Objective:To explore the efficient extraction method of organic selenium from selenium-rich tea and its occurrence form.Methods:The continuous dialysis method and the subtraction method were used to optimize the extraction method of organic selenium. At the same time, the four proteins (water-soluble, salt-soluble, alcohol-soluble, alkali-soluble proteins) were sequentially extracted according to the classification and properties of Osborne soluble proteins. In vitro simulation technology was used to simulate the digestion process of selenium in selenium-rich tea in the gastrointestinal fluid, and the bioavailability of human intake of selenium and the occurrence form of organic selenium were further analyzed by atomic fluorescence spectrometer-liquid chromatography. Results:The total selenium content of selenium-rich tea was (303.12 ± 1.19) μg/kg. The contents of organic selenium measured by the continuous dialysis method and the subtraction method were (154.76 ± 9.47) and (265.02 ± 6.55) μg/kg, respectively, the difference was statistically significant ( t=- 2.56, P < 0.05). The contents of four proteins in descending order were alkali-soluble protein (29.79 g/100 g), water-soluble protein (2.52 g/100 g), salt-soluble protein (2.15 g/100 g), and alcohol-soluble protein (1.04 g/100 g), respectively. After digestion simulation of gastrointestinal fluid, the selenium content of tea samples was (203.01 ± 3.16) μg/kg, and the bioavailability of selenium was 66.97%. The content of selenomethionine (SeMet) in alcohol-soluble protein was (13.87 ± 3.21) μg/kg, and the content of selenocysteine (SeCys) was (0.82 ± 0.38) μg/kg; the content of SeMet in alkali-soluble protein was (2.59 ± 2.16) μg/kg. Conclusions:In the extraction method of organic selenium from selenium-rich tea, subtraction method is better than continuous dialysis method. SeMet in selenium-rich tea can be detected in alcohol-soluble and alkali-soluble proteins, and SeCys can be detected in alcohol-soluble protein.

Objective: To investigate the therapeutic effect of free superficial circumflex iliac artery perforator (SCIP)flap for reconstruction of soft tissue defects secondary to resection of retromolar and lateral buccal squamous cell carcinoma. Methods: From January 2014 to January 2017, eight patients with retromolar and lateral buccal squamous cell carcinoma received radical resection and reconstructed with SCIP flap immediately. CTA and color Doppler sonography were routinely performed before the surgery. According to the size of the defect in the recipient area, the flap vascularized by the perforator vessel was carefully prepared and transferred to the buccal-pharynx-palate composite defect. The recipient area and donor area were sutured tightly after arteriovenous anastomosis under microscope. The survival and functional recovery of the flap were observed after operation. Results: The flap sizes ranged from 5 cm× 6 cm to 7 cm×9 cm.The mean diameter of the superficial circumflex iliac arteries was 0.65 mm. And the mean diameter of the veins was 1.2 mm. The mean arterial pedicle length was 7.0 cm, and the venous pedicle length was 8.0 cm. Eight flaps were all survived. The shape of the buccal-parapharyngeal-palate was good and the mouth opening was normal after operation. Conclusions Superficial circumflex iliac artery perforator flap was a good choice for repairing the defect of parapharyngeal squamous cell carcinoma in the posterior molar region.

OBJECTIVE：To study the effects of sulforaphane on the prolifera tion and apoptosis of human renal tubular epithelial cells HK- 2 induced by high glucose ，and to investigate its mechanism primarily. METHODS ：HK-2 cells were divided into normal group ，high glucose group ，irbesartan group （positive control ，1 μmol/L），sulforaphane low ，medium and high concentration groups （10，20，40 μmol/L）. The cells in normal group were cultured in DMEM medium for 96 hours. T he cells in other groups were cultured in high glucose DMEM medium （containing 40 mmol/L glucose ）for 48 hours. After inducing cell injury，the cells were added with corresponding drugs for 48 hours. Survival rate and apoptotic rate of cells were detected. mRNA expression of cyclin D 1，caspase-3，Bcl-2 and Bax as well as protein expression of p-mTOR ，p-AMPK，p-Akt and p-PI 3K were also determined. In addition ，HK-2 cells were divided into normal group ，high glucose group ，sulforaphane high concentration group（40 μmol/L），acardicin group （AMPK agonist ，1 mmol/L），sulforaphane high concentration+compound C group （sulforaphane 40 μmol/L+AMPK inhibitor compound C 40 μmol/L），perifoxine group （Akt inhibitor ，19.95 μmol/L）、sulforaphane high concentration+SC 79 group（sulforaphane 40 μmol/L+Akt agonist SC79 4 μmol/L）. After cultured with the same method ， protein expression of p-mTOR ，p-AMPK，p-Akt and p-PI 3K were detected in HK- 2 cells. RESULTS ：Compared with normal group，survival rate of HK- 2 cells，mRNA expression of cyclin D 1 and Bcl- 2 as well as protein expression of p-AMPK were decreased significantly in high glucose group （P＜0.05）；apoptotic rate ，mRNA expression of caspase- 3 and Bax ，protein expression of p-mTOR ，p-Akt and p-PI 3K in HK- 2 cells were increased significantly （P＜0.05）. Compared with high glucose group，above indexes of sulforaphane low ，medium and high concentration groups ，irbesartan group were all improved significantly （P＜0.05）；the improvement of above indexes in sulforaphane medium and high concentration groups were significantly better those of sulforaphane low concentration group （P＜0.05）. There was no significant difference in above indexes between sulforaphane high concentration group and irbesartan group （P＞0.05）. Compared with sulforaphane high concentration group，there were no significant difference in the protein expression of p-AMPK ，p-mTOR in acardicin group and p-mTOR ，p-Akt and p-PI 3K in perifoxine group （P＞0.05）；the protein expression of p-AMPK in sulforaphane high concentration+compound C group was decreased significantly （P＜0.05），while the protein expression of p-mTOR was increased significantly （P＜0.05）；the protein expression of p-mTOR 、p-Akt、p-PI3K in sulforaphane high concentration+SC 79 group were increased significantly （P＜ 0.05）. CONCLUSIONS ：Sulforaphane can promote the proliferation of renal tubular epithelial cells and inhibit its apoptosis ；its mechanism may be associated with up-regulating the expression of p-AMPK and down-regulating the expression of p-mTOR ，p-Akt and p-PI 3K.

This study aimed to explore the relationship between comorbidity factors and in-hospital mortality related to factors in patients with carbapenem-resistant Klebsiella pneumoniae (CRKP) pneumonia. This study collected clinical data from 218 patients with CRKP pneumonia in Beijing hospital from November 2011 to December 2023, analyzed the number of comorbidities carried by CRKP pneumonia patients, comorbidity patterns, Charlson Comorbidity Index (CCI) scores, and comorbidity of underlying diseases, and explored the relationship between various indicators and comorbidity factors and in-hospital mortality in CRKP pneumonia patients. The Ward.D cluster analysis was performed on the comorbidities of patients and used to draw heatmaps. Using a multiple logistic regression model, a nomogram model was constructed to predict in-hospital mortality in patients with CRKP pneumonia. This study included 218 patients with CRKP pneumonia. The results showed that there were significant differences in the age ( P=0.003), comorbidities such as heart failure ( P<0.001), arrhythmia ( P=0.002), chronic liver disease ( P=0.003), chronic kidney disease ( P=0.002), CCI score ( P=0.007), total number of comorbidities ( P<0.001), and comorbidity patterns (respiratory/immune/psychiatric disease patterns and cardiovascular/tumor/metabolic disease patterns, P=0.003) between the survival and death groups of CRKP pneumonia patients. The multiple logistic regression showed that cardiovascular/tumor/metabolic disease patterns ( P=0.030), CCI score ( P=0.040), concomitant heart failure ( P=0.011), and concomitant arrhythmia ( P=0.025) were independent risk factors for in-hospital mortality in patients with CRKP pneumonia. The nomogram model for predicting the risk of in-hospital mortality in patients with CRKP pneumonia, constructed based on the identified risk factors, had an area under the ROC curve of 0.758. Both the ROC curve and validation curve indicated that the nomogram model had stable performance in predicting in-hospital mortality in patients with CRKP pneumonia. In summary, comorbidity factors are risk factors for predicting in-hospital mortality in patients with CRKP pneumonia, and the role of comorbidity factors in in-hospital mortality in patients with CRKP pneumonia should be taken seriously.

This study aimed to explore the relationship between comorbidity factors and in-hospital mortality related to factors in patients with carbapenem-resistant Klebsiella pneumoniae (CRKP) pneumonia. This study collected clinical data from 218 patients with CRKP pneumonia in Beijing hospital from November 2011 to December 2023, analyzed the number of comorbidities carried by CRKP pneumonia patients, comorbidity patterns, Charlson Comorbidity Index (CCI) scores, and comorbidity of underlying diseases, and explored the relationship between various indicators and comorbidity factors and in-hospital mortality in CRKP pneumonia patients. The Ward.D cluster analysis was performed on the comorbidities of patients and used to draw heatmaps. Using a multiple logistic regression model, a nomogram model was constructed to predict in-hospital mortality in patients with CRKP pneumonia. This study included 218 patients with CRKP pneumonia. The results showed that there were significant differences in the age ( P=0.003), comorbidities such as heart failure ( P<0.001), arrhythmia ( P=0.002), chronic liver disease ( P=0.003), chronic kidney disease ( P=0.002), CCI score ( P=0.007), total number of comorbidities ( P<0.001), and comorbidity patterns (respiratory/immune/psychiatric disease patterns and cardiovascular/tumor/metabolic disease patterns, P=0.003) between the survival and death groups of CRKP pneumonia patients. The multiple logistic regression showed that cardiovascular/tumor/metabolic disease patterns ( P=0.030), CCI score ( P=0.040), concomitant heart failure ( P=0.011), and concomitant arrhythmia ( P=0.025) were independent risk factors for in-hospital mortality in patients with CRKP pneumonia. The nomogram model for predicting the risk of in-hospital mortality in patients with CRKP pneumonia, constructed based on the identified risk factors, had an area under the ROC curve of 0.758. Both the ROC curve and validation curve indicated that the nomogram model had stable performance in predicting in-hospital mortality in patients with CRKP pneumonia. In summary, comorbidity factors are risk factors for predicting in-hospital mortality in patients with CRKP pneumonia, and the role of comorbidity factors in in-hospital mortality in patients with CRKP pneumonia should be taken seriously.