Objective To evaluate the value of the periportal free air(PPFA) sign at computed tomography(CT) in distinguishing between upper and lower gastrointestinal(GI) tract perforation. Methods CT images of 62 patients with surgically proven GI tract perforation were retrospectively analyzed. 62 cases included upper and lower GI tract perforation in 35 cases and 27 cases,respective-ly. When there was free air in the periportal area,it was defined as positive periportal free air(PPFA) sign. The difference of PPFA sign in upper and lower GI tract perforation, and the sensitivity, specificity, positive predictive value, negative predictive value and ac-curacy of PPFA sign in diagnosing gastrointestinal perforation were analysed respectively. Results The PPFA sign was seen in 33 of 35(94%) patients with upper GI tract perforation,but only in 10 of 27 (37%) patients with lower GI tract perforation,there was sig-nificant difference between them(P<0.05). For diagnosis of super GI perforation with PPFA sign, the sensitivity, specificity, positive predictive value,negative predictive value and accuracy were 94% (33/35), 63%(17/27), 770%(33/43), 89%(17/19) and 81% (50/ 62), respectively. Conclusion The PPFA sign is a useful finding in distinguishing between upper and lower GI tract perforation.

Objective To evaluate the effect and potential mechanism of Shikonin on hormone-induced osteoporosis in rats.Methods RAW264.7 cell lines were treated with indicated concentrations of Shikonin,and the effects of Shikonin on cell viability were evaluated by CCK8 assay.Then the cells were divided into five groups:control group,dexamethasone(osteoporosis agent)group,dexamethasone + recombinant human parathyroid(anti-osteoporosis agent)group,dexamethasone + Shikonin 0.3 μmol·L-1 group,and dexamethasone + Shikonin 1.2 μmol·L-1 group.The effect of Shikonin on osteoclast function was evaluated by TRAP staining and bone resorption area measurement.The rat model of osteoporosis induced by dexamethasone was established,and divided into five groups(n=8):dexamethasone group,dexamethasone + PTH group,dexamethasone + Shikonin 0.3 μmol·L-1 group and dexamethasone + Shikonin 1.2 μmol·L-1 group,while control group was set up,then each group given separately 0.9%NaCl 6 mL·kg-1,PTH 20 μg·kg-1 3 days,Shikonin 0.5 mg·kg-1 day(0.3 μmol·L-1),Shikonin 2 mg·kg-1 day(1.2 μmol·L-1),and 0.9%NaCl 6 mL·kg-1for 3 weeks.ELISA was used to detect Serum type I collagen(CTX),Cathepsin K(Cathepsin K)and oxidative stress related indicators.HE staining was used to detect the changes of bone structure,and dual-energy X-ray scanning was used to detect the changes of bone density(BMD).Western blot and immunofluorescence were used to detect the effect of Shikonin on NF-κB/MAPKs signaling pathway,Western blot and qRT-PCR were used to detect the expression of RANKL-related proteins and mRNA,and Western blot was used to detect the blocking effect of Shikonin on RANKL/TRAF6.Results 1.2 μmol·L-1 Shikonin had the least damage to cells.Shikonin decreased the number of TRAP positive cells(P<0.05),decreased bone absorption area(P<0.05).and decreased the expression of CTX and Cathepsin K(P<0.05),and in 1.2 μmol·L-1 group decreased more significantly(P<0.05).Shikonin increased rat femur BMD(P<0.05),and increased more significantly in 1.2 μmol·L-1 group(P<0.01).Shikonin reversed the reduction and thinning of bone trabeculae induced by dexamethasone.The expression of SOD and GSH in rats increased(P<0.05),while the expression of MDA decreased(P<0.05).Shikonin inhibited the phosphorylation of NF-κB pathway related proteins in vitro.Shikonin inhibited the expression of RANK,RANKL,TRAF6,c-fos and NFATc1 protein and mRNA.Moreover,Shikonin blocked the expression of TRAF6.Conclusion Shikonin can ameliorate glucocorticoid induced osteoporosis by inhibiting RANKL/RANK/TRAF6 and its mediated NF-κB/MAPKs signaling pathway and oxidative stress.

Objective:To assess the value of amide proton transfer weighted (APTw) imaging in the evaluation of pH changes in infarct core (IC) and ischemic penumbra (IP) in subacute cerebral infarction.Methods:The data of twenty-three subacute cerebral infarction patients with unilateral steno-occlusive disease of the middle cerebral artery (subacute infarction group) from April to November 2019 in the First Affiliated Hospital of Dalian Medical University were prospectively analyzed. Fifteen healthy volunteers were enrolled in this study as the control group. All subjects underwent conventional MRI, DWI, 3D-pseudo continuous arterial spin labeling (3D-pCASL) and APTw sequences. Based on DWI images, relative cerebral blood flow (rCBF) and APTw images to determine the region of IC, blood flow penumbra [cerebral blood flow(CBF)-DWI mismatch area, IP CBF] and metabolic penumbra (APTw-DWI mismatched area, IP APT). 3D ROIs were used to semi-automatically measure the APTw signals and the volume of IC and IP CBF of the patients in subacute infarction group. The comparison of APTw signals between the infarct side and the contralateral side in the subacute infarction group, the comparison of bilateral APTw signals in the control group, and the comparison of APTw signals in the IC and IP CBF regions were performed by paired-sample t test or Wilcoxon signed-rank test. The paired-sample t test or Mann-Whitney U test was used to compare the APTw signals between the two groups. The Friedman test was applied to compare the difference of volumes among IP CBF1.5, IP CBF2.5 and IP APT . Results:There was no significant difference of the APTw signals among the IC, the contralateral side in the subacute infarction group and the control group ( P>0.05). The APTw signals of IP CBF and IC of the infarction group were statistically different ( P<0.05). Compared with the contralateral side of IP CBF1.5 (3.7±1.7, -1.84±1.48, 5.57±2.75), the APTwmax (3.07±1.41, t=-3.012, P=0.006), APTw min [-1.30 (-1.74, -0.57), Z=-2.099, P=0.036], and APTwmax-min(4.51±2.58, t=-3.273, P=0.003) signals in the IP CBF1.5 were decreased ( P<0.05). Compared with the contralateral side of IP CBF2.5 [-1.53 (-2.80, -0.91), 5.31±2.61], the APTw min [-1.08 (-1.60, -0.49), Z=-2.616, P=0.009] and APTwmax-min (4.41±2.72, t=-3.228, P=0.004) signals in the IP CBF2.5 were decreased. The volumes of IP CBF1.5 [107.51(50.08, 138.61)mm 3], IP APT [99.00 (53.27, 121.335) mm 3] and IP CBF2.5 [89.91 (51.53, 139.87) mm 3] were successively reduced (χ2=7.913, P=0.019), and the volume of IP CBF2.5 was significantly smaller than that of IP CBF1.5 ( P=0.037). Conclusion:The acid-base metabolism in the IC of subacute cerebral infarction is not obvious, but the blood flow penumbra has local acid-base metabolism imbalance, and the range of metabolic penumbra coincides with the blood flow penumbra.

Objective To investigate the effect of Trichomonas vaginalis macrophage migration inhibitory factor (TvMIF) on THP-1 macrophages.. Methods Recombinant TvMIF protein was prokaryotic expressed and purified, and endotoxin was removed after identification. Following exposure to TvMIF at concentrations of 0, 1, 5, 10, 50 and 100 ng/mL, the cytotoxicity of the recombinant TvMIF protein to THP-1 macrophages was tested using cell counting kit (CCK)-8 assay, and the apoptosis of THP-1 macrophages and reactive oxygen species (ROS) were detected using flow cytometry. The relative expression of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3), caspase-1, interleukin-1β (IL-1β) and IL-18 genes was quantified using real-time fluorescent quantitative PCR (qPCR) assay, and the expression of caspase-1, NLRP3, gasdermin D (GSDMD), gasdermin D N-terminal (GSDMD-NT) and pro-IL-1β proteins were determined using Western blotting assay. Results Sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) displayed successful expression and purification of the recombinant TvMIF protein with a molecular weight of 15.5 kDa, and the endotoxin activity assay showed the successful removal of endotoxin in the recombinant TvMIF protein (endotoxin concentration < 0.1 EU/mL), which was feasible for the subsequent studies on protein functions. Flow cytometry revealed that the recombinant TvMIF protein at a concentration of 10 ng/mL and less promoted the apoptosis of THP-1 macrophages, and the highest apoptotic rate of THP-1 macrophages was seen following exposure to the recombinant TvMIF protein at a concentration of 5 ng/mL, while the recombinant TvMIF protein at concentrations of 50 and100 ng/mL inhibited the apoptosis of THP-1 macrophages. Exposure to the recombinant TvMIF protein at a concentration 1 ng/mL resulted in increased ROS levels in THP-1 macrophages. qPCR assay quantified significantly elevated caspase-1, NLRP3, IL-18 and IL-1β expression in THP-1 macrophages 8 hours post-treatment with the recombinant TvMIF protein at a concentration 1 ng/mL, and Western blotting determined increased caspase-1, NLRP3, pro-IL-1β, GSDMD and GSDMD-NT protein expression in THP-1 macrophages following exposure to the recombinant TvMIF protein at a concentration 1 ng/mL. Pretreatment with MCC950 significantly reduced GSDMD and GSDMD-NT protein expression. Conclusions High-concentration recombinant TvMIF protein inhibits macrophage apoptosis, while low-concentration recombinant TvMIF protein activates NLRP3 inflammasome and promotes macrophage pyroptosis.