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Biomedical subjects

C Beall

Publications and source records attributed to C Beall.

At least 19 recordsLinked to original sources
PubMed2006

Cancer incidence among semiconductor and electronic storage device workers.

AIMS: To evaluate cancer incidence among workers at two facilities in the USA that made semiconductors and electronic storage devices. METHODS: 89 054 men and women employed by International Business Machines (IBM) were included in the study. We compared employees' incidence rates with general population rates and examined incidence patterns by facility, duration of employment, time since first employment, manufacturing era, potential for exposure to workplace environments other than offices and work activity. RESULTS: For employees at the semiconductor manufacturing facility, the standardised incidence ratio (SIR) for all cancers combined was 81 (1541 observed cases, 95% confidence interval (CI) 77 to 85) and for those at the storage device manufacturing facility the SIR was 87 (1319 observed cases, 95% CI 82 to 92). The subgroups of employees with > or =15 years since hiring and > or =5 years worked had 6-16% fewer total incidents than expected. SIRs were increased for several cancers in certain employee subgroups, but analyses of incidence patterns by potential exposure and by years spent and time since starting in specific work activities did not clearly indicate that the excesses were due to occupational exposure. CONCLUSIONS: This study did not provide strong or consistent evidence of causal associations with employment factors. Data on employees with long potential induction time and many years worked were limited. Further follow-up will allow a more informative analysis of cancer incidence that might be plausibly related to workplace exposures in the cohort.

Adult↗
PubMed2001

Mortality among employees at a petrochemical research facility.

BACKGROUND: This retrospective follow-up study evaluated mortality during 1970-1996 among 6,956 employees at a petrochemical research facility in Illinois. METHODS: Standardized mortality ratios (SMRs) compared employees' mortality rates with those of the Illinois general population. Poisson regression procedures estimated rate ratios for various subject subgroups compared to other facility employees. RESULTS: Subjects had 267 observed/524 expected deaths (SMR = 51) from all causes combined and a large deficit of deaths from all cancers (76/136, SMR = 56) and from most other major diseases. Other results included fewer than expected brain cancers (1/4.0, SMR = 25) and a slight increase in colorectal cancer (20/14, SMR = 139) that was concentrated in white male scientists employed for one of the three main companies at the facility (SMR = 295, RR = 2.6). CONCLUSIONS: The deficit of brain cancer deaths contrasts with an excess incidence seen in a companion study. Subjects' generally favorable mortality experience probably reflects socioeconomic advantages of employees relative to the Illinois general population.

Adult↗
PubMed2001

Cancer incidence among employees at a petrochemical research facility.

This investigation evaluated cancer incidence among workers at a petrochemical research facility in Illinois. A cluster of brain cancer and other intracranial tumors had occurred at the facility before the study began. The subjects were 5641 people who had worked at the facility from 1970 through 1996 and who had lived in Illinois at any time between 1986 and 1997. Data on cancer cases came primarily from the Illinois State Cancer Registry. Analyses compared the 1986-to-1997 cancer incidence rates of employees with Illinois general population rates. Subjects had 18% fewer than expected total cancers (125 observed/153 expected cases; standardized incidence ratio [SIR], 82; 95% confidence interval [CI], 68 to 98), which was primarily attributed to a large deficit of lung cancer (10/26; SIR, 39; CI, 19 to 72). Brain cancer was increased in the overall study group (6/2.7; SIR, 222; CI, 81 to 484). This excess was restricted to white men who were scientists or technicians for one of the three companies at the facility (6/0.8; SIR, 750; CI, 275 to 1633); all cases in this group had worked in the "500 building complex" (6/0.6; SIR, 968; CI, 355 to 2106). Subjects also had an increased incidence of thyroid cancer (7/2.6; SIR, 265; CI, 106 to 546) that was not concentrated in particular occupational or building groups. The brain cancer incidence patterns indicated that an unidentified occupational exposure might have been responsible for the excess. Chance, socioeconomic factors leading to better case detection in facility employees than in the general population, and confounding by potential nonoccupational risk factors are plausible explanations of the observed increase in thyroid cancer.

Adult↗
PubMed2001

Cancer and benign tumor incidence among employees in a polymers research complex.

