Dr. Xiaobin  Wang  Md image

Dr. Xiaobin Wang Md

2300 Children's Plaza, Box 157
Chicago IL 60614
312 737-7738
Medical School: Other - Unknown
Accepts Medicare: No
Participates In eRX: No
Participates In PQRS: No
Participates In EHR: No
License #:
NPI: 1861447021
Taxonomy Codes:

Request Appointment Information

Awards & Recognitions

About Us

Practice Philosophy


Medical Malpractice Cases

None Found

Medical Board Sanctions

None Found


None Found


KLF7 regulates satellite cell quiescence in response to extracellular signaling. - Stem cells (Dayton, Ohio)
Retaining muscle stem satellite cell (SC) quiescence is important for the maintenance of stem cell population and tissue regeneration. Accumulating evidence supports the model where key extracellular signals play crucial roles in maintaining SC quiescence or activation, however, the intracellular mechanisms that mediate niche signals to control SC behavior are not fully understood. Here, we reported that KLF7 functioned as a key mediator involved in low-level TGF-β signaling and canonical Notch signaling-induced SC quiescence and myoblast arrest. The data obtained showed that KLF7 was upregulated in quiescent SCs and non-proliferating myoblasts. Silence of KLF7 promoted SCs activation and myoblasts proliferation, but overexpression of KLF7 induced myogenic cell arrest. Notably, the expression of KLF7 was regulated by TGF-β and Notch3 signaling. Knockdown of KLF7 diminished low-level TGF-β and canonical Notch signaling-induced SC quiescence. Investigation into the mechanism revealed that KLF7 regulation of SC function was dependent on p21 and acetylation of Lys227 and/or 231 in the DNA binding domain of KLF7. Our study provides new insights into the regulatory network of muscle stem cell quiescence. This article is protected by copyright. All rights reserved.© 2016 AlphaMed Press.
Mathematical Modeling of the Biomarker Milieu to Characterize Preterm Birth and Predict Adverse Neonatal Outcomes. - American journal of reproductive immunology (New York, N.Y. : 1989)
To identify preterm neonates at risk for adverse neonatal outcomes.A nested case-control study from the prospectively followed Boston Birth Cohort of mother-neonate pairs was performed. A classification model for preterm-born neonates was derived from 27 cord blood biomarkers using orthogonal projections to latent structures discriminant analysis. Predictive relationships were made between biomarkers and adverse outcomes using logistic regression.From 926 births (53% of which were preterm), using weighted values for 27 biomarkers, a score was created that classified 73% of preterm deliveries. Soluble TNF-R1, NT-3, MCP-1, BDNF, IL-4, MMP-9, TREM-1, TNF-α, IL-5 and IL-10 were most influential. Our model was more sensitive for birth <34 weeks (sensitivity 89.5%, specificity 76.9%). IL-10, TNF-α, BDNF, NT-3, MMP-9, sTNF-R1 and MCP-1 were significantly predictive of NEC, IVH, sepsis and infections.We developed a novel mathematical model of 27 biomarkers associated with adverse neonatal outcomes in neonates born preterm.© 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
Maternal BMI, gestational diabetes, and weight gain in relation to childhood obesity: The mediation effect of placental weight. - Obesity (Silver Spring, Md.)
High prepregnancy body mass index (BMI), excessive gestational weight gain (GWG), and gestational diabetes mellitus (GDM) are associated with the risk of childhood obesity. This study aims to examine the extent to which these effects may be mediated through the placenta.Data included 33,893 mothers and their singleton infants from birth to 7 years old (total 154,590 visits) in the Collaborative Perinatal Project, a U.S. multicenter prospective cohort study from 1959 to 1976. The placentas were weighed after removing cord and membranes. We performed sequential generalized estimating equation-linear models excluding and including placental weight to evaluate its mediation effect.In this population, 21.7% of mothers had overweight or obesity, 17.3% had excessive GWG, and 350 (1%) had diagnosed GDM; in addition, 7.2% children had obesity. After adjustment for prepregnancy BMI and other covariates, childhood BMI was 0.23 (95% CI: 0.05, 0.40) kg/m(2) higher for children born to mothers with GDM versus those without GDM. Inclusion of placental weight in the model attenuated the association by 52% to 0.11 (95% CI: -0.06, 0.28) and similarly attenuated the associations with childhood BMI for GWG by 25% and maternal prepregnancy BMI by 17%.Placental weight partly mediates the effects of prepregnancy BMI, excessive GWG, and GDM on childhood BMI.© 2016 The Obesity Society.
