Interventions to facilitate return to work in adults with adjustment disorders

BACKGROUND: Adjustment disorders are a frequent cause of sick leave and various interventions have been developed to expedite the return to work (RTW) of individuals on sick leave due to adjustment disorders. OBJECTIVES: To assess the effects of interventions facilitating RTW for workers with acute or chronic adjustment disorders. SEARCH METHODS: We searched the Cochrane Depression, Anxiety and Neurosis Review Group's Specialised Register (CCDANCTR) to October 2011; the Cochrane Central Register of Controlled Trials (CENTRAL) to Issue 4, 2011; MEDLINE, EMBASE, PsycINFO and ISI Web of Science, all years to February 2011; the WHO trials portal (ICTRP) and ClinicalTrials.gov in March 2011. We also screened reference lists of included studies and relevant reviews. SELECTION CRITERIA: We selected randomised controlled trials (RCTs) evaluating the effectiveness of interventions to facilitate RTW of workers with adjustment disorders compared to no or other treatment. Eligible interventions were pharmacological interventions, psychological interventions (such as cognitive behavioural therapy (CBT) and problem solving therapy), relaxation techniques, exercise programmes, employee assistance programmes or combinations of these interventions. The primary outcomes were time to partial and time to full RTW, and secondary outcomes were severity of symptoms of adjustment disorder, work functioning, generic functional status (i.e. the overall functional capabilities of an individual, such as physical functioning, social function, general mental health) and quality of life. DATA COLLECTION AND ANALYSIS: Two authors independently selected studies, assessed risk of bias and extracted data. We pooled studies that we deemed sufficiently clinically homogeneous in different comparison groups, and assessed the overall quality of the evidence using the GRADE approach. MAIN RESULTS: We included nine studies reporting on 10 psychological interventions and one combined intervention. The studies included 1546 participants. No RCTs were found of pharmacological interventions, exercise programmes or employee assistance programmes. We assessed seven studies as having low risk of bias and the studies that were pooled together were comparable. For those who received no treatment, compared with CBT, the assumed time to partial and full RTW was 88 and 252 days respectively. Based on two studies with a total of 159 participants, moderate-quality evidence showed that CBT had similar results for time (measured in days) until partial RTW compared to no treatment at one-year follow-up (mean difference (MD) -8.78, 95% confidence interval (CI) -23.26 to 5.71). We found low-quality evidence of similar results for CBT and no treatment on the reduction of days until full RTW at one-year follow-up (MD -35.73, 95% CI -113.15 to 41.69) (one study with 105 participants included in the analysis). Based on moderate-quality evidence, problem solving therapy (PST) significantly reduced time until partial RTW at one-year follow-up compared to non-guideline based care (MD -17.00, 95% CI -26.48 to -7.52) (one study with 192 participants clustered among 33 treatment providers included in the analysis), but we found moderate-quality evidence of no significant effect on reducing days until full RTW at one-year follow-up (MD -17.73, 95% CI -37.35 to 1.90) (two studies with 342 participants included in the analysis). AUTHORS' CONCLUSIONS: We found moderate-quality evidence that CBT did not significantly reduce time until partial RTW and low-quality evidence that it did not significantly reduce time to full RTW compared with no treatment. Moderate-quality evidence showed that PST significantly enhanced partial RTW at one-year follow-up compared to non-guideline based care but did not significantly enhance time to full RTW at one-year follow-up. An important limitation was the small number of studies included in the meta-analyses and the small number of participants, which lowered the power of the analyses

A Micro-Raman Spectroscopic Study of Hydrazine-Treated Human Dental Calculus

Hydrazine has been used to remove organic components and to isolate the mineral(s) from human calculus. Micro-Raman measurements were performed on the mineral phase. After the hydrazine-treatment, not only a large reduction in fluorescence but also an increase in Raman signal was observed. The treatment was essential in minimizing thermally-induced chemical changes which could otherwise occur to the original calculus mineral due to the intense laser light. The Raman spectral features of the mineral were nearly all identical among the Raman spectra obtained at many randomly-selected sites by the micro-Raman microbe with a lateral resolution of approximately 1 μm, and were consistent with those of impure hydroxyapatite containing CO32- and HPO42-. The spectra contained typical hydroxyapatite bands including PO43- bands of the v1, v2, v3 and v4 modes and one OH- stretch band. Other minor bands due to the CO32- v1 and v3 modes and bands possibly due to the HPO42- v1, v2 and v4 modes were observable by the technique despite the hydrazine-treatment that could in principle remove the HPO4 and CO3 ions from the mineral. In comparison with pure synthetic hydroxyapatite, the intensity of the OH- stretch band relative to that of the PO43- v1 band was approximately 70% weaker, and the bandwidth of the phosphate v1 band was 200% broader, reflecting various crystal imperfections presumably present in the calculus mineral

Increasing the susceptibility of the rat 208F fibroblast cell line to radiation-induced apoptosis does not alter its clonogenic survival dose-response.

Recent studies have suggested a correlation between the rate and incidence of apoptosis and the radiation response of particular cell lines. However, we found that increasing the rate of induction of apoptosis in the fibroblast line 208F, by transfecting it with human c-myc, did not lead to a change in its clonogenic survival dose-response for either gamma-irradiation or 125I-induced DNA damage. It was also found that expression of mutant (T24) Ha-ras in the 208F line appeared to decrease the level of apoptosis per mitosis after irradiation and inhibited the formation of nucleosomal ladders, but did not affect either the onset of the morphological features of apoptosis or the clonogenic survival dose-response of the cells to either gamma-irradiation or 125I-induced DNA damage. Our findings suggest that it may be incorrect to make predictions about the radiosensitivity of cells based only on knowledge of their mode of death

Origin Of The Far Off-Axis GRB171205A

We show that observed properties of the low luminosity GRB171205A and its afterglow, like those of most other low-luminosity (LL) gamma ray bursts (GRBs) associate with a supernova (SN), indicate that it is an ordinary SN-GRB, which was produced by inverse Compton scattering of glory light by a highly relativistic narrowly collimated jet ejected in a supernova explosion and viewed from a far off-axis angle. As such, VLA/VLBI follow-up radio observations of a superluminal displacement of its bright radio afterglow from its parent supernova, will be able to test clearly whether it is an ordinary SN-GRB viewed from far off-axis or it belongs to a distinct class of GRBs, which are different from ordinary GRBs, and cannot be explained by standard fireball models of GRBs as ordinary GRBsComment: 5 pages, 6 figures, updated data in Fig. 3, Corrected GRB angular distance used in Fig.

Enhanced activity of desilicated Cu-SSZ-13 for the selective catalytic reduction of NOx and its comparison with steamed Cu-SSZ-13

Mesoporous Cu-SSZ-13 was created by first synthesizing zeolite H-SSZ-13 and subsequently desilicating the material by base leaching using NaOH in different concentrations. The catalyst materials were prepared by ion exchanging the leached samples back to their acidic form using NH4NO3, and to their active Cu form by ion exchanging them with CuSO4. For comparison, H- and Cu-SSZ-13 were steamed using a wide variety of different conditions. Using a 0.10 M NaOH solution for base leaching, it was found that Cu-SSZ-13 becomes more active in the selective catalytic reduction of NOx with NH3 (NH3-SCR) over the entire temperature region but especially in the low temperature region (<200 °C). This increase could be explained by a decrease in pore diffusion limitations due to the introduction of mesopores on the outside of the zeolite crystals but keeping the chemical environment of the catalyst nearly the same as that of the parent material. Higher base leaching concentrations do, however, lead to a decrease in the amount of Brønsted acid sites, pore volume and accessible surface area, accompanied by a decrease in NH3-SCR activity. Ar physisorption coupled with SEM and confocal fluorescence microscopy in combination with two differently sized fluorescent organic probe molecules (i.e., 4-(4-dimethyl-aminostyryl)-1-methyl-pyridinium-iodide and 4-(4-dicyclohexyl-aminostyryl)-1-methyl-pyridinium-iodide) show an increase in the external surface area due to the creation of mesopores. The development of mesoporosity starts from the crystal surface and continues into the crystal with increasing alkaline solution strength, but under our conditions it never reaches the center. On the other hand, zeolite steaming did not successfully introduce mesoporosity and mainly managed to deactivate the Cu-SSZ-13 zeolite catalysts

On small proofs of Bell-Kochen-Specker theorem for two, three and four qubits

The Bell-Kochen-Specker theorem (BKS) theorem rules out realistic {\it non-contextual} theories by resorting to impossible assignments of rays among a selected set of maximal orthogonal bases. We investigate the geometrical structure of small $v-l$ BKS-proofs involving $v$ real rays and $l$ $2n$-dimensional bases of $n$-qubits ($1< n < 5$). Specifically, we look at the parity proof 18-9 with two qubits (A. Cabello, 1996), the parity proof 36-11 with three qubits (M. Kernaghan & A. Peres, 1995 \cite{Kernaghan1965}) and a newly discovered non-parity proof 80-21 with four qubits (that improves work of P. K Aravind's group in 2008). The rays in question arise as real eigenstates shared by some maximal commuting sets (bases) of operators in the $n$-qubit Pauli group. One finds characteristic signatures of the distances between the bases, which carry various symmetries in their graphs.Comment: version to appear in European Physical Journal Plu

Nucleosomes in pancreatic cancer patients during radiochemotherapy

Nucleosomes appear spontaneously in elevated concentrations in the serum of patients with malignant diseases as well as during chemo- and radiotherapy. We analyzed whether their kinetics show typical characteristics during radiochemotherapy and enable an early estimation of therapy efficacy. We used the Cell Death Detection Elisaplus ( Roche Diagnostics) and investigated the course of nucleosomes in the serum of 32 patients with a local stage of pancreatic cancer who were treated with radiochemotherapy for several weeks. Ten of them received postsurgical therapy, 21 received primary therapy and 1 received therapy for local relapse. Blood was taken before the beginning of therapy, daily during the first week, once weekly during the following weeks and at the end of radiochemotherapy. The response to therapy was defined according to the kinetics of CA 19-9: a decrease of CA 19-9 650% after radiochemotherapy was considered as `remission'; an increase of >= 100% ( which was confirmed by two following values) was defined as `progression'. Patients with `stable disease' ranged intermediately. Most of the examined patients showed a decrease of the concentration of nucleosomes within 6 h after the first dose of radiation. Afterwards, nucleosome levels increased rapidly, reaching their maximum during the following days. Patients receiving postsurgery, primary or relapse therapies did not show significant differences in nucleosome values during the time of treatment. Single nucleosome values, measured at 6, 24 and 48 h after the application of therapy, could not discriminate significantly between patients with no progression and those with progression of disease. However, the area under the curve of the first 3 days, which integrated all variables of the initial therapeutic phase, showed a significant correlation with the progression-free interval ( p = 0.008). Our results indicate that the area under the curve of nucleosomes during the initial phase of radiochemotherapy could be valuable for the early prediction of the progression-free interval. Copyright (C) 2005 S. Karger AG, Basel

