Intrahepatic paracrine signaling by cardiotrophin-like cytokine factor 1 ameliorates diet-induced NASH in mice.

BACKGROUND AND AIMS: The mammalian liver harbors heterogeneous cell types that communicate via local paracrine signaling. Recent studies have delineated the transcriptomic landscape of the liver in NASH that provides insights into liver cell heterogeneity, intercellular crosstalk, and disease-associated reprogramming. However, the nature of intrahepatic signaling and its role in NASH progression remain obscure. APPROACH AND RESULTS: Here, we performed transcriptomic analyses and identified cardiotrophin-like cytokine factor 1 (CLCF1), a member of the IL-6 family cytokines, as a cholangiocyte-derived paracrine factor that was elevated in the liver from diet-induced NASH mice and patients with NASH. Adenovirus-associated virus-mediated overexpression of CLCF1 in the liver ameliorated NASH pathologies in two diet-induced NASH models in mice, illustrating that CLCF1 induction may serve an adaptive and protective role during NASH pathogenesis. Unexpectedly, messenger RNA and protein levels of leukemia inhibitory factor receptor (LIFR), a subunit of the receptor complex for CLCF1, were markedly downregulated in NASH liver. Hepatocyte-specific inactivation of LIFR accelerated NASH progression in mice, supporting an important role of intrahepatic cytokine signaling in maintaining tissue homeostasis under metabolic stress conditions. CONCLUSIONS: Together, this study sheds light on the molecular nature of intrahepatic paracrine signaling during NASH pathogenesis and uncovers potential targets for therapeutic intervention.

The rice germin-like protein OsGLP1 participates in acclimation to UV-B radiation.

Exposure to ultraviolet B radiation (UV-B) stress can have serious effects on the growth and development of plants. Germin-like proteins (GLPs) may be involved in different abiotic and biotic stress responses in different plants, but little is known about the role of GLPs in UV-B stress response and acclimation in plants. In the present study, knockout of GLP 8-14 (OsGLP1) using the CRISPR/Cas9 system resulted in mutant rice (Oryza sativa L.) plants (herein called glp1) that exhibited UV-B-dependent formation of lesion mimic in leaves. Moreover, glp1 grown under solar radiation (including UV-B) showed decreased plant height and increased leaf angle, but we observed no significant differences in phenotypes between wild-type (WT) plants and glp1 grown under artificial light lacking UV-B. Fv/Fm, Y (II) and the expression of many genes, based on RNA-seq analysis, related to photosynthesis were also only reduced in glp1, but not in WT, after transfer from a growth cabinet illuminated with artificial white light lacking UV-B to growth under natural sunlight. The genes-associated with flavonoid metabolism as well as UV resistance locus 8 (OsUVR8), phytochrome interacting factor-like 15-like (OsPIF3), pyridoxal 5'-phosphate synthase subunit PDX1.2 (OsPDX1.2), deoxyribodipyrimidine photolyase (OsPHR), and deoxyribodipyrimidine photolyase family protein-like (OsPHRL) exhibited lower expression levels, while higher expression levels of mitogen-activated protein kinase 5-like (OsMPK3), mitogen-activated protein kinase 13-like (OsMPK13), and transcription factor MYB4-like (OsMYB4) were observed in glp1 than in WT after transfer from a growth cabinet illuminated with artificial white light to growth under natural sunlight. Therefore, mutations in OsGLP1 resulted in rice plants more sensitive to UV-B and reduced expression of some genes for UV-B protection, suggesting that OsGLP1 is involved in acclimation to UV-B radiation.

Dietary risk factors for inflammatory bowel disease in Shanghai: A case-control study.