The Association of Maternal Obesity and Diabetes With Autism and Other Developmental Disabilities. - Pediatrics
Obesity and diabetes are highly prevalent among pregnant women in the United States. No study has examined the independent and combined effects of maternal prepregnancy obesity and maternal diabetes on the risk of autism spectrum disorder (ASD) in parallel with other developmental disorders (DDs).This study is based on 2734 children (including 102 ASD cases), a subset of the Boston Birth Cohort who completed at least 1 postnatal study visit at Boston Medical Center between 1998 and 2014. Child ASD and other DDs were based on physician diagnoses as documented in electronic medical records. Risks of ASD and other DDs were compared among 6 groups defined by maternal prepregnancy obesity and diabetes status by using Cox proportional hazard regression controlling for potential confounders.When examined individually, maternal prepregnancy obesity and pregestational diabetes (PGDM) were each associated with risk of ASD. When examined in combination, only mothers with obesity and PGDM (hazard ratio 3.91, 95% confidence interval 1.76-8.68) and those with obesity and gestational diabetes (hazard ratio 3.04, 95% confidence interval 1.21-7.63) had a significantly increased risk of offspring ASD. Intellectual disabilities (IDs), but not other DDs, showed a similar pattern of increased risk associated with combined obesity and PGDM. This pattern of risk was mostly accounted for by cases with co-occurring ASD and ID.Maternal prepregnancy obesity and maternal diabetes in combination were associated with increased risk for ASD and ID. ASD with ID may be etiologically distinct from ASD without ID.Copyright © 2016 by the American Academy of Pediatrics.
Imatinib promotes apoptosis of giant cell tumor cells by targeting microRNA-30a-mediated runt‑related transcription factor 2. - Molecular medicine reports
Giant cell tumor (GCT) is an aggressive type of bone tumor consisting of multinucleated osteoclast‑like giant cells. Imatinib is a selective inhibitor for certain type III tyrosine kinase receptor family members with a variety of beneficial effects. The purpose of the present study was to determine the therapeutic potential and underlying mechanism of imatinib against GCT. In the present study, cell viability and apoptosis in GCT were analyzed using the MTT assay, flow cytometry and DAPI staining assay. Caspase‑3 and ‑9 activity in GCT cells were analyzed with colorimetric assay kits. In addition, the expression levels of runt‑related transcription factor 2 (RunX2) protein and microRNA‑30a (miR‑30a) in GCT cells were detected using western blotting and quantitative polymerase chain reaction, respectively. Results from the present study demonstrated that imatinib treatment inhibited cell viability, increased cell apoptosis, and significantly promoted caspase‑3 and ‑9 activity in GCT. In addition, imatinib treatment decreased the RunX2 protein expression level. Notably, imatinib was demonstrated to increase miR‑30a expression. However, upregulation of miR‑30a expression reduced the RunX2 protein expression level, and downregulation of miR‑30a expression reversed the anticancer effect of imatinib on GCT, increasing the expression level of RunX2 protein in GCT. The results of the present study indicate that imatinib promotes apoptosis of GCT cells by targeting the miR‑30a‑mediated RunX2 signaling pathway.
Adiposity trajectory and its associations with plasma adipokine levels in children and adolescents-A prospective cohort study. - Obesity (Silver Spring, Md.)
This study aimed to examine the associations of longitudinal adiposity measures with two adipokines, leptin and adiponectin, and their ratio in children and adolescents.A total of 953 children and adolescents participated in a 6-year longitudinal study. Body mass index (BMI), percentage body fat (%BF), and fat mass index (FMI) were used to assess adiposity status.After adjusting for possible confounders, our regression models revealed that BMI, %BF, and FMI, in both the baseline and follow-up surveys were independently associated with a higher level of leptin and the leptin/adiponectin ratio at the follow-up survey, whereas the significant association with adiponectin only partly existed in adiposity measures at the follow-up visit. Moreover, the longitudinal change in adiposity measures was found to be a significant predictor for follow-up plasma adipokine levels. Compared with the low→low group, the medium→medium group, up-trend group, and high→high group all showed a significantly increased level of leptin and leptin/adiponectin ratio. The up-trend group and high→high group also had significantly decreased adiponectin levels.These findings highlight the importance of adiposity surveillance and the utility of adipokines as biomarkers for adverse metabolic consequences of childhood adiposity.© 2015 The Obesity Society.
Proteinuria Is an Independent Risk Factor for First Incident Stroke in Adults Under Treatment for Hypertension in China. - Journal of the American Heart Association
Conflicting evidence exists regarding whether reduced estimated glomerular filtration rate (eGFR) and proteinuria are independent risk factors for stroke and its subtypes in hypertensive patients. This study investigated the association of these renal measures with first incident stroke in adults under treatment for hypertension in China.The study included 19 599 adults aged 45 to 75 years who participated in the China Stroke Primary Prevention Trial. Baseline eGFR was calculated using the Chronic Kidney Disease Epidemiology Collaboration creatinine equation. Proteinuria was assessed by qualitative dipstick urinalysis and in a subset by the quantitative albumin-creatinine ratio method. Cox regression analysis was used to examine the effects of eGFR and proteinuria on the risk of first incident stroke. During a median of 4.5 years of follow-up, a total of 585 first strokes (472 ischemic strokes) were identified. Compared to participants without proteinuria, participants with proteinuria (trace or more by dipstick) had a 35% increased risk of first stroke: the adjusted hazard ratio (HR) (95% CI) was 1.35 (1.09-1.66, P=0.005). The results were robust in subgroup analyses. In a subset with data on proteinuria measured by quantitative albumin-creatinine ratio, a similar association was found. In both independent and combined analyses with proteinuria, eGFR was not significantly associated with stroke.In adults under treatment for hypertension in China, baseline proteinuria measured by dipstick or quantitative albumin-creatinine ratio, but not reduced eGFR, was found to be an independent risk factor for first incident stroke and ischemic stroke.© 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.
Hyperhomocysteinemia predicts renal function decline: a prospective study in hypertensive adults. - Scientific reports
Hyper-homocysteinemia (HHcy) is associated with microalbuminuria and glomerular injury in general and diabetic populations. However, HHcy's role in hypertensive patients was not studied. We investigated whether HHcy is an independent risk factor for renal function decline and development of chronic kidney disease (CKD) in hypertensive men and women. This was a community-based prospective cohort study of 2,387 hypertensive adults without CKD at baseline, with a mean follow-up of 4.4 years. Baseline and follow-up levels of plasma Hcy, folate, vitamin B12, blood pressure and other pertinent covariables were obtained. CKD was defined as an estimated glomerular filtration rate (eGFR) <60 ml/min/per 1.73 m(2) and an eGFR decline rate >1 ml/min/per 1.73 m(2)/year. There was a graded association between Hcy tertiles and eGFR decline. Subjects in the 3(rd) tertile of Hcy levels had an accelerated rate of eGFR decline and an increased risk of incident CKD, as compared with those in the 1st tertile, after adjusting for age, gender, baseline diabetes, SBP, BMI, smoking, dyslipidemia, eGFR, folate and vitamin B12 levels. In conclusion, in this prospective cohort of Chinese hypertensive adults, elevated baseline plasma Hcy can serve as an independent biomarker to predict renal function decline and incident CKD.
