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Aims: To assess the excess risk of cardiovascular disease (CVD) associated with different criteria for metabolic health, and the interplay of body size, insulin sensitivity and metabolic health with CVD risk. Materials and Methods: We conducted a prospective study involving 115 638 participants from the China Cardiometabolic Disease and Cancer Cohort (4C) Study. Metabolic health was defined using three different definitions: (1) insulin sensitivity defined by homeostatic model assessment of insulin resistance index; (2) absence of metabolic syndrome according to the National Cholesterol Education Program Adult Treatment Panel III criteria; and (3) simultaneous absence of metabolic abnormalities (diabetes, hypertension, dyslipidaemia). The primary endpoint was a composite of incident CVD events comprising the first occurrence of myocardial infarction, stroke, heart failure, or cardiovascular death. Results: During a mean 3.61‐year follow‐up period, obese individuals with insulin sensitivity (multivariable‐adjusted hazard ratio [HR] 1.69, 95% confidence interval [CI] 1.37–2.08), or without metabolic syndrome (HR 1.46, 95% CI 1.13–1.89) still exhibited increased CVD risks, when compared to their normal‐weight counterparts. Otherwise, those with obesity but simultaneous absence of metabolic abnormalities demonstrated similar CVD risk compared to normal‐weight individuals (HR 0.91, 95% CI 0.53–1.59). CVD risk increased with the number of abnormalities across body mass index categories, regardless of insulin sensitivity. Conclusions: This study emphasizes the need for refined definitions of metabolic health and advocates for meticulous screening for metabolic abnormalities to reduce cardiovascular risks, even in individuals with normal weight and insulin sensitivity. [ABSTRACT FROM AUTHOR]

Tomatoes are frequently challenged by various pathogens, among which Phytophthora capsici (P. capsici) is a destructive soil‐borne pathogen that seriously threatens the safe production of tomatoes. Plant growth‐promoting rhizobacteria (PGPR) positively induced plant resistance against multiple pathogens. However, little is known about the role and regulatory mechanism of PGPR in tomato resistance to P. capsici. Here, we identified a new strain Serratia plymuthica (S. plymuthica), HK9‐3, which has a significant antibacterial effect on P. capsici infection. Meanwhile, stable colonization in roots by HK9‐3, even under P. capsici infection, improved tomato growth parameters, root system architecture, photosynthetic capacity, and boosted biomass. Importantly, HK9‐3 colonization significantly alleviated the damage caused by P. capsici infection through enhancing ROS scavenger ability and inducing antioxidant defense system and pathogenesis‐related (PR) proteins in leaves, as evidenced by elevating the activities of peroxidase (POD), superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), phenylalanine ammonia lyase (PAL), polyphenol oxidase (PPO), and chitinase, β‐1,3‐glucanase, and increasing the transcripts of POD, SOD, CAT, APX1, PAL1, PAL2, PAL5, PPO2, CHI17 and β‐1,3‐glucanase genes. Notably, HK9‐3 colonization not only effectively improved soil microecology and soil fertility, but also significantly enhanced fruit yield by 44.6% and improved quality. Our study presents HK9‐3 as a promising and effective solution for controlling P. capsici infection in tomato cultivation while simultaneously promoting plant growth and increasing yield, which may have implications for P. capsici control in vegetable production. [ABSTRACT FROM AUTHOR]

Hollow polymer microfibers with variable microstructural and hydrophilic properties were proposed as building elements to create axon‐mimicking phantoms for validation of diffusion tensor imaging (DTI). The axon‐mimicking microfibers were fabricated in a mm‐thick 3D anisotropic fiber strip, by direct jet coaxial electrospinning of PCL/polysiloxane‐based surfactant (PSi) mixture as shell and polyethylene oxide (PEO) as core. Hydrophilic PCL‐PSi fiber strips were first obtained by carefully selecting appropriate solvents for the core and appropriate fiber collector rotating and transverse speeds. The porous cross‐section and anisotropic orientation of axon‐mimicking fibers were then quantitatively evaluated using two ImageJ plugins—nearest distance (ND) and directionality based on their scanning electron microscopy (SEM) images. Third, axon‐mimicking phantom was constructed from PCL‐PSi fiber strips with variable porous‐section and fiber orientation and tested on a 3T clinical MR scanner. The relationship between DTI measurements (mean diffusivity [MD] and fractional anisotropy [FA]) of phantom samples and their pore size and fiber orientation was investigated. Two key microstructural parameters of axon‐mimicking phantoms including normalized pore distance and dispersion of fiber orientation could well interpret the variations in DTI measurements. Two PCL‐PSi phantom samples made from different regions of the same fiber strips were found to have similar MD and FA values, indicating that the direct jet coaxial electrospun fiber strips had consistent microstructure. More importantly, the MD and FA values of the developed axon‐mimicking phantoms were mostly in the biologically relevant range. [ABSTRACT FROM AUTHOR]

Saikosaponin‐D (SSD), an active ingredient in Bupleurum chinense, exerts anticancer effects in various cancers by inhibiting cancer proliferation and inducing apoptosis. However, whether SSD can induce other forms of cell death is unknown. The current study aims to demonstrate that SSD can induce pyroptosis in non‐small‐cell lung cancer. In this study, HCC827 and A549 non‐small‐cell lung cancer cells were treated with different concentrations of SSD for 1.5 h. HE and TUNEL staining were used to verify cell damage caused by SSD. Immunofluorescence and western blotting were performed to verify the effect of SSD on the NF‐κB/NLRP3/caspase‐1/gasdermin D (GSDMD) pathway. Changes in inflammatory factors were detected by ELISAs. Finally, the reactive oxygen species (ROS) scavenger N‐acetylcysteine (NAC) was introduced to verify that SSD induces pyroptosis through the ROS/NF‐κB pathway. The results of the HE and TUNEL staining showed that SSD resulted in balloon‐like swelling of NSCLC cells accompanied by increased DNA damage. Immunofluorescence and western blot assays confirmed that SSD treatment activated the NLRP3/caspase‐1/GSDMD pathway, stimulated an increase in ROS levels and activated NF‐κB in lung cancer cells. The ROS scavenger N‐acetylcysteine significantly attenuated SSD‐induced NF‐κB/NLRP3/caspase‐1/GSDMD pathway activation and inhibited the release of the inflammatory cytokines IL‐1β and IL‐18. In conclusion, SSD induced lung cancer cell pyroptosis by inducing ROS accumulation and activating the NF‐κB/NLRP3/caspase‐1/GSDMD pathway. These experiments lay the foundation for the application of SSD in the treatment of non‐small‐cell lung cancer and regulation of the lung cancer immune microenvironment. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Diabetes is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Evidence regarding the impact of education on diabetes risk is scarce in developing countries. We aimed to explore the association between education and diabetes within a large population in China and to identify the possible mediators between them. Methods: Information on educational level and lifestyle factors was collected through questionnaires. Diabetes was diagnosed from self‐report and biochemical measurements. A structural equation model was constructed to quantify the mediation effect of each mediator. Results: Compared with their least educated counterparts, men with college education had a higher risk of diabetes (odds ratio [OR] 1.19; 95% confidence interval [CI], 1.12–1.27), while college‐educated women were less likely to have diabetes (OR 0.77; 95% CI, 0.73–0.82). Obesity was the strongest mediator in both genders (proportion of mediation: 11.6% in men and 23.9% in women), and its association with education was positive in men (β[SE] 0.0387 [0.0037]) and negative in women (β[SE] −0.0824 [0.0030]). Taken together, all behavioral factors explained 12.4% of the excess risk of diabetes in men and 33.3% in women. Conclusions: In a general Chinese population, the association between education level and diabetes was positive in men but negative in women. Obesity was the major mediator underlying the education disparities of diabetes risk, with a stronger mediation effect among women. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Diabetes is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Diabetes is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Dysbiosis of the laryngeal microbiota has been demonstrated to the development of head and neck squamous cell carcinoma (HNSCC), but the association of Fusobacterium and Fusobacterium nucleatum (F. nucleatum) with DNA mismatch repair (MMR) and microsatellite instability (MSI) has not been investigated. Methods: The abundance of Fusobacterium and F. nucleatum, the status of deficient MMR (dMMR) and MSI, and MMR‐related gene expression were analyzed in 171 HNSCC tissues, 61 paired para‐tumor tissues, and 60 vocal cord polyp tissues. The molecular mechanism of F. nucleatum and MMR‐related gene expression were investigated in two human HNSCC cell lines (Tu 686 and FD‐LSC‐1). Results: Our results demonstrated that a high Fusobacterium abundance was detected in the HNSCC tissues and was exaggerated in the recurrent patients. We further found that a high Fusobacterium abundance was detected in the HNSCC tissues with dMMR and MSI. The Fusobacterium abundance was negatively correlated with the expression of MLH1, MSH2, and MSH6 in the HNSCC tissues. The Fusobacterium abundance was closely associated with the F. nucleatum abundance in the HNSCC tissues. F. nucleatum increased miR‐205‐5p expression to suppress MLH1, MSH2, and MSH6 expression via the TLR4‐ and MYD88‐dependent innate immune signaling pathway, resulting in dMMR, DNA damage, and cell proliferation in HNSCC. Conclusions: F. nucleatum impacts HNSCC epigenetic changes in tissues with dMMR to promote DNA damage and cell proliferation by suppressing MMR‐related gene expression via the TLR4/MYD88/miR‐205‐5p signaling pathway, which is valuable in the development of efficient strategies for HNSCC prevention and treatment. LAY SUMMARY: This study clearly indicates that Fusobacterium induced head and neck squamous cell carcinoma (HNSCC) aggressiveness to affect poor prognosis in HNSCC patients by epigenetic alteration of DNA mismatch repair (MMR) and microsatellite instability. Moreover, the research has shown that Fusobacterium nucleatum (F. nucleatum) impacts HNSCC epigenetic changes in tissues with deficient MMR to promote DNA damage and cell proliferation by suppressing MMRrelated gene expression via the TLR4/MYD88/miR‐205‐5p signaling pathway. [ABSTRACT FROM AUTHOR]

In the past decade, self‐healing polymer materials, being researched and utilized in many fields, have attracted more and more attention. In this work, self‐healing siloxane elastomer (SPUR) with flexible cross‐linked networks were designed through the reaction of amino‐functionalized polyether, isocyanate and α‐siloxane, which endowed elastomer with intermolecular hydrogen bond. Herein, these hydrogen bonds can break and reorganize via a simple thermal treatment to gain self‐healing and post‐processing actions. The self‐healing performance of the elastomer is confirmed through tensile test and SEM surface analysis. Consistent with our experiments, the researches show that siloxane modified polyurea elastomers (SPUR) congaing higher content of amino‐functionalized polyether with 2000 molecular weights (PEA20) show much better flexibility and healing efficiency. Also, the polyurea can be quickly cured without any metal catalyst due to the presence of α‐siloxane, which is a highlight of this article, and it is better than the related literature reported so far. Through tensile test and healing performance test, SPUR1 possessing the both remarkable strength and elasticity was obtained (elongation at break 530 %, tensile stress 5.26 MPa). In addition, it has relatively satisfied healing efficiency 30 % and excellent thermal stability. In view of such intermolecular hydrogen bond, we have developed a special self‐healing polymer material with tunable performance by varying the monomer ratio between amino‐functionalized polyether PEA9 (the molecular weight Mn=900 Da) and PEA20 (Mn=2000 Da). A variety of self‐healing polymer materials can be lightly synthesized on account of the wide extent of commercial activities of raw materials such as primary amine, silane and isocyanate. Therefore, self‐healable polymer elastomers are exceptionally popular in a rank of fields, such as coatings, construction, aerospace, flexible electronics, automobile, medical device and lithium‐ion batteries. [ABSTRACT FROM AUTHOR]

This article, titled "Front Cover," is based on a study conducted in China called the China Cardiometabolic Disease and Cancer Cohort (4C) study. The study examines the relationship between body size, insulin sensitivity, metabolic health, and the risk of cardiovascular disease in Chinese adults. The study involved a large number of participants and provides insights into these important health factors. The article is authored by a diverse group of researchers and provides valuable information for individuals conducting research on these topics. [Extracted from the article]

Loss of nephron primary cilia due to disruption of the Ift88 gene results in sex‐ and age‐specific phenotypes involving renal cystogenesis, blood pressure (BP) and urinary Na+ excretion. Previous studies demonstrated that male mice undergoing induction of nephron‐specific Ift88 gene disruption at 2 months of age developed reduced BP and increased salt‐induced natriuresis when pre‐cystic (2 months post‐induction) and became hypertensive associated with frankly cystic kidneys by 9 months post‐induction; in contrast, female Ift88 KO mice manifested no unique phenotype 2 months post‐induction and had mildly reduced BP 9 months post‐induction. The current study utilized these Ift88 KO mice to investigate associated changes in renal Na+ transporter and channel protein expression. At 2 months post‐induction, pre‐cystic male Ift88 KO mice had reduced high salt diet associated total NKCC2 levels while female mice had no alterations in Na+ transporters or channels. At 9 months post‐induction, cystic male Ift88 KO mice had increased total and phosphorylated NHE3 levels together with reduced NKCC2, phosphorylated and/or total NCC, and ENaC‐α expression on normal and high salt diets. In contrast, female Ift88 KO mice at 9 months post‐induction had no changes in Na+ transporters or channels beyond an increase in phosphorylated‐NCC during high salt intake. Thus, reduced BP in pre‐cystic, and elevated BP in renal cystic, male Ift88 KO mice are associated with unique sex‐dependent changes in nephron Na+ transporter/channel expression. [ABSTRACT FROM AUTHOR]

Background: Gestational hyperglycemia increases the risk of diabetes in later life. However, the risk of future cardiovascular diseases (CVD) related to gestational hyperglycemia remains inconclusive. The purpose of this study was to investigate the impact of gestational hyperglycemia on the subsequent risk of CVD and its modifying factors among elderly Chinese women. Methods: We conducted a case‐control study of elderly women from the baseline survey of Risk Evaluation of cAncers in Chinese diabeTic Individuals: a lONgitudinal (REACTION) study. Women with gestational hyperglycemia (n = 82), and controls matched by age and study site (n = 410) were included. Information on CVD, including reported coronary heart disease, stroke, or myocardial infarction, was collected through an interviewer‐assisted questionnaire. Results: Women with gestational hyperglycemia were more likely to develop diabetes (odds ratio [OR], 2.51; 95% confidence interval [CI], 1.50‐4.18) and CVD (OR, 1.98; 95% CI, 1.05‐3.74). Even without progressing to type 2 diabetes, gestational hyperglycemia was associated with an increased risk of CVD (OR, 2.88; 95% CI, 1.18‐7.00). However, subgroup analysis indicated that compared with those without gestational hyperglycemia or hypertension, women with both gestational hyperglycemia and hypertension had higher risk of CVD (OR, 3.98; 95% CI, 1.65‐9.58), whereas the risk estimate did not significantly change in women with gestational hyperglycemia alone (OR, 2.15; 95% CI, 0.71‐6.57). Stratified analysis indicated that among those with overweight/obesity, inactive physical activity, or unhealthy dietary habits, gestational hyperglycemia increased the risk of CVD. Conclusions: In elderly Chinese women, gestational hyperglycemia was associated with an increased risk of CVD in later life. This association was independent of the progression to diabetes and might be modified by lifestyle factors and hypertension. [ABSTRACT FROM AUTHOR]

Arundinaria gigantea commonly referred to as giant cane (GC) shows potential to be a sustainable, renewable, and low‐cost source for natural cellulose fibers and biocomposites. GC is considered a weed and is found extensively, particularly along river banks and also as canopy under forest trees. The grass is made up of stems (culms) that resemble bamboo but with smaller diameters. In this study, the possibility of extracting natural cellulose fibers from the culms and also to utilize the culms directly as reinforcement for polypropylene (PP) biocomposites has been explored. Natural cellulose fibers extracted from the culms had cellulose content of about 50%. The fibers had considerably high tensile strength of 543 MPa and elongation of 5.6%. Biocomposites with varying tensile and flexural properties could be obtained depending on the proportion of the reinforcement and matrix and density of the biocomposites. Furthermore, reinforcing PP with GC increased acoustic sorption but decreased thermal conductivity. GC offers potential to develop fibers and biocomposites with desired properties as a substitute to the conventional lignocellulosic fibers obtained from fiber crops. [ABSTRACT FROM AUTHOR]

Background: Age at menarche was reported to be associated with the risk of diabetes. However, the impact of ideal cardiovascular health metrics (ICVHMs) on the association between age at menarche and adulthood diabetes risk was unclear. Methods: We included 121 431 women from the nationwide, population‐based cohort of the REACTION study (Risk Evaluation of Cancers in Chinese Diabetic Individuals: a Longitudinal Study). The diagnosis of diabetes was based on the oral glucose tolerance test (OGTT) and glycosylated hemoglobin (HbA1c) measurement. Logistic regression and multiplicative interaction analysis were conducted to investigate the potential interaction effect between age at menarche and ICVHMs on the development of diabetes. Results: The multivariable‐adjusted odds ratios of diabetes across categories of age at menarche (<14, 14‐17, and > 17 years) were 1.22 (95% confidence interval [CI]: 1.17, 1.28), 1.00 (reference), and 0.89 (95% CI: 0.85, 0.93), respectively. In subgroup analysis, significant interactions were detected between total cholesterol/blood pressure levels and age at menarche regarding the risk of diabetes (P for interaction =.0091 and.0019, respectively). The increased risk associated with age at menarche <14 years was observed in participants with three or fewer ICVHMs, but not in women with four or more ICVHMs (P for interaction =.0001). Conclusions: Age at menarche was inversely associated with the risk of diabetes in adulthood in Chinese women, and it appeared to be modified by the presence of ICVHMs. Further studies are needed to clarify the precise interrelationship and the generalizability of our results. [ABSTRACT FROM AUTHOR]

Background: Early life exposure to famine and adulthood obesity increased the risk of nonalcoholic fatty liver disease (NAFLD) in adulthood. However, the joint effects on adulthood NAFLD risk are not clear. Aim: This study aimed to explore the joint effects of famine exposure and adulthood obesity on NAFLD risk in later life. Methods: We included 7632 subjects aged ≥40 years from a community‐dwelling population. Participants were divided into 4 famine exposure groups according to the birth year, including nonexposed (1963‐1974), fetal‐exposed (1959‐1962), childhood‐exposed (1949‐1958) and adolescent‐exposed (1941‐1948). General obesity was assessed by body mass index (BMI: overweight ≥24.0 kg/m2, obesity ≥28.0 kg/m2) and abdominal obesity assessed by waist‐to‐hip ratio (WHR, men/women: moderate ≥0.90/0.85, high ≥0.95/0.90). Results: Compared with nonexposed, fetal‐ and childhood‐exposed participants show an increased risk of NAFLD with multivariable‐adjusted odds ratio (OR) and 95% confidence interval (CI) of 1.28 (1.02‐1.61) and 1.40 (1.04‐1.88) respectively. After further adjusting BMI and WHR, the increased risk was observed only in childhood‐exposed participants (OR = 1.46, 95% CI = 1.04‐2.05). Significant interaction between famine exposure and general obesity on the risk of NAFLD was observed in women (P for interaction =.02). No significant interactions were detected between famine exposure and abdominal obesity (all P for interaction >.05). Compared with normal‐BMI and ‐WHR participants, those with both general and abdominal obesity in adulthood had 20.74 (95% CI: 12.00‐35.96), 14.45 (8.76‐23.86), 23.02 (16.28‐32.57) and 13.04 (8.30‐20.48)‐fold higher risk in nonexposed, fetal‐, childhood‐ and adolescent‐exposed groups respectively. Conclusion: Coexistence of early life famine exposure and adulthood obesity was associated with a higher risk of NAFLD. [ABSTRACT FROM AUTHOR]

Background: Emerging evidence indicated that sleep characteristics may play important roles in the development of metabolic disorders. However, little is known as to the association between bedtime and the risk of non-alcoholic fatty liver disease (NAFLD) in individuals with pre-diabetes and diabetes.Methods: In a prospective cohort of 10 375 adults aged ≥40 years, 1960 of 3484 eligible pre-diabetic and diabetic individuals were identified for the current study. NAFLD was diagnosed using liver ultrasonography at baseline and at follow-up. Information on bedtime was obtained at baseline using a standard questionnaire.Results: We documented 433 incident cases of NAFLD among this study population. In multivariable-adjusted logistic regression model, later bedtime was associated with increased risk of NAFLD (29% increased risk per hour of later bedtime). Compared to individuals with bedtime ≤20:00, the odds ratios (95% confidence intervals) of NAFLD for bedtime of 20:00-22:00 and ≥22:00 were 1.56 (1.04-2.34) and 2.05 (1.31-3.20), respectively. In the subgroup analysis, significant associations were observed among those who were overweight or physically inactive, or those with metabolic syndrome or elevated 10-year risks for atherosclerotic cardiovascular disease. When estimating the joint effect of bedtime and other sleep characteristics, higher risk of incident NAFLD was observed in groups of late bed/early rise, late bed/napping (yes), late bed/bad sleeper, or late bed/shorter sleep durations.Conclusions: Later bedtime was significantly associated with an increased risk of incident NAFLD in adults with pre-diabetes and diabetes, underscoring the importance of sleep behaviour management in the prevention of NAFLD. [ABSTRACT FROM AUTHOR]

Background: This study investigated the association between birth weight and diabetes in a Chinese population, and the effects of body mass index (BMI) and lifestyle factors in later life on this association. Methods: Data from 49 118 participants aged ≥40 years with recalled birth weight from the Risk Evaluation of cAncers in Chinese diabeTic Individuals: a lONgitudinal (REACTION) study, a nationwide population‐based cohort, were used. Diabetes diagnosis was based on oral glucose tolerance tests and HbA1c measurements. Logistic regression models were used to evaluate the association of birth weight and risk of diabetes in later life. Results: Increased risk of diabetes was associated with lower or higher birth weight. Compared with individuals with a birth weight of 2500 to 3499 g, the odds ratios (ORs) and 95% confidence intervals (CIs) of diabetes for individuals with a birth weight of <2500, between 3500 and 3999, and ≥4000 g were 1.28 (1.11‐1.47), 1.11 (1.04‐1.19), and 1.20 (1.07‐1.34), respectively. Significant associations were prominent in participants with a current BMI ≥24 kg/m2, but not detected in those with a normal BMI (OR 1.20 [95% CI 0.96‐1.49], 1.11 [95% CI 0.98‐1.25], and 1.10 [95% CI 0.89‐1.37], respectively). Moreover, there was no increased risk of diabetes in individuals with a low birth weight but with healthy dietary habits (OR 0.94; 95% CI 0.68‐1.29) or ideal physical activity (OR 1.41; 95% CI 0.97‐2.04). Conclusions: A U‐shaped association was observed between birth weight and the risk of diabetes. Healthy lifestyles (healthy dietary habits or ideal physical activity) may eliminate the negative effects of low birth weight in the development of diabetes, but not the effect of high birth weight. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Diabetes is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Isotactic polypropylene (iPP) fibers containing silica nanocapsules (described as SNCs) were prepared with twin‐screw extruder. Modification of silica nanocapsules was hydrolyzed with octadecyltrimethoxysilane in order to improve the interaction between capsules and the hydrophobic PP matrix. Characterization of iPP/SNCs blends were performed by transmission electron microscopy, field‐emission scanning electron microscopy (FE‐SEM), differential scanning calorimetry, thermogravimetric analysis, X‐ray diffraction, and tensile strength tests. Dispersion quality of silica nanocapsules was examined using FE‐SEM. As a result, the modified silica nanocapsules with octadecyltrimethoxysilane (SNCs‐C18) could be well dispersed into iPP matrix because of the hydrophobic surface of modified capsules. The incorporation of all the SNCs samples showed little influence on the crystallization behavior, thermal stability of iPP and mechanical properties. By contrast, the presence of unmodified SNCs in iPP showed a negative effect on mechanical properties due to the poor interface interaction between the inorganic and organic phases. This study presented a successful potential applied for encapsulation. POLYM. COMPOS., 39:762–769, 2018. © 2016 Society of Plastics Engineers [ABSTRACT FROM AUTHOR]

Aloe vera is a widely used natural herb from which many sorts of commercial products have been derived using different preparation technologies. Aloe whole-leaf powder is one of the most popular subtypes. The long-term impact of aloe products has already been reported; however, there have been few studies about short-term exposure, and especially about the relative impact of Aloe vera whole-leaf freeze-dried powder ( AWFP). To provide more toxicological data and to document the early changes induced by AWFP, in this study 120 SD rats were divided into four groups (control and 400/1200/2000 mg/kg treatment groups) and were administered AWFP once daily by oral gavage for 28 consecutive days, followed by a two week recovery phase. The results showed that AWFP could induce soft/loose changes in faeces. Significantly decreased white blood cell (WBC) counts, associated with reduced lymphocyte counts were also noted. The relative organ weight, including both organ-to-body weight ratio and organ-to-brain weight ratio of kidneys, was significantly increased in 2000 mg/kg compared with that in controls. Histopathologically, pigmentation in the kidneys and increased mucosal thickness in colon were also noted in a dose response groups. Other changes observed in the study were not considered to be treatment related, and 400 mg/kg was considered as the no-observed-adverse-effect level. The study provided clear evidence of treatment-related changes with a short-term exposure to AWFP. This is also the first report of the early colon morphologic changes associated with stool changes noted previously in-life phase, providing additional toxicity data which will contribute to our understanding about the short-term usage of AWFP as a remedy. [ABSTRACT FROM AUTHOR]

Summary ADAM23, a member of a disintegrin and metalloprotease (ADAM) family, has been reported to be expressed in several types of tumours. The exact role of ADAM23 and the possible mechanisms in which it is involved in non-small-cell lung carcinoma (NSCLC) remains unclear. Therefore, this study was designed to explore the expression of ADAM23 and its correlation with promoter methylation in NSCLC. Immunohistochemistry and RT-PCR together with Western blotting methods were used to analyse the expression of ADAM23 in 52 cancer tissue samples and eight benign pulmonary lesions as well as four cell lines. The methylated status of ADAM23 gene was determined with methylation-specific PCR (MSP). The results of immunohistochemistry showed that the expression of ADAM23 protein was lower in NSCLC than that in corresponding normal tissues and benign pulmonary lesions (38.5% vs. 86.5% and 87.5%, P < 0.05), and decreased as NSCLC progressed. Meanwhile, methylation of ADAM23 gene was observed in 21 of 52 NSCLC tissues (40.4%), much higher than that of adjacent normal tissues (7.6%) and benign pulmonary lesions (0/8). In the cancer tissues of ADAM23-negative samples, the rate of ADAM23 gene methylation was 50.3% (17/32). ADAM23 expression and its promoter methylation were negatively associated ( r = −0.328, P = 0.017). Moreover, weak expression of ADAM23 in methylated cancer cells increased after treatment with 5-aza-2′-deoxycytidine (5-Aza-2′-dC), confirming that methylation was responsible for the gene downregulation. Our results demonstrate that the expression level of ADAM23 is likely to be involved in the progression of NSCLC and its downregulation is probably correlated with promoter methylation. These findings may provide potential diagnostic and prognostic information about NSCLC. [ABSTRACT FROM AUTHOR]