The American College of Radiology recently published the appropriateness criteria for initial imaging assessment of chronic pancreatitis （CP） and acute inflammation superimposed on CP （ACP）. These criteria systematically elaborate on the role of various imaging modalities in diagnosing CP and ACP， assessing disease severity， identifying underlying causes， and evaluating complications， in order to provide guidance for effective management of CP patients through early and accurate imaging techniques and with reference to clinical and laboratory assessments. This article gives an excerpt of the key statements from the criteria.

ObjectiveThis study aimed to evaluate the effects of cycloastragenol （CAG） on mitochondrial dysfunction during cardiac remodeling and to elucidate its regulatory role in myocardial energy metabolic homeostasis and the associated transcriptional regulatory axis. MethodsA rat model of heart failure （HF） was established by ligation of the left anterior descending coronary artery. Rats were randomly divided into a control group， a model group， a captopril group （3.25 mg·kg^-1）， a low-dose CAG group （10 mg·kg^-1， CAG-L）， and a high-dose CAG group （20 mg·kg^-1， CAG-H）. After 28 days of treatment， left ventricular ejection fraction （LVEF）， left ventricular fractional shortening （LVFS）， left ventricular end-diastolic diameter （LVIDd）， and left ventricular end-systolic diameter （LVIDs） were assessed by echocardiography. Serum levels of N-terminal pro-brain natriuretic peptide （NT-proBNP）， creatine kinase-MB （CK-MB）， cardiac troponinⅠ （cTnI）， interleukin-1β （IL-1β）， interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， and cyclic adenosine monophosphate （cAMP） were measured by enzyme-linked immunosorbent assay （ELISA）. Hematoxylin-eosin （HE） and Masson's trichrome staining were used to evaluate myocardial histopathology and fibrosis. Wheat germ agglutinin （WGA）， reactive oxygen species （ROS）， and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling （TUNEL） staining were performed to assess cardiomyocyte hypertrophy， oxidative stress， and apoptosis. Adenosine triphosphate （ATP） content and the activities of mitochondrial respiratory chain complexes Ⅰ-Ⅳ were determined by colorimetric assays. The mRNA expression of α-smooth muscle actin （α-SMA）， Col Ⅰ， and Col Ⅲ was detected by Real-time quantitative polymerase chain reaction （Real-time PCR）， while the protein levels of β₂-adrenergic receptor （ADRB2）， protein kinase A （PKA）， phosphorylated cAMP response element-binding protein/total cAMP response element-binding protein （p-CREB/CREB）， peroxisome proliferator-activated receptor γ coactivator-1α （PGC-1α）， nuclear respiratory factor 1 （NRF1）， and mitochondrial transcription factor A （TFAM） were analyzed by Western blot. ResultsCompared with the control group， the model group exhibited significantly decreased LVEF， LVFS， and ATP levels （P<0.05）， and markedly increased LVIDd， LVIDs， NT-proBNP， CK-MB， cTnI， IL-1β， IL-6， TNF-α， ROS levels， TUNEL-positive rate， Col deposition area， and the mRNA expression of α-SMA， Col Ⅰ， and Col Ⅲ （P<0.05）. In addition， the activities of mitochondrial respiratory chain complexes Ⅰ-Ⅳ， the protein expression of ADRB2， PKA， p-CREB， PGC-1α， NRF1， and TFAM， as well as the cAMP content， were significantly reduced （P<0.05）. Compared with the model group， both low- and high-dose CAG significantly increased LVEF and LVFS， and decreased LVIDd， LVIDs， and the levels of NT-proBNP， CK-MB， and cTnI （P<0.05）. CAG treatment alleviated myocardial disarray and Collagen deposition， and downregulated the mRNA expression of α-SMA， Col Ⅰ， and Col Ⅲ. The treatment markedly reduced ROS generation and the TUNEL-positive rate （P<0.05）， thereby attenuating cardiomyocyte hypertrophy and inflammatory responses. Furthermore， CAG treatment increased ATP content and the activities of mitochondrial respiratory chain complexes Ⅰ-Ⅳ， accompanied by upregulation of PGC-1α， NRF1， TFAM， ADRB2， PKA， and p-CREB protein expression as well as cAMP levels （P<0.05）. The CAG-H group showed the most pronounced improvements， which were superior to those of the captopril group and the CAG-L group. ConclusionCycloastragenol delays adverse cardiac remodeling and improves cardiac function by activating the ADRB2-mediated GPCR/cAMP/PKA/CREB signaling pathway， enhancing the PGC-1α/NRF1/TFAM activity， promoting mitochondrial energy metabolism remodeling， and suppressing oxidative stress， inflammation， and myocardial fibrosis.

ObjectiveThis study aimed to evaluate the effects of cycloastragenol （CAG） on mitochondrial dysfunction during cardiac remodeling and to elucidate its regulatory role in myocardial energy metabolic homeostasis and the associated transcriptional regulatory axis. MethodsA rat model of heart failure （HF） was established by ligation of the left anterior descending coronary artery. Rats were randomly divided into a control group， a model group， a captopril group （3.25 mg·kg^-1）， a low-dose CAG group （10 mg·kg^-1， CAG-L）， and a high-dose CAG group （20 mg·kg^-1， CAG-H）. After 28 days of treatment， left ventricular ejection fraction （LVEF）， left ventricular fractional shortening （LVFS）， left ventricular end-diastolic diameter （LVIDd）， and left ventricular end-systolic diameter （LVIDs） were assessed by echocardiography. Serum levels of N-terminal pro-brain natriuretic peptide （NT-proBNP）， creatine kinase-MB （CK-MB）， cardiac troponinⅠ （cTnI）， interleukin-1β （IL-1β）， interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， and cyclic adenosine monophosphate （cAMP） were measured by enzyme-linked immunosorbent assay （ELISA）. Hematoxylin-eosin （HE） and Masson's trichrome staining were used to evaluate myocardial histopathology and fibrosis. Wheat germ agglutinin （WGA）， reactive oxygen species （ROS）， and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling （TUNEL） staining were performed to assess cardiomyocyte hypertrophy， oxidative stress， and apoptosis. Adenosine triphosphate （ATP） content and the activities of mitochondrial respiratory chain complexes Ⅰ-Ⅳ were determined by colorimetric assays. The mRNA expression of α-smooth muscle actin （α-SMA）， Col Ⅰ， and Col Ⅲ was detected by Real-time quantitative polymerase chain reaction （Real-time PCR）， while the protein levels of β₂-adrenergic receptor （ADRB2）， protein kinase A （PKA）， phosphorylated cAMP response element-binding protein/total cAMP response element-binding protein （p-CREB/CREB）， peroxisome proliferator-activated receptor γ coactivator-1α （PGC-1α）， nuclear respiratory factor 1 （NRF1）， and mitochondrial transcription factor A （TFAM） were analyzed by Western blot. ResultsCompared with the control group， the model group exhibited significantly decreased LVEF， LVFS， and ATP levels （P<0.05）， and markedly increased LVIDd， LVIDs， NT-proBNP， CK-MB， cTnI， IL-1β， IL-6， TNF-α， ROS levels， TUNEL-positive rate， Col deposition area， and the mRNA expression of α-SMA， Col Ⅰ， and Col Ⅲ （P<0.05）. In addition， the activities of mitochondrial respiratory chain complexes Ⅰ-Ⅳ， the protein expression of ADRB2， PKA， p-CREB， PGC-1α， NRF1， and TFAM， as well as the cAMP content， were significantly reduced （P<0.05）. Compared with the model group， both low- and high-dose CAG significantly increased LVEF and LVFS， and decreased LVIDd， LVIDs， and the levels of NT-proBNP， CK-MB， and cTnI （P<0.05）. CAG treatment alleviated myocardial disarray and Collagen deposition， and downregulated the mRNA expression of α-SMA， Col Ⅰ， and Col Ⅲ. The treatment markedly reduced ROS generation and the TUNEL-positive rate （P<0.05）， thereby attenuating cardiomyocyte hypertrophy and inflammatory responses. Furthermore， CAG treatment increased ATP content and the activities of mitochondrial respiratory chain complexes Ⅰ-Ⅳ， accompanied by upregulation of PGC-1α， NRF1， TFAM， ADRB2， PKA， and p-CREB protein expression as well as cAMP levels （P<0.05）. The CAG-H group showed the most pronounced improvements， which were superior to those of the captopril group and the CAG-L group. ConclusionCycloastragenol delays adverse cardiac remodeling and improves cardiac function by activating the ADRB2-mediated GPCR/cAMP/PKA/CREB signaling pathway， enhancing the PGC-1α/NRF1/TFAM activity， promoting mitochondrial energy metabolism remodeling， and suppressing oxidative stress， inflammation， and myocardial fibrosis.

Objective To compare the dosimetric differences between volumetric modulated arc therapy(VMAT)and intensity modulated radiation therapy(IMRT)in the irradiation of chest wall and upper and lower clavicle regions after radical mastectomy for breast cancer.Methods A total of 100 patients who were scheduled to receive radiotherapy after radical mastectomy were included and selected as research subjects.Patients were divided into the VMAT group and the IMRT group by random number table method,with 50 cases in each group.The target dose parameters,exposure dose of organs at risk,monitor unit(MU)and treatment time were compared between the two groups.Results There were no statistical differences in V95 and V110 between the VMAT group and the IMRT group(P＞0.05).The D2%in the VMAT group was lower than that of the IMRT group,while D98%and D50%were higher in the VMAT group than those in the IMRT group(P＜0.05).Target area uniformity and target area conformity were better in the VMAT group than those in the IMRT group(P＜0.05).There were no significant differences in mean cardiac dose(Dmean)and ipsilateral lung V5 and V10 between the VMAT group and the IMRT group(P＞0.05).The heart V20 and V30,contralateral lung Dmean,maximum spinal cord dose(Dmax),contralateral breast Dmean,ipsilateral lung Dmean,V20,V30 and mean MU were lower in the VMAT group than those in the IMRT group,and the treatment time was shorter than that in the IMRT group(P＜0.05).Conclusion In the irradiation treatment of chest wall and upper and lower clavicle regions after radical mastectomy,VMAT demonstrates superior dosimetric characteristics and higher treatment efficiency compared with IMRT,particularly in terms of target area uniformity,target area conformity and exposure doses to organs at risk.

Objective To compare the dosimetric differences between volumetric modulated arc therapy(VMAT)and intensity modulated radiation therapy(IMRT)in the irradiation of chest wall and upper and lower clavicle regions after radical mastectomy for breast cancer.Methods A total of 100 patients who were scheduled to receive radiotherapy after radical mastectomy were included and selected as research subjects.Patients were divided into the VMAT group and the IMRT group by random number table method,with 50 cases in each group.The target dose parameters,exposure dose of organs at risk,monitor unit(MU)and treatment time were compared between the two groups.Results There were no statistical differences in V95 and V110 between the VMAT group and the IMRT group(P＞0.05).The D2%in the VMAT group was lower than that of the IMRT group,while D98%and D50%were higher in the VMAT group than those in the IMRT group(P＜0.05).Target area uniformity and target area conformity were better in the VMAT group than those in the IMRT group(P＜0.05).There were no significant differences in mean cardiac dose(Dmean)and ipsilateral lung V5 and V10 between the VMAT group and the IMRT group(P＞0.05).The heart V20 and V30,contralateral lung Dmean,maximum spinal cord dose(Dmax),contralateral breast Dmean,ipsilateral lung Dmean,V20,V30 and mean MU were lower in the VMAT group than those in the IMRT group,and the treatment time was shorter than that in the IMRT group(P＜0.05).Conclusion In the irradiation treatment of chest wall and upper and lower clavicle regions after radical mastectomy,VMAT demonstrates superior dosimetric characteristics and higher treatment efficiency compared with IMRT,particularly in terms of target area uniformity,target area conformity and exposure doses to organs at risk.

Objective:To evaluate the role of interferon regulatory factor 3 (IRF3) in renal fibrosis in a mouse model of renal ischemia-reperfusion injury.Methods:Twelve male C57BL/6J wild-type mice and 12 macrophage IRF3 conditional knockout C57BL/6J mice, aged 8-10 weeks, weighing 20-25 g, were divided into 2 groups ( n=6 each) using a random number table method: wild-type sham operation group (WT-Sham group) and wild-type renal ischemia-reperfusion injury group (WT-I/R group); IRF3 conditional knockout sham operation group (cKO-Sham group) and IRF3 conditional knockout I/R group (cKO-I/R group). The model of renal I/R injury was established by occluding bilateral renal pedicles for 45 min followed by reperfusion in anesthetized animals. The orbital blood samples and renal tissues were collected at 14 days of reperfusion for determination of the concentrations of blood urea nitrogen (BUN) and creatinine (Cr) in serum, expression of fibronectin, collagen-I, alpha-smooth muscle actin (α-SMA) (by immunofluorescence), F4/80-α-SMA double positive cell count, and mRNA expression of interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and transforming growth factor-β1 (TGF-β1) in renal tissues (by real-time polymerase chain reaction) and for observation of pathological changes which were scored. The area of renal fibrosis was measured. Results:For two types of mice, compared with group Sham, the levels of serum BUN and Cr, area of renal fibrosis and renal injury score were significantly increased, the expression of fibronectin, COL-Ⅰ and α-SMA protein and IL-6, IL-1β, TNF-α and TGF-β1 mRNA was up-regulated, and the F4/80-α-SMA dual positive cell count was increased in group WT-I/R ( P<0.05). Compared with group WT-I/R, the concentrations of BUN and Cr in serum, area of renal fibrosis and renal injury score were significantly decreased, the expression of fibronectin, COL-Ⅰ and α-SMA protein and IL-6, IL-1β, TNF-α and TGF-β1 mRNA was down-regulated, and the F4/80-α-SMA dual positive cell count was decreased in cKO-I/R group ( P<0.05). Conclusions:IRF3 is involved in the process of renal fibrosis in a mouse model of renal ischemia-reperfusion injury, and the mechanism may be associated with the promotion of inflammatory responses and the transformation of macrophages into myofibroblasts.

Objective To explore the application value of CT-based radiomics in differentiating pneumonia-type mucinous adenocarcinoma(PTMA)from organizing pneumonia(OP).Methods A total of 52 PTMA patients and 102 OP patients were retrospectively included and randomly divided into training set(n=124)and test set(n=30)in an 8∶2 ratio.Eight PTMA patients and 22 OP patients from another hospital during the same period were included as external validation set(n=30).Clinical characteristics and CT signs of the patients were selected to construct the clinical model.Radiomics features were extracted and dimensionality reduction was performed through the least absolute shrinkage and selection operator(LASSO)algorithm.A radiomics model was constructed and the Radiomics score(Radscore)was calculated.The Radscore was combined with clinical factors to establish the combined model and a nomogram was illustrated.The models' fitting degree was analyzed by the calibration curve,while their efficacy was evaluated by the receiver operating characteristic(ROC)curve and decision curve analysis(DCA).Results The clinical model,established based on the border,cystic space and bronchial leafless tree sign,achieved area under the curve(AUC)of 0.850,0.782,and 0.759 in the training set,test set,and external validation set,respectively.Thirteen features were obtained to construct the radiomics model,with AUC of 0.925,0.865,and 0.830,respectively.The AUC of the combined model were 0.970,0.905,and 0.864,respectively,in which the calibration curve demonstrated good model fitting.DCA indicated that the combined model had the greatest clinical net benefit.Conclusion The combined model based on CT radiomics can effectively distinguish PTMA from OP.

Objective:To evaluate the role of interferon regulatory factor 3 (IRF3) in renal fibrosis in a mouse model of renal ischemia-reperfusion injury.Methods:Twelve male C57BL/6J wild-type mice and 12 macrophage IRF3 conditional knockout C57BL/6J mice, aged 8-10 weeks, weighing 20-25 g, were divided into 2 groups ( n=6 each) using a random number table method: wild-type sham operation group (WT-Sham group) and wild-type renal ischemia-reperfusion injury group (WT-I/R group); IRF3 conditional knockout sham operation group (cKO-Sham group) and IRF3 conditional knockout I/R group (cKO-I/R group). The model of renal I/R injury was established by occluding bilateral renal pedicles for 45 min followed by reperfusion in anesthetized animals. The orbital blood samples and renal tissues were collected at 14 days of reperfusion for determination of the concentrations of blood urea nitrogen (BUN) and creatinine (Cr) in serum, expression of fibronectin, collagen-I, alpha-smooth muscle actin (α-SMA) (by immunofluorescence), F4/80-α-SMA double positive cell count, and mRNA expression of interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and transforming growth factor-β1 (TGF-β1) in renal tissues (by real-time polymerase chain reaction) and for observation of pathological changes which were scored. The area of renal fibrosis was measured. Results:For two types of mice, compared with group Sham, the levels of serum BUN and Cr, area of renal fibrosis and renal injury score were significantly increased, the expression of fibronectin, COL-Ⅰ and α-SMA protein and IL-6, IL-1β, TNF-α and TGF-β1 mRNA was up-regulated, and the F4/80-α-SMA dual positive cell count was increased in group WT-I/R ( P<0.05). Compared with group WT-I/R, the concentrations of BUN and Cr in serum, area of renal fibrosis and renal injury score were significantly decreased, the expression of fibronectin, COL-Ⅰ and α-SMA protein and IL-6, IL-1β, TNF-α and TGF-β1 mRNA was down-regulated, and the F4/80-α-SMA dual positive cell count was decreased in cKO-I/R group ( P<0.05). Conclusions:IRF3 is involved in the process of renal fibrosis in a mouse model of renal ischemia-reperfusion injury, and the mechanism may be associated with the promotion of inflammatory responses and the transformation of macrophages into myofibroblasts.

Objective To investigate the preventive efficacy of recombinant human granulocyte-macrophage colony-stimulating factor(rhGM-CSF)combined with Kangfuxin liquid on radiation dermatitis in breast cancer patients underwent radiotherapy.Methods A total of 90 breast cancer patients were randomized into the control group(45 cases,rhGM-CSF alone)and the observation group(45 cases,rhGM-CSF+Kangfuxin liquid).Both groups received radiotherapy.The incidence of radiation dermatitis,the time of first occurrence,the healing time and severity of radiation dermatitis(graded by RTOG criteria)were compared between the two groups.Skin growth factors[epidermal growth factor(EGF),basic fibroblast growth factor(bFGF),transforming growth factor-β(TGF-β)]were measured via enzyme linked immunosorbent assay(ELISA)before radiotherapy and 2 weeks after radiotherapy.The quality of life of patients was assessed using the EORTC QLQ-C30 V3.0 questionnaire.Results The incidence of radiation dermatitis was significantly lower in the observation group(35.56%,16/45)than that in the control group(68.89%,31/45,P＜0.05),and the first occurrence time of dermatitis was later,the healing time was shorter,and the severity grade of dermatitis was lower(P＜0.05).Two weeks after radiotherapy,levels of EGF,bFGF,TGF-β and the scores of QLQ-C30 increased in both groups,and those of the observation group were significantly higher than the control group(P＜0.05).Conclusion Combining rhGM-CSF with Kangfuxin liquid can effectively prevent radiation dermatitis in breast cancer patients by reducing incidence and severity,delaying onset time,accelerating healing,and improving quality of life.