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旨在促进微波技术在花生油生产中的应用，比较了3种炒籽方式(微波、电磁、燃气)压榨花生油的色泽、酸值、风味物质含量、VE含量以及感官评价的差异，并考察了微波物料输送频率对花生油色泽、酸值和风味物质组成的影响。结果表明：微波炒籽压榨花生油的酸值和风味物质含量明显高于燃气炒籽和电磁炒籽，色泽也更深，VE含量更高（430.87 mg/kg），且消费者喜爱度最高；随着微波物料输送频率的降低，花生油的色泽逐渐加深，酸值略有升高，风味物质数量和含量均逐渐增加，其中吡嗪类物质占比最高（39.54%～46.55%）。微波作为一种高效、快速、绿色的新型产香技术在浓香花生油的加工中具有明显的优势和良好的应用前景。In order to promote the application of microwave technology in the production of peanut oil, the differences in color, acid value, flavor substance content, VE content, and sensory evaluation of oil obtained from peanut respectively fried by microwave frying method, electromagnetic frying method, and gas frying method were compared,and the effects of the materials conveying frequency of microwave on the color, acid value and flavor substances composition of peanut oil were investigated.The results showed that the acid value and flavor substance content of oil obtained from microwave fried peanut were significantly higher than those from gas fried peanut and electromagnetic fried peanut, the color was deeper, the VE content was the highest (430.87 mg/kg), and consumers liked it the most. With the decrease of materials conveying frequency of microwave, the color of peanut oil gradually became darker, the acid value slightly increased, and the kind and content of flavor substances gradually increased, in which pyrazines accounted for the highest proportion (39.54%-46.55%). Microwave, as an efficient, fast and green new aroma production technology, has obvious advantages and good application prospects in the processing of fragrant peanut oil.

为制备风味品质较优的小榨花生油，在不同炒籽条件下处理花生仁，压榨制备小榨花生油。对小榨花生油进行感官评价，基于主成分分析（PCA）分析炒籽条件与小榨花生油风味类型的相关性，并对小榨花生油风味物质含量进行了测定。结果表明：炒籽温度低于160 ℃时小榨花生油呈生香味、甜香味，风味弱，在炒籽温度160~165 ℃时呈甜香味、熟坚果味，在炒籽温度170 ℃时开始表现出煳味，并且随着炒籽温度的升高煳味增大；当入炒水分由4.09%升高到7.12%时，小榨花生油的风味类型没有明显改变，风味强度略有增加；在炒籽温度145~160 ℃条件下，醛类和吡嗪类化合物为主要呈味物质，在炒籽温度165 ℃以上时，吡嗪类化合物是最主要的呈味物质，并且随着炒籽温度的升高，吡嗪类化合物占比呈现逐渐增加趋势，醛类化合物占比呈现逐渐降低趋势；在入炒水分4.09%和7.12%、炒籽温度145～175 ℃条件下，风味物质总量分别为15.7~43.2 mg/kg和115~39.8 mg/kg。综上，选择165 ℃的炒籽温度，可得到具有较好风味品质的小榨花生油。 In order to prepare pressed flavor peanut oil with better flavor quality, peanut kernels were processed under different roasting conditions, and pressed flavor peanut oil was prepared by pressing. The sensory index of pressed flavor peanut oil was evaluated, and the correlation between the roasting conditions and the flavor types of pressed flavor peanut oil was analyzed based on the principal component analysis(PCA). The flavor substance content of pressed flavor peanut oil was determined. The results showed that when the roasting temperature was lower than 160 ℃, the pressed flavor peanut oil presented raw flavor and sweet flavor, and the flavor was weak. When the roasting temperature was 160-165 ℃, it presented sweet flavor and fried nut flavor. When the roasting temperature was 170 ℃, it began to show paste flavor which increased with the increase of roasting temperature. When the roasting water content increased from 4.09% to 7.12%, the flavor type of pressed flavor peanut oil did not change significantly, and the flavor intensity slightly increased. Under the condition of roasting temperature of 145-160 ℃, aldehydes and pyrazines were the main flavoring substances. When the roasting temperature was above 165 ℃, pyrazines were the most important flavoring substances. With the increase of roasting temperature, pyrazines content gradually increased, while aldehydes content gradually decreased. Under the conditions of roasting water content 4.09% and 7.12%, and roasting temperature from 145 ℃ to 175 ℃, the total amounts of flavor substances were 15.7-43.2 mg/kg and 11.5-39.8 mg/kg respectively. In conclusion, pressed flavor peanut oil with good flavor quality can be obtained by selecting the appropriate roasting temperature of 165 ℃.

Aim: Blood–brain barrier (BBB) disorder is one of the early findings in cognitive impairments. We have recently found that Porphyromonas gingivalis bacteraemia can cause cognitive impairment and increased BBB permeability. This study aimed to find out the possible key virulence factors of P. gingivalis contributing to the pathological process. Materials and Methods: C57/BL6 mice were infected with P. gingivalis or gingipains or P. gingivalis lipopolysaccharide (P. gingivalis LPS group) by tail vein injection for 8 weeks. The cognitive behaviour changes in mice, the histopathological changes in the hippocampus and cerebral cortex, the alternations of BBB permeability, and the changes in Mfsd2a and Cav‐1 levels were measured. The mechanisms of Ddx3x‐induced regulation on Mfsd2a by arginine‐specific gingipain A (RgpA) in BMECs were explored. Results: P. gingivalis and gingipains significantly promoted mice cognitive impairment, pathological changes in the hippocampus and cerebral cortex, increased BBB permeability, inhibited Mfsd2a expression and up‐regulated Cav‐1 expression. After RgpA stimulation, the permeability of the BBB model in vitro increased, and the Ddx3x/Mfsd2a/Cav‐1 regulatory axis was activated. Conclusions: Gingipains may be one of the key virulence factors of P. gingivalis to impair cognition and enhance BBB permeability by the Ddx3x/Mfsd2a/Cav‐1 axis. [ABSTRACT FROM AUTHOR]

The association between Porphyromonas gingivalis infection and oral squamous cell carcinoma (OSCC) has been established by numerous epidemiological studies. However, the underlying mechanism specific to this connection remains unclear. By bioinformatical analysis, we identified ZFP36 as a potentially significant co‐expressed gene in both the OSCC gene database and the persistent infection model of P. gingivalis. To further investigate the role of ZFP36, we established a cell model that human immortalized oral epithelial cells (HIOECs) that were sustainedly infected by P. gingivalis (MOI = 1) for a duration of 30 weeks. Our findings indicated that sustained infection with P. gingivalis inhibited the expression of ZFP36 protein and induced changes in the biological behaviour of HIOECs. The mechanism investigation demonstrated the potential role of ZFP36 in regulating the cancer‐related biological behaviour of HIOECs. Subsequent studies revealed that highly expressed CCAT1 could serve as a molecular scaffold in the formation of the ZFP36/CCAT1/MK2 complex. This complex formation enhanced the binding abundance of MK2 and ZFP36, thereby promoting the inhibition of ZFP36 protein phosphorylation. To summarize, low expression of ZFP36 protein under persistent P. gingivalis infection enhances the cancer‐related biological behaviour of HIOECs. [ABSTRACT FROM AUTHOR]

Aim: To assess the relationship between dietary antioxidant intake and periodontal health in US adults and the potential role of mitochondrial function. Materials and Methods: We performed a cross‐sectional study using data from the National Health and Nutrition Examination Survey (NHANES) 2011–2014. Dietary antioxidant intake was evaluated using three diet‐related indices: dietary oxidative balance score (DOBS), dietary total antioxidant capacity (DTAC) of antioxidant vitamins and composite dietary antioxidant index (CDAI). Periodontal parameters included attachment loss (AL) and probing pocket depth (PPD). Mitochondrial dysfunction was assessed using the methylmalonic acid (MMA) level. Weighted multivariable linear regression analyses were employed to investigate the association between dietary antioxidant intake and periodontal status. Additionally, exploratory mediation analyses were conducted to determine the mediating effect of MMA on the association. Results: Totally, 5520 participants were included in our study. Participants with higher DOBS and DTAC scores had lower mean AL/PPD and MMA values. CDAI was negatively associated with mean AL and PPD. Furthermore, MMA mediated 9.4% and 4.9% of the associations between DOBS and mean AL and mean PPD, respectively. MMA also accounted for 7.2% and 3.3% of the association between DTAC and mean AL and PPD, respectively. Conclusions: The findings support that dietary antioxidant intake helps in improving periodontal health, possibly and partially by enhancing mitochondrial function. [ABSTRACT FROM AUTHOR]

Background: To examine the relationship between the systemic immune‐inflammation index (SII) and periodontitis and to investigate possible effect modifiers. Methods: Data used in the present cross‐sectional study are from the National Health and Nutrition Examination Survey (NHANES) 2009–2014 (N = 10,301). The SII was calculated using the following formula: (neutrophils count × platelet count)/lymphocytes count. The category of periodontitis was defined by the Centers for Disease Control and Prevention and American Academy of Periodontology (CDC/AAP) classification. We employed natural cubic spline and multivariable logistic regression analyses to evaluate the associations of the SII with periodontitis. Results: The associations between SII and periodontal health followed a J‐shape (p < 0.001). The risk of periodontitis tended to reduce with the increment of log2(SII) in participants with log2(SII) ≤ 8.66 (odds radio [OR] = 0.83; 95% CI: 0.69–0.999), especially among non‐Hispanic Whites (OR = 0.70; 95% CI: 0.52–0.95), and increased with the increment of log2(SII) in participants with log2(SII) > 8.66 (OR = 1.19; 95% CI: 1.02–1.38). A similar trend was also observed between the SII and the number of sites with probing pocket depth (PPD) ≥4 mm and clinical attachment loss (CAL) ≥ 3 or 5 mm. Furthermore, we found a significantly stronger correlation between lymphocytes and either neutrophils or platelets in individuals with log2(SII) > 8.66, as opposed to those with log2(SII) ≤ 8.66. Conclusions: There is a J‐shaped association between SII and periodontitis in US adults, with an inflection point of log2(SII) at 8.66, which may provide potential adjunctive treatment strategies for periodontitis with different immune response states. Further prospective trials are still required to confirm our findings. [ABSTRACT FROM AUTHOR]