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Biomedical subjects

L M Brown

Publications and source records attributed to L M Brown.

At least 127 records · Page 7Linked to original sources
PubMed1988

Occupational risk factors for laryngeal cancer on the Texas Gulf Coast.

Analyses are reported from a case-control interview study of incident laryngeal cancer on the Gulf Coast of Texas. Study subjects were 183 white men with squamous cell carcinoma of the larynx and 250 frequency matched controls. Occupational exposures were examined controlling for potential confounding by cigarette smoking and alcohol consumption. Significantly elevated risks were seen for men employed in the public services industry [transportation, communication, utilities, sanitary service; relative risk (RR), 1.6]; in metal fabricating (RR, 2.1), construction (RR, 1.7), and maintenance (RR, 2.7) occupations; and for workers potentially exposed to paint (RR, 1.8) and diesel or gasoline fumes (RR, 1.5). Elevated risks of border-line significance were seen for men employed as woodworkers/furniture makers (RR, 8.1) and for those with occupational exposure to asbestos (RR, 1.5). When asbestos was categorized by intensity of exposure, a significant positive gradient was found.

Alcohol Drinking↗
PubMed1988

Culture of in vitro fertilized rabbit ova.

Embryonic development of in-vitro fertilized rabbit ova was assessed following in-vitro culture in four different serum supplemented media. A mixture of Basal Medium Eagle (BME) and Ham's F10 medium (1:1) provided better support for in-vitro development than Ham's F10, BME, or regular acidic saline (RAS). In-vitro embryonic development in the BME/Ham's F10 mixture was synchronous with in-vivo development through at least 55 hr of culture. After 54 hr of culture, embryos transferred to the oviduct of a synchronous pseudopregnant recipient were able to implant at the same rate as simultaneously transferred embryos grown in vivo. BME/Ham's F10 supplemented with 10% newborn calf serum was highly supportive of rabbit embryo development following in-vitro fertilization.

Animals↗
PubMed1988

The effect of selective type A or type B monoamine oxidase inhibition on the intrasynaptosomal deamination of (3H)serotonin in rat spinal cord tissue.

The degree to which the type A and type B forms of monoamine oxidase participate in the intraneuronal deamination of (3H)serotonin (5-HT) was examined in synaptosomal-rich fractions of rat spinal cord tissue. Synaptosomes were labeled with (3H)5-HT and superfused with physiological buffers containing selective concentrations of a type A (clorgyline) or a type B (deprenyl) MAO inhibitor. The efflux of (3H)5-HT and newly-formed (3H)5-hydroxyindoleacetic acid (5-HIAA) was determined and compared to controls over time. In control samples, a slight decline in (3H)5-HT efflux occurred over the experimental superfusion period. However, a stable formation and efflux of (3H)5-HIAA was seen during this same period of time. When clorgyline was added to the superfusion buffer, a rapid decline in superfusate levels of (3H)5-HIAA was observed. Similar experiments in the presence of deprenyl were without effect. In order to elevate cytoplasmic concentrations of (3H)5-HT and therefore increase its chances for interaction with nerve terminal MAO, reserpine was added to the superfusion buffer. Reserpine caused a greater than 3-fold increase in (3H)5-HIAA formation with no change in (3H)5-HT efflux. Clorgyline inhibited this increase in (3H)5-HIAA formation but deprenyl was again without effect. In the presence of clorgyline, reserpine also caused an increase in (3H)5-HT efflux. These results strongly support the notion that 5-HT deamination within rat spinal cord nerve terminals occurs primarily, if not exclusively, through an interaction with type A MAO.

Animals↗
PubMed1988

Base rates of post-concussional symptoms.

Several cognitive, physical and psychological symptoms have been reported as common sequelae of head injury. However, these data have been reported largely in absence of established base rates. This study employed self-report and relative report questionnaires to assess base rates of these symptoms in uninjured subjects. Chi square analysis was used to compare the rate of symptoms reported by head injured subjects, relatives of head injured subjects, uninjured subjects and relatives of uninjured subjects. In most cases, no significant difference was found between the symptoms reported by the head injured group and the uninjured group. These results demonstrate the importance of establishing base rates of symptoms in non-clinical populations prior to drawing conclusions about symptoms in clinical populations.

Journal Article↗
PubMed1987

Testicular cancer in young men: the search for causes of the epidemic increase in the United States.

A case-control study of 271 men with testicular cancer and 259 controls was conducted in the Washington, DC area to evaluate whether suggested risk factors could be responsible for the epidemic increases in testicular cancer in young men. No substantial risks were associated with a history of groin hernia operation, the common childhood diseases, allergies, x rays below the waist, venereal disease, vasectomy, or external means of elevating the temperature of the testis. Excess risks were associated with a history of undescended testis (RR = 3.7, CI = 1.5-9.5), testicular trauma (RR = 2.6, CI = 1.6-4.2), and mumps orchitis (RR = 5.8, CI = 0.7-129.7). It is unlikely, however, that any of these conditions has increased sufficiently over time to markedly affect the testicular cancer incidence patterns. Therefore, while the risk factors identified in this paper are of epidemiological interest, they do not account for the increase in testicular cancer in young men.

Adolescent↗
PubMed1986

Testicular cancer in the United States: trends in incidence and mortality.

The patterns of incidence and mortality of testicular cancer in the United States indicate substantial differences by age, race, time period, and geographical region. An epidemic increase over time in the risk of testicular cancer is noted for young men aged 15-44, with the most recent birth cohorts showing the greatest rate of increase. Indeed, some of the evidence suggests the possibility of two separate increases, one apparent from at least the late 1930's through the late 1950's and the second appearing in the late 1970's. The incidence data for blacks also show a young adult peak, even though the rates for whites are four to five times higher than for blacks at all ages except early childhood. Mortality rates for older men consistently declined over the 30-year period, while rates for younger men showed a dramatic drop only for the most recent time period. Aetiological factors yet to be determined may be responsible for the increasing incidence of testicular cancer in young adults. Survival factors appear to explain the age-specific differences between the incidence and mortality curves over time.

Adolescent↗
PubMed1986

Prenatal and perinatal risk factors for testicular cancer.

In an attempt to determine the risk factors responsible for the dramatic increases in testicular cancer incidence in young adults, mothers of testicular cancer cases and controls were questioned about in utero exposures, pregnancy-related conditions, and perinatal factors during their pregnancies with the 202 cases and the 206 controls. The strongest risk factor was low birth weight with a greater than 12-fold risk (confidence interval = 2.8 to 78.1) for subjects weighing 5 lb or less at birth compared to those who weighed over 5 lb. A statistically significant 2-fold increase in risk was associated with unusual bleeding or spotting during pregnancy, regardless of whether medication was taken for this condition. Other exposures during pregnancy associated with a statistically significant increase in risk were: use of "sedatives"; alcohol consumption; and exposure to X-rays. No excess risk was associated with the use of hormones during pregnancy. The findings for birth weight and abnormal uterine bleeding suggest that significant compromise of the normal maternal-fetal environment may be associated with subsequent increase in risk of testicular cancer. However, this increase in risk is not great enough to explain the dramatic increases in testicular cancer that have occurred in young adults.

Birth Weight↗
PubMed1985

Familial testicular cancer and urogenital developmental anomalies.

In a case-control study of testicular cancer, 6 of 269 cases (2.2%) reported a first-degree relative with testicular cancer, compared to 1 of 259 controls (0.4%). Fathers and brothers of testicular cancer cases had a six-fold elevated risk of developing a testicular malignancy compared to men in the general population. Cryptorchidism was reported in a first-degree relative in 1 (17%) of the familial cases versus 7 of 259 (2.7%) controls and 14 of 263 (5.3%) cases with a negative family history for testicular cancer. One half of the 6 familial cases reported a first-degree relative with a groin hernia (all surgically repaired before age 12), compared to 12.7% of 259 controls and 10.3% of 263 nonfamilial cases. Three familial clusters identified through the case-control study were selected for clinical evaluation. One of the 6 surviving males with testicular cancer in these 3 families had undergone orchiopexy and inguinal herniorrhaphy at age 6 years, and one had a hydrocele associated with his testicular tumor. Of the 12 living fathers and brothers of these 6 men, 3 reported childhood inguinal hernias, two with coexisting hydroceles. One additional hernia and two additional hydroceles were detected during urologic evaluation of these healthy relatives. The high prevalence of cryptorchidism, inguinal hernias, and hydroceles among men in these families suggests that an underlying alteration in urogenital embryogenesis may be associated with the familial predisposition to testicular neoplasia.

Adult↗
PubMed1985

Testicular cancer risk among young men: role of cryptorchidism and inguinal hernia.

The role of cryptorchidism (undescended testis) and inguinal hernia in the etiology of testicular cancer among men aged 18-42 years was evaluated in a case-control study of 271 cases and 259 controls referred to three collaborating medical centers in the Washington, DC, area. The relative risk of testicular cancer for men who reported a history of an undescended testis was 3.7 (95% confidence interval = 1.6-8.6). The risk increased with increasing age at correction; the risk was highest for those men whose cryptorchid testis was never corrected. Among unilateral cryptorchids, no increased risk of testicular cancer was observed for the normally descended testis. There was only a slight excess risk for men without cryptorchidism who had a herniorrhaphy; however, those who underwent a hernia operation after age 7 had a significantly elevated risk of testicular cancer on the same side as the hernia. This case-control study is the first one to support the clinical recommendations for early surgical correction of cryptorchidism and inguinal hernia. Data from this study suggest that the excess cancer risk associated with cryptorchidism is due to internal factors that affect the undescended testis rather than to some underlying developmental abnormality.

Adolescent↗
PubMed1984

Structural studies of the waves in striated muscle fibres shortened passively below their slack length.

Isolated skeletal muscle fibres of Rana pipiens were shortened below their slack length by longitudinal compression in a gelatine block, and examined by light and electron microscopy. Waves appeared sharply when the striation spacing (S) reached a critical value (about 2 microns) and increased in height with further compression down to S = 1.6 microns while the resting band pattern was maintained. The waves were plane, helical or irregular, with wave lengths of 5-15 striations. The Z lines usually ran perpendicular to the direction of the myofibrils to form wedge-shaped sarcomeres. The bending occurred mainly in the I band. The thin filaments ran stiffly for about 30 nm from the Z line and then bent toward the A band. The thick filaments bent very slightly, particularly at their tips. The edges of the A band were indistinct, and there were no dense lines at the A-I junction. The appearance of the individual sarcomeres resembled those in relaxed myofibrils at slack length, with no Cm bands. The H zone was only seen occasionally in the slack and wavy fibres examined. In very thin sections the individual thin filaments were seen to end in the pseudo-H zone, and not to cross the M line. There was a single array of not more than six thin filaments round each thick one in transverse sections of the M-line region. These observations suggest that the narrowing of the bands observed in fresh wavy fibres is due mainly to the obliquity of the myofibrils, and that the sarcomere length measured parallel to their axis is longer than the striation spacing. The relationship between sarcomere length and the length of the thin-filament complex is discussed.

Animals↗
PubMed1984

Sarcomere and filament lengths in passive muscle fibres with wavy myofibrils.

Longitudinal compression of isolated skeletal muscle fibres of Rana pipiens caused waves to appear sharply at a critical striation spacing which was slightly less than the slack length measured at the same point. Both slack length and critical length varied between fibres and along the length of one fibre, being shortest near the tendons. The critical length varied from 1.93 to 2.11 microns. The troponin periodicity (Pdiff) was measured in embedded material by light diffraction of calibrated electron micrographs. Comparison between the troponin periodicities in a fibre made wavy at one end and stretched at the other showed that longitudinal compression did not cause shortening of the thin filaments. Comparison between Pdiff and the troponin periodicity of fresh muscle provided an estimate of the artefact mainly caused by shrinkage during specimen preparation. It varied from 3 to 11%. The gaps between the ends of the thin filaments in the M-line region were estimated from sarcomere length (corrected for shrinkage) and the assumed in vivo values for total thin-filament length or the length between the last troponin lines (1.975 microns and 1.925 microns respectively). The estimates were confirmed by a few direct measurements of thin-filament length and periodicity. Sarcomere length varied from fibre to fibre, from 1.91 to 2.12 microns, except at the inside of bends in wedge-shaped sarcomeres where it fell to 1.86 microns in some cases. This indicates that in one fibre the tips of the thin filaments overlapped at the level of the last troponin lines, while, at the other extreme, the tips of the thin filaments only just reached the bare zone of the thick filaments. The origin of the resistance to sliding and the force which restores an actively shortened fibre to its slack length are discussed. While there may be a well-defined barrier to sliding at the point where the troponins of opposite polarity meet, there must also be an additional length-dependent resistance to account for the appearance of waves at longer sarcomere lengths. The formation of waves is interpreted as a buckling phenomenon in which a longitudinal compressive force is applied to the myofibrils which have a finite stiffness bending and a finite elastic restraint against lateral displacement. The bending stiffness is largely and perhaps entirely accounted for by contributions from (1) the stiffness of the individual filaments and (2) the stiffness of myofibrils calculated from their Young's modulus.

Animals↗
PubMed1984

Lung cancer in relation to environmental pollutants emitted from industrial sources.

A case-control study of residents who lived in the vicinity of a primary zinc smelter and a large steel manufacturing plant in eastern Pennsylvania was undertaken to investigate the role of environmental pollutants in the etiology of lung cancer. Lifetime residential, occupational, and smoking histories were obtained from the next of kin of 335 white male lung cancer cases and 332 white male controls. Soil samples were collected and analyzed for content in ppm of arsenic, copper, lead, manganese, zinc, and cadmium. Relative risks were determined according to distance of residence from the zinc smelter and the steel plant, and according to residence in areas with heavy and light levels of various pollutants. Two-fold risks for lung cancer were associated with residence near the zinc smelter and with residence in areas with heavy levels of arsenic and cadmium, although the number of individuals living in these higher risk areas was small. These increases were not explained by the effects of cigarette smoking or by employment in the zinc or steel industry. No excess risk was associated with living near the steel plant. The limited size of the study precludes causal interpretation, but the findings suggest the need for further investigation of metallic air pollution and lung cancer.

Adult↗
PubMed1984

Combined granulocyte and platelet transfusions: inter-relationship between granulocyte and platelet recoveries in the presence and absence of complicating factors.

191 combined collections of granulocytes (PMN) and platelets (PLT) obtained by discontinuous cytapheresis were given to 23 patients with acute myeloid leukaemia (AML). The circulation in recipients of the concomitantly transfused cells was compared by measuring the % recovery of PMN at 1 h, and of PLT at 1 and 20 h. The recovery of both cells was greatly reduced in transfusions accompanied by a transfusion reaction. Fever in recipients had no effect on the recovery of either cell, but PMN recovery was significantly higher in patients receiving oral prednisolone. Alloimmunization to PLT, defined as recovery levels less than 15% at 1 h and/or less than 10% at 20 h, was recorded in 42 transfusions, and PMN recovery was significantly reduced in this group. In transfusions where PMN recovery was 'low' (less than 5%); the recovery of the coincidentally transfused PLT was significantly reduced only in transfusions accompanied by a reaction. These results emphasize the deleterious effects of transfusion reactions and suggest that donor PMN frequently circulate less well in recipients alloimmunized to PLT from the same donor.

Blood Group Incompatibility↗