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L Davis

Publications and source records attributed to L Davis.

At least 73 records · Page 4Linked to original sources
PubMed1999

Surveillance of work-related asthma in selected U.S. states using surveillance guidelines for state health departments--California, Massachusetts, Michigan, and New Jersey, 1993-1995.

PROBLEM/CONDITION: Cases of work-related asthma (WRA) are sentinel health events that indicate the need for preventive intervention. WRA includes new-onset asthma caused by workplace exposure to sensitizers or irritants and preexisting asthma exacerbated by workplace exposures. REPORTING PERIOD: This report reviews cases of WRA identified by state health departments from January 1, 1993, through December 31, 1995, as well as follow-up investigations of cases and associated workplaces conducted through June 30, 1998. DESCRIPTION OF THE SYSTEMS: State-based surveillance and intervention programs for WRA are conducted in California, Massachusetts, Michigan, and New Jersey as part of the Sentinel Event Notification Systems for Occupational Risks (SENSOR) cooperative agreement program, initiated by CDC's National Institute for Occupational Safety and Health (NIOSH). RESULTS: From 1993 through 1995, a total of 1,101 cases of WRA were identified by SENSOR surveillance staff members in California, Massachusetts, Michigan, and New Jersey. Of these 1,101 cases, 19.1% were classified as work-aggravated asthma, and 80.9% were classified as new-onset asthma. Objective evidence substantiating asthma work-relatedness was documented in the medical records of 3.4% of WRA cases identified in the two states (Michigan and New Jersey) where medical records are routinely reviewed for this information. Indoor air pollutants, dusts, cleaning materials, lubricants (e.g., metalworking fluids), and diisocyanates were among the most frequently reported causes of WRA. In addition, a well-recognized cause of occupational asthma - natural rubber latex - was identified in a new setting, the healthcare industry. The most common industries associated with WRA cases included transportation equipment manufacturing (19.3%), health services (14.2%), and educational services (8.7%). Air sampling for agents known to induce occupational asthma was performed in Michigan for comparison with established federal time-weighted average exposure limits. Sixteen (13.4%) of 119 workplaces tested had airborne concentrations exceeding NIOSH recommended exposure limits (RELs); 11 (9.1%) of 121 workplaces had concentrations exceeding permissible exposure limits (PELs) of the Michigan Occupational Safety and Health Act (MIOSHA) program. INTERPRETATION: The surveillance data findings confirm well-recognized causes of asthma and have identified new putative causes (e.g., cleaning materials and metalworking fluids). Because the surveillance program depends on physicians' recognizing asthma work-relatedness and reporting diagnosed cases, the data are considered an underestimate of the magnitude of the WRA problem. The data also indicate that physicians are not commonly performing objective physiologic tests to substantiate a WRA diagnosis. Workplace findings suggest a need to evaluate existing exposure standards for specific agents known to induce occupational asthma (e.g., diisocyanates). Case-based surveillance can help improve the recognition, control, and prevention of WRA. The SENSOR model also provides a mechanism for workers and physicians to request workplace investigations aimed at primary prevention for other workers. PUBLIC HEALTH ACTION: NIOSH and state health department representatives are working to establish a long-term agenda for state-based surveillance of work-related conditions and hazards. The results from the SENSOR WRA programs described in this report support inclusion of WRA as a priority condition warranting surveillance at the state level.

Asthma↗
PubMed1999

Allelic loss on chromosome 6Q in primary prostate cancer.

Molecular genetic analyses of human prostate cancer (CaP) has revealed frequent loss of specific chromosome regions suggesting the presence of putative tumor suppressor gene(s) (TSG) on these chromosome loci whose inactivation may play a role in prostate tumorigenesis. To understand the role of 6q alterations in CaP, we have undertaken a comprehensive analysis of proximal 6q. Genomic DNA from tumor and normal prostate tissues from radical prostatectomy specimens of 38 patients were analyzed by polymerase chain reaction (PCR) for 13 polymorphic microsatellite loci on 6q. Allelic losses of 1 or more polymorphic loci were detected in 11 of 38 patients (29%). Six of 11 tumors showing any 6q deletion were found to have allelic losses at D6S1056 and D6S300 loci. Our results revealed a 1.5 megabase interval between D6S1056 and D6S300 at 6q16.3-21 as the minimal region of deletion, which may contain the putative TSG involved in prostate tumorigenesis. One of the tumor samples demonstrated homozygous deletion at a distal location D6S314 (6q23-24), suggesting another locus potentially associated with CaP. Although the relationship of 6q loss of heterozygosity (LOH) with various clinico-pathologic variables, i.e., cancer recurrence or pathologic stage, did not reveal a statistically significant association, the risk for 6q LOH to non-organ confined (pT3) disease was 5-fold higher than for organ confined disease.

