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Articles by S Zheng
Total Records ( 8 ) for S Zheng
  B. L Carter , M Rogers , J Daly , S Zheng and P. A. James
 

Background  Team-based care is the strategy that has had the greatest effect on improving blood pressure (BP). The purpose of this systematic review was to determine the potency of interventions for BP involving nurses or pharmacists.

Methods  A MEDLINE search for controlled clinical trials that involved a nurse or pharmacist intervention was conducted. Mean reductions in systolic (S) and diastolic (D) BP were determined by 2 reviewers who independently abstracted data and classified the different intervention components.

Results  Thirty-seven articles met the inclusion criteria. Education about BP medications was significantly associated with a reduction in mean BP (–8.75/–3.60 mm Hg). Other strategies that had large effect sizes on SBP include pharmacist treatment recommendations (–9.30 mm Hg), intervention by nurses (–4.80 mm Hg), and use of a treatment algorithm (–4.00 mm Hg). The odds ratios (95% confidence intervals) for controlled BP were: nurses, 1.69 (1.48-1.93); pharmacists within primary care clinics, 2.17 (1.75-2.68); and community pharmacists, 2.89 (1.83-4.55). Mean (SD) reductions in SBP were: nursing studies, 5.84 (8.05) mm Hg; pharmacists in clinics, 7.76 (7.81) mm Hg; and community pharmacists, 9.31 (5.00) mm Hg. There were no significant differences between the nursing and pharmacy studies (P ≥ .19).

Conclusions  Team-based care was associated with improved BP control, and individual components of the intervention appeared to predict potency. Implementation of new hypertension guidelines should consider changes in health care organizational structure to include important components of team-based care.

  C. A Weber , M. E Ernst , G. S Sezate , S Zheng and B. L. Carter
 

Background  Pharmacist-physician comanagement of hypertension has been shown to improve office blood pressures (BPs). We sought to describe the effect of such a model on 24-hour ambulatory BPs.

Methods  We performed a prospective, cluster-randomized, controlled clinical trial, enrolling 179 patients with uncontrolled hypertension from 5 primary care clinics in Iowa City, Iowa. Patients were randomized by clinic to receive pharmacist-physician collaborative management of hypertension (intervention) or usual care (control) for a 9-month period. In the intervention group, pharmacists helped patients to identify barriers to BP control, counseled on lifestyle and dietary modifications, and adjusted antihypertensive therapy in collaboration with the patients' primary care providers. Patients were seen by pharmacists a minimum of every 2 months. Ambulatory BP was measured at baseline and at study end.

Results  Baseline and end-of-study ambulatory BP profiles were evaluated for 175 patients. Mean (SD) ambulatory systolic BPs (SBPs), reported in millimeters of mercury, were reduced more in the intervention group than in the control group: daytime change in () SBP, 15.2 (11.5) vs 5.5 (13.5) (P < .001); nighttime SBP, 12.2 (14.8) vs 3.4 (13.3) (P < .001); and 24-hour SBP, 14.1 (11.3) vs 5.5 (12.5) (P < .001). More patients in the intervention group than in the control group had their BP controlled at the end of the study (75.0% vs 50.7%) (P < .001), as defined by overall 24-hour ambulatory BP monitoring.

Conclusion  Pharmacist-physician collaborative management of hypertension achieved consistent and significantly greater reduction in 24-hour BP and a high rate of BP control.

Trial Registration  clinicaltrials.gov Identifier: NCT00201045

  E. A Houseman , B. C Christensen , M. R Karagas , M. R Wrensch , H. H Nelson , J. L Wiemels , S Zheng , J. K Wiencke , K. T Kelsey and C. J. Marsit
 

Motivation: Integration of various genome-scale measures of molecular alterations is of great interest to researchers aiming to better define disease processes or identify novel targets with clinical utility. Particularly important in cancer are measures of gene copy number DNA methylation. However, copy number variation may bias the measurement of DNA methylation. To investigate possible bias, we analyzed integrated data obtained from 19 head and neck squamous cell carcinoma (HNSCC) tumors and 23 mesothelioma tumors.

Results: Statistical analysis of observational data produced results consistent with those anticipated from theoretical mathematical properties. Average beta value reported by Illumina GoldenGate (a bead-array platform) was significantly smaller than a similar measure constructed from the ratio of average dye intensities. Among CpGs that had only small variations in measured methylation across tumors (filtering out clearly biological methylation signatures), there were no systematic copy number effects on methylation for three and more than four copies; however, one copy led to small systematic negative effects, and no copies led to substantial significant negative effects.

Conclusions: Since mathematical considerations suggest little bias in methylation assayed using bead-arrays, the consistency of observational data with anticipated properties suggests little bias. However, further analysis of systematic copy number effects across CpGs suggest that though there may be little bias when there are copy number gains, small biases may result when one allele is lost, and substantial biases when both alleles are lost. These results suggest that further integration of these measures can be useful for characterizing the biological relationships between these somatic events.

  Y. K Wang , Y. L Zhu , F. M Qiu , T Zhang , Z. G Chen , S Zheng and J. Huang
 

Cancer stem cells (CSCs) play an important role in carcinogenesis, resistance to treatment and may lead to cancer recurrence and metastasis. However, the molecular mechanism of CSC involved in these events needs to be further elucidated. In this study, CD133+ colon cancer cells were cultured, which showed CSC properties both in vitro and in vivo from metastatic tissue. Upstream molecules in Akt and mitogen-activated protein kinase (MAPK) pathways were preferentially expressed in these CD133+ cells, as revealed by a global gene chip. The kinase activities of Akt and extracellular signal-regulated kinase (Erk)1/2 were also significantly upregulated in CD133+ cells. In addition, the clonogenic growth of CD133+ cell was reduced greatly by inhibiting the activity of Akt and Erk1/2. The results revealed the Akt and MAPK pathways were involved in the tumorigenesis of CD133+ colon cancer cells, suggesting that molecules in these two pathways might be potential targets in the future therapy.

  Y Tang , S Zheng and A. Chen
 

Nonalcoholic steatohepatitis (NASH) is commonly found in patients with obesity and is often accompanied with abnormally elevated levels of plasma leptin, i.e. hyperleptinemia. A relatively high population of NASH patients develops hepatic fibrosis, even cirrhosis. Hepatic stellate cells (HSCs) are the major effector cells during liver fibrogenesis and could be activated by leptin. The antioxidant curcumin, a phytochemical from turmeric, has been shown to suppress HSC activation in vitro and in vivo. This project is to evaluate the effect of curcumin on leptin-induced HSC activation and to elucidate the underlying mechanisms. We hypothesize that curcumin abrogates the stimulatory effect of leptin on HSC activation by interrupting leptin signaling and attenuating leptin-induced oxidative stress. Curcumin eliminates the stimulatory effects of leptin on regulating expression of genes closely relevant to HSC activation. Curcumin interrupts leptin signaling by reducing phosphorylation levels of leptin receptor (Ob-R) and its downstream intermediators. In addition, curcumin suppresses gene expression of Ob-R in HSCs, which requires the activation of endogenous peroxisome proliferator-activated receptor- and de novo synthesis of glutathione. In conclusion, our results demonstrate that curcumin abrogates the stimulatory effect of leptin on HSC activation in vitro by reducing the phosphorylation level of Ob-R, stimulating peroxisome proliferator-activated receptor- activity, and attenuating oxidative stress, leading to the suppression of Ob-R gene expression and interruption of leptin signaling. These results provide novel insights into therapeutic mechanisms of curcumin in inhibiting HSC activation and intervening liver fibrogenesis associated with hyperleptinemia in NASH patients.

  L Jin , D Martynowski , S Zheng , T Wada , W Xie and Y. Li
 

The retinoic acid-related orphan receptor (ROR) has important roles in development and metabolic homeostasis. Although the biological functions of ROR have been studied extensively, no ligands for ROR have been identified, and no structure of ROR has been reported. In this study, we showed that hydroxycholesterols promote the recruitment of coactivators by ROR using biochemical assays. We also report the crystal structures of the ROR ligand-binding domain bound with hydroxycholesterols. The structures reveal the binding modes of various hydroxycholesterols in the ROR pocket, with the receptors all adopting the canonical active conformation. Mutations that disrupt the binding of hydroxycholesterols abolish the constitutive activity of ROR. Our observations suggest an important role for the endogenous hydroxycholesterols in modulating ROR-dependent biological processes.

  C Zhang , S Zheng , Y Wang , Y Zhao , J Zhu and L. Ge
 

Cleidocranial dysplasia (CCD) is a dominantly inherited skeletal dysplasia caused by mutations in the osteoblast-specific transcription factor-encoding gene, RUNX2. To correlate different RUNX2 mutations with CCD clinical spectrum, we studied six independent Chinese CCD patients. In five patients, mutations were detected in the coding region of the RUNX2 gene, including two frameshift mutations and three missense mutations. Of these mutations, four were novel and one had previously been reported. All the detected mutations were exclusively clustered within the Runt domain that affected conserved residues in the Runt domain. In vitro green fluorescent protein fusion studies showed that the three mutations—R225L, 214fs and 172fs—interfered with nuclear accumulation of RUNX2 protein, while T200I mutation had no effect on the subcellular distribution of RUNX2. There was no marked phenotypic difference between patients in craniofacial and clavicles features, while the expressivity of supernumerary teeth in our patient cohort had a striking variation, even among family members. The occurrence of intrafamilial clinical variability raises the view that hypomorphic effects and genetic modifiers may alter the clinical expressivity of these mutations. Our results provide new genetic evidence that mutations involved in RUNX2 contribute to CCD.

  S Zheng , W Li , M Xu , X Bai , Z Zhou , J Han , J. Y. J Shyy and X. Wang
 

Ischemia induces angiogenesis as a compensatory response. Although ischemia is known to causes synthesis and release of calcitonin gene-related peptide (CGRP), it is not clear whether CGRP regulates angiogenesis under ischemia and how does it function. Thus we investigated the role of CGRP in angiogenesis and the involved mechanisms. We found that CGRP level was increased in the rat hindlimb ischemic tissue. The expression of exogenous CGRP by adenovirus vectors enhanced blood flow recovery and increased capillary density in ischemic hindlimbs. In vitro, CGRP promoted human umbilical vein endothelial cell (HUVEC) tube formation and migration. Further more, CGRP activated AMP-activated protein kinase (AMPK) both in vivo and in vitro, and pharmacological inhibition of CGRP and cAMP attenuated the CGRP-activated AMPK in vitro. CGRP also induced endothelial nitric oxide synthase (eNOS) phosphorylation in HUVECs at Ser1177 and Ser633 in a time-dependent manner, and such effects were abolished by AMPK inhibitor Compound C. As well, Compound C blocked CGRP-enhanced HUVEC tube formation and migration. These findings indicate that CGRP promotes angiogenesis by activating the AMPK-eNOS pathway in endothelial cells.

 
 
 
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