both treatment groups. Preadmission therapy with aspirin was associated with a lower in-hospital infarction rate (19% vs. 34%, p = 0.01). CONCLUSIONS: The presence of transient myocardial ischemia in patients with unstable angina is associated with a significantly higher incidence of myocardial infarction or death in hospital. Combined therapy with heparin and aspirin compared with aspirin alone makes no difference in the development of these events, nor does it reduce the development of transient myocardial ischemia.

Adult↗
PubMed1994

Early and longitudinal evaluations of treated infants and children and untreated historical patients with congenital toxoplasmosis: the Chicago Collaborative Treatment Trial.

Between December 1981 and May 1991, 44 infants and children with congenital toxoplasmosis were referred to our study group. A uniform approach to evaluation and therapy was developed and is described herein along with the clinical characteristics of these infants and children. In addition, case histories that illustrate especially important clinical features or previously undescribed findings are presented. Factors that contributed to the more severe disabilities included delayed diagnosis and initiation of therapy; prolonged, concomitant neonatal hypoxia and hypoglycemia; profound visual impairment; and prolonged, uncorrected increased intracranial pressure with hydrocephalus and compression of the brain. Years after therapy was discontinued, three children developed new retinal lesions (without loss of visual acuity when therapy for Toxoplasma gondii was initiated promptly), and three children experienced a new onset of afebrile seizures. Most remarkable were the normal developmental, neurological, and ophthalmologic findings at the early follow-up evaluations of many--but not all--of the treated children despite severe manifestations, such as substantial systemic disease, hydrocephalus, microcephalus, multiple intracranial calcifications, and extensive macular destruction detected at birth. These favorable outcomes contrast markedly with outcomes reported previously for children with congenital toxoplasmosis who were untreated or treated for only 1 month.

Animals↗
PubMed1994

Nuclear localization of the PEP protein tyrosine phosphatase.

PEP is an intracellular protein tyrosine phosphatase expressed primarily by cells of hematopoietic origin that can be divided structurally into a catalytic domain and a large carboxy-terminal domain. The carboxy-terminal domain is enriched in proline, glutamic acid, serine, and threonine residues (PEST sequences) and contains a nonperfect tandem repeat sequence enriched in proline residues and a carboxy terminus enriched in basic amino acids. Here we show that PEP is diffusely expressed in lymphoid tissues, consistent with expression by many different cell types. Analysis of the PEP protein identifies a nuclear localization sequence within the extreme carboxy terminus. Transfer of 18 amino acids from the carboxy terminus of PEP to beta-galactosidase conferred nuclear localization, indicating that this sequence was sufficient for nuclear localization. Proteins enriched in PEST sequences are often rapidly degraded. However, pulse-chase analysis indicates that PEP has a half-life of greater than 5 h.

Amino Acid Sequence↗
PubMed1994

Glucose given after hypoxic ischemia does not affect brain injury in piglets.

BACKGROUND AND PURPOSE: Giving glucose before hypoxic ischemia worsens brain injury in piglets. Does giving glucose after hypoxic ischemia affect severity of injury? METHODS: Forty-three 0- to 3-day-old pigs were used. All piglets received 2 U/kg insulin before injury to prevent stress-induced hyperglycemia. Hypoxic ischemic brain damage was induced by clamping both carotid arteries and reducing arterial blood pressure to two thirds of normal by hemorrhage at time 0. At 15 minutes the fraction of inspired oxygen (FIO2) was reduced to 6%. At 30 minutes FIO2 was increased to 100%, the carotids were released, and the withdrawn blood was reinfused. The piglets were then randomized to receive either 2 mL/kg of 50% dextrose followed by 2 mL/kg per hour for 2 hours or an equal volume of saline. RESULTS: Neurological examination scores (20 is normal, 5 is brain dead, by blinded observer) at 1 day postinjury were similar in the two groups: glucose, median 15.5 (25th percentile, 12.2; 75th percentile, 18); controls, 15.6 (9.3, 18). Piglets were killed at 3 days with brain preservation at death. Pathological examination scores (sum of scores from cortex, hippocampus, and basal ganglia: 30 is normal, 3 is total necrosis) by blinded observer were similar in the two groups: glucose, 26 (18, 28); controls, 25 (16.5, 28); NS. CONCLUSIONS: Although elevated glucose levels during hypoxic ischemic injury worsen brain injury in the piglet, elevated glucose levels after injury do not affect the severity of the injury.