Adult↗
PubMed1999

Clinical value of mammography for symptomatic women 35 years of age and younger.

OBJECTIVE: This retrospective observational study was designed to answer the following question: Is mammography clinically effective in the evaluation of women </=35 years old with breast symptoms or findings. STUDY DESIGN: A retrospective review was undertaken of 1908 consecutive initial mammogram reports of symptomatic women </=35 years old who came to a referral breast clinic. The clinic records were analyzed for the working diagnoses and management plans before and after the input of the initial mammogram reports. RESULTS: Of the 4160 initial mammograms of women who came (1992-1995) to the Breast Diagnostic Center at Women's and Children Hospital, Los Angeles, Calif, 1908 were of women </=35 years old. The mammogram reports were reviewed and tabulated by age group for mammography recommendations. The working diagnoses and management plans in the center's charts were retrospectively evaluated before and after the mammogram reports to ascertain whether the mammogram reports altered clinical management in this patient population and age group. No clinically unsuspected cancers were perceived by mammography performed at the center in women </=35 years old. (All of the 23 invasive cancers were palpable and had prior diagnoses after fine-needle aspiration biopsy.) The initial mammogram reports did not change the working diagnosis or clinical management of these cases in this patient population and clinic setting. Ultrasonography was recommended by the radiologists in 37% of the study cases. CONCLUSIONS: Routine initial mammography was not cost-effective or clinically beneficial in the evaluation of breast symptoms or findings and management of the cases of women </=35 years old who came to our center.

Adenocarcinoma↗
PubMed1999

Do heavy smokers benefit from higher dose nicotine patch therapy?

Heavy smokers (N = 408, smoking more than 25 cigarettes/day) were randomized to receive high-dose (25 mg) or standard-dose (15 mg) nicotine patch therapy delivered during the daytime only (16 hr) for a period of 6 weeks. Treatment effects of each dose were similar. The percentages of participants not smoking at 2-, 6-, and 12-month follow-ups were 26 versus 20, 14 versus 16, and 14 versus 14 for the 15-mg and 25-mg doses, respectively. The higher dose was well tolerated, and adverse event profiles for both treatment doses were very similar. Stepwise Cox proportional hazards analyses indicated that initial postrandomization craving and baseline scores on the Center for Epidemiological Studies Depression Instrument predicted time-to-relapse during treatment; only initial craving predicted relapse over the entire study interval (12 months). The results of this trial do not support the routine use of higher dose nicotine patch therapy in the treatment of nicotine dependence.

Administration, Cutaneous↗
PubMed1999

Expression of peroxisome proliferator-activated receptor gamma (PPARgamma) in human transitional bladder cancer and its role in inducing cell death.

The present study examined the expression and role of the thiazolidinedione (TZD)-activated transcription factor, peroxisome proliferator-activated receptor gamma (PPARgamma), in human bladder cancers. In situ hybridization shows that PPARgamma mRNA is highly expressed in all human transitional epithelial cell cancers (TCCa's) studied (n=11). PPARgamma was also expressed in five TCCa cell lines as determined by RNase protection assays and immunoblot. Retinoid X receptor alpha (RXRalpha), a 9-cis-retinoic acid stimulated (9-cis-RA) heterodimeric partner of PPARgamma, was also co-expressed in all TCCa tissues and cell lines. Treatment of the T24 bladder cancer cells with the TZD PPARgamma agonist troglitazone, dramatically inhibited 3H-thymidine incorporation and induced cell death. Addition of the RXRalpha ligands, 9-cis-RA or LG100268, sensitized T24 bladder cancer cells to the lethal effect of troglitazone and two other PPAR- activators, ciglitazone and 15-deoxy-delta(12,14)-PGJ2 (15dPGJ(2)). Troglitazone treatment increased expression of two cyclin-dependent kinase inhibitors, p21(WAF1/CIP1) and p16(INK4), and reduced cyclin D1 expression, consistent with G1 arrest. Troglitazone also induced an endogenous PPARgamma target gene in T24 cells, adipocyte-type fatty acid binding protein (A-FABP), the expression of which correlates with bladder cancer differentiation. In situ hybridization shows that A-FABP expression is localized to normal uroepithelial cells as well as some TCCa's. Taken together, these results demonstrate that PPARgamma is expressed in human TCCa where it may play a role in regulating TCCa differentiation and survival, thereby providing a potential target for therapy of uroepithelial cancers.

