BACKGROUND:Fewer ethical issues exist in adult stem cells, and some operating technologies are relatively mature. Therefore, to construct tissue-engineered salivary glands using adult stem cells is very attractive and seductive with an extremely important application prospect. OBJECTIVE:To establish a rat model of salivary gland injury by ligation of the main excretory duct of the submandibular gland and to explore the existing feasibility and location of adult stem cells in the injured models. METHODS:The main excretory duct of the right submandibular glands was ligated in Sprague-Dawley rats. After 1 week, rats were kil ed to remove the bilateral glands that were then subject to hematoxylin-eosin staining, PAS glycogen staining and immunohistochemical staining for determination of CK-19, Bcl-2, Ki-67. After that, we compared the normal submandibular gland with the damaged model after ligation of main excretory duct. RESULTS AND CONCLUSION:The rats showed differences in the volume and mass of the affected and normal submandibular glands. The normal submandibular gland was oval, ruddy, smooth, soft with an intact envelop. After ligation, the injured submandibular gland appeared to have atrophy with dark red in color, irregular morphology, envelop congestion, and rough texture;the surrounding vessels showed compensatory expansion. PAS-positive gland cells disappeared, CK-19-postive smal duct epithelial cells proliferated, and laminin-positive cells that were rarely found in the normal gland existed around the duct. In addition, Bcl-2/Ki-67 positive cells were both increased. These findings indicate that stem/progenitor cells may be located in the periductal area of the submandibular gland;and the model of submandibular gland injury established by ligation of the main excretory duct is effective to activate stem/progenitor cells in the submandibular gland.

Objective To investigate the relationship between mRNA expression of DMBT1 in breast cancer tissues and clinicopathological characteristics of patients with breast cancer.Methods 60 cases of breast cancer tissues,30 cases of breast paracancerous hyperplasia tissues and 30 cases of breast paracancerous normal tissues were selected,then reverse transcription-polymerase chain reaction (RT-PCR) were performed to detect the differential expression of DMBT1 in mRNA levels.Furthermore,its relationship with clinicopathological characteristics of patients with breast cancer was analyzed.Results 44 out of 60 breast cancer tissues were detected no or low expression of DMBT1 (73.3％),and 16 out of 60 cases were found normal expression of DMBT1(26.7％).There were statistically significant differences between paracancerous normal tissues and breast cancer tissues,also between paracancerous hyperplasia tissues and breast cancer tissues (x2 =11.72,P =0.000 62 ; x2 =15.99,P =0.000 06).No significant difference was found between the low expression of DMBT1 with the age of patients (x2 =1.733,P =0.188),the size of tumor (x2 =0.776,P =0.378) and the histological grade of tissues (x2 =1.000,P =0.316).However,the loss rates of DMBT1 mRNA expression in patients with lymph node metastasis and clinical stage Ⅲ were higher than that in patients without metastasis and clinicalⅠ-Ⅱstage (x2 =4.885,P =0.026 ; x2 =4.600,P =0.032).Conclusion Low expression of DMBT1 mRNA is closely associated with the metastasis and clinical stage of breast cancer.

Alcoholic liver disease(ALD), with its increasing morbidity and mortality, has seriously and extensively affected the health of people worldwide. Methyl ferulic acid(MFA) has been proven to significantly inhibit alcohol-induced lipid production in L02 cells through the AMP-activated protein kinase(AMPK) pathway, but its in-depth mechanism remains unclear. This study aimed to further clarify the mechanism of MFA in improving lipid accumulation in L02 cells through the microRNA-378b(miR-378b)-mediated calcium/calmodulin-dependent protein kinase kinase 2(CaMKK2)-AMPK signaling pathway based on existing researches. L02 cells were induced by 100 mmol·L~(-1) ethanol for 48 h to establish the model of ALD in vitro, and 100, 50, and 25 μmol·L~(-1) concentration of MFA was treated. MiR-378b plasmids(containing the overexpression plasmid-miR-378b mimics, silence plasmid-miR-378b inhibitor, and their respective negative control-miR-378b NCs) were transfected into L02 cells by electroporation to up-regulate or down-regulate the levels of miR-378b in L02 cells. The levels of total cholesterol(TC) and triglyceride(TG) in cells were detected by commercial diagnostic kits and automatic biochemical analyzers. The expression levels of miR-378b in L02 cells were detected by real-time quantitative polymerase chain reaction(qRT-PCR). CaMKK2 mRNA levels were detected by PCR, and protein expressions of related factors involved in lipid synthesis, decomposition, and transport in lipid metabolism were detected by Western blot. The results displayed that ethanol significantly increased TG and TC levels in L02 cells, while MFA decreased TG and TC levels. Ethanol up-regulated the miR-378b level, while MFA effectively inhibited the miR-378b level. The overexpression of miR-378b led to lipid accumulation in ethanol-induced L02 cells, while the silence of miR-378b improved the lipid deposition induced by ethanol. MFA activated the CaMKK2-AMPK signaling pathway by lowering miR-378b, thus improving lipid synthesis, decomposition, and transport, which improved lipid deposition in L02 cells. This study shows that MFA improves lipid deposition in L02 cells by regulating the CaMKK2-AMPK pathway through miR-378b.
Humans ; Ethanol/toxicity* ; AMP-Activated Protein Kinases/metabolism* ; Fatty Liver ; Triglycerides ; MicroRNAs/genetics* ; Calcium-Calmodulin-Dependent Protein Kinase Kinase/genetics*

Using isolated rat hearts perfused on a langendorff apparatus,ischemic preconditioning (IP) was investigated with 5 min normothermic (at 37℃) or hypothermic (at 30 ℃) ischemia, followed by 10 min of reperfusion before the arrest period, as an adjunct to St. Thomas crystalloid cardioplegia during 180 min ischemia. After basline functional data were obtained, IP was induced 1 control hearts underwent no IP. Results showed that IP improved functional recovery from ischemia during 45 min reperfusion in normothermic ischemic preconditioning group (NP) comparing with normothermic control (NC),P

Objective: To evaluate an innovative surgical approach for submandibular gland resection with minimal invasive incision. Methods:With cutaneous incision of 30 mm in the submandibular area, six patients with chronic sialadenitis of submandibular gland were treated with this approach. Anterior facial vein and facial artery were maintained without ligation. Results:The operation time is ranged from 40 to 80 minutes. There were no facial nerve injuries. Furthermore, the surgical stigmata was minimized. Conclusion:The modified minimal incision for submandibular gland resection has less wound and better cosmesis.

Objective:To evaluate the clinical safety and effectiveness of heavy specific gravity levobupivacaine in spinal block.Method:30 selective general surgical patients of ASAⅠ～Ⅱin obstetrics and gynecology were randomly di- vided into levobupivacaine group(L group)and bupivacaine group(B group).After opening the venous channel and transfusing equilibrium liquid 30 mins,the T 4-5 space was selected as the puncture site for the epidural puncture.The 2 medicaments were injected in the rate of 0.1 ml/s respectively.Then the anesthetizing onset time,maintenance time,time of motion blockade and restoration,effect of anesthesia,variations of blood pressure and heart rate and adverse drug reac- tion were observed.Result:The onset time was 82.61?22.10 s in L group and 59.30?21.50s in B group,respectively. The variations of SBP,DBP and HR in L group were less than those in B group.There was no significant difference in the 2 groups in maintenance time,time of motion blockade and restoration and effect of anesthesia.Conclusion:Compared with bupivacaine,heavy specific gravity levobupivacaine can make the same anesthesia effect with a steadier blood circulation. The specific gravity levobupivacaine is a safe and feasible drug for spinal anesthesia.

Objective To obtain the intestines absorption of TPGS-CS/PTX polymeric micelles in rats, a drug-loaded micelle system was established by a kind of amphiphilic copolymer, D-α-tocopherol polyethylene glycol 1000 succinate-chitosan (TPGS-CS) was prepared by grafting D-α-tocopherol polyethyleneglycol 1000 succinate (TPGS) as the donor of the micelle hydrophobic group on chitosan (CS) as bioadhesive material, and loading paclitaxel as model drug. Methods TPGS was activated by its hydroxy-terminal carboxylation with succinic anhydride (SA) and 4-dimethylaminopyridine (DMAP). The TPGS-CS copolymer was prepared by the amidation of free amino groups on CS. The chemical structure of the TPGS-CS grafted copolymer was characterized by Fourier transform-infrared spectroscopy (FT-IR) and Nuclear magnetic resonance spectroscopy (NMR). The polymer micelle loading paclitaxel was selected as model drug and TPGS-CS/PTX was prepared by ultrasonic emulsification method. The encapsulation efficacy (EE) and drug loading (DL) were determined by high performance liquid chromatography (HPLC). The particle size, Zeta potential, and size distribution of the micelle system were measured by dynamic light scattering (DLS). The surface morphology of the micelles was investigated by Transmission electron microscopy (TEM). The in vivo intestines absorption rate (Ka) of paclitaxel-loaded TPGS-CS micelle was calculated in rats. Results The results of FT-IR and 1H NMR indicated that the copolymer (TPGS-CS) was synthesized. The TEM result showed that the formed particles were uniform in shape without aggregation. The Ka of TPGS-CS/PTX was 20 percent higher in comparison to the reference preparation, it indicated that this polymeric micelles could increase bioavailability. Conclusion The proposed TPGS-CS copolymer was successfully synthesized in this experiment, and the drug-loaded micelles prepared by ultrasonic emulsification exhibited good characteristics compared with the reference preparation, the Ka of paclitaxel was increased to some extent to promote oral absorption of the drug.

