Emerging probing perspective of two-dimensional materials physics: terahertz emission spectroscopy.

Terahertz (THz) emission spectroscopy (TES) has emerged as a highly effective and versatile technique for investigating the photoelectric properties of diverse materials and nonlinear physical processes in the past few decades. Concurrently, research on two-dimensional (2D) materials has experienced substantial growth due to their atomically thin structures, exceptional mechanical and optoelectronic properties, and the potential for applications in flexible electronics, sensing, and nanoelectronics. Specifically, these materials offer advantages such as tunable bandgap, high carrier mobility, wideband optical absorption, and relatively short carrier lifetime. By applying TES to investigate the 2D materials, their interfaces and heterostructures, rich information about the interplay among photons, charges, phonons and spins can be unfolded, which provides fundamental understanding for future applications. Thus it is timely to review the nonlinear processes underlying THz emission in 2D materials including optical rectification, photon-drag, high-order harmonic generation and spin-to-charge conversion, showcasing the rich diversity of the TES employed to unravel the complex nature of these materials. Typical applications based on THz emissions, such as THz lasers, ultrafast imaging and biosensors, are also discussed. Step further, we analyzed the unique advantages of spintronic terahertz emitters and the future technological advancements in the development of new THz generation mechanisms leading to advanced THz sources characterized by wide bandwidth, high power and integration, suitable for industrial and commercial applications. The continuous advancement and integration of TES with the study of 2D materials and heterostructures promise to revolutionize research in different areas, including basic materials physics, novel optoelectronic devices, and chips for post-Moore's era.

Machine-learning models are superior to severity scoring systems for the prediction of the mortality of critically ill patients in a tertiary medical center.

BACKGROUND: Intensive care unit (ICU) mortality prediction helps to guide therapeutic decision making for critically ill patients. Several scoring systems based on statistical techniques have been developed for this purpose. In this study, we developed a machine-learning model to predict patient mortality in the very early stage of ICU admission. METHODS: This study was performed with data from all patients admitted to the intensive care units of a tertiary medical center in Taiwan from 2009 to 2018. The patients' comorbidities, co-medications, vital signs, and laboratory data on the day of ICU admission were obtained from electronic medical records. We constructed random forest and extreme gradient boosting (XGBoost) models to predict ICU mortality, and compared their performance with that of traditional scoring systems. RESULTS: Data from 12,377 patients was allocated to training (n = 9901) and testing (n = 2476) datasets. The median patient age was 70.0 years; 9210 (74.41%) patients were under mechanical ventilation in the ICU. The areas under receiver operating characteristic curves for the random forest and XGBoost models (0.876 and 0.880, respectively) were larger than those for the Acute Physiology and Chronic Health Evaluation II score (0.738), Sequential Organ Failure Assessment score (0.747), and Simplified Acute Physiology Score II (0.743). The fraction of inspired oxygen on ICU admission was the most important predictive feature across all models. CONCLUSION: The XGBoost model most accurately predicted ICU mortality and was superior to traditional scoring systems. Our results highlight the utility of machine learning for ICU mortality prediction in the Asian population.

mRNA expression and functional analysis of chicken IFIT5 after infected with Newcastle disease virus.

Innate immunity is the first line against the invasion of pathogenic microorganisms. Over the past several years, the antiviral activity and mechanisms of the IFIT5 gene have been confirmed in mammals. However, more information is needed on the role of IFIT5 in response to viral infection in chickens. In this study, we examined the mRNA expression profile of chicken IFIT5 (chIFIT5) in different tissues and explored how chIFIT5 transduces upstream signaling to the downstream adaptor. Relative mRNA expression level of chIFIT5 was the highest in spleen and expression level of chIFIT5 was significantly up-regulated following Newcastle disease virus (NDV) infection, and polyinosinic:polycytidylic acid [poly (I:C)]- and poly(deoxyadenylic-thymidylic) [poly (dA:dT)]-triggered antiviral immune responses. Chicken MDA5, MAVS, and IRF7 positively regulated the mRNA expression of chIFIT5. Overexpression of chIFIT5 could promote IRF7- and NF-κB-mediated gene expression following NDV infection or transfection with poly (I:C). These results suggested that chIFIT5 is an important enhancer of the innate immunity response.

Infusion of Human Mesenchymal Stem Cells Improves Regenerative Niche in Thioacetamide-Injured Mouse Liver

BACKGROUND@#This study investigated whether xenotransplantation of human Wharton’s jelly-derived mesenchymal stem cells (WJ-MSCs) reduces thioacetamide (TAA)-induced mouse liver fibrosis and the underlying molecular mechanism. @*METHODS@#Recipient NOD/SCID mice were injected intraperitoneally with TAA twice weekly for 6 weeks before initial administration of WJ-MSCs. Expression of regenerative and pro-fibrogenic markers in mouse fibrotic livers were monitored post cytotherapy. A hepatic stallate cell line HSC-T6 and isolated WJ-MSCs were used for in vitro adhesion, migration and mechanistic studies. @*RESULTS@#WJ-MSCs were isolated from human umbilical cords by an explant method and characterized by flow cytometry. A single infusion of WJ-MSCs to TAA-treated mice significantly reduced collagen deposition and ameliorated liver fibrosis after 2-week therapy. In addition to enhanced expression of hepatic regenerative factor, hepatocyte growth factor, and PCNA proliferative marker, WJ-MSC therapy significantly blunted pro-fibrogenic signals, including Smad2, RhoA, ERK. Intriguingly, reduction of plasma fibronectin (pFN) in fibrotic livers was noted in MSC-treated mice. In vitro studies further demonstrated that suspending MSCs triggered pFN degradation, soluble pFN conversely retarded adhesion of suspending MSCs onto type I collagen-coated surface, whereas pFN coating enhanced WJ-MSC migration across mimicked wound bed. Moreover, pretreatment with soluble pFN and conditioned medium from MSCs with pFN strikingly attenuated the response of HSC-T6 cells to TGF-b1-stimulation in Smad2 phosphorylation and RhoA upregulation. @*CONCLUSION@#These findings suggest that cytotherapy using WJ-MSCs may modulate hepatic pFN deposition for a better regenerative niche in the fibrotic livers and may constitute a useful anti-fibrogenic intervention in chronic liver diseases.

Infusion of Human Mesenchymal Stem Cells Improves Regenerative Niche in Thioacetamide-Injured Mouse Liver

BACKGROUND@#This study investigated whether xenotransplantation of human Wharton’s jelly-derived mesenchymal stem cells (WJ-MSCs) reduces thioacetamide (TAA)-induced mouse liver fibrosis and the underlying molecular mechanism. @*METHODS@#Recipient NOD/SCID mice were injected intraperitoneally with TAA twice weekly for 6 weeks before initial administration of WJ-MSCs. Expression of regenerative and pro-fibrogenic markers in mouse fibrotic livers were monitored post cytotherapy. A hepatic stallate cell line HSC-T6 and isolated WJ-MSCs were used for in vitro adhesion, migration and mechanistic studies. @*RESULTS@#WJ-MSCs were isolated from human umbilical cords by an explant method and characterized by flow cytometry. A single infusion of WJ-MSCs to TAA-treated mice significantly reduced collagen deposition and ameliorated liver fibrosis after 2-week therapy. In addition to enhanced expression of hepatic regenerative factor, hepatocyte growth factor, and PCNA proliferative marker, WJ-MSC therapy significantly blunted pro-fibrogenic signals, including Smad2, RhoA, ERK. Intriguingly, reduction of plasma fibronectin (pFN) in fibrotic livers was noted in MSC-treated mice. In vitro studies further demonstrated that suspending MSCs triggered pFN degradation, soluble pFN conversely retarded adhesion of suspending MSCs onto type I collagen-coated surface, whereas pFN coating enhanced WJ-MSC migration across mimicked wound bed. Moreover, pretreatment with soluble pFN and conditioned medium from MSCs with pFN strikingly attenuated the response of HSC-T6 cells to TGF-b1-stimulation in Smad2 phosphorylation and RhoA upregulation. @*CONCLUSION@#These findings suggest that cytotherapy using WJ-MSCs may modulate hepatic pFN deposition for a better regenerative niche in the fibrotic livers and may constitute a useful anti-fibrogenic intervention in chronic liver diseases.

Polymorphism in MC1R, TYR and ASIP genes in different colored feather chickens.

Coat color genetics successfully adapted and applied to different animal species, which provides a good demonstration of the concept of comparative genetics. In this study, we sequenced 945 bp fragments of melanocortin 1 receptor (MC1R) gene, 421 bp fragments of exon 1 of tyrosinase (TYR) gene and 266 bp fragments of exon 3 of agouti signaling protein (ASIP) gene for 250 individuals with five plumage color patterns. We detected a total of three SNPs (T398A, T637C, and G920C) in MC1R and built six haplotypes (H1-H6) based on the three SNPs. H5 and H6 haplotypes were mainly concentrated in white and grey chicken. And diplotypes H2H3 occurred in white feather and black-speckle feather with the same frequency. Moreover, a total of three SNPs (C47G, T120C, and T172C) in TYR were found and built six haplotypes (P1-P6) based on the three SNPs. Among them, haplotype P2, P3 and P6 were not occurred in black chicken, the diplotypes P1P6 and P4P6 were only distributed in white, gray and black-speckled feather. We only detected one SNP (T168C) in ASIP gene and found that genotype TT was advantage genotype in the different plumage color groups of chickens. Collectively, our study suggested an association between plumage color and genetic variation of MC1R, TYR and ASIP in chicken.

Nerve growth factor upregulates sirtuin 1 expression in cholestasis: a potential therapeutic target

This study investigated the regulatory role of nerve growth factor (NGF) in sirtuin 1 (SIRT1) expression in cholestatic livers. We evaluated the expression of NGF and its cognate receptors in human livers with hepatolithiasis and the effects of NGF therapy on liver injury and hepatic SIRT1 expression in a bile duct ligation (BDL) mouse model. Histopathological and molecular analyses showed that the hepatocytes of human diseased livers expressed NGF, proNGF (a precursor of NGF), TrkA and p75NTR, whereas only p75NTR was upregulated in hepatolithiasis, compared with non-hepatolithiasis livers. In the BDL model without NGF therapy, p75NTR, but not TrkA antagonism, significantly deteriorated BDL-induced liver injury. By contrast, the hepatoprotective effect of NGF was abrogated only by TrkA and not by p75NTR antagonism in animals receiving NGF therapy. Intriguingly, a positive correlation between hepatic SIRT1 and NGF expression was found in human livers. In vitro studies demonstrated that NGF upregulated SIRT1 expression in mouse livers and human Huh-7 and rodent hepatocytes. Both NGF and proNGF induced protective effects against hydrogen peroxide-induced cytotoxicity in Huh-7 cells, whereas inhibition of TrkA and p75NTR activity prevented oxidative cell death. Mechanistically, NGF, but not proNGF, upregulated SIRT1 expression in human Huh-7 and rodent hepatocytes via nuclear factor (NF)-κB activity, whereas NGF-induced phosphoinositide-3 kinase/Akt, extracellular signal–regulated kinase and NF-κB signaling and SIRT1 activity were involved in its hepatoprotective effects against oxidative injury. These findings suggest that pharmacological manipulation of the NGF/SIRT1 axis might serve as a novel approach for the treatment of cholestatic disease.

Imaging features of an intraosseous arteriovenous malformation in the tibia

Primary intraosseous arteriovenous malformations (AVMs) are rare and have only been occasionally reported. We herein report a histologically proven case of primary intraosseous AVM in the tibia, which mimicked a fibrous tumour on radiography. This presentation carries a risk of triggering acute large haemorrhage through unnecessary biopsy. In intraosseous AVM, the magnetic resonance (MR) imaging features typical of a soft tissue AVM are absent, making diagnosis difficult. In this report, peculiar MR features in the presence of a connecting vessel between the normal deep venous system of the lower extremity and the tumour provide a clue for the early diagnosis of primary intraosseous AVM.

[Curative effects of extrusive and Fogarty balloon catheter embolectomy in acute femoral vein thrombosis: experiment with rabbits].

OBJECTIVE: To compare the influence extrusive and Fogarty balloon catheter embolectomy on the patency rate of bloodstream and the damage of the wall of vein in acute femoral vein thrombosis. METHODS: Eighty rabbits were randomly divided into 4 groups: Group A (n = 25) undergoing ligation of unilateral femoral to establish acute femoral vein thrombosis model and treated by extrusion of the hind leg muscles 24 h after the operation, Group B (n = 25) treated by Fogarty balloon catheter embolectomy 24 h after establishment of the thrombosis model, Group C (n = 25) undergoing sham operation, and Group D (n = 5) as normal controls.7, 14, and 28 days after the treatment digital subtraction angiography (DSA) was conducted to observe the patency rate of the vessel.1, 4, 7, 14, and 28 days after the treatment specimens of the thrombotic and corresponding sections of the veins were collected from the 4 groups (on days 1 and 7 for Group D) to undergo transmission electron microscopy (TEM) and scanning electron microscopy (SEM). Quantitative reverse transcription and polymerase chain reaction was used to detect the level of tissue thromboplastin (TF). ELISA was used to detect the levels of thromboxane B(2), (TXB(2)) and 6-keto-prostaglandin F1alpha (PGF1alpha). RESULTS: Occlusion was seen in 3 femoral veins of Group B and one femoral vein of Group (P < 0.01), and the other veins were all patent. TEM and SEM showed that the endothelial cell injury was slight in Group A, and aggravated in Group B. TF mRNA expression could be seen 1 day after the treatment in Groups A, B, and C, and peaked on the day 7, and not found in Group D at any time points (all P < 0.01); and the TF mRNA levels at different time points of Group A were all significantly lower than those of Group B (all P < 0.01). The TXB(2) expression levels on days 1 and 7 of Groups A, B, and C were all significantly higher than those of Group D; especially those of Group B (all P < 0.01). The 6-keto-PGF(1)alpha levels on days 1 and 7 of Group D were both significantly higher than those of Groups A, B, and C (all P < 0.01). CONCLUSION: Compared with Fogarty balloon catheter embolectomy, extrusion embolectomy can discard the thrombus more thoroughly and guarantee the patency rate of bloodstream. Both extrusion embolectomy and Fogarty balloon catheter embolectomy, especially the latter, cause damage to the blood vessel endothelium.

Establishment and application of oncogene over expressed human epithelial cell transformation model / 中华预防医学杂志

<p><b>OBJECTIVE</b>To establish human bronchial epithelial cell lines over expressing oncogene and to investigate its application in detection of carcinogen-induced cell transformation.</p><p><b>METHODS</b>Mediated by retrovirus infection, human telomerase catalytic subunit, hTERT was introduced into immortal human bronchial epithelial cells (16HBE) and followed by introduction of the oncogenic allele H-Ras(V12), or c-Myc or empty vector, creating cell lines 16HBETR, 16HBETM and 16HBETV, respectively. Biological characteristics of these cell lines including morphology, proliferation, and chromosomal aberration were examined to access whether they were transformed. Soft agar experiment and nude mice subcutaneous injection were performed using pre-transformed 16HBE cells induced by known carcinogens, nickel sulfate (NiSO4) and 7, 8, -dihydrodiol-9, 10-epoxide benzo[a] pyrene (BPDE).</p><p><b>RESULTS</b>With detection of telomerase activity and Western blotting, the expression of target proteins was verified. Thus, the transgenic 16HBE cell lines were successfully established. Cells expressing oncogene H-Ras or c-Myc grew 30.3% or 10.4% faster than control cells. However, these cells failed to form colonies in soft agar or form tumor in nude mice. 16HBETR, 16HBETM cells obtained transformed phenotype at 5 wks, 11 wks, respectively after treatment with BPDE, which are 15 wks and 9 wks earlier than control cells 16HBETV (20 wks). Meanwhile, 16HBETR, 16HBETM cells obtained transformed phenotype at 11 wks, 14 wks, respectively after treatment with nickel sulfate, which are 21 wks and 18 wks earlier than control cells (32 wks).</p><p><b>CONCLUSION</b>With the advantage of shorter latency, transgenic human cell transformation models could be used in potent carcinogen screening and applied to chemical-carcinogenesis mechanism study.</p>