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PubMed1986

Saunders v. State.

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Euthanasia, Passive↗
PubMed1990

Photoperiodic diapause in Drosophila melanogaster involves a block to the juvenile hormone regulation of ovarian maturation.

Females of Drosophila melanogaster held under short-day photoperiods at a moderately low temperature (12 degrees) enter a state of ovarian diapause in which yolk deposition in the oocytes is suspended (D. S. Saunders, V. C. Henrich, and L. I. Gilbert, Proc. Natl. Acad. Sci. USA 86, 3748-3752, 1989). An enzyme-linked immunosorbent assay (ELISA) using polyclonal antibodies raised against D. melanogaster yolk polypeptides (YPs) showed that diapausing flies synthesize and accumulate YPs in the hemolymph, but very little in the ovary. Nondiapausing females at the same temperature but at long days, and short-day flies in which diapause was broken by an upshift in temperature or topical application of juvenile hormone (JH), showed enhanced titers of YPs in the ovaries, suggesting stimulating uptake. Determinations of juvenile hormone bisepoxide (JHB3) and JH III synthesis in vitro by single excised corpora allata showed that glands from nondiapausing flies or corpora allata from flies in which diapause had been broken synthesized JH at a rate about four times higher than glands from diapausing flies. Corpora allata incubated in medium supplemented with farnesoic acid showed an increase in the rate of JH synthesis, but the increase was relatively greater with corpora allata from nondiapausing flies. Glands from diapausing flies presented the appearance of newly emerged or "immature" glands. Ovarian diapause is terminated at 12 degrees LD 10:14 in 7 days following topical application of either JH III or JHB3 at a concentration of about 0.5 micrograms per fly, diapause termination being expressed by an increased rate of vitellogenesis and by an increase in the number of fully developed eggs per vitellogenic female. It is concluded that the short-day-elicited diapause in D. melanogaster results from a "block" to the JH-stimulated uptake of yolk proteins from the hemolymph, caused by a reduced rate of JH synthesis by the corpus allatum. Photoperiodic regulation of the corpus allatum may be mediated via the brain.

Animals↗
PubMed1993

Wilms tumor genes.

Multiple 'WT' genes exist. The WT1 gene at chromosomal band 11p13 has been cloned and is known to be important in the etiology of at least some tumors by virtue of the identification of both germline and somatic mutations in WT patients. Genes at 11p15 and 16q are also involved, either as initiating or tumor progression events. An unlocalized familial predisposition gene is also known to be important etiologically. The identification of several genes that are involved in the etiology or progression of WT, the preferential loss of maternally derived alleles in tumor tissue, and the observed reduction to 11p homozygosity in normal tissue DNA from some patients, all strikingly indicate that a simple, one-locus-'two-hit' genetic model for WT is inadequate. The question is not if this model needs to be modified, but how it should be modified, or if it is even valid enough to be a starting point for understanding the genetics of Wilms tumor. To begin to address this, several questions can be asked. Do all Wilms tumors carry mutations at the WT1 locus? Do both alleles at the WT1 locus need to be inactivated or lost for tumorigenesis? Or, instead, do some WT1 mutations act dominantly? Do patients with bilateral disease carry germline mutations as originally hypothesized, or, as more recently suggested, is bilateral disease the result of early somatic mutations, genomic imprinting, or multifactorial inheritance? Must mutations at an 11p15 locus and/or 11p15 LOH accompany WT1 mutations, or do 11p13 and 11p15 mutations act independently of each other? Have tumors from familial WT cases (who do not carry germline WT1 mutations) sustained somatic mutations at the WT1 locus, the 11p15 locus or the 16q locus? Conversely, do tumors from sporadic WT patients carry somatic mutations at the non-11p familial predisposition gene? Will most tumors be found to carry mutations at the same one or two loci, but differ only with regard to whether the mutations are somatic or germline? Are effects of genomic imprinting layered over, so to speak, a framework of classically mendelian mutations, or in some cases is imprinting the mechanism by which genes are inactivated or their normal function modulated? Although not definitive, there are data that bear on some of these questions. Germline mutations have been observed in patients with bilateral tumors, but may not prove to be a universal feature of bilateral disease.(ABSTRACT TRUNCATED AT 400 WORDS)

Genes, Wilms Tumor↗
PubMed1979

Happenings.

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Attitude to Health↗
PubMed2001

Costs of care for irritable bowel syndrome patients in a health maintenance organization.

OBJECTIVES: The aims of this study were: 1) to determine the total costs of care and costs related to lower GI-related problems for patients who received a diagnosis of irritable bowel syndrome (IBS), and 2) to compare them to age- and sex-matched population controls and patients treated for inflammatory bowel disease (IBD) or gastroesophageal reflux disease (GERD). METHODS: Use and cost data were obtained through the computerized information systems of a large staff-model health maintenance organization on three groups of patients diagnosed in 1994 or 1995 with IBS, IBD, or GERD; and an age- and sex-matched control group of patients without any of these listed diagnoses. The IBS patient group was compared to the three comparison groups on components of total and IBS-related costs. RESULTS: Total costs of care for IBS patients were 49% higher than population controls during the year starting with the visit at which IBS patients were identified. In the index year, every component of total costs except inpatient care was significantly higher for IBS patients than for population controls. The costs of care for lower GI problems were significantly higher for patients with IBS than for population controls across a range of services. However, only 33% of the difference in total costs of care between IBS patients and population controls was due to lower GI-related services in the index year. In the subsequent years, lower GI-related services accounted for 18% and 20% of the total cost difference between IBS patients and population controls. The total costs of care as well as the components of costs of care were generally higher for IBD patients than for IBS patients, but were comparable for GERD and IBS patients. CONCLUSIONS: Patients with IBS show sustained increases in health care costs relative to population controls for both lower GI services and care unrelated to lower GI problems. However, the majority of the excess in health care costs resulted from medical care not directly related to lower GI problems.

Adolescent↗
PubMed2000

Stimulation of plasminogen activator and inhibitor in the lymphatic endothelium.

Chromogenic assays, immunoblotting, and Northern blot hybridization methods were employed to assess the effects of various agonists on the production of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) by the lymphatic endothelium (LEC). Fibrin autography showed that plasminogen-dependent fibrinolytic activity occurred at M(r) of 110 kDa, which represents a complex of tPA with PAI-1, and 65- and 55-kDa bands corresponding to tPA and uPA, respectively. The fractionation of lymph collected from ovine lymphatic vessels also produced a prominent lytic band of approximately 110 kDa, suggesting the formation of PA/PAI complexes in lymph. The stimulation of various agonists produced large-scale increases in tPA mRNA, as shown by Northern blot hybridization analyses. The effects of ECGF, histamine, and LPS on the presence of tPA and on enhancing the levels of mRNA reached maximum activity at 4 h and declined to levels below that of controls by 8 h. However, phorbol-treated cells exhibited reduced levels of tPA mRNA at 4 h, but was significantly increased by 8 h. A large-scale increase in PAI-1 mRNA steady-state levels was also stimulated by the agonists used in these studies. Both the 3.4- and 2.4-kb species of PAI-1 mRNA were increased. These observations demonstrated that tPA and PAI-1 are produced and secreted by LEC monolayer cultures and are also present in lymph.

Animals↗
PubMed1997

Racial variation in retinopathy of prematurity. The Cryotherapy for Retinopathy of Prematurity Cooperative Group.

OBJECTIVES: To determine and compare the incidence of severe, vision-threatening retinopathy of prematurity (ROP) in black and white low-birth-weight infants. DESIGN: Prospective cohort study. SETTING: Seventy neonatal intensive care units in 23 US participating centers in the Multicenter Trial of Cryotherapy for Retinopathy of Prematurity. PATIENTS: A total of 4099 premature infants weighing less than 1251 g at birth were enrolled to evaluate the natural history of ROP. This 'Natural History' cohort included 2158 white infants and 1584 black infants who were followed up prospectively according to a Natural History protocol. MAIN OUTCOME MEASURES: Incidence and severity of acute ROP. RESULTS: While ROP occurred with similar frequency in all racial subgroups, severe ROP was less common in black infants. One hundred sixty (7.4%) of 2158 white infants reached threshold ROP (defined as at least 5 contiguous or 8 cumulative clock-hours of stage 3 retinopathy in zone 1 or zone 2 in the presence of "plus disease" [dilation and tortuosity of the posterior pole blood vessels]), but only 51 (3.2%) of 1584 black infants progressed to threshold ROP. Using multiple logistic regression analysis, race emerged as a highly significant factor (P < .001) in the development of threshold disease, even when birth weight, gestational age status at delivery, sex, multiple births, and transport status were considered. CONCLUSIONS: Severe, vision-threatening ROP occurs with greater frequency in low-birth-weight white infants than in low-birth-weight black infants who are seemingly at equivalent risk. The reason for this disparity is unknown. We speculate that differences in retinal pigmentation may confer relative protection against free radical-mediated phototoxic injury in black infants.

Birth Weight↗
PubMed2000

Quantum mechanical interpretation of nitrite reduction by cytochrome cd1 nitrite reductase from Paracoccus pantotrophus.

The reduction of nitrite to nitric oxide in respiratory denitrification is catalyzed by a cytochrome cd(1) nitrite reductase in Paracoccus pantotrophus (formerly known as Thiosphaera pantotropha LMD 92.63). High-resolution structures are available for the fully oxidized [Fülöp, V., Moir, J. W., Ferguson, S. J., and Hajdu, J. (1995) Cell 81, 369-377; Baker, S. C., Saunders, N. F., Willis, A. C., Ferguson, S. J., Hajdu, J., and Fülöp, V. (1997) J. Mol. Biol. 269, 440-455] and fully reduced forms of this enzyme, as well as for various intermediates in its catalytic cycle [Williams, P. A., Fülöp, V., Garman, E. F., Saunders, N. F., Ferguson, S. J., and Hajdu, J. (1997) Nature 389, 406-412]. On the basis of these structures, quantum mechanical techniques (QM), including density functional methods (DFT), were combined with simulated annealing (SA) and molecular mechanics techniques (MM) to calculate the electronic distribution of molecular orbitals in the active site during catalysis. The results show likely trajectories for electrons, protons, substrates, and products in the process of nitrite reduction, and offer an interpretation of the reaction mechanism. The calculations indicate that the redox state of the d(1) heme and charges on two histidines in the active site orchestrate catalysis locally. Binding of nitrite to the reduced iron is followed by proton transfer from His345 and His388 to one of the oxygens of nitrite, creating a water molecule and an [Fe(II)-NO(+)] complex. Valence isomerization within this complex gives [Fe(III)-NO]. The release of NO from the ferric iron is influenced by the protonation state of His345 and His388, and by the orientation of NO on the d(1) heme. Return of Tyr25 to a hydrogen-bonding position between His345 and His388 facilitates product release, but a rebinding of Tyr25 to the oxidized iron may be bypassed in steady-state catalysis.

Binding Sites↗
PubMed1997

Concordance between ICD-10 alcohol and drug use disorder criteria and diagnoses as measured by the AUDADIS-ADR, CIDI and SCAN: results of a cross-national study.

Agreement between the AUDADIS-ADR, CIDI and SCAN in case identification for ICD-10 alcohol and drug use disorders and diagnostic criteria was investigated in three countries, Luxembourg, Greece and the US. Overall, agreement for ICD-10 dependence diagnoses between the three instruments was fair to good for alcohol, opioids and cocaine, but generally lower for dependence diagnoses for other substance. In contrast, concordance between instruments for harmful use diagnoses was extremely poor for all substances. Implications of these major findings are discussed in terms of the relationship between prevalence, reliability and concordance and indications and cautions regarding cross-instrument comparisons.

Adult↗
PubMed1987

Ventilatory responses to inhaled carbon dioxide at rest and during exercise in man.

1. Rapid steady-state CO2 responses were determined in six normal subjects at rest and five subjects at four different work loads up to 125 W, by injecting pure CO2 at constant flow into a small mixing chamber in the inspiratory limb of a breathing circuit. 2. The time course of the response of ventilation (V) and mean alveolar PCO2 (PACO2) was checked in separate experiments, where the flow rate of injected CO2 was changed abruptly and the effects were followed for 10 min. 3. V and PACO2 were measured every breath, and the results ensemble-averaged for each subject (two or three runs per subject) and then for the groups as a whole, in 30 s or 60 s time bins. 4. PACO2 during exercise was estimated by graphical reconstruction from the sloping alveolar plateau, and separately by the empirical equation of Jones, Robertson & Kane [1]. At rest, PACO2 was assumed equal to end-tidal PCO2 (PetCO2). 5. With the constant inflow technique, 4 min was required to reach steady-state V and PACO2 during exercise, and 6 min at rest. 6. At rest, with 4 min steps (doubtful steady state) the averaged CO2 response was concave up. With 6 min steps the response was almost linear. In neither case was the deviation from linearity statistically significant. 7. During exercise, the averaged CO2 responses were essentially isocapnic at work loads greater than 75 W with either method of deriving PACO2.

Adult↗