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Generation of arbitrarily spin polarized muon pairs is investigated via polarized $e^-e^+$ collision. We calculate the fully spin-resolved cross section ${\rm d}\sigma_{e^-e^+\rightarrow \mu^-\mu^+}$ and utilize the Monte Carlo method of binary collision to describe the production and polarization processes of muon pairs. We find that, due to the dependence of mixed helicities on the scattering angle, arbitrarily polarized muon pairs with both of the longitudinal and transverse spin components can be produced. The collision of tightly collimated electron and positron beams with highly longitudinal polarization and nC charge can generate about $40\%$ muon pairs with longitudinal polarization and about $60\%$ muon pairs with transverse polarization. The compact high-flux $e^-e^+\rightarrow\mu^-\mu^+$ muon source could be implemented through the next-generation laser-plasma linear collider, and would be essential to facilitate the investigation of fundamental physics and the measurement technology in broad areas.

Forest land plays a vital role in global climate, ecosystems, farming and human living environments. Therefore, forest biomass estimation methods are necessary to monitor changes in the forest structure and function, which are key data in natural resources research. Although accurate forest biomass measurements are important in forest inventory and assessments, high-density measurements that involve airborne light detection and ranging (LiDAR) at a low flight height in large mountainous areas are highly expensive. The objective of this study was to quantify the aboveground biomass (AGB) of a plateau mountainous forest reserve using a system that synergistically combines an unmanned aircraft system (UAS)-based digital aerial camera and LiDAR to leverage their complementary advantages. In this study, we utilized digital aerial photogrammetry (DAP), which has the unique advantages of speed, high spatial resolution, and low cost, to compensate for the deficiency of forestry inventory using UAS-based LiDAR that requires terrain-following flight for high-resolution data acquisition. Combined with the sparse LiDAR points acquired by using a high-altitude and high-speed UAS for terrain extraction, dense normalized DAP point clouds can be obtained to produce an accurate and high-resolution canopy height model (CHM). Based on the CHM and spectral attributes obtained from multispectral images, we estimated and mapped the AGB of the region of interest with considerable cost efficiency. Our study supports the development of predictive models for large-scale wall-to-wall AGB mapping by leveraging the complementarity between DAP and LiDAR measurements. This work also reveals the potential of utilizing a UAS-based digital camera and LiDAR synergistically in a plateau mountainous forest area.

Hepatocellular carcinoma (HCC) is a deadly form of liver cancer with limited treatment options. The c-Myc transcription factor is a pivotal player in hepatocarcinogenesis, but the mechanisms underlying c-Myc oncogenic activity in the liver remain poorly delineated. Mammalian target of rapamycin complex 2 (mTORC2) has been implicated in cancer by regulating multiple AGC kinases, especially AKT proteins. In the liver, AKT1 and AKT2 are widely expressed. While AKT2 is the major isoform downstream of activated phosphoinositide 3-kinase and loss of phosphatase and tensin homolog-induced HCC, the precise function of AKT1 in hepatocarcinogenesis is largely unknown. In the present study, we demonstrate that mTORC2 is activated in c-Myc-driven mouse HCC, leading to phosphorylation/activation of Akt1 but not Akt2. Ablation of Rictor inhibited c-Myc-induced HCC formation in vivo. Mechanistically, we discovered that loss of Akt1, but not Akt2, completely prevented c-Myc HCC formation in mice. Silencing of Rictor or Akt1 in c-Myc HCC cell lines inhibited phosphorylated forkhead box o1 expression and strongly suppressed cell growth in vitro. In human HCC samples, c-MYC activation is strongly correlated with phosphorylated AKT1 expression. Higher expression of RICTOR and AKT1, but not AKT2, is associated with poor survival of patients with HCC. In c-Myc mice, while rapamycin, an mTORC1 inhibitor, had limited efficacy at preventing c-Myc-driven HCC progression, the dual mTORC1 and mTORC2 inhibitor MLN0128 effectively promoted tumor regression by inducing apoptosis and necrosis. Conclusion: Our study indicates the functional contribution of mTORC2/Akt1 along c-Myc-induced hepatocarcinogenesis, with AKT1 and AKT2 having distinct roles in HCC development and progression; targeting both mTORC1 and mTORC2 may be required for effective treatment of human HCC displaying c-Myc amplification or overexpression.

Laser-driven brilliant controllable polarized $\gamma$-photon sources open the way for designing compact $\gamma\gamma$ collider, which enable the large yield of linear Breit-Wheeler (LBW) pairs in a single shot and thus provide an opportunity for the investigation of polarized LBW process. In this work we investigate the polarization characteristics of LBW pair production via our developed spin-resolved binary collision simulation method. Polarization of $\gamma$-photons modifies the kinematics of scattering particles and induces the correlated energy-angle shift of LBW pairs, and the latter's polarization characteristic depends on the helicity configures of scattering particles. Our method confirms that the polarized $\gamma\gamma$ collider with an asymmetric setup can be performed with currently achievable laser facilities to produce abundant polarized LBW pairs, fulfilling the detection power of polarimetries. The precise knowledge of polarized LBW process is in favor of the calibration and monitor of polarized $\gamma\gamma$ collider, and could enhance the opacity of $\gamma$-photons in high-energy astrophysical objects to exacerbate the inconsistency between some observations and standard models.

Generation of arbitrarily spin-polarized lepton (here refer in particular to electron and positron) beams has been investigated in the single-shot interaction of high-energy polarized $\gamma$ photons with an ultraintense asymmetric laser pulse via nonlinear Breit-Wheeler (BW) pair production. We develop a fully spin-resolved semi-classical Monte Carlo method to describe the pair creation and polarization in the local constant field approximation. In nonlinear BW process the polarization of created pairs is simultaneously determined by the polarization of parent $\gamma$ photons, the polarization and asymmetry of scattering laser field, due to the spin angular momentum transfer and the asymmetric spin-dependent pair production probabilities, respectively. In considered all-optical method, dense GeV lepton beams with average polarization degree up to about $80\%$ (adjustable between the transverse and longitudinal components) can be obtained with currently achievable laser facilities, which could be used as injectors of the polarized $e^{+}e^{-}$ collider to search for new physics beyond the Standard Model.

Hepatocellular carcinoma (HCC) is a deadly malignancy with limited treatment options. Activation of the AKT/mTOR cascade is one of the most frequent events along hepatocarcinogenesis. mTOR is a serine/threonine kinase and presents in two distinct complexes: mTORC1 and mTORC2. While mTORC1 has been extensively studied in HCC, the functional contribution of mTORC2 during hepatocarcinogenesis has not been well characterized, especially in vivo. Pten expression is one of the major mechanisms leading to the aberrant activation of the AKT/mTOR signaling. Here, we show that concomitant downregulation of Pten and upregulation of c-Met occurs in a subset of human HCC, mainly characterized by poor prognosis. Using CRISPR-based gene editing in combination with hydrodynamic injection, Pten was deleted in a subset of mouse hepatocytes (sgPten). We found that loss of Pten synergizes with overexpression of c-Met to promote HCC development in mice (sgPten/c-Met). At the molecular level, sgPten/c-Met liver tumor tissues display increased AKT and mTOR signaling. Using Rictor conditional knockout mice, we demonstrate that sgPten/c-Met-driven HCC development strictly depends on an intact mTORC2 complex. Our findings therefore support the critical role of mTORC2 in hepatocarcinogenesis. sgPten/c-Met mouse model represents a novel valuable system that can be used for the development of targeted therapy against this deadly malignancy.

A new process based on gas bubble supported organic liquid membrane extraction technology was suggested to treat the auro-cyanide wastewaters. The results show that, not only the high-concentration copper(I) in the auro-cyanide wastewaters can be recovered satisfactorily, but the very low concentration gold(I) can also be extracted efficiently by the suggested gas bubble supported organic liquid membrane extraction technology. The recovery of copper(I), gold(I) and cyanide can reach 99%, 99%, and 91.9%, respectively. The raffinates after bubbling extraction can be returned back to the mineral separation process for reusing and recycling in the factories, so that almost zero discharge of the cyanide wastewaters comes true. The Cu(I) and Au(I) in the loaded organic phase can be stripped by acidic thiourea and then the regenerated organic phase can be returned back for reusing. Zinc powder is used to recover gold(I) and copper(I) in the thiourea solutions. Then, gold and copper can be separated by two-steps of dissolving the zinc powder replacement residues with dilute acid. The total recovery of gold(I) and copper(I) can reach 98.06% and 94.74%, respectively. The raffinates after the zinc powder replacement process can be used to produce zinc sulphide products. The total recovery of zinc reaches 96%. The suggested new process based on gas bubble supported organic liquid membrane extraction technology is economical and with a low processing cost. It is also environmental friendly and might find potential industrial application in the future., A new process based on gas bubble supported organic liquid membrane extraction technology was suggested to treat the auro-cyanide wastewaters. The results show that, not only the high-concentration copper(I) in the auro-cyanide wastewaters can be recovered satisfactorily, but the very low concentration gold(I) can also be extracted efficiently by the suggested gas bubble supported organic liquid membrane extraction technology. The recovery of copper(I), gold(I) and cyanide can reach 99%, 99%, and 91.9%, respectively. The raffinates after bubbling extraction can be returned back to the mineral separation process for reusing and recycling in the factories, so that almost zero discharge of the cyanide wastewaters comes true. The Cu(I) and Au(I) in the loaded organic phase can be stripped by acidic thiourea and then the regenerated organic phase can be returned back for reusing. Zinc powder is used to recover gold(I) and copper(I) in the thiourea solutions. Then, gold and copper can be separated by two-steps of dissolving the zinc powder replacement residues with dilute acid. The total recovery of gold(I) and copper(I) can reach 98.06% and 94.74%, respectively. The raffinates after the zinc powder replacement process can be used to produce zinc sulphide products. The total recovery of zinc reaches 96%. The suggested new process based on gas bubble supported organic liquid membrane extraction technology is economical and with a low processing cost. It is also environmental friendly and might find potential industrial application in the future.

BackgroundHepatocellular carcinoma (HCC) is a leading cause of cancer related deaths worldwide. The PI3K cascade is one of the major signaling pathways underlying HCC development and progression. Activating mutations of PI3K catalytic subunit alpha (PIK3CA) and/or loss of Pten often occur in human HCCs. Serum and glucocorticoid kinase 3 (SGK3) belongs to the SGK family of AGK kinases and functions in parallel to AKT downstream of PI3K. Previous studies have shown that SGK3 may be the major kinase responsible for the oncogenic potential of PIK3CA helical domain mutants, such as PIK3CA(E545K), but not kinase domain mutants, such as PIK3CA(H1047R).MethodsWe investigated the functional contribution of SGK3 in mediating activated PIK3CA mutant or loss of Pten induced HCC development using Sgk3 knockout mice.ResultsWe found that ablation of Sgk3 does not affect PIK3CA(H1047R) or PIK3CA(E545K) induced lipogenesis in the liver. Using PIK3CA(H1047R)/c-Met, PIK3CA(E545K)/c-Met, and sgPten/c-Met murine HCC models, we also demonstrated that deletion of Sgk3 moderately delays PIK3CA(E545K)/c-Met driven HCC, while not affecting PIK3CA(H1047R)/c-Met or sgPten/c-Met HCC formation in mice. Similarly, in human HCC cell lines, silencing of SGK3 reduced PIK3CA(E545K) -but not PIK3CA(H1047R)- induced accelerated tumor cell proliferation.ConclusionAltogether, our data suggest that SGK3 plays a role in transducing helical domain mutant PIK3CA signaling during liver tumor development.

