Objective: To analyze the clinical efficacy of Acarbose on type 2 diabetes mellitus combined with postprandial hypotension (PPH) in elderly patient. Methods: A total of 60 elderly patients with type 2 diabetes mellitus and PPH who were diagnosed and treated at our hospital from July 2016 to December 2017 were enrolled in this study.Patients were given Acarbose intervention for two weeks.The changes of blood pressure, heart rate and blood glucose before and after treatment were monitored, and the therapeutic effects and side effects were evaluated. Results: After Acarbose intervention, postprandial systolic pressure (F=9.311, P=0.033), diastolic pressure (F=8.710, P=0.026) and mean arterial pressure (F=7.710, P=0.021) were decreased significantly in elderly patients with type 2 diabetes mellitus and PPH by comparison with those before intervention.There was no significant difference in heart rate fluctuation(F=8.091, P=0.069)and in fasting blood glucose level(t=0.209, P=0.120)before and after treatment.The 2-hour postprandial blood glucose level was lower in elderly patients with diabetes mellitus and PPH after treatment of acarbose than before treatment [(7.9±0.9)mmol/L vs. (8.9±1.9)mmol/L, t=18.310, P=0.003]. The incidence rate of PPH was 100.0% before treatment, and decreased to 43.3% (26/60) after acarbose intervention (χ²=51.430, P=0.000). There were 5 patients with adverse reactions, and the incidence rate of adverse reactions was 8.3%(5/60), and no patients had cerebral ischemia. Conclusions Acarbose can alleviate postprandial blood pressure, decrease the fluctuation of postprandial blood glucose and reduce the incidence of PPH, which has a high safety.It may be one of the effective measures in treating diabetes mellitus combined with postprandial hypotension in the elderly.

Objective: To invest the status of symptom clusters in patients with cancer receiving FOLFOX6 chemotherapy during the course of chemotherapy. Methods: Total 100 patients with cancer receiving FOLFOX6 chemotherapy were investigated using MD. Anderson Symptom Inventory-Chinese (MDASI-C). Results: The top severity of symptoms were lack of appetite and nausea during chemotherapy; weary was the highest score during the intermission of chemotherapy. Exploratory factor analysis showed four main symptom clusters: gastrointestinal symptom clusters, physical symptom clusters, mental symptom clusters and subjective feeling clusters. There were no significant difference in the scores of subjective feeling clusters between chemotherapy and the first day after discharge (P>0.05), other symptom clusters also declined slowly; the symptom clusters began to ease significantly from the three day after discharge (P<0.05). Conclusion Patients with cancer suffer from multiple symptoms during FOLFOX6 chemotherapy and during the intermission of chemotherapy. The results are good for establishing early predictions of symptom clusters in intermission of chemotherapy.

OBJECTIVE To investigate the hepato-protective mechanism of thymoquinone (TQ) onthe development of acetaminophen (APAP)- induced liver injury. METHODS In vivo, male kunming mice were injected with a single dose of 300 mg·kg-1 APAP. Some mice were pretreated with TQ (5 or 20 mg·kg-1) and N-acetylcysteine (NAC, 300 mg·kg-1) 2 h before APAP injection. Mice were euthanized at 2 h, 6 h, 12 h after APAP treatment. In vitro, human Chang liver cells were incubated with 3.125, 6.25 or 12.5 μmol·L-1 TQ, 10 μmol·L-1 SP600125 and 500 μmol·L-1 AICAR in the presence of APAP for 24 h. Cell viability were analyzed by MTT assay, protein expressions were assessed by Western blot. RESULTS TQ pretreatment significantly reduced serum aminotransferase and increased hepatic gluta?thione (GSH) and glutathione peroxidase (GSH-PX) activities, while significantly inhibited interleukin-1β(IL-1β) levels. TQ significantly inhibited c-Jun N-terminal kinase (JNK), extracellular signal regulated kinase (ERK) and P38 phosphorylation induced by APAP. Moreover, TQ inhibited phosphatidylinositol 3- kinase (PI3K)/mammalian target of rapamycin (mTOR) signaling activation and activated AMPK phosphorylation induced by APAP. In addition, TQ inhibited signal transducer and activator of transcription 3 (STAT3) phosphorylation on APAP-induced liver injury. In vitro, APAP enhanced JNK phosphorylation and attenuated AMPK phosphorylation in Chang liver cells, and these effects were blocked by pretreatment with TQ, SP600125 (JNK inhibitor) and AICAR (AMPK activator). CONCLUSION Our findings suggest that TQ may actively prevent APAP-induced liver injury, and this effect may be mediated by JNK and AMPK signaling pathways.

OBJECTIVE To investigate the mechanism of SIRT1/AMPK signaling pathway between hepatocytes and hepatic stellate cells (HSCs). METHODS Normal human Chang liver cells and human hepatic stellate cell line, LX-2 cells were treated with SRT1720 (10 μmol·L-1) and AICAR (500 μmol·L-1) prior to ethanol (50 mmol·L-1) for 24 and 48 h. Cell viability was analyzed by methyl thiazolyl tetrazolium assay. SIRT1, AMPK and p-AMPK mRNA levels for 24 h and 48 h were analyzed by RT-PCR, SIRT1, AMPK and p-AMPK protein expressions in the supernatant at 24 and 48 h was detected by Western blot. RESULTS SRT1720 and AICAR effectively decreased LX-2 cell viabilities and exhibited scarcely little toxicity in human Chang liver cells. SRT1720 and AICAR attenuated collagen-I, α-smooth muscle actin (α-SMA) levels, activated liver kinase B-1 (LKB1) and AMPK phosphorylation in ethanol treated LX-2 cells. Meanwhile, SRT1720 and AICAR enhanced SIRT1 expression mediated by ethanol both in Chang liver cells and LX-2 cells. Furthermore, SRT1720 and AICAR suppressed the expression of sterol regulatory element-binding protein-1 (SREBP-1) to regulate fatty acid synthesis. CONCLUSION SIRT1 agonist and AMPK agonist blocked the crosstalk between hepatocytes and HSCs via SIRT1/AMPK signaling pathway to modulate hepatocytes accumulation of lipid and HSCs activation.

Objective To learn the quality of life (QOL) and mental health status of the physically disabled people in Zhejiang Province,in order to provide evidence for improving the quality of life and mental health of the physically disabled people.Methods Using questionnaires and interviews to make household surveys of 950 physically disabled people.The questionnaire included the brief quality of life scale (SF-36) and the general health questionnaire (GHQ-28) in the anxiety and depression scale,physical and mental health status.The basic information and other living conditions of physically disabled people were collected through interviews.Results A total of 907 valid questionnaires were recovered,and the effective response rate was 95.47％.Scores of QOL of 907 physically disabled people was 60.89,and anxiety and depression scores were more than 4 points and there was a high score on anxious and depression.The scores of quality of life,anxiety and depression were not statistically significant between males and females(P ＞0.05).There were significant differences in all dimensions of SF-36 and anxiety and depression in different levels of physically disabled people(P ＜ 0.01).There was a significant negative correlation between the quality of life and anxiety and depression in physically disabled people(rs =-0.626、-0.639,P ＜ 0.01).The multiple linear regression showed that physiological function,role physical,physical pain and general health were the influencing factors of anxiety of the physically disabled people,and role physical,physical pain and general health were the influencing factors of depression of the physically disabled people.Condusion The quality of life of physically disabled people were comparably poor,and presented anxiety,depression and other psychological problems.Physical function status directly affects the quality of life and mental health status.

Objective:To explore the possible mechanism of Yanghe Huayantang in reversing the drug resistance of breast cancer by observing the effect of Yanghe Huayantang on the transplant tumor of tamoxifen （TAM）-resistant breast cancer and its influences on the interaction pathway of estrogen receptor （ER）/phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）/mammalian rapamycin target protein （mTOR）. Method:Fifty mice were randomly divided into 5 groups： blank group， model group， Yanghe Huayantang group， everolimus group， and Yanghe Huayantang+everolimus group. The model of kidney deficiency was established by bilateral ovariectomy， and the blank group was treated with sham operation. Three days after the establishment of the model， all the five groups of mice were inoculated with breast cancer TAM drug-resistant cells （MCF-7/TAM^-） to establish breast cancer TAM -resistant transplanted tumor model. After successful modeling， Yanghe Huayantang group received intragastric administration of Yanghe Huayantang （traditional Chinese medicine preparation 20 mL·kg^-1）， everolimus group received intraperitoneal injection of everolimus （10 mg·kg^-1）. Yanghe Huayantang + everolimus group received Yanghe Huayantang by intragastric administration and everolimus by intraperitoneal injection. The blank group and model group received intragastric administration and intraperitoneal injection of phosphate buffer （PBS）. Drug administration was lasted for 28 days in all groups， once a day. After administration， the tumor tissue was separated and weighed， and the tumor inhibition rate was calculated. Hematoxylin-eosin （HE） staining was used to observe the pathological changes of tumor tissue. Immunofluorescence and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） were used to detect the expression of PI3K， Akt， mTOR， ER protein and mRNA in tumor tissue. Result:Compared with the model group， the tumor volume and tumor weight of Yanghe Huayantang group decreased significantly on the 12th， 20th and 28th days （P<0.01）， and the tumor inhibition rate increased significantly （P<0.01）.Yanghe Huayantang group significantly reduced the density of tumor cells and caused tumor cell necrosis. Compared with the model group， Yanghe Huayantang group， everolimus group and Yanghe Huayantang+everolimus group inhibited the expression of PI3K， Akt， mTOR protein and mRNA （P<0.05， P<0.01）. Compared with the blank group， Yanghe Huayantang group， everolimus group and Yanghe Huayantang+everolimus group all inhibited the protein and mRNA expression of ER， and mRNA expression of ER in Yanghe Huayantang+everolimus group was significantly lower than that in the model group （P<0.01）. Conclusion:Yanghe Huayantang can inhibit the growth of TAM-resistant breast cancer. The mechanism may be that Yanghe Huayantang can reverse the TAM resistance of breast cancer by down-regulating the expression of key molecules of ER/PI3K/Akt/mTOR cross-signal pathway.

OBJECTIVETo evaluate the advantages, disadvantages and their indications of total nasal reconstruction with different techniques.

METHODSA series of total nasal reconstruction were treated with four methods from 1975 to 2003. These methods were tubed flap of arm,midline forehead flap with skin graft, midline forehead flap with bilateral frontotemporal flaps for repairing the donor site, and expanded forehead flap.

RESULTSAll of the patients were treated successfully. The shape and function of the reconstructed noses were satisfactory. However, the traditional forehead flap with skin graft may leave a unsightly big and black scar on the forehead. The technique of the tubed flap of arm could provide enough tissue without remaining forehead scar and be easily shaped, