Loss of RSR1 function increases the abscisic acid content and improves rice quality performance at high temperature.

Rice starch regulator1 (RSR1) participates in the regulation of starch synthesis in rice, but it's function on starch synthesis and quality formation in response to high temperature is unknown. RSR1 mutation resulted in a significant increase in the abscisic acid (ABA) content in rice grains under both normal and high temperature, and the effect of high temperature on grain filling and quality formation of the rsr1 mutants was significantly reduced. The grain size, 1000-kernels weight, amylose content, gelatinization temperature, and starch viscosity of the rsr1 mutants were less sensitive to high temperature. Loss of RSR1 function increased the expression levels of starch synthesis-related genes and reduced their responses to high temperature to some extent. Besides, the percentage of germinated seeds from rsr1 mutants was significantly lower than that of the wild-type, and the difference was more significant under ABA treatment. The shoot lengths of the rsr1 mutants were remarkably shorter than those of the wild-type, which was further exacerbated by ABA treatment. These results indicated that loss function of RSR1 can improve rice quality performance at high temperature by moderately increasing the ABA content of rice grains, which provides theoretical significance for the cultivation of better-quality rice with high-temperature resistance.

Anthracene and tetraphenylsilane based conjugated porous polymer nanoparticles for sensitive detection of nitroaromatics in water.

Conjugated porous polymers (CPPs) are a kind of promising sensing materials for the detection of nitroaromatic compounds, but their sensing applications in aqueous media are limited because of their poor dispersity or solubility in water. In this study, we prepared anthracene and tetraphenylsilane based CPPs named PSiAn by conventional Suzuki coupling and Suzuki-miniemulsion polymerization, respectively. The structure, morphology and porosity of the CPPs were characterized by Fourier Transform infrared spectroscopy (FT-IR), proton nuclear magnetic resonance (1H NMR), transmission electron microscope (TEM) and N2 sorption isotherm, respectively. Both of the CPPs have porous structure which is beneficial for the adsorption and diffusion of the analytes within them. The particle size of PSiAn nanoparticles prepared by Suzuki-miniemulsion polymerization is 10-40 nm from the TEM image, which facilitates the dispersion in the aqueous phase. Combined with the porosity and nanoparticle morphology, PSiAn nanoparticles realized the efficient photoluminescence (PL) sensing of nitroaromatic explosives in aqueous phase. The limit of detection (LOD) and limit of quantitation (LOQ) of PSiAn nanoparticles for 2,4,6-trinitrophenol (TNP) detection in the pure aqueous phase are 0.33 µM and 1.11 µM, respectively. Meanwhile, the good selectivity and anti-interference in presence of other nitro-compounds were observed. Furthermore, the spike/recovery test for the TNP detection in real water samples by PL sensing based on PSiAn nanoparticles indicates the quantitative recovery of TNP from 100.74 % to 101.00 %. The electrochemical test, ultraviolet-visible absorption spectra, excitation and emission spectra, and time-resolved PL spectra were investigated to explore the PL sensing mechanism. As a result, it is found that the fluorescence inner filter effect might be the predominant quenching mechanism during the detection of nitrophenolic compounds such as TNP and 4-nitrophenol (4-NP).

Long non-coding RNA EGOT is associated with 131iodine sensitivity and contributes to thyroid cancer progression by targeting miR-641/PTEN axis.

Thyroid cancer is a prevalent endocrine malignancy around the world. Radioactive 131iodine (131I) therapy is widely applied in TC patients, but the resistance affects its effectiveness in the clinics. Long non-coding RNA (lncRNA) EGOT has been reported to induce an inhibitory effect on cancer progression, but the specific function of EGOT in 131I resistance of TC cells remains unclear. Here, we successfully established 131I-resistant TC cells and evaluated the impact of EGOT on 131I resistance in the cells. Our data showed that EGOT and PTEN expression was reduced but the miR-641 expression was enhanced in 131I-resistant TC cells. EGOT inhibited viability, induced apoptosis and enhanced DNA damage in 131I-resistant TC cells. Mechanically, we identified that EGOT induced PTEN expression by targeting miR-641 in 131I-resistant TC cells. Moreover, the depletion of PTEN and miR-641 mimic reversed EGOT-relieved 131I resistance of TC cells in vitro. Thus, we conclude that lncRNA EGOT attenuated 131I resistance of TC cells by targeting miR-641/PTEN axis. The clinical functions of EGOT in TC therapy deserve to be validated in future exploration.