The aim of this paper is to reveal the change of the brain function for nicotine addicts after smoking cessation, and explore the basis of neural physiology for the nicotine addicts in the process of smoking cessation. Fourteen subjects, who have a strong dependence on nicotine, have agreed to give up smoking and insist on completing the test, and 11 volunteers were recruited as the controls. The resting state functional magnetic resonance imaging and the regional homogeneity (ReHo) algorithm have been used to study the neural activity before and after smoking cessation. A two factors mixed design was used to investigate within-group effects and between-group effects. After 2 weeks' smoking cessation, the increased ReHo value were exhibited in the brain area of supplementary motor area, paracentral lobule, calcarine, cuneus and lingual gyrus. It suggested that the synchronization of neural activity was enhanced in these brain areas. And between-group interaction effects were appeared in supplementary motor area, paracentral lobule, precentral gyrus, postcentral gyrus, and superior frontal gyrus. The results indicate that the brain function in supplementary motor area of smoking addicts would be enhanced significantly after 2 weeks' smoking cessation.

Aim To investigate the protective effect of mogroside V on hydrogen peroxide ( H,02 )-induced oxidative stress response in mouse islet (3 cells MIN6 and the relation of its mechanism to PI3K/Akt signa¬ling pathway.Methods MIN6 cells were treated with 500 (jimol • L_1 H,(), after mogroside V,and cell via¬bility was detected by MTT.The release of reactive ox¬ygen species ( ROS) and apoptotic percentage of MIN6 cells were determined by flow cytometry.The expres¬sions of apoptosis-related factor Bel-2 , proliferation-re¬lated factor PCNA, protein Akt and p-Akt were deter¬mined by Western blot.Results H,02 restrained the proliferation of MIN6 cells obviously, induced ROS pro¬duction and apoptosis, and reduced the expression of Bel-2 and PCN A.The expressions of protein Akt and p-Akt decreased.After treatment of mogroside V , the release of ROS decreased, and the apoptosis of MIN6 cells was inhibited.The expression levels of apoptosis- related protein Bcl-2 and proliferation-related protein PCN A were reversed.The expressions of protein Akt and P-Akt increased.The viability of MIN6 cells in¬duced by H,0, increased.In addition, mogroside V partly reversed the apoptosis induction and ROS pro¬duction of Akt inhibitor MK2206 (5 jjimol • L"1 ) on MIN6 cells.Conclusions Mogroside V has protec¬tive effect on H202-induced oxidative damage in MIN6 cells and its mechanism is related to PI3K/Akt signa¬ling pathway.

Objective PINK1 and Parkin are directly invoveled in the regulation and maintenance of mitochondrial functional morphology. We aim to explore the effect of Wnt2 overexpression on PINK1^B9 Mutant Drosophila and its mechanism in this study. Methods The GAL4-UAS system was used to construct the normal control flies（W1118/ + ；MHC-GAL4/+）, PINK1^B9 transgenic Drosophila model flies（UAS-PINK1^B9 /y；MHC-GAL4 / +；Parkinson's disease model of Drosophila melanogaster), the Wnt2 overexpression flies（UAS-PINK1^B9 /y；MHC-GAL4 / Wnt2 OE） and the Wnt2 RNAi flies（UAS-PINK1^B9 /y；MHC-GAL4 /Wnt2）. On the 5th day, the abnormal wings phenotype rate and flying rate of flies were observed. The contents of Ndufs3 proteins were detected by Western blot. The mRNA expression levels of PGC-1α, Nrf1 and TFAM related to mitochondrial metabolism and synthesis were detected by real-time fluorescence quantitative PCR. The morphology of mitochondria was observed by electron microscopy. Complex I and Complex II function was detected by high-resolution mitochondrial respiratory system. Results Compared with the normal control flies, PINK1^B9 transgenic Drosophila model flies showed increased abnormal wings phenotype rate([1.87±0.06]% vs [68.79±0.70]%), decreased flying rate([ 97.51±0.52)% vs(3.95±0.53)%], and the differences were statistically significant(P<0.05); Compared with PINK1^B9 transgenic Drosophila model flies, the Wnt2 RNAi flies showed decreased abnormal wings phenotype rate[(10.14±1.72)%], increased flying rate([41.83±2.57]%)(P<0.05). Compared with the normal control flies, PINK1^B9 transgenic Drosophila model flies showed decreased expression levels of PGC-1α and Nrf1,Ndufs3 proteins, Complex I and Complex II(P<0.05);On the contrary, the Wnt2 RNAi flies showed increased trends compared with PINK1^B9 transgenic Drosophila model flies(P<0.05). Conclusion Overexpression of Wnt2 protects PINK1^B9 transgenic Drosophila models, which is related to the improvement of mitochondrial function.