Animals↗
PubMed1993

Evidence of surface antigen detachment during incubation of cells with immunomagnetic beads.

We have studied the attachment of immunomagnetic beads to different cells, with particular interest in cells that did not, as expected, appear to bind antibody-coated beads. Through the use of immunofluorescence and laser scanning confocal microscopy it was possible to demonstrate that beads can detach significant amounts of antigen from the surface of cells. This results in the appearance of antigen-depleted yet viable cells. Moreover, the detached antigen is found to be bound to beads and is associated with fragments of cell membrane which can also carry other (non-bead binding) cell surface proteins. After reculturing, antigen-depleted cells can recover their normal levels of surface antigen. Our results demonstrate the existence of an immunobead-induced cell membrane detachment phenomenon that can lead to the removal of all of a specific surface antigen without killing the cells, as judged by both vital staining and reculturing. An important aspect of this phenomenon is that immunoidentification of immunobead-selected populations of cells will give erroneous results. This may thus be of significance for the immunobead-based cell depletion methods that are used in medicine.

Antigens, CD↗
PubMed1993

Solution conformation of the (+)-trans-anti-[BPh]dA adduct opposite dT in a DNA duplex: intercalation of the covalently attached benzo[c]phenanthrene to the 5'-side of the adduct site without disruption of the modified base pair.

Benzo[c]phenanthrene diol epoxide can covalently bind to the exocyclic amino group of deoxyadenosine to generate [BPh]dA adducts where the polycyclic aromatic hydrocarbon is attached to the major groove edge of DNA. This paper reports on NMR-energy minimization structural studies of the (+)-trans-anti-[BPh]dA adduct positioned opposite dT in the sequence context d(C5-[BPh]A6-C7).d-(G16-T17-G18) at the 11-mer duplex level. The exchangeable and nonexchangeable protons of the benzo[c]phenanthrenyl moiety and the nucleic acid were assigned following analysis of two-dimensional NMR data sets in H2O and D2O solution. The solution structure of the (+)-trans-anti-[BPh]dA.dT 11-mer duplex has been determined by incorporating intramolecular and intermolecular proton-proton distances defined by upper and lower bounds deduced from NOESY data sets as restraints in energy minimization computations. The covalently attached benzo[c]phenanthrene ring intercalates to the 5'-side of the [BPh]-dA6 lesion site without disruption of the flanking Watson-Crick dC5.dG18 and [BPh]dA6.dT17 base pairs. The observed buckling of the intercalation cavity reflects the selective overlap of the intercalated phenanthrenyl ring with dT17 and dG18 bases on the unmodified strand. The structure provides new insights into how a polycyclic aromatic hydrocarbon covalently attached to the major groove edge of deoxyadenosine can still unidirectionally intercalate into the helix without disruption of the modified base pair. Our study establishes that among the contributing factors are a propeller-twisted [BPh]dA6.dT17 base pair, displacement of the carcinogen-DNA linkage bond from the plane of the dA6 base, the specific pucker adopted by the benzylic ring, and the propeller-like nonplanar geometry for the aromatic phenanthrenyl ring system. Our combined experimental-computational studies to date have now identified three structural motifs adopted by covalent polycyclic aromatic hydrocarbon-DNA adducts with their distribution determined by the chiral characteristics of individual stereoisomers and by whether the covalent adducts are generated at the minor or the major groove edge of the helix.

Base Sequence↗
PubMed1993

The p27 catalytic subunit of the apolipoprotein B mRNA editing enzyme is a cytidine deaminase.

The messenger RNA for apolipoprotein B undergoes a discrete and specific C to U editing of nucleotide 6666. This generates a stop translation codon and defines the carboxyl terminus of apolipoprotein B48. A 27-kDa rat intestinal protein that does not itself edit apolipoprotein B mRNA, but confers editing activity on chick intestinal extracts that do not have intrinsic editing activity, has recently been identified and its cDNA cloned (Teng, B., Burant, C. F., and Davidson, N. O. (1993) Science 260, 1816-1819). Here we show that p27 is homologous in the zinc coordinating region of the active site to cytidine deaminases from Escherichia coli, Bacillus subtilis, yeast, and man and to deoxycytidylate deaminases from T2 and T4 bacteriophages and man. p27 expressed in Xenopus laevis oocyte extracts has cytidine deaminase activity and specifically confers editing activity on chick intestinal extracts. The homologous E. coli cytidine deaminase does not confer editing activity. The zinc-specific chelating agent o-phenanthroline abolishes p27 activity and site-specific apolipoprotein B mRNA editing in rat enterocyte editing extracts. We conclude that p27 is the catalytic subunit of the apolipoprotein B mRNA editing enzyme and is a zinc-containing cytidine deaminase.

APOBEC-1 Deaminase↗
PubMed1993

Use of density perturbation to isolate immunologically distinct populations of cells.

Experiments have been carried out to demonstrate that, using antibody coated-Dynabeads as a model system for density labelling MOLT-4 T cells, the overall density of cells can be increased such that the cells that bind particles can be separated on isopycnic isotonic density gradients from cells that bind fewer particles. The increase in density is dependent on the cell volume and the number of particles bound. After centrifugation, cells with bound particles were found at positions in the gradient that reflected their increased density. Observed density ranges for cells with particular numbers of particles bound coincided closely with calculated expected density ranges. These results indicate the potential for separation of different subpopulations of cells on the basis of the immunological identity of the surface of cells using density perturbation methods involving antibody coated-density particles.

Cell Separation↗
PubMed1993

Expression of Xist during mouse development suggests a role in the initiation of X chromosome inactivation.

The mouse Xist gene maps to the X inactivation center (Xic) region and is expressed exclusively from the inactive X chromosome. It is thus a candidate gene for the Xic. We show that the onset of Xist expression in mouse development precedes X chromosome inactivation and may therefore be a cause rather than merely a consequence of X inactivation. The earliest Xist expression in morulae and blastocysts is imprinted, resulting in specific expression of the paternal Xist allele. Imprinted Xist expression may thus be the cause of nonrandom inactivation of the paternal X in trophectoderm. Strong Xce alleles can act to reduce the effect of imprinted Xist expression in the trophectoderm. The imprint on Xist expression is lost shortly before gastrulation when random X inactivation occurs. Our data support a direct role for Xist in the initiation of X inactivation.

Aging↗
PubMed1993

Apolipoprotein B mRNA editing is associated with UV crosslinking of proteins to the editing site.

Apolipoprotein (apo) B100 mRNA undergoes editing of C-6666 to a U residue, which generates a stop-translation codon and defines the carboxyl terminus of apoB48. To aid purification of the editing enzyme we have undertaken UV crosslinking of a 32P-labeled substrate for apoB mRNA editing in vitro to proteins in an enterocyte editing extract. Proteins of 60 (p60) and 43 (p43) kDa, prominent among crosslinking bands, were competed for by unlabeled substrate, but not by nonspecific RNA, and did not crosslink to antisense RNA. Editing in vitro and UV crosslinking were inhibited by NaCl and vanadyl ribonucleoside complexes and by chemical modification of sulfhydryl, imidazolium, and guanidinium groups on the protein. The editing activity copurified predominantly with p60. To define the binding site for p60 on the substrate RNA, a series of scanning and point mutant RNAs, previously used to define nucleotides 6671-6681 as essential for editing, were used in competition studies with wild-type substrate. Results demonstrated that p60 binding is centered on nucleotides 6671-6674. We suggest that p60 contains the RNA-recognition component of the apoB mRNA-editing enzyme.

Animals↗
PubMed1993

Isolation of porcine IgE, and preparation of polyclonal antisera.

High Titre, Ascaris specific, porcine reaginic antibody was induced by combining parasitic infestation and antigen challenge. The reagin was characterised as being heat labile at 56 degrees C, possessing long term skin sensitising activity, and as having physicochemical properties similar to IgE in other species. Porcine IgE was purified by conventional immunochemical techniques, and an epsilon chain isolate prepared using SDS-PAGE gel excision and electro elution. Antisera raised against the intact IgE molecule and its epsilon chain were rendered monospecific by immunoabsorption and characterised by reverse cutaneous anaphylaxis (RCA) testing, passive cutaneous anaphylaxis inhibition, immunohistology and Western blotting. These antisera are currently being used to study the regulation of IgE responses in the pig.

Animals↗
PubMed1993

Calculation of volume flow rate by the proximal isovelocity surface area method: simplified approach using color Doppler zero baseline shift.

OBJECTIVES: The goal of this study was to develop an accurate, simplified proximal isovelocity surface area (PISA) method for calculating volume flow rate using lower blue-red interface velocity produced by a color Doppler zero baseline shift technique. BACKGROUND: The Doppler color proximal isovelocity surface area method has been shown to be accurate for calculating the volume flow rate (Q) across a narrowed orifice by the formula Q = PISA x Blue-red interface velocity. A hemispheric model is generally used to calculate proximal isovelocity surface area (PISA = 2 pi a2, where a = the radius corresponding to the blue-red interface velocity). Although a hemispheric model is simple, requiring measurement of one radius, it may underestimate the actual volume flow rate because, in the general case, the shape of a proximal isovelocity surface area is hemielliptic. Although a hemielliptic model is generally more accurate for calculating proximal isovelocity surface area, it is more complex, requiring measurement of two orthogonal radii. METHODS: Sixteen in vitro constant flow model studies were performed using planar circular orifices (diameter range 6 to 16 mm). The blue-red interface velocity was changed from 3 to 54 cm/s using color Doppler zero baseline shift. RESULTS: 1) With decreasing blue-red interface velocity, the size of the proximal isovelocity surface area was increased, and its shape changed from hemielliptic to hemispheric. 2) With the blue-red interface velocity in the range 11 to 15 cm/s, the proximal isovelocity surface area became nearly hemispheric; however, it was difficult to determine the blue-red interface radius at a blue-red interface velocity < 10 cm/s because of interface fluctuations. 3) Calculated volume flow rate using the hemispheric proximal isovelocity surface area model with a single radius was relatively accurate at a blue-red interface velocity of 11 to 15 cm/s (mean percent difference from actual volume flow rate was -3.6%). CONCLUSIONS: Because the shape of the proximal isovelocity surface area is nearly hemispheric at a blue-red interface velocity of 11 to 15 cm/s, volume flow rate can be accurately calculated in this proximal isovelocity surface area interface velocity range (produced by zero baseline shift) by measuring a single-interface radius. This approach should be clinically useful for calculating the volume flow rate across stenotic and regurgitant valves and across shunt defects.

Blood Flow Velocity↗
PubMed1993

A phase II trial of concomitant human interleukin-2 and interferon-alpha-2a in patients with disseminated malignant melanoma.

Interleukin-2 (IL-2) and alpha-interferon have each shown antitumor activity in patients with disseminated malignant melanoma. Because animal studies suggest enhanced activity for the combination over each agent used alone, this trial using a relatively low-dose outpatient regimen was undertaken. IL-2 at a dose of 2 x 10(6) U/m2/day (Roche units) was given by continuous intravenous infusion for 4 days a week with interferon-alpha-2a at a dose of 6 x 10(6) U/m2/day given by s.c. or i.m. injection on days 1 and 4 of each treatment week. One cycle consisted of 4 consecutive weeks of treatment followed by a 2-week rest period. Fourteen patients were entered in this study. No complete or partial responses were seen. One patient required dose reduction because of grade 3 diarrhea and two patients had interruption of treatment because of central-line-related sepsis. Fatigue was common in all patients. This low-dose combination regimen of IL-2 and alpha-interferon does not appear to be better than the single agents used alone in optimal dosage.

Adult↗