Adsorption of Different Ionic Types of Polyacrylamide on Montmorillonite Surface: Insight from QCM-D and Molecular Dynamic Simulation.

This study investigates the interaction between montmorillonite and polyacrylamide (PAM) with different ionic types using quartz crystal microbalance with dissipation monitoring (QCM-D) and molecular dynamics (MD) simulations. The goal was to understand the effect of ionicity and ionic type on polymer deposition on montmorillonite surfaces. The results of the QCM-D analysis showed that a decrease in pH led to an increase in the adsorption of montmorillonite on the alumina surface. The ranking of adsorption mass on alumina and pre-adsorbed montmorillonite alumina surfaces was found to be cationic polyacrylamide (CPAM) > polyacrylamide (NPAM) > anionic polyacrylamide (APAM). The study also found that CPAM had the strongest bridging effect on montmorillonite nanoparticles, followed by NPAM, while APAM had a negligible bridging effect. The MD simulations showed that ionicity had a significant influence on the adsorption of polyacrylamides. The cationic functional group N(CH3)3+ had the strongest attraction interaction with the montmorillonite surface, followed by the hydrogen bonding interaction of the amide functional group CONH2, and the anionic functional group COO- had a repulsive interaction. The results suggest that at high ionicity levels, CPAM can be adsorbed on the montmorillonite surface, while at low ionicity levels, APAM may still be adsorbed with a strong coordination trend.

Efficacy and safety of a fourth dose of the COVID-19 vaccine in kidney transplant recipients: A systematic review and meta-analysis.

BACKGROUND: Kidney transplant recipients (KTRs) who become infected with SARS-CoV-2 are at greater risk of serious illness and death than the general population. To date, the efficacy and safety of the fourth dose of the COVID-19 vaccine in KTRs have not been systematically discussed. METHODS: This systematic review and meta-analysis included articles from PubMed, Embase, the Cochrane Library, Web of Science, China National Knowledge Infrastructure, and Wanfang Med Online published before May 15, 2022. Studies evaluating the efficacy and safety of a fourth dose of the COVID-19 vaccine in kidney transplant recipients were selected. RESULTS: Nine studies were included in the meta-analysis, with a total of 727 KTRs. The overall pooled seropositivity rate after the fourth COVID-19 vaccine was 60% (95% CI, 49%-71%, I2 = 87.83%, p > 0.01). The pooled proportion of KTRs seronegative after the third dose that transitioned to seropositivity after the fourth dose was 30% (95% CI, 15%-48%, I2 = 94.98%, p < 0.01). CONCLUSIONS: The fourth dose of the COVID-19 vaccine was well tolerated in KTRs with no serious adverse effects. Some KTRs showed a reduced response even after receiving the fourth vaccine dose. Overall, the fourth vaccine dose effectively improved seropositivity in KTRs, as recommended by the World Health Organization for the general population.

Antarctic krill (Euphausia superba) oil high internal phase emulsions improved the lipid quality and gel properties of surimi gel.

