We propose a new single image Super Resolution (SR) algorithm via Bayesian modeling with a natural image prior modeled by a high-order Markov Random Field (MRF). SR is one of the long-standing and active topics in image processing community. It is of great use in many practical applications, such as astronomical observation, medical imaging and the adaptation of low-resolution contents onto highresolution displays. One category of the conventional approaches for image super resolution is formulating the problem with Bayesian modeling techniques and then obtaining its Maximum-A-Posteriori (MAP) solution, which actually boils down to a regularized regression task. Although straightforward, this approach can not exploit the full potential offered by the probabilistic modeling, as only the posterior mode is sought. On the other hand, current Bayesian SR approaches using the posterior mean estimation typically use very simple prior models for natural images to ensure the computational tractability. In this paper, we present a Bayesian image SR approach with a flexible high-order MRF model as the prior for natural images. The Minimum Mean Square Error (MMSE) criteria is used for estimating the HR image. A Markov Chain Monte Carlo (MCMC) based sampling algorithm is presented for obtaining the MMSE solution. The proposed method can not only enjoy the benefits offered by the flexible prior, but also has the advantage of making use of the probabilistic modeling to perform a posterior mean estimation, thus is less sensitive to the local minima problem as the MAP solution. Experimental results indicate that the proposed method can generate competitive or better results than state-of-the-art SR algorithms.

Hepatocellular carcinoma (HCC) typically relies on angiogenesis for its malignant behavior, including growth and metastasis. Vasohibin 2 (VASH2) was previously identified as an angiogenic factor, but its role in tumorigenesis is unknown. Using quantitative PCR and western blot analyses, we found that VASH2 is overexpressed in HCC cells and tissues. Using chromatin immunoprecipitation, we detected histone modifications at the putative VASH2 promoter, with increased H3K4 trimethylation and H3 acetylation and decreased H3K27 trimethylation, suggesting that epigenetic mechanisms are responsible for the deregulated VASH2 transcription in HCC. Knockdown of VASH2 via siRNA inhibited the proliferation of the hepatoma cell lines by delaying cell cycle progression and increasing apoptosis. Importantly, we found VASH2 secreted in the culture supernatant, and co-expression of its secretory chaperone small vasohibin-binding protein (SVBP) further enhanced VASH2 secretion. The supernatant from HepG2 cells expressing VASH2 enhanced the proliferation, migration and tube formation of human umbilical vein endothelial cells, and knockdown of VASH2 significantly inhibited these effects. In an in vivo study using a nude mouse model, we found that exogenous VASH2 significantly contributed to tumor growth, microvessel density and hemoglobin concentration in the tumors. Further analyses showed that the VASH2-mediated increase in the transcription of fibroblast growth factor-2, vascular endothelial growth factor and vasohibin 1 may be the mechanism underlying these effects. Taken together, these data indicate that VASH2 is abnormally expressed in HCC cells as a result of histone modifications and that VASH2 contributes to the angiogenesis in HCC via an SVBP-mediated paracrine mechanism. These results indicate a novel and important role for VASH2 in HCC angiogenesis and malignant transformation.Oncogene advance online publication, 21 May 2012; doi:10.1038/onc.2012.177.

OBJECTIVE Prospective case-control study, undertaken to investigate serum cytokine and chemokine concentrations during all clinical phases and in different clinical types of haemorrhagic fever with renal syndrome (HFRS). METHODS Serum was collected at various disease phases from patients with HFRS (n = 35) and healthy control subjects (n = 10). Tumour necrosis factor (TNF)-α, interleukin (IL)-6, IL-4, interferon (IFN)-γ, IL-8, interferon inducible protein-10 (IP-10) and chemokine (C-C motif) ligand 5 (also known as 'regulated upon activation, normal T-cell expressed and secreted'[RANTES]) were quantified using commercial enzyme-linked immunosorbent assay kits. RESULTS Serum concentrations of TNF-α, IL-6, IFN-γ, IL-8, IP-10 and RANTES (but not IL-4) were significantly higher in patients compared with controls. Highest concentrations were generally found during the febrile, hypotensive and oliguric disease phases, as well as in clinically severe and critical cases. CONCLUSION Serum concentrations of proinflammatory cytokines and chemokines increased in line with disease severity in HFRS patients.

