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Articles by F Gao
Total Records ( 7 ) for F Gao
  K. S Nunley , F Gao , A. C Albers , S. J Bayliss and D. H. Gutmann
 

Objective  To evaluate the predictive utility of the number and morphologic appearance of isolated café au lait macules (CALMs) in establishing the diagnosis of neurofibromatosis type 1 (NF1) in a cohort of children referred to an NF1 subspecialty clinic.

Design  Retrospective study of patients seen between the years 2004 and 2007.

Setting  Tertiary care neurofibromatosis referral clinic at St Louis Children's Hospital.

Patients  The study population comprised 110 patients who presented with CALMs and no other diagnostic features of NF1. The median number of CALMs at initial presentation was 6, while the median age of the patients was 33 months. The median age at the last follow-up examination was 76.5 months.

Main Outcome Measures  Number and morphologic appearance of CALMs and diagnosis of NF1.

Results  Thirty-four of the children met diagnostic criteria for NF1 during the study period. Thirty-two children met criteria prior to age 72 months, and 2 children met criteria after 72 months. The mean number of CALMs at presentation in children eventually diagnosed as having NF1 (11.8 CALMs) was significantly higher than the mean number of CALMs in children not diagnosed as having NF1 (4.6 CALMs). Of the 44 children who had 6 or more typical CALMs at presentation, 34 children met criteria for NF1. Sixty-eight patients had CALMs described as "typical," while 42 patients had "atypical" CALMs. Only 2 patients with atypical CALMs met criteria for NF1.

Conclusion  The majority of patients with 6 or more CALMs will eventually meet diagnostic criteria for NF1, typically by age 6 years, and this likelihood increases with increasing number and typical morphologic appearance of CALMs.

  M. A Kass , M. O Gordon , F Gao , D. K Heuer , E. J Higginbotham , C. A Johnson , J. K Keltner , J. P Miller , R. K Parrish , M. R Wilson and for the Ocular Hypertension Treatment Study Group
 

Objective  To compare the safety and efficacy of earlier vs later treatment in preventing primary open-angle glaucoma (POAG) in individuals with ocular hypertension.

Methods  One thousand six hundred thirty-six individuals with intraocular pressure (IOP) from 24 to 32 mm Hg in 1 eye and 21 to 32 mm Hg in the fellow eye were randomized to observation or to topical ocular hypotensive medication. Median time of treatment in the medication group was 13.0 years. After a median of 7.5 years without treatment, the observation group received medication for a median of 5.5 years. To determine if there is a penalty for delaying treatment, we compared the cumulative proportions of participants who developed POAG at a median follow-up of 13 years in the original observation group and in the original medication group.

Main Outcome Measures  Cumulative proportion of participants who developed POAG.

Results  The cumulative proportion of participants in the original observation group who developed POAG at 13 years was 0.22 (95% confidence interval [CI], 0.19-0.25), vs 0.16 (95% CI, 0.13-0.19) in the original medication group (P = .009). Among participants at the highest third of baseline risk of developing POAG, the cumulative proportion who developed POAG was 0.40 (95% CI, 0.33-0.46) in the original observation group and 0.28 (95% CI, 0.22-0.34) in the original medication group. There was little evidence of increased adverse events associated with medication.

Application to Clinical Practice  Absolute reduction was greatest among participants at the highest baseline risk of developing POAG. Individuals at high risk of developing POAG may benefit from more frequent examinations and early preventive treatment.

Trial Registration  clinicaltrials.gov Identifier: NCT00000125

  B. D Sumer , B. R Gastman , B Nussenbaum , F Gao and B. H. Haughey
 

Objective  To determine the functional outcome in patients undergoing pharyngeal reconstruction with free tissue transfer with the intent of functional laryngeal preservation.

Design  Retrospective medical record review.

Setting  Academic tertiary care hospital.

Patients  The study population comprised 45 patients who underwent a major pharyngeal resection with or without a partial laryngeal resection (2 patients died perioperatively, leaving 43 to evaluate). The majority (n = 35 [81%]) had advanced (T3 or T4) primary tumors at presentation and underwent subsequent reconstruction using free tissue transfer at a tertiary care hospital.