In the study, high internal phase emulsions (HIPEs) prepared from Antarctic krill oil (AKO) were added into surimi and the effects on gel properties, lipid quality and stability were investigated. It is found that HIPEs-added groups exhibited higher gel strength and lower cooking loss than Oil-added counterparts. HIPEs-added groups had higher proportion of capillary water, and microstructure of HIPEs-added gels showed fewer large voids and small size droplets. HIPEs-added groups also showed less pronounced myosin heavy chain band. HIPEs- and Oil-added gels showed > 3500 mg/kg EPA + DHA and 0.4-0.8 mg/kg astaxanthin, and most HIPEs-added groups had higher levels of them but lower TBARS values. Results suggest AKO-HIPEs could reduce the intervention by lipids on myosin crosslinking during gelation, and protect fatty acids and asxtanthin from oxidation due to oxygen-isolation led by their high accumulation. Thus, AKO-HIPEs can be applied to fortify ω-3 PUFA and maintain good gel properties in surimi product.

Variation of rice starch structure and physicochemical properties in response to high natural temperature during the reproductive stage.

Climate warming affects rice growth at different phenological stages, thereby increasing rice chalkiness and protein content and reducing eating and cooking quality (ECQ). The structural and physicochemical properties of rice starch played important roles in determining rice quality. However, differences in their response to high temperature during the reproductive stage have been rarely studied. In the present study, they were evaluated and compared between two contrasting natural temperature field conditions, namely, high seasonal temperature (HST) and low seasonal temperature (LST), during the reproductive stage of rice in 2017 and 2018. Compared with LST, HST significantly deteriorated rice quality, including increased grain chalkiness, setback, consistence, and pasting temperature and reduced taste values. HST considerably reduced the total starch and increased the protein content. Likewise, HST significantly reduced the short amylopectin chains [degree of polymerization (DP) <12] and increased the long amylopectin chains (DP > 12) and relative crystallinity. The starch structure, total starch content, and protein content explained 91.4%, 90.4%, and 89.2% of the total variations in pasting properties, taste value, and grain chalkiness degree, respectively. In conclusion, we suggested that rice quality variations were closely associated with the changes in chemical composition content (total starch and protein content) and starch structure in response to HST. These results indicated that we should improve the resistance of rice to high temperature during the reproductive stage to improve the fine structure of rice starch in further breeding and practice.

CircLRP6 contributes to prostate cancer growth and metastasis by binding to miR-330-5p to up-regulate NRBP1.

BACKGROUND: Circular RNA low-density lipoprotein receptor-related protein 6 (circLRP6) is considered as an oncogene in many types of cancers. However, the function and mechanisms of circLRP6 in prostate cancer (PCa) tumorigenesis remain largely undefined. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot assays were conducted to assess the expression of circLRP6, microRNA (miR)-330-5p, and nuclear receptor binding protein 1 (NRBP1). Cell counting kit-8 (CCK-8), colony formation, 5-ethynyl-2'-deoxyuridine (EDU) incorporation, flow cytometry, transwell, wound healing, and western blot assays were performed to detect cell proliferation, apoptosis, and metastasis in vitro. Subcutaneous tumor growth was observed in nude mice to investigate the role of circLRP6 in vivo. The targeting relationship between miR-330-5p and NRBP1 or circLRP6 was verified using dual-luciferase reporter, pull-down, and RNA immunoprecipitation (RIP) assays. Immunohistochemistry was employed to test relative protein expression. RESULTS: CircLRP6 was highly expressed in PCa tissues and cells, knockdown of circLRP6 impaired PCa cell growth and metastasis in vitro by affecting cell proliferation, apoptosis, invasion, migration, and epithelial-mesenchymal transition (EMT). Mechanistic studies showed that circLRP6 could competitively bind with miR-330-5p to prevent the degradation of its target gene NRBP1. Rescue assay suggested that miR-330-5p inhibition reversed the inhibitory effects of circLRP6 knockdown on PCa cell growth and metastasis. Moreover, overexpression of miR-330-5p suppressed PCa progression via NRBP1. Notably, tumor formation assay indicated that circLRP6 silencing impeded tumor growth and EMT in vivo. CONCLUSION: Our findings demonstrated that circLRP6 promoted PCa tumorigenesis and metastasis through miR-330-5p/NRBP1 axis, suggesting a potential therapeutic target for PCa.

