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W R Williams

Publications and source records attributed to W R Williams.

At least 37 records · Page 2Linked to original sources

Segregation analysis of cancer in families of childhood soft-tissue-sarcoma patients.

This paper presents the analysis of familial cancer data collected in a hospital-based study of 159 childhood soft-tissue-sarcoma patients. Two different statistical models detected excess aggregation of cancer, which could be explained by a rare dominant gene. For each kindred, we estimated the probability of the observed cancer distribution under the dominant-gene model and identified 12 families that are the most likely to be segregating the gene. Two of those families have confirmed germ-line mutations in the p53 tumor-suppressor gene. The relative risk of affection for children who are gene carriers was estimated to be 100 times the background rate. Females were found to have a slightly higher age-specific penetrance, but maternal and paternal lineages made equal contributions to the evidence in favor of the dominant gene. The proband's histology, ethnicity, and age at diagnosis were evaluated to determine whether any of these altered the probability of affection in family members. Only embryonal rhabdomyosarcoma was found to be a significant covariate under the dominant-gene model. While molecular genetic studies of familial cancer will eventually provide answers to the questions of genetic heterogeneity, age- and site-specific penetrance, mutation rates, and gene frequency, information from statistical models is useful for setting priorities and defining hypotheses.

Adolescent↗

Inhalation and nasal challenge in the diagnosis of aspirin-induced asthma.

Inhalation and nasal aspirin challenge has been investigated in asthma patients with co-existing rhinitis. Eight of 39 asthma patients were diagnosed as aspirin-sensitive on the basis of inhalation challenge. Seven aspirin-sensitive asthmatics were subjected to nasal aspirin provocation. During nasal challenge, all seven patients experienced a fall in FEV1 of at least 15%, two showed a significant increase (greater than 400%) in nasal airways resistance (NAR) and one developed urticaria. No significant changes in FEV1 or NAR were observed in nine normal subjects after aspirin inhalation and nasal challenge. There were no significant changes in FEV1 or NAR in six aspirin-tolerant asthmatics when aspirin was given intranasally. The results of this study show that aspirin nasal provocation impairs lung function in aspirin-sensitive asthmatics. In comparison with inhalation challenge responses are generally milder and easier to control. Nasal challenge is also less time-consuming than other methods of aspirin challenge and is therefore more suitable for routine use.

Adult↗

Aspirin-sensitive asthma: significance of the cyclooxygenase-inhibiting and protein-binding properties of analgesic drugs.

The in vitro release of endogenous and exogenous PgF2 alpha from plasma and serum proteins by aspirin and other analgesic drugs has been studied by RIA and equilibrium-dialysis techniques, respectively. Before aspirin addition, the mean plasma level of PgF2 alpha measured by RIA was significantly lower in aspirin-sensitive asthma (ASA) patients (11.3 +/- 6.5 pg/ml; n = 8) than in aspirin-tolerant asthma (ATA) patients (25.0 +/- 11.4 pg/ml; n = 21). After aspirin addition (50 micrograms/ml) the mean PgF2 alpha level detected in plasma by RIA was higher in ASA patients (97.6 +/- 5.5 pg/ml) than in ATA patients (66.9 +/- 4.5). The binding of [3H]PgF2 alpha to serum protein was significantly inhibited by NSAIDs but not by paracetamol (0.2-1.0 mM). These results implicate PgF2 alpha and the protein-binding property of analgesic drugs in the pathogenesis of aspirin-sensitive asthma.

Acetaminophen↗

In vitro tests for the diagnosis of aspirin-sensitive asthma.

In patients with aspirin-sensitive asthma, no significant changes in plasma beta-thromboglobulin or bicyclic prostaglandin (PG) E2 were observed during aspirin challenge. The addition of aspirin to platelet suspensions from patients with aspirin-sensitive asthma produced no detectable chemiluminescence. Small concentrations of aspirin generated PGF2 alpha but not PGE2 or PGD2 from plasma in vitro. PGF2 alpha levels were significantly higher in plasma from aspirin-sensitive patients and distinguished aspirin-sensitive from aspirin-tolerant patients with asthma. The results of this study suggest that the displacement of protein-bound PGF2 alpha may be of importance in the pathogenesis of aspirin-induced asthma.

Adult↗

Laser fluorometric detection of porphyrin methyl esters for high-performance thin-layer chromatography.

A new detection method is presented for the determination of porphyrins present in biological materials. Separation is accomplished by high-performance thin-layer chromatography after esterification of individual carboxylic acid porphyrins. Detection is achieved by utilizing one of the visible lines of an argon-ion laser for fluorometric excitation. Good selectivity and detectability are demonstrated for the determination of porphyrin profiles in human urine. The detection limits for uro-, heptacarboxy-, hexacarboxy-, pentacarboxy-, copro-, and mesoporphyrin methyl esters are in the 18-35 pg range.

Carboxylic Acids↗

Aspirin-like effects of selected food additives and industrial sensitizing agents.

A number of food additives and industrial chemicals, responsible for inducing symptoms of intolerance in some individuals, have been studied in tests measuring platelet activation by noradrenaline. All the investigated agents inhibited platelet aggregation and this was associated with inhibition of the cyclo-oxygenase-thromboxane pathway. Suboptimal inhibitory concentrations of the agents studied had additive inhibitory effects on platelet aggregation when they were tested in pairs, or when tested with salicylate or aspirin. The results support the theory that some food additives and industrial chemicals induce intolerance because of their aspirin-like properties.

Adolescent↗

Genetic analysis of childhood sarcoma.

A survey of cancer in 159 3-year survivors of childhood soft tissue sarcoma and their relatives revealed a cancer excess in first-degree relatives primarily due to cancers occurring before the age of 35 years and a highly significant excess in relatives of patients with second malignant neoplasms. Tumors of soft tissue and bone, breast, and brain were in excess in relatives and as second malignant neoplasms in patients. To determine the most likely explanation for the observed cancer distribution, we applied segregation analysis under a unified version of the mixed model. The observed data were most compatible with a rare autosomal dominant gene with high penetrance (gene carriers had a 50% probability of cancer by age 30, increasing to 90% by age 60) as compared with a chance occurrence or a multifactorial explanation. We contrasted the relative odds of observing each pedigree under a sporadic, multifactorial, or major gene model, and identified 11 pedigrees in which familial clustering of cancer was significant, with the distribution of cancer strongly favoring a major gene in 9 pedigrees. The tumors in these kindreds have been associated with alterations in specific genetic loci by tumor-specific genetic analysis. In particular, we observed soft tissue sarcoma, osteosarcoma and premenopausal ductal breast carcinoma tumors, perhaps attributable to loss of the Rb-1 suppressor gene on chromosome 13q, in the same patients and families. Study of the cancer predisposition segregating in 10 families by genetic linkage with markers of chromosome 13q and the Rb-1 gene have to date given negative LOD scores at 0 = 0 of Z = -1.2 to -13.0.(ABSTRACT TRUNCATED AT 250 WORDS)

Bone Neoplasms↗

Chronic beryllium disease in identical twins.

Identical male twins born in 1959 have developed chronic beryllium disease. Twin 1 was exposed to beryllium for more than 3 years. The diagnosis was first suspected at the time of his post-employment chest radiograph. Twin 2 was exposed for 21 months and ceased employment at the same time as his brother. His post-employment examination was normal. Thirty months later he developed an unusual skin rash which biopsy showed to be granulomatous. Further investigations proved the diagnosis. Both men have reduced tear secretion measured with Schirmer's test, a feature not previously reported in this condition. Bronchoalveolar lavage and laser microprobe mass spectrometry (LAMMS) were used as aids to the diagnosis. Sarcoidosis has been reported in identical twins, suggesting genetic susceptibility, which may also be of importance in chronic beryllium disease.

Adult↗

Effects of theophylline, beta-adrenergic stimulants and prednisolone on platelet and urine cyclic guanosine monophosphate (cGMP).

Experiments were carried out to investigate the effects of anti-asthma drugs on cGMP levels. In vitro, theophylline (5 X 10(-4) M) increased basal and 5-hydroxytryptamine stimulated cGMP formation by platelets (p less than 0.05) while salbutamol and prednisolone produced no change. No significant differences were found in urine cGMP levels in healthy subjects, after short term treatment with theophylline, isoprenaline or prednisolone. Urinary cGMP levels were lower than normal in the majority (7/10) of asthma patients tested and in female patients this difference was significant (p less than 0.05). Severity of asthma symptoms were not found to be associated with particular changes in urinary cGMP levels. Fluctuations in the cGMP levels were, however, greater (p less than 0.01) in asthma patients with a more unstable respiratory condition. The differences between in vitro and in vivo results may demonstrate that beta-stimulants and theophylline have different acute and chronic effects on cGMP formation, or show that in vivo these drugs primarily affect tissue enzymes that differ from those on platelets.

Adrenergic beta-Agonists↗

Heritable fraction of unilateral Wilms tumor.

Heritability of the unilateral-sporadic (non-familial) form of Wilms tumor was examined in the offspring of 96 long-term survivors of the neoplasm. No Wilms tumor has developed in any of the 179 offspring of these patients. The maximum likelihood estimate of a hereditary Wilms tumor in our patients is zero and the corresponding 95% upper confidence limit ranges between 0.06 and 0.11, depending on penetrance. Among their offspring, the 95% upper bound of the risk of Wilms tumor is 0.02. These figures can be applied in genetic counseling of other survivors of unilateral-sporadic Wilms tumor.

Humans↗

The genetic implications of long-term survival of childhood cancer. A conceptual framework.

