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 effects of glycogen synthase kinase-3β (GSK3β)/eukaryotic extension factor kinase 2 (eEF2K) signaling pathway on the process of pulmonary fibrosis through in vivo experiments, and find new ideas for clinical treatment of pulmonary fibrosis. Methods: The pulmonary fibrosis model of C57BL/6 male mice was induced by bleomycin with intratracheal injection at the dose of 2 mg/kg. After 14 days of modeling, animals were divided into model group, negative inhibition group and inhibition group (n=5 for each group), and control group was not processed. The inhibition group was treated with TDZD-8 (4 mg/kg) after modeling, the negative inhibition group was given DMSO solution after modeling, and the samples were collected after 28 days. Hematoxylin-eosin staining method was used to detect lung fibrosis in mice and scored according to Ashcroft scale. Expression levels of GSK3β, p-GSK3β, eEF2K, p-eEF2K (Ser70, Ser392, Ser470), precursor protein of matrix metalloproteinase-2 (pro-MMP-2), matrix metalloproteinase-2 (MMP-2), collagen I (Col I), collagen Ⅲ (Col Ⅲ) and α-smooth muscle actin (α-SMA) were detected by Western blot. Results: Compared with control group, the fibrosis score was up-regulated, the expression levels of GSK3β, p-GSK3β, p-eEF2K (Ser70, Ser392, Ser470), pro-MMP-2, MMP-2, Col I, Col Ⅲ and α-SMA were increased, while that of eEF2K was decreased in model group (P＜0.05). Compared with model group, the fibrosis score, expression levels of GSK3β, p-GSK3β, p-eEF2K (Ser70, Ser392, Ser470), pro-MMP-2, MMP-2, Col I, Col Ⅲ and α-SMA were decreased, but the expression level of eEF2K was increased in inhibition group (P＜0.05). Conclusion: GSK3β can activate eEF2K by phosphorylation at the sites of Ser70, Ser392 and Ser470, increase the contents of fibrosis indicators, promote the formation of pulmonary fibrosis, and aggravate lung tissue lesions.
Animals ; Collagen ; Collagen Type I ; Elongation Factor 2 Kinase/metabolism* ; Eukaryota/metabolism* ; Fibrosis ; Glycogen Synthase Kinase 3 beta ; Male ; Matrix Metalloproteinase 2/metabolism* ; Mice ; Mice, Inbred C57BL ; Pulmonary Fibrosis/chemically induced* ; Signal Transduction

Objective:To study the effects of isoproterenol(Iso) on the proliferation of cultured submandibular gland cells of SD rats. Methods:Submandibular gland cells of SD rats were primarily cultured. The cells were exposed to Iso at 10 -3 g/L continuously for 8 days or intermittently(2 h each day for 8 days). The cell proliferation was sutdied by bromodeoxyuridine Brdu labeling and cell counting.Results:Iso increased cell proliferation(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 prepare an acellular matrix from trachea of rabbits and SD rats, and to investigate its biocompatibility.Methods: A modified detergent and enzyme link extraction procedure was performed to remove cells from the trachea of SD rats and rabbits. The histology, topography of inner-surface and biocompatibility were studied by morphological observation,cell culture and in vivo transplantation respectively.Results:The acellular trachea matrix did not inhibit the growth and amylase secretion of allogenic salivary gland cells cultured on it.The allogenically transplanted acellular trachea matrix did not result in inflammation reaction of the host tissue,could integrate with surrounding tisses.Conclusion:The acellular trachea matix is biocompatible.

s Objective: To study the feasibility of allogeneic tra ns plantation of myoblasts of SD rats for the reconstruction of facial muscle de fects. Methods: Myoblasts obtained from the forelimbs and hindlimbs of neonatal SD rats were purified and cultured. 5?10 4 myoblasts w ere seeded onto each of type Ⅰcollagen sponges in the size of 1.5 mm?0.8 mm? 0.5 cm. The myoblasts/sponge constructs were transplanted into the facial muscl e defects of syngeneic mutured rats and observed with microscopy,immunohistoche mistry and electromyography (EMG).Result:Myoblasts attac hed and kept alive on type I collagen for at lest 3～4 days in culture. 4 and 8 w eeks after transplantation,muscle like tissue with blood vessles was observed i n the implants. Expression of actin and myosin in the implants was similar to th at in the control muscle.8 weeks after implantation,the spike wave (mV) on the g rafted side and control side was 0.7?0.3 and 2.7?0.6 ( P

