The 1960 and 1964 Jacksonville Riots

As the 1950 ended and a new decade began, leaders of the civil rights movement grew impatient. Nearly six year had passed since the United State Supreme Court had laid the foundation for ending segregation. Nevertheless, for African Americans little had changed. Blacks continued to languish at the bottom of American society, systematically denied the legal protection afforded to even America\u27s newest immigrants. Forced to endure second-rate educational and social services, southern blacks increased the pressure on policy makers

The Fourteenth Amendment: The Great Equalizer of the American People

The Fourteenth Amendment to the United States Constitution, which was ratified on July 28, 1868, demonstrated the change in attitude, which hit many Americans after the chaotic Civil War. It was America’s first attempt to legally challenge White supremacist ideas by creating a truly equal multiracial society. With its emphasis on equal protection and equal justice, the Fourteenth Amendment was intended to be the great equalizer of American people, legally changing African American men into White men so that they could enjoy all the rights, privileges, and immunities of United States citizenship. However, determining the meaning of equality uncovered the racism which characterized Americans. Even though the Fourteenth Amendment changed the law, it could not change White Americans who refused to accept African American equality. The dichotomy in American racial ideas was summed up by two Democratic slogans. First, “The Union as It Is, the Constitution as It Was” represented many American’s desire to return to a prewar constitutional status quo with Whites in a favored position. The other slogan captured in the 1866 Cincinnati Enquirer, “Slavery is dead, . . . the negro is not, there is the misfortune” underscored the real problem. Abolishing slavery did not solve America’s race problem. The Civil War changed American racial laws, but it did not change American racial attitudes. It was not until the Warren Court’s decision in Brown v. Board of Education that the courts finally instituted Fourteenth Amendment principles and attempted to legally create racial equality, as well as color blindness when dispensing justice and carrying out social policy

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570

Unemployment and its association with health-relevant actions: investigating the role of time perspective with German census data

Schunck R, Rogge B. Unemployment and its association with health-relevant actions: investigating the role of time perspective with German census data. International Journal of Public Health. 2010;55(4):271-278.Objective In this study, we seek to explain how unemployment is related to an increase in health-damaging actions. A short time perspective, that is an orientation towards the present rather than the future, is hypothesised to account for this effect. The concept of time perspective is located within an action theoretical framework and the hypothesis is tested empirically. Methods We investigated the unemployed people’s smoking behaviour and body-mass index (BMI) using German microcensus data from 2003. Data from 77,766 respondents (88.60% employed and 11.40% unemployed) were analysed. Multivariate regression analysis was applied to test our hypotheses. Results Unemployment is associated with a 46% higher probability to smoke and with a 0.37 unit increase in BMI compared to employment. The likelihood of smoking steadily increases with the duration of unemployment, while only unemployment spells of 4 years and longer are significantly related to BMI. Yet, the smoking probability of those unemployed who have a long time perspective is 74% lower and their BMI is 1.81 lower than those who do not have a long time perspective. Conclusion Unemployment is negatively associated with health-relevant actions. This effect varies according to persons’ time perspectives. Our approach delivers an innovative view on why unemployed individuals exercise more health-damaging actions than the employed

Mapping the human genetic architecture of COVID-19

The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3–7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease