Art Dent

Tom has been a Columbia Basin resident most of his life. He became a professional pilot in 1976, and soon after founded Tom Dent Aviation, which offered aerial application, pilot service and flight instruction for area agriculture and industry. Tom lives with his family on the Flying T Ranch,...

Dent came to Emory from Hunter College of the City University of New York in New York City, where she served as acting provost and vice president for academic affairs as well as vice president for student success and learning innovation.

Art Dent

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At Hunter College, Dent was co-chair of the Presidential Task Force for the Advancement of Racial Equity. Important to her work at Emory, Dent believes strongly in the role of the library and museum in civic outreach and has a deep understanding of libraries and museums as centers of community empowerment and civic responsibility. Dent is an active scholar who travels, conducts and publishes high-impact research, and presents globally. She has a robust and consistent record of scholarly achievement in the areas of chronic poverty and literacy, rural African libraries, and literacy culture development and is a Fulbright Scholar.

The chromatin field has been galvanized in the last several years by the identification of histone acetyltransferases (HATs), histone deacetylases (HDACs), histone methyltransferases (HMTs), and other chromatin modifying enzymes. It has been further stimulated by the discovery of modified-histone binding motifs in nonhistone proteins and the realization that regulatory switches are created by the cross-regulation of particular modifications. However, the functions of many histone modifying enzymes in vivo are still not well defined. Nor is it clear whether post-translational modifications in other proteins are cross-regulated as they are in histones. Research in the Dent lab addresses these important questions using a combination of genetic, molecular, and biochemical approaches and a variety of model systems, including Saccharomyces cerevesiae, mice, embryonic stem cells, and tissue culture cell lines.

The diagnosis is established in a male proband with the typical clinical findings and a family history consistent with X-linked inheritance who has a pathogenic variant in either CLCN5 (known as Dent disease 1) or in OCRL (known as Dent disease 2). Heterozygous females are usually asymptomatic, but some exhibit LMW proteinuria and hypercalciuria, and others with kidney stones have also been described. Heterozygous females are most likely to be identified by familial molecular genetic testing related to a male proband.

Surveillance: Monitor at least annually urinary calcium excretion, renal function (glomerular filtration rate), and the parameters used to stage CKD (i.e., blood pressure, hematocrit/hemoglobin, and serum calcium and phosphorous concentrations). Monitor more frequently when CKD is evident.

Dent disease is inherited in an X-linked manner. The father of an affected male will not have the disease nor will he be hemizygous for the pathogenic variant. If the mother of the proband has a pathogenic variant, the chance of transmitting it in each pregnancy is 50%. Males who inherit the pathogenic variant will be affected; females who inherit the pathogenic variant will be carriers and will usually not be significantly affected. Affected males pass the pathogenic variant to all of their daughters (who become carriers) and none of their sons. Carrier testing for at-risk female relatives and prenatal and preimplantation genetic testing are possible if the pathogenic variant in the family has been identified.

Male proband. The diagnosis of Dent disease is established in a male proband with the identification of a hemizygous pathogenic variant in either CLCN5 (Dent disease 1) or OCRL (Dent disease 2) by molecular genetic testing (see Table 2).

A multigene panel that includes CLCN5, OCRL, and other genes of interest (see Differential Diagnosis) can also be considered as a first step. Note: (1) The genes included in the panel and the diagnostic sensitivity of the testing used for each gene vary by laboratory and are likely to change over time. (2) Some multigene panels may include genes not associated with the condition discussed in this GeneReview; thus, clinicians need to determine which multigene panel is most likely to identify the genetic cause of the condition while limiting identification of variants of uncertain significance and pathogenic variants in genes that do not explain the underlying phenotype. (3) Methods used in a panel may include sequence analysis, deletion/duplication analysis, and/or other non-sequencing-based tests.

Glomerular disease. Some individuals with Dent disease 1 with more severe proteinuria were found to have focal segmental glomerulosclerosis (FSGS) or global sclerosis on kidney biopsy [Copelovitch et al 2007, Frishberg et al 2009]. Most cases of FSGS are idiopathic, but FSGS can be seen in association with obesity or progressive chronic kidney disease of any cause. FSGS associated with Dent disease can be identified by the prominent low molecular weight (LMW) proteinuria and confirmed by genetic testing.

It is appropriate to evaluate male relatives at risk for Dent disease 1 (caused by mutation of CLCN5) or Dent disease 2 (caused by mutation of OCRL) in order to identify as early as possible those who would benefit from initiation of treatment and preventive measures.

Note: Molecular genetic testing may be able to identify the family member in whom a de novo pathogenic variant arose, information that could help determine genetic risk status of the extended family.

Once the CLCN5 or OCRL pathogenic variant has been identified in an affected family member, prenatal testing for a pregnancy at increased risk and preimplantation genetic testing are possible.

Normal gene product. The clC-5 isoform NP_000075.1, encoded by transcript NM_000084.2, comprises 746 amino acids. The protein is a voltage-dependent two chloride/proton exchanger. In human kidney, it is expressed in proximal tubular cells, in alpha and beta intercalated cells of the cortical collecting tubule, and in the thick ascending limb of Henle's loop. The protein localizes in the intracellular subapical endosomes that are involved in the reabsorption of low molecular weight proteins filtered through the glomerulus, which are normally completely reabsorbed [Smith et al 2009]. The function of the protein is to modulate the chloride concentration during proton transport [Carraro-Lacroix et al 2010, Novarino et al 2010].

Dent was originally known as Challensville in the 19th century, named for the local minister Rev. James Challenge.[4] A post office called Challensville was established in 1843, the name was changed to Dent in 1846 at the urging of local resident and then-state representative Charles Reemelin. Reemelin was said to have disliked naming places after people and instead thought that "Dent" represented the geography of the area, with the depression of the land just east of Harrison Pike. The Dent post office closed in 1904.[5] The present name "Dent" is after its setting in a valley (or dent).[6]

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Dent continued to serve as an Aide-de-Camp to General Grant after the Civil War. When Grant became President in 1869, Dent served as a "Military Secretary" at the White House for four years. In this role he oversaw incoming mail and managed all White House visitors for President Grant. After leaving this position during Grant's second term in office, Dent went on to serve another ten years in the U.S. Army at various posts around the country, retiring in 1883 at the rank of Colonel after serving forty years in the Army. As he faced impending death from thorat cancer in 1885, General Grant wished to set aside a small gift for his longtime friend and brother-in-law. In a letter to Dent the following year, Frederick Dent Grant included a $500 check and stated that his father had been "very fond of you."

The DENT ECHO supports and educates primary oral health care providers in the delivery of quality and effective dental care for patients across the state of Texas by facilitating an engaging dialogue between subject matter experts and Texas dental care providers.

Join this growing community of oral health professionals to discuss challenging cases and solutions with colleagues in dentistry while learning about the latest developments from the field.

Session summary: The session described the use of anesthesia and analgesia in the dental practice and cover the main reasons for anesthesia failure in the clinic. Mechanisms of action for the most commonly used analgesics were discussed. Guidance on how to formulate a flexible prescription plan for post-operative pain management was also provided.

Session summary: In the third session of the DENT ECHO featured didactics on Integrating Dental and Medical Health Care by Dr. Luis Yepes, DDS. This was followed by a case presentation and discussion with Carlos Escobar, DDS AEGD resident at UT Health San Antonio School of Dentistry.

The University of Texas Health Science Center at San Antonio, also called UT Health San Antonio, is a leading academic health center with a mission to make lives better through excellence in advanced academics, life-saving research and comprehensive clinical care including health, dental and cancer services.

My research over the last 20 years has focused on novel and emerging therapies for breast cancer as well as treatment-related toxicities including cardiotoxicity. I have led, as the principal investigator for Canada, a global phase III breast cancer trial, and I have been actively involved in steering committees at the International level. I have been a co-investigator of a number of investigator-initiated peer-reviewed funded studies and have been an active member of grant review boards including the Canadian Institute for Health Research (CIHR) and the Canadian Breast Cancer Foundation (CBCF). At the national level, I served for several years as a member of the clinical guidance panel for breast cancer for the Pan Canadian Drug Review. At Duke Health, my research will focus on identifying patients who are at risk of experiencing cancer therapy-related to cardiac dysfunction as well as optimizing cardiac health in order to provide optimal cancer therapy. 2351a5e196