Main Outcome Measures  The rate of functional larynx preservation, best swallow score based on the Functional Outcome Swallowing Scale, and need for tracheostomy. Thirteen independent variables relevant to function and 6 postoperative outcome variables were studied following treatment, and their correlation with laryngeal function was determined.

Results  Of the 43 patients, 35 (81%) had T3 (n = 9) or T4 (n = 26) squamous cell carcinoma at presentation. There was 100% flap survival. Thirty-one patients (72%) tolerated an oral diet, with 24 (56%) achieving an exclusively oral diet. Only a history of gastroesophageal reflux disease had a statistically significant correlation with poor swallowing; having had a cranial nerve removed did not achieve statistical significance (P = .06). The majority of patients had their best swallow by 10 months. Of the 43 patients, 42 (97%) achieved native laryngeal speech and 36 (84%) were decannulated. The need for a tracheostomy did not correlate with any of the preoperative independent variables.

Conclusions  Free tissue transfer allows for successful reconstruction of complex pharyngeal defects that functionally threaten the remaining larynx. In properly selected patients, functional laryngeal preservation, decannulation, and use of laryngeal speech can be reliably achieved. Excellent swallowing function can less reliably be predicted.

  J. S Burchfield , J. W Dong , Y Sakata , F Gao , H. P Tzeng , V. K Topkara , M. L Entman , N Sivasubramanian and D. L. Mann
 

Background— Activation of both type 1 and type 2 tumor necrosis factor (TNF) receptors (TNFR1 and TNFR2) confers cytoprotection in cardiac myocytes. Noting that the scaffolding protein TNF receptor–associated factor 2 (TRAF2) is common to both TNF receptors, we hypothesized that the cytoprotective responses of TNF were mediated through TRAF2.

Methods and Results— Mice with cardiac-restricted overexpression of low levels of TNF (MHCsTNF3) and TRAF2 (MHC-TRAF2LC) and mice lacking TNFR1, TNFR2, and TNFR1/TNFR2 were subjected to ischemia (30 minutes) reperfusion (30 minutes) injury ex vivo using a Langendorff apparatus. MHCsTNF3 mice were protected against ischemia-reperfusion injury as shown by a significant 30% greater left ventricular developed pressure, 80% lower creatine kinase release, and Evans blue dye uptake compared with littermates. The extent of ischemia-reperfusion induced injury was similar in wild-type, TNFR1, and TNFR2 deficient mice; however, mice lacking TNFR1/TNFR2 had a significant 40% lower left ventricular developed pressure, a 65% greater creatine kinase release, and 40% greater Evans blue dye uptake compared with littermates. Interestingly, MHC-TRAF2LC mice had a significant 50% lower left ventricular developed pressure, a 70% lower creatine kinase release, and 80% lower Evans blue dye uptake compared with littermate controls after ischemia-reperfusion injury. Biochemical analysis of the MHC-TRAF2LC hearts showed that there was activation of nuclear factor-kappaB but not c-Jun N-terminal kinase activation.

Conclusion— Taken together, these results suggest that TNF confers cytoprotection in the heart through TRAF2-mediated activation of nuclear factor-B.

  K Ganguly , M Depner , C Fattman , K Bein , T. D Oury , S. C Wesselkamper , M. T Borchers , M Schreiber , F Gao , E von Mutius , M Kabesch , G. D Leikauf and H. Schulz
 

Polymorphisms in Superoxide dismutase 3, extracellular (SOD3) have been associated with reduced lung function and susceptibility to chronic obstructive pulmonary disease (COPD) in adults. Previously, we identified SOD3 as a contributing factor to altered ventilation efficiency (dead space volume/total lung capacity) in mice. Because SOD3 protects the extracellular matrix of the lung, we hypothesized that SOD3 variants also may influence postnatal lung function development. In this study, SOD3 transcript and protein localization were examined in mouse strains with differing ventilation efficiency [C3H/HeJ (high), JF1/Msf (low)] during postnatal lung development. Compared with C3H/HeJ mice, JF1/Msf mice had Sod3 promoter single nucleotide polymorphisms (SNPs) that could affect transcription factor binding sites and a decline in total lung SOD3 mRNA during postnatal development. In adult JF1/Msf mice, total lung SOD3 activity as well as SOD3 transcript and protein in airway epithelial and alveolar type II cells and the associated matrix decreased. In children (n = 1,555; age 9–11 yr), two common SOD3 SNPs, one located in the promoter region [C/T affecting a predicted aryl hydrocarbon receptor-xenobiotic response element (AhR-XRE) binding motif] and the other in exon 2 (Thr/Ala missense mutation), were associated with decreased forced expiratory volume in 1 s (FEV1), and the promoter SNP was associated with decreased maximal expiratory flow at 25% volume (MEF25). In vitro, a SOD3 promoter region-derived oligonucleotide containing the C variant was more effective in competing with the nuclear protein-binding capacity of a labeled probe than that containing the T variant. Along with the previous associated risk of lung function decline in COPD, these findings support a possible role of SOD3 variants in determining lung function in children.

  D. J Pappas , G Coppola , P. A Gabatto , F Gao , D. H Geschwind , J. R Oksenberg and S. E. Baranzini
 

Type I interferons (IFNs) are pleiotropic cytokines that modulate both innate and adaptive immune responses. They have been used to treat autoimmune disorders, cancers, and viral infection and have been demonstrated to elicit differential responses within cells, despite sharing a single receptor. The molecular basis for such differential responses has remained elusive. To identify the mechanisms underlying differential type I IFN signaling, we used whole genome microarrays to measure longitudinal transcriptional events within human CD4+ T cells treated with IFN-2b or IFN-β1a. We identified differentially regulated genes, analyzed them for the enrichment of known promoter elements and pathways, and constructed a network module based on weighted gene coexpression network analysis (WGCNA). WGCNA uses advanced statistical measures to find interconnected modules of correlated genes. Overall, differential responses to IFN in CD4+ T cells related to three dominant themes: migration, antigen presentation, and the cytotoxic response. For migration, WGCNA identified subtype-specific regulation of pre-mRNA processing factor 4 homolog B and eukaryotic translation initiation factor 4A2, which work at various levels within the cell to affect the expression of the chemokine CCL5. WGCNA also identified sterile -motif domain-containing 9-like (SAMD9L) as critical in subtype-independent effects of IFN treatment. RNA interference of SAMD9L expression enhanced the migratory phenotype of activated T cells treated with IFN-β compared with controls. Through the analysis of the dynamic transcriptional events after differential IFN treatment, we were able to identify specific signatures and to uncover novel genes that may underpin the type I IFN response.

  M. J Xie , Y. G Ma , F Gao , Y. G Bai , J. H Cheng , Y. M Chang , Z. B Yu and J. Ma
 

Cerebral arterial remodeling is one of the critical factors in the occurrence of postspaceflight orthostatic intolerance. We hypothesize that large-conductance calcium-activated K+ (BKCa) channels in vascular smooth muscle cells (VSMCs) may play an important role in regulating cerebrovascular adaptation during microgravity exposure. The aim of this work was to investigate whether activation of BKCa channels is involved in regulation of apoptotic remodeling of cerebral arteries in simulated microgravity rats. In animal studies, Sprague-Dawley rats were subjected to 1-wk hindlimb unweighting to simulate microgravity. Alterations of BKCa channels in cerebral VSMCs were investigated by patch clamp and Western blotting; apoptosis was assessed by electron microscopy and terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick-end labeling (TUNEL). To evaluate the correlation of BKCa channel and apoptosis, channel protein and cell nucleus were double-stained. In cell studies, hSlo+β1 channel was coexpressed into human embryonic kidney 293 (HEK293) cells to observe the effects of BKCa channels on apoptosis. In rats, enhanced activities and expression of BKCa channels were found to be correlated with increased apoptosis in cerebral VSMCs after simulated microgravity. In transfected HEK293 cells, activation of cloned BKCa channel induced apoptosis, whereas inhibition of cloned BKCa channel decreased apoptosis. In conclusion, activation of BKCa channels is associated with increased apoptosis in cerebral VSMCs of simulated microgravity rats.

 
 
 
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