Drug-loaded nanoparticles have shown great potential in the study of carriers for disease-targeting drug delivery. Drug-loaded nanoparticles are excellent in keeping the drug in the systemic circulation for a prolonged period of time, introducing targeting molecules to improve targeting efficiency and to reduce side effects. A general review on active drug targeting of cancerous diseases by nanoparticles functionalized with ligands to folate receptors is presented including the (1) materials and methods for nanoparticle preparation,(2) methods for drug encapsulation,(3) surface functionalization of the nanoparticle with ligand to folate receptors, and (4) in vitro and in vivo experiments.

PurposeTo evaluate the visual and anatomical results of surgery for macular hole-related retinal detachment (MHRD) after phacoemulsification cataract extraction.MethodsData for all patients who underwent surgery for MHRD after phacoemulsification cataract extraction from 1 December 1998 to 30 September 2008 in one hospital were evaluated. Patient characteristics, best-corrected visual acuity (VA) preoperatively and at last examination, surgical technique, anatomical success, and follow-up period were extracted and analysed statistically.ResultsA total of 13 625 eyes of 10 076 patients who had phacoemulsification cataract surgery were included. In the follow-up period, 10 cases of MHRD in nine patients were observed, of which seven eyes had high myopia. The mean axial length was 30.97±1.36 mm (29.19, 32.97) and mean myopia was-19.35±1.93 (-7.5,-3.5) dioptres. Overall anatomical success was achieved in 90%(9 out of 10 eyes). There was no statistically significant difference (P=0.240) between the logarithm of the MAR VA before the phacoemulsification cataract extraction and after MHRD surgical repair. VA increased in three eyes but decreased in the other seven after MHRD surgery.ConclusionsAs a primary procedure, vitreous surgery combined with other necessary adjunct procedures such as membrane peeling and retinal tamponade seems to be successful in achieving anatomical success. However, VA improvement is dependent on the type of macular lesion and not the surgical procedure.Eye advance online publication, 18 May 2012; doi:10.1038/eye.2012.87.

The unfolded protein response (UPR) is generally activated in solid tumors and results in tumor cell anti-apoptosis and drug resistance. However, tumor-specific UPR transducers are largely unknown. In the present study, we identified CD147, a cancer biomarker, as an UPR inducer in hepatocellular carcinoma (HCC). The expression of the major UPR target, Bip, was found to be positively associated with CD147 in human hepatoma tissues. By phosphorylating FAK and Src, CD147-enhanced TFII-I tyrosine phosphorylation at Tyr248. CD147 also induced p-TFII-I nuclear localization and binding to the Bip promoter where endoplasmic reticulum (ER) stress response element 1 (ERSE1)(-82/-50) is the most efficient target of the three ERSEs, thus increasing transcription of Bip. Furthermore, by inducing UPR, CD147 inhibited HCC cell apoptosis and decreased cell Adriamycin chemosensitivity, thus decreasing the survival rate of hepatoma-bearing nude mice. Together, these results reveal pivotal roles for CD147 in modulating the UPR in HCC and raise the possibility that CD147 is a target that promotes HCC cell apoptosis and increases the sensitivity of tumors to anti-cancer drugs. Therefore, CD147 inhibition provides an opportunity to enhance the efficacy of existing agents and represents a novel target for HCC treatment.Cell Death and Differentiation advance online publication, 18 May 2012; doi:10.1038/cdd.2012.60.

