Combined effects of cadmium and sulfamethoxazole on Eisenia fetida: Insights into accumulation, subcellular partitioning, biomarkers and toxicological responses.

Cadmium (Cd) and sulfamethoxazole (SMX) frequently coexist in farmlands, yet their synergistic toxicological impacts on terrestrial invertebrates remain unexplored. In this study, earthworms were exposed to artificial soils percolated with Cd (5 mg/kg), SMX (5 mg/kg) or combination of them for 7 days, followed by a 12-day elimination phase in uncontaminated soil. The uptake of Cd and SMX by the earthworms, along with their subcellular distribution, was meticulously analyzed. Additionally, a suite of biomarkers-including superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), and weight loss-were evaluated to assess the health status of the earthworms and the toxicological effects of the Cd and SMX mixture. Notably, the cotreatment with Cd and SMX resulted in a significantly higher weight loss in Eisenia fetida (41.25 %) compared to exposure to Cd alone (26.84 %). Moreover, the cotreatment group exhibited substantially higher concentrations of Cd in the total internal body, fraction C (cytosol), and fraction E (tissue fragments and cell membranes) in Eisenia fetida compared to Cd alone counterparts. The combined exposure also significantly elevated the SMX levels in the total body and fraction C compared with the SMX-only treated earthworms. Additionally, Eisenia fetida subjected to the combined treatment showed markedly increased activities of SOD, CAT, and MDA compared to those treated with Cd alone. The effect addition indices (EAIs), ranging from 1.00 to 2.23, unequivocally demonstrated a synergistic effect of the combined treatments. Interestingly, relocating the earthworms to clean soil did not mitigate the observed adverse effects. These findings underscore the increased risk posed by the Cd-SMX complex to terrestrial invertebrates in agricultural areas.

Autotrophic denitrification of NO for effectively recovering N2O through using thiosulfate as sole electron donor.

To reclaim nitrous oxide (N2O) as an energy resource economically, this study developed an autotrophic denitrification-based system with thiosulfate (S2O32-) and nitric oxide (NO) as electron donor and acceptor, respectively. NO from flue gases is absorbed on Fe(II)EDTA to overcome its low solubility in liquid phase by forming Fe(II)EDTA-NO. Short-term batch tests and long-term continuous experiments were conducted to investigate the N2O production profile and NO conversion efficiency from thiosulfate-based denitrification under varied Fe (II)EDTA-NO conditions (5-20 mM). Up to 39% of NO was converted to gaseous N2O at 20 mM Fe(II)EDTA-NO amid batch test due to the inhibition of key enzymatic activities by NO and the acidic conditions following thiosulfate oxidation. Higher Fe(II)EDTA-NO levels induced lower enzymatic activities with N2OR being suppressed harder than NOR. Microbial diversity was reduced in the continuous thiosulfate-driven Fe(II)EDTA-NO-based denitrification system. NO-resistant bacteria and sulfide-tolerant denitrifiers were enriched, facilitating NO conversion to N2O thereafter.

Sulfur-driven autotrophic denitrification of nitric oxide for efficient nitrous oxide recovery.

Nitrous oxide (N2 O) was previously deemed as a potent greenhouse gas but is actually an untapped energy source, which can accumulate during the microbial denitrification of nitric oxide (NO). Compared with the organic electron donor required in heterotrophic denitrification, elemental sulfur (S0 ) is a promising electron donor alternative due to its cheap cost and low biomass yield in sulfur-driven autotrophic denitrification. However, no effort has been made to test N2 O recovery from sulfur-driven denitrification of NO so far. Therefore, in this study, batch and continuous experiments were carried out to investigate the NO removal performance and N2 O recovery potential via sulfur-driven NO-based denitrification under various Fe(II)EDTA-NO concentrations. Efficient energy recovery was achieved, as up to 35.5%-40.9% of NO was converted to N2 O under various NO concentrations. N2 O recovery from Fe(II)EDTA-NO could be enhanced by the low bioavailability of sulfur and the acid environment caused by sulfur oxidation. The NO reductase (NOR) and N2 O reductase (N2 OR) were inhibited distinctively at relatively low NO levels, leading to efficient N2 O accumulation, but were suppressed irreversibly at NO level beyond 15 mM in continuous experiments. Such results indicated that the regulation of NO at a relatively low level would benefit the system stability and NO removal capacity during long-term system operation. The continuous operation of the sulfur-driven Fe(II)EDTA-NO-based denitrification reduced the overall microbial diversity but enriched several key microbial community. Thauera, Thermomonas, and Arenimonas that are able to carry out sulfur-driven autotrophic denitrification became the dominant organisms with their relative abundance increased from 25.8% to 68.3%, collectively.

Exosomal lncRNA HOTTIP Mediates Antiviral Effect of Tenofovir Alafenamide (TAF) on HBV Infection.

INTRODUCTION: Chronic hepatitis B (CHB) virus (HBV) infection has emerged as a global health burden affecting nearly 292 million people. Tenofovir alafenamide (TAF) is an effective treatment for CHB patients. However, the detailed mechanism underlying the antiviral activity of TAF remains unclear. METHODS: In this study, we investigated the antiviral effect of exosomes derived from the serum of CHB patients treated with TAF (Exo-serum) and TAF-treated macrophages (MP) (Exo-MP(TAF)). RESULTS: RNAseq analysis was also performed to determine the associated long non-coding RNAs (lncRNAs). The results demonstrated that both Exo-serum and Exo-MP(TAF) could be taken up by HepAD38 cells and exhibited potent antiviral activities, as manifested by significantly downregulating the levels of hepatitis B surface antigen, hepatitis B e antigen, HBV DNA, and covalently closed circular DNA. The antiviral effect of Exo-serum was more potent than those of TAF treatment alone. RNAseq analysis revealed that lncRNA HOTTIP was upregulated significantly in Exo-serum. Further, lncRNA HOTTIP knockdown reversed the antiviral effect of Exo-MP(TAF) on HepAD38 cells, whereas lncRNA HOTTIP knockdown exerted the opposite roles. DISCUSSION: Taken together, these results suggest that exosomal lncRNA HOTTIP is essential for the antiviral activity of TAF and provide a novel understanding of the exosome-mediated mechanism underlying HBV infection.

Role of digestive protease enzymes and related genes in host plant adaptation of a polyphagous pest, Spodoptera frugiperda.

The evolutionary success of phytophagous insects depends on their ability to efficiently exploit plants as a source of energy for survival. Herbivorous insects largely depend on the efficiency, flexibility, and diversity of their digestive physiology and sophistication of their detoxification system to use chemically diverse host plants as food sources. The fall armyworm, Spodoptera frugiperda (J.E. Smith), is a polyphagous pest of many commercially important crops. To elucidate the ability of this insect pest to adapt to host plant mechanisms, we evaluated the impact of primary (corn) and alternate (rice) host plants after 11 generations on gut digestive enzymatic activity and expression profiles of related genes. Results indicated that the total protease and class-specific trypsin- and chymotrypsin-like protease activity of S. frugiperda significantly differed among host plant treatments. The class-specific protease profiles greatly differed in S. frugiperda midguts upon larval exposure to different treatments with inhibitors compared with treatments without inhibitors. Similarly, the single and cumulative effects of the enzyme-specific inhibitors TLCK, TPCK, and E-64 significantly increased larval mortality and reduced larval growth/mass across different plant treatments. Furthermore, the quantitative reverse transcription polymerase chain reaction results revealed increased transcription of two trypsin (SfTry-3, SfTry-7) and one chymotrypsin gene (Sfchym-9), which indicated that they have roles in host plant adaptation. Knockdown of these genes resulted in significantly reduced mRNA expression levels of the trypsin genes. This was related to the increased mortality observed in treatments compared with the dsRED control. This result indicates possible roles of S. frugiperda gut digestive enzymes and related genes in host plant adaptation.

Biological Reduction of Nitric Oxide for Efficient Recovery of Nitrous Oxide as an Energy Source.

Chemical absorption-biological reduction based on Fe(II)EDTA is a promising technology to remove nitric oxide (NO) from flue gases. However, limited effort has been made to enable direct energy recovery from NO through production of nitrous oxide (N2O) as a potential renewable energy rather than greenhouse gas. In this work, the enhanced energy recovery in the form of N2O via biological NO reduction was investigated by conducting short-term and long-term experiments at different Fe(II)EDTA-NO and organic carbon levels. The results showed both NO reductase and N2O reductase were inhibited at Fe(II)EDTA-NO concentration up to 20 mM, with the latter being inhibited more significantly, thus facilitating N2O accumulation. Furthermore, N2O accumulation was enhanced under carbon-limiting conditions because of electron competition during short-term experiments. Up to 47.5% of NO-N could be converted to gaseous N2O-N, representing efficient N2O recovery. Fe(II)EDTA-NO reduced microbial diversity and altered the community structure toward Fe(II)EDTA-NO-reducing bacteria-dominated culture during long-term experiments. The most abundant bacterial genus Pseudomonas, which was able to resist the toxicity of Fe(II)EDTA-NO, was significantly enriched, with its relative abundance increased from 1.0 to 70.3%, suggesting Pseudomonas could be the typical microbe for the energy recovery technology in NO-based denitrification.

Revisiting Microplastics in Landfill Leachate: Unnoticed Tiny Microplastics and Their Fate in Treatment Works.

Due to the environmental risks caused by microplastics, understanding the sources and characteristics of microplastics and cutting off their routes into the environment are crucial. However, so far, studies on microplastics in the landfill leachate system (a major pathway of microplastics into the environment) are still limited, especially for tiny particles <50 µm that might have higher risks to the environment. This study investigated the microplastics in landfill leachate and in leachate treatment works, with a size detection limit down to 10 µm. The results showed that the microplastics particle and mass concentrations in the untreated leachate were 235.4 ± 17.1 item/L and 11.4 ± 0.8 µg/L, respectively, with tiny particles (<50 µm) accounting for over 50%. Overall, 27 polymeric materials were detected in leachate samples, with polyethylene and polypropylene being the most abundant in the untreated leachate. The neutral buoyancy of microplastics (average density: 0.94 g/cm3), together with irregular shapes, suggested they may be difficult to be removed by sedimentation. Further exploring the fate of microplastics in leachate treatment works showed that the membrane treatment effectively reduced microplastics loading to 0.14% for particle and 0.01% for mass, but the average particle density rose. The differences in polymeric materials distribution at different sampling locations and the presence of membrane-related polymer in membrane treatment effluent suggested tiny microplastics could be generated and released from membrane systems. Moreover, this study discovered that the sludge dewatering liquor could contain a high amount of microplastics, and the estimated particle loading was about 3.6 times higher than that in dewatered sludge. This suggested a new approach to microplastics mitigation through separating microplastics from the sludge dewatering liquor before its recirculation.

Intercropping Rosemary (Rosmarinus officinalis) with Sweet Pepper (Capsicum annum) Reduces Major Pest Population Densities without Impacting Natural Enemy Populations.

Intercropping of aromatic plants provides an environmentally benign route to reducing pest damage in agroecosystems. However, the effect of intercropping on natural enemies, another element which may be vital to the success of an integrated pest management approach, varies in different intercropping systems. Rosemary, Rosmarinus officinalis L. (Lamiaceae), has been reported to be repellent to many insect species. In this study, the impact of sweet pepper/rosemary intercropping on pest population suppression was evaluated under greenhouse conditions and the effect of rosemary intercropping on natural enemy population dynamics was investigated. The results showed that intercropping rosemary with sweet pepper significantly reduced the population densities of three major pest species on sweet pepper, Frankliniella intonsa, Myzus persicae, and Bemisia tabaci, but did not affect the population densities of their natural enemies, the predatory bug, Orius sauteri, or parasitoid, Encarsia formosa. Significant pest population suppression with no adverse effect on released natural enemy populations in the sweet pepper/rosemary intercropping system suggests this could be an approach for integrated pest management of greenhouse-cultivated sweet pepper. Our results highlight the potential of the integration of alternative pest control strategies to optimize sustainable pest control.

Rosmarinus officinialis L. (Lamiales: Lamiaceae), a Promising Repellent Plant for Thrips Management.

A number of thrips species are among the most significant agricultural pests globally. Use of repellent intercrop plants is one of the key components in plant-based 'push-pull' strategies to manage pest populations. In this study, the behavioral responses of three thrips species, Frankliniella occidentalis (Pergande), Frankliniella intonsa (Trybom), and Thrips palmi Karny (Thysanoptera: Thripidae) to Rosmarinus officinalis were investigated in Y-tube olfactometer bioassays and cage experiments. In addition, the major volatile compounds from rosemary were identified and the effect of the individual compounds on thrips behavior was evaluated. Females and males of the three thrips species were significantly repelled by the volatiles from cut rosemary leaves. The presence of rosemary plants significantly reduced settlement of females of the three thrips species and eggs laid by F. occidentalis females on target host plants. In total, 47 compounds were identified in the volatiles collected from the cut leaves of rosemary plants. The responses of the three thrips species to 10 major volatile compounds showed significant differences. However, α-pinene, the most abundant volatile, was repellent to F. occidentalis and F. intonsa. Eucalyptol, the second most abundant volatile, showed significant repellent activity to all the three thrips species. Our findings showed that rosemary is a promising repellent plant against the three thrips pests we tested, which could be a good candidate for 'push' plants in plant-based 'push-pull' strategies. The identified volatile compounds that accounted for the repellent activity could be developed as repellents for sustainable thrips management.

Preparation and textural properties of white salted noodles made with hard red winter wheat flour partially replaced by different levels of cross-linked phosphorylated RS4 wheat starch.

BACKGROUND: Resistant starch (RS) has health benefits and can be used as a functional ingredient in various food products. Kansas hard red winter (HRW) wheat is conventionally used for bread making and this is attributed to its strong gluten network. To develop Asian white salted noodles with a high RS content, HRW wheat flour was partially replaced with cross-linked phosphorylated RS4 wheat starch. Vital wheat gluten or wheat protein isolate was added to compensate for textural changes due to the addition of RS. RESULTS: The maximum recommended level of RS4 starch to replace HRW wheat flour was 40%. The substitution of 10-40 parts of RS4 for flour did not change hardness in cooked noodles but it did reduce their extensibility, cohesiveness, and springiness, which was probably due to the non-swelling properties of RS4. At 40 parts of RS4 replacement, supplementation of 2-8 parts of vital wheat gluten or wheat protein isolate in the composite flour notably enhanced the hardness and extensibility of cooked noodles, whereas cohesiveness and springiness were minimally affected. Supplemental vital wheat gluten produced a thicker protein network than endogenous protein or added wheat protein isolate, giving cooked noodles greater breaking force and distance. CONCLUSION: RS4 could be used as a functional ingredient to replace up to 40% of hard wheat flour for making Asian noodles while maintaining their hardness after cooking. The extensibility of cooked noodles with high RS4 could be noticeably enhanced by supplementation with vital wheat gluten in the composite flour (RS/flour = 40/60). © 2020 Society of Chemical Industry.

Activating PPARγ Increases NQO1 and γ-GCS Expression via Nrf2 in Thrombin-activated Microglia.

The present study aimed to explore the molecular mechanisms underlying the increase of nicotinamide adenine dinucleotide phosphate:quinine oxidoreductase 1 (NQO1) and γ-glutamylcysteine synthetase (γ-GCS) in brain tissues after intracerebral hemorrhage (ICH). The microglial cells obtained from newborn rats were cultured and then randomly divided into the normal control group (NC group), model control group (MC group), rosiglitazone (RSG) intervention group (RSG group), retinoic-acid intervention group (RSG+RA group), and sulforaphane group (RSG+SF group). The expression levels of NQO1, γ-GCS, and nuclear factor E2-related factor 2 (Nrf2) were measured by real-time polymerase chain reaction (RT-PCR) and Western blotting, respectively. The results showed that the levels of NQO1, γ-GCS and Nrf2 were significantly increased in the MC group and the RSG group as compared with those in the NC group (P<0.01). They were found to be markedly decreased in the RSG+RA group and increased in the RSG+SF group when compared with those in the MC group or the RSG group (P<0.01). The RSG+SF group displayed the highest levels of NQO1, γ-GCS, and Nrf2 among the five groups. In conclusion, a medium dose of RSG increased the anti-oxidative ability of thrombin-activated microglia by increasing the expression of NQO1 and γ-GCS. The molecular mechanisms underlying the increase of NQO1 and γ-GCS in thrombin-activated microglia may be associated with the activation of Nrf2.

Relationships among resistin, adiponectin, and leptin and microvascular complications in patients with type 2 diabetes mellitus.

OBJECTIVE: To investigate the relationships among serum resistin, adiponectin, and leptin and microvascular complications in patients with type 2 diabetes mellitus (T2DM). METHODS: A total of 120 patients with T2DM were divided into non-microangiopathy and microangiopathy groups. Sixty age- and sex-matched healthy subjects were used as a normal control (NC) group. Body height, body mass, waist circumference, and blood pressure were determined, and waist/hip ratio (WHR), body mass index, blood glucose, lipids, resistin, leptin, adiponectin, free fatty acids (FFA), high-sensitivity C-reactive protein (hs-CRP), fasting insulin, hemoglobin A1c, and homeostatic model assessment of insulin resistance (HOMA-IR) were compared among the three groups. RESULTS: Serum levels of resistin, leptin, FFA, and hs-CRP were significantly higher and levels of adiponectin were significantly lower in patients in the non-microangiopathy (n = 60) and microangiopathy groups (n = 60) compared with the NC group (n = 60). Serum resistin and leptin levels in patients with T2DM were positively correlated with WHR, hs-CRP, FFA, HOMA-IR, and triglycerides, but negatively correlated with high-density lipoprotein-cholesterol (HDL-C). Serum adiponectin levels in patients with T2DM were negatively correlated with WHR, hs-CRP, FFA, HOMA-IR, and triglycerides, but positively correlated with HDL-C. CONCLUSION: Serum resistin, adiponectin, and leptin levels correlate with the occurrence of T2DM and microvascular complications.

Silencing lncRNA TUG1 Alleviates LPS-Induced Mouse Hepatocyte Inflammation by Targeting miR-140/TNF.

Hepatitis is a major public health problem that increases the risk of liver cirrhosis and liver cancer. Numerous studies have revealed that long non-coding RNAs (lncRNAs) exert essential function in the inflammatory response of multiple organs. Herein, we aimed to explore the effect of lncRNA TUG1 in LPS-induced hepatocyte inflammation response and further illuminate the underlying mechanisms. Mice were intraperitoneally injected with LPS, and the liver inflammation was evaluated. Microarray showed that lncRNA TUG1 was upregulated in LPS-induced hepatocyte inflammation. qRT-PCR and immunofluorescence assay indicated a significant increase of TUG1 in mice with LPS injection. Functional analysis showed that si-TUG1 inhibited LPS-induced inflammation response in mice liver, inhibited apoptosis level, and protected liver function. Then, we knock down TUG1 in normal human hepatocyte AML12. Consistent with in vivo results, si-TUG1 removed the injury of LPS on AML12 cells. Furthermore, TUG1 acted as a sponge of miR-140, and miR-140 directly targeted TNFα (TNF). MiR-140 or si-TNF remitted the beneficial effects of TUG1 on LPS-induced hepatocyte inflammation response both in vitro and in vivo. Our data revealed that deletion of TUG1 protected against LPS-induced hepatocyte inflammation via regulating miR-140/TNF, which might provide new insight for hepatitis treatment.

GSTO1 regards as a meritorious regulator in cutaneous malignant melanoma cells.

BACKGROUND: Glutathione S-transferase omega 1 (GSTO1), as a member of the glutathione S-transferase (GST) family genes, has been discovered to be up-regulated in several cancer cell lines which exhibited strong aggressiveness. However, the function of GSTO1 on cutaneous malignant melanoma (CMM) has not been illuminated. METHODS: Outcome of expression level and prognosis of GSTO1 were obtained from Oncomine and TCGA database. The specific effects of GSTO1 on the characteristics and regulatory mechanism of CMM cells were demonstrated by cell counting kit-8, colony formation, flow cytometry, and transwell assays in vitro. Western blot was employed to analyze the expression of proliferating cell nuclear antigen (PCNA), p53 and epithelial-to-mesenchymal (EMT) related proteins. RESULTS: We observed that GSTO1 was up-regulated in CMM samples when compared with the corresponding controls. Moreover, patients in CMM with high expression of GSTO1 were more likely to have a poor prognosis. Through in vitro experiments, silenced GSTO1 resulted in inhibition of CMM cells growth and aggressiveness, increased cell apoptosis, and blocked cell cycle. Finally, the expression of PCNA, p53 and EMT-related proteins were changed due to reduction of GSTO1. CONCLUSIONS: To sum up, our outcomes exhibited that weakening GSTO1 reduced the proliferation and mobility of CMM cells, increased the apoptosis ability of CMM cells, and arrested cell cycle at G1 phase, which can be achieved by affecting the expression of PCNA, p53 and the EMT process. This discovery provided a new perspective for elucidating the mechanism of CMM, and offered theoretical support for searching clinical therapeutic targets in the future.

Id-1 expression in colorectal adenocarcinoma tissues and its clinical significance.

BACKGROUND: This study aims to investigate the expression of Id-1 in human colorectal adenocarcinoma tissues and explore its correlation with the clinical pathological parameters of colorectal cancer. METHODS: The Id-1 mRNA and protein expression levels of 50 specimens of normal colorectal tissues and 50 specimens of colorectal adenocarcinoma tissues were detected using reverse-transcription polymerase chain reaction and western blot. Furthermore, Id-1 protein was detected using immunohistochemistry. The correlation between the expression of Id-1 and clinicopathologic features was analyzed. RESULTS: The mRNA expression level of Id-1 in colorectal adenocarcinoma tissues and normal colorectal tissues was 0.96 ± 0.03 vs. 0.20 ± 0.04, respectively; and the difference was statistically significant (P=0.011). Furthermore, Id-1 protein expression was higher in colorectal adenocarcinoma tissues than in normal colorectal tissues (0.82 ± 0.04 vs. 0.31 ± 0.02, P=0.020). In addition, the positive protein expression rate of Id-1 was higher in colorectal adenocarcinoma tissues than in normal colorectal tissues (72.00% vs. 24.00%, X2=23.431, P=0.000). The expression of Id-1 was correlated with the depth of tumor invasion, TNM stage, lymph node metastasis, vessel invasion, and liver metastasis (P<0.01). However, this expression was not correlated with tumor size and differentiation degrees (P>0.05). CONCLUSIONS: The high Id-1 expression in colorectal adenocarcinoma tissues play an important role in the process of cancer, and is expected to become a new tumor monitoring indicator for clinical diagnosis, treatment, and prognosis judgment.

A study of the impact of inhibitors of DNA binding-1 on proliferation and migration in human colon carcinoma cells.

This study aims to explore the effect of an inhibitor of DNA binding-1 (Id-1) on the proliferation and migration of human colon carcinoma cell line SW480 and HT-29. SW480 and HT-29 cells transfected with Id-1-interference sequence were assigned to the experimental groups (inhibition groups 1 and 2), and SW480 and HT-29 cells with blank interference sequence (blank groups) and blank load transfection (blank load groups) were assigned as the control groups. The expression of Id-1 in six groups was detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. Cell proliferation in vitro was assessed by MTT assay. RT-PCR and Western blot results demonstrated that the mRNA and protein expressions of Id-1 in the inhibition group 1 were lower than those in the blank group 1 and blank load group 1. RT-PCR and Western blot results revealed that the mRNA and protein expressions of Id-1 were lower in the inhibition group 2 than in the blank group 2 and blank load group 2. The results of the growth curve revealed that proliferation ability was significantly weaker from the third day in the inhibition groups 1 and 2 than in the blank group and blank load group. Transwell chamber experiment and Matrigel invasion assay revealed that the number of Transwell cells significantly decreased in the inhibition groups 1 and 2 than in the blank groups and blank load groups (P < 0.01). Id-1 significantly promotes the proliferation and migration of human colon carcinoma cell lines SW480 and HT-29.

Id-1 expression in colorectal adenocarcinoma tissues and its clinical significance

SUMMARY BACKGROUND: This study aims to investigate the expression of Id-1 in human colorectal adenocarcinoma tissues and explore its correlation with the clinical pathological parameters of colorectal cancer. METHODS: The Id-1 mRNA and protein expression levels of 50 specimens of normal colorectal tissues and 50 specimens of colorectal adenocarcinoma tissues were detected using reverse-transcription polymerase chain reaction and western blot. Furthermore, Id-1 protein was detected using immunohistochemistry. The correlation between the expression of Id-1 and clinicopathologic features was analyzed. RESULTS: The mRNA expression level of Id-1 in colorectal adenocarcinoma tissues and normal colorectal tissues was 0.96 ± 0.03 vs. 0.20 ± 0.04, respectively; and the difference was statistically significant (P=0.011). Furthermore, Id-1 protein expression was higher in colorectal adenocarcinoma tissues than in normal colorectal tissues (0.82 ± 0.04 vs. 0.31 ± 0.02, P=0.020). In addition, the positive protein expression rate of Id-1 was higher in colorectal adenocarcinoma tissues than in normal colorectal tissues (72.00% vs. 24.00%, X2=23.431, P=0.000). The expression of Id-1 was correlated with the depth of tumor invasion, TNM stage, lymph node metastasis, vessel invasion, and liver metastasis (P<0.01). However, this expression was not correlated with tumor size and differentiation degrees (P>0.05). CONCLUSIONS: The high Id-1 expression in colorectal adenocarcinoma tissues play an important role in the process of cancer, and is expected to become a new tumor monitoring indicator for clinical diagnosis, treatment, and prognosis judgment.

RESUMO OBJETIVO: O objetivo deste estudo é investigar a expressão de Id-1 em tecidos de adenocarcinoma colorretal em humanos e investigar sua correlação com os parâmetros patológicos clínicos de câncer colorretal. MÉTODOS: Os níveis de expressão de proteína e mRNA Id-1 em 50 amostras de tecido colorretal normal e 50 amostras de tecido de adenocarcinoma colorretal foram detectados através de reação em cadeia de polimerase precedida de transcrição reversa e western blot. Além disso, a proteína Id-1 foi detectada através de imuno-histoquímica. A correlação entre a expressão de Id-1 e características clínico-patológicas foi analisada. RESULTADOS: O nível de expressão de mRNA Id-1 em tecidos de adenocarcinoma colorretal e tecidos colorretais normais foi de 0,96 ± 0,03 versus 0,20 ± 0,04, respectivamente; a diferença foi estatisticamente significativa (P= 0,011). Além disso, a expressão da proteína Id-1 foi maior em tecidos de adenocarcinoma colorretal do que em tecidos colorretais normais (0,82 ± 0,04 versus 0,31 ± 0,02, P= 0,020). Além disso, a taxa de expressão positiva de proteínas Id-1 foi maior em tecidos de adenocarcinoma colorretal do que em tecidos colorretais normais (72,00% vs. 24,00%, X2=23,431, p=0,000). A expressão de Id-1 foi correlacionada com a profundidade da invasão tumoral, estágio TNM, metástases linfonodais, invasão vascular e metástase hepática (P<0,01). Todavia, essa expressão não se correlacionou com o tamanho do tumor e graus de diferenciação (P>0,05). CONCLUSÃO: A alta expressão de Id-1 em tecidos de adenocarcinoma colorretal desempenham um importante papel no processo do câncer, e é esperado que se torne um novo indicador de monitoramento de tumores para o diagnóstico clínico, tratamento e estimativa de prognóstico.

