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Juvenile Probation in the United States : Current Practices and How It Can Be Improved
Ira M. Schwartz,Peter Jones,David Schwartz. 한국보호관찰학회 2009 보호관찰 Vol.9 No.2
소년사법에 신경회로망을 이용한 선구적 연구는 미국에서 진행되었는데, 우리는 신경회로망 기술이 다른 나라에서도 적용되면 미국의 경우만큼의 성과가 있을지 궁금하다. 한국에서도 그러한 성과가 있을지 살펴보는 것은 흥미로운 일이 아닐 수 없다. 나의 동료들과 나는 그 가능성에 대해 낙관적이며 체계적 방법으로 조심스레 가능성을 타진하는 것이 중요하다고 생각한다. 그러므로 우리는 한국의 보호관찰 관계자들이 우리와 유사한 연구의 진행을 고려해볼 것을 권하고자 한다. 의미 있는 결과를 산출하기 위해 종종 수년이 소요되는 전통적인 기존의 연구방법과 달리, 신경회로망을 활용한 연구는 비교적 저렴한 수행비용이 들며, 1년 이내에 완료 할 수 있는 장점이 있다. 신경회로망 기반 모델을 형성할 만큼 의 충분한 데이터가 필요할 뿐이며, 모델 형성 후 현장에서 검증 절차를 거치고 기존의 도구와 비교하면 일단락된다. 또한 이와 같은 연구를 수행하기 위해 새로운 데이터를 수집할 필요가 없다. 예를 들어, 미국에서 신경회로망을 이용하였던 연구는 소년사법과 사회복지 기관에서 일상적으로 수집되는 자료를 활용하여 수행되었으므로 새로운 데이터를 수집하거나 기존의 자료 축적체계를 수정할 필요가 없었다. 한국 소년사법 자료와 그 수집과정에 대해 아는 바가 없으나, 이미 수집된 자료만으로도 이연구가 수행될 수 있을 것으로 생각한다.
Persistent pain is dependent on spinal mitochondrial antioxidant levels.
Schwartz, Erica S,Kim, Hee Young,Wang, Jigong,Lee, Inhyung,Klann, Eric,Chung, Jin Mo,Chung, Kyungsoon The Society 2009 The Journal of neuroscience Vol.29 No.1
<P>Reactive oxygen species (ROS) scavengers have been shown to relieve persistent pain; however, the mechanism is not clearly understood. Superoxide produced from mitochondrial oxidative phosphorylation is considered the major source of ROS in neurons during excitation where mitochondrial superoxide levels are normally controlled by superoxide dismutase (SOD-2). The present study hypothesizes that capsaicin-induced secondary hyperalgesia is a consequence of superoxide build-up in spinal dorsal horn neurons and SOD-2 is a major determinant. To test this hypothesis, the spinal levels of SOD-2 activity, inactivated SOD-2 proteins, and mitochondrial superoxide were measured and correlated to the levels of capsaicin-induced secondary hyperalgesia in mice with and without SOD-2 manipulations. The data suggest that superoxide accumulation is a culprit in the abnormal sensory processing in the spinal cord in capsaicin-induced secondary hyperalgesia. Our studies also support the notion that SOD-2 nitration is a critical mechanism that maintains elevated superoxide levels in the spinal cord after capsaicin treatment. Finally, our findings suggest a therapeutic potential for the manipulation of spinal SOD-2 activity in pain conditions.</P>
Schwartz, David L,Powis, Garth,Thitai-Kumar, Arun,He, Yi,Bankson, James,Williams, Ryan,Lemos, Robert,Oh, Junghwan,Volgin, Andrei,Soghomonyan, Suren,Nishii, Ryuichi,Alauddin, Mian,Mukhopadhay, Uday,Pen American Association for Cancer Research, Inc 2009 Molecular Cancer Therapeutics Vol.8 No.4
<P>Hypoxia inducible factor-1 (HIF-1) promotes tumor cell adaptation to microenvironmental stress. HIF-1 is up-regulated in irradiated tumors and serves as a promising target for radiosensitization. We initially confirmed that the orally bioavailable HIF-1 inhibitor PX-478 reduces HIF-1 protein levels and signaling in vitro in a dose-dependent manner and provides direct radiosensitization of hypoxic cancer cells in clonogenic survival assays using C6 glioma, HN5 and UMSCCa10 squamous cells, and Panc-1 pancreatic adenocarcinoma cell lines. However, PX-478 yields striking in vivo tumor sensitization to single-dose irradiation, which cannot be explained by incremental improvement in direct tumor cell killing. We show that PX-478 prevents postradiation HIF-1 signaling and abrogates downstream stromal adaptation in C6 and HN5 reporter xenografts as measured by serial ultrasound, vascular magnetic resonance imaging, and hypoxia response element-specific micro-positron emission tomography imaging. The primacy of indirect PX-478 in vivo effects was corroborated by our findings that (a) either concurrent or early postradiation sequencing of PX-478 provides roughly equivalent sensitization and (b) constitutive vascular endothelial growth factor expression maintains refractory tumor vessel function and progression following combined radiation and PX-478. These results confirm that disruption of postradiation adaptive HIF-1 signaling by PX-478 imparts increased therapeutic efficacy through blockade of HIF-1-dependent reconstitution of tumor stromal function. Successful translation of targeted HIF-1 radiosensitization to the clinical setting will require specific consideration of tumor microenvironmental effects and mechanisms.</P>
Schwartz, Pierre-Olivier,Biniek, Laure,Zaborova, Elena,Heinrich, Benoî,t,Brinkmann, Martin,Leclerc, Nicolas,Mé,ry, Sté,phane American Chemical Society 2014 JOURNAL OF THE AMERICAN CHEMICAL SOCIETY - Vol.136 No.16
<P>Perylenediimide-based donor–acceptor co-oligomers are particularly attractive in plastic electronics because of their unique electro-active properties that can be tuned by proper chemical engineering. Herein, a new class of co-oligomers has been synthesized with a dyad structure (AD) or a triad structure (DAD and ADA) in order to understand the correlations between the co-oligomer molecular architecture and the structures formed by self-assembly in thin films. The acceptor block A is a perylene tetracarboxyl diimide (PDI), whereas the donor block D is made of a combination of thiophene, fluorene, and 2,1,3-benzothiadiazole derivatives. D and A blocks are linked by a short and flexible ethylene spacer to ease self-assembling in thin films. Structural studies using small and wide X-ray diffraction and transmission electron microscopy demonstrate that AD and ADA lamellae are made of a double layer of co-oligomers with overlapping and strongly π-stacked PDI units because the sectional area of the PDI is about half that of the donor block. These structural models allow rationalizing the absence of organization for the DAD co-oligomer and therefore to draw general rules for the design of PDI-based dyads and triads with proper self-assembling properties of use in organic electronics.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/jacsat/2014/jacsat.2014.136.issue-16/ja4129108/production/images/medium/ja-2013-129108_0012.gif'></P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/ja4129108'>ACS Electronic Supporting Info</A></P>