Alitretinoin↗
PubMed1999

Effect of Withania somnifera on cytokine production in normal and cyclophosphamide treated mice.

Administration of an extract from the powdered root of the plant Withania somnifera (Family: Solanaceae) enhanced the levels of Interferon gamma (IFN-gamma) (75.87 pg/ml), Interleukin-2 (IL-2) (14.16 pg/ml) and Granulocyte macrophage colony stimulating factor (GM-CSF) (49.22 pg/ml) in normal Balb/c mice. The lowered levels of IFN gamma--(30 pg/ml), IL-2 (4.5 pg/ml) and GM-CSF (19.12 pg/ml) after treatment with cyclophosphamide (CTX) was reversed by the administration of Withania somnifera extract (IFN gamma--74 pg/ml; IL-2 7.5 pg/ml; GM-CSF 35.47 pg/ml). Withania extract lowered the levels of Tumour necrosis factor alpha (TNF alpha) production. Administration of bonemarrow cells from donor mice treated with Withania extract increased the spleen nodular colonies in irradiated mice (8.33) compared to those treated with normal bonemarrow cells (3.03). The number of nodular colonies increased significantly when these animals were continued with Withania extract treatment. These results indicate the immunopotentiating and myeloprotective effect of Withania somnifera as seen from the enhancement of cytokine production and stem cell proliferation and its differentiation.

Animals↗
PubMed1999

Endothelin B receptor modulates inflammatory pain and cutaneous inflammation.

The role of endothelin B (ET(B)) receptors in inflammation and nociception was examined using ET(B) receptor knockout mice. Genotyping studies were used with tissues from ET(B)((+/+)), ET(B)((+/-)), and ET(B)((-/-)) mice to confirm the loss of ET(B) receptors. Algesia induced by phenylbenzoquinone was evident in the (+/+) mice, reduced by approximately 80% in the (+/-) mice, and absent in the (-/-) mice. Phenylbenzoquinone-induced algesia in (+/+) mice was inhibited 74% by the ET(B) receptor-selective antagonist A192621 (25 mg/kg p.o.), but unaffected by the ET(A) receptor-selective antagonist SB 234551 (25 mg/kg p.o.). Noninflammatory pain, induced by hotplate, was equivalent between (+/+) and (-/-) mice. The cutaneous inflammatory response to topical arachidonic acid (AA) also was evaluated. Whereas (+/+) mice had a marked inflammatory response to AA, the (+/-), and (-/-) mice had significantly reduced fluid phase responses (37 and 65% inhibition, respectively). Neutrophil infiltration also was reduced in the (+/-) and (-/-) mice (51 and 65% reduction, respectively). Topical administration of A192621 (500 microg/ear) in (+/+) mice inhibited AA-induced swelling (39%), whereas SB 234551 (500 microg/ear) was without effect. Collectively, these results implicate the ET(B) receptor in mediation of inflammatory pain and cutaneous inflammatory responses in mice.

Animals↗
PubMed1998

Prostaglandin E2 inhibits renal collecting duct Na+ absorption by activating the EP1 receptor.

PGE2 exerts potent diuretic and natriuretic effects on the kidney. This action is mediated in part by direct inhibition of collecting duct Na+ absorption via a Ca++-coupled mechanism. These studies examine the role the Ca++-coupled PGE-E EP1 receptor plays in mediating these effects of PGE2 on Na+ transport. Rabbit EP1 receptor cDNA was amplified from rabbit kidney RNA. Nuclease protection assays demonstrated highest expression of EP1 mRNA in kidney, followed by stomach, adrenal, and ileum. In situ hybridization, demonstrated renal expression of EP1 mRNA was exclusively over the collecting duct. In fura-2-loaded microperfused rabbit cortical collecting duct, EP1 active PGE analogs were 10-1, 000-fold more potent in raising intracellular Ca++ than EP2, EP3, or EP4-selective compounds. Two different EP1 antagonists, AH6809 and SC19220, completely blocked the PGE2-stimulated intracellular calcium increase. AH6809 also completely blocked the inhibitory effect of PGE2 on Na+ absorption in microperfused rabbit cortical collecting ducts. These studies suggest that EP1 receptor activation mediates PGE2-dependent inhibition of Na+ absorption in the collecting duct, thereby contributing to its natriuretic effects.