Fabrication of stable high-performance urchin-like CeO2/ZnO@Au hierarchical heterojunction photocatalyst for water remediation.

In this paper, the urchin-like CeO2/ZnO@Au photocatalyst was rationally designed and prepared through hydrothermal method, chemical precipitation and photo reduction deposition. The optimal photocatalyst (CZA8) degraded Rhodamine B (RhB), 4-nitrophenol (4-NP) and Naproxen (NPX) about 100% within 20 min, 91.4% within 60 min and 88.9% within 30 min under Xe lamp illumination, respectively. Besides, the CZA8 possesses outstanding photo corrosion resistance capacity which has been verified with the cycle degradation experiments. The photocatalyst displays excellent light response and efficient separation of photo-induced carriers due to the fabrication of type-II heterojunction, the presence of surface plasmon resonance (SPR) effect and as well as the oxygen vacancy. The oxygen vacancy was systematically characterized by XPS, PL and Raman. Moreover, the photocatalytic degradation pathways are proposed based on the LC-MS results. Finally, a novel photocatalytic mechanism for photocatalytic oxidation of RhB, 4-NP and NPX is discussed and schematically illuminated.

Downregulation of Transmembrane protein 40 by miR-138-5p Suppresses Cell Proliferation and Mobility in Clear Cell Renal Cell Carcinoma.

BACKGROUND: Clear cell renal cell carcinoma (ccRCC) represents approximately 70% of RCC,as the most frequent histological subtype of RCC. MiR-138-5p, a tumor-related microRNA (miRNA), has been reported to be implicated in the diverse types of human malignancies, but its role in ccRCCremains unclear. OBJECTIVE: The study was designed to investigate the functional behaviors and regulatory mechanisms of miR-138-5p in ccRCC. MATERIALS AND METHODS: Quantitative real-time PCR and western blotting analyses were performed to determine the expression of miR-138-5p and TMEM40 in ccRCC tissues. Pearson's correlation coefficient was utilized to evaluate the correlation between miR-138-5p and TMEM40 expression. The function of miR-138-5p and TMEM40 in the cell proliferation, migration and invasion of ccRCC cells (786-O and ACHN) was assessed by CCK-8, colony formation, wound healing and transwell assay, respectively. A luciferase reporter assay was performed to confirm the direct binding of miR-138-5p to the target gene TMEM40. RESULTS: We found the expression of miR-138-5p was significantly down-regulated, while TMEM40 was remarkably up-regulated in ccRCC tissues. TMEM40 expression was discovered to be inversely correlated with miR-138-5p expression in ccRCC tissues. Functional studies demonstrated that miR-138-5p overexpression or TMEM40 knockdown significantly suppressed ccRCC cell proliferation, migration and invasion in vitro. Notably, we experimentally confirmed that miR-138-5p directly recognizes the 3'-UTR of the TMEM40 transcript and down-regulated its expression in ccRCC cells. CONCLUSIONS: Taken together, our findings provide the first clues regarding the role of miR-138-5p as a tumor suppressor in ccRCC by directly targeting of TMEM40.

6PGD Upregulation is Associated with Chemo- and Immuno-Resistance of Renal Cell Carcinoma via AMPK Signaling-Dependent NADPH-Mediated Metabolic Reprograming.

BACKGROUND: The essential role of 6-phosphogluconate dehydrogenase (6PGD), the enzyme catalyzing the oxidative pentose phosphate pathway, in tumor growth and metabolism has garnered attention in recent years. In this work, we are the first to demonstrate that aberrant activation of 6PGD is a feature in renal cell carcinoma (RCC) and is critically involved in renal carcinogenesis and chemo- and immuno-resistance. MATERIALS AND METHODS: 6PGD expression and activity were systematically analyzed in normal and malignant renal cells and tissues. The roles of 6PGD and its downstream mechanism were investigated using gain-of-function and loss-of-function approaches. RESULTS: 6PGD expression and enzyme activity were increased in RCC cells and patients' samples. Activation of 6PGD via gain-of-function approach promoted growth of normal kidney but not RCC cells, and alleviated the efficacy of chemotherapeutic (e.g., 5-FU) and immunotherapeutic (e.g., IFN-α) agents. In contrast, 6PGD inhibition using siRNA knockdown and pharmacological inhibitor physcion augmented the inhibitory effects of 5-FU and IFN-α in RCC. Mechanistic studies demonstrated that 6PGD inhibition activated AMPK signaling, leading to ACC1 enzyme inhibition and reduction of lipid synthesis. In addition, 6PGD inhibition disrupted NADPH and NADH homeostasis in RCC cells as shown by the decreased level of NADPH and NADH, and suppressed SIRT-1 activity. AMPK inhibition by siRNA knockdown reversed the inhibitory effects of physcion, demonstrating that the effect of 6PGD inhibition is AMPK activation dependent. CONCLUSIONS: Our work provides preclinical evidence that 6PGD inhibition may represent a potential therapeutic strategy to augment the efficacy of RCC standard of care drugs.

Inhibition of the CDK4/6-Cyclin D-Rb Pathway by Ribociclib Augments Chemotherapy and Immunotherapy in Renal Cell Carcinoma.

Renal cell carcinoma (RCC) is the most aggressive type of genitourinary cancer and is resistant to current therapies. Identifying drugs that enhance the efficacy of RCC standard-of-care drugs at sublethal concentrations is an alternative therapeutic strategy. Ribociclib is an orally available cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitor that is approved for the treatment of breast cancer. In this work, we demonstrate that ribociclib at clinically achievable concentrations inhibits proliferation of 7 out of 9 tested RCC cell lines, with IC50 range from 76 to 280 nM. In addition, ribociclib induces apoptosis of RCC cells, but with less potency compared to its antiproliferative activity. The combination of ribociclib with chemotherapeutic or immunotherapeutic agents is synergistic in RCC cell lines. Of note, ribociclib demonstrates selective anti-RCC activity by sparing normal kidney cells and fibroblast cells. Consistent with the in vitro findings, ribociclib inhibits RCC growth at the dosage that does not lead to toxicity in mice and enhances the in vivo efficacy of RCC standard-of-care drugs. Mechanistically, we show that ribociclib remarkably inhibits phosphorylation of retinoblastoma protein (Rb) at various sites, leading to the suppression of transcription of E2F target genes in RCC cells. Our findings clearly demonstrate the potency and selectivity of ribociclib in RCC preclinical models, via inhibition of the CDK4/6-cyclin D/Rb pathway. Our findings support a clinical trial for the combination of ribociclib with chemo/immunotherapy in RCC.

miR-135a inhibits malignant proliferation and diffusion of non-small cell lung cancer cells by down-regulating ROCK1 protein.

OBJECTIVE: To seek the clinical significance and regulatory mechanism of miR-135a and Rho-associated protein kinase 1 (ROCK1) in non-small cell lung cancer (NSCLC). METHODS: NSCLC cells were purchased, and miR-135a-mimics, miR-135a-inhibitor, miR-NC, si-ROCK1 and Sh-ROCK1 were transfected into NSCLC cells HCC827 and NCI-H524. qRT-PCR and Western blot were used to detect the expression of miR-135a, ROCK1, Bax, Caspase3, Bcl-2, N-cadherin, vimentin and E-cadherin. MTT, scratch test, Transwell and flow cytometry were used to analyze the cell proliferation, migration, invasion and apoptosis. RESULTS: miR-135a was low expressed in serum of NSCLC group, while ROCK1 was opposite. miR-135a low level or ROCK1 high level was associated with poor prognosis of NSCLC and lower 3-year OS. Over-expression of miR-135a and inhibition of ROCK1 expression could control malignant growth and diffusion of cells and expression of Bcl-2, N-cadherin and vimentin proteins, and promote apoptosis and expression of Bax, Caspase3 and E-cadherin proteins. After transfection of miR-135a-mimics+sh-ROCK1 to HCC827 and NCI-H524, the malignant proliferation and diffusion behavior of the cells were not different from those of the miR-NC group with no transfection sequence. The double luciferase report revealed that miR-135a has a targeting relationship with ROCK1. CONCLUSION: miR-135a is abnormally down-regulated in NSCLC. As a serum indicator, miR-135a has the potential to diagnose NSCLC and predict prognosis. The up-regulated expression of miR-135a protein can down-regulate the ROCK1 protein, inhibit the malignant proliferation, migration, invasion, EMT and other diffusion behaviors of NSCLC cells, and increase the apoptosis ability of cells.

Long noncoding RNA SNHG22 increases ZEB1 expression via competitive binding with microRNA-429 to promote the malignant development of papillary thyroid cancer.

Long noncoding RNA termed small nucleolar RNA host gene 22 (SNHG22) is a crucial regulator in epithelial ovarian carcinoma. Nevertheless, the regulatory functions of SNHG22 in papillary thyroid cancer (PTC) progression and its mechanisms of action remain poorly defined. Therefore, the present study aimed to investigate the role of SNHG22 in the malignant phenotype of PTC and determine whether SNHG22 regulates PTC progression via a ceRNA mechanism. SNHG22 expression in PTC was detected using reverse transcription-quantitative polymerase chain reaction analysis. The biological actions of SNHG22 silencing in PTC cells were evaluated both in vitro (using Cell Counting Kit-8 assay, flow cytometry analysis, and cell migration and invasion assays) and in vivo (using tumorigenicity assay). Herein, high SNHG22 expression was observed in PTC tissues and cell lines. This high SNHG22 level was closely associated with unfavorable clinicopathological characteristics and worse overall survival in patients with PTC. SNHG22 knockdown effectively suppressed PTC cell proliferation, migration, and invasion in vitro; accelerated cell apoptosis; and hindered tumor growth in vivo. Mechanistic experiments revealed that SNHG22 directly interacts with microRNA-429 (miR-429) as an miRNA sponge and positively modulates ZEB1 expression. Rescue assays found that miR-429 inhibition or ZEB1 upregulation can offset the actions of SNHG22 knockdown in PTC cells. In sum, SNHG22, miR-429, and ZEB1 form an interactive regulatory network with cancer-promoting roles in PTC cells, suggesting that the SNHG22/miR-429/ZEB1 pathway is a novel diagnostic and therapeutic target.

Knockdown of lncRNA TUG1 Enhances Radiosensitivity of Prostate Cancer via the TUG1/miR-139-5p/SMC1A Axis.

BACKGROUND: Prostate cancer (PCa) is a common malignant tumor of the urinary system in males. LncRNA taurine-upregulated gene 1 (TUG1) has been verified to play a crucial role in progression and prognosis of PCa. However, the functional mechanism of TUG1 remains unclear with radiosensitivity of PCa. METHODS: Quantitative real-time PCR (qRT-PCR) was conducted to measure the transcription levels of genes. 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis were employed to assess cell proliferation and apoptosis, respectively. Moreover, colony formation assay was used to measure colony survival. Western blot was performed to detect the relative proteins expression. The interaction among variables was predicted by online tool starbase, and then confirmed using the dual luciferase reporter assay. A xenograft mouse model was constructed to investigate the effect of TUG1 on tumor growth in vivo. RESULTS: The levels of lncRNA TUG1 and SMC1A were remarkably increased, while miR-139-5p was downregulated in PCa. Patients with high expression of TUG1 showed a lower survival rate and poor prognosis. Knockdown of TUG1 inhibited PCa cell proliferation and colony survival fraction, and promoted apoptosis. Downregulation of miR-139-5p reversed the effects of TUG1 deletion on proliferation, apoptosis and colony survival fraction in PCa cells treated with 4 Gy of X-ray radiation. Moreover, TUG1 sponged miR-139-5p to regulate SMC1A expression. SMC1A deletion blocked the effects of TUG1 on the progression of PCa cells treated with 4 Gy of X-ray radiation. The tumor volume and weight were illustriously reduced with radiation and TUG1 silencing in xenograft model. CONCLUSION: Knockdown of lncRNA TUG1 enhanced radiosensitivity in PCa via the TUG1/miR-139-5p/SMC1A axis. It may become a promising target for PCa treatment.