BACKGROUND AND OBJECTIVES: Inflammatory bowel disease (IBD) is a multifactorial condition involving the complex interplay of genomics, microbiota, immunology, environment, and personal behaviors, particularly diet. METHODS AND STUDY DESIGN: A case-control study in a tertiary referral hospital. Fifty patients with IBD and 50 controls without gastrointestinal diseases were enrolled consecutively from October 1, 2016, to December 31, 2017. Sociodemographic and Food Frequency Questionnaires (FFQs) were completed, and dietary risk factors for IBD were identified. RESULTS: Six major foods were associated with the recurrent incidence of IBD (p<0.05): chili, fish, milk, nuts, eggs, and fruit. Logistic regression analysis revealed that eating chili and drinking milk more than three times weekly increased the risk of relapse, as did eating fish and nuts one or two times weekly. Eating fruit more than once weekly reduced the risk of IBD. Fish, seafood, vegetables, nuts, beef, and fruit, along with a history of food allergy, were associated with a high risk of clinically recurrent IBD. Dietary patterns featuring seafood and nuts also increased the risk of relapse. CONCLUSIONS: The consumption of chili, milk, fish, and nuts beyond moderate weekly frequencies increased the risk of IBD, whereas fruit consumption was consistently protective against IBD development. Relapse susceptibility was also associated with a history of food allergy. Thus, IBD risk management can involve more personalized and less restrictive dietary patterns, as well as the enforcement of weekly dose thresholds. Uncertainty remains regarding association differentials between ulcerative colitis (UC) and Crohn's disease (CD).

hnRNPU/TrkB Defines a Chromatin Accessibility Checkpoint for Liver Injury and Nonalcoholic Steatohepatitis Pathogenesis.

BACKGROUND AND AIMS: Nonalcoholic steatohepatitis (NASH) is a progressive liver disease that is characterized by liver injury, inflammation, and fibrosis. NASH pathogenesis is linked to reprogramming of chromatin landscape in the liver that predisposes hepatocytes to stress-induced tissue injury. However, the molecular nature of the putative checkpoint that maintains chromatin architecture and preserves hepatocyte health remains elusive. APPROACH AND RESULTS: Here we show that heterogeneous nuclear ribonucleoprotein U (hnRNPU), a nuclear matrix protein that governs chromatin architecture and gene transcription, is a critical factor that couples chromatin disruption to NASH pathogenesis. RNA-seq and chromatin immunoprecipitation-seq studies revealed an extensive overlap between hnRNPU occupancy and altered gene expression during NASH. Hepatocyte-specific inactivation of hnRNPU disrupted liver chromatin accessibility, activated molecular signature of NASH, and sensitized mice to diet-induced NASH pathogenesis. Mechanistically, hnRNPU deficiency stimulated the expression of a truncated isoform of TrkB (TRKB-T1) that promotes inflammatory signaling in hepatocytes and stress-induced cell death. Brain-derived neurotrophic factor treatment reduced membrane TRKB-T1 protein and protected mice from diet-induced NASH. CONCLUSIONS: These findings illustrate a mechanism through which disruptions of chromatin architecture drive the emergence of disease-specific signaling patterns that promote liver injury and exacerbate NASH pathogenesis.

Training non-native vowel perception: In quiet or noise.

Noise makes speech perception much more challenging for non-native listeners than for native listeners. Training for non-native speech perception is usually implemented in quiet. It remains unclear if background noise may benefit or hamper non-native speech perception learning. In this study, 51 Chinese-native listeners were randomly assigned into three groups, including vowel training in quiet (TIQ), vowel training in noise (TIN), and watching videos in English as an active control. Vowel identification was assessed before (T1), right after (T2), and three months after training (T3) in quiet and various noise conditions. Results indicated that compared with the video watching group, the TIN group improved vowel identification in both quiet and noise significantly more at T2 and at T3. In contrast, the TIQ group improved significantly more in quiet and also in non-speech noise conditions at T2, but the improvement did not hold at T3. Moreover, compared to the TIQ group, the TIN group showed significantly less informational masking at both T2 and T3 and less energetic masking at T3. These results suggest that L2 speech training in background noise may improve non-native vowel perception more effectively than TIQ background only. The implications for non-native speech perception learning are discussed.

Zbtb7b engages the long noncoding RNA Blnc1 to drive brown and beige fat development and thermogenesis.