Genome-wide methylation profiling reveals new biomarkers for prognosis prediction of glioblastoma. - Journal of cancer research and therapeutics
To identify a specific hypermethylated molecular biomarker for human malignant glioblastoma prognosis.Genome-wide methylation profiling was performed on 33 tumors and 3 normal glioblastoma samples using the Infinium HumanMethylation450 microarray. Cluster analysis was carried out in these samples according to the differentiated methylated genes. DNA methylation of selected significant candidates was subsequently validated to analyze the association of methylation status of these genes with overall survival as well as gene expression.We found 217 hypermethylated CpG sites located in 210 respective genes with significant differences in short- and long-term survival (STS and LTS) samples (P < 0.01). Cluster analysis revealed fine clustering of genes with LTS and STS. Of these, we selected 10 most hypermethylated genes, including IL11, RRAD, MS4A6A, SNAPC2, ALDH1A3, ADCY1, MMS19L, NDUFB8, POMC, and THSD4, to perform cluster analysis. It came out with the same fine classification and with survival time of these patients. The top ranking genes were further examined to compare their methylation status with the overall survival rate of patients, as well as with gene expression levels.We obtained a featured global profiling of DNA methylation in glioblastoma. Our findings strongly indicate that epigenetic silencing of IL11, RRAD, MS4A6A, SNAPC2, and ALDH1A3 are common events in glioblastoma which could be used as novel biomarkers for the prognosis of glioblastoma.
Effect of folic acid supplementation on risk of new-onset diabetes in adults with hypertension in China: Findings from the China Stroke Primary Prevention Trial (CSPPT). - Journal of diabetes
The aim of the present post hoc analysis of the China Stroke Primary Prevention Trial (CSPPT) was to evaluate the effect of folic acid supplementation on the risk of new-onset diabetes in hypertensive adults in China.In all, 20 702 hypertensive adults with no history of stroke and/or myocardial infarction (MI) were randomly assigned to receive double-blind daily treatment with tablets containing either: (i) 10 mg enalapril and 0.8 mg folic acid (n = 10 348); or (ii) 10 mg enalapril alone (n = 10 354). New-onset diabetes was defined as either self-reported physician-diagnosed diabetes or the use of glucose-lowering drugs during the follow-up period of the CSPPT.Over a median treatment duration of 4.5 years, new-onset diabetes occurred in 198 (2.0%) and 214 (2.1%) subjects in the enalapril-folic acid and enalapril groups, respectively (hazard ratio [HR] 0.92; 95% confidence interval [CI] 0.76-1.12). Similar results were observed when analyses were limited to subjects with baseline fasting glucose (FG) <7.0 mmol/L (HR 0.85; 95% CI 0.62-1.14). Furthermore, there was no significant group difference in: (i) the risk of new-onset FG ≥7.0 mmol/L (defined as FG <7.0 at baseline and ≥7.0 mmol/L at the last visit; relative risk [RR] 1.07; 95% CI 0.96-1.20); or (ii) the composite of new-onset diabetes or new-onset FG ≥7.0 mmol/L (RR = 1.06; 95% CI 0.95-1.19).Among adults with hypertension with no history of stroke and/or MI in China, folic acid supplementation had no significant effect on the risk of new-onset diabetes.© 2016 Ruijin Hospital, Shanghai Jiaotong University School of Medicine and John Wiley & Sons Australia, Ltd.

Map & Directions

2300 Children's Plaza, Box 157 Chicago, IL 60614
View Directions In Google Maps

Nearby Doctors

2555 N. Clark St.
Chicago, IL 60614
773 293-3320
2300 Childrens Plaza # 107
Chicago, IL 60614
312 276-6060
467 W Deming St Lincoln Park Primary Care
Chicago, IL 60614
773 279-9125
1960 N Lincoln Park W 2Nd Floor
Chicago, IL 60614
773 273-3131
2400 N Sheffield Ave
Chicago, IL 60614
773 800-0320
2300 Childrens Place
Chicago, IL 60614
773 804-4415
2536 N Lincoln Ave
Chicago, IL 60614
773 805-5455
1610 W Fullerton Ave
Chicago, IL 60614
773 689-9200
2300 N Childrens Plz Box 28
Chicago, IL 60614
773 804-4000
2551 N Clark St Suite 700
Chicago, IL 60614
773 487-7008