Quasi-free Compton Scattering and the Polarizabilities of the Neutron

Differential cross sections for quasi-free Compton scattering from the proton and neutron bound in the deuteron have been measured using the Glasgow/Mainz tagging spectrometer at the Mainz MAMI accelerator together with the Mainz 48 cm $\oslash$ $\times$ 64 cm NaI(Tl) photon detector and the G\"ottingen SENECA recoil detector. The data cover photon energies ranging from 200 MeV to 400 MeV at $\theta^{LAB}_\gamma=136.2^\circ$. Liquid deuterium and hydrogen targets allowed direct comparison of free and quasi-free scattering from the proton. The neutron detection efficiency of the SENECA detector was measured via the reaction $p(\gamma,\pi^+ n)$. The "free" proton Compton scattering cross sections extracted from the bound proton data are in reasonable agreement with those for the free proton which gives confidence in the method to extract the differential cross section for free scattering from quasi-free data. Differential cross sections on the free neutron have been extracted and the difference of the electromagnetic polarizabilities of the neutron have been obtained to be $\alpha-\beta= 9.8\pm 3.6(stat){}^{2.1}_1.1(syst)\pm 2.2(model)$ in units $10^{-4}fm^3$. In combination with the polarizability sum $\alpha +\beta=15.2\pm 0.5$ deduced from photoabsorption data, the neutron electric and magnetic polarizabilities, $\alpha_n=12.5\pm 1.8(stat){}^{+1.1}_{-0.6}\pm 1.1(model)$ and $\beta_n=2.7\mp 1.8(stat){}^{+0.6}_{-1.1}(syst)\mp 1.1(model)$ are obtained. The backward spin polarizability of the neutron was determined to be $\gamma^{(n)}_\pi=(58.6\pm 4.0)\times 10^{-4}fm^4$

Compton Scattering by the Proton using a Large-Acceptance Arrangement

Compton scattering by the proton has been measured using the tagged-photon facility at MAMI (Mainz) and the large-acceptance arrangement LARA. The new data are interpreted in terms of dispersion theory based on the SAID-SM99K parameterization of photo-meson amplitudes. It is found that two-pion exchange in the t-channel is needed for a description of the data in the second resonance region. The data are well represented if this channel is modeled by a single pole with mass parameter m(sigma)=600 MeV. The asymptotic part of the spin dependent amplitude is found to be well represented by pi-0-exchange in the t-channel. A backward spin-polarizability of gamma(pi)=(-37.1+-0.6(stat+syst)+-3.0(model))x10^{-4}fm^4 has been determined from data of the first resonance region below 455 MeV. This value is in a good agreement with predictions of dispersion relations and chiral pertubation theory. From a subset of data between 280 and 360 MeV the resonance pion-photoproduction amplitudes were evaluated leading to a E2/M1 multipole ratio of the p-to-Delta radiative transition of EMR(340 MeV)=(-1.7+-0.4(stat+syst)+-0.2(model))%. It was found that this number is dependent on the parameterization of photo-meson amplitudes. With the MAID2K parameterization an E2/M1 multipole ratio of EMR(340 MeV)=(-2.0+-0.4(stat+syst)+-0.2(model))% is obtained

Endogenous Formaldehyde Is a Hematopoietic Stem Cell Genotoxin and Metabolic Carcinogen

Endogenous formaldehyde is produced by numerous biochemical pathways fundamental to life, and it can crosslink both DNA and proteins. However, the consequences of its accumulation are unclear. Here we show that endogenous formaldehyde is removed by the enzyme alcohol dehydrogenase 5 (ADH5/GSNOR), and Adh5−/− mice therefore accumulate formaldehyde adducts in DNA. The repair of this damage is mediated by FANCD2, a DNA crosslink repair protein. Adh5−/−Fancd2−/− mice reveal an essential requirement for these protection mechanisms in hematopoietic stem cells (HSCs), leading to their depletion and precipitating bone marrow failure. More widespread formaldehyde-induced DNA damage also causes karyomegaly and dysfunction of hepatocytes and nephrons. Bone marrow transplantation not only rescued hematopoiesis but, surprisingly, also preserved nephron function. Nevertheless, all of these animals eventually developed fatal malignancies. Formaldehyde is therefore an important source of endogenous DNA damage that is counteracted in mammals by a conserved protection mechanism.Medical Research Council de Reino Unido. MC_U105178811Instituto de Salud Carlos III (ISCIII) de España. CP12/03273Ministerio de Economía y Competitividad de España. BFU2013-041457-PNational Institute of Environmental Health Sciences (NIEHS) de los Estados Unidos. P42 ES005948 y P30 ES010126Texas Commission for Environmental Quality. Estados Unidos. 582-12-2186