Invalid Forensic Science Testimony and Wrongful Convictions

This is the first study to explore the forensic science testimony by prosecution experts in the trials of innocent persons, all convicted of serious crimes, who were later exonerated by post-conviction DNA testing. Trial transcripts were sought for all 156 exonerees identified as having trial testimony by forensic analysts, of which 137 were located and reviewed. These trials most commonly included testimony concerning serological analysis and microscopic hair comparison, but some included bite mark, shoe print, soil, fiber, and fingerprint comparisons, and several included DNA testing. This study found that in the bulk of these trials of innocent defendants - 82 cases or 60% - forensic analysts called by the prosecution provided invalid testimony at trial - that is, testimony with conclusions misstating empirical data or wholly unsupported by empirical data. This was not the testimony of a mere handful of analysts: this set of trials included invalid testimony by 72 forensic analysts called by the prosecution and employed by 52 laboratories, practices, or hospitals from 25 states. Unfortunately, the adversarial process largely failed to police this invalid testimony. Defense counsel rarely cross-examined analysts concerning invalid testimony and rarely obtained experts of their own. In the few cases in which invalid forensic science was challenged, judges seldom provided relief. This evidence supports efforts to create scientific oversight mechanisms for reviewing forensic testimony and to develop clear scientific standards for written reports and testimony. The scientific community can through an official government entity promulgate standards to ensure the valid presentation of forensic science in criminal cases and thus the integrity and fairness of the criminal process

Invalid Forensic Science Testimony and Wrongful Convictions

This is the first study to explore the forensic science testimony by prosecution experts in the trials of innocent persons, all convicted of serious crimes, who were later exonerated by post-conviction DNA testing. Trial transcripts were sought for all 156 exonerees identified as having trial testimony by forensic analysts, of which 137 were located and reviewed. These trials most commonly included testimony concerning serological analysis and microscopic hair comparison, but some included bite mark, shoe print, soil, fiber, and fingerprint comparisons, and several included DNA testing. This study found that in the bulk of these trials of innocent defendants - 82 cases or 60% - forensic analysts called by the prosecution provided invalid testimony at trial - that is, testimony with conclusions misstating empirical data or wholly unsupported by empirical data. This was not the testimony of a mere handful of analysts: this set of trials included invalid testimony by 72 forensic analysts called by the prosecution and employed by 52 laboratories, practices, or hospitals from 25 states. Unfortunately, the adversarial process largely failed to police this invalid testimony. Defense counsel rarely cross-examined analysts concerning invalid testimony and rarely obtained experts of their own. In the few cases in which invalid forensic science was challenged, judges seldom provided relief. This evidence supports efforts to create scientific oversight mechanisms for reviewing forensic testimony and to develop clear scientific standards for written reports and testimony. The scientific community can through an official government entity promulgate standards to ensure the valid presentation of forensic science in criminal cases and thus the integrity and fairness of the criminal process

Linux implementation of the MEP protocol for the LHCb experiment

We present a kernel implementation of the LHCb MEP protocol. MEP is implemented in the IP stack as a loadable module. This allows for better monitoring at the network level and can potentially reduce the overhead associated with the reception of the data

ALMA data suggest the presence of a spiral structure in the inner wind of CW Leo

(abbreviated) We aim to study the inner wind of the well-known AGB star CW Leo. Different diagnostics probing different geometrical scales have pointed toward a non-homogeneous mass-loss process: dust clumps are observed at milli-arcsec scale, a bipolar structure is seen at arcsecond-scale and multi-concentric shells are detected beyond 1". We present the first ALMA Cycle 0 band 9 data around 650 GHz. The full-resolution data have a spatial resolution of 0".42x0".24, allowing us to study the morpho-kinematical structure within ~6". Results: We have detected 25 molecular lines. The emission of all but one line is spatially resolved. The dust and molecular lines are centered around the continuum peak position. The dust emission has an asymmetric distribution with a central peak flux density of ~2 Jy. The molecular emission lines trace different regions in the wind acceleration region and suggest that the wind velocity increases rapidly from about 5 R* almost reaching the terminal velocity at ~11 R*. The channel maps for the brighter lines show a complex structure; specifically for the 13CO J=6-5 line different arcs are detected within the first few arcseconds. The curved structure present in the PV map of the 13CO J=6-5 line can be explained by a spiral structure in the inner wind, probably induced by a binary companion. From modeling the ALMA data, we deduce that the potential orbital axis for the binary system lies at a position angle of ~10-20 deg to the North-East and that the spiral structure is seen almost edge-on. We infer an orbital period of 55 yr and a binary separation of 25 au (or ~8.2 R*). We tentatively estimate that the companion is an unevolved low-mass main-sequence star. The ALMA data hence provide us for the first time with the crucial kinematical link between the dust clumps seen at milli-arcsecond scale and the almost concentric arcs seen at arcsecond scale.Comment: 22 pages, 18 Figures, Astronomy & Astrophysic

Understanding phenotypic variation in rodent models with germline Apc mutations

Adenomatous Polyposis Coli (APC) is best known for its crucial role in colorectal cancer suppression. Rodent models with various Apc mutations have enabled experimental validation of different Apc functions in tumors and normal tissues. Since the development of the first mouse model with a germline Apc mutation in the early 1990s, twenty other Apc mouse and rat models have been generated. This article compares and contrasts currently available Apc rodent models with particular emphasis on providing potential explanations for their reported variation in three areas: 1) intestinal polyp multiplicity, 2) intestinal polyp distribution, and 3) extra intestinal phenotypes

Distribution of Water Vapor in Molecular Clouds

We report the results of a large-area study of water vapor along the Orion Molecular Cloud ridge, the purpose of which was to determine the depth-dependent distribution of gas-phase water in dense molecular clouds. We find that the water vapor measured toward 77 spatial positions along the face-on Orion ridge, excluding positions surrounding the outflow associated with BN/KL and IRc2, display integrated intensities that correlate strongly with known cloud surface tracers such as CN, C2H, 13CO J =5-4, and HCN, and less well with the volume tracer N2H+. Moreover, at total column densities corresponding to Av < 15 mag., the ratio of H2O to C18O integrated intensities shows a clear rise approaching the cloud surface. We show that this behavior cannot be accounted for by either optical depth or excitation effects, but suggests that gas-phase water abundances fall at large Av. These results are important as they affect measures of the true water-vapor abundance in molecular clouds by highlighting the limitations of comparing measured water vapor column densities with such traditional cloud tracers as 13CO or C18O. These results also support cloud models that incorporate freeze-out of molecules as a critical component in determining the depth-dependent abundance of water vapor

SWAS observations of comet 9P/Tempel 1 and Deep Impact

On 4 July 2005 at 1:52 UT the Deep Impact mission successfully completed its goal to hit the nucleus of 9P/Tempel 1 with an impactor, forming a crater on the nucleus and ejecting material into the coma of the comet. The 370 kg impactor collided with the sunlit side of the nucleus with a relative velocity of 10.2 km/s. NASA's Submillimeter Wave Astronomy Satellite (SWAS) observed the 1(10)-1(01) ortho-water ground-state rotational transition in comet 9P/Tempel 1 before, during, and after the impact. No excess emission from the impact was detected by SWAS. However, the water production rate of the comet showed large natural variations of more than a factor of three during the weeks before the impact.Comment: to appear in the proceedings of the IAU Symposium No. 231: "Astrochemistry - Recent Successes and Current Callenges". Typo corrected in author affiliation lis

Constitutive Musashi1 expression impairs mouse postnatal development and intestinal homeostasis

Evolutionarily conserved RNA-binding protein Musashi1 (Msi1) can regulate developmentally relevant genes. Here we report the generation and characterization of a mouse model that allows inducible Msi1 overexpression in a temporal and tissue-specific manner. We show that ubiquitous Msi1 induction in ∼5-wk-old mice delays overall growth, alters organ-to-body proportions, and causes premature death. Msi1-overexpressing mice had shortened intestines, diminished intestinal epithelial cell (IEC) proliferation, and decreased growth of small intestine villi and colon crypts. Although Lgr5-positive intestinal stem cell numbers remained constant in Msi1-overexpressing tissue, an observed reduction in Cdc20 expression provided a potential mechanism underlying the intestinal growth defects. We further demonstrated that Msi1 overexpression affects IEC differentiation in a region-specific manner, with ileum tissue being influenced the most. Ilea of mutant mice displayed increased expression of enterocyte markers, but reduced expression of the goblet cell marker Mucin2 and fewer Paneth cells. A higher hairy and enhancer of split 1:mouse atonal homolog 1 ratio in ilea from Msi1-overexpressing mice implicated Notch signaling in inducing enterocyte differentiation. Together, this work implicates Msi1 in mouse postnatal development of multiple organs, with Notch signaling alterations contributing to intestinal defects. This new mouse model will be a useful tool to further elucidate the role of Msi1 in other tissue settings