Brown and beige adipocytes convert chemical energy into heat through uncoupled respiration to defend against cold stress. Beyond thermogenesis, brown and beige fats engage other metabolic tissues via secreted factors to influence systemic energy metabolism. How the protein and long noncoding RNA (lncRNA) regulatory networks act in concert to regulate key aspects of thermogenic adipocyte biology remains largely unknown. Here we developed a genome-wide functional screen to interrogate the transcription factors and cofactors in thermogenic gene activation and identified zinc finger and BTB domain-containing 7b (Zbtb7b) as a potent driver of brown fat development and thermogenesis and cold-induced beige fat formation. Zbtb7b is required for activation of the thermogenic gene program in brown and beige adipocytes. Genetic ablation of Zbtb7b impaired cold-induced transcriptional remodeling in brown fat, rendering mice sensitive to cold temperature, and diminished browning of inguinal white fat. Proteomic analysis revealed a mechanistic link between Zbtb7b and the lncRNA regulatory pathway through which Zbtb7b recruits the brown fat lncRNA 1 (Blnc1)/heterogeneous nuclear ribonucleoprotein U (hnRNPU) ribonucleoprotein complex to activate thermogenic gene expression in adipocytes. These findings illustrate the emerging concept of a protein-lncRNA regulatory network in the control of adipose tissue biology and energy metabolism.

Long intergenic non-protein-coding RNA 1567 (LINC01567) acts as a "sponge" against microRNA-93 in regulating the proliferation and tumorigenesis of human colon cancer stem cells.

BACKGROUND: Cancer stem cells (CSCs) are considered to be the major factor in tumor initiation, progression, metastasis, recurrence and chemoresistance. Maintaining the stemness and promoting differentiation of these cells involve various factors. Recently, long non-coding RNAs (lncRNAs) have been identified as new regulatory factors in human cancer cells. However, the function of lncRNAs in colon CSCs is still unknown. METHODS: Primary colon cancer cells were maintained in serum-free medium to form spheres and CD133+/CD166+/CD44+ spheroid cells were selected using FACS technique. Then we detected growth curve, colony formation, invasion and migration ability, and tumorigenicity of CD133+/CD166+/CD44+ cells. LOCCS-siRNA and pcDNA-LOCCS plasmid vectors were constructed and transfected to evaluate impact of the lncRNA. We also performed dual luciferase reporter assay to verify the interaction of LOCCS and miR-93. RESULTS: The research explored lncRNA expression and the regulatory role of novel lncRNAs in colon CSCs. Using the stem cell markers CD133, CD166 and CD44, we found a subpopulation of highly tumorigenic human colon cancer cells. They displayed some characteristics of stem cells, including the ability to proliferate and form colonies, to resist chemotherapeutic drugs, and to produce xenografts in nude mice. We also found an lncRNA, LOCCS, with obviously upregulated expression in colon CSCs. Knockdown of LOCCS reduced cell proliferation, invasion, migration, and generation of tumor xenografts. Furthermore, microRNA-93 (miR-93) and Musashi-1 mediated the tumor suppression of LOCCS knockdown. CONCLUSIONS: There was reciprocal repression between LOCCS and miR-93. Research on mechanisms suggested direct binding, as a predicted miR-93 binding site was identified in LOCCS. This comprehensive analysis of LOCCS in colon CSCs provides insight for elucidating important roles of the lncRNA-microRNA functional network in human colon cancer.

MicroRNA-139-5p Suppresses 3T3-L1 Preadipocyte Differentiation Through Notch and IRS1/PI3K/Akt Insulin Signaling Pathways.

MicroRNAs (miRNAs) participate in the regulation of adipogenesis. Identification of the full repertoire of miRNAs expressed in adipose tissue is likely to significantly improve our understanding of adipose tissue growth and development. Here, miR-139-5p was identified as an inhibitor of 3T3-L1 adipocyte differentiation with significantly down-regulating the expression levels of adipogenic marker genes PPAR γ (P < 0.01), aP2 (P < 0.01) and FAS (P < 0.01). Importantly, flow cytometry and EdU incorporation assay indicated that this inhibition was partly due to the dysfunction of clonal expansion. Furthermore, we firstly demonstrated that miR-139-5p blocked adipogenesis via directly targeted the 3' untranslated regions (UTRs) of Notch1 and IRS1 mRNAs, a key member of Notch signaling and IRS1/PI3K/Akt insulin signaling, respectively. In addition, the overexpression of Notch1 or IRS1 partially restored the suppressive effects miR-139-5p on differentiation of 3T3-L1 cells. To our knowledge, this was the first report that miR-139-5p functioned negatively by targeting Notch1 and IRS1 during 3T3-L1 adipogenesis, regulating the transition from clonal expansion to terminal differentiation.

MicroRNA-139-5p regulates C2C12 cell myogenesis through blocking Wnt/ß-catenin signaling pathway.

MicroRNAs (miRNAs) are novel and potent regulators in myogenesis. However, the molecular mechanisms that many miRNAs regulate myoblast proliferation and differentiation which are largely unknown. Here, we found that miR-139-5p increased during C2C12 myoblast proliferation, while presenting an inverse trend during C2C12 myoblast differentiation. Flow cytometry and EdU incorporation assay showed that miR-139-5p slowed down the growth of C2C12 cells. Additional study demonstrated that ectopic introduction of miR-139-5p into C2C12 cells blocked myoblast differentiation. Importantly, we demonstrated for the first time that Wnt1, which is associated with the Wnt/ß-catenin signaling pathway, was a direct target of miR-139-5p. Moreover, we found that the expression level of Wnt1 was suppressed significantly (p < 0.01) by miR-139-5p, which triggered inhibition of Wnt/ß-catenin signaling through upregulation of glycogen synthase kinase 3 beta (GSK-3ß; p < 0.05) and downregulation of p-GSK-3ß (p < 0.01), ß-catenin (p < 0.05), and nuclear ß-catenin (p < 0.01). Taken together, these results suggest that miR-139-5p is an important negative regulator in myogenesis through blocking the Wnt1-mediated Wnt/ß-catenin signaling pathway.

Vowel identification in temporal-modulated noise for native and non-native listeners: Effect of language experience.

A previous study found that English vowel identification in babble was significantly different between Chinese-native listeners in China and in the U.S. One possible explanation is that native English experiences might change Chinese-native listeners' ability to take advantage of the temporal modulation in noise for their English vowel perception. As a follow-up, the current study explored whether there was a difference between the two groups of Chinese listeners in using temporal gaps in noise for English vowel identification. Vowel identification in temporally modulated noise and a temporal modulation transfer function (TMTF) was measured for American-English-native listeners (EN), Chinese-native listeners in the U.S. (CNU), and Chinese-native listeners in China (CNC). The results revealed that TMTFs were similar across the three groups, indicating that psychophysical temporal processing was independent of listeners' language backgrounds. However, for vowel identification in noise, EN and CNU listeners showed significantly greater masking release from the temporal modulation of noise than CNC listeners at low signal-to-noise ratios (e.g., -12 dB). Altogether, native English experiences may change the use of temporal cues in noise for English vowel identification for Chinese-native listeners.

A dorsal visual route necessary for global form perception: evidence from neuropsychological fMRI.

Hierarchical models of visual processing assume that global pattern recognition is contingent on the progressive integration of local elements across larger spatial regions, operating from early through intermediate to higher-level cortical regions. Here, we present results from neuropsychological fMRI that refute such models. We report two patients, one with lesions to intermediate ventral regions and the other with damage around the intraparietal sulcus (IPS). The patient with ventral damage showed normal behavioral and BOLD responses to global Glass patterns. The patient with IPS damage was impaired in discriminating global patterns and showed a lack of significant responses to these patterns in intermediate visual regions spared by the lesion. However, this patient did show BOLD activity to translational patterns, where local element relations are important. These results suggest that activation of intermediate ventral regions is not necessary to code global patterns; instead global patterns are coded in a heterarchical fashion. High-level regions of dorsal cortex are necessary to generate global pattern coding in intermediate ventral regions; in contrast, local integration processes are not sufficient.

MiR-15a/b promote adipogenesis in porcine pre-adipocyte via repressing FoxO1.

Diabetes and many other metabolism syndromes are closely related to obesity. To reveal the underlying mechanism of fat deposition, an increasing number of studies are focusing on the functions of miRNAs during adipocytes development. Previous studies have proved that miR-15a/b play important roles in multiple physiological processes; however, their functions during adipogenesis remain unclear. To reveal this, we detected the expression profiles of miR-15a/b during adipogenesis in porcine pre-adipocyte, and found that their expression levels increased in the early stage of adipocyte differentiation and dropped after day 4. Moreover, over-expression of miR-15a/b in porcine pre-adipocytes promoted adipocyte differentiation and lipid accumulation. Target genes of miR-15a/b were predicted and examined, which revealed that Forkhead box protein O1 (FoxO1) is the target gene of miR-15a/b. The inhibition of FoxO1 expression level caused by miR-15a/b over-expression had a positive effect on adipogenesis. Thus, we conclude that miR-15a/b promote adipogenesis in porcine pre-adipocyte via repressing FoxO1.

Serum erythropoietin: a useful biomarker for coronary collateral development and potential target for therapeutic angiogenesis among the patients with coronary chronic total occlusion.

The study was to investigate the association of endogenous erythropoietin (EPO) and coronary collateral development. Forty-nine patients (31 with chronic total occlusion (CTO), 18 with normal coronary artery) were consecutively enrolled. The serum EPO was positively related with Rentrop class. Increased serum EPO was one of the independent predictors of good collateral development (odds ratio 1.31; p = 0.025). A significantly positive correlation was seen between serum EPO and vascular endothelial growth factor (VEGF) levels (r = 0.96, p < 0.001). Circulatory EPO may be a useful biomarker for coronary collateral development and potential target for therapeutic angiogenesis in patients with CTO.

English vowel identification in long-term speech-shaped noise and multi-talker babble for English and Chinese listeners.

The identification of 12 English vowels was measured in quiet and in long-term speech-shaped noise (LTSSN) and multi-talker babble for English-native (EN) listeners and Chinese-native listeners in the U.S. (CNU) and China (CNC). The signal-to-noise ratio was manipulated from -15 to 0 dB. As expected, EN listeners performed significantly better in quiet and noisy conditions than CNU and CNC listeners. Vowel identification in LTSSN was similar between CNU and CNC listeners; however, performance in babble was significantly better for CNU listeners than for CNC listeners, indicating that exposing non-native listeners to native English may reduce informational masking of multi-talker babble.

[Demethylation pattern of PD-1 gene in promoter region is associated with the PD-1 expression on peripheral blood mononuclear cells in chronic hepatitis B patients].

OBJECTIVE: To observe the expression variations and influencing factors of programmed death one (PD-1) and DNA demethylation of PD-1 promoter on peripheral blood mononuclear cells (PBMCs) in chronic hepatitis B (CHB) patients and further investigate the relationship between the demethylation pattern of PD-1 gene in promoter region and the PD-1 expression on PBMC in CHB patients. METHODS: A total of 162 subjects, including 144 CHB patients and 18 healthy blood donors, were enrolled. The expression of PD-1 on PBMCs was detected by flow cytometry. And the serum HBV markers, HBV DNA load and liver function were also measured. DNA of PBMCs was treated with sodium bisulfite; the PD-1 promoter fragments were amplified by polymerase chain reaction (PCR) and then transformed into Escherichia coli. Positive clones were selected for sequencing and the methylation status of fragments of PD-1 promoter was examined. RESULTS: With the PD-1 expression in normal controls (10.8% ± 4.4%) as a baseline level, the expression of PD-1 in CHB patients significantly increased. In CHB patients, the serum expression of PD-1 in PBMCs from patients with positive HBeAg (27.1% ± 18.4%) was much higher than that from those with negative HBeAg (19.6% ± 15.6%). And the expression level of PD-1 was not correlated with serum HBV DNA load and serum level of alanine aminotransferase. The results of bisulfite genomic sequencing showed that demethylation probability of some CG points in PD-1 promoter region (-601, -553, -538, -483, -463, -317 bp) were significantly correlated with PD-1 expression level (P < 0.05). CONCLUSION: The demethylation pattern of PD-1 gene in promoter region is associated with the PD-1 expression on PBMC in CHB patients.

[Dynamic changes in PD-1, TLR3, and TLR4 surface expression on peripheral blood mononuclear cells in chronic hepatitis C patients undergoing peg-IFNalpha-2a plus ribavirin combination therapy].

OBJECTIVE: To investigate the dynamic changes in expression of programmed death (PD)-1, Toll-like receptor (TLR)3, and TLR4 on the surface of peripheral blood mononuclear cells (PBMCs) in patients with chronic hepatitis C (CHC) that occur in response to pegylated-interferon alpha-2a (peg-IFNalpha-2a) plus ribavirin (RBV) combination therapy, and to analyze the relation to achievement of sustained virological response (SVR). METHODS Twenty-three CHC patients and 10 healthy controls were enrolled in the study. All CHC patients underwent 48 weeks of combination therapy with peg-IFNalpha-2a (180 microg, subcutaneous injection, once weekly) plus RBV (15 microg/kg, oral, once daily). Total PBMCs were isolated from both groups (CHC patients at treatment week 0, 12, 24, and 48 and post-treatment week 24; controls at enrollment) and subjected to flow cytometric analysis of PD-1, TLR3, and TLR4 surface expression. In addition, serum levels of alanine aminotransferase (ALT) and hepatitis C virus (HCV) RNA levels were analyzed by enzymatic assay and the AmpliPrep/COBAS (Roche) nucleic acid amplification test, respectively. SVR was defined as undetectable levels of HCV RNA at post-treatment week 24. Intergroup differences were assessed by one-way ANOVA. RESULTS: The expression ratios of PD-1, TLR4 and PD-1: TLR4 on PBMCs were significantly higher in CHC patients before therapy than in the healthy controls (45.20 +/- 7.12% vs. 16.82 +/- 4.13%, 58.45 +/- 15.13% vs. 21.09 +/- 2.89%, and 35.54 +/- 7.69% vs. 14.12 +/- 2.89%; all P < 0.05). In contrast, the expression ratios of TLR3 and PD-1:TLR3 were slightly, but not significantly, higher in CHC patients before therapy than in the healthy controls (P > 0.05). During the course of peg-IFNalpha-2a plus RBV combination therapy, the expression ratios of PD-1 and TLR4 on PBMCs showed a decreasing trend, while TLR3 expression showed an increasing trend. Furthermore, CHB patients who achieved SVR at post-treatment week 24 had a significantly different expression ratio of PD-1 and TLR3 than those who did not achieve SVR (P < 0.05). CONCLUSION: Surface expression of PD-1, TLR4, and PD-1:TLR4 is up-regulated in the total PBMCs of CHC patients. Peg-IFNalpha-2a plus RBV treatment-induced suppression of HCV replication results in a significant reduction in PD-1 and TLR4 expression on the surface of PBMCs, but a remarkably elevated level of TLR3 expression. The dynamic change in PD-1 and TLR3 expression on PBMCs that occurs during antiviral therapy may be related to achievement of SVR.

A Large Institutional Study on Outcomes and Complications after Transcatheter Closure of a Perimembranous-Type Ventricular Septal Defect in 890 Cases.

PURPOSE: To investigate the incidence, cause, and prevention of complications associated with interventional therapy for perimembranous ventricular septal defects (pmVSDs). METHODS: A retrospective analysis was performed on 890 patients with pmVSDs after interventional therapy. The complications were then analyzed by electrocardiography and echocardiography during or after interventional therapy. During the follow-up period of 12-52 (mean of 26.9 ± 21.6) months, the technical success rate was 97.9% (871/890). RESULTS: The incidence of serious complication was 1.12% (10/890), including five cases of third-degree atrioventricular block, two of severe tricuspid valve regurgitation, one of cerebral infarction in the basal ganglia area, and two of femoral artery thrombosis. No death was reported during patient follow-up. CONCLUSIONS: Transcatheter closure of pmVSDs in selected patients was found to be effective and safe. KEY WORDS: Complication; Interventional therapy; Ventricular septal defect.

Hepatic-Targeted Nano-enzyme with Resveratrol Loading for Precise Relief of Nonalcoholic Steatohepatitis.