The decay B[over ¯]_{s}^{0}→J/ψK^{+}K^{-} is investigated using 0.16  fb^{-1} of data collected with the LHCb detector using 7 TeV pp collisions. Although the J/ψϕ channel is well known, final states at higher K^{+}K^{-} masses have not previously been studied. In the K^{+}K^{-} mass spectrum we observe a significant signal in the f_{2}^{'}(1525) region as well as a nonresonant component. After subtracting the nonresonant component, we find B(B[over ¯]_{s}^{0}→J/ψf_{2}^{'}(1525))/B(B[over ¯]_{s}^{0}→J/ψϕ)=(26.4±2.7±2.4)%.

The objectives of this experiment were to evaluate procedures that may be used to predict the concentration of standardized ileal digestible (SID) Lys in distillers dried grains with solubles (DDGS) fed to pigs and to evaluate the accuracy of a published equation to predict SID Lys in DDGS. Twenty-one sources of DDGS were analyzed (as-fed basis) for CP (23.8 to 33.6%; CV = 8.3%), Lys (0.69 to 1.17%; CV = 12.4%), and furosine (0.02 to 0.22%; CV = 91.4%). The concentration of reactive Lys (%, as-fed basis) was calculated as: analyzed Lys (%)- furosine (%) ÷ 0.32 × 0.40, and ranged from 0.47 to 1.15%(CV = 20.7%) in the 21 sources of DDGS. Twenty-one diets that each contained 60.0% of one source of DDGS as the sole source of CP and AA were formulated. An N-free diet was also formulated and used to determine basal endogenous losses of CP and AA. Twenty-two barrows with an initial BW of 45.2 kg (SD = 3.1 kg) were fitted with a T-cannula in the distal ileum and allotted to a 22 × 10 Youden square design with the 22 diets and 10 periods. The SID of CP and AA were calculated for each source of DDGS. The SID of CP ranged from 69.8 to 79.6%, and the SID of Lys from 45.3 to 74.1%. The concentration of SID Lys in the 21 samples of DDGS was highly related to the concentration of analyzed Lys (P < 0.001; r(2)= 0.849) and with the concentration of reactive Lys in the samples (P < 0.001; r(2)= 0.898). In contrast, the concentration of SID Lys in the 21 sources of DDGS was not related to the concentration of CP in the samples (P = 0.558; r(2)= 0.021). However, values for SID Lys were in good agreement with values predicted using a published prediction equation. In conclusion, analyzed Lys in DDGS, but not CP, may be used to predict the concentration of SID Lys in DDGS fed to pigs. However, analysis of furosine in addition to Lys and subsequent calculation of reactive Lys improves the prediction accuracy of digestible Lys concentration in DDGS.

Incidence of kidney cancer is on the rise, and a better understanding of molecular mechanisms involved in the cancer invasion and metastasis is required for the development of curative therapeutics. In this study, we report that the proinflammatory cytokine prostaglandin E2 (PGE2) induces the malignant SN12C, but not benign HK2 kidney cell invasion. The PGE2 increases SN12C cell invasion through a signal pathway that encompasses EP2 and EP4, Akt, small GTPase RalA and Ral·GTP inactivator RGC2. The results support the idea that targeted interference of EP2/EP4 signal to RalA·GTP may provide benefit to patients diagnosed with advanced kidney cancer.Oncogene advance online publication, 14 May 2012; doi:10.1038/onc.2012.161.

Biomaterials that can drive stem cells to an appropriate differentiation level and decrease apoptosis of transplanted cells are needed in regenerative medicine. Nanomaterials are promising novel materials for such applications. Here we reported that carboxylated multiwalled carbon nanotube (MWCNT 1) promotes myogenic differentiation of mouse myoblast cells and inhibits cell apoptosis under the differentiation conditions by regulating basic helix-loop-helix transcription factors. MWCNT 1 attenuates bone morphogenetic protein receptor (BMPR) signaling activity by binding to BMPR2 and attenuating the phosphorylation of BMPR1. This molecular understanding allowed us to tune stem cell differentiation to various levels by chemical modifications, demonstrating human control of biological activities of nanoparticles and opening an avenue for potential applications of nanomaterials in regenerative medicine.