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<channel rdf:about="http://hdl.handle.net/2144/939">
<title>Clinical Science</title>
<link>http://hdl.handle.net/2144/939</link>
<description/>
<items>
<rdf:Seq>
<rdf:li rdf:resource="http://hdl.handle.net/2144/4511"/>
<rdf:li rdf:resource="http://hdl.handle.net/2144/4364"/>
<rdf:li rdf:resource="http://hdl.handle.net/2144/4363"/>
<rdf:li rdf:resource="http://hdl.handle.net/2144/3446"/>
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</items>
<dc:date>2013-03-24T16:35:33Z</dc:date>
</channel>
<item rdf:about="http://hdl.handle.net/2144/4511">
<title>A transitional opioid program to engage hospitalized drug users</title>
<link>http://hdl.handle.net/2144/4511</link>
<description>A transitional opioid program to engage hospitalized drug users
Shanahan, CW; Beers, D; Alford, DP; Brigandi, E; Samet, JH
BACKGROUND:&#13;
Many opioid-dependent patients do not receive care for addiction issues when hospitalized for other medical problems. Based on 3 years of clinical practice, we report the Transitional Opioid Program (TOP) experience using hospitalization as a "reachable moment" to identify and link opioid-dependent persons to addiction treatment from medical care.&#13;
METHODS:&#13;
A program nurse identified, assessed, and enrolled hospitalized, out-of-treatment opioid-dependent drug users based on their receipt of methadone during hospitalization. At discharge, patients transitioned to an outpatient interim opioid agonist program providing 30-day stabilization followed by 60-day taper. The nurse provided case management emphasizing HIV risk reduction, health education, counseling, and medical follow-up. Treatment outcomes included opioid agonist stabilization then taper or transfer to long-term opioid agonist treatment.&#13;
RESULTS:&#13;
From January 2002 to January 2005, 362 unique hospitalized, opioid-dependent drug users were screened; 56% (n = 203) met eligibility criteria and enrolled into the program. Subsequently, 82% (167/203) presented to the program clinic post-hospital discharge; for 59% (119/203) treatment was provided, for 26% (52/203) treatment was not provided, and for 16% (32/203) treatment was not possible (pursuit of TOP objectives precluded by medical problems, psychiatric issues, or incarceration). Program patients adhered to a spectrum of medical recommendations (e.g., obtaining prescription medications, medical follow-up).&#13;
CONCLUSIONS:&#13;
The Transitional Opioid Program (TOP) identified at-risk hospitalized, out-of-treatment opioid-dependent drug users and, by offering a range of treatment intensity options, engaged a majority into addiction treatment. Hospitalization can be a "reachable moment" to engage and link drug users into addiction treatment.
doi: 10.1007/s11606-010-1311-3; PMID: 20237960 [PubMed - indexed for MEDLINE] PMCID: PMC2896583
</description>
<dc:date>2010-08-01T00:00:00Z</dc:date>
</item>
<item rdf:about="http://hdl.handle.net/2144/4364">
<title>Inhibitory Effects of Robo2 on Nephrin: A Crosstalk between Positive and Negative Signals Regulating Podocyte Structure</title>
<link>http://hdl.handle.net/2144/4364</link>
<description>Inhibitory Effects of Robo2 on Nephrin: A Crosstalk between Positive and Negative Signals Regulating Podocyte Structure
Fan, Xueping; Li, Qinggang; Pisarek-Horowitz, Anna; Rasouly, Hila Milo; Wang, Xiangling; Bonegio, Ramon G.; Wang, Hang; McLaughlin, Margaret; Mangos, Steve; Kalluri, Raghu; Holzman, Lawrence B.; Drummond, Iain A.; Brown, Dennis; Salant, David J.; Lu, Weining
Robo2 is the cell surface receptor for the repulsive guidance cue Slit and is involved in axon guidance and neuronal migration. Nephrin is a podocyte slit- diaphragm protein that functions in the kidney glomerular filtration barrier. Here, we report that Robo2 is expressed at the basal surface of mouse podocytes and colocalizes with nephrin. Biochemical studies indicate that Robo2 forms a complex with nephrin in the kidney through adaptor protein Nck. In contrast to the role of nephrin that promotes actin polymerization, Slit2-Robo2 signaling inhibits nephrin-induced actin polymerization. In addition, the amount of F-actin associated with nephrin is increased in Robo2 knockout mice that develop an altered podocyte foot process structure. Genetic interaction study further reveals that loss of Robo2 alleviates the abnormal podocyte structural pheno- type in nephrin null mice. These results suggest that Robo2 signaling acts as a negative regulator on neph- rin to influence podocyte foot process architecture.
</description>
<dc:date>2012-07-26T00:00:00Z</dc:date>
</item>
<item rdf:about="http://hdl.handle.net/2144/4363">
<title>Noninvasive Assessment of Antenatal Hydronephrosis in Mice Reveals a Critical Role for Robo2 in Maintaining Anti-Reflux Mechanism</title>
<link>http://hdl.handle.net/2144/4363</link>
<description>Noninvasive Assessment of Antenatal Hydronephrosis in Mice Reveals a Critical Role for Robo2 in Maintaining Anti-Reflux Mechanism
Wang, Hang; Li, Qinggang; Liu, Juan; Mendelsohn, Cathy; Salant, David J.; Lu, Weining
Antenatal hydronephrosis and vesicoureteral reflux (VUR) are common renal tract birth defects. We recently showed that disruption of the Robo2 gene is associated with VUR in humans and antenatal hydronephrosis in knockout mice. However, the natural history, causal relationship and developmental origins of these clinical conditions remain largely unclear. Although the hydronephrosis phenotype in Robo2 knockout mice has been attributed to the coexistence of ureteral reflux and obstruction in the same mice, this hypothesis has not been tested experimentally. Here we used noninvasive high- resolution micro-ultrasonography and pathological analysis to follow the progression of antenatal hydronephrosis in individual Robo2-deficient mice from embryo to adulthood. We found that hydronephrosis progressed continuously after birth with no spontaneous resolution. With the use of a microbubble ultrasound contrast agent and ultrasound-guided percutaneous aspiration, we demonstrated that antenatal hydronephrosis in Robo2-deficient mice is caused by high-grade VUR resulting from a dilated and incompetent ureterovesical junction rather than ureteral obstruction. We further documented Robo2 expression around the developing ureterovesical junction and identified early dilatation of ureteral orifice structures as a potential fetal origin of antenatal hydronephrosis and VUR. Our results thus demonstrate that Robo2 is crucial for the formation of a normal ureteral orifice and for the maintenance of an effective anti-reflux mechanism. This study also establishes a reproducible genetic mouse model of progressive antenatal hydronephrosis and primary high- grade VUR.
</description>
<dc:date>2011-09-20T00:00:00Z</dc:date>
</item>
<item rdf:about="http://hdl.handle.net/2144/3446">
<title>Introducing Annals of Surgical Innovation and Research</title>
<link>http://hdl.handle.net/2144/3446</link>
<description>Introducing Annals of Surgical Innovation and Research
Matteotti, Ronald; Gagner, Michel; Becker, James
</description>
<dc:date>2007-02-20T00:00:00Z</dc:date>
</item>
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