Diary of the Rev. John Ward, A. M., vicar of Stratford-upon-Avon, extending from 1648 to 1679. From the original mss. preserved in the library of the Medical society of London.

Microfilmed for preservation

John Ward, M. D..

Mode of access: Internet.

Sketch of the Life of William Blanchard Towne

Sketch of the life of William Blanchard Towne.

London marriage licences 1521-1869.

Memoir of Col. Joseph Lemuel Chester ... by John Ward Dean.

Boston College Law School 75th Celebration Event Salutes J. Donald Monan, S.J., Chancellor of Boston College

On September 13, 2005, in front of a standing-room only crowd of students and faculty, J. Donald Monan, S.J., accepted the Boston College Law School's 75th anniversary Distinguished Service Award from Dean John Garvey for more than thirty years of dedication to the school. Currently Chancellor of Boston College, a position he acquired in 1996, Monan holds the distinction of having been Boston College president for 24 years, the longest tenure in school history.

Can't Get No Satisfaction: Lessons Learned while Developing an Assessment of Faculty Awareness and Attitudes towards Library Services

The presentation was offered as part of the CUNY Library Assessment Conference, Reinventing Libraries: Reinventing Assessment, held at the City University of New York in June 2014.

Clinical and molecular phenotype of Aicardi-Goutières syndrome

Aicardi-Goutières syndrome (AGS) is a genetic encephalopathy whose clinical features mimic those of acquired in utero viral infection. AGS exhibits locus heterogeneity, with mutations identified in genes encoding the 3′→5′ exonuclease TREX1 and the three subunits of the RNASEH2 endonuclease complex. To define the molecular spectrum of AGS, we performed mutation screening in patients, from 127 pedigrees, with a clinical diagnosis of the disease. Biallelic mutations in TREX1, RNASEH2A, RNASEH2B, and RNASEH2C were observed in 31, 3, 47, and 18 families, respectively. In five families, we identified an RNASEH2A or RNASEH2B mutation on one allele only. In one child, the disease occurred because of a de novo heterozygous TREX1 mutation. In 22 families, no mutations were found. Null mutations were common in TREX1, although a specific missense mutation was observed frequently in patients from northern Europe. Almost all mutations in RNASEH2A, RNASEH2B, and RNASEH2C were missense. We identified an RNASEH2C founder mutation in 13 Pakistani families. We also collected clinical data from 123 mutation-positive patients. Two clinical presentations could be delineated: an early-onset neonatal form, highly reminiscent of congenital infection seen particularly with TREX1 mutations, and a later-onset presentation, sometimes occurring after several months of normal development and occasionally associated with remarkably preserved neurological function, most frequently due to RNASEH2B mutations. Mortality was correlated with genotype; 34.3% of patients with TREX1, RNASEH2A, and RNASEH2C mutations versus 8.0% RNASEH2B mutation-positive patients were known to have died (P = .001). Our analysis defines the phenotypic spectrum of AGS and suggests a coherent mutation-screening strategy in this heterogeneous disorder. Additionally, our data indicate that at least one further AGS-causing gene remains to be identified. © 2007 by The American Society of Human Genetics. All rights reserved.

2010 International consensus algorithm for the diagnosis, therapy and management of hereditary angioedema

ABSTRACT: