1.2 News Article About US Supreme Court Justices Rule in Favor of Lloyd Gaines by 6 to 2 Vote in The Call Newspaper

Following the decision, northern newspapers hailed it as “the Supreme Court speaking out in defense of the quality of human rights.” The Kansas City Call, one of the leading black newspapers in Missouri, declared, “If keeping the races separate is so important to Missourians that coeducation is unthinkable then let them count the cost!” The NAACP’s long-term plan for casting financial burden upon the Jim Crow states was now a reality.

2.1 Lloyd Gaines close up image

Charles Hamilton Houston and other NAACP attorneys assembled in early October 1939 to take depositions in preparation for the hearing scheduled a week later in Columbia to determine whether the university had complied with the Gaines decision. Attorneys took depositions from all of the instructors of the new LU law school as their preparation for the court proceedings wound down. The deposition of Lloyd Gaines was next. Attorneys planned to ask Gaines whether he considered Lincoln to be as good of a law school as Missouri and whether he planned to enroll. Called for questioning, Gaines did not respond. He could not be located anywhere. Lloyd’s mother, Callie Gaines, recalled that in January her son “left here to go to Kansas City to make a speech. That’s the last I saw of him.” While in Kansas City, Gaines spoke at the Centennial Methodist Church. He also looked for work, but not finding any caught a train for Chicago, telling people in Kansas City that he would stay a few days and return home.

2.3 Eddie Mae Page, Friend of Lloyd Gaines in Chicago

During this time Lloyd Gaines took meals at the home of Eddie Mae Page; a friend from St. Louis. Running low on funds, he stayed at the Alpha Phi Alpha house where members took up a collection for him. On a rainy night, March 19, 1939, Lloyd Gaines told friends that he was going to buy stamps and would be right back. To this day, Lloyd L. Gaines has never been located.

2.4 "The Strange Disappearance of Lloyd Gaines"

The May 1951 Ebony Magazine Article "The Strange Disappearance of Lloyd Gaines"

2. 6 Memorial for Lloyd Gaines, St. Peter's Cemetery, Normandy, St. Louis County, Missouri

What happened to Gaines? There are many ideas ranging from being murdered or lynched, being bribed to run away, or disappearing on his own to get away from the pressure of celebrity. That final possibility was brought about by Dr. Greene, who claimed that a man who sounded like Gaines had phoned him while in Mexico and wished to meet. The man never showed up. A recent theory is one of where Lloyd was kidnapped by opponents of the Gaines court decision who took him to Jefferson City and lynched him in McClung Park. All of these theories are speculation and the fact remains that Lloyd Gaines’ whereabouts are a mystery to this day.

3.3 University of Missouri awarded a law degree to Lloyd Gaines in 2006

In 2006, a law degree was posthumously awarded to Lloyd and accepted by his nephew, George Gaines.

3.2 Lloyd L. Gaines/Marian O'Fallon Oldham Black Culture Center at University of Missouri

Lloyd Gaines’ memory has been honored most notably by the University of Missouri. In 1995, a law scholarship in his name was established at the institution. Also, in 2001, MU opened the Gaines/Oldham Black Culture at MU which shares his name.

3.4 University of Missouri Doctor of Law Degree to Lloyd Lionel Gaines

On May 13, 2006, University of Missouri awarded Lloyd Gaines Doctor of Law degree.

3.5 The Missouri State Supreme Court Conferred a Honorary Law License for Lloyd Gaines.

On September 28th, 2006, the Missouri State Supreme Court conferred a posthumous law license for Mr. Gaines.

Exhibit: Lloyd Gaines: The Man, The Mission & The Mystery

This Exhibit is on display at Inman E. Page Library Room 317 and online at Blue Tiger Commons: http://bluetigercommons.lincolnu.edu/lgaines_exhibit/

A “REVOLTA” DE JEÚ E A ESTELA DE DÃ: Um Estudo Em 2 Reis 10,28-36

A pesquisa tem por objetivo trabalhar o evento da Revolta de Jeú, em conjunto com a Estela de Dã, tendo como ponto de partida para tal, a exegese da perícope de 2 Reis 10-28,36. A história Deuteronomista apresenta o ato da Revolta de Jeú como sendo um feito demasiadamente importante, na restauração do culto a Javé em Israel, a partir de um contexto onde o culto a outras divindades, em Israel Norte, estava em pleno curso. No entanto, a partir da análise conjunta da Estela de Dã, que tem como provável autor o rei Hazael de Damasco, somos desafiados a ler esta história pelas entrelinhas não contempladas pelo texto, que apontam para uma participação ativa de Hazael, nos desfechos referentes a Revolta de Jeú, como sendo o responsável direto que proporcionou a subida de Jeú ao trono em Israel, clarificando desta forma este importante período na história Bíblica. Para tal análise, observar-se-á três distintos tópicos, ligados diretamente ao tema proposto: (1) A Revolta de Jeú e a Redação Deuteronomista, a partir do estudo exegético da perícope de 2 Reis 10,28-36, onde estão descritas informações pontuais sobre período em que Jeú reinou em Israel; (2) Jeú e a Estela de Dã, a partir da apresentação e análise do conteúdo da Estela de Dã, tratando diretamente dos desdobramentos da guerra em Ramote de Gileade, de onde se dá o ponto de partida à Revolta de Jeú; e por fim (3) O Império da Síria, onde a partir da continuidade da análise do conteúdo da Estela de Dã, demonstraremos a significância deste reino, além de apontamentos diretamente ligados ao reinado de Hazael, personagem mui relevante no evento da Revolta de Jeú.

Tumor necrosis factor α plays a central role in immune-mediated clearance of adenoviral vectors

Adenovirus (Ad) gene transfer vectors are rapidly cleared from infected hepatocytes in mice. To determine which effector mechanisms are responsible for elimination of the Ad vectors, we infected mice that were genetically compromised in immune effector pathways [perforin, Fas, or tumor necrosis factor α (TNF-α)] with the Ad vector, Ad5-chloramphenicol acetyl transferase (CAT). Mice were sacrificed at 7–60 days postinfection, and the levels of CAT expression in the liver determined by a quantitative enzymatic assay. When the livers of infected mice were harvested 28 days postinfection, the levels of CAT expression revealed that the effectors most important for the elimination of the Ad vector were TNF-α > Fas > perforin. TNF-α did not have a curative effect on infected hepatocytes, as the administration of TNF-α to infected severe combined immunodeficient mice or to infected cultures in vitro had no specific effect on virus persistence. However, TNF-α-deficient mice demonstrated a striking reduction in the leukocytic infiltration early on in the infection, suggesting that TNF-α deficiency resulted in impaired recruitment of inflammatory cells to the site of inflammation. In addition, the TNF-deficient mice had a significantly reduced humoral immune response to virus infection. These results demonstrate a dominant role of TNF-α in elimination of Ad gene transfer vectors. This result is particularly important because viral proteins that disable TNF-α function have been removed from most Ad vectors, rendering them highly susceptible to TNF-α-mediated elimination.

Presence of an inducible HIV-1 latent reservoir during highly active antiretroviral therapy

Although highly active antiretroviral therapy (HAART) in the form of triple combinations of drugs including protease inhibitors can reduce the plasma viral load of some HIV-1-infected individuals to undetectable levels, it is unclear what the effects of these regimens are on latently infected CD4+ T cells and what role these cells play in the persistence of HIV-1 infection in individuals receiving such treatment. The present study demonstrates that highly purified CD4+ T cells from 13 of 13 patients receiving HAART with an average treatment time of 10 months and with undetectable (<500 copies HIV RNA/ml) plasma viremia by a commonly used bDNA assay carried integrated proviral DNA and were capable of producing infectious virus upon cellular activation in vitro. Phenotypic analysis of HIV-1 produced by activation of latently infected CD4+ T cells revealed the presence in some patients of syncytium-inducing virus. In addition, the presence of unintegrated HIV-1 DNA in infected resting CD4+ T cells from patients receiving HAART, even those with undetectable plasma viremia, suggests persistent active virus replication in vivo.

T cell functions in granulocyte/macrophage colony-stimulating factor deficient mice

Immunological functions were analyzed in mice lacking granulocyte/macrophage colony-stimulating factor (GM-CSF). The response of splenic T cells to allo-antigens, anti-mouse CD3 mAb, interleukin 2 (IL-2), or concanavalin A was comparable in GM-CSF +/+ and GM-CSF −/− mice. To investigate the responses of CD8+ and CD4+ T cells against exogenous antigens, mice were immunized with ovalbumin peptide or with keyhole limpet hemocyanin (KLH). Cytotoxic CD8+ T cells with specificity for ovalbumin peptide could not be induced in GM-CSF −/− mice. After immunization with KLH, there was a delay in IgG generation, particularly IgG2a, in GM-CSF −/− mice. Purified CD4+ T cells from GM-CSF −/− mice immunized with KLH showed impaired proliferative responses and produced low amounts of interferon-γ (IFN-γ) and IL-4 when KLH-pulsed B cells or spleen cells were used as antigen presenting cells (APC). When enriched dendritic cells (DC) were used as APC, CD4+ T cells from GM-CSF −/− mice proliferated as well as those from GM-CSF +/+ mice and produced high amounts of IFN-γ and IL-4. To analyze the rescue effect of DC on CD4+ T cells, supernatants from (i) CD4+ T cells cultured with KLH-pulsed DC or (ii) DC cultured with recombinant GM-CSF were transferred to cultures of CD4+ T cells and KLH-pulsed spleen cells from GM-CSF −/− mice. Supernatants from both DC sources contained a factor or factors that restored proliferative responses and IFN-γ production of CD4+ T cells from GM-CSF −/− mice.

Endogenous tumor necrosis factor protects the adult cardiac myocyte against ischemic-induced apoptosis in a murine model of acute myocardial infarction

Previous studies have shown that proinflammatory cytokines, such as tumor necrosis factor (TNF), are expressed after acute hemodynamic overloading and myocardial ischemia/infarction. To define the role of TNF in the setting of ischemia/infarction, we performed a series of acute coronary artery occlusions in mice lacking one or both TNF receptors. Left ventricular infarct size was assessed at 24 h after acute coronary occlusion by triphenyltetrazolium chloride (TTC) staining in wild-type (both TNF receptors present) and mice lacking either the type 1 (TNFR1), type 2 (TNFR2), or both TNF receptors (TNFR1/TNFR2). Left ventricular infarct size as assessed by TTC staining was significantly greater (P < 0.005) in the TNFR1/TNFR2-deficient mice (77.2% ± 15.3%) when compared with either wild-type mice (46.8% ± 19.4%) or TNFR1-deficient (47.9% ± 10.6%) or TNFR2-deficient (41.6% ± 16.5%) mice. Examination of the extent of necrosis in wild-type and TNFR1/TNFR2-deficient mice by anti-myosin Ab staining demonstrated no significant difference between groups; however, the peak frequency and extent of apoptosis were accelerated in the TNFR1/TNFR2-deficient mice when compared with the wild-type mice. The increase in apoptosis in the TNFR1/TNFR2-deficient mice did not appear to be secondary to a selective up-regulation of the Fas ligand/receptor system in these mice. These data suggest that TNF signaling gives rise to one or more cytoprotective signals that prevent and/or delay the development of cardiac myocyte apoptosis after acute ischemic injury.