miR-758-3p suppresses human bladder cancer cell proliferation, migration and invasion by targeting NOTCH2.

MicroRNAs (miRs) are widely involved in regulating tumor development and progression. miR-758-3p has been reported to suppress the progression of various cancer types, including hepatocellular carcinoma. However, whether miR-758-3p has a role in bladder cancer (BC) has not been previously reported, and was thus investigated in the present study. It was revealed that miR-758-3p was downregulated in BC tissues and cell lines. Transfection with miR-758-3p mimics suppressed the proliferation, migration and invasion of BC cells, and inhibition of miR-758-3p had the opposite effect. In terms of the underlying mechanisms, a luciferase reporter assay revealed that Notch receptor 2 (NOTCH2) is a direct target gene of miR-758-3p in BC cells. Transfection with miR-758-3p mimics decreased the mRNA and protein levels of NOTCH2. Furthermore, an inverse correlation between miR-758-3p and NOTCH2 levels was identified. Finally, overexpression of NOTCH2 significantly rescued the proliferation, migration and invasion of BC cells transfected with miR-758-3p mimics. Taken together, the present study indicated that miR-758-3p suppresses BC cell proliferation, migration and invasion by targeting NOTCH2.

Effects of high temperature on the fine structure of starch during the grain-filling stages in rice: mathematical modeling and integrated enzymatic analysis.

BACKGROUND: High temperature during the grain-filling stage is an important factor that can affect grain quality by altering the composition and structure of starch in rice. Therefore, it is important to study the regulatory mechanism of high temperature on rice starch biosynthesis. RESULTS: Two japonica cultivars, the waxy rice Taihunuo and non-waxy Nangeng 5055 were used to examine the effect of high temperature on the fine structure of starch during the grain-filling stage. Analysis of starch chain length distribution indicated that exposure to a high temperature increased the content of starch with medium-long chains and decreased the starch with short chains in both rice varieties. The differences of amylopectin synthesis responding to high temperature between waxy and non-waxy rice can shed light on the interactions of amylose and amylopectin synthesis under high temperature conditions. In the non-waxy variety, the amylose biosynthesis may affect the short and medium-long amylopectin biosynthesis under high temperature. A mathematical fitting model was used to interpret the fine structure of amylopectin and a series of parameters with enzymatical significance (ß and γ) were obtained. The fitting results showed that the waxy and non-waxy rice had similar responses to high temperature. The variations of the parameter response to high temperature was more remarkable in Taihunuo. Activity analysis of starch synthesis-related enzymes during the grain-filling stage demonstrated the reliability of model fitting results. CONCLUSION: The influences of high temperature on the fine structure of starch are similar between waxy and non-waxy rice. Amylose biosynthesis may affect amylopectin biosynthesis under high temperature. © 2018 Society of Chemical Industry.

CSE1L participates in regulating cell mitosis in human seminoma.

OBJECTIVES: CSE1L has been reported to be highly expressed in various tumours. Testicular germ cell tumours are common among young males, and seminoma is the major type. However, whether CSE1L has functions in the seminoma is unclear. MATERIALS AND METHODS: The expression of CSE1L was detected by immunohistochemistry in seminoma tissues and non-tumour normal testis tissues from patients. CSE1L distribution during cell mitosis was determined by immunofluorescent staining with CSE1L, α-tubulin and γ-tubulin antibodies. The effects of Cse1L knockdown on cell proliferation and cell cycle progression were determined by Cell Counting Kit-8 assay, flow cytometry, PH3 staining and bromodeoxyuridine incorporation assay. RESULTS: CSE1L was significantly enriched in the seminoma tissue compared with the non-tumour normal testis tissue. CSE1L also co-localized with α-tubulin in the cells with a potential to divide. In the seminoma cell line TCam-2, CSE1L was associated with the spindles and the centrosomes during cell division. The knockdown of CSE1L in TCam-2 cells attenuated the cells' proliferative capacity. Cell cycle assay revealed that the CSE1L-deficient cells were mainly arrested in the G0/G1 phase and moderately delayed in the G2/M phase. The proportion of cells with multipolar spindle and abnormal spindle geometry was obviously increased by CSE1L expression silencing in the TCam-2 cells. CONCLUSIONS: Overall, these findings showed that CSE1L plays a pivotal role in maintaining cell proliferation and cell division in seminomas.

Comprehensive analysis of marker gene detection and computed tomography for the diagnosis of human lung cancer.

Non-small cell lung cancer (NSCLC) is one of leading causes of cancer-associated mortality, with a high number of cases caused by metastasis. The early diagnosis of cancer contributes to the successful treatment of patients with lung cancer. The aim of the present study was to analyze the efficacy of marker gene detection and computed tomography (CT) in diagnosing human lung cancer. Lung cancer marker genes, including carcinoembryonic antigen (CEA), cancer antigen 125 (CA125), tissue polypeptide antigen (TPA), pro-gastrin-releasing peptide (ProGRB), cytokeratin fragment 21-1 (Cyfra21-1) and neuron-specific enolase (NSE), were analyzed in patients with lung cancer. The tumor size was evaluated using CT, and the association between lung serum levels of marker gene protein expression and tumor size was investigated. A total of 328 patients with lung cancer were identified, including 204 adenocarcinoma, 75 large cell carcinoma and 49 squamous cell carcinoma cases. All patients were indicated to have a high serum level of CEA, CA125, TPA, ProGRB, Cyfra21-1 and NSE, compared with the normal range. Immunohistochemistry demonstrated higher expression levels of CEA, CA125, TPA, ProGRB, Cyfra21-1 and NSE in lung tumor tissues, compared with the normal range. Results indicated that CT was able to diagnose tumor size for patients with lung cancer. The CEA and CA125 expression levels were associated with CT-diagnosed adenocarcinoma tumor size. Large cell carcinoma tumor size was associated with serum levels of CEA, TPA and ProGRB. Results indicated that Cyfra21-1 and NSE were associated with the squamous cell carcinoma cases, as demonstrated using CT. In conclusion, these results indicated that comprehensive analysis of marker gene detection and CT results may be used to diagnose human lung cancer.

Targeting mitochondria by anthelmintic drug atovaquone sensitizes renal cell carcinoma to chemotherapy and immunotherapy.

Targeting mitochondria respiration is an effective therapeutic strategy in renal cell carcinoma (RCC). Atovaquone is a FDA-approved antibiotic but is also known as a mitochondrial inhibitor. We found that atovaquone inhibited proliferation and induced apoptosis of RCC cells. Mechanistically, atovaquone inhibits mitochondrial respiration in a concentration-dependent and time-dependent manner, via targeting mitochondrial respiratory complex III. Although increased glycolysis was observed in atovaquone-treated cells, atovaquone decreased ATP levels. As a consequence of mitochondrial respiration inhibition, reactive oxygen species levels were increased by atovaquone. The complete rescue of atovaquone's effects by an antioxidant suggests the important role of oxidative stress in the action of atovaquone in RCC. Importantly, atovaquone enhanced the in vitro and in vivo efficacy of 5-fluorouracil (5-FU) and interferon-α (IFN-α). Our preclinical findings suggest that atovaquone is a useful addition for RCC treatment. Our work also further demonstrates that RCC is more dependent on mitochondrial respiration than glycolysis.