Hepatocellular carcinoma (HCC) is the most common type of liver cancer and has limited treatment options. Snail family transcriptional repressor 1 (SNAI1) is a master regulator of epithelial-mesenchymal transition (EMT) and has been implicated in HCC initiation and progression. However, the precise role of SNAI1 and the way it contributes to hepatocarcinogenesis have not been investigated in depth, especially in vivo. Here, we analyzed the functional relevance of SNAI1 in promoting hepatocarcinogenesis in the context of the AKT/c-Met-driven mouse liver tumor model (AKT/c-Met/SNAI1). Overexpression of SNAI1 did not accelerate AKT/c-Met-induced HCC development or induce metastasis in mice. Elevated SNAI1 expression rather led to the formation of cholangiocellular (CCA) lesions in the mouse liver, a phenotype that was paralleled by increased activation of Yap and Notch. Ablation of Yap strongly inhibited AKT/c-Met/SNAI-induced HCC and CCA development, whereas inhibition of the Notch pathway specifically blocked the CCA-like phenotype in mice. Intriguingly, overexpression of SNAI1 failed to induce EMT, indicated by strong E-cadherin expression and lack of vimentin expression by AKT/c-Met/SNAI tumor cells. SNAI1 mRNA levels strongly correlated with the expression of CCA markers, including SOX9, CK19, and EPCAM, but not with EMT markers such as E-CADHERIN and ZO-1, in human HCC samples. Overall, our findings suggest SNAI1 regulates the CCA-like phenotype in hepatocarcinogenesis via regulation of Yap and Notch. SIGNIFICANCE: These findings report a new function of SNAI1 to promote cholangiocellular transdifferentiation instead of epithelial-mesenchymal transition in hepatocellular carcinoma.

A 3d model of crank connecting rod of a single cylinder internal combustion engine (ICE) is established, whose force analysis was carried out in ADAMS/VIEW using virtual prototyping method. It was found that the results between the analysis and the theoretical calculation results were basically consistent, indicating that the established model is correct and reliable. In order to reduce the inertia force and torque of this ICE, the uniaxial balance method was used to carry out the vibration reduction design based on the balance shaft. The results of virtual experiments showed that the single cylinder internal combustion engine with a balance shaft can greatly reduce the inertia excitation force as well as improve the vibration.

Intrahepatic cholangiocarcinoma (iCCA) is a deadly malignancy with limited treatment options. Gain-of-function mutations in K-Ras is a very frequent alteration, occurring in ~15 to 25% of human iCCA patients. Here, we established a new iCCA model by expressing activated forms of Notch1 (NICD) and K-Ras (K-RasV12D) in the mouse liver (K-Ras/NICD mice). Furthermore, we investigated the therapeutic potential of MEK inhibitors in vitro and in vivo using human CCA cell lines and K-Ras/NICD mice, respectively. Treatment with U0126, PD901, and Selumetinib MEK inhibitors triggered growth restraint in all CCA cell lines tested, with the most pronounced growth suppressive effects being observed in K-Ras mutant cells. Growth inhibition was due to reduction in proliferation and massive apoptosis. Furthermore, treatment of K-Ras/NICD tumor-bearing mice with PD901 resulted in stable disease. At the molecular level, PD901 efficiently inhibited ERK activation in K-Ras/NICD tumor cells, mainly leading to increased apoptosis. Altogether, our study demonstrates that K-Ras/NICD mice represent a novel and useful preclinical model to study K-Ras-driven iCCA development and the effectiveness of MEK inhibitors in counteracting this process. Our data support the usefulness of MEK inhibitors for the treatment of human iCCA.

