Richmond, VA, United States
Richmond, VA, United States

Virginia Commonwealth University is a public research university located in Richmond, Virginia. VCU was founded in 1838 as the medical department of Hampden–Sydney College, becoming the Medical College of Virginia in 1854. In 1968, the Virginia General Assembly merged MCV with the Richmond Professional Institute, founded in 1917, to create Virginia Commonwealth University. Today, more than 31,000 students pursue 222 degree and certificate programs through VCU's 13 schools and one college. The VCU Health System supports the university's health care education, research and patient care mission.With a record $256 million in sponsored research funding in the fiscal year 2011, VCU is designated as a research university with very high research activity by the Carnegie Classification of Institutions of Higher Education. A broad array of university-approved centers and institutes of excellence, involving faculty from multiple disciplines in public policy, biotechnology and health care discoveries, supports the university's research mission. Twenty-eight graduate and first-professional programs are ranked by U.S. News and World Report as among the best in the country. VCU's athletic teams compete in Division I of the NCAA and are collectively known as the VCU Rams. They are members of the Atlantic 10 Conference. The VCU campus includes historic buildings such as the Ginter House, now used by the school's provost. Wikipedia.


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Patent
Virginia Commonwealth University | Date: 2016-03-24

A compound having the formula:


A family of compounds which function as selective ligands for the serotonin receptor 2B (5-HT_(2B)) is identified. Some of the compounds are synthetic non-natural ligands which have a relatively strong interaction with 5-HT2B compared to naturally occurring compounds (some of which are identified for the first time herein as ligands for 5-HT_(2B)). Because the compounds, both naturally occurring and synthetically produced, function as ligands for 5-HT_(2B )they will have application in, for example, the treatment and/or prevention of nervous system disorders such as Alzheimers disease.


Patent
Virginia Commonwealth University | Date: 2016-08-25

The system includes various embodiments of components, including (1) a sensor array, (2) a processor, (3) a transmitter, (4) a receiver-stimulator, and (5) an implantable electrode array. The gustatory implant system generates tastant fingerprints by detecting tastants with an array of chemical sensors and then transmitting variable spatiotemporal stimulation patterns for an electrode array with electrode stimulating points positioned at different locations in the gustatory cortex (e.g., stimulating the chorda tympanic nerve). Different patterns of activity in the gustatory cortex are thereby generated which mimic the sense of taste in a subject. Once trained the system should be usable by a subject to detect or correctly identify or perceive one or more tastes. The system may also include an external electronic device for processing and displaying information to monitor ingestion of various substances in a subject.


Patent
Virginia Commonwealth University | Date: 2015-05-06

L27 in Staphylococcus aureus and other Firmicutes is encoded with an N-terminal extension that is not present in most Gram-negative organisms and is absent from mature ribosomes. We have identified a cysteine protease, conserved among bacteria containing the L27 N-terminal extension, which performs post-translational cleavage of L27. The provided methods have utility for the development of new therapeutic antibiotics that target this novel pathway in order to kill pathogenic Firmicutes and related bacteria.


Patent
Virginia Commonwealth University | Date: 2015-03-25

Constructs and monitoring systems to assess the level of molecules that bind to thrombin (e.g. thrombin regulators and inhibitors) are provided. The constructs are nanosensors comprising i) a thrombin molecule to which is bound a reporter ligand comprising a fluorescent label, ii) a fluorescence-quenching metal nanoparticle, and, optionally iii) a fluorescence-quenching dye molecule attached to one or both of the nanoparticle and the thrombin molecule. The binding of a thrombin regulator or inhibitor to the thrombin molecule displaces the reporter ligand, and the signal from the fluorescent label increases. The increase is proportional to the concentration of thrombin-binding molecule in the sample.


Patent
Virginia Commonwealth University and The Regents Of The University Of Colorado | Date: 2016-08-31

In one example implementation, a method includes receiving, at a computing device, a request to grant a set of requested permissions to an application installed on the computing device, and sending, from the computing device, a permission query request to a recommendation server, where the permission query request includes an identifier for the application, and the set of requested permissions. The method may also include receiving, at the computing device, from the recommendation server, a set of permission recommendations, where the set of permission recommendations indicates whether the recommendation server recommends granting each requested permission from the set of requested permissions. The method may also include displaying the set of requested permissions and the set of permission recommendations, determining a set of granted permissions for the application, granted by a user of the computing device, from the set of requested permissions, and setting the permissions for the application on the computing device using the set of granted permissions.


