Search

The material master data catalogue in large hospitals may well exceed 50'000 articles required at one or another location for patient diagnosis and treatment. Most hospitals use a commercial material management IT system to deal with orders, eProcurement, incoming goods, warehouse management, internal commissioning and distribution. An analysis in three Swiss hospitals (including a hospital chain) demonstrated however, that despite existing standards maintenance of the material master data catalogue is often done manually based on different incoming formats such as csv, mail etc. We present components, which may enable seamless master data update using standardized formats and discuss in detail current barriers within hospital supply to give finally recommendations how to overcome them.

Background: Vascular endothelial growth factor (VEGF) is one of several angiogenic factors expressed in cirrhosis and during progression to malignancy, that seem to play a major role in hepatocellular carcinoma development. Lately, another angiogenic factor, epidermal growth factor-like domain multiple 7 (EGFL7), has attracted interest due to its possible relationship with hepatocellular carcinoma metastasis., Aims: To evaluate expression of VEGF and EGFL7 in human hepatocellular carcinoma, compared to corresponding cirrhotic surrounding tissue., Methods: Tumoural and cirrhotic tissue was harvested from 12 consecutive patients undergoing surgical resection. VEGF and EGFL7 were assessed by immunofluorescence and quantitative reverse transcriptase-polymerase chain reaction, compared with normal controls., Results: Both angiogenic factors were over-expressed in cirrhotic livers compared to normal controls. VEGF and EGFL7 expressions did not differ according to disease aetiology, nodule size or other clinical variables. While VEGF expression was constant, regardless of tumour differentiation stage and unchanged compared to surrounding cirrhotic tissue, EGFL7 expression increased in less differentiated hepatocellular carcinoma., Conclusions: The preferential expression of EGFL7 in less differentiated hepatocellular carcinoma compared to VEGF, suggests a possible important role of this angiogenic factor in a later oncogenic and infiltrative/metastatic phase., (Copyright © 2015 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.)

Leptin is an adipocytokine that reduces ischemic damage in several organs including brain and heart. STAT3 activation is a key step for the attainment of leptin effects in various tissues. We evaluated the possible effect of leptin on liver viability and STAT3 activation, in a rat model of ischemia-reperfusion injury. Rat livers, flushed and stored with Belzer solution (4° C for 24 h), were warmly reperfused (3.5 ml/min/g liver for 1 h at 37° C with O(2) ) with Krebs-Ringer bicarbonate. Treatment group underwent an identical protocol with the adjunct of Leptin (10 ng/ml). Liver effluent was harvested to assess LDH and AST output. Liver tissue was used for pSTAT3 expression (western blot and immunostaining), optical microscopy, TUNEL, and Cell Death Detection assays. The pSTAT3 expression was enhanced by administration of leptin. In parallel, LDH and AST output were reduced (P = 0.04 and P = 0.02 for LDH and AST, respectively). Optical microscopy, TUNEL, and Cell Death Detection assay results demonstrated increased viability in livers treated with leptin in comparison with others (Optical microscopy P = 0.02; TUNEL P = 0.01; Cell death Detection assay P = 0.003). In conclusion, cold storage and reperfusion with leptin reduce liver ischemia-reperfusion injury. This effect is associated with an increased expression of pSTAT-3., (© 2012 The Authors. Transplant International © 2012 European Society for Organ Transplantation.)

Cholestasis, induced by liver ischemia-reperfusion injury (IRI), is characterized by dilatation of bile canaliculi and loss of microvilli. Tauroursodeoxycholic acid (TUDCA) is an anti-cholestatic agent, modulating protein kinase C (PKC) alpha pathway. PKC reduces ischemic damage in several organs, its isoform alpha modulates ezrin, a key protein in the maintenance of cell lamellipoidal extensions. We evaluated the effects of TUDCA on cholestasis, canalicular changes and PKCalpha-ezrin expression in a rat model of liver IRI. Livers flushed and stored with Belzer solution or Belzer + 10 mm TUDCA (4 degrees C for 6 h) were reperfused (37 degrees C with O(2)) with Krebs-Ringer bicarbonate + 2.5 micromol/min of Taurocholate or TUDCA. Bile was harvested for bile flow assessment. Liver tissue was employed for Electron Microscopy (EM) and for PKCalpha and ezrin immunoblot and immunofluorescence. The same experiments were conducted with the PKCalpha inhibitor Go-6976. TUDCA-treated livers showed increased bile flow (0.25+/-0.17 vs. 0.042+/-0.02 microl/min/g liver, P<0.05) and better preservation of microvilli and bile canalicular area at EM. These effects were associated with increased PKCalpha and ezrin expression (P=0.03 and P=0.04 vs. control respectively), as also confirmed by immunofluorescence data. PKCalpha inhibition abolished these TUDCA effects. TUDCA administration during IRI reduces cholestasis and canalicular damage in the liver modulating PKCalpha-ezrin pathway.

