The Phantom Five Years

For centuries, Vincent de Paul’s birth year was held to be 1576. Pierre Coste’s research established that it was actually 1581, and that Vincent knew his age and referred to it consistently. There are many reasons for the five-year difference in tradition. As was common at the time, Vincent lied about his age at ordination, being nineteen and not the requisite age of twenty-four. Early biographers either left his comments about his age undated or tampered with sources to make them add up to his traditional age of eighty-five at his death

Vincent de Paul\u27s Discernment of His Own Vocation And That of the Congregation of the Mission

Vincent de Paul discovered his vocation and that of the Congregation in several ways. These were fulfilling the Church’s needs, seeking evidence of God’s will in events, and obeying God’s will, either as mandated by superiors or by following inspiration that responded to events. Such inspiration was always carefully examined before being put into practice. These elements are traced through Vincent’s life and career. Through work with Pierre de Berulle, he saw the need for properly formed priests, especially for country parishes. His ministry on the Gondi estates, especially the mission at Folleville, further convinced him of the poor’s need for priests. When no one else would undertake rural missions, Vincent’s obedience compelled him to act on inspiration and to found the Congregation. As part of efforts to reform the clergy, the archbishop obliged the community to give retreats to ordinands. Again, Vincent was led by obedience. His seminary work was an inspiration in response to the same need for priests, but he only began after consulting Cardinal Richelieu

Vincent de Paul\u27s View of Common Life in the Congregation of the Mission

For Vincent de Paul, community life enabled the Congregation to follow Jesus’s example, both in the work of evangelization and in the development of Christlike virtues that supported the work. To be effective missionaries—to travel and to share the life of the poor while evangelizing them—confreres were to embrace poverty. They also were to model Christian behavior for others by demonstrating it among themselves; this was accomplished through the virtues of uniformity, patience, and fraternal charity. Uniformity meant that the confreres were to have the same judgments and practice. Patience called for the tolerance of each other’s faults and the awareness of one’s own faults. Fraternal charity was the most important virtue. Confreres had to show each other Christian love to spread that love through missions. The order of the day is described to show how virtues were to be cultivated. The regimentation of community life and the ways it contributed to the apostolate are also explained

Segregated Catholicism: The Origins of Saint Katharine\u27s Parish, New Orleans

The complicated history of the establishment of Saint Katharine’s, a black parish in New Orleans, is recounted. For reasons explained in the article, the city’s Catholic churches were originally racially integrated. There were two groups of blacks in New Orleans: colored Creoles (the term they used for themselves) and African Americans. Colored Creoles were people of Afro-French descent and they were Catholic. African Americans were Protestant and worshipped in separate churches from whites. This was partly because of racism in the white community and partly because African Americans wanted to control their own religious affairs. Francis Janssens, the archbishop, wanted blacks to control their churches and he wanted to win African American converts. Moreover, he believed there were many defections among colored Creoles. He saw the solution to all of this in Saint Katharine’s establishment, though he stressed that black Catholics were free to choose between it and their home parishes. The colored Creoles opposed segregation for any reason and therefore opposed Saint Katharine’s. The negotiations for its establishment with the Vincentians and with Katharine Drexel, who provided funds, are described in detail. Saint Katharine’s was dedicated in 1895. With the advent of official segregation, it became a successful parish

A New Look At An Old Temptation: Saint Vincent de Paul\u27s Temptation Against Faith and Resolution to Serve the Poor

According to Vincent de Paul’s first biographer, Louis Abelly, Vincent prayed to have a temptation against faith transferred to him to free a doctor of theology who was originally suffering from it. The temptation continued for three or four years until Vincent resolved to serve poor persons. While many biographers have accepted this story, its truth is doubtful for many reasons besides those that follow. Vincent never spoke of having this temptation himself. He never would have prayed for a transfer of temptation without advice from his spiritual director, and this advice would not have been given. The temptation would have occurred during a year that he said was the happiest of his life. At the time that the temptation would have ended, Vincent was not serving the poor. Instead, he was reforming clergy, converting heretics, and serving the Gondi family. It is well documented that Vincent’s work with persons who were poor developed out of responses to unanticipated needs and events, not as a result of an astonishing conversion

God is Wonderful in All His Works : A Contemporary Account of Vincentian Activity in the District of Cape Girardeau, Missouri, 1828-1850

John Francis McGerry recounts the Vincentians’ role in establishing Catholicism in the Cape Girardeau region. He describes John Timon’s ministry, which mostly consisted of baptisms, work with condemned prisoners, and various efforts to help the Daugherty family, including purchasing their land. McGerry also relates how John Mary Odin and John Brands worked with non-Catholics and converts despite anti-Catholic prejudice. Finally, McGerry gives details regarding the building and beginning of Saint Vincent’s College at Cape Girardeau

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

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

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization 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