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Biomedical subjects

K Patel

Publications and source records attributed to K Patel.

At least 145 records · Page 8Linked to original sources
PubMed1997

Artemether in moderate to severe malaria: a multicenter trial in India.

154 patients suffering from acute attack of moderate to severe malaria caused by Plasmodium falciparum were treated with 480 mg artemether, administered intramuscularly (i.m.) in six equally divided doses at 12 hour intervals. Results showed a rapid parasite clearance. Mean parasite clearance time (PCT) was found to be 23.65 +/- 1.57 hours. Mean fever clearance time (FCT) was 35.28 +/- 1.7 hours. Adverse drug events (ADE) were mild and self-limiting. Recrudescence rate (RR) among the patients followed up was 4.55%. We conclude that artemether is a safe and effective anti-malarial agent for the treatment of moderate and severe cases of P. falciparum malaria.

Acute Disease↗
PubMed1996

Cloning and early dorsal axial expression of Flik, a chick follistatin-related gene: evidence for involvement in dorsalization/neural induction.

We have cloned and sequenced a chick gene, Flik (follistatin-like) that appears to be the homolog of the mammalian TSC36. The ORF encodes a secreted protein of approx 38 kDa, containing a single cysteine-rich domain that shows a strong relationship with the second of the four from which Follistatin is constructed. The remainder of the Flik protein shows no strong family affinities. We describe here the normal expression pattern of the gene during primitive streak and neurula stages. We also give revised data for early neurectodermal expression of chick follistatin (Connolly et al., 1995, Developmental Genetics 17(1), 65-77) and follow the new ectopic expression of both genes during the induction of a second neural axis, after grafting of Hensen's node into a peripheral position in a host blastoderm. Both genes mark the organizer (node and/or mesodermal head process) and early neural plate, and could thus be involved in intercellular signaling during mesodermal dorsalization and neural induction. Flik expression appears earlier than that of follistatin however, and unlike that of follistatin, it is maintained strongly in the dorsal midline with intensity smoothly declining into presumptive lateral regions. We show that both genes are upregulated in host tissue in the neighborhood of node grafts, but whereas follistatin is transcribed after 8-10 hr in host epiblast that has formed new neural plate, Flik is expressed within 4 hr in this region, sometimes detectable before the first structural changes (columnarization) of neuralization. Thus, although ectodermal Flik expression is later confined within neural plate, and mesodermal expression concentrated in dorsal axial tissue, its early distribution is consistent with the idea that the encoded protein may first be involved in generating a graded system that positions the boundaries of both neural and dorsal axial mesodermal territories. The results are discussed in relation to this hypothesis and to other recent findings regarding control of vertebrate dorsoventral patterning.

Amino Acid Sequence↗
PubMed1996

The expression and regulation of follistatin and a follistatin-like gene during avian somite compartmentalization and myogenesis.

We report on the normal and experimentally altered expression of two structurally related genes, Follistatin and Follistatin-like (Flik), in the somites of avian embryos. In normal chick embryos, Follistatin expression can first be seen in the cells of the dorsolateral somite quarter. During somite maturation, the cells of the dorsomedial quarter also express this gene. Within the dermomyotome it seems that only the muscle precursors are Follistatin-positive. The migrating precursors of limb and tongue muscle as well as the myotome cells show Follistatin expression. The manipulation experiments reveal that the expression of Follistatin in the somites can be inhibited by notochord signals. This effect can be mimicked by sonic hedgehog protein. Flik is expressed in the dorsomedial compartment of the somite and later on in the myotome. Unlike Follistatin, Flik expression requires signals emanating from the neural tube. Notochordal influences do not alter Flik expression. The expression of both genes does not depend on signals of intermediate or lateral mesoderm. Since the products of both genes are proposed to antagonize TGF-beta superfamily proteins during gastrulation and neuralization, we postulate that during myogenesis follistatin and flik counteract inhibiting effects of related molecules on muscle differentiation.

Animals↗
PubMed1996

A former hockey player with knee and calf pain.

