Hip fractures in elderly--ten years analysis

Geriatric hip fractures (GHP) are the major problem in the geriatric traumatology and it is estimated that treatment of GHF will spend a large amount of health care resources. The aim of this retrospective study was to compare differences in incidence of operatively treated patients with GHF, type of treatment depending of the type of fracture, early postoperative mortality, length of stay and costs of used implants within a 10 years period. Surgically treated 2478 patients, older than 65 years with hip fractures were included in the study. Patients were grouped according to the type of fracture (femoral neck fracture or intertrochanteric femoral fracture) and used implant. Results showed increasing trend in GHF in our County in the last 10 years. There was a shifting trend in used implants, and new surgical techniques were used more commonly in the last few years. In observed period there were no significant changes in revision surgery and length of hospital stay. The mortality decreased, especially in males, but generally it was not in correlation with used implant. At the 10-years period increase in patients with GHF of 179% was followed with 4 time higher increase in implant prices. Present reimbursement in health care system does not calculate the difference of implant costs in hospital expenses, therefore proper usage of modern implants and careful planning in the treatment of GHF is necessary.     

Protein kinase C-mediated endothelial barrier regulation is caveolin-1-dependent

Protein kinase C (PKC) is activated in response to various inflammatory mediators and contributes significantly to the endothelial barrier breakdown. However, the mechanisms underlying PKC-mediated permeability regulation are not well understood. We prepared microvascular myocardial endothelial cells from both wild-type (WT) and caveolin-1-deficient mice. Activation of PKC by phorbol myristate acetate (PMA) (100 nM) for 30 min induced intercellular gap formation and fragmentation of VE-cadherin immunoreactivity in WT but not in caveolin-1-deficient monolayers. To test the effect of PKC activation on VE-cadherin-mediated adhesion, we allowed VE-cadherin-coated microbeads to bind to the endothelial cell surface and probed their adhesion by laser tweezers. PMA significantly reduced bead binding to 78±6% of controls in WT endothelial cells without any effect in caveolin-1-deficient cells. In WT cells, PMA caused an 86±18% increase in FITC-dextran permeability whereas no increase in permeability was observed in caveolin-1-deficient monolayers. Inhibition of PKC by staurosporine (50 nM, 30 min) did not affect barrier functions in both WT and caveolin-1-deficient MyEnd cells. Theses data indicate that PKC activation reduces endothelial barrier functions at least in part by the reduction of VE-cadherin-mediated adhesion and demonstrate that PKC-mediated permeability regulation depends on caveolin-1.     

Unusual entropy-driven affinity of Chromobacterium violaceum lectin CV-IIL toward fucose and mannose

The purple pigmented bacterium Chromobacterium violaceum is a dominant component of tropical soil microbiota that can cause rare but fatal septicaemia in humans. Its sequenced genome provides insight into the abundant potential of this organism for biotechnological and pharmaceutical applications and allowed an ORF encoding a protein that is 60% identical to the fucose binding lectin (PA-IIL) from Pseudomonas aeruginosa and the mannose binding lectin (RS-IIL) from Ralstonia solanacearum to be identified. The lectin, CV-IIL, has recently been purified from C. violaceum [Zinger-Yosovich, K., Sudakevitz, D., Imberty, A., Garber, N. C., and Gilboa-Garber, N. (2006) Microbiology 152, 457-463] and has been confirmed to be a tetramer with subunit size of 11.86 kDa and a binding preference for fucose. We describe here the cloning of CV-IIL and its expression as a recombinant protein. A complete structure-function characterization has been made in an effort to analyze the specificity and affinity of CV-IIL for fucose and mannose. Crystal structures of CV-IIL complexes with monosaccharides have yielded the molecular basis of the specificity. Each monomer contains two close calcium cations that mediate the binding of the monosaccharides, which occurs in different orientations for fucose and mannose. The thermodynamics of binding has been analyzed by titration microcalorimetry, giving dissociation constants of 1.7 and 19 microM for alpha-methyl fucoside and alpha-methyl mannoside, respectively. Further analysis demonstrated a strongly favorable entropy term that is unusual in carbohydrate binding. A comparison with both PA-IIL and RS-IIL, which have binding preferences for fucose and mannose, respectively, yielded insights into the monosaccharide specificity of this important class of soluble bacterial lectins.     

Tropospheric ozone-induced structural changes in leaf mesophyll cell walls in grapevine plants

The structural changes in leaves of grapevine plants (Vitis vinifera L.) exposed to different ozone concentrations were investigated. Ozone fumigations were performed in open-top chambers at four different ozone levels (charcoal-filtered air (F), ambient air (N), ambient air + 25 mm³m⁻³ ozone (O-25) and ambient air + 50 mm³m⁻³ ozone (O-50)). The leaves of plants from chambers with increased ozone concentrations (O-25 and O-50) were significantly thicker than the controls (F), owing to increased thickness of the mesophyll layer. Observing O-50 leaves, it was found that the mesophyll cell wall displayed structural changes. In some places cell wall thickness increased up to 1 μm. We found callose deposits on the inner side of the cell walls of mesophyll cells. These data are in accord with the concept that the mesophyll cell wall acts as a barrier against the penetration of tropospheric ozone into the cells.     