The detection of several intracranial tumors among employees in one building complex (C500) at a petrochemical research facility prompted investigation of a possible workplace cause. This retrospective follow-up study included 1847 subjects, of whom 1735 had worked in C500. Medical records, death certificates, and Illinois State Cancer Registry data confirmed self-reported cancers and tumors. Analyses compared the subjects' cancer and benign intracranial tumor incidence rates with national general population rates. C500 employees had 15% fewer than expected total cancers (92 observed/108 expected; standardized incidence ratio [SIR], 85; 95% confidence interval [95% CI], 69 to 104). An excess of brain cancer (6/2.0; SIR, 302; 95% CI, 111 to 657) was concentrated among white men who had 10 or more years since hire and 5 or more years of C500 employment (4/0.7; SIR, 602; 95% CI, 165 to 1552) and who had worked in a particular building of C500 (5/0.7; SIR, 735; 95% CI, 239 to 1716). An excess of benign intracranial tumors (6/1.6; SIR, 385; 95% CI, 142 to 839) was not restricted to a single type of tumor and was not concentrated in any particular building. Occupational exposure may have caused the increased rate of brain cancer but is a less likely explanation for the elevated rate of benign intracranial tumors.

Adult↗
PubMed2001

Case-control study of intracranial tumors among employees at a petrochemical research facility.

This case-control study evaluated the relation between potential exposure to chemical and physical agents and the occurrence of intracranial tumors among employees at a petrochemical research facility. Cases were employees with glioma (n = 6) or benign intracranial tumors (n = 6). Controls (n = 119) were individually matched to cases on gender and birth year, and they were alive and did not have an intracranial tumor at the case's diagnosis date. Exposure information came from interviews with subjects or surrogates and from corporate records on agents used in research projects. Analyses computed matched odds ratios (ORs) and corresponding 95% confidence intervals (CIs) for self-reported exposure to 15 agents and project-based estimates of exposure to 29 agents. For gliomas, the OR was elevated for self-reported exposure to ionizing radiation (OR, 15.7; CI, 1.4 to 179.4), n-hexane (OR, infinity; CI, 1.4 to infinity), organometallics (OR, 9.4; CI, 1.5 to 59.7), and amines other than nitrosamines (OR, 6.0; CI, 1.0 to 35.7). The OR also was elevated for project-based potential use of ionizing radiation (OR, 9.6; CI, 1.7 to 55.2) and for potential use of n-hexane lasting at least 4 years (OR, 16.2; CI, 1.1 to 227.6). For benign intracranial tumors, the OR was elevated only for self-reported exposure to ionizing radiation (OR, 5.4; CI, 1.7 to 43.1) and other amines (OR, 5.2; CI, 0.9 to 29.5). Occupational exposure may have contributed to the glioma excess, but the specific causal agents remain unknown. The study indicated that benign intracranial tumors were unlikely to be work-related.

Adult↗
PubMed1999

Case-series investigation of intracranial neoplasms at a petrochemical research facility.

BACKGROUND: From 1970 through 1997, 17 intracranial neoplasms were identified among 6,800 employees of a petrochemical research facility. This investigation describes the case-series. METHODS: The intracranial neoplasms were identified by self reports and record linkages, and were confirmed by medical records and a pathology review. Standardized incidence ratios (SIRs) compare observed and expected numbers of cases according to certain work characteristics. RESULTS: Overall, there were 17 observed and 10.5 expected intracranial neoplasms, including 11/4.7 benign intracranial tumors and 6/5.9 brain cancers. All brain cancers occurred among male research scientists or technicians. Four had worked at some time on the same floor of one building (SIR=12.6, 95% CI=3.4-32.1), and several had worked on a research project with at least one other brain cancer case. The benign intracranial neoplasm cases did not have common building assignments or work activities. CONCLUSIONS: The occurrence pattern of brain cancers, but not that of benign tumors, suggests a possible occupational etiology.

Adenoma↗
PubMed1996

Brain tumors among electronics industry workers.

We evaluated the relation between work experience in the United States operations of an electronics company and brain tumor mortality, focusing on video display terminal (VDT) development jobs. Subjects were 149 brain tumor cases and 591 matched controls selected from a company registry of all employees dying between 1975 and 1989. Company databases and interviews with company personnel constituted the basis for work histories, including information on whether subjects had held VDT development jobs. Subjects who worked at plants with hardware or VDT development operations had slightly but imprecisely elevated odds ratios (OR). The study found no meaningful association between VDT development work and brain tumor mortality. Other results included an elevated OR for 10 or more years of employment in engineering/technical jobs [OR = 1.7; 95% confidence interval (CI) = 1.0-3.0] or in programming jobs (OR = 2.8; 95% CI = 1.1-7.0). The OR for glioma for all subjects who had accrued 5 years of programming work 10 years before the case's death was 3.9 (95% CI = 1.2-12.4). These associations were limited in large part to one of four division groups. Also, only male programmers experienced an elevated OR. These patterns indicate that the associations may be due to chance, although unidentified causal exposures present in a subset of engineering/technical and programming jobs cannot be ruled out.

Adult↗
PubMed1995

Mortality patterns among women in the motor vehicle manufacturing industry.

This retrospective follow-up study evaluated the mortality experience of 11,271 women employed in a large motor vehicle manufacturing company in 1973. Company computerized personnel records were used to identify subjects and to obtain their employment histories. Follow-up through December 31, 1985, was conducted using company, state, and national data sources. The mortality rates of the cohort were compared with the rates of the U.S. general population of white or black women, adjusting for age and calendar time and using the standardized mortality ratio (SMR) as the measure of association. The overall mortality rate of the cohort was lower than the U.S. rate by 15% among whites (SMR = 85, 95% confidence interval (CI) = 78-93) and by 40% among blacks (SMR = 59, CI = 49-70). Among whites, the low mortality rate was due primarily to deficits of noncancer deaths, although a 32% deficit also was observed for breast cancer (SMR = 68, CI = 48-92). Black female workers had 40% fewer deaths than expected overall, and their all cancer SMR also was below expectation (SMR = 82, CI = 60-109). Despite evidence of a strong healthy worker effect among women in the motor vehicle manufacturing industry, the study found excesses of lung cancer among white women in assembly jobs (SMR = 158, CI = 107-226) and of pancreatic cancer among white assembly workers in upholstery and trim operations (SMR = 302, CI = 97-704).

Adult↗
PubMed1994

Cancer mortality among women employed in motor vehicle manufacturing.

This article summarizes published data on employment and cancer patterns in the motor vehicle manufacturing (MVM) industry and presents results from a new study of female MVM workers. Historically, female MVM employees worked primarily in aerospace; electric and electronic equipment manufacturing; and paint, plastic, and trim operations. Women are now moving into vehicle assembly and metal parts production. Investigations of cancer have focused on men and reported excesses of lung cancer in foundry operations, of gastrointestinal cancer in metal processing operations involving exposure to machining fluids, and of colorectal cancer in wood pattern making. Numbers of women were insufficient for a meaningful evaluation of their cancer patterns. A recent study found that white women employed at a MVM company, compared to the female general US population, had small excesses of lung cancer (standardized mortality ratio (SMR) = 1.26; 95% confidence interval (CI) = 0.96-1.63) and of colorectal cancer (SMR = 1.27, 95% CI = 0.87-1.78) and a deficit of breast cancer (SMR = 0.68, 95% CI = 0.48-0.92). The lung cancer increase was concentrated among women in assembly jobs (SMR = 1.58, 95% CI = 1.07-2.26); the colorectal cancer increase, among women in nonproduction jobs (SMR = 1.78, 95% CI = 0.97-2.98); and the breast cancer deficit, among women in production-related jobs (SMR = 0.60, 95% CI = 0.37-0.91). Further investigation is needed to determine if these patterns are due to the occupational environment and to clarify causes of cancer among women in the MVM industry.

Automobiles↗
PubMed1993

Ultrastructure of developing flight muscle in Drosophila. I. Assembly of myofibrils.

In order to evaluate the effects of specific mutations on sarcomere assembly and function in vivo, we describe the course of normal development of Drosophila indirect flight muscle (IFM) in staged pupae using electron microscopy. We find that no contractile assemblies remain in larval muscle remnants invaded by imaginal myoblasts, establishing that myofibrils in IFM assemble de novo. Stress-fiber-like structures or other template structures are not prominent before or during sarcomere assembly. By 42 hr pupation (eclosion approximately 112 hr), thick and thin filaments have appeared simultaneously in slender, interdigitated arrays between regularly spaced Z-bodies. Each tiny, uniformly striated myofibril forms within a "sleeve" of microtubules, and both microtubules and myofibrils are attached to the cell membrane at each end of the fiber from the initial stages of assembly. Later in pupation, the microtubule "sleeves" disassemble. Sarcomere number appears to remain constant. We saw no evidence that terminal sarcomeres are sites for addition of new sarcomeres or that Z-lines split transversely, producing new, very short sarcomeres. Rather, initial thick and thin filaments and sarcomeres are much shorter than adult length. Sarcomere length increases smoothly and coordinately from approximately 1.7 to approximately 3.2 microns, reflecting increase in filament lengths and indicating that myosin and actin molecules must be incorporated into filaments after sarcomere formation. Myofilaments are not seen scattered in the cytoplasm at any time, nor do we detect filaments that could be in the process of being "trolleyed" along myofibrils into positions of lateral register. Myofibril diameter increases uniformly from approximately 4-thick filaments to approximately 36-thick filaments across, by peripheral addition of myofilaments. At each successive stage, all sarcomeres in a fiber attained similar length and diameter. Initial thick filaments are solid but within several hours these and all subsequently assembled thick filaments appear hollow. Initial Z-bodies do not show any internal lattice and are more irregularly shaped than adult Z-discs.

Animals↗
PubMed1993

Ultrastructure of developing flight muscle in Drosophila. II. Formation of the myotendon junction.

Using ultra-thin section electron microscopy, the development of the myotendon junction (MTJ) of Drosophila indirect flight muscle (IFM) is described for the first time. The MTJ is a cell-cell junction between the IFM and epithelial tendon cells. The terminal Z-band of each myofibril forms a uniform junction with a tendon cell; each junction shows a precise sequence of folding and elaboration in which microtubule arrays in both cell types play a prominent role. Upon IFM/tendon cell contact (by approximately 32 hr pupation), numerous flat, focal dense plaques form between muscle and tendon cell membranes. In the muscle, transient arrays of microtubules, which will form "sleeves" around the developing myofibrils, delineate the perimeter of these focal plaques. Each of the dense plaques enlarges and develops into the modified terminal Z-band (MT-Z) of a myofibril, linking the thick and thin filaments of the highly ordered terminal sarcomere to the membrane via a dense feltwork. As these plaques develop into the MT-Z, the perimeter of each plaque advances, leaving the central region deeply indented. Between 50-75 hr pupation, secondary folds appear in each MTJ, and tendon cell microtubules that will form the tendon elements attach to specific dense sites on the secondary folds of the junctional membrane opposite the MT-Z. By 100 hr pupation, each MTJ develops numerous sharp folds, thereby tightly interdigitating the muscle and tendon cell. Amorphous density associated with the junctional membranes assumes a crystalline array that includes the membrane cytoskeletons of both cells and the extracellular matrix. At the end of pupation (approximately 112 hr), the final link between tendon cell and cuticle is formed as the tiny, dense-tipped microvilli in contact with the cuticle are replaced by extracellular tonofibrils, dense shafts that fill deep pits in the tendon cell and extend deeply into the cuticle. The tendon cell microtubules become bundled and decorated by fine "feather" filaments and the free ends of these microtubule bundles become linked to the membrane surrounding the pits.

Animals↗
PubMed1992

Isolation of a Drosophila gene encoding glutathione S-transferase.

We have isolated a Drosophila gene, DmGST-2, that encodes glutathione S-transferase, a homo- or heterodimeric enzyme thought to be involved in detoxification of xenobiotics, including known carcinogens. The encoded protein has a primary sequence that is more similar to mammalian placental and nematode GSTs than that of a previously described Drosophila GST gene, herein referred to as DmGST-1. We provide a physical map of the gene and show that it specifies at least two mRNAs, measuring 1.9 and 1.6 kb, which differ only in the lengths of their 3' untranslated regions. Both of the mRNAs are present during all developmental stages. In situ hybridization of the DmGST-2 gene to larval polytene chromosomes places it within the 53F subdivision of chromosome 2, and Southern blotting to chromosomal DNA indicates that the gene has no close relatives within the Drosophila genome. Our results make possible molecular genetic approaches for further elaborating the function of glutathione S-transferases in insect development and physiology, in the metabolism of plant toxins, and in conferring insecticide resistance.

Amino Acid Sequence↗
PubMed1992

Knowledge about aging and Alzheimer's disease among baccalaureate nursing students.

Alzheimer's disease (AD) is a debilitating disease that poses many physical, social, psychological, and management problems for family and professional caregivers. Nursing students' ability to meet this challenge was measured using Palmore's (1988) Facts on Aging Quiz, Version 2 (FAQ2) and the Alzheimer's Disease Knowledge (ADK) Test developed by Dieckmann, Zarit, Zarit, and Gatz (1988). No significant difference in ADK Test scores was found for students who had previous personal or educational experiences with AD. However, older students, seniors, and those who reported knowing more about AD had significantly better scores on the ADK Test. Knowledge about AD was not found to be related to knowledge of aging, and subjects as a group were found to exhibit a negative bias toward the elderly as measured by Palmore's FAQ2.

