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Biomedical subjects

J Meyers

Publications and source records attributed to J Meyers.

At least 19 recordsLinked to original sources
PubMed2001

Restricted growth of avirulent avian reovirus strain 2177 in macrophage derived HD11 cells.

The replication of two pathotypes of avian reovirus, 1733 and 2177 in transformed chicken lymphoid and myeloid cell lines was examined, showing that only the macrophage cell line, HD11, supports replication. The virulent strain 1733 causes a lytic infection producing 100-1000 fold more virus than the avirulent strain 2177. Cells infected with strain 2177 display delayed viral RNA and protein synthesis as well as a suppressed expression of the major capsid protein muB. These features may contribute to the lower virulence of the strain 2177 in their natural host in vivo.

Animals↗
PubMed2001

Interleukin-4 up-regulates mouse mammary tumor virus expression yet is not required for in vivo virus spread.

The mouse mammary tumor virus (MMTV) superantigen induces T-cell production of cytokines, such as interleukin-4, which in turn increase MMTV transcription. However, interleukin-4 is not required for in vivo virus spread, because mice lacking interleukin-4 or the STAT6 transcription factor showed wild-type infection of lymphoid and mammary tissue. In spite of this, mammary tumor incidence was decreased in STAT6 null mice.

Animals↗
PubMed2001

An instrument to measure musculoskeletal symptoms among immigrant Hispanic farmworkers: validation in the nursery industry.

We report on the construction and psychometrics of a survey measure of musculoskeletal symptomatology for use with Spanish-speaking immigrant farmworkers. Survey development included focus groups with workers, forward and backward translations, and pilot testing. The final survey includes a body diagram and items about symptom severity, frequency, and duration and about self-treatment, medical care, and job tasks. We report on the initial test of the survey with 213 commercial nursery workers in Southern California. Fifty-five percent of the workers reported pain, with 30% reporting back pain, 21% reporting upper extremity pain, 19% reporting lower extremity pain, and 10% reporting neck and shoulder pain. A composite symptom score exhibited acceptable test-retest reliability (r = 0.41, p < 0.01) over the annual agricultural cycle. Greater symptomatology was associated with greater frequency of self-treatment (r = 0.42, p < 0.01), seeking professional health care (t = 2.49, p < 0.05), and exposure to high-risk jobs (OR = 2.1, p < 0.05, CI = 1.0 to 4.4), supporting the validity of composite score.

Adolescent↗
PubMed2000

The psychiatric interview in the emergency department.

Psychiatric assessment of patients in the emergency department requires a psychological and medical approach. Acute medical problems must be investigated immediately, before a more nuanced exploration of emotional, cognitive, and behavioral aspects of these patients is undertaken. A multidimensional, nonreductive description then guides the treatment and disposition of patients in the emergency department.

Diagnosis, Differential↗
PubMed1999

Mutations in the KCNQ4 gene are responsible for autosomal dominant deafness in four DFNA2 families.

We have previously found linkage to chromosome 1p34 in five large families with autosomal dominant non-syndromic hearing impairment (DFNA2). In all five families, the connexin31 gene ( GJB3 ), located at 1p34 and responsible for non-syndromic autosomal dominant hearing loss in two small Chinese families, has been excluded as the responsible gene. Recently, a fourth member of the KCNQ branch of the K+channel family, KCNQ4, has been cloned. KCNQ4 was mapped to chromosome 1p34 and a single mutation was found in three patients from a small French family with non-syndromic autosomal dominant hearing loss. In this study, we have analysed the KCNQ4 gene for mutations in our five DFNA2 families. Missense mutations altering conserved amino acids were found in three families and an inactivating deletion was present in a fourth family. No KCNQ4 mutation could be found in a single DFNA2 family of Indonesian origin. These results indicate that at least two and possibly three genes responsible for hearing impairment are located close together on chromosome 1p34 and suggest that KCNQ4 mutations may be a relatively frequent cause of autosomal dominant hearing loss.

Amino Acid Sequence↗
PubMed1998

A single nucleotide polymorphism in the matrix metalloproteinase-1 promoter creates an Ets binding site and augments transcription.

Matrix metalloproteinases (MMPs) facilitate cellular invasion by degrading the extracellular matrix, and their regulation is partially dependent on transcription. Binding sites for members of the Ets family of transcription factors are present within MMP promoters and are potent positive regulators. We report a single nucleotide polymorphism at -1607 bp in the MMP-1 promoter, where an additional guanine (G) creates an Ets binding site, 5'-GGA-3'. This polymorphism displays significantly higher transcription in normal fibroblasts and in melanoma cells than the 1 G polymorphism, and it binds substantially more nuclear extract and recombinant ETS-1. Analysis of control DNAs from the Center d'Etude du Polymorphisme Humain pedigrees reveals that this polymorphism is not a mutation, with a frequency of the 2 G polymorphism at 30%. In contrast, in eight tumor cell lines, this frequency increased to 62.5% (P < 0.0001). Thus, this MMP-1 polymorphism contributes to increased transcription, and cells expressing the 2 G polymorphism may provide a mechanism for more aggressive matrix degradation, thereby facilitating cancer progression.

Binding Sites↗
PubMed1997

Linkage analysis of progressive hearing loss in five extended families maps the DFNA2 gene to a 1.25-Mb region on chromosome 1p.

Thus far, 13 genes for autosomal dominant hearing loss have been localized to specific chromosomal regions, but none of the genes has been cloned. Only a single family has been linked to each of these loci, with the exception of DFNA2. DFNA2 was originally mapped in two extended families originating from Indonesia and the United States. In this study we report linkage to DFNA2 in three additional large families with autosomal dominant hearing loss from Belgium and The Netherlands. These five DFNA2 families show a similar progressive sensorineural hearing loss, starting in the high frequencies and also affecting the middle and low frequencies later in life. Combining the information from all linked families, the candidate region that is most likely to contain the DFNA2 gene was reduced to a 1.25-Mb region between markers D1S432 and MYCL1. Different haplotypes segregating with the hearing loss were found in all five families, suggesting that different mutations are present in the same gene. These results indicate that DFNA2 is most likely an important gene for autosomal dominant hearing loss.

Alleles↗
PubMed1997

Conduct disorder, substance dependence, and adolescent motherhood.

Of 26 teenage mothers in a nonclinical sample, one-third were found to have a diagnosis of conduct disorder; of these, two-thirds were also diagnosed with substance abuse or dependence. Conduct disorder as a risk factor for adolescent pregnancy and substance use is discussed, as are the implications for preventive intervention.

Adolescent↗
PubMed1997

Enhancement of compliance among patients with hypertension.

Studies of patient compliance with medical advice consistently demonstrate a high level of noncompliance. Not following recommendations can have serious negative consequences in the management of disease. This study was an assessment of the effect on compliance of a longitudinal, individualized educational program for patients with hypertension in a managed care setting. A before-and-after self-paired design was used to assess the behavior of 107 patients with hypertension. Trained nurses using an interactive interview format reinforced prescribed treatment and provided appropriate printed material to participants. Brief telephone follow-up interviews at prescribed intervals were used to elicit problems, provide additional education, and reinforce compliance behaviors. Most of the patients who participated showed a statistically significant (P < 0.01) decrease in both systolic and diastolic blood pressure. There was also an effect on various recommended behaviors, including compliance with medication taking, ideal body weight, salt restriction, stress, and exercise. A statistically significant relation existed between improved compliance with individual behavior changes and decreased blood pressure (P < 0.01). Elderly persons were particularly likely to show statistically significant reductions in blood pressure (75.4% versus 50.0%). A chi 2 test indicated that those differences were significant at the 0.01 level. A relatively inexpensive, office-based educational protocol can have a statistically significant effect on treatment compliance among patients with hypertension. The intervention has particular implications for geriatric patients, whose high blood pressure is disproportionately represented.

Adult↗
PubMed1996

Nosocomial infections with vancomycin-resistant Enterococcus faecium in liver transplant recipients: risk factors for acquisition and mortality.

