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Biomedical subjects

W Lane

Publications and source records attributed to W Lane.

At least 19 recordsLinked to original sources
PubMed2002

An outbreak of viral gastroenteritis following environmental contamination at a concert hall.

In January 1999, an outbreak of viral gastroenteritis affected more than 300 people who attended a metropolitan concert hall over a 5-day period. Norwalk-like virus (NLV) was confirmed in faecal samples by reverse transcription polymerase chain reaction assay. The index case was a concert attendee who vomited in the auditorium and adjacent male toilet. Gastrointestinal illness occurred among members of 8/15 school parties who attended the following day. Children who sat on the same level of the auditorium as the index case were much more likely to be ill than those seated elsewhere (relative risk 7.1, 95% confidence interval 5.4-9.2. P < 0.001). The majority of other reported cases had not been present on the evening of the vomiting incident. Disinfection procedure was poor and the disinfectant used contained no sodium hypochlorite. Transmission most likely occurred through direct contact with contaminated fomites. The outbreak has implications for disinfection procedures following vomiting incidents at public venues.

Adult↗
PubMed2001

EBNA-LP associates with cellular proteins including DNA-PK and HA95.

EBNA-LP-associated proteins were identified by sequencing proteins that immunoprecipitated with Flag epitope-tagged EBNA-LP (FLP) from lymphoblasts in which FLP was stably expressed. The association of EBNA-LP with Hsp70 (72/73) was confirmed, and sequences of DNA-PK catalytic subunit (DNA-PKcs), HA95, Hsp27, prolyl 4-hydroxylase alpha-1 subunit, alpha-tubulin, and beta-tubulin were identified. The fraction of total cellular HA95 that associated with FLP was very high, while progressively lower fractions of the total DNA-PKcs, Hsp70, Hsp 27, alpha-tubulin, and beta-tubulin specifically associated with EBNA-LP as determined by immunoblotting with antibodies to these proteins. EBNA-LP bound to two domains in the DNA-PKcs C terminus and DNA-PKcs associated with the EBNA-LP repeat domain. DNA-PKcs that was bound to EBNA-LP phosphorylated p53 or EBNA-LP in vitro, and the phosphorylation of EBNA-LP was inhibited by Wortmannin, a specific in vitro inhibitor of DNA-PKcs.

DNA-Activated Protein Kinase↗
PubMed2000

Autocrine stimulation of VEGFR-2 activates human leukemic cell growth and migration.

Emerging data suggest that VEGF receptors are expressed by endothelial cells as well as hematopoietic stem cells. Therefore, we hypothesized that functional VEGF receptors may also be expressed in malignant counterparts of hematopoietic stem cells such as leukemias. We demonstrate that certain leukemias not only produce VEGF but also express functional VEGFR-2 in vivo and in vitro, resulting in the generation of an autocrine loop that may support leukemic cell survival and proliferation. Approximately 50% of freshly isolated leukemias expressed mRNA and protein for VEGFR-2. VEGF(165) induced phosphorylation of VEGFR-2 and increased proliferation of leukemic cells, demonstrating these receptors were functional. VEGF(165) also induced the expression of MMP-9 by leukemic cells and promoted their migration through reconstituted basement membrane. The neutralizing mAb IMC-1C11, specific to human VEGFR-2, inhibited leukemic cell survival in vitro and blocked VEGF(165)-mediated proliferation of leukemic cells and VEGF-induced leukemic cell migration. Xenotransplantation of primary leukemias and leukemic cell lines into immunocompromised nonobese diabetic mice resulted in significant elevation of human, but not murine, VEGF in plasma and death of inoculated mice within 3 weeks. Injection of IMC-1C11 inhibited proliferation of xenotransplanted human leukemias and significantly increased the survival of inoculated mice. Interruption of signaling by VEGFRs, particularly VEGFR-2, may provide a novel strategy for inhibiting leukemic cell proliferation.

Animals↗
PubMed1999

Investigation of an outbreak of gastroenteritis at a hospital for patients with learning difficulties.

Eighty of the 460 patients and staff (attack rate 22%) in a long-stay hospital for patients with learning difficulties became ill in a general outbreak of gastrointestinal infection that followed a buffet style party on one ward. Illness in the cohort of 47 resident patients, relations, and staff who attended that party was associated with having eaten ham, coleslaw, bread rolls, and cheese and pineapple on sticks. Food from the hospital kitchen was supplemented by food brought in and prepared on the ward by staff and patients. The investigation suggested that food items were contaminated either during preparation by staff and patients or during the party when people served themselves. Microbiological and virological investigations were negative, but small round structured virus was thought to be responsible. Hospitals could do more to prevent outbreaks of foodborne infection by undertaking risk assessment as required by the Food Safety Act (General Food Hygiene) Regulations 1995. Purchasers of hospital infection control should ensure compliance with this legislation.

Cohort Studies↗
PubMed1998

NAT, a human complex containing Srb polypeptides that functions as a negative regulator of activated transcription.

A complex that represses activated transcription and contains the human homologs of the yeast Srb7, Srb10, Srb11, Rgr1, and Med6 proteins was isolated. The complex is devoid of the Srb polypeptides previously shown to be components of the yeast Mediator complex that functions in transcriptional activation. The complex phosphorylates the CTD of RNA polymerase II (RNAPII) at residues other than those phosphorylated by the kinase of TFIIH. Moreover, the complex specifically interacts with RNAPII. The interaction is not mediated by the CTD of RNAPII, but is precluded by phosphorylation of the CTD. Our results indicate that the complex is a subcomplex of the human RNAPII holoenzyme. We suggest that the RNAPII holoenzyme is a transcriptional control panel, integrating and responding to specific signals to activate or repress transcription.

Amino Acid Sequence↗
PubMed1998

A campylobacter outbreak associated with stir-fried food.

An outbreak of gastrointestinal illness affecting 12 of 29 customers of a 'Hawaiian' theme restaurant specializing in stir-fried food occurred in Cardiff, Wales in February 1997. Campylobacter jejuni serotype HS50 phage type 49 (PT49) was isolated from 5 cases. A total of 47 isolates of C. jejuni HS50 PT49 were identified from Wales during 1997, of which 11 were isolated in late February or early March and from the Cardiff area. In the outbreak, illness was associated with eating stir-fried chicken pieces (relative risk 4.81, 95% confidence interval (CI) 0.76-30.44, P=0.03) and a dose-response relationship between risk of illness and amount of chicken consumed was observed (chi2-test for linear trend 3.96, P=0.047). Undercooking of chicken was probably due to a combination of inadequate cooking time and use of large chicken pieces. This is the first time that stir-fried food has been associated with a campylobacter outbreak. The incident also illustrates the value of routine campylobacter subtyping in supporting outbreak investigation.

Campylobacter Infections↗
PubMed1994

Specific binding of the transglutaminase, platelet factor XIII, to HSP27.

HSP27, the unique mammalian low molecular weight heat shock protein, is prominently phosphorylated upon activation of a wide variety of cells and has a role in thermotolerance, growth events, and regulation of actin cytoskeletal dynamics. In thrombin-stimulated platelets, HSP27 is rapidly and prominently phosphorylated in a manner highly correlated with platelet secretion. However, the function of HSP27 and the identity of proteins that interact with HSP27 remain unknown. To identify specific HSP27-protein interactions, a recombinant fusion protein affinity reagent was constructed and used to identify proteins associating with HSP27 from human platelet lysates and erythroleukemia cells. An 84-kDa protein was found to associate specifically with HSP27 and was isolated from platelet lysates, resolved on preparative gels, transferred to nitrocellulose, subjected to enzymatic digestion, and microsequenced. A 20-amino acid sequence derived from p84 proved identical to amino acids 484-503 of the transglutaminase, platelet Factor XIII. Immunoblotting studies were used to confirm the binding of FXIII from fresh platelet lysates to the HSP27 fusion protein. FXIII also was shown to coprecipitate with HSP27 in immunoprecipitation studies and to colocalize with HSP27 in immunofluorescence studies of intact glass-activated platelets. The data thus demonstrate specific binding of platelet FXIII to HSP27 and suggest that HSP27 may participate in the cellular localization and/or enzymatic regulation of platelet FXIII.

Amino Acid Sequence↗
PubMed1994

What the contract doesn't say.

Even when a PPO contract looks acceptable at first glance, hidden snags can await the unwary. A family physician who is an experienced negotiator points out possible "sleepers"--unstated conditions that aren't in your best interests.

Contract Services↗
PubMed1993

Value of bedside plating of semiquantitative cultures for diagnosis of central venous catheter-related infections in ICU patients.

We compared semiquantitative central venous catheter tip cultures plated at the bedside with those cultured in the laboratory, to determine if bedside plating provides a significantly better yield. Paired segments of 197 catheter tips from 92 surgical and medical ICU patients were evaluated prospectively. A total of 31 catheter tip cultures were positive for > or = 15 organisms per agar plate, with 10 of these being simultaneously positive at the bedside and in the laboratory. Cultures were exclusively positive in 18 cases plated immediately at the bedside, whereas laboratory plating resulted in only 3 exclusively positive cases. This discrepancy was statistically significant (p < 0.005). Compared with bedside plating, the sensitivity and specificity of sending catheters to the laboratory were 36 percent and 98 percent, respectively. These results indicate that the practice of sending central venous catheter tips to the laboratory for routine culture should be reconsidered in favor of bedside plating.

Adult↗
PubMed1992

Aromatic trivalent arsenicals: covalent yet reversible reagents for the agonist binding site of nicotinic receptors.

The agonist binding site of nicotinic acetylcholine receptors (AChRs) includes a disulfide bond that is easily reduced with dithiothreitol to a pair of thiols, and can be then either reoxidized with dithiobis(nitrobenzoic acid) (DTNB) or irreversibly alkylated with bromoacetylcholine (BAC). Aromatic trivalent arsenicals form stable complexes with pairs of appropriately-spaced thiols, but not single thiols. Furthermore, once complexed in proteins, trivalent arsenicals can be removed with dimercaptans, such as 2,3-dimercaptopropanesulfonic acid (DMPS). In an effort to develop reagents that will covalently, yet reversibly label AChRs, we investigated the effects of two model arsenicals, p-aminophenyldichloroarsine (APA) and 4-bromoacetyl-aminophenylarsenoxide (BAPA) on two types of nicotinic receptors: AChRs from Torpedo electroplax and neuronal receptors from chick retina. APA and BAPA significantly decrease the number of 125I-alpha-bungarotoxin binding sites in reduced Torpedo AChRs. Furthermore, arsenylation of neuronal and Torpedo receptors with APA or BAPA (1) prevents reoxidation with DTNB, (2) is reversible with DMPS, and (3) protects against irreversible alkylation by BAC. In Torpedo receptors, the EC50 of protection against BAC alkylation with APA or BAPA is approximately 30 nM. APA arsenylation of Torpedo receptors persists up to 20 h, but can be reversed at any time with DMPS. These results suggest that heterobifunctional arsenicals could anchor labeling groups in the agonist binding site in order to map the agonist binding site, quantitate receptors, or purify and reconstitute functional receptors.

Acetylcholinesterase↗