This report describes the case of a young Romanian patient who developed a severe exacerbation of pulmonary tuberculosis during interferon-alpha treatment for chronic hepatitis D. While this occurrence underscores that clinical guidelines should be applied with caution in immigrants from underdeveloped countries, due to the possible presence of unrecognized or unreported comorbidity, the mechanisms for an interferon-related exacerbation of pulmonary tuberculosis are also examined. We propose that IFN-induced weight loss and anorexia may have played an important role in promoting clinical manifestations of tuberculosis in our patient.

Biliary lipids output is reduced after liver transplantation and tends to normalize thereafter. Cyclosporine A (CyA) is reported to interfere with the normal bile-restoring process after liver grafting, but data are inconclusive, in particular regarding the comparison with the other widely used calcineurin inhibitor tacrolimus (TCR). Furthermore, previous researches were conducted in patients taking multiple immunosuppressive therapies and with a short follow up. In this study we readdressed this issue by comparing biliary lipids in the first 3 months after liver transplant, in 20 patients randomized to receive immunosuppression with CyA or TCR monotherapy. Bile samples, harvested through a T-tube at days 1, 3, 7, 15, 30, 60 and 90 were assessed for cholesterol, phospholipids, and total and individual concentrations of bile acids (BA). Liver and kidney function tests were evaluated as well. We found no differences between CyA and TCR in biochemical findings or in total biliary BAs, cholesterol, and phospholipids. However, CyA-treated patients showed lower levels of glycochenodeoxycholic acid at day 15, compared to those treated with TCR (P < 0.04). This difference normalized thereafter, without any biochemical or clinical effect at 3-month follow up.

Bell's palsy is caused by a nuclear and/or infranuclear lesion of the facial nerve, producing an ipsilateral deficit of the facial muscles. The etiology is unknown. Bell's palsy has a frequency of 20:100000 individuals/year, a familiarity of 1-2% of cases, and a recurrence rate of 9% of cases. We studied 33 children (mean age 9.1 years) admitted to our Division during the period 1991-1994 because of Bell's palsy. We propose our personal diagnostic and therapeutical trial: in every patient a full neurological and otoscopic examination, and an audioimpedenzometric test. Treatment is then commenced with prednisone (1 mg/kg/day p.o. for 5-10 days and gradual reduction in 5 days), vitamins B1, B6 and B12 p.o. for 30 days, and local treatment with artificial tears, and occlusive bandage at nighttime until the lagophthalmus is resolved. Electromyography-electroneurography, and brain CT-scan are carried out after 15 days and 21 days respectively of treatment, if neurological deficit is unchanged. 80 to 90% of patients are reported to recover spontaneously from Bell's palsy. With our approach we achieved a 100% recovery rate within an average of 3 weeks (range: 1 week to 5 months).

We followed 94 preterm infants (G.A. < 37 weeks) small for gestational age (SGA) born from 1980 to 1987 in Pavia and admitted to the Neonatal Intensive Care Unit of S. Matteo Hospital (Pavia). A control group matched for gestational age of 94 preterm appropriate for gestational age (AGA) was also studied. Neurological examination was carried out at 40 weeks postmenstrual age and at 3, 6, 9, 12, 24, 36 months of age with the method of Amiel-Tison and Grenier (1986). Psychomotor development was assessed using Brunet-Lezine's Scale until 1985 and after Bayley Scales of Infant Development. Intrauterine mortality was 23.40% in the SGA group and 5.32% in the AGA group (p = 0.0003); neonatal mortality was 18% in the SGA group and 6.62% in the AGA group (p < 0.01). 42 SGA (80.8%) and 58 AGA (79.5%) were completely normal (group A) at 36 months, but SGA infants showed transient neurological abnormalities (TNA) more frequently than the control group (30.7% vs 6.8% - p < 0.001). 5 SGA (9.6%) and 10 AGA (13.7%) had minor abnormalities (group B); no SGA children and only one AGA had diplegia (group C); 3 SGA (5.8%) and 4 AGA (5.5%) were considered to have severe handicap (group D) SGA children had a higher incidence of epilepsy (3.8% vs 0) than AGA (group E). These results show that in our group of SGA preterm infants the union of intrauterine growth retardation and prematurity compromise the possibility of survival.(ABSTRACT TRUNCATED AT 250 WORDS)