The effects of crown venting or pre‐cementing of CAD/CAM‐constructed all‐ceramic crowns luted on YTZ implants on marginal cement excess

Objectives

The purpose of this study was to analyze the cement excess produced when cementing CAD/CAM‐fabricated lithium disilicate (L) or zirconium dioxide (Z) crowns using adhesive cement (A) or resin‐modified glass ionomer cement (B). Three different cementation techniques were applied: palatal venting (PV), pre‐cementation with custom analogs (CA), and conventional standard procedure (SP).

Materials and Methods

Seventy‐two crowns (36 each material) were assigned to 12 experimental groups depending on the restoration material (L, Z), type of cement (A, B), and cementation technique (PV, CA, SP). Weight measurements were taken during cementation, and the amounts of excess cement, cement retained in crown, and relative excess cement were calculated and statistically analyzed.

Results

A significant direct relation between the amounts of cement applied and excess cement was observed in groups CA and SP. Vented crowns showed least amounts of marginal excess cement (0.8 ± 0.3 μl) followed by CA (4.2 ± 1.1 μl) and SP (8.8 ± 2.5 μl; p < .001). In CA, 32.1% less excess cement (95%CI: 28.4, 35.7) was produced than in the SP group (p < .001), but 27.4% more than in the PV group (95%CI: 23.8,31.0; p < .001). Overall, slightly smaller amounts of adhesive cement (A) than of glass ionomer cement (B) were retained in crowns.

Conclusions

Using crown venting was the most effective measure to reduce the amount of marginal excess cement, followed using a pre‐cementation device. To keep the marginal excess cement of one‐piece zirconia implants to a minimum, both techniques should be considered for clinical application.     

An Uncommon Presentation of Metastatic Melanoma: A Case Report

Metastases to the spleen are rare and are generally part of a multi-visceral metastatic disease. The most common sources of splenic metastases include breast, lung and colorectal malignancies as well as melanoma and ovarian carcinoma. Solitary splenic metastasis is very uncommon.We present a case of a 44-year-old man who presented at our department for gallstones symptoms. He had a past medical history of neck cutaneous melanoma (T3bN0M0—Stage IIb). He had not attended follow-up schedule for personal reasons. However, abdominal ultrasound revealed the presence of a solitary solid lesion in the spleen. Preoperative workup was completed with CT scan that confirmed the presence of a large splenic lesion with subcapsular fluid collection, also compatible with a post-traumatic lesion.Preoperative findings could not exclude malignancy and patient was therefore submitted to surgery. At laparoscopy, a condition of peritoneal melanosis was present. Splenectomy was carried out. Histological report confirmed the peritoneal melanosis and the diagnosis of metastatic spleen lesion from melanoma. Patient was observed, but died of metastatic disease 14 months after surgery.Splenic metastases are uncommon. Isolated metastases from melanoma are rare and could be found several months after primary diagnosis of melanoma. Surgery remains the most effective treatment, especially for metachronous disease, offering the best chance of long-term survival. Prognosis remains poor, as metachronous disease is indicative of aggressive widespread of the disease.     

Maternal investment, life histories, and the costs of brain growth in mammals

Brain size variation in mammals correlates with life histories: larger-brained species have longer gestations, mature later, and have increased lifespans. These patterns have been explained in terms of developmental costs (larger brains take longer to grow) and cognitive benefits (large brains enhance survival and increase lifespan). In support of the developmental cost hypothesis, we show that evolutionary changes in pre- and postnatal brain growth correlate specifically with duration of the relevant phases of maternal investment (gestation and lactation, respectively). We also find support for the hypothesis that the rate of fetal brain growth is related to the energy turnover of the mother. In contrast, we find no support for hypotheses proposing that costs are accommodated through direct tradeoffs between brain and body growth, or between brain growth and litter size. When the duration of maternal investment is taken into account, adult brain size is uncorrelated with other life history traits such as lifespan. Hence, the general pattern of slower life histories in large-brained species appears to be a direct consequence of developmental costs.     

Efficacy of a dual chamber defibrillator with atrial antitachycardia functions in treating spontaneous atrial tachyarrhythmias in patients with life-threatening ventricular tachyarrhythmias.

BACKGROUND: Atrial fibrillation has a high incidence in patients wearing an implantable cardioverter defibrillator for ventricular tachyarrhythmias and may lead to palpitations, heart failure, angina, stroke and inappropriate defibrillator discharge. The aim of the study was to evaluate the efficacy of a dual chamber defibrillator with atrial antitachycardia functions in treating spontaneous atrial tachyarrhythmias. METHODS: One hundred and twelve patients, 88 male, mean age 64+/-11 years, were enrolled. Seventy-six had ischaemic heart disease, 21 idiopathic dilated cardiomyopathy, nine other heart diseases, six no structural heart disease. The mean left ventricular ejection fraction was 40+/-11%. Sixty-two had prior atrial tachyarrhythmias. RESULTS: Follow-up lasted 11+/-9 months (range 1-42). Among 933 ventricular tachyarrhythmia episodes, 100% of ventricular fibrillation and 92% of ventricular tachycardia were successfully cardioverted. Among 414 detected sustained atrial tachyarrhythmias, 195 were classified as atrial tachycardia (47.1%), 192 as atrial fibrillation (46.4%) and 27 (6.5%) as sinus rhythm. The detection-positive predictive value was 93.5%. Therapy success rates: antitachy pacing on atrial tachycardia = 71.3% (crude estimate); 66.1% (adjusted estimate); 50 Hertz on atrial fibrillation=36.2% (crude estimate); 13.5% (adjusted estimate); atrial shock on atrial fibrillation = 62.5% (mean energy 7.8+/-14.1J). Shock efficacy was 32% when delivered energy was < or = 2 atrial defibrillation threshold at implant and 92% when >2. Duration of successfully treated atrial episodes was significantly lower than that of unsuccessfully treated (6+/-26 min vs 42+/-60). CONCLUSIONS: Atrial antitachy pacing and shock therapies demonstrated very high efficacy in treating atrial tachyarrhythmias in defibrillator patients.     

The EUROclass trial: defining subgroups in common variable immunodeficiency

The heterogeneity of common variable immunodeficiency (CVID) calls for a classification addressing pathogenic mechanisms as well as clinical relevance. This European multicenter trial was initiated to develop a consensus of 2 existing classification schemes based on flowcytometric B-cell phenotyping and the clinical course. The clinical evaluation of 303 patients with the established diagnosis of CVID demonstrated a significant coincidence of granulomatous disease, autoimmune cytopenia, and splenomegaly. Phenotyping of B-cell subpopulations confirmed a severe reduction of switched memory B cells in most of the patients that was associated with a higher risk for splenomegaly and granulomatous disease. An expansion of CD21(low) B cells marked patients with splenomegaly. Lymphadenopathy was significantly linked with transitional B-cell expansion. Based on these findings and pathogenic consideration of B-cell differentiation, we suggest an improved classification for CVID (EUROclass), separating patients with nearly absent B cells (less than 1%), severely reduced switched memory B cells (less than 2%), and expansion of transitional (more than 9%) or CD21(low) B cells (more than 10%). Whereas the first group contains all patients with severe defects of early B-cell differentiation, severely reduced switched memory B cells indicate a defective germinal center development as found in inducible constimulator (ICOS) or CD40L deficiency. The underlying defects of expanded transitional or CD21(low) B cells remain to be elucidated. This trial is re-gistered at http://www.uniklinik-freiburg.de/zks/live/uklregister/Oeffentlich.html as UKF000308.     

Atorvastatin induces apoptosis by a caspase‐9‐dependent pathway: an in vitro study on activated rat hepatic stellate cells

Background: Statins are shown to have cholesterol‐independent properties such as anti‐inflammation and immunomodulation. Activated hepatic stellate cells (HSCs) acquire the capacity to synthesize matrix proteins in damaged liver. We tested the hypothesis that atorvastatin may be capable of inducing apoptosis in HSCs. Methods: Primary cultures of rat HSCs were exposed to atorvastatin, mevalonic acid and U0126. Quantification of living, apoptotic and necrotic HSCs was performed by flow cytometry and laser‐scan microscopy. Cell‐cycle analysis was performed by flow cytometry. Pro‐ and anti‐apoptotic factors were investigated by Western blot and electrophoresis mobility shift assay. Protease activity of caspases was calculated using a colorimetric kit. Results: Atorvastatin leads to a G2‐arrest and induces apoptosis in activated HSCs. Atorvastatin‐mediated apoptosis could be blocked by co‐administration of mevalonic acid and U0126. No effects of atorvastatin on gene expression of CD95, CD95L, NF‐κB, p53 and p21WAF1 could be observed. Atorvastatin‐induced apoptosis in activated HSCs is related to an increased protease activity of caspase‐9 and ‐3. Gene expression of the major proteins of the bcl‐system shows that truncated Bid is involved in apoptosis mediated by atorvastatin. By blocking the extracellular signal‐regulated protein kinase (ERK1/2) activation by adding U0126, we could prevent the apoptosis induced by atorvastatin. By Western blot we could not detect any change in the activation of c‐jun N‐terminal kinase (JNK). Conclusions: Atorvastatin induces apoptosis in activated HSCs acting through an ERK‐dependent cleavage of Bid and a highly increased protease activity of caspase‐9 and ‐3. JNK is not involved in atorvastatin‐mediated apoptosis in HSCs.     

