Objective To explore MSCT appearances of lung lacerating injury.Methods The MSCT findings of lung lacerating injury in 31 patients were analyzed retrospective.Results The lung lacerating injury of the 31 cases with 67 lesions in total was found,18 of whom were located on the back side of lung near the pleura,11 of whom had solitary lesion and 20 of whom had multiple ones. The MSCT findings included lung cavity in 9 eases,liquid airbag cavity in 1 7 and lung hematoma in 5 .The pulmonary contusion with different degrees was found in all 3 1 cases.Dynamic observation showed the cavities and hematoma could be transformed into each other.Conclusion MSCT is the best method for diagnosis and observation of lung lacerating injury and helpful for the guide of clinical treatment.

Objective To discuss the expressions and clinical significance of p53 and p33ING1b in human psoriasis and basal cell carcinoma (BCC). Methods Immunohistochemistry EnVision technique was used to detect the expressions of p53 and p33ING1b in samples of 36 psoriasis vulgaris, 28 BCC and 14 normal skins. Results The expression of p53 increased while p33ING1b had a degressive expression in the control group, the psoriasis group and the BCC group. It was found significant statistical difference between the two groups (all P < 0.05). Prominent positive correlation between p53 and p33ING1b were found in both psoriasis group and BCC group (all P<0.05). Conclusions p53 coacts with p33ING1b at local lesions of abnormal proliferative diseases . It′s one of the most prominent mechanisms contributing to deviant cell proliferation.

Objective Toexplore the expression and significance of microRNA-155 (miR-155) in psoriasis vulgaris. Methods Areal-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) method with TaqMan probe technology was performed to detect miR-155 expression in skin lesion area and nonskinlesionalarea of 35 patients with psoriasis vulgaris , compared with that of 30 normal controls. The correlations among miR-155 expression, psoriasis area and severity index (PASI) score and Interleukin-17A(IL-17A)expression were studied. Results The expressions of miR-155 and IL-17A in lesional and non-lesionalgroups were higher than that of control group (all P < 0.01). Also expressions in lesional skin were higher than non-lesional skin (both P < 0.01). In skin lesion group, significant positive correlations existed betweenmiR-155 or IL-17A expression and PASI score as well as miR-155 and IL-17A expression (all P < 0.05). Conclusions Up-expression of miR-155 was relevant to psoriasis development , which is related withthe hyperfunctionof Th17 cells in psoriasis.

Objective To explore the expression alteration and significance of inteleukin (IL)-37 in pso-riasis valguris (PV) patients. Methods Patients with PV had been treated with oral acitretin for 8 weeks. PASI score, ELISA and qRT-PCR were used to exam the data of 38 patients (PV group) and 32 controls (control group). Results IL-37 in PV group was significantly higher than that in control group (P < 0.001) and IL-37 changed slightly after 4 weeks of treatment(P > 0.05) but decreased obviously after 8 weeks(P < 0.001). Signif-icant correlations existed among PASI scores, IL-37, IFN-γ and IL-17, as well as among IL-37 and IFN-γ, IL-17 (P < 0.05). Conclusions The increase of IL-37 is relevant to PV development and is associated with pa-tients’ conditions, IFN-γ and IL-17 but the alteration of IL-37 is not related with IL-4.

Objective To investigate the inhibitory effect of gallic acid(GA)on lipopolysaccharide(LPS)-induced inflammatory responses in human THP1 macrophages.Methods THP1 monocytes were differentiated into macrophages with phorbol myristate acetate.A macrophage inflammation model was established with LPS induction,and GA was added at different concentrations.The safe concentrations of LPS and GA for THP1 cells were screened using the CCK-8 method,and a normal group,model group(100 μg/L LPS),and GA group(100 μg/L LPS+different concentrations of GA)were set up.ELISA was used to detect the levels of interleukin(IL)-6,tumor necrosis factor-α(TNF-α),and IL-1β in the cell culture media of each group.The microplate method was used to detect lactate dehydrogenase(LDH)activity and NO content in the cell cultures,and fluorescence staining was used to detect the reactive oxygen species(ROS)levels,cell damage,and changes in mitochondrial transmembrane potential in each group.Western blot was performed to detect the levels of cyclooxygenase-2(COX-2),HMGB1,c-Jun amino-terminal kinase(JNK),extracellular-regulated protein kinase(ERK),P38 mitogen-activated protein kinase(P38),nuclear transcription factor-KB(NF-κB),NOD-like receptor protein 3(NLRP3),Caspase-1,IL-1β,and gasdermin D(GSDMD).Results Compared with the normal group,the model cell group's secretion of IL-6,TNF-α,IL-1β,and NO was increased(P＜0.05);the secretion of COX-2,HMGB1,p-ERK,p-JNK,and p-P38 and expression of p-NF-KB,NLRP3,Caspase-1,IL-1β were elevated(P＜0.05);expression of GSDMD protein activation fragment was reduced(P＜0.05);ROS generation and cellular damage were significantly increased;mitochondrial transmembrane potential was significantly lower;and LDH activity was elevated(P＜0.05).In comparison with the model group,the GA group cells'secretion of IL-6,TNF-α,IL-1β,and NO was decreased(P＜0.05);expression of COX-2,HMGB1,p-ERK,p-JNK,p-P38,p-NF-κB,NLRP3,Caspase-1,and IL-1β was decreased(P＜0.05);GSDMD protein activation fragment expression level was increased(P＜0.05);ROS generation and cellular damage were decreased;mitochondrial transmembrane potential gradually increased;and LDH activity was decreased(P＜0.05).Conclusions GA had an inhibitory effect on the LPS-induced inflammatory response in THP1 macrophages,and its anti-inflammatory mechanism may involve the MAPK and NF-κB signaling pathways.

Objective:To examine the relationship between sarcopenia and DNA methylation in the promoter of the growth differentiation factor 15(GDF15)gene in elderly individuals.Methods:This cross-sectional study collected data from 865 elderly individuals aged 65 years and above who underwent physical examination at the Yuetang Town Community Medical Center in Yangzhou City between May and September 2020.The verification set included 431 males and 434 females with an age range of 65-100 years and a mean age of(76.0±5.9)years.The diagnosis of sarcopenia was based on the consensus diagnostic criteria of the Asian Sarcopenia Working Group in 2019.The study included 295 cases in the non-sarcopenia group and 470 cases in the sarcopenia group.The study selected 50 non-sarcopenia patients and 50 age-gender matched sarcopenia patients as the explore set for DNA methylation sequencing of the GDF15 gene.The sequencing results were then verified using the methylation-specific polymerase chain(PCR)method in the verification center.Additionally, serum GDF15 levels were detected using the enzyme-linked immunosoradsorption method.The study analyzed the correlation between GDF15 methylation levels, serum GDF15 levels, and sarcopenia.Results:The study found that individuals with sarcopenia had lower levels of body mass index(BMI), appendicular skeletal muscle mass(ASMI), grip strength, and gait speed in both the discovery and validation sets compared to those without sarcopenia( P<0.05). Additionally, the DNA methylation of GDF15 was found to be lower in the sarcopenic group compared to the non-sarcopenic group[93.7%(79.6%, 98.0%) vs.97.7%(95.3%, 99.0%), Z=-9.294, P<0.01]. The results of the correlation analysis indicate a positive relationship between the methylation level and appendicular skeletal muscle mass( r=0.206, P<0.01), grip strength( r=0.297, P<0.01), and gait speed( r=0.383, P<0.01). Conversely, there was a negative correlation between the methylation level and serum GDF15 level( r=-0.249, P<0.05). The study conducted ROC analysis to determine the predictive ability of GDF15 methylation for sarcopenia found that the area under the curve was 0.700 with a cut-off score of 92.7%.Furthermore, binary regression analysis revealed that low GDF15 methylation( OR=1.136, 95% CI: 1.098~1.175, P<0.01)was linked to a higher risk of sarcopenia, even after adjusting for age, sex, and BMI.The serum GDF15 level was higher in the sarcopenic group compared to the non-sarcopenic group[(0.665±0.432)pg/L vs.(0.465±0.211)pg/L( t=-2.452, P<0.05)]. Additionally, it was observed that the methylation of GDF15 was negatively correlated with the serum GDF15 level( r=-0.249, P<0.05). Conclusions:A low level of GDF15 methylation has been found to be linked with a higher risk of sarcopenia, suggesting that measuring GDF15 methylation could potentially serve as a biomarker for diagnosing sarcopenia.

Objective:To discuss the effect of Boschnikia rossica polysaccharides rapa polysaccharides(BRPS)on lipopolysaccharide(LPS)-induced inflammatory responses in the THP-1 macrophages,and to clarify its mechanism.Methods:The THP-1 monocytes were differentiated into the macrophages,and the inflammation model was established using LPS to induce the THP-1 macrophages.CCK-8 method was used to detect the survial rates of the THP-1 macrophages after treated with different concentrations(0,100,200,500,1 000,and 2 000 μg·L-1)of LPS and different concentrations(0,12.5,25.0,50.0,100.0,and 200.0 mg·L-1)of BRPS to select the concentrations for the subsequent experiments.The THP-1 macrophages were divided into blank group,model group,low dose of BRPS group(25.0 mg·L-1 BRPS),medium dose of BRPS group(50.0 mg·L-1 BRPS),and high dose of BRPS group(100.0 mg·L-1 BRPS).P38 inhibitor SB203580,ERK inhibitor U0126,c-Jun N-terminal kinase(JNK)inhibitor SP600125,and nuclear factor of kappa B(NF-κB)inhibitor BAY11-7082 were used to verify the effects on THP-1 cells.The THP-1 cells were divided into control group,LPS group,inhibitor group,100.0 mg·L-1 BRPS group,and inhibitor+100.0 mg·L-1 BRPS group.ELISA method was used to detect the levels of tumor necrosis factor α(TNF-α),interleukin(IL)-6,and IL-1β in culture fluid of the THP-1 macrophages in various groups;DCFH-DA fluorescence probe method was used to detect the reactive oxygen species(ROS)levels in the THP-1 macrophages in various groups;Hoechst33342/PI fluorescence staining method was used to detect the membrane damage in the THP-1 macrophages in various groups;JC-1 fluorescence staining was used to observe mitochondrial membrane potential in the THP-1 macrophages in various groups;Western blotting method was used to detect the expression levels of cyclooxygenase-2(COX-2),high mobility group protein B1(HMGB1),NOD-like receptor thermal protein domain assciated protein 3(NLRP3),cysteinyl aspartate specific protease(Caspase)-1,gasdermin D(GSDMD)-N,IL-1β,mitogen-activated protein kinase(MAPK),and nuclear factor-kappa B(NF-κB)related proteins in the THP-1 macrophages in various groups.Results:The CCK-8 method results showed that when the LPS concentration was 100-2 000 μg·L-1,the survival rates of the THP-1 macrophages were over 90%.Compared with 0 μg·L-1 LPS group,the IL-6 levels in culture fluid of the THP-1 macrophages in 100,200,500,1 000,and 2 000 μg·L-1 LPS group were increased(P<0.05),indicating a significant enhancement of the inflammatory response in the macrophages,so 100 μg·L-1 LPS was used to construct the inflammation model.After treated with 12.5,25.0,50.0,100.0,and 200.0 mg·L-1 BRPS,the survival rates of the THP-1 macrophage were 91.2%,93.8%,91.4%,90.6%,and 91.8%,respectively,so 25.0,50.0,and 100.0 mg·L-1 BRPS were selected as the drug concentrations for low,medium,and high doses of BRPS groups in the subsequent experiments.The ELISA results showed that compared with blank group,the levels of IL-6,TNF-α,and IL-1β in culture fluid of the THP-1 macrophages in model group were increased(P<0.05);compared with model group,the levels of IL-6,TNF-α,and IL-1β in low,medium,and high doses of BRPS groups were decreased(P<0.05).The DCFH-DA fluorescence probe method results showed that compared with blank group,the ROS level in the THP-1 macrophages in model group was increased(P<0.05);compared with model group,the ROS levels in low,medium,and high doses of BRPS groups were decreased(P<0.05).The Hoechst33342/PI fluorescence staining results showed that compared with blank group,the degree of membrane damage in the THP-1 macrophages in model group was increased;compared with model group,the degrees of membrane damage in low,medium,and high doses of BRPS groups were decreased.The JC-1 fluorescence staining results showed that compared with blank group,the mitochondrial membrane potential in the THP-1 macrophages in model group was decreased significantly;compared with model group,the mitochondrial membrane potential in low,medium,and high doses of BRPS groups were increased gradually.The Western blotting results showed that compared with blank group,the expression levels of COX-2,HMGB1,NLRP3,Caspase 1,GSDMD-N,and IL-1β proteins and the ratios of p-P38/P38,p-ERK/ERK,p-JNK/JNK,and p-NF-κB/NF-κB in the THP-1 macrophages in model group were increased(P<0.05);compared with model group,the expression levels of HMGB1,NLRP3,Caspase-1,GSDMD-N,and IL-1β proteins and the ratios of p-P38/P38,p-ERK/ERK,p-JNK/JNK,and p-NF-κB/NF-κB in the THP-1 macrophages in medium and high doses of BRPS groups were decreased(P<0.05),the expression levels of NLRP3,Caspase-1,and IL-1β proteins in the cells in low dose of BRPS group were decreased(P<0.05),the expression level of COX-2 protein in the cells in high dose of BRPS group was decreased(P<0.05).Compared with control group,the ratios of p-P38/P38,p-ERK/ERK,p-JNK/JNK,and p-NF-κB/NF-κB,and the expression level of IL-1β protein in the THP-1 macrophages in LPS group were increased(P<0.05);compared with LPS group,the ratios of p-P38/P38,p-ERK/ERK,p-JNK/JNK,and p-NF-κB/NF-κB,and the expression level of IL-1β protein in the THP-1 macrophages in inhibitor group,100 mg·L-1 BRPS group,and inhibitor+100 mg·L-1 BRPS group were decreased(P<0.05);compared with inhibitor group,the ratios of p-P38/P38,p-ERK/ERK,p-JNK/JNK,and p-NF-κB/NF-κB in the THP-1 macrophages in inhibitor+100 mg·L-1 BRPS group were decreased(P<0.05).Conclusion:BRPS inhibits the inflammatory response of the THP-1 macrophages,which may be related to the MAPK and NF-κB signaling pathways regulated by BRPS.