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Articles by J. R Turner
Total Records ( 3 ) for J. R Turner
  J. P Lopez , J. R Turner and L. H. Philipson
 

A key step in regulating insulin secretion is insulin granule trafficking to the plasma membrane. Using live-cell time-lapse confocal microscopy, we observed a dynamic association of insulin granules with filamentous actin and PIP2-enriched structures. We found that the scaffolding protein family ERM, comprising ezrin, radixin, and moesin, are expressed in β-cells and target both F-actin and PIP2. Furthermore, ERM proteins are activated via phosphorylation in a glucose- and calcium-dependent manner. This activation leads to a translocation of the ERM proteins to sites on the cell periphery enriched in insulin granules, the exocyst complex docking protein Exo70, and lipid rafts. ERM scaffolding proteins also participate in insulin granule trafficking and docking to the plasma membrane. Overexpression of a truncated dominant-negative ezrin construct that lacks the ERM F-actin binding domain leads to a reduction in insulin granules near the plasma membrane and impaired secretion. Conversely, overexpression of a constitutively active ezrin results in more granules near the cell periphery and an enhancement of insulin secretion. Diabetic mouse islets contain less active ERM, suggestive of a novel mechanism whereby impairment of insulin granule trafficking to the membrane through a complex containing F-actin, PIP2, Exo70, and ERM proteins contributes to defective insulin secretion.

  J Neily , P. D Mills , N Eldridge , E. J Dunn , C Samples , J. R Turner , A Revere , R. G DePalma and J. P. Bagian
 

Objective  To describe incorrect surgical procedures reported from Veterans Health Administration (VHA) Medical Centers from 2001 to mid-2006 and provide proposed solutions for preventing such events.

Design  Descriptive study.

Setting  Veterans Health Administration Medical Centers.

Participants  Veterans of the US Armed Forces.

Interventions  The VHA instituted an initial directive, "Ensuring Correct Surgery and Invasive Procedures," in January 2003. The directive was updated in 2004 to include non–operating room (OR) invasive procedures and incorporated requirements of The Joint Commission Universal Protocol for preventing wrong-site operations.

Main Outcome Measures  The categories included 5 incorrect event types (wrong patient, side, site, procedure, or implant), major or minor surgical procedures, location in or out of the OR, therapeutic or diagnostic events, adverse event or close call, inpatient or ambulatory events, specialty department, body segment, and severity and probability of harm.

Results  We reviewed 342 reported events (212 adverse events and 130 close calls). Of these, 108 adverse events (50.9%) occurred in an OR, and 104 (49.1%) occurred elsewhere. When examining adverse events only, ophthalmology and invasive radiology were the specialties associated with the most reports (45 [21.2%] each), whereas orthopedics was second to ophthalmology for number of reported adverse events occurring in the OR. Pulmonary medicine cases (such as wrong-side thoracentesis) and wrong-site cases (such as wrong spinal level) were associated with the most harm. The most common root cause of events was communication (21.0%).

Conclusions  Incorrect ophthalmic and orthopedic surgical procedures appear to be overrepresented among adverse events occurring in ORs. Outside the OR, adverse events by invasive radiology were most frequently reported. Incorrect surgical procedures are not only an OR challenge but also a challenge for events occurring outside of the OR. We support earlier communication based on crew resource management to prevent surgical adverse events.

  A Mykoniatis , L Shen , M Fedor Chaiken , J Tang , X Tang , R. T Worrell , E Delpire , J. R Turner , K. S Matlin , P Bouyer and J. B. Matthews
 

In secretory epithelial cells, the basolateral Na+-K+-2Cl cotransporter (NKCC1) plays a major role in salt and fluid secretion. Our laboratory has identified NKCC1 surface expression as an important regulatory mechanism for Cl secretion in the colonic crypt cell line T84, a process also present in native human colonic crypts. We previously showed that activation of protein kinase C (PKC) by carbachol and phorbol 12-myristate 13-acetate (PMA) decreases NKCC1 surface expression in T84 cells. However, the specific endocytic entry pathway has not been defined. We used a Madin-Darby canine kidney (MDCK) cell line stably transfected with enhanced green fluorescent protein (EGFP)-NKCC1 to map NKCC1 entry during PMA exposure. At given times, we fixed and stained the cells with specific markers (e.g., dynamin II, clathrin heavy chain, and caveolin-1). We also used chlorpromazine, methyl-β-cyclodextrin, amiloride, and dynasore, blockers of the clathrin, caveolin, and macropinocytosis pathways and the vesicle "pinchase" dynamin, respectively. We found that PMA caused dose- and time-dependent NKCC1 endocytosis. After 2.5 min of PMA exposure, ~80% of EGFP-NKCC1 endocytic vesicles colocalized with clathrin and ~40% colocalized with dynamin II and with the transferrin receptor, the uptake of which is also mediated by clathrin-coated vesicles. We did not observe significant colocalization of EGFP-NKCC1 endocytic vesicles with caveolin-1, a marker of the caveolae-mediated endocytic pathway. We quantified the effect of each inhibitor on PMA-induced EGFP-NKCC1 endocytosis and found that only chlorpromazine and dynasore caused significant inhibition compared with the untreated control (61% and 25%, respectively, at 2.5 min). Together, these results strongly support the conclusion that PMA-stimulated NKCC1 endocytosis is associated with a clathrin pathway.

 
 
 
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