233 research outputs found
Screening for cervical neoplasia in Mamelodi lessons from an unscreened population
No Abstract
Fracture of the pancreas in two patients after a go‐kart accident
BackgroundAfter blunt abdominal trauma, an isolated injury to the pancreatic duct is uncommon. Physical signs and laboratory parameters are often inaccurate, and missing this diagnosis can cause serious clinical problems.Case outlinesTwo young women (aged 18 and 20 years) are reported who sustained isolated trauma to the pancreatic duct in go‐kart accidents. Each patient sustained a fracture of the pancreas. This injury was diagnosed only after a period of clinical observation with repeated laboratory parameters, ultrasound and CT scan. Pancreatic tissue was conserved by performing a pancreaticojejunostomy.DiscussionAfter any episode of blunt abdominal trauma, isolated injury to the pancreatic duct should be considered. Serum analysis, ultrasonography and CT scanning can be helpful in early diagnosis. Preservation of pancreatic tissue can be achieved with a good clinical outcome
Implementing glucose control in intensive care: a multicenter trial using statistical process control
Implementing glucose control in intensive care: a multicenter trial using statistical process control
Risk factors for necrotizing enterocolitis in neonates: A systematic review of prognostic studies
Background: Necrotizing enterocolitis (NEC) is a severe multifactorial disease in preterm neonates associated with high morbidity and mortality. Better insight into prognostic values of the many reported factors associated with NEC is needed to enable identification of neonates at risk for NEC. The aim was to systematically review the literature to identify independent risk factors for NEC from the literature. Methods: Medline, Cochrane, Embase, Pubmed and Google Scholar were searched systematically for cohort studies reporting prognostic factors for NEC in neonates using multivariable analysis. Studies were scored with the Quality In Prognosis Studies tool (QUIPS). Results: From 5154 initial hits, 14 prognostic studies were included, with various designs. Study quality was rated high in th
Hypo-osmotic cell swelling activates the p38 MAP kinase signalling cascade
Hypo-osmotic swelling of human Intestine 407 cells leads to a significant increase of intracellular MAPKAP-kinase 2 activity and Hsp27 phosphorylation. Pre-treatment of the cells with the p38 MAP kinase inhibitor SB-203580 blocks this activation, indicating that the hypotonicity-induced activation of MAPKAP kinase 2 is, similarly to that described for hyperosmotic treatment, the result of an activated p38 MAP kinase cascade. The activation of MAPKAP kinase 2 proceeds with kinetics similar to that of one of the first physiological responses of hypo-osmotic treatment, the opening of compensatory Cl- channels. However, inhibition of the p38 MAP kinase cascade does not block the osmo-sensitive anion efflux and, vice versa, activation of p38 MAP kinase by cytokines and anisomycin does not increase the efflux. These results indicate that the p38 MAP kinase cascade is not directly involved in Cl- channel activation but instead may play a role in subsequent cellular repair processes
Protein tyrosine phosphorylation is involved in osmoregulation of ionic conductances
Using the human Intestine 407 cell line as a model, we investigated a
possible role for tyrosine kinase(s) in regulating the ion efflux pathways
induced by hyposmotic stimulation (regulatory volume decrease, RVD).
Pretreatment of 125I(-)-and 86Rb(+)-loaded cells with the phosphotyrosine
phosphatase inhibitor sodium orthovanadate (200 microM) potentiated
isotope efflux triggered by mild hypotonicity (10-20%) but did not further
increase the efflux in response to more vigorous osmotic stimulation (30%
hypotonicity). The tyrosine kinase inhibitors herbimycin A and genistein
largely reduced the osmoshock-induced efflux in both control and
vanadate-pretreated cells, while not affecting calcium-activated 86Rb+
efflux. Potentiation of the RVD response by vanadate was confirmed by
direct measurements of hypotonicity-induced changes in cell volume.
Hypotonic shock alone triggered a rapid and transient increase in tyrosine
phosphorylation of several proteins as well as phosphorylation of
mitogen-activated protein kinase. Furthermore, the potentiating effects of
vanadate on hypotonicity-induced ion efflux and mitogen-activated protein
(MAP) kinase phosphorylation were mimicked by epidermal growth factor.
Neither vanadate nor epidermal growth factor provoked a RVD-like ionic
response under isotonic conditions. These results indicate that tyrosine
phosphorylation is an essential step in the RVD response and suggest a
novel role of growth factors in the cellular defense against osmotic
stress
Endogenous type II cGMP-dependent protein kinase exists as a dimer in membranes and can Be functionally distinguished from the type I isoforms
In mammalian tissues two types of cGMP-dependent protein kinase (cGK) have
been identified. In contrast to the dimeric cGK I, cGK II purified from
pig intestine was shown previously to behave as a monomer. However,
recombinant rat cGK II was found to have hydrodynamic parameters
indicative of a homodimer. Chemical cross-linking studies showed that pig
cGK II in intestinal membranes h
Isotype-specific activation of cystic fibrosis transmembrane conductance regulator-chloride channels by cGMP-dependent protein kinase II
Type II cGMP-dependent protein kinase (cGKII) isolated from pig intestinal
brush borders and type I alpha cGK (cGKI) purified from bovine lung were
compared for their ability to activate the cystic fibrosis transmembrane
conductance regulator (CFTR)-Cl- channel in excised, inside-out membrane
patches from NIH-3T3 fibroblasts and from a rat intestinal cell line
(IEC-CF7) stably expressing recombinant CFTR. In both cell models, in the
presence of cGMP and ATP, cGKII was found to mimic the effect of the
catalytic subunit of cAMP-dependent protein kinase (cAK) on opening
CFTR-Cl-channels, albeit with different kinetics (2-3-min lag time,
reduced rate of activation). By contrast, cGKI or a monomeric cGKI
catalytic fragment was incapable of opening CFTR-Cl- channels and also
failed to potentiate cGKII activation of the channels. The cAK activation
but not the cGKII activation was blocked by a cAK inhibitor peptide. The
slow activation by cGKII could not be ascribed to counteracting protein
phosphatases, since neither calyculin A, a potent inhibitor of phosphatase
1 and 2A, nor ATP gamma S (adenosine 5'-O-(thiotriphosphate)), producing
stable thiophosphorylation, was able to enhance the activation kinetics.
Channels preactivated by cGKII closed instantaneously upon removal of ATP
and kinase but reopened in the presence of ATP alone. Paradoxically,
immunoprecipitated CFTR or CF-2, a cloned R domain fragment of CFTR (amino
acids 645-835) could be phosphorylated to a similar extent with only minor
kinetic differences by both isotypes of cGK. Phosphopeptide maps of CF-2
and CFTR, however, revealed very subtle differences in site-specificity
between the cGK isoforms. These results indicate that cGKII, in contrast
to cGKI alpha, is a potential activator of chloride transport in
CFTR-expressing cell types
Necrotising enterocolitis and mortality in preterm infants after introduction of probiotics: A quasi-experimental study
Evidence on the clinical effectiveness of probiotics in the prevention of necrotising enterocolitis (NEC) in preterm infants is conflicting and cohort studies lacked adjustment for time trend and feeding type. This study investigated the association between the introduction of routine probiotics (Lactobacillus acidophilus and Bifidobacterium bifidum; Infloran ®) on the primary outcome 'NEC or death'. Preterm infants (gestational age <32 weeks or birth weight <1500 gram) admitted before (Jan 2008-Sep 2012; n = 1288) and after (Oct 2012-Dec 2014; n = 673) introduction of probiotics were compared. Interrupted time series logistic regression models were adjusted for confounders, effect modification by feeding type, seasonality and underlying temporal trends. Unadjusted and adjusted analyses showed no difference in 'NEC or death' between the two periods. The overall incidence of NEC declined from 7.8% to 5.1% (OR 0.63, 95% CI 0.42-0.93, p = 0.02), which was not statistically significant in the adjusted models. Introduction of probiotics was associated with a reduced adjusted odds for 'NEC or sepsis or death' in exclusively breastmilk-fed infants (OR 0.43, 95% CI 0.21-0.93, p = 0.03) only. We conclude that introduction of probiotics was not associated with a reduction in 'NEC or death' and that type of feeding seems to modify the effects of probiotics
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