Citation: Foot and Ankle Clinics. 2014, 19(2), 245-58
Author: Wood EV, Walker CR, Hennessy MS
Abstract: Arthrodesis of the first metatarsophalangeal joint is a reliable operation in
the treatment of selected cases of hallux valgus. It corrects deformity of
hallux valgus and metatarsus primus varus, leading to good functional results
with a low complication rate. It is a technique well suited to patients with
hallux valgus associated with degenerative changes or severe deformity, and
those for whom primary hallux valgus surgery has failed.
Link to PubMed record
Tuesday, 30 December 2014
Wednesday, 24 December 2014
WUTH publication: Zinc induced damage to kidney proximal tubular cells: studies on chemical speciation leading to a mechanism of damage
Citation: Journal of Trace Elements in medicine and biology. 2013 Jul;27(3):242-8
Author: Sargazi M, Shenkin A, Roberts NB
Abstract: This study was carried out to investigate whether zinc can potentiate renal toxicity using monolayer cultures of kidney proximal tubular cells and if so to establish the chemical species and the mechanism involved.
METHODS: Zinc was prepared as the citrate complex at pH 7.4 in phosphate buffered saline. Monolayers of kidney proximal tubular cells under standard cell culture conditions were exposed to zinc concentrations of 0, 5 10, 20, 50 and 100 μmol/L. To assess cellular damage, thiazol blue (MTT) uptake, NAG and LDH release, DAPI staining and Tunel assay were used. Cytoprotective agents: trolox, cysteine, glutathione, ascorbic acid and sodium selenite were used to investigate if the damage was reversible.
RESULTS: Incubation of kidney cells with zinc citrate showed a dose related reduction in cell viability (p<0.005) associated with cellular uptake of zinc ions. After 24 h incubation with 100 μmol/L Zn citrate, NAG release was not significantly different compared to the control whereas LDH increased 3 fold. DAPI staining showed apoptotic bodies within the cells confirmed by Tunel assay using flow cytometry. Electron microscopy showed significant morphological changes including loss of brush border, vacuolated cytoplasm and condensed nuclei. Trolox almost completely (>85±5%) and sodium selenite partially recovered (40±4%) the viability of cells exposed to Zn but no protection was observed with other cytoprotectants, e.g. glutathione, cysteine or ascorbic acid. In conclusion zinc can induce damage to kidney cells by a mechanism dependent on zinc ions entering the cell, binding to the cell organelles and disrupting cellular processes rather than damage initiated by free radical and ROS production.
Link to PubMed record.
Author: Sargazi M, Shenkin A, Roberts NB
Abstract: This study was carried out to investigate whether zinc can potentiate renal toxicity using monolayer cultures of kidney proximal tubular cells and if so to establish the chemical species and the mechanism involved.
METHODS: Zinc was prepared as the citrate complex at pH 7.4 in phosphate buffered saline. Monolayers of kidney proximal tubular cells under standard cell culture conditions were exposed to zinc concentrations of 0, 5 10, 20, 50 and 100 μmol/L. To assess cellular damage, thiazol blue (MTT) uptake, NAG and LDH release, DAPI staining and Tunel assay were used. Cytoprotective agents: trolox, cysteine, glutathione, ascorbic acid and sodium selenite were used to investigate if the damage was reversible.
RESULTS: Incubation of kidney cells with zinc citrate showed a dose related reduction in cell viability (p<0.005) associated with cellular uptake of zinc ions. After 24 h incubation with 100 μmol/L Zn citrate, NAG release was not significantly different compared to the control whereas LDH increased 3 fold. DAPI staining showed apoptotic bodies within the cells confirmed by Tunel assay using flow cytometry. Electron microscopy showed significant morphological changes including loss of brush border, vacuolated cytoplasm and condensed nuclei. Trolox almost completely (>85±5%) and sodium selenite partially recovered (40±4%) the viability of cells exposed to Zn but no protection was observed with other cytoprotectants, e.g. glutathione, cysteine or ascorbic acid. In conclusion zinc can induce damage to kidney cells by a mechanism dependent on zinc ions entering the cell, binding to the cell organelles and disrupting cellular processes rather than damage initiated by free radical and ROS production.
Link to PubMed record.
Thursday, 18 December 2014
“Merry Christmas” from the Library
Take
time for yourself, this festive season, and borrow one of our fiction books.
You
can even borrow 3 in addition to your standard borrowing allowance.
Short
of time? Why not try a ‘quick read’ easy reads that take approximately 2-3 hrs.
With
over 1000 to choose from why wait any longer?
Tuesday, 16 December 2014
WUTH publication: Rectal mucocoele following subtotal colectomy for colitis
Citation: Annals of the Royal College of Surgeons of England. 2014, 96(6), e13-4
Author: Appleton N, Day N, Walsh C
Abstract: We present a unique case of a rectal mucocoele affecting a patient several years after his subtotal colectomy for ulcerative colitis. This was secondary to both a benign anorectal stenosis and a benign mucus secreting rectal adenoma. This case highlights the importance of surveillance in such patients.
Link to PubMed record
Author: Appleton N, Day N, Walsh C
Abstract: We present a unique case of a rectal mucocoele affecting a patient several years after his subtotal colectomy for ulcerative colitis. This was secondary to both a benign anorectal stenosis and a benign mucus secreting rectal adenoma. This case highlights the importance of surveillance in such patients.
Link to PubMed record
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