Stony Brook University

About: Stony Brook University is a education organization based out in Stony Brook, New York, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 32534 authors who have published 68218 publications receiving 3035131 citations. The organization is also known as: State University of New York at Stony Brook & SUNY Stony Brook.

Flowchart techniques for structured programming

Abstract: With the advent of structured programming and GOTO-less programming a method is needed to model computation in simply ordered structures, each representing a complete thought possibly defined in terms of other thoughts as yet undefined. A model is needed which prevents unrestricted transfers of control and has a control structure closer to languages amenable to structured programming. We present an attempt at such a model.

Chemotherapeutic Approaches for Targeting Cell Death Pathways

Abstract: For several decades, apoptosis has taken center stage as the principal mechanism of programmed cell death in mammalian tissues. It also has been increasingly noted that conventional chemotherapeutic agents not only elicit apoptosis but other forms of nonapoptotic death such as necrosis, autophagy, mitotic catastrophe, and senescence. This review presents background on the signaling pathways involved in the different cell death outcomes. A re-examination of what we know about chemotherapy-induced death is vitally important in light of new understanding of nonapoptotic cell death signaling pathways. If we can precisely activate or inhibit molecules that mediate the diversity of cell death outcomes, perhaps we can succeed in more effective and less toxic chemotherapeutic regimens.

The functions of self-injury in young adults who cut themselves: clarifying the evidence for affect regulation

Abstract: The functions of non-suicidal self-injury were examined in 39 young adults with a history of skin-cutting and other self-injurious behaviors including banging, burning, and severe scratching. Consequences, affect-states, and reasons associated with self-injury were assessed by a structured interview. Results indicate that self-injury is associated with improvements in affective valence and decreases in affective arousal. Specifically, participants tended to feel overwhelmed, sad, and frustrated before self-injury, and relieved and calm after self-injury. Further, these affective changes predict lifetime frequency of self-injury, suggesting that they reinforce the behavior. Finally, although reasons for self-injury related to both affect-regulation (e.g., to release emotional pressure that builds up inside of me) and self-punishment (e.g., to express anger at myself) were endorsed by a majority of participants, affect-regulation reasons were overwhelmingly rated as primary and self-punishment reasons as secondary.

CoREST: A functional corepressor required for regulation of neural-specific gene expression

Abstract: Several genes encoding proteins critical to the neuronal phenotype, such as the brain type II sodium channel gene, are expressed to high levels only in neurons. This cell specificity is due, in part, to long-term repression in nonneural cells mediated by the repressor protein REST/NRSF (RE1 silencing transcription factor/neural-restrictive silencing factor). We show here that CoREST, a newly identified human protein, functions as a corepressor for REST. A single zinc finger motif in REST is required for CoREST interaction. Mutations of the motif that disrupt binding also abrogate repression. When fused to a Gal4 DNA-binding domain, CoREST functions as a repressor. CoREST is present in cell lines that express REST, and the proteins are found in the same immunocomplex. CoREST contains two SANT (SW13/ADA2/NCoR/TFIIIB B) domains, a structural feature of the nuclear receptor and silencing mediator for retinoid and thyroid human receptors (SMRT)-extended corepressors that mediate inducible repression by steroid hormone receptors. Together, REST and CoREST mediate repression of the type II sodium channel promoter in nonneural cells, and the REST/CoREST complex may mediate long-term repression essential to maintenance of cell identity.