Long noncoding RNA HOTAIR silencing inhibits invasion and proliferation of human colon cancer LoVo cells via regulating IGF2BP2.

Colon cancer is one of the most life-threatening malignancies worldwide. Long noncoding RNA (lncRNA) HOX transcript antisense RNA (HOTAIR) is a cancer-associated biomarker involved in the metastasis and prognosis of several cancers. However, whether and how HOTAIR affects colon cancer progression is still unclear. Consequently, we used RNA interference to knock down HOTAIR to explore its effects on human colon cancer cells. The dual luciferase reporter gene assay was initially used for testify the regulating relationship between lncRNA HOTAIR and insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2). We determined the expressions of HOTAIR, IGF2BP2, E-cadherin, and vimentin. Meanwhile, cell growth, cycle and apoptosis, migration, and invasion were assayed. LoVo cells were transplanted into nude mice, and tumor formation and microvessel density were evaluated. LncRNA HOTAIR positively regulated IGF2BP2. Besides, the expressions of HOTAIR and E-cadherin and the apoptosis were increased, while the expressions of IGF2BP2 and vimentin, the growth, invasion and migration of LoVo cells, the average tumor weight, and microvessel density value were decreased. Of importance, overexpressed IGF2BP2 could reverse the above impacts. Taken together, the current study indicates that silencing of HOTAIR could inhibit the invasion, proliferation, and migration, and promote apoptosis of colon cancer LoVo cells through suppressing IGF2BP2 and the epithelial-mesenchymal transition.

Evaluation of Vascular Remodeling in Carotid Atherosclerosis Among Type 2 Diabetes Mellitus Patients Using High-Frequency Ultrasonography Combined with Serum Resistin.

Diabetes remains a long standing public health issue among the Chinese population, with an incidence of up to 11.6%, of which type 2 diabetes mellitus (T2DM) accounts for 85%-95%. During this study, we aimed to elucidate the value of high-frequency ultrasonography (HFUS) combined with serum resistin on vascular remodeling (VR) in carotid atherosclerosis (CA) among patients suffering from T2DM. A total of 432 T2DM were recruited and assigned into the short T2DM duration group (<5 years), middle T2DM duration group (5~10 years) and long T2DM duration group (>10 years), while another 172 healthy cases were recruited as the control group. The intima-media thickness (IMT) as well as plaque score, detection rate and type were detected by the HFUS. The respective blood pressure readings were measured and pulse pressure was calculated accordingly. The serum resistin level, remodeling incidence and type, levels of total cholesterol (TC), fasting blood glucose (FBG), low-density lipoprotein cholesterol (LDL-C), high-density liproprotein cholesterol (HDL-C), and triglyceride (TG) were measured. The correlation between IMT, the plaque detection rate and blood pressure were analyzed. A receiver operating characteristic (ROC) curve was constructed in order to evaluate the impact of VR in CA on T2DM patients who were solely using HFUS and serum resistin respectively, as well as a combination of HFUS with serum resistin. As In comparison with the control group, the short, middle and long T2DM duration groups all displayed increased IMT, plaque score and detection rate, serum resistin level and VR incidence, especially for the long T2DM duration group. Levels of TC, TG, FBG and LDL-C were much higher while HDL-C was lower among patients with T2DM than those in the control group. A positive correlation was detected between the disease course and IMT. The detection rate of plaque with thickening IMT exhibited upregulated levels when compared to those with normal IMT. The HFUS, serum resistin and HFUS combined with serum resistin respective areas under the ROC curve were 0.873, 0.867 and 0.923, respectively, suggesting that the combination of HFUS and serum resistin was superior to that of individual HFUS or individual serum resistin in regard to the impact of VR in CA on T2DM patients. The results of this study revealed that the combination of HFUS and serum resistin was superior to individual HFUS or individual serum resistin in relation to its ability to evaluate the impact of VR in CA in patients with T2DM.