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Articles by S Wu
Total Records ( 8 ) for S Wu
  S Wu , X Shen and C. J. Geyer

Several sparseness penalties have been suggested for delivery of good predictive performance in automatic variable selection within the framework of regularization. All assume that the true model is sparse. We propose a penalty, a convex combination of the L1- and L-norms, that adapts to a variety of situations including sparseness and nonsparseness, grouping and nongrouping. The proposed penalty performs grouping and adaptive regularization. In addition, we introduce a novel homotopy algorithm utilizing subgradients for developing regularization solution surfaces involving multiple regularizers. This permits efficient computation and adaptive tuning. Numerical experiments are conducted using simulation. In simulated and real examples, the proposed penalty compares well against popular alternatives.

  P Wang , J Liu , Y Li , S Wu , J Luo , H Yang , R Subbiah , J Chatham , O Zhelyabovska and Q. Yang

Rationale: Peroxisome proliferator-activated receptors (PPARs) (, , and /β) are nuclear hormone receptors and ligand-activated transcription factors that serve as key determinants of myocardial fatty acid metabolism. Long-term cardiomyocyte-restricted PPAR deficiency in mice leads to depressed myocardial fatty acid oxidation, bioenergetics, and premature death with lipotoxic cardiomyopathy.

Objective: To explore the essential role of PPAR in the adult heart.

Methods and Results: We investigated the consequences of inducible short-term PPAR knockout in the adult mouse heart. In addition to a substantial transcriptional downregulation of lipid metabolic proteins, short-term PPAR knockout in the adult mouse heart attenuated cardiac expression of both Cu/Zn superoxide dismutase and manganese superoxide dismutase, leading to increased oxidative damage to the heart. Moreover, expression of key mitochondrial biogenesis determinants such as PPAR coactivator-1 were substantially decreased in the short-term PPAR deficient heart, concomitant with a decreased mitochondrial DNA copy number. Rates of palmitate and glucose oxidation were markedly depressed in cardiomyocytes of PPAR knockout hearts. Consequently, PPAR deficiency in the adult heart led to depressed cardiac performance and cardiac hypertrophy.

Conclusions: PPAR is an essential regulator of cardiac mitochondrial protection and biogenesis and PPAR activation can be a potential therapeutic target for cardiac disorders.

  T. J Vachharajani , S Moossavi , L Salman , S Wu , I. D Maya , A. S Yevzlin , A Agarwal , K. D Abreo , J Work and A. Asif

The foundation of endovascular procedures by nephrologists was laid in the private practice arena. Because of political issues such as training, credentialing, space and equipment expenses, and co-management concerns surrounding the performance of dialysis-access procedures, the majority of these programs provided care in an outpatient vascular access center. On the basis of the improvement of patient care demonstrated by these centers, several nephrology programs at academic medical centers have also embraced this approach. In addition to providing interventional care on an outpatient basis, academic medical centers have taken a step further to expand collaboration with other specialties with similar expertise (such as with interventional radiologists and cardiologists) to enhance patient care and research. The enthusiastic initiative, cooperative, and mutually collaborative efforts used by academic medical centers have resulted in the successful establishment of interventional nephrology programs. This article describes various models of interventional nephrology programs at academic medical centers across the United States.

  A Aguilar , S Wu and F. De Luca

Cytochrome P450 oxidoreductase (POR) is the electron donor for microsomal cytochrome P450 enzymes and other non-P450 enzymes. Targeted deletion of POR expression in mice leads to a variety of embryonic defects, including bone abnormalities. In addition, POR mutations in humans are associated with impaired steroidogenesis and skeletal malformations. Yet, little is known on the mechanisms underlying the skeletal abnormalities secondary to impaired POR activity. In our study, rat chondrocytes transfected with POR-specific short interfering RNAs exhibited decreased cell proliferation and differentiation and induced apoptosis. In addition, the reduced expression of POR in chondrocytes caused decreased intracellular cholesterol content. The addition of cholesterol in the culture medium prevented the POR small interfering RNA (siRNA)-mediated effects on chondrocyte proliferation, differentiation, and apoptosis. Because cholesterol is required for normal activity of the hedgehog proteins, we evaluated the effects of POR siRNAs on the expression of Indian hedgehog (Ihh), an important regulator of chondrogenesis. POR siRNA-transfected chondrocytes exhibited reduced Ihh expression, with such effect being neutralized by cholesterol. Lastly, recombinant human/mouse Ihh prevented the POR siRNA-mediated effects on chondrocyte proliferation, differentiation, and apoptosis. Our findings suggest that the bone malformations associated with defective POR activity are due to reduced cholesterol synthesis and, in turn, reduced Ihh expression in chondrocytes.

  S Wu , W Wang , X Kong , L. M Congdon , K Yokomori , M. W Kirschner and J. C. Rice

Although the PR-Set7/Set8/KMT5a histone H4 Lys 20 monomethyltransferase (H4K20me1) plays an essential role in mammalian cell cycle progression, especially during G2/M, it remained unknown how PR-Set7 itself was regulated. In this study, we discovered the mechanisms that govern the dynamic regulation of PR-Set7 during mitosis, and that perturbation of these pathways results in defective mitotic progression. First, we found that PR-Set7 is phosphorylated at Ser 29 (S29) specifically by the cyclin-dependent kinase 1 (cdk1)/cyclinB complex, primarily from prophase through early anaphase, subsequent to global accumulation of H4K20me1. While S29 phosphorylation did not affect PR-Set7 methyltransferase activity, this event resulted in the removal of PR-Set7 from mitotic chromosomes. S29 phosphorylation also functions to stabilize PR-Set7 by directly inhibiting its interaction with the anaphase-promoting complex (APC), an E3 ubiquitin ligase. The dephosphorylation of S29 during late mitosis by the Cdc14 phosphatases was required for APCcdh1-mediated ubiquitination of PR-Set7 and subsequent proteolysis. This event is important for proper mitotic progression, as constitutive phosphorylation of PR-Set7 resulted in a substantial delay between metaphase and anaphase. Collectively, we elucidated the molecular mechanisms that control PR-Set7 protein levels during mitosis, and demonstrated that its orchestrated regulation is important for normal mitotic progression.

  J Doupis , T. E Lyons , S Wu , C Gnardellis , T Dinh and A. Veves

Objective: We investigated the association between inflammation, microvascular reactivity, and the development of peripheral diabetic neuropathy.

Research Design and Methods: We studied three groups: 55 healthy control subjects, 80 nonneuropathic patients, and 77 neuropathic diabetic patients. We also subdivided the neuropathic patients into a subgroup of 31 subjects with painless neuropathy and 46 with painful neuropathy. We measured the foot skin endothelium-dependent and -independent vasodilation, the nerve axon reflex-related vasodilation (NARV), and inflammatory cytokines and biochemical markers of endothelial function.

Results: The endothelium-dependent and -independent vasodilation and NARV were lower in the neuropathic group (P < 0.05). NARV was further reduced in the subgroup of painless neuropathy when compared to painful neuropathy (P < 0.05). Compared to the other two groups, the neuropathic group also had higher serum levels of PDGF AA/BB (P < 0.05), RANTES (P < 0.01), leptin (P < 0.0001), osteoprotegerin (P < 0.01), G-CSF (P < 0.05), sE-Selectin (P < 0.01), sICAM (P < 0.0001), sVCAM (P < 0.001), CRP (P < 0.0001), TNF (P < 0.05), and fibrinogen (P < 0.05). Patients with painful neuropathy had higher sICAM-1 (P < 0.05) and CRP levels (P < 0.01) when compared to painless neuropathy. No major changes in the above results were observed in 78 diabetic patients who were seen for a second visit 21 months after the first visit.

Conclusions: Peripheral diabetic neuropathy is associated with increased biochemical markers of inflammation and endothelial dysfunction. Painful neuropathy is associated with further increase in inflammation and markers of endothelial dysfunction and preservation of the nerve axon reflex.

  H. M Conklin , S Helton , J Ashford , R. K Mulhern , W. E Reddick , R Brown , M Bonner , B. W Jasper , S Wu , X Xiong and R. B. Khan

Objective To investigate the methylphenidate (MPH) response rate among childhood survivors of acute lymphoblastic leukemia (ALL) and brain tumors (BTs) and to identify predictors of positive MPH response. Methods Cancer survivors (N = 106; BT = 51 and ALL = 55) identified as having attention deficits and learning problems participated in a 3-week, double-blind, crossover trial consisting of placebo, low-dose MPH (0.3 mg/kg), and moderate-dose MPH (0.6 mg/kg). Weekly teacher and parent reports on the Conners’ Rating Scales were gathered. Results Following moderate MPH dose, 45.28% of the sample was classified as responders. Findings revealed that more problems endorsed prior to the medication trial on parent and teacher ratings were predictive of positive medication response (p < .05). Conclusions MPH significantly reduces attention problems in a subset of childhood cancer survivors. Parent and teacher ratings may assist in identifying children most likely to respond to MPH so prescribing may be optimally targeted.

  V Pastukh , H Chen , S Wu , C. J Jong , M Alexeyev and S. W. Schaffer

Hypernatremia exerts multiple cellular effects, many of which could influence the outcome of an ischemic event. To further evaluate these effects of hypernatremia, isolated neonatal cardiomyocytes were chronically incubated with medium containing either normal (142 mM) or elevated sodium (167 mM) and then transferred to medium containing deoxyglucose and the electron transport chain inhibitor amobarbital. Chronic hypernatremia diminished the degree of calcium accumulation and reactive oxygen species generation during the period of metabolic inhibition. The improvement in calcium homeostasis was traced in part to the downregulation of the CaV3.1 T-type calcium channel, as deficiency in the CaV3.1 subtype using short hairpin RNA or treatment with an inhibitor of the CaV3.1 variant of the T-type calcium channel (i.e., diphenylhydantoin) attenuated energy deficiency-mediated calcium accumulation and cell death. Although hyperosmotically stressed cells (exposed to 50 mM mannitol) had no effect on T-type calcium channel activity, they were also resistant to death during metabolic inhibition. Both hyperosmotic stress and hypernatremia activated Akt, suggesting that they initiate the phosphatidylinositol 3-kinase/Akt cytoprotective pathway, which protects the cell against calcium overload and oxidative stress. Thus hypernatremia appears to protect the cell against metabolic inhibition by promoting the downregulation of the T-type calcium channel and stimulating cytoprotective protein kinase pathways.

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