Our tendency to see the world of psychiatric illness in dichotomous and opposing terms has three major sources: the philosophy of Descartes, the state of neuropathology in late nineteenth century Europe (when disorders were divided into those with and without demonstrable pathology and labeled, respectively, organic and functional), and the influential concept of computer functionalism wherein the computer is viewed as a model for the human mind-brain system (brain-hardware, mind-software). These mutually re-enforcing dichotomies, which have had a pernicious influence on our field, make a clear prediction about how 'difference-makers' (aka causal risk factors) for psychiatric disorders should be distributed in nature. In particular, are psychiatric disorders like our laptops, which when they dysfunction, can be cleanly divided into those with software versus hardware problems? I propose 11 categories of difference-makers for psychiatric illness from molecular genetics through culture and review their distribution in schizophrenia, major depression and alcohol dependence. In no case do these distributions resemble that predicted by the organic-functional/ hardware-software dichotomy. Instead, the causes of psychiatric illness are dappled, distributed widely across multiple categories. We should abandon Cartesian and computer-functionalism-based dichotomies as scientifically inadequate and an impediment to our ability to integrate the diverse information about psychiatric illness our research has produced. Empirically based pluralism provides a rigorous but dappled view of the etiology of psychiatric illness. Critically, it is based not on how we wish the world to be but how the difference-makers for psychiatric illness are in fact distributed. © 2012 Macmillan Publishers Limited All rights reserved.


Kendler K.S.,Virginia Commonwealth University
Molecular Psychiatry | Year: 2013

Psychiatric genetics has taught us a great deal about the nature of psychiatric disorders. Traditional family, twin and adoption studies have demonstrated the substantial role of genetic factors in their etiology, clarified the role of genetic factors in comorbidity, elucidated development pathways, and documented the importance of gene-environment correlation and interaction. We have also received some hard lessons when we were unable to detect replicable genes of large effect size and found that our much-valued candidate genes did not live up to their expected promise. With more mature molecular and statistical methods, we are entering now a different era. Statistical analyses of aggregate molecular signals are validating earlier heritability estimates. Replicated findings from genome-wide association studies are beginning to emerge, as are discoveries of large-effect size rare genomic variants. The number of such findings is likely to soon grow dramatically. The most pressing question facing the field is what biological picture these results will reveal. I articulate four possible scenarios that reflect (i) no, (ii) minimal, (iii) moderate and (iv) high biological coherence in the replicated molecular variant findings, which are soon likely to emerge. I discuss the factors that will likely influence these patterns, including the problems of etiological heterogeneity and multiple realizability. These findings could provide critical insights into the underlying biology of our psychiatric syndromes and potentially permit us to perceive, 'through a glass darkly,' the levels of the mind-brain system that are disordered. © 2013 Macmillan Publishers Limited All rights reserved.


Meot-Ner M.,Virginia Commonwealth University
Chemical Reviews | Year: 2012

A study was conducted to provide detailed information about strong ionic hydrogen bonds (IHB). These strong hydrogen bonds were critical in ionic clusters and nucleation, in electrolytes, ion solvation, and acid-base chemistry, in the structures of ionic crystals, surfaces, silicates, and clays. IHBs were also important in bioenergetics including protein folding, enzyme-active centers, formation of membranes and proton transport, and biomolecular recognition. The energetics of IHB interactions were isolated and studied quantitatively in the gas phase. These studies led to a fundamental understanding of relations between strong ionic hydrogen bond strengths and molecular structure and the solvation of ions in the critical inner shells, and acid-base phenomena and bioenergetics.


Gewirtz D.A.,Virginia Commonwealth University
Cancer Research | Year: 2014

It is generally thought that autophagy has two primary and opposing functions in tumor cells in response to stress induced by chemotherapy or radiation. One is the cytoprotective function that can in theory be inhibited for therapeutic advantage by sensitizing the cells to these treatment modalities. The other is the cytotoxic function that is generally not observed with conventional treatment modalities, but that may function to promote tumor cell killing either alone or in association with apoptosis. In this commentary/review, we advance the premise that autophagy is actually populated by at least two additional players. One we have termed the nonprotective form of autophagy, where the cell is apparently carrying out autophagy-mediated degradative functions, but where autophagy inhibition does not lead to perceptible alterations in drug or radiation sensitivity. The other is what we now term the cytostatic form of autophagy in that its activation results in prolonged growth inhibition as well as reduced clonogenic survival (loss of reproductive capacity) but in the absence of actual loss of cell viability through apoptosis or necrosis; however, as is the case with cytototoxic autophagy, inhibition of cytostatic autophagy protects the tumor cell from the agent (drugs or radiation) that promotes the autophagic response. In view of current clinical efforts to exploit autophagy inhibition as a therapeutic strategy for sensitization of malignancies to chemotherapy and radiation, it is critical to recognize that if chemotherapy and/or radiation actually promote autophagy in patient tumors, the autophagy is not of necessity cytoprotective in function. © 2014 AACR.

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