A 37-year-old man presented with severe pain in his left knee and calf. He had no other joint pain, fever, chills, or dysuria. He had previously gone to another hospital, where x-rays of the knees and legs reportedly showed inflammation and arthritis. He had been given oxycodone-acetaminophen, but the pain continued.

Acute Disease↗
PubMed1996

CD98: a type II transmembrane glycoprotein expressed from the beginning of primitive and definitive hematopoiesis may play a critical role in the development of hematopoietic cells.

In our search for cell surface markers expressed on hematopoietic stem cells and/or very early progenitor cells we found that the Joro 177 monoclonal antibody (MoAb) bound to most hematopoietic cells in day 8/8.5 yolk sac, day 12 fetal liver, and day 13 fetal thymocytes; it stained hematopoietic stem cells and less immature lymphoid, myeloid, and erythroid-lineage cells, but not most thymocytes and splenic lymphocytes in adult mice. Joro 177 MoAb stimulated tyrosine phosphorylation of an integral of 124-kD protein and induced homotypic aggregation of lymphoid progenitor cells. Importantly, Joro 177 MoAb inhibited cell survival/growth and consequently the generation of lymphoid, myeloid, and erythroid lineage cells in vitro from early Lin- hematopoietic precursors. Joro 177 MoAb induced apoptosis of hematopoietic progenitor cells. Molecular cloning and expression indicated that Joro 177 MoAb recognizes a type II transmembrane protein, which is the mouse homologue of the human CD98 heavy chain gene. We suggest that CD98 is a cell membrane receptor involved in the control of cell survival/death of hematopoietic cells.

Amino Acid Sequence↗
PubMed1996

Experience with a hospital-wide outbreak of vancomycin-resistant enterococci.

BACKGROUND: Vancomycin-resistant enterococci (VRE) were first detected in our institution in 1991. An outbreak was recognized in late 1992 when there was a sudden rise in the number of patients per month with VRE. Little information exists concerning the natural history of infection with these pathogens, and the effect of antimicrobial therapy is unclear. Recent guidelines emphasize prudent use of vancomycin and prompt institution of barrier precautions to limit the spread of vancomycin resistance. METHODS: Data were obtained by review of microbiologic and clinical records. Patients were categorized according to site of infection, and outcome of therapy was assessed. Hospital antibiotic usage was analyzed to determine any correlation with the outbreak. Infection control measures instituted in 1993 included patient isolation, environmental cleaning, and a reemphasis of barrier precautions. Surveillance cultures were performed to assess the extent of the outbreak in January 1995. RESULTS: VRE were detected in clinical cultures from 159 patients from 1991 through 1994. Mortality rate was 48%, but in most cases death could not be attributed to enterococcal infection. Patients with wound infections healed without specific therapy. Many patients with bacteremia had resolution with ampicillin or without specific therapy. Patients were widely scattered throughout the hospital from the beginning of the outbreak. Hospital usage of cefotaxime correlated with the number of cases. Infection control measures were not successful. Surveillance culture results in January 1995 revealed that 53% of all medical and surgical inpatients had fecal colonization with VRE. Genetic analysis of selected isolates revealed that one strain predominated, but at least seven distinct strains were identified. CONCLUSIONS: Our data suggest that many infections with VRE resolve without specific therapy. The infection control measures we used were ineffective, possibly because of the multiple strains present in our hospital. Isolation of all patients with VRE is impractical when there is widespread fecal carriage.

Adult↗
PubMed1996

Incidental paranasal sinus inflammatory changes in a British population.

A retrospective study was carried out to determine the prevalence of abnormality in the paranasal sinuses in a British population having magnetic resonance imaging (MRI) scans for neurological signs and symptoms. The T2-weighted scans of 130 patients were studied. Abnormalities in the paranasal sinuses show as high signal on the T2-weighted scans and thus are clearly seen. Abnormalities included mucosal thickening, fluid levels, sinus opacification and retention cysts/polyps. Of the patients studied, 49.2 per cent showed one or more abnormality. Mucosal thickening was the most common abnormality noted and the ethmoid sinuses the most commonly affected.

Adolescent↗
PubMed1996

An inbred colony of oncogene transgenic mice: diversity of tumours and potential as a therapeutic model.

Transgenic mice carrying the activated rat c-neu oncogene under transcriptional control of the MMTV promoter were backcrossed to BALB/c mice, with the aim of developing a model for cancer therapy. A total of 86 of 268 transgene-positive mice in the first five generations developed 93 histologically diverse tumours (median age of onset 18 months). The cumulative incidence of breast tumours at 24 months was 18%, and overall tumour incidence 31%. As well as expected c-neu expressing breast cancers, lymphomas and Harderian gland carcinomas developed. Virgin mice had fewer mammary tumours than those with two litters. Breast carcinomas metastasised to the lungs, and lymphomas were widely disseminated. The tumours showed a range of architectural patterns, which resembled human breast cancers or lymphomas. This diversity was reflected in S-phase fraction and aneuploidy. Breast tumours transplanted to nude mice showed variable responses to interferon (IFN)-alpha and gamma. A tumour transplanted to BALB/c mice responded to interleukin (IL)-12. There was significant decline in transgene positivity with successive generations. The diversity, histological and biological resemblance to human cancer suggests that the model has potential for evaluating novel therapies. However, further genetic and environmental manipulations are required to increase tumour incidence and decrease age of onset.

Animals↗
PubMed1996

Manipulation of a hospital antimicrobial formulary to control an outbreak of vancomycin-resistant enterococci.

Infection control practices are not uniformly successful in limiting outbreaks of vancomycin-resistant enterococci (VRE). Despite the implementation of barrier precautions for VRE-infected patients, nearly one-half of the inpatients at our center were found to have gastrointestinal colonization by VRE. In an attempt to control the outbreak, we altered the antibiotic formulary by restricting the use of cefotaxime and vancomycin and adding beta-lactamase inhibitors to replace third-generation cephalosporins. The use of clindamycin was also restricted because of a concomitant outbreak of Clostridium difficile colitis. After 6 months, the average monthly use of cefotaxime, ceftazidime, vancomycin, and clindamycin had decreased by 84%, 55%, 34%, and 80%, respectively (P < .02). The point prevalence of fecal colonization with VRE decreased from 47% to 15% (P < .001), and the number of patients whose clinical specimens were culture positive also gradually decreased. A change in antibiotic use appears to have significantly affected our VRE outbreak when previous measures failed.

Ampicillin↗
PubMed1996

Acute myeloid leukaemia complicated by anergic tuberculosis.

A case of acute myeloid leukaemia presenting as pyrexia of unknown origin and weight loss with pancytopenia is described. Initial investigations revealed trilineage myelodysplasia which evolved into acute myeloid leukaemia within 2 weeks of presentation. He was commenced on a standard induction regimen consisting of idarubicin, Ara-C and thioguanine. Throughout his hospital stay he remained febrile. In spite of exhaustive investigations no cause for the pyrexia was found nor did he respond to any form of treatment. He died after 9 weeks in hospital. His post-mortem examination revealed widespread disseminated tuberculosis without any reactive inflammatory tissue response or granuloma formation.

Acute Disease↗
PubMed1996

Comparison of five selective media for identifying fecal carriage of vancomycin-resistant enterococci.

There is no uniformly accepted method for detecting colonization with vancomycin-resistant enterococci (VRE). The sensitivities of five culture methods were determined for patients known to harbor VRE. Of 189 inpatients, 101 were found to harbor VRE by at least one method. Three methods detected fewer than half of the cultures. Campylobacter agar identified 70% of patients. Enterococcosel broth (containing vancomycin and aztreonam) identified 88% and may be preferred over other media for routine surveillance.

Anti-Bacterial Agents↗
PubMed1996

Rapid diagnosis of respiratory syncytial virus infections in immunocompromised adults.

Although rapid antigen detection methods for the documentation of respiratory syncytial virus (RSV) infections are widely used with pediatric patients, these tests have not been prospectively evaluated in immunocompromised (IC) adults. For bone marrow transplant recipients and adult patients undergoing chemotherapy for leukemia who had recent onset of respiratory symptoms, respiratory samples (combined nasal wash [NW]-throat swab [TS], endotracheal tube [ET] aspirate, or bronchoalveolar lavage [BAL] samples) were collected for simultaneous culture and rapid antigen detection with the Directigen test kit (Becton Dickinson, Cockeysville, Md.). NW specimens from hospitalized pediatric patients with suspected RSV infection were also evaluated. Viral quantitation was performed on aliquots of the original specimens. A total of 539 samples from 372 adult patients were evaluated. RSV was isolated from 56 specimens (40 NW-TS, 7 ET aspirate, and 9 BAL specimens). By using culture as the "gold standard," rapid antigen detection had a sensitivity of 15% for adult NW-TS specimens, 71.4% for ET aspirate specimens, and 88.9% for BAL specimens; the specificity was > or = 97% for all specimen types. Significantly greater viral quantities were present in pediatric NW specimens than in adult NW specimens. In adults, more virus was present in BAL and ET aspirate specimens than in NW-TS specimens. Rapid detection of antigen respiratory samples obtained from the lower respiratory tracts of IC adults is sensitive and specific, but detection in upper respiratory tract samples is insensitive. The lower sensitivity of antigen detection in NW-TS specimens may be due to decreased viral load. A BAL specimen is more sensitive than an NW-TS specimen for the rapid diagnosis of RSV disease in IC adults.

Adult↗
PubMed1996

Expression and regulation of Cek-8, a cell to cell signalling receptor in developing chick limb buds.

The Eph-related receptor tyrosine kinase gene, Cek-8, is expressed in mesenchyme at the tip of chick limb buds, with high levels of transcripts posteriorly and apically but fading out anteriorly. Expression of Cek-8 in distal mesenchyme is regulated by apical ridge- and FGF-polarising signals and retinoic acid, and is uniform across the anteroposterior axis in talpid3 mutants. These data indicate that Cek-8 expression responds to regulatory signals during limb patterning and suggest that this receptor tyrosine kinase may have a role in coordinating responses to signals in the progress zone of early buds. Later on in limb development, Cek-8 expression is associated with cell condensations that form tendons and their attachments to cartilage rudiments and then in developing feather buds.

Animals↗
PubMed1995

Modulation of interleukin-6-induced plasma protein secretion in hepatoma cells by p53 species.

The ability of p53 species (wild-type and mutant) to modulate the "differentiated" response of human hepatoma cell lines Hep3B and HepG2 to interleukin-6 (IL-6) was investigated. Transient transfection experiments were carried out in Hep3B and HepG2 cell cultures in which IL-6 was used to activate a beta-fibrinogen (beta Fib) enhancer/reporter construct containing two copies of the 36-base pair IL-6-response element (IL-6RE) (p beta FibCAT). Cotransfection with constitutive expression vectors for wild-type (wt) human or murine p53 inhibited the activation of the p beta FibCAT reporter by IL-6 in both Hep3B and HepG2 cells. Several mutant p53 species either did not inhibit the activation of p beta FibCAT or up-regulated the response. Hepatoma cell lines stably expressing the Val-135 temperature-sensitive mutant of murine p53 (wt-like at 32.5 degrees C and mutant-like at 37 degrees C) were derived from Hep3B cells and tested for the temperature-sensitive phenotype of their ability to synthesize and secrete fibrinogen and alpha 1-antichymotrypsin in response to IL-6. In an experimental protocol in which the parental Hep3B cells did not show a significant difference in plasma protein secretion at the two temperatures, hepatoma line 3 (p53Val-135+) had a greater response to IL-6 at 37 degrees C than parental Hep3B cells, while line 3 cells had a reduced response to IL-6 at 32.5 degrees C. Similarly, hepatoma lines 1 and 2 (both p53Val-135+) had reduced IL-6 responsiveness at 32.5 degrees C, whereas line 22 (transfected with pSVneo alone) and the parental Hep3B cells did not. These data indicate that mutations in p53 contained in tumor cells can modulate the "differentiated" response of these cells to cytokines.

Animals↗