Nonalcoholic steatohepatitis (NASH) is characterized by massive lipid deposition in hepatocytes and is often associated with hepatic inflammation and other severe metabolic syndromes. The intervention of NASH can prevent its further progression into hepatocarcinoma. In this study we have successfully constructed liver-targeted Ce-based hollow mesoporous nanocarriers loaded with bioactive drugs. This may provide an effective approach for eliminating NASH. Liver-section-specific targeting was realized by covalently linked galactose (Gal), which can be specifically recognized by receptors in the membranes of hepatocytes. Meanwhile, resveratrol (Res), a drug used to treat NASH, was efficiently loaded into the pores and cavity of CeO2 (Res@H-CeO2 -Gal). In steatotic HepG2 cells (free fatty acid induction), this nanosystem was found to enhance cellular Res internalization for improved anti-lipogenesis activity. In mice with NASH, Res@H-CeO2 -Gal increased Res delivery to liver sections for a reduction in lipid accumulation and enhanced anti-inflammatory activity from the antioxidant capacity of Ce-based nanocarriers. This effectively recovered NASH mice to the normal state. These findings show that the hepatic targeting and Res delivery nanoplatform could act as a safe and promising strategy for the elimination of NASH and other liver diseases.

Effects of Thermal Treatment on the Mechanical Properties of Bamboo Fiber Bundles.

Bamboo is known as a typical kind of functional gradient natural composite. In this paper, fiber bundles were extracted manually from various parts of the stem in the radial direction, namely the outer, middle, and inner parts. After heat treatment, the mechanical properties of the fiber bundles were studied, including the tensile strength, elastic modulus, and fracture modes. The micromechanical properties of the fiber cell walls were also analyzed. The results showed that the mean tensile strength of the bamboo fiber bundles decreased from 423.29 to 191.61 MPa and the modulus of elasticity increased from 21.29 GPa to 27.43 GPa with the increase in temperature. The elastic modulus and hardness of the fiber cell walls showed a positive correlation with temperature, with the modulus of elasticity and the hardness increasing from 15.96 to 18.70 GPa and 0.36 to 0.47 GPa, respectively. From the outside to the inside of the bamboo stems, the tensile strength and elastic modulus showed a slight decrease. The fracture behavior of the fiber bundles near the outside approximates ductile fracture, while that of the bundles near to the inside tend to be a brittle fracture. The fracture surfaces of the bamboo bundles and the single fibers became smoother after heat treatment. The results show that bamboo fiber bundles distributed near the outside are most suitable for industrial development under heat treatment at 180 °C. Therefore, this study can provide a reasonable scientific basis for the selective utilization, functional optimization, and bionic utilization of bamboo materials, which has very important theoretical and practical significance.

Effects of conversion of natural forest to plantations on the abundance of nitrite reducing genes in soil aggregates in subtropical forest region.

Large proportion of natural forest has been transformed into plantations in subtropical regions, with consequences on forest ecosystem structure and function. In order to understand the responses of two nitrite reducing genes (nirK and nirS) in N2O production to forest conversion, we collected soil samples from Castanopsis carlesii natural forest, Cunninghamia lanceolata plantation and Pinus massoniana plantation and examined the abundance of nirK and nirS genes in soils and aggregates. Results showed that forest conversion increased soil pH, while decreased soil ammonium content. Forest conversion did not influence the mass proportion of soil aggregates. The abundance of nirK and nirS genes varied in aggregates with different particle sizes. The abundance of nirK and nirS genes was the highest in small macraoaggregates and the lowest in the silt-clay particles. Moreover, the abundance of nirK was significantly higher than that of nirS in soils of all forest types, indicating that nirK dominated in the acidic forest soils. Conversion of natural forest to plantations significantly increased the abundance of nirK and nirS genes in the bulk soil and aggregates, indicating that forest conversion would be beneficial for the growth of microorganisms bearing nirK and nirS genes, which might be associated with the increases of soil pH. Taken together, conversion of natural forest to C. lanceolata plantation or P. massoniana plantation significantly increased the abundance of nirK and nirS in soils and aggregates, but did not affect the mass proportions of aggregates.