Scanning mutations of the 5'UTR regulatory sequence of L-ferritin by denaturing high-performance liquid chromatography: identification of new mutations

Hereditary hyperferritinaemia cataract syndrome is an autosomal dominant disorder caused by heterogeneous mutations of the iron regulatory element (IRE) in the ferritin l-chain mRNA. The mutations are rare and fast DNA scanning would facilitate diagnosis. The aim of the study was to compare the analytical performances of two fast DNA scanning techniques: denaturing high-performance liquid chromatography (DHPLC) and double-gradient denaturing gradient gel electrophoresis (DG-DGGE). We analysed the sequence encoding the 5' untranslated flanking region of ferritin l-chain mRNA, which includes an IRE stem loop structure. The two systems unambiguously identified all the 12 accessible mutations in a single run, including the difficult C-G transversions. DHPLC and DG-DGGE identified seven abnormal patterns in DNA samples from 47 subjects with unexplained hyperferritinaemia; all had mutations in the IRE sequence, including two not reported before: C36G and A37G. The scanning of 250 DNA samples from subjects genotyped for HFE led to the identification of four new mutations, all outside the IRE structure: C10T, C16T, C90T and del-T156. We conclude that DHPLC, similar to DG-DGGE, detects all the mutations in the l-ferritin 5'UTR sequence in a single run, and that various mutations occur outside the IRE structure.     

Work Ability Index in Israeli Hospital Nurses: Applicability of the Adapted Questionnaire

Background/Study Context: The Work Ability Index (WAI) questionnaire is widely used for evaluation of the work ability of workers. This is the first application of the validated Hebrew version of this questionnaire to Israeli nurses in order to evaluate factors affecting their work ability.

Methods: A cross-sectional study was conducted among 515 nurses from two general hospitals in Israel (87.3% female).

Results: A significant negative correlation was found between the WAI score and age, years in current job, and number of reported diagnoses. The most frequently reported illnesses (as diagnosed by a physician) were musculoskeletal disorders, endocrine/metabolic diseases, and cardiovascular diseases. Agreement between illnesses as diagnosed by a physician and as self-reported by nurses was low, especially with respect to mental/emotional stress, (kappa statistics = 16.4%, p < .001).

Conclusions: Mean WAI score found in Israeli hospital nurses is relatively high as compared with that of European nurses. It gradually decreases with age. The WAI questionnaire enables the early identification of those nurses with compromised work ability and who are in need of assistance in order to prevent early retirement. As retirement age is currently advancing, keeping elderly workers in the workforce is of prime importance.     

MRP4 over-expression has a role on both reducing nitric oxide-dependent antiplatelet effect and enhancing ADP induced platelet activation

The impact of inhibition of multidrug resistance protein 4 (MRP4) on nitric oxide (NO) resistance and on ADP-induced platelet aggregation is unknown. The aim of this investigation was to verify whether platelet NO resistance correlates with MRP4 expression and evaluate whether this can be reduced by in vitro MRP4 inhibition mediated by cilostazol. Moreover, we assessed if inhibition of MRP4-mediated transport reduces ADP-induced platelet reactivity. The inhibitory effect of sodium nitroprusside (SNP), a NO-donor that enhances cyclic guanosine monophosphate (cGMP) cytosolic concentration, was assessed in platelets obtained from aspirin treated patients and in a control population. The inhibitory effect of SNP was evaluated by ADP-induced aggregation in SNP-treated platelets. The impact of MRP4 on ADP-induced platelet aggregation was performed in high on aspirin residual platelet reactivity (HARPR) patients and compared to healthy volunteers (HV), and a control cohort (CTR). In aspirin-treated patients with high levels of MRP4, reduced SNP inhibition was found compared to those with low levels of MRP4. MRP4 inhibition by cilostazol significantly reduced ADP-induced platelet aggregation in HARPR population, and to a lesser extent in HV and CTR populations. In conclusion, cilostazol can mitigate the hyper-reactive platelet phenotype of HARPR patients by reducing residual ADP-induced platelet aggregation and increasing NO-dependent endothelial antiplatelet effects.