Absorption↗
PubMed1998

Cardiac hypertrophy in chronically anemic fetal sheep: Increased vascularization is associated with increased myocardial expression of vascular endothelial growth factor and hypoxia-inducible factor 1.

OBJECTIVE: Our purpose was to determine whether the increase in fetal cardiac mass and cardiac output in chronic anemia is accompanied by changes in capillary density or size or changes in levels of vascular endothelial growth factor and hypoxia-inducible factor 1, a basic helix-loop-helix transcription factor that has previously been shown to activate vascular endothelial growth factor gene transcription when cultured cells are subjected to hypoxia. STUDY DESIGN: Anemia was induced in near-term ovine fetuses by daily isovolemic hemorrhage. In five fetuses the heart was arrested in diastole, isolated, and fixed at physiologic pressures with adenosine-paraformaldehyde, and morphometric measurements of capillaries were made. In six fetuses cardiac expression of vascular endothelial growth factor and hypoxia-inducible factor 1 protein was detected by Western analysis and vascular endothelial growth factor messenger ribonucleic acid by Northern blot analysis. Eleven age-matched fetuses served as controls. RESULTS: The anemic fetuses compared with controls had a lower hematocrit (14.8% +/- 0.7% vs 35.3% +/- 1.5%) and a greater heart-to-body weight ratio (10.5 +/- 1.1 vs 7.7 +/- 0.5 gm/kg). The minimal capillary diameter was increased and the intercapillary distance was decreased in both right and left ventricles of anemic fetuses compared with controls. Vascular endothelial growth factor protein was increased 4.5-fold, vascular endothelial growth factor messenger ribonucleic acid 3.2-fold, and hypoxia-inducible factor 1alpha protein 3.8-fold in ventricular tissue from anemic fetuses. CONCLUSIONS: In chronic fetal anemia cardiac hypertrophy is accompanied by anatomic changes in myocardial capillary morphometry along with induction of hypoxia-inducible factor 1 and vascular endothelial growth factor. These results provide evidence for a pathway by which anemia-hypoxia may stimulate myocardial vascularization.

Anemia↗
PubMed1998

Suppressive effect of cyclophosphamide-induced toxicity by Withania somnifera extract in mice.

Administration of Withania somnifera extract (Solanaceae) was found to significantly reduce leucopenia induced by cyclophosphamide (CTX) treatment. The total WBC count on the 12th day of the CTX-treated group was 3720 cells/mm3 and that of CTX along with Withania was 6120 cells/mm3. Treatment of Withania along with CTX was found to significantly (P < 0.001) increase the bone marrow cellularity (13.1 x 10(6) cells/femur) compared to CTX alone treated group (8 x 10(6) cells/femur). Administration of Withania extract increased the number of alpha-esterase positive cells (1130/4000 cells) in the bone marrow of CTX treated animals, compared to the CTX-alone treated group (687/4000 cells). The major activity of Withania somnifera may be the stimulation of stem cell proliferation. These studies indicate that Withania somnifera could reduce the cyclophosphamide induced toxicity and its usefulness in cancer therapy.

Animals↗
PubMed1998

Yeast meiotic mutants proficient for the induction of ectopic recombination.

A screen was designed to identify Saccharomyces cerevisiae mutants that were defective in meiosis yet proficient for meiotic ectopic recombination in the return-to-growth protocol. Seven mutants alleles were isolated; two are important for chromosome synapsis (RED1, MEK1) and five function independently of recombination (SPO14, GSG1, SPOT8/MUM2, 3, 4). Similar to the spoT8-1 mutant, mum2 deletion strains do not undergo premeiotic DNA synthesis, arrest prior to the first meiotic division and fail to sporulate. Surprisingly, although DNA replication does not occur, mum2 mutants are induced for high levels of ectopic recombination. gsg1 diploids are reduced in their ability to complete premeiotic DNA synthesis and the meiotic divisions, and a small percentage of cells produce spores. mum3 mutants sporulate poorly and the spores produced are inviable. Finally, mum4-1 mutants produce inviable spores. The meiotic/sporulation defects of gsg1, mum2, and mum3 are not relieved by spo11 or spo13 mutations, indicating that the mutant defects are not dependent on the initiation of recombination or completion of both meiotic divisions. In contrast, the spore inviability of the mum4-1 mutant is rescued by the spo13 mutation. The mum4-1 spo13 mutant undergoes a single, predominantly equational division, suggesting that MUM4 functions at or prior to the first meiotic division. Although recombination is variably affected in the gsg1 and mum mutants, we hypothesize that these mutants define genes important for aspects of meiosis not directly related to recombination.

Alleles↗
PubMed1998

Yeast dom34 mutants are defective in multiple developmental pathways and exhibit decreased levels of polyribosomes.

The DOM34 gene of Saccharomyces cerevisiae is similar to genes found in diverse eukaryotes and archaebacteria. Analysis of dom34 strains shows that progression through the G1 phase of the cell cycle is delayed, mutant cells enter meiosis aberrantly, and their ability to form pseudohyphae is significantly diminisehd. RPS30A, which encodes ribosomal protein S30, was identified in a screen for high-copy suppressors of the dom34delta growth defect. dom34delta mutants display an altered polyribosome profile that is rescued by expression of RPS30A. Taken together, these data indicate that Dom34p functions in protein translation to promote G1 progression and differentiation. A Drosophila homolog of Dom34p, pelota, is required for the proper coordination of meiosis and spermatogenesis. Heterologous expression of pelota in dom34delata mutants restores wild-type growth and differentiation, suggesting conservation of function between the eukaryotic members of the gene family.

Amino Acid Sequence↗
PubMed1997

Nicotine patch and self-help video for cigarette smoking cessation.

A total of 424 smokers were randomized in a 2 x 2 factorial experiment. A pharmacologic factor contained 2 levels: transdermal nicotine path (TNP; 21 mg) and placebo. A self-help behavioral treatment factor contained 2 levels: video-enhanced self-help treatment manual and self-help treatment manual only. At 2 months, TNP produced a higher level of abstinence (36%) than placebo (20%), p < .001. No other comparison was significant. In secondary analyses, (at 2 months) and compliance with patch treatment regimen (at 2, 6, and 12 months) were associated with less relapse. Although nicotine replacement therapy has improved our ability to produce smoking cessation, the production of sustained, longer term abstinence remains an elusive goal.

Administration, Cutaneous↗
PubMed1997

Vertebral osteomyelitis due to Pseudallescheria boydii.

A case of primary vertebral osteomyelitis due to an opportunistic fungus, Pseudallescheria boydii, in a child with acute myeloid leukemia, is reported. To our knowledge this is the first such case in a child, and only the second reported case in the international literature of primary spinal osteomyelitis due to this organism. We discuss the problems presented by this case both in terms of diagnosis and management. We also discuss the role of surgery and systemic antifungal chemotherapy in the treatment of deep infections due to Pseudallescheria boydii.

Child, Preschool↗
PubMed1997

Micronuclei containing whole chromosomes harbouring the selectable gene do not lead to mutagenesis.

Loss of heterozygosity is one genetic change observed in many tumours. We do not know whether the loss of chromosomal material through micronucleus formation is a viable mechanism associated with, and possibly leading to, genetic disease. Previously, we treated L5178Y mouse lymphoma cells with four aneugens. Although these aneugens induced micronuclei containing predominantly whole chromosomes, they did not induce mutations at Tk1, the selectable gene, under the same non-toxic conditions in which they induced micronuclei. This suggested that the induction of micronuclei containing whole chromosomes was not an early event leading to phenotypically expressed mutations in these cells under the conditions used. However, it is possible that chromosome 11, on which Tk1 resides, may be under-represented in the micronucleus population. To find out the frequency of induction of micronuclei containing chromosome 11, we applied fluorescence in situ hybridization using a chromosome 11 paint to micronuclei induced by colcemid and vinblastine. We found that the numbers of micronuclei containing chromosome 11 are more than sufficient to be detectable as mutations if these micronuclei lead to viable mutants. We conclude that the formation of micronuclei containing whole chromosomes does not lead to viable, dividing mutants in this system.

Animals↗