Liver cancer comprises a group of malignant tumors, among which hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC) are the most common. ICC is especially pernicious and associated with poor clinical outcome. Studies have shown that a subset of human ICCs may originate from mature hepatocytes. However, the mechanisms driving the trans-differentiation of hepatocytes into malignant cholangiocytes remain poorly defined. We adopted lineage tracing techniques and an established murine hepatocyte-derived ICC model by hydrodynamic injection of activated forms of AKT (myr-AKT) and Yap (YapS127A) proto-oncogenes. Wild-type, Notch1 flox/flox , and Notch2 flox/flox mice were used to investigate the role of canonical Notch signaling and Notch receptors in AKT/Yap-driven ICC formation. Human ICC and HCC cell lines were transfected with siRNA against Notch2 to determine whether Notch2 regulates biliary marker expression in liver tumor cells. We found that AKT/Yap-induced ICC formation is hepatocyte derived and this process is strictly dependent on the canonical Notch signaling pathway in vivo. Deletion of Notch2 in AKT/Yap-induced tumors switched the phenotype from ICC to hepatocellular adenoma-like lesions, while inactivation of Notch1 in hepatocytes did not result in significant histomorphological changes. Finally, in vitro studies revealed that Notch2 silencing in ICC and HCC cell lines down-regulates the expression of Sox9 and EpCAM biliary markers. Notch2 is the major determinant of hepatocyte-derived ICC formation in mice.

Hepatocellular carcinoma (HCC) is a deadly malignancy with limited treatment options. Recently, it was found that Dasatinib treatment led to synthetic lethality in c-Myc high-expressing human cancer cells due to inhibition of p-Lyn. Overexpression of c-Myc is frequently seen in human HCC. We investigated the sensitivity to Dasatinib in vitro using HCC cell lines and in vivo using c-Myc mouse HCC model. We found that HCC cell line responsiveness to Dasatinib varied significantly. However, there was no correlation between c-Myc expression and IC50 to Dasatinib. In c-Myc-induced HCC in mice, tumors continued to grow despite Dasatinib treatment, although the eventual tumor burden was lower in Dasatinib treatment cohort. Molecular analyses revealed that Dasatinib was effective in inhibiting p-Src, but not p-Lyn, in HCC. Importantly, we found that in HCC cell lines as well as c-Myc mouse HCC, Dasatinib treatment induced up regulation of activated/phosphorylated (p)-focal adhesion kinase(FAK). Concomitant treatment of HCC cell lines with Dasatinib and FAK inhibitor prevented Dasatinib-induced FAK activation, leading to stronger growth restraint. Altogether, our results suggest that Dasatinib may have limited efficacy as single agent for HCC treatment. Combined treatment with Dasatinib with FAK inhibitor might represent a novel therapeutic approach against HCC.

Background & aimsIntrahepatic cholangiocarcinoma (ICC) is a lethal malignancy without effective treatment options. MLN0128, a second generation pan-mTOR inhibitor, shows efficacy for multiple tumor types. We evaluated the therapeutic potential of MLN0128 vs. gemcitabine/oxaliplatin in a novel ICC mouse model.MethodsWe established a novel ICC mouse model via hydrodynamic transfection of activated forms of AKT (myr-AKT) and Yap (YapS127A) protooncogenes (that will be referred to as AKT/YapS127A). Genetic approaches were applied to study the requirement of mTORC1 and mTORC2 in mediating AKT/YapS127A driven tumorigenesis. Gemcitabine/oxaliplatin and MLN0128 were administered in AKT/YapS127A tumor-bearing mice to study their anti-tumor efficacy in vivo. Multiple human ICC cell lines were used for in vitro experiments. Hematoxylin and eosin staining, immunohistochemistry and immunoblotting were applied for the characterization and mechanistic study.ResultsCo-expression of myr-AKT and YapS127A promoted ICC development in mice. Both mTORC1 and mTORC2 complexes were required for AKT/YapS127A ICC development. Gemcitabine/oxaliplatin had limited efficacy in treating late stage AKT/YapS127A ICC. In contrast, partial tumor regression was achieved when MLN0128 was applied in the late stage of AKT/YapS127A cholangiocarcinogenesis. Furthermore, when MLN0128 was administered in the early stage of AKT/YapS127A carcinogenesis, it led to disease stabilization. Mechanistically, MLN0128 efficiently inhibited AKT/mTOR signaling both in vivo and in vitro, inducing strong ICC cell apoptosis and only marginally affecting proliferation.ConclusionsThis study suggests that mTOR kinase inhibitors may be beneficial for the treatment of ICC, even in tumors that are resistant to standard of care chemotherapeutics, such as gemcitabine/oxaliplatin-based regimens, especially in the subset of tumors exhibiting activated AKT/mTOR cascade. Lay summary: We established a novel mouse model of intrahepat

UnlabelledHepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC) are the most prevalent types of primary liver cancer. These malignancies have limited treatment options, resulting in poor patient outcomes. Metabolism reprogramming, including increased de novo lipogenesis, is one of the hallmarks of cancer. Fatty acid synthase (FASN) catalyzes the de novo synthesis of long-chain fatty acids from acetyl-coenzyme A and malonyl-coenzyme A. Increased FASN expression has been reported in multiple tumor types, and inhibition of FASN expression has been shown to have tumor-suppressing activity. Intriguingly, we found that while FASN is up-regulated in human HCC samples, its expression is frequently low in human ICC specimens. Similar results were observed in mouse ICC models induced by different oncogenes. Ablating FASN in the mouse liver did not affect activated AKT and Notch (AKT/Notch intracellular domain 1) induced ICC formation in vivo. Furthermore, while both HCC and ICC lesions develop in mice following hydrodynamic injection of AKT and neuroblastoma Ras viral oncogene homolog oncogenes (AKT/Ras), deletion of FASN in AKT/Ras mice triggered the development almost exclusively of ICCs. In the absence of FASN, ICC cells might receive lipids for membrane synthesis through exogenous fatty acid uptake. In accordance with the latter hypothesis, ICC cells displayed high expression of fatty acid uptake-related proteins and robust long-chain fatty acid uptake.ConclusionOur data demonstrate that FASN dependence is not a universal feature of liver tumors: while HCC development is highly dependent of FASN and its mediated lipogenesis, ICC tumorigenesis can be insensitive to FASN deprivation; our study supports novel therapeutic approaches to treat this pernicious tumor type with the inhibition of exogenous fatty acid uptake. (Hepatology 2016;63:1900-1913).

In experimental myocardial infarction (MI), a rise in cell counts of circulating monocyte subsets contributes to impaired myocardial healing and to atherosclerotic plaque destabilization. In humans, the prognostic role of monocyte subsets in patients suffering ST-elevation MI (STEMI) is still unclear. In the present study, we aimed to determine the kinetics of the 3 monocyte subsets (classical CD14++CD16-, intermediate CD14++CD16+, and nonclassical CD14+CD16++ monocytes), as well as the subset-specific monocyte-platelet aggregates (MPA), in acute STEMI followed by primary percutaneous coronary intervention (PCI), and their relationships with cardiovascular outcomes during a 2-year follow-up.Monocyte subsets and MPA were measured in 100 STEMI patients receiving primary PCI on days 1, 2, 3, 5, and 7 of symptom onset, which were compared with 60 stable coronary heart disease patients and 35 healthy volunteers. From day 1 to day 7, significant increases in the counts of CD14++CD16+ monocytes and CD14++CD16+ MPA were observed, with peak levels on day 2. During a median follow-up of 2.0 years, 28 first cardiovascular events (defined as cardiovascular death, nonfatal ischemic stroke, recurrent MI, need for emergency or repeat revascularization, and rehospitalization for heart failure) were recorded. After adjustment for confounders, CD14++CD16+ monocytosis (day 1 [HR: 3.428; 95% CI: 1.597-7.358; P = 0.002], day 2 [HR: 4.835; 95% CI: 1.106-21.13; P = 0.04], day 3 [HR: 2.734; 95% CI: 1.138-6.564; P = 0.02], and day 7 [HR: 2.647; 95% CI: 1.196-5.861; P = 0.02]), as well as increased levels of CD14++CD16+ MPA measured on all time points (days 1, 2, 3, 5, and 7), had predictive values for adverse cardiovascular events.In conclusion, our data show the expansion of the CD14++CD16+ monocyte subset during acute phase of STEMI has predictive values for 2-year adverse cardiovascular outcomes in patients treated with primary PCI. Future studies will be warranted to elucidate whether C

