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101.
102.
Kuan-Ying A. Huang Pramila Rijal Lisa Schimanski Timothy J. Powell Tzou-Yien Lin John W. McCauley Rodney S. Daniels Alain R. Townsend 《The Journal of clinical investigation》2015,125(7):2631-2645
The selective pressure that drives antigenic changes in influenza viruses is thought to
originate from the human immune response. Here, we have characterized the B cell
repertoire from a previously vaccinated donor whose serum had reduced neutralizing
activity against the recently evolved clade 6B H1N1pdm09 viruses. While the response was
markedly polyclonal, 88% of clones failed to recognize clade 6B viruses; however, the
ability to neutralize A/USSR/90/1977 influenza, to which the donor would have been exposed
in childhood, was retained. In vitro selection of virus variants with representative
monoclonal antibodies revealed that a single amino acid replacement at residue K163 in the
Sa antigenic site, which is characteristic of the clade 6B viruses, was responsible for
resistance to neutralization by multiple monoclonal antibodies and the donor serum. The
K163 residue lies in a part of a conserved surface that is common to the hemagglutinins of
the 1977 and 2009 H1N1 viruses. Vaccination with the 2009 hemagglutinin induced an
antibody response tightly focused on this common surface that is capable of selecting
current antigenic drift variants in H1N1pdm09 influenza viruses. Moreover, amino acid
replacement at K163 was not highlighted by standard ferret antisera. Human monoclonal
antibodies may be a useful adjunct to ferret antisera for detecting antigenic drift in
influenza viruses. 相似文献
103.
104.
105.
Michael A. Weber MD Ernesto L. Schiffrin MD William B. White MD Samuel Mann MD Lars H. Lindholm MD John G. Kenerson MD John M. Flack MD Barry L. Carter Pharm D Barry J. Materson MD C. Venkata S. Ram MD Debbie L. Cohen MD Jean‐Claude Cadet MD Roger R. Jean‐Charles MD Sandra Taler MD David Kountz MD Raymond R. Townsend MD John Chalmers MD Agustin J. Ramirez MD George L. Bakris MD Jiguang Wang MD Aletta E. Schutte MD John D. Bisognano MD Rhian M. Touyz MD Dominic Sica MD Stephen B. Harrap MD 《Journal of clinical hypertension (Greenwich, Conn.)》2014,16(1):14-26
106.
I. Filges E. Nosova E. Bruder S. Tercanli K. Townsend W.T. Gibson B. Röthlisberger K. Heinimann J.G. Hall C.Y. Gregory‐Evans W.W. Wasserman P. Miny J.M. Friedman 《Clinical genetics》2014,86(3):220-228
Gene discovery using massively parallel sequencing has focused on phenotypes diagnosed postnatally such as well‐characterized syndromes or intellectual disability, but is rarely reported for fetal disorders. We used family‐based whole‐exome sequencing in order to identify causal variants for a recurrent pattern of an undescribed lethal fetal congenital anomaly syndrome. The clinical signs included intrauterine growth restriction (IUGR), severe microcephaly, renal cystic dysplasia/agenesis and complex brain and genitourinary malformations. The phenotype was compatible with a ciliopathy, but not diagnostic of any known condition. We hypothesized biallelic disruption of a gene leading to a defect related to the primary cilium. We identified novel autosomal recessive truncating mutations in KIF14 that segregated with the phenotype. Mice with autosomal recessive mutations in the same gene have recently been shown to have a strikingly similar phenotype. Genotype–phenotype correlations indicate that the function of KIF14 in cell division and cytokinesis can be linked to a role in primary cilia, supported by previous cellular and model organism studies of proteins that interact with KIF14. We describe the first human phenotype, a novel lethal ciliary disorder, associated with biallelic inactivating mutations in KIF14. KIF14 may also be considered a candidate gene for allelic viable ciliary and/or microcephaly phenotypes. 相似文献
107.
108.
Kristine Yaffe MD Manjula Kurella‐Tamura MD MPH Lynn Ackerson PhD Tina D. Hoang MSPH Amanda H. Anderson PhD Mark Duckworth MPH Alan S. Go MD Marie Krousel‐Wood MD MSPH John W. Kusek PhD James P. Lash MD Akinlolu Ojo MD PhD Nancy Robinson PhD Ashwini R. Sehgal MD James H. Sondheimer MD Susan Steigerwalt MD Raymond R. Townsend MD the CRIC Study Investigators 《Journal of the American Geriatrics Society》2014,62(9):1623-1629
109.
Sreekanth Vemulapalli Jamy Ard George L. Bakris Deepak L. Bhatt Alan S. Brown William C. Cushman Keith C. Ferdinand John M. Flack Jerome L. Fleg Barry T. Katzen John B. Kostis Suzanne Oparil Chet B. Patel Carl J. Pepine Ileana L. Piña Krishna J. Rocha-Singh Raymond R. Townsend Eric D. Peterson Robert M. Califf Manesh R. Patel 《American heart journal》2014
110.
Mice are a widely utilized in vivo model for translational salivary gland research but must be used with caution. Specifically, mouse salivary glands are similar in many ways to human salivary glands (i.e., in terms of their anatomy, histology, and physiology) and are both readily available and relatively easy and affordable to maintain. However, there are some significant differences between the two organisms, and by extension, the salivary glands derived from them must be taken into account for translational studies. The current review details pertinent similarities and differences between human and mouse salivary glands and offers practical guidelines for using both for research purposes. 相似文献