The risk factors for acquisition of and mortality due to nosocomial infection with vancomycin-resistant Enterococcus faecium (VREF) in orthotopic liver transplant (OLT) recipients were studied at a tertiary care hospital; 32 VREF-infected OLT patients (cases) were compared with 33 randomly selected OLT recipients (controls). More antibiotics were administered preoperatively to cases (mean, 4 antibiotics per patient for 474 antibiotic-days) than to controls (mean, 1.8 antibiotics per patient for 131 antibiotic-days). Cases were more likely than controls to have received vancomycin therapy preoperatively and to have been hospitalized in the intensive care unit (ICU) preoperatively. Logistic regression revealed that the risk factors for acquisition of VREF infection were surgical reexploration and a prolonged stay in the surgical ICU postoperatively. In the cases, the risk factors for mortality were admission to the ICU preoperatively and hemodialysis. The mortality rate associated with polymicrobial bloodstream infections was 100% despite appropriate therapy. Sixteen and 18 cases received parenteral chloramphenicol and doxycycline, respectively, for treatment of VREF infection. There were no hematologic adverse effects attributed to chloramphenicol treatment. DNA analysis of selected E. faecium isolates suggested that infections were due to multiple clones. In summary, the source of VREF infection in OLT patients is the gastrointestinal tract. Antibiotic selective pressure may contribute to colonization. Infection with VREF is a predictor of morbidity and mortality in OLT patients.

Anti-Bacterial Agents↗
PubMed1995

The blue light-responsive AthH2 gene of Arabidopsis thaliana is primarily expressed in expanding as well as in differentiating cells and encodes a putative channel protein of the plasmalemma.

According to our previous studies the Arabidopsis gene AthH2 which is inducible by blue light and phytohormones codes for an intrinsic membrane protein. It bears a resemblance to several distinct channel proteins of plant and animal species classified as the MIP/NOD-26/GlpF family. In the present study biochemical analyses and electron microscopic immunochemistry were used to elucidate the subcellular location of the AthH2 protein. The results clearly demonstrate that it is an exclusive constituent of the plasmalemma. Furthermore, the expression of the AthH2 gene in transgenic Arabidopsis plants containing the promoter region of AthH2 fused to the beta-glucuronidase (gus) reporter gene was studied. The in situ localization of gus activity revealed that the specific promoter is temporally activated by light in expanding and/or differentiating cells comprising newly formed tissues and organs: root elongation zone, guard cells of stomata, vascular bundle sheaths, filaments of stamen and young siliques. Several sites of gus expression coincide spatially with those of in situ hybridization and the immunocytochemical reaction, respectively, suggesting that the AthH2 promoter had correctly responded to light as an important exogenous factor with relevance to the complex pattern of differentiation. Studies with protoplasts from plants transformed with an antisense construct revealed a water transport capacity of the AthH2 protein.

Arabidopsis↗
PubMed1994

The importance of social interaction: a new perspective on social epidemiology, social risk factors, and health.

Social epidemiology research has provided persuasive evidence of the link between the social environment--especially socioeconomic status--and health outcomes, but has failed to identify underlying mechanisms that might account for the association. The research may have been limited to date by its reliance on traditional epidemiological methods that emphasize a search for specific causal factor-disease relationships. It is time to take the research evidence and recast it to find practical solutions. We argue that the human development perspective supplies a framework for understanding the critical interaction between elements of social environment and health: Analyzing the social epidemiological research from this perspective can help to explain why and how the most potent factor, socioeconomic status, affects health outcomes. Equally important, this alternative perspective also presents health education practice implications.

Epidemiologic Methods↗
PubMed1993

Long-term follow-up of patients with invasive fungal disease who received adjunctive therapy with recombinant human macrophage colony-stimulating factor.

Mortality of bone marrow transplant (BMT) patients who develop invasive fungal infection is greater than 80%. Long-term follow-up of 46 consecutive BMT patients who received recombinant human macrophage colony-stimulating factor (rhM-CSF) as adjunctive therapy with standard antifungal treatment who were entered into phase I/II trials at The Fred Hutchinson Cancer Research Center is reported. rhM-CSF (100 micrograms/m2 to 2,000 micrograms/m2; Chiron/Cetus Corporation, Emeryville, CA) was administered from day 0 to 28 after determination of progressive fungal disease. Results of long-term follow-up of fungal infection, relapse, and survival were compared with 58 similar historical controls. Multivariable analysis of the patients who received rhM-CSF showed two factors that significantly correlated with poor survival: Karnofsky score < or = 20% and Aspergillus infection. Overall, survival of patients who received rhM-CSF was greater than that of historical patients (27% v 5%) and was entirely because of a 50% survival rate in patients with Candida infection and Karnofsky scores greater than 20%. Prospective, randomized, controlled trials to determine efficiency of rhM-CSF are indicated and should be directed at patients with invasive candidiasis.

Adult↗
PubMed1992

Activation-driven T cell death. II. Quantitative differences alone distinguish stimuli triggering nontransformed T cell proliferation or death.

Clonal deletion is the major mechanism by which T cell tolerance is achieved in vivo. The process of activation-driven cell death, originally characterized with T cell hybridomas, likely represents the mechanism of clonal deletion because it shares a number of properties with the in vivo process, especially the ability to be triggered in an Ag-specific manner, the cell-autonomous nature of the response, and its sensitivity to the drug cyclosporin A. We now have extended our analysis of activation-driven cell death to clonal populations of nontransformed T cells. Activation-driven cell death can be induced in nontransformed T lymphocytes by combinations of mitogenic stimuli. In particular, two mitogenic stimuli at high dose, one a lymphokine and the other delivered via the TCR or another activation structure, are required to induce activation-driven cell death. Activation-driven cell death is an active cell suicide process with attributes typical of physiological cell death, including early nuclear disintegration and a requirement for macromolecular synthesis, and is distinct from death by factor deprivation. Susceptibility to the induction of cell death by antigenic or activating stimulation is a common aspect of most T cells and is consistent with observations that clonal deletion can occur throughout T cell ontogeny. Most importantly, the alternative cellular responses of cell death and cell proliferation in nontransformed T cells appear to be triggered solely as a function of quantitative differences in the doses of identical stimuli. This can be viewed as a dose-dependent switch that determines cell fate. Developmental regulation of this switch may explain the processes of positive and negative selection during T cell ontogeny and also provide a mechanistic rationale for a strategy of selective anti-tumor therapy.

Animals↗
PubMed1992

Susceptibility to cell death is a dominant phenotype: triggering of activation-driven T-cell death independent of the T-cell antigen receptor complex.

The failure of Thy-1 and Ly-6 to trigger interleukin-2 production in the absence of surface T-cell antigen receptor complex (TCR) expression has been interpreted to suggest that functional signalling via these phosphatidylinositol-linked alternative activation molecules is dependent on the TCR. We find, in contrast, that stimulation of T cells via Thy-1 or Ly-6 in the absence of TCR expression does trigger a biological response, the cell suicide process of activation-driven cell death. Activation-driven cell death is a process of physiological cell death that likely represents the mechanism of negative selection of T cells. The absence of the TCR further reveals that signalling leading to activation-driven cell death and to lymphokine production are distinct and dissociable. In turn, the ability of alternative activation molecules to function in the absence of the TCR raises another issue: why immature T cells, thymomas, and hybrids fail to undergo activation-driven cell death in response to stimulation via Thy-1 and Ly-6. One possibility is that these activation molecules on immature T cells are defective. Alternatively, susceptibility to activation-driven cell death may be developmentally regulated by TCR-independent factors. We have explored these possibilities with somatic cell hybrids between mature and immature T cells, in which Thy-1 and Ly-6 are contributed exclusively by the immature partner. The hybrid cells exhibit sensitivity to activation-driven cell death triggered via Thy-1 and Ly-6. Thus, the Thy-1 and Ly-6 molecules of the immature T cells can function in a permissive environment. Moreover, with regard to susceptibility to Thy-1 and Ly-6 molecules of the immature T cells can function in a permissive environment. Moreover, with regard to susceptibility to Thy-1 and Ly-6 triggering, the mature phenotype of sensitivity to cell death is genetically dominant.

Animals↗
PubMed1992

Genome digestion is a dispensable consequence of physiological cell death mediated by cytotoxic T lymphocytes.

We examined virally transformed murine fibroblast clones as targets for cytotoxic T lymphocyte (CTL)-triggered lysis and genome digestion. Strikingly, while all clones were essentially equivalent in the ability to be lysed, one clone, SV3T3-B2.1, failed to exhibit genome digestion associated with CTL attack. Other aspects of the physiological cell death process, including loss of adhesion and nuclear envelope breakdown (lamin phosphorylation and solubilization), were not altered in this clone. The absence of genome digestion associated with CTL-induced cell death correlated with the absence of endodeoxyribonuclease activity in the nuclei of that clone. Characterization of the activity affected identifies a calcium-dependent, DNase I-like endonuclease of approximately 40 kDa, normally present constitutively in all cell nuclei, as the enzyme responsible for genome digestion associated with CTL-mediated cell death. These observations indicate that neither genome digestion per se nor its consequences [such as activation of poly(ADP-ribose) polymerase] are essential for cell death resulting from the triggering of this cell suicide process.

Animals↗