Adult↗
PubMed1991

From genes to tensile forces: genetic dissection of contractile protein assembly and function in Drosophila melanogaster.

Myofibrils, the contractile organelles of skeletal muscle, are highly ordered and precisely regulated actomyosin networks. Investigations of myofibril assembly are revealing the cellular mechanisms by which contractile components are arranged and regulated. In order to facilitate this research we have developed formal molecular genetics for myofibrillar proteins of Drosophila flight muscle. Presently, mutations can be used systematically to perturb or eliminate any of the classical myofibrillar proteins within these fibers, and the in vivo consequences can be conveniently evaluated using protein electrophoresis, electron microscopy, or by assaying flight performance. Here we review some recent progress.

Animals↗
PubMed1990

Drosophila melanogaster troponin-T mutations engender three distinct syndromes of myofibrillar abnormalities.

In vertebrates troponin complexes interact co-operatively with tropomyosin dimers to modulate skeletal muscle contraction. In order further to investigate troponin assembly and function in vivo, we are developing molecular genetic approaches. Here we report characterization of the gene that encodes Drosophila tropinin-T and analyses of muscle defects engendered by several mutant alleles. We found that the Drosophila troponin-T locus specifies at least three proteins having sequences similar to vertebrate troponin-T. All are significantly larger than any avian or mammalian isoforms, however, due to a highly acidic carboxy-terminal extension. Comparisons of the chromosomal arrangements of vertebrate and Drosophila troponin-T genes revealed that the location of one intron-exon boundary is conserved. This observation and the similarity of vertebrate and Drosophila troponin-T primary sequences suggest that the respective proteins are homologous, and that troponin-T pre-dates the divergence of vertebrate and invertebrate organisms. In situ hybridization of the Drosophila troponin-T gene to polytene chromosomes demonstrated that it resides within subdivision 12A of the X chromosome, precisely where upheld and indented thorax flight muscle mutations have been mapped previously. We determined the nucleotide sequences of troponin-T genes in five extant mutants. All have deleterious alterations, directly establishing that upheld and indented thorax muscle abnormalities are due to defective troponin-T. Two of the alleles, upheld2 and upheld3, apparently disrupt RNA splicing and eliminate most or all troponin-T from flight and jump muscles, while the remaining three alleles change the identities of single amino acids of troponin-T. Electron microscopy of mutant muscles revealed that the two null alleles eliminate thin filaments, except where they are bound by electron-dense material presumed to be Z-disc proteins. Two of the point mutations, upheld101 and indented thorax3, do not perturb assembly of myofibrils, but cause their degeneration within days after muscles begin to be utilized. The final mutation, upheldwhu, reduces the diameter of the myofibril lattice by approximately one-half. We propose hypotheses to explain how each troponin-T mutation engenders the observed myofibrillar defects.

Alleles↗
PubMed1990

Genetic approaches to myofibril form and function in Drosophila.

Myofibrils, the contractile organelles of muscle, are apt subjects for studies on the formation and function of actomyosin networks. Molecular genetic approaches are advancing our understanding of myofibril structure and assembly, and may offer a novel and useful approach for investigating the crossbridge cycle. We review recent progress in Drosophila.

Animals↗
PubMed1989

Formation of reverse rigor chevrons by myosin heads.

The uniform angle and conformation of myosin subfragment 1 (S1) bound to actin filaments (F-actin) attest to the precise alignment and stereospecificity of the binding of these two contractile proteins. Because actin filaments are polar, myosin heads must swing or rotate about the head-tail junction in order to bind. Electron microscopy of isolated thick filaments and of myosin molecules suggests that the molecules are flexible, but myosin fragments and crossbridges have been reported not to interact with inappropriately oriented actin filaments. Here we describe myofibrillar defects engendered by a site-directed mutation within the flight-muscle-specific actin gene of the fruitfly Drosophila. The mutation apparently retards sarcomere assembly: peripheral thick and thin filaments are misregistered and not incorporated into the Z-line. Therefore, a myosin filament encounters thin filaments with the 'wrong' polarity. We show that myosin heads tethered in a single thick filament can bind with opposite rigor crossbridge angles to flanking thin filaments, which are apparently of opposite polarities. Preservation of identical actomyosin interfaces requires that sets of heads originating from opposite sides of the thick filament swivel 180 degrees relative to each other, implying that myosin crossbridges are as flexible as isolated molecules.

Actins↗