Objective To study the expression of Survivin in breast carcinoma combined with prognosis of ten-year follow-up.Methods The expression of Survivin was investigated by immunohistochemistry in 60 cases of breast cancer and 20 tumor surrounding tissue.All the cases were performed with prognosis of tenyear follow-up.Results The expression rate of Survivin in breast carcinoma(68.3%)was higher than that in fibroadenoma of bast tissue(25%)(χ2=20.03,P＜0.01).Survivin didn't experss in tumor surrounding tissue.There Was no relationship among the expression of Survivin and the histological differentiation,clinical staging,and lymph node metastasis of breast carcinoma.The expression of Survivin was correlated with the survival years of patients.Conclusion The expression of Survivin was up-regulated in breast carcinoma,which indicated that survivin may play an important role of the genesis and development of breast cancer,but it may play negative correlated with breast carcinoma.

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*

Objective To identify the risk factors of corneal endothelial cell injury caused by phacoemulsification, so as to provide the evidence for formulating interventions for prevention of corneal endothelial cell injury among cataract patients. Methods A total 248 eyes from 212 cataract patients that underwent phacoemulsification were selected as study subjects. The associations of subjects’ age, gender, left/right eye, pupillary diameter, grades of lens nucleus hardness, duration of phacoemulsification, total ultrasound energy, total infusion fluid amount with endothelial cell loss were evaluated using univariate analysis, and the independent risk factors for corneal endothelial cell injury caused by phacoemulsification were identified using multiple linear regression analysis. Results The density of endothelial cells was (2282.4 ± 412.16) cells/mm² prior to phacoemulsification and (1921.77 ± 125.46) cells/mm² months after phacoemulsification in 239 affected eyes, and the proportion of endothelial hexagonal cells was (54.41 ± 7.22)% prior to phacoemulsification and (45.62 ± 3.58)% months after phacoemulsification (χ² = 5.43, P < 0.05). The incidence of corneal endothelial cell injury was 15.5% in 239 affected eyes. Univariate analysis showed that advanced age, small pupillary diameter, long duration of phacoemulsification, high grades of lens nucleus hardness and high total ultrasound energy were associated with endothelial cell loss, while gender and surgical eyes (left or right eye) were not associated with endothelial cell loss. Multiple linear regression analysis revealed that high grades of lens nucleus hardness, high total infusion fluid amount, long duration of phacoemulsification and high total ultrasound energy were independent risk factors for endothelial cell loss. Conclusions Lens nucleus hardness, high totalinfusion fluid amount, long duration of phacoemulsification and high total ultrasound energy are independent risk factors for endothelial cell loss caused by phacoemulsification.

OBJECTIVETo comparatively study the curative effects of combined massage-smouldering-washing therapy (MSW) and mini-invasive surgery in treating knee osteoarthritis (KOA) of mild-moderate degree so as to provide a suitable therapeutic protocol.

METHODSSixty patients with KOA were assigned to two groups. The treatment group was treated with MSW once a day for 10 days as one course, and 4 courses were applied totally with an interval of 3 days between courses. The control group was treated with mini-invasive surgery by arthroscopic mopping, followed with post-operational intra-articular cavity injection with sodium hyaluronate injection, 20 mg every week for 5 times continuously. The therapeutic effect and the changes in scores of clinical symptoms and signs before and after treatment in the two groups were observed and compared.

RESULTSOutcome of 3-month follow-up showed the effective rate was 90% in the treatment group and 93.33% in the control group; scores of clinical symptoms and signs effectively improved in both groups, but the improvement on the 4 items (joint pain, swelling, soreness of loin and knee, and cold aversion of knee) was superior in the treatment group, while that on the other 4 items (pain during squatting or half-squatting, up stairs or down stairs, joint stiffiness and joint kinetic capacity) was superior in the control group (P < 0.05).

CONCLUSIONBoth MSW and mini-invasive surgery have definite curative effect on KOA but with different particularities.

Adult ; Aged ; Aged, 80 and over ; Combined Modality Therapy ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Knee Joint ; physiopathology ; surgery ; Male ; Massage ; Middle Aged ; Minimally Invasive Surgical Procedures ; Osteoarthritis, Knee ; drug therapy ; physiopathology ; surgery ; therapy