This article outlines a conceptual framework for considering the genetic implications of childhood cancer and taking into account genetic predisposition as well as the genotoxic effects of cancer treatment. The primary consequences by which genetic effects are measured are somatic genetic damage, second tumors in the proband, germline genetic damage, and reproductive outcomes. Studies of retinoblastoma and rhabdomyosarcoma are offered as models for examining the etiology of genetic effects and defining the risks for a second malignant neoplasm. The conclusion from these studies is that there is a small subgroup of patients for whom the genetic implications of long-term survival are significant. Characteristics of this subgroup and the risks involved in treatment are defined. More optimistically, the data indicate that for the majority of patients, the risks involved in mutagenic and carcinogenic agents used in the treatment of childhood cancer are small. The authors conclude that treatment-related effects vary according to the genetic background of the proband.

Adolescent↗

Genetic epidemiology of familial aggregation of cancer.

Literature pertaining to genetic epidemiological studies of familial cancer has been reviewed from a historical perspective. Although interest in the question of heritability of cancer was extant at least as early as the beginning of the nineteenth century, early investigators were unable to produce consistent and meaningful evidence pertaining to the issue because of unsystematic methods of data collection and inadequate methods of data analysis. During the early twentieth century, developments in the fields of genetics, statistics, and epidemiology provided concepts and methods that permitted investigators to recognize important deficiencies in past studies, and to design others in which the critical comparisons could be made between patient groups and control groups. Registries of cancer incidence in large populations became available in several countries in the middle twentieth century, providing a standard "control group" for comparison. Large surveys of site-specific cancer experience in families, rigorously designed and analyzed, found for most kinds of cancers a two- to threefold increased risk for close relatives of propositi. These studies also reemphasized the great difficulty in obtaining even minimally complete family health history information, and the importance of verifying all reported cases with medical or vital records. Although clinical and laboratory investigation will be necessary to understand the mechanisms by which human genes may predispose to cancer, epidemiological approaches can estimate the extent to which genetic etiological factors may be present in a population, whether a general population or one defined by other factors under investigation. Population-based studies are already of practical significance to the clinical geneticist in the estimation of risk of eventual cancer development in unaffected family members, and can be expected to continue to identify specific groups and characteristics associated with genetic cancer predisposition. Finally, segregation and linkage analysis and their present applications to family studies of cancer were reviewed. As a result of the increasing number of DNA polymorphisms that are becoming available due to developments in molecular biology, the human gene map can be expected to be well defined in the near future, and investigation of families using segregation and linkage analysis will then be instrumental in defining the role of heredity in the development of cancer in human populations.

Age Factors↗

cGMP levels in chronic cadmium disease and osteoarthritis.

To investigate the effect of cadmium on guanyl cyclase activity, urine levels of the nucleotide cGMP were measured in patients with bone and renal lesions resulting from chronic cadmium exposure, in patients with osteoarthritis and in a normal age-matched control population. The effects of cadmium, zinc and mercury salts on blood mononuclear cell cGMP production were also studied in vitro. The two patient groups exhibited clear differences in cGMP excretion. Lower urine cGMP (59%, P less than 0.01) and creatinine values (43%, P less than 0.01) were found in cadmium-exposed patients and higher cGMP values (56%, P less than 0.05) in patients with osteoarthritis, compared to the control group. Creatinine adjusted cGMP values were also lower in cadmium-exposed patients (28%, P less than 0.05) and higher in patients with osteoarthritis (130%, P less than 0.01). In vitro, a 10 h exposure of mononuclear cells to cadmium or mercury salts depressed guanyl cyclase activity in most experiments. At 10(-4) M, mercury was consistently more inhibitory in all cultures (95%, P less than 0.01). As cadmium has a potential for inhibiting guanyl cyclase activity in human tissue, the low urine cGMP values found in patients with cadmium disease may be attributable to chronic cadmium exposure. High guanyl cyclase activity in patients with osteoarthritis may be associated with inflammation.

Aged↗

Formation of extracellular cGMP in blood mononuclear and platelet cell preparations.

The addition of inorganic acids to cell suspensions of mononuclear cells and platelets significantly increased concentrations of cGMP in supernatant fractions (3-6 X basal level). Increases in supernatant cGMP with the addition of 10(-4) M adrenaline (19 X basal level) 10(-5) M 5-HT (33 X) and 5 mM ascorbic acid (38 X) were detectable after acidification of the cell suspensions. Agonist and acid concentrations at termination of the incubations were important in determining cGMP concentrations in supernatants. The results suggest that cGMP is formed on the exterior surface of the cell membrane and therefore has an extracellular, rather than intracellular, role in transmission of the membrane stimulus for cell activation.

Ascorbic Acid↗

Pseudo-leptospires in broncho-alveolar lavage fluid and blood cell cultures.

Two types of microscopic filaments were observed in mucous and fluid obtained by broncho-alveolar lavage (BAL). Filaments in mucous smears were probably cilia from desquamated ciliated epithelial cells. Those in BAL fluid, resembling leptospira, may originate from platelets as similar filaments were produced in vitro by exposing platelets to thrombin.

Blood Platelets↗