A 3-year longitudinal study of quality-of-life outcomes of elderly patients with implant- and tooth-supported fixed partial dentures in posterior dental regions

doi: 10.1111/j.1741‐2358.2011.00592.x
A 3‐year longitudinal study of quality‐of‐life outcomes of elderly patients with implant‐ and tooth‐supported fixed partial dentures in posterior dental regions Background: Clinical studies have mainly been focused on oral health‐related quality‐of‐life (OHRQoL) outcomes of removable dentures. Objective: To evaluate therapy of elderly patients with implant‐supported fixed partial dentures (IFPD) and tooth‐supported fixed partial dentures (FPD) in the posterior dental regions. Patients and methods: The OHIP49 was used to measure OHRQoL in 64 patients with IFPD and 38 patients with FPD, before, 3 weeks and 3 years after rehabilitation. A control group (CG) consisted of 62 individuals. Results: The Oral Health Impact Profile questionnaire (OHIP) follow‐up scores of the patients with FPD and the patients with IFPD were significantly smaller in comparison with the baseline scores (p < 0.01). The OHIP scores were further reduced at the 3‐year follow‐up. The patients with IFPD had significantly higher scores than the patients with FPD and the CG at the baseline and at the follow‐ups. In the patients with FPD, both age groups (≤60 and >60) showed equal improvement of the OHRQoL. In the IFPD group, patients older than 60 years showed better improvement (p < 0.05). There were no significant differences dependent on gender and antagonistic teeth (p > 0.05). Conclusion: The FPD and the IFPD treatment showed significant improvement of OHRQoL. The FPD treatment improved OHRQoL equally in both age groups, while the IFPD treatment improved OHRQoL better in older patients.     

Does life along the sea carry greater risk of thyroid cancer?

Aim of this study was to determine whether there are any differences between coastal and inland Dalmatia in incidence rates and clinical characteristics of thyroid cancer. Data on 651 persons who suffer from and have undergone surgery for thyroid cancer have been analysed. All patients lived in Dalmatia between 1997 and 2006. Data were collected via surveys, insight into medical histories and results of histopathological analysis. In Dalmatia, in the overall sample, there are no statistically significant differences in incidence between coastal and inland areas (chi2=3.03; df=1; p=0.082). Somewhat higher overall incidence has been recorded in the inland (8.5%000) than in the coastal Dalmatia (7.3%000). In the overall sample, in Dalmatia, women make up 81.4% of patients and papillary cancer accounts for 80.0% of all thyroid cancers. The ratio of papillary to folicullar cancer is 7.8:1 in coastal and 4.2:1 in inland Dalmatia. Papillary and medullary types are more common in the coastal area and follicular and anaplastic cancer types in the inland area and the differences are statistically significant (p>0.033). Epidemiological characteristics of thyroid cancer in coastal Dalmatia are in accordance with the characteristics of this cancer as described in iodine-sufficient areas: the most common type is papillary cancer, and the ratio of papillary to follicular is 7.8:1. Sex-wise, the coastal area records a higher ratio of male patients (1:3.8) than the inland area (1:7.1). There are no statistically significant differences in thyroid cancer incidence rates between coastal and inland Dalmatia. Epidemiological characteristics of thyroid cancer in inland Dalmatia are in some ways more similar to those of continental Croatia. This result could be the consequence of previous iodine insufficiency in inland Dalmatia.     

Relocalization of Junctional Adhesion Molecule A during Inflammatory Stimulation of Brain Endothelial Cells

Junctional adhesion molecule A (JAM-A) is a unique tight junction (TJ) transmembrane protein that under basal conditions maintains endothelial cell-cell interactions but under inflammatory conditions acts as a leukocyte adhesion molecule. This study investigates the fate of JAM-A during inflammatory TJ complex remodeling and paracellular route formation in brain endothelial cells. The chemokine (C-C motif) ligand 2 (CCL2) induced JAM-A redistribution from the interendothelial cell area to the apical surface, where JAM-A played a role as a leukocyte adhesion molecule participating in transendothelial cell migration of neutrophils and monocytes. JAM-A redistribution was associated with internalization via macropinocytosis during paracellular route opening. A tracer study with dextran-Texas Red indicated that internalization occurred within a short time period (～10 min) by dextran-positive vesicles and then became sorted to dextran-positive/Rab34-positive/Rab5-positive vesicles and then Rab4-positive endosomes. By ～20 min, most internalized JAM-A moved to the brain endothelial cell apical membrane. Treatment with a macropinocytosis inhibitor, 5-(N-ethyl-N-isopropyl)amiloride, or Rab5/Rab4 depletion with small interfering RNA oligonucleotides prevented JAM-A relocalization, suggesting that macropinocytosis and recycling to the membrane surface occur during JAM-A redistribution. Analysis of the signaling pathways indicated involvement of RhoA and Rho kinase in JAM-A relocalization. These data provide new insights into the molecular and cellular mechanisms involved in blood-brain barrier remodeling during inflammation.     

Bcs1, a AAA protein of the mitochondria with a role in the biogenesis of the respiratory chain

The family of AAA+ proteins in eukaryotes has many members in various cellular compartments with a broad spectrum of functions in protein unfolding and degradation. The mitochondrial AAA protein Bcs1 plays an unusual role in protein translocation. It is involved in the topogenesis of the Rieske protein, Rip1, and thereby in the biogenesis of the cytochrome bc(1) complex of the mitochondrial respiratory chain. Bcs1 mediates the export of the folded FeS domain of Rip1 across the mitochondrial inner membrane and the insertion of its transmembrane segment into an assembly intermediate of the cytochrome bc(1) complex. We discuss structural elements of the Bcs1 protein compared to other AAA proteins in an attempt to understand the mechanism of its function. In this context, we discuss human diseases caused by mutations in Bcs1 that lead to different properties of the protein and subsequently to different symptoms.