The Touch And Go Camera System (TAGCAMS) is a three-camera-head instrument onboard NASA’s OSIRIS-REx asteroid sample return mission spacecraft. The purpose of TAGCAMS is to facilitate navigation to ...the target asteroid, (101955) Bennu; confirm acquisition of the asteroid sample; document asteroid sample stowage; and provide supplementary imaging for OSIRIS-REx science investigations.
During the almost two-year OSIRIS-REx outbound cruise phase we pursued nine TAGCAMS imaging campaigns to check, calibrate and characterize the camera system’s performance before asteroid arrival and proximity operations began in late 2018. The TAGCAMS in-flight calibration dataset provides the relevant information to enable the three cameras to complete their primary observation goals during asteroid operations. The key performance parameters that we investigated in flight included: linearity, responsivity (both point source and extended body), dark current, hot pixels, pointing, image geometry transformation, image quality and stray light. Analyses of the in-flight performance either confirmed the continued applicability of the TAGCAMS ground test results or substantially improved upon the ground test knowledge. In addition, the TAGCAMS calibration observations identified the source of a spacecraft outgassing feature that guided successful remediation efforts prior to asteroid arrival.
Abstract Purpose We aimed to validate a family history screening questionnaire in an Australian primary care population designed to identify people at increased risk for breast, ovarian, colorectal, ...and prostate cancer; melanoma; ischemic heart disease; and type 2 diabetes. Methods We prospectively validated the questionnaire in 6 general practices in Perth, Western Australia among 526 patients aged 20 to 50 years who responded to a single invitation from their general practice. They completed the 15-item questionnaire before a reference standard 3-generation pedigree was obtained by a genetic counselor blinded to the questionnaire responses. We calculated diagnostic performance statistics for the questionnaire using the pedigree as the reference standard. Results A combination of 9 questions had the following diagnostic performance, expressed as value (95% CI), to identify increased risk of any of the 7 conditions: area under the receiver operating characteristic curve 84.6% (81.2%-88.1%), 95% sensitivity (92%-98%), and 54% specificity (48%-60%). The combination of questions to detect increased risk had sensitivity of 92% (84%-99%) and 96% (93%-99%) for the 5 and 6 conditions applicable only to men and women, respectively. The specificity was 63% (28%-52%) for men and 49% (42%-56%) for women. The positive predictive values were 67% (56%-78%) and 68% (63%-73%), and the false-positive rates were 9% (0.5%-17%) and 9% (3%-15%) for men and women, respectively. Conclusions This simple family history screening questionnaire shows good performance for identifying primary care patients at increased disease risk because of their family history. It could be used in primary care as part of a systematic approach to tailored disease prevention.
Juno’s JunoCam Images of Europa Hansen, C. J.; Ravine, M. A.; Schenk, P. M. ...
The planetary science journal,
03/2024, Letnik:
5, Številka:
3
Journal Article
Recenzirano
Odprti dostop
Abstract On 2022 September 29 the Juno spacecraft passed Europa at 355 km, the first close pass since the Galileo flyby in 2000. Juno’s visible-light imager, JunoCam, collected four images, enabling ...cartographic, topographic, and surface geology analysis. The topography along the terminator is consistent with previously reported features that may indicate true polar wander. A bright band was discovered, and indicates global symmetry in the stress field that forms bright bands on Europa. The named feature Gwern is shown not to be an impact crater. Surface change detection shows no changes in 22 yr, although this is a difficult task considering differences between the JunoCam and Galileo imagers and very different viewing geometries. No active eruptions were detected.
Although autosomal dominant polycystic kidney disease type 2 (PKD2) is known to have a milder clinical phenotype than PKD1, neither disorder has been compared with an unaffected control population in ...terms of survival. We report the findings of a multicentre survey that aimed to define more precisely the survival and clinical expression of PKD1 and PKD2.
Clinical data from 333 people with PKD1 (31 families) were compared with data from 291 people with PKD2 (31 families) and 398 geographically matched controls. Survival analysis was used to compare age-at event data. Differences in the prevalence of complications were assessed by logistic regression.
Median age at death or onset of end-stage renal disease was 53·0 years (95% CI 51·2–54·8) in individuals with PKD1, 69·1 years (66·9–71·3) in those with PKD2, and 78·0 years (73·8–82·2) in controls. Women with PKD2 had a significantly longer median survival than men (71·0 67·4–74·8
vs 67·3 64·9–69·7 years), but no sex influence was apparent in PKD1. Age at presentation with kidney failure was later in PKD2 than in PKD1 (median age 74·0 67·2–80·8
vs 54·3 52·7–55·9 years). PKD2 patients were less likely to have hypertension (odds ration 0·25 95% CI 0·15–0·42), a history of urinary-tract infection. (0·50 0·31–0·83), or haematuria (0·59 0·35–0·98).
Although PKD2 is clinically milder than PKD1, it has a deleterious impact on overall life expectancy and cannot be regarded as a benign disorder.
Location of mutations within the PKD2 gene influences clinical outcome.
Since the cloning of the gene for autosomal dominant polycystic kidney disease type 2 (PKD2), approximately 40 different ...mutations of that gene have been reported to be associated with the disease. The relationship between the PKD2 genotype and phenotype, however, remains unclear.
Detailed clinical information was collected for PKD2 families in which the underlying mutation had been identified. Logistic regression analysis was employed to assess the influence of age and sex on hypertension, hematuria, renal calculi, and urinary tract infections, and a clinical phenotype score was computed. Patients were then grouped according to the relative location of their mutation within the cDNA sequence, and differences in the mean phenotypic score between groups were tested for statistical significance by means of a multiple pairwise t-test.
While phenotypic scores for each mutational group revealed a considerable degree of intragroup variability, the variability in phenotypic scores was significantly higher between mutational groups than within groups. A group-wise comparison of the mean phenotypic scores confirmed the observation of significant nonlinear variation in disease severity, with high- and low-scoring mutational groups interspersed along the gene sequence.
The identification of groups of mutations in the PKD2 gene, which differ significantly with respect to clinical outcome, is to our knowledge the first description of a genotype/phenotype correlation in autosomal dominant polycystic kidney disease. It also provides evidence against complete loss of function of the mutant PKD2 gene product.
Recently the second gene for autosomal dominant poly-cystic kidney disease (ADPKD), located on chromosome 4q21-q22, has been cloned and characterized. The gene encodes an integral membrane protein, ...polycystin-2, that shows amino acid similarity to the PKD1 gene product and to the family of voltage-activated calcium (and sodium) channels. We have systematically screened the gene for mutations by single-strand conformation—polymorphism analysis in 35 families with the second type of ADPKD and have identified 20 mutations. So far, most mutations found seem to be unique and occur throughout the gene, without any evidence of clustering. In addition to small deletions, insertions, and substitutions leading to premature translation stops, one amino acid substitution and five possible splice-site mutations have been found. These findings suggest that the first step toward cyst formation in PKD2 patients is the loss of one functional copy of polycystin-2.
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