Barkhausen noise emission of AISI 304 stainless steel originating from strain induced martensite by shot peening

This study deals with magnetic Barkhausen noise emission produced by strain-induced martensite generated during shot peening of austenitic AISI 304 stainless steel. The transformation from the paramagnetic to ferromagnetic state and the corresponding birth of the magnetic domain structure are important with respect to irreversible motion of domain walls and the corresponding Barkhausen noise emission. Barkhausen noise is investigated and explained with respect to the residual stress state as well as the micro-structure expressed in terms of the martensite fraction, its crystallite size, preferred orientation, surface topography, and microhardness. The strength of the Barkhausen noise is mainly linked with the number of shot peening cycles, corresponding Almen intensity, and the associated volume fraction of strain-induced martensite as well as the extent of its depth. The role of the residual stress state in the martensite phase is minor. Surface strengthening expressed in terms of the microhardness in the near-surface region is very high for the medium shot peening intensity. A remarkable decrease in the near-surface microhardness as well as the presence of heavily thinned folds indicate over shot peen-ing and surface microcracking in the case of a longer shot peening time and the corre-sponding higher Almen intensity.Web of Science2076274

Prognostic significance of endogenous adhesion/growth-regulatory lectins in lung cancer

Objective: To determine the expression of endogenous adhesion/growth-regulatory lectins and their binding sites using labeled tissue lectins as well as the binding profile of hyaluronic acid as an approach to define new prognostic markers. Methods: Sections of paraffin-embedded histological material of 481 lungs from lung tumor patients following radical lung excision processed by a routine immunohistochemical method (avidin-biotin labeling, DAB chromogen). Specific antibodies against galectins-1 and - 3 and the heparin-binding lectin were tested. Staining by labeled galectins and hyaluronic acid was similarly visualized by a routine protocol. After semiquantitative assessment of staining, the results were compared with the pT and pN stages and the histological type. Survival was calculated by univariate and multivariate methods. Results: Binding of galectin-1 and its expression tended to increase, whereas the parameters for galectin-3 decreased in advanced pT and pN stages at a statistically significant level. The number of positive cases was considerably smaller among the cases with small cell lung cancer than in the group with non-small-cell lung cancer, among which adenocarcinomas figured prominently with the exception of galectin-1 expression. Kaplan-Meier computations revealed that the survival rate of patients with galectin-3-binding or galectin-1-expressing tumors was significantly poorer than that of the negative cases. In the multivariate calculations of survival lymph node metastases ( p < 0.0001), histological type ( p = 0.003), galectin-3-binding capacity ( p = 0.01), galectin-3 expression ( p = 0.03) and pT status ( p = 0.003) proved to be independent prognostic factors, not correlated with the pN stage. Conclusion: The expression and the capacity to bind the adhesion/growth regulatory galectin-3 is defined as an unfavorable prognostic factor not correlated with the pTN stage. Copyright (C) 2005 S. Karger AG, Basel

High temperature superconductivity (Tc onset at 34K) in the high pressure orthorhombic phase of FeSe

We have studied the structural and superconducting properties of tetragonal FeSe under pressures up to 26GPa using synchrotron radiation and diamond anvil cells. The bulk modulus of the tetragonal phase is 28.5(3)GPa, much smaller than the rest of Fe based superconductors. At 12GPa we observe a phase transition from the tetragonal to an orthorhombic symmetry. The high pressure orthorhombic phase has a higher Tc reaching 34K at 22GPa.Comment: 15 pages, 4 figure

Upper critical field, lower critical field and critical current density of FeTe0.60Se0.40 single crystal

The transport and magnetic studies are performed on high quality FeTe0.60Se0.40 single crystals to determine the upper critical fields (Hc2), lower critical field (Hc1) and the Critical current density (Jc). The value of upper critical field Hc2 are very large, whereas the activation energy as determined from the slope of the Arrhenius plots are was found to be lower than that in the FeAs122 superconductor. The lower critical field was determined in ab direction and c direction of the crystal, and was found to have a anisotropy of 'gamma'{=(Hc1//c) / (Hc1//b)} ~ 4. The magnetic isotherms measured up to 12 Tesla shows the presence of fishtail behavior. The critical current densities at 1.8K of the single crystal was found to almost same in both ab and c direction as 1X105 Amp/cm2 in low field regime.Comment: 9 pages, 6 figure

\u3cem\u3eRPGRIP1\u3c/em\u3e and Cone-Rod Dystrophy in Dogs

Cone–rod dystrophies (crd) represent a group of progressive inherited blinding diseases characterized by primary dysfunction and loss of cone photoreceptors accompanying or preceding rod death. Recessive crd type 1 was described in dogs associated with an RPGRIP1 exon 2 mutation, but with lack of complete concordance between genotype and phenotype. This review highlights role of the RPGRIP1, a component of complex protein networks, and its function in the primary cilium, and discusses the potential mechanisms of genotype–phenotype discordance observed in dogs with the RPGRIP1 mutation

Midkine is a NF-κB-inducible gene that supports prostate cancer cell survival

BackgroundMidkine is a heparin-binding growth factor that is over-expressed in various human cancers and plays important roles in cell transformation, growth, survival, migration, and angiogenesis. However, little is known about the upstream factors and signaling mechanisms that regulate midkine gene expression.MethodsTwo prostate cancer cell lines LNCaP and PC3 were studied for their expression of midkine. Induction of midkine expression in LNCaP cells by serum, growth factors and cytokines was determined by Western blot analysis and/or real-time quantitative reverse-transcription - polymerase chain reaction (RT-PCR). The cell viability was determined by the trypan blue exclusion assay when the LNCaP cells were treated with tumor necrosis factor alpha (TNFalpha) and/or recombinant midkine. When the LNCaP cells were treated with recombinant midkine, activation of intracellular signalling pathways was determined by Western blot analysis. Prostate tissue microarray slides containing 129 cases (18 normal prostate tissues, 40 early stage cancers, and 71 late stage cancers) were assessed for midkine expression by immunohistochemical staining.ResultsWe identified that fetal bovine serum, some growth factors (epidermal growth factor, androgen, insulin-like growth factor-I, and hepatocyte growth factor) and cytokines (TNFalpha and interleukin-1beta) induced midkine expression in a human prostate cancer cell line LNCaP cells. TNFalpha also induced midkine expression in PC3 cells. TNFalpha was the strongest inducer of midkine expression via nuclear factor-kappa B pathway. Midkine partially inhibited TNFalpha-induced apoptosis in LNCaP cells. Knockdown of endogenous midkine expression by small interfering RNA enhanced TNFalpha-induced apoptosis in LNCaP cells. Midkine activated extracellular signal-regulated kinase 1/2 and p38 mitogen-activated protein kinase pathways in LNCaP cells. Furthermore, midkine expression was significantly increased in late stage prostate cancer, which coincides with previously reported high serum levels of TNFalpha in advanced prostate cancer.ConclusionThese findings provide the first demonstration that midkine expression is induced by certain growth factors and cytokines, particularly TNFalpha, which offers new insight into understanding how midkine expression is increased in the late stage prostate cancer

Evaluation of gait symmetry in poliomyelitis subjects : Comparison of a conventional knee ankle foot orthosis (KAFO) and a new powered KAFO.

Background: Compared to able-bodied subjects, subjects with post polio syndrome and poliomyelitis demonstrate a preference for weight-bearing on the non-paretic limb, causing gait asymmetry. Objectives: The purpose of this study was to evaluate the gait symmetry of the poliomyelitis subjects when ambulating with either a drop- locked knee ankle foot orthosis (KAFO) or a newly developed powered KAFO. Methods: Seven subjects with poliomyelitis who routinely wore conventional KAFOs participated in this study, and received training to enable them to ambulate with the powered KAFO on level ground, prior to gait analysis. Results: There were no significant differences in the gait symmetry index (SI) of step length (P=0.085), stance time (P=0.082), double limb support time (P=0.929) or speed of walking (p=0.325) between the two test conditions. However, using the new powered KAFO improved the SI in step width (P=0.037), swing time (P=0.014), stance phase percentage (P=0.008) and knee flexion during swing phase (p≤0.001) compared to wearing the dropped locked KAFO. Conclusion: The use of a powered KAFO for ambulation by poliomyelitis subjects affects gait symmetry in the base of support, swing time, stance phase percentage and knee flexion during swing phase

Are German patients burdened by the practice charge for physician visits ('Praxisgebuehr')? A cross sectional analysis of socio-economic and health related factors

<p>Abstract</p> <p>Background</p> <p>In 2004, a practice charge for physician visits ('Praxisgebuehr') was implemented in the German health care system, mainly in order to reduce expenditures of sickness funds by reducing outpatient physician visits. In the statutory sickness funds, all adults now have to pay € 10 at their first physician visit in each 3 month period, except for vaccinations and preventive services. This study looks at the effect of this new patient fee on delaying or avoiding physician visits, with a special emphasis on different income groups.</p> <p>Methods</p> <p>Six representative surveys (conducted between 2004 and 2006) of the Bertelsmann Healthcare Monitor were analysed, comprising 7,769 women and men aged 18 to 79 years. The analyses are based on stratified analyses and logistic regression models, including a focus on the subgroup having a chronic disease.</p> <p>Results</p> <p>Two results can be highlighted. First, avoiding or delaying a physician visit due to this fee is seen most often among younger and healthier adults. Second, those in the lowest income group are much more affected in this way than the better of. The multivariate analysis in the subgroup of respondents having a chronic disease shows, for example, that this reaction is reported 2.45 times more often in the lowest income group than in the highest income group (95% CI: 1.90–3.15).</p> <p>Conclusion</p> <p>The analyses indicate that the effects of the practice charge differ by socio-economic group. It would be important to assess these effects in more detail, especially the effects on health care quality and health outcomes. It can be assumed, however, that avoiding or delaying physician visits jeopardizes both, and that health inequalities are increasing due to the practice charge.</p

The G67E mutation in hMLH1 is associated with an unusual presentation of Lynch syndrome

Germline mutations in the mismatch repair (MMR) genes are associated with Lynch syndrome, also known as hereditary non-polyposis colorectal cancer (HNPCC) syndrome. Here, we characterise a variant of hMLH1 that confers a loss-of-function MMR phenotype. The mutation changes the highly conserved Gly67 residue to a glutamate (G67E) and is reminiscent of the hMLH1-p.Gly67Arg mutation, which is present in several Lynch syndrome cohorts. hMLH1-Gly67Arg has previously been shown to confer loss-of-function (Shimodaira et al, 1998), and two functional assays suggest that the hMLH1-Gly67Glu protein fails to sustain normal MMR functions. In the first assay, hMLH1-Gly67Glu abolishes the protein's ability to interfere with MMR in yeast. In the second assay, mutation of the analogous residue in yMLH1 (yMLH1-Gly64Glu) causes a loss-of-function mutator phenotype similar to yMLH1-Gly64Arg. Despite these molecular similarities, an unusual spectrum of tumours is associated with hMLH1-Gly67Glu, which is not typical of those associated with Lynch syndrome and differs from those found in families carrying the hMLH1-Gly67Arg allele. This suggests that hMLH1 may have different functions in certain tissues and/or that additional factors may modify the influence of hMLH1 mutations in causing Lynch syndrome