Background Cryoablation is one of the local therapies for hepatocellular carcinoma (HCC), but its safety and effect has not been studied in patients with Child class A or B and Barcelona Clinic Liver Cancer (BCLC) stage C HCC. Metastasis-associated in colon cancer-1 (MACC1) overexpression has been associated with poor prognosis of HCC, but its predictive value to post-cryoablation outcomes remains unknown in patients with BCLC stage C HCC. Methods This study assessed the safety and outcomes of cryoablation measured by time to progression (TTP) and overall survival (OS), and predictive value of MACC1 mRNA and protein overexpression in tumorous tissue to post-cryoablation outcomes in 120 advanced HCC patients with child-pugh class A or B by quantitative polymerase chain reaction and immunohistochemical staining. The potenial correlation of MACC1 and c-Met expression to tumor cell proliferation and apoptosis was also analyzed. Results The cryoablation in patients with advanced unresectable HCC resulted in a median TTP and OS of 5.5 (4.2- 6.7) months and 10.5 (9.0-12.0) months, respectively and no significant complications, comparable to the historical report for RFA therapy. The MACC1 mRNA and nuclear protein expression was significantly increased in tumorous tissues in these patients than that in normal liver tissue controls. Higher expression of MACC1 mRNA and nuclear protein in tumorous tissues in these patients was associated with shorter post cryoablation median TTP and OS than that with lower MACC1 expression. Conclusions Cryoablation is a safe and effective therapeutic option for patients with advanced HCC and Child-pugh class A or B cirrhosis; and a higher intratumoral expression of MACC1 or nuclear translocation predicts poor outcomes of cryotherapy in these patients.

Photoluminescence (PL) and time-resolved PI, were employed to study the steady and transient optical properties of cubic InxGa1-xN epilayers grown by MBE. The results suggest that the PL transitions in InGaN epilayers are mainly from localized exciton states. The localization energies are estimated to be 60 meV, independent of In composition. The PL decay is characterized by a hi-exponential dependence. The fast process (50 ps at 12K) is related to the fast relaxation of excitons, while a slower contribution (200-270 ps at 12K) is attributed to the decay process of localized excitons.

PURPOSE: The objective of this study was to perform a systematic review and meta-analysis of the effects of statins on mortality for patients with non-severe pneumonia or severe pneumonia. METHODS: PubMed, EMBASE, Cochrane Database of Systematic Reviews, Cochrane central register of controlled trials and Clinicaltrials.gov were searched for the association between statins and non-severe/severe pneumonia. Eligible articles were analyzed in Stata 12.0. RESULTS: The database search yielded a total of 566 potential publications, 24 studies involving 312,309 patients met the eligibility criteria. Pooled unadjusted data showed that statin use was associated with lower mortality after non-severe pneumonia (odds ratio [OR] 0.70, 95% confidence interval [CI], 0.66-0.73), but not severe pneumonia (OR 1.05; 95% CI, 0.86-1.28). However, this protective effect of statins was weakened using adjusted estimates (OR 0.78, 95% CI, 0.75-0.82). Besides, protective effect of statins was attenuated by confounders in a subgroup analysis, especially when accounting for pneumonia severity indicators (OR 0.88; 95% CI, 0.80-0.96). CONCLUSIONS: Statin use was associated with reduced mortality after non-severe pneumonia but not severe pneumonia and this protective effect was weakened in subgroups. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.