OBJECTIVETo explore the best technique parameters on preparing evening primrose oil microspheres by spray drying technique.

METHODGC and internal standard method were used to determine the content of gamma-linolenic acid methyl esters, the technological parameters were investigated by orthogonal experimental design with the yield and entrapment rate as indexes.

RESULTThe charging rate as 3 mL x min(-1), atomizing pressure as 100 kPa and the temperature of inlet as 105 degrees C were the best technique parameters.

CONCLUSIONEvening primrose oil microspheres accorded with the expecting demand. The main influencing factor is the charging rate. Spray drying is reasonable and practical for preparing evening primrose oil microspheres.

Chromatography, Gas ; Feasibility Studies ; Linear Models ; Microspheres ; Oenothera biennis ; chemistry ; Plant Oils ; chemistry ; isolation & purification ; Reproducibility of Results ; Sensitivity and Specificity ; gamma-Linolenic Acid ; analysis

Diabetic kidney disease (DKD) is the most common complication of diabetes mellitus (DM). Qianjin Wenwu decoction (QWD), a well-known traditional Korean medicine, has been used for the treatment of DKD, with satisfactory therapeutic effects. This study was designed to investigate the active components and mechanisms of action of QWD in the treatment of DKD. The results demonstrated that a total of 13 active components in five types were found in QWD, including flavonoids, flavonoid glycosides, phenylpropionic acids, saponins, coumarins, and lignins. Two key proteins, TGF-β1 and TIMP-1, were identified as the target proteins through molecular docking. Furthermore, QWD significantly suppressed Scr and BUN levels which increased after unilateral ureteral obstruction (UUO). Hematoxylin & eosin (H&E) and Masson staining results demonstrated that QWD significantly alleviated renal interstitial fibrosis in UUO mice. We also found that QWD promoted ECM degradation by regulating MMP-9/TIMP-1 homeostasis to improve renal tubulointerstitial fibrosis and interfere with the expression and activity of TGF- β1 in DKD treatment. These findings explain the underlying mechanism of QWD for the treatment of DKD, and also provide methodological reference for investigating the mechanism of traditional medicine in the treatment of DKD.
Rats ; Mice ; Animals ; Ureteral Obstruction/metabolism* ; Kidney/metabolism* ; Tissue Inhibitor of Metalloproteinase-1/metabolism* ; Molecular Docking Simulation ; Rats, Sprague-Dawley ; Kidney Diseases/drug therapy* ; Extracellular Matrix/metabolism* ; Flavonoids/metabolism* ; Fibrosis

Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

Objective:To investigate the prognostic value of N-terminal B-type brain natriuretic peptide precursor (NT-proBNP), cardiac troponin I (cTnI) and aVL lead T-wave changes in acute coronary syndrome (ACS).Methods:Clinical data of 162 patients with ACS admitted to the Emergency Chest Pain Center of the Affiliated Hospital of Jining Medical University from January 2020 to December 2021 were retrospectively collected, including 84 patients with unstable angina pectoris (UAP) and 46 patients with ST-segment elevation myocardial infarction (STEMI). 32 patients with non-ST elevation myocardial infarction (NSTEMI); There were 66 patients with single-vessel disease, 70 patients with double-vessel disease, 26 patients with multi-vessel disease, and 51 patients with major cardiovascular adverse events (MACE). The levels of NT-proBNP, cTnI and T-wave change ratio of aVL lead were compared in different patients.Results:The NT-proBNP and cTnI of UAP patients were 510.42(365.56, 630.54)pg/ml and 8.20(6.50, 10.50)ng/ml, respectively, which were significantly lower than those of STEMI and NSTEMI patients (all P<0.05). There was no significant difference in NT-proBNP and cTnI between STEMI and NSTEMI patients (all P>0.05). The T-wave change proportions of NT-proBNP, cTnI and aVL leads in patients with multi-vessel lesions were 804.90(680.87, 980.05)pg/ml, 13.90(10.12, 15.65)ng/ml and 88.46%(23/26), respectively. It was significantly higher than that in patients with single and double vessel lesions (all P<0.05). The T-wave change ratio of NT-proBNP, cTnI and aVL leads in patients with double-vessel disease was 680.84(525.50, 810.62)pg/ml, 10.40(8.92, 13.60)ng/ml and 67.14%(47/70), respectively, which was significantly higher than that in patients with single-vessel disease (all P<0.05). The proportions of T-wave changes of NT-proBNP, cTnI and aVL leads in MACE patients were 744.54(621.17, 905.54)pg/ml, 12.21(8.65, 15.54)ng/ml and 86.27%(44/51), respectively. It was significantly higher than those without MACE (all P<0.05). The area under receiver operating characteristic (ROC) curve of NT-proBNP, cTnI and aVL lead T-wave changes independently and jointly predicted the occurrence of MACE were 0.937, 0.677, 0.706 and 0.799, respectively, among which NT-proBNP had a higher value in predicting the occurrence of MACE. Conclusions:The T-wave changes of NT-proBNP, cTnI and aVL leads are related to the type of lesions, the number of lesions and the occurrence of MACE in ACS patients, and NT-proBNP has a high value in predicting prognosis.

Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

Regardless of the underlying etiology, renal fibrosis is the final histological outcome of progressive kidney disease. Unilateral ureteral obstruction (UUO) is an ideal and reproducible experimental rodent model of renal fibrosis, which is characterized by tubulointerstitial inflammatory responses, accumulation of extracellular matrix, tubular dilatation and atrophy, and fibrosis. The magnitude of UUO-induced renal fibrosis is experimentally manipulated by the species chosen, animal age, and the severity and duration of the obstruction, while relief of the obstruction allows the animal to recover from fibrosis. The pathogenesis of renal fibrosis is complex and multifactorial and is orchestrated by activation of renin-angiotensin system (RAS), oxidative stress, inflammatory response, transforming growth factor beta 1-Smad pathway, activated myofibroblasts, cell death (apoptosis, autophagy, ferroptosis, and necroptosis), destruction of intracellular organelles, and signaling pathway. The current therapeutic approaches have limited efficacy. Inhibition of RAS and use of antioxidants and antidiabetic drugs, such as inhibitors of sodium-glucose cotransporter 2 and dipeptidyl peptidase-4, have recently gained attention as therapeutic strategies to prevent renal scarring. This literature review highlights the state of the art regarding the molecular mechanisms relevant to the management of renal fibrosis caused by UUO.

PURPOSE: Several studies have compared the effects of coronary stenting and coronary-artery bypass grafting (CABG) on left main coronary artery (LMCA) disease. However, there are limited data on the long-term outcomes of these two interventions in diabetic patients. MATERIALS AND METHODS: We evaluated 56 patients with LMCA stenosis who underwent drug-eluting stent (DES) implantation and 116 patients who underwent CABG in a single hospital in China between January 2004 and December 2006. We compared long-term major adverse cardiac events (death; a "serious outcome" composite of death, myocardial infarction, or stroke; and target-vessel revascularization). RESULTS: In-hospital (30-day) mortality was 0% for the DES group and 3.4% for the CABG group (p=0.31). There was no difference between the two groups in terms of risk of death [hazard ratio for stenting group, 0.49; 95% confidence interval (CI), 0.13-1.63; p=0.55] or risk of serious outcome (hazard ratio for DES group, 1.11; 95% CI, 0.39-1.45; p=0.47). The target-vessel revascularization rate was higher in the DES group than in the CABG group (hazard ratio, 3.67; 95% CI, 1.24-11.06; p=0.018). CONCLUSION: In this cohort of diabetic patients with LMCA stenosis, there was no difference in composite endpoints between patients receiving DESs and those undergoing CABG. However, stenting was associated with higher rates of target-vessel revascularization than CABG. DES implantation in diabetic patients with LMCA disease was found to be at least as safe as CABG.
Angioplasty, Balloon, Coronary/*methods ; Coronary Stenosis/*therapy ; Diabetes Mellitus ; *Drug-Eluting Stents ; Female ; Humans ; Male ; Middle Aged ; Treatment Outcome

To investigate the relationship between cytoskeleton and hyposmotic membrane stretch-induced increase in muscarinic current, the role of actin microfilament in hyposmotic membrane stretch-induced increase in muscarinic current was studied with the whole-cell patch clamp technique in guinea-pig gastric myocytes. In this study, the muscarinic current was induced by carbachol (50 micromol/L) or GTPgammaS (0.5 mmol/L). The results showed that hyposmotic superfusate (202 mOsmol/L) increased carbachol-induced current (I(CCh)) by 145+/-27% and increased GTPgammaS-induced current by 183+/-30%; but in the presence of cytochalasin-B (Cyt-B, 20 micromol/L), an actin cytoskeleton disruptor, hyposmotic membrane stretch increased I(CCh) by 70+/-6%. However, hyposmotic membrane stretch induced increase in I(CCh) was potentiated to 545+/-81% by phalloidin (20 micromol/L), an actin microfilament stabilizer. The results demonstrated that hyposmotic membrane stretch increased the muscarinic currents induced by carbachol or GTPgammaS and that the actin microfilament is involved in the process in guinea-pig gastric myocytes.
Actin Cytoskeleton ; physiology ; Animals ; Carbachol ; pharmacology ; Female ; Guinea Pigs ; Male ; Membrane Potentials ; drug effects ; Myocytes, Smooth Muscle ; physiology ; Osmotic Pressure ; Patch-Clamp Techniques ; Pyloric Antrum ; cytology ; Receptors, Muscarinic ; physiology

Objective:An early diagnosis model of acute aortic dissection (AAD) was established based on chest pain center database.Methods:The clinical data of patients who attended Chest Pain Center of Department of Emergency in Affiliated Hospital of Jining Medical University of Shandong Province from January 2020 to December 2020 were retrospectively collected. Patients were divided into AAD and non-AAD groups according to whether or not AAD was diagnosed. The clinical related indicators of the two groups were compared. The research indicators with statistical differences between the two groups were included in multivariate Logistic regression analysis, and the early diagnosis of AAD nomogram model was established. The receiver operating characteristic (ROC) curve of the model was used to evaluate the prediction accuracy, and the Homser-Lemeshow statistics were used to test the goodness of fit for the model. A total of 630 patients with chest pain who visited the hospital from January 2021 to March 2021 were also collected for external validation of the model. The t-test of independent samples was used to compare the measurement data of normal distribution, nonparametric test was used to compare the measurement data of skewness distribution, and χ 2 test was used to compare the counting data between groups. Results:A total of 2 738 patients were included, of which 4.09% (112/2 738) were AAD patients. Univariate analysis showed that in AAD group, male morbidity (74.11%(83/112)), hypertension history (70.54%(79/112)), aortic disease history (10.71%(12/112)), family history of aortic disease (4.46%(5/112)), sudden onset of symptoms (76.79%(86/112)), percentage of patients with laceration pain (38.39%(43/112)), patients with back pain (66.07%(74/112)), patients with abdominal pain (16.96%(19/112)), systolic blood pressure ((159.44±30.94) mmHg), bilateral blood pressure/pulse asymmetry (23.21% (26/112)), incidence of complicated neurological signs (7.14%(8/112)) and D-dimer (3.57(2.10, 6.62) mg/L) were significantly higher than those in non-AAD group (59.56%(1 564/2 626), 46.23%(1 214/2 626), 0.23%(6/2 626), 0.08%(2/2 626), 35.99%(945/2 626), 0.08%(2/2 626), 3.08%(81/2 626), 3.81%(100/2 626), (142.46±27.90) mmHg, 0.15%(4/2 626), 0.27%(7/2 626), 0.31(0.20, 0.50) mg/L). Age ((57.95±14.35) years old) and CK-MB (1.50(0.90, 3.25) μg/L) were significantly lower than those in the non-AAD group ((61.94±15.77) years, 2.50(1.24, 4.81) μg/L). The differences were statistically significant (the statistical values were χ 2=9.47, χ 2=25.46, χ 2=180.80, χ 2=81.11, χ 2=76.17, χ 2=975.60, χ 2=798.00, χ 2=44.72, t=6.28, χ 2=527.20, χ 2=93.22, Z=14.09, t=2.61, and Z=3.51, respectively; P values were 0.002, <0.001, <0.001, <0.001, <0.001, <0.001, <0.001, <0.001, <0.001, <0.001, <0.001, <0.001, 0.009, and <0.001, respectively). Multivariate analysis showed that history of hypertension ( OR=3.088, 95% CI:1.294-7.374), history of aortic disease ( OR=20.771, 95% CI:2.132-202.361), family history of aortic disease ( OR=266.425, 95% CI:17.610-4 030.851), sudden onset of symptoms ( OR=3.538, 95% CI:1.643-7.619), laceration pain ( OR=1 771.971, 95% CI:204.048-15 387.935), back pain ( OR=61.550,95% CI:27.987-135.367), abdominal pain ( OR=12.325, 95% CI:4.201-36.161), systolic blood pressure ( OR=1.026, 95% CI:1.013-1.039), bilateral blood pressure/pulse asymmetry ( OR=338.357, 95% CI:60.704-1 885.949) and D-dimer ( OR=1.241, 95% CI:1.176-1.309) were independent factors for the diagnosis of AAD in patients with chest pain (P values were 0.011, 0.009, <0.001, 0.001, <0.001, <0.001, <0.001, <0.001, <0.001, and <0.001, respectively). Furthermore, the nomogram model was constructed. ROC curve analysis showed that the area under the curve was 0.976 ( P<0.01), the specificity was 94.52%, and the sensitivity was 91.96%. The statistics of Homser-lemeshow was used to test the goodness of fit, which shows that the model can be fitted well (χ 2=2.928, P=0.939). The prediction model was verified by external validation data, and the area under the ROC curve was 0.934 ( P<0.01), indicating that the model had good prediction performance. Conclusions:History of hypertension, history of aortic disease, family history of aortic disease, sudden onset of symptoms, laceration pain, back pain, abdominal pain, systolic blood pressure, bilateral blood pressure/pulse asymmetry and D-dimer were independent factors for the diagnosis of AAD in patients with acute chest pain. The AAD early diagnosis nomogram model based on the above factors has good predictive performance.