Petition for a Writ of Habeas Corpus

Sheppard exhausted his available state remedies as required by Title 28, USC, Section 2254. On May 31, 1956, the Supreme Court of Ohio affirmed his conviction, 165 0.S. 293; a petition for rehearing was denied on July 5, 1956. The Supreme Court of the United States denied certiorari, 352 U.S. 910; a petition for rehearing was denied, 352 U.S. 955 . A petition for a writ of habeas corpus was dismissed by the Supreme Court of Ohio, 170 0.S. 551 (1958). Sheppard asserted there were no further avenues of revue open to him in the courts of Ohio, and any proceeding therein would be unavailing, for the Ohio courts generally are so biased and prejudiced against him that he will be denied relief in any event. The petition states that Ohio violated Sheppard\u27s federal constitutional right to a fair and impartial trial, and more specifically his federal constitutional right to counsel. Sheppard\u27s repeated motions for change of venue to a district or locale not saturated by the massive prejudicial and inflammatory publicity stimulated were likewise denied. Claims of the petition focused on the personal influences of the local court judge, reelection publicity, and the local media\u27s inflammatory published opinions amongst numerous incidents of abuse of power by government officials. As a result of the facts and circumstances set forth, petitioner was denied a fair and impartial trial, and was further denied the equal protection of the laws of the state of Ohio; petitioner\u27s trial was not a trial at all, but a sham proceeding conducted and controlled by persons of official responsibility whose primary purpose was to satisfy the populace which had been convinced by irresponsible news media that petitioner was guilty despite the marked lack of evidence tending to prove such guilt; petitioner was subjected to trial by newspaper, and was subjected specifically to the perverted power of the Cleveland Press, which sought to and did cause petitioner to be convicted in violation of his constitutional rights

Affidavit of Poverty and Motion to Proceed in Forma Pauperis in Habeas Corpus Proceedings

While incarcerated in the Ohio State Penitentiary serving a sentence of life imprisonment, Sam Sheppard submitted this affidavit and motion claiming his liberty was restrained in violation of the United States Constitution. Sheppard, insolvent, made this affidavit for the purpose of availing himself of the rights and privileges afforded indigents under Title 28 U.S. C., § 1915

Petition for a Writ of Habeas Corpus

Sheppard exhausted his available state remedies as required by Title 28, USC, Section 2254. On May 31, 1956, the Supreme Court of Ohio affirmed his conviction, 165 0.S. 293; a petition for rehearing was denied on July 5, 1956. The Supreme Court of the United States denied certiorari, 352 U.S. 910; a petition for rehearing was denied, 352 U.S. 955 . A petition for a writ of habeas corpus was dismissed by the Supreme Court of Ohio, 170 0.S. 551 (1958). Sheppard asserted there were no further avenues of revue open to him in the courts of Ohio, and any proceeding therein would be unavailing, for the Ohio courts generally are so biased and prejudiced against him that he will be denied relief in any event. The petition states that Ohio violated Sheppard\u27s federal constitutional right to a fair and impartial trial, and more specifically his federal constitutional right to counsel. Sheppard\u27s repeated motions for change of venue to a district or locale not saturated by the massive prejudicial and inflammatory publicity stimulated were likewise denied. Claims of the petition focused on the personal influences of the local court judge, reelection publicity, and the local media\u27s inflammatory published opinions amongst numerous incidents of abuse of power by government officials. As a result of the facts and circumstances set forth, petitioner was denied a fair and impartial trial, and was further denied the equal protection of the laws of the state of Ohio; petitioner\u27s trial was not a trial at all, but a sham proceeding conducted and controlled by persons of official responsibility whose primary purpose was to satisfy the populace which had been convinced by irresponsible news media that petitioner was guilty despite the marked lack of evidence tending to prove such guilt; petitioner was subjected to trial by newspaper, and was subjected specifically to the perverted power of the Cleveland Press, which sought to and did cause petitioner to be convicted in violation of his constitutional rights

Modern microwave methods in solid state inorganic materials chemistry: from fundamentals to manufacturing

No abstract available

Virus-Infection or 5′ppp-RNA Activates Antiviral Signal through Redistribution of IPS-1 Mediated by MFN1

In virus-infected cells, RIG-I-like receptor (RLR) recognizes cytoplasmic viral RNA and triggers innate immune responses including production of type I and III interferon (IFN) and the subsequent expression of IFN-inducible genes. Interferon-β promoter stimulator 1 (IPS-1, also known as MAVS, VISA and Cardif) is a downstream molecule of RLR and is expressed on the outer membrane of mitochondria. While it is known that the location of IPS-1 is essential to its function, its underlying mechanism is unknown. Our aim in this study was to delineate the function of mitochondria so as to identify more precisely its role in innate immunity. In doing so we discovered that viral infection as well as transfection with 5′ppp-RNA resulted in the redistribution of IPS-1 to form speckle-like aggregates in cells. We further found that Mitofusin 1 (MFN1), a key regulator of mitochondrial fusion and a protein associated with IPS-1 on the outer membrane of mitochondria, positively regulates RLR-mediated innate antiviral responses. Conversely, specific knockdown of MFN1 abrogates both the virus-induced redistribution of IPS-1 and IFN production. Our study suggests that mitochondria participate in the segregation of IPS-1 through their fusion processes

Multiple Interferon Stimulated Genes Synergize with the Zinc Finger Antiviral Protein to Mediate Anti-Alphavirus Activity

The zinc finger antiviral protein (ZAP) is a host factor that mediates inhibition of viruses in the Filoviridae, Retroviridae and Togaviridae families. We previously demonstrated that ZAP blocks replication of Sindbis virus (SINV), the prototype Alphavirus in the Togaviridae family at an early step prior to translation of the incoming genome and that synergy between ZAP and one or more interferon stimulated genes (ISGs) resulted in maximal inhibitory activity. The present study aimed to identify those ISGs that synergize with ZAP to mediate Alphavirus inhibition. Using a library of lentiviruses individually expressing more than 350 ISGs, we screened for inhibitory activity in interferon defective cells with or without ZAP overexpression. Confirmatory tests of the 23 ISGs demonstrating the largest infection reduction in combination with ZAP revealed that 16 were synergistic. Confirmatory tests of all potentially synergistic ISGs revealed 15 additional ISGs with a statistically significant synergistic effect in combination with ZAP. These 31 ISGs are candidates for further mechanistic studies. The number and diversity of the identified ZAP-synergistic ISGs lead us to speculate that ZAP may play an important role in priming the cell for optimal ISG function

Domestication of Campylobacter jejuni NCTC 11168

Reference and type strains of well-known bacteria have been a cornerstone of microbiology research for decades. The sharing of well-characterized isolates among laboratories has run in parallel with research efforts and enhanced the reproducibility of experiments, leading to a wealth of knowledge about trait variation in different species and the underlying genetics. Campylobacter jejuni strain NCTC 11168, deposited at the National Collection of Type Cultures in 1977, has been adopted widely as a reference strain by researchers worldwide and was the first Campylobacter for which the complete genome was published (in 2000). In this study, we collected 23 C . jejuni NCTC 11168 reference isolates from laboratories across the UK and compared variation in simple laboratory phenotypes with genetic variation in sequenced genomes. Putatively identical isolates, identified previously to have aberrant phenotypes, varied by up to 281 SNPs (in 15 genes) compared to the most recent reference strain. Isolates also display considerable phenotype variation in motility, morphology, growth at 37 °C, invasion of chicken and human cell lines, and susceptibility to ampicillin. This study provides evidence of ongoing evolutionary change among C. jejuni isolates as they are cultured in different laboratories and highlights the need for careful consideration of genetic variation within laboratory reference strains. This article contains data hosted by Microreact

Th1-Th17 Cells Mediate Protective Adaptive Immunity against Staphylococcus aureus and Candida albicans Infection in Mice

We sought to define protective mechanisms of immunity to Staphylococcus aureus and Candida albicans bloodstream infections in mice immunized with the recombinant N-terminus of Als3p (rAls3p-N) vaccine plus aluminum hydroxide (Al(OH3) adjuvant, or adjuvant controls. Deficiency of IFN-γ but not IL-17A enhanced susceptibility of control mice to both infections. However, vaccine-induced protective immunity against both infections required CD4+ T-cell-derived IFN-γ and IL-17A, and functional phagocytic effectors. Vaccination primed Th1, Th17, and Th1/17 lymphocytes, which produced pro-inflammatory cytokines that enhanced phagocytic killing of both organisms. Vaccinated, infected mice had increased IFN-γ, IL-17, and KC, increased neutrophil influx, and decreased organism burden in tissues. In summary, rAls3p-N vaccination induced a Th1/Th17 response, resulting in recruitment and activation of phagocytes at sites of infection, and more effective clearance of S. aureus and C. albicans from tissues. Thus, vaccine-mediated adaptive immunity can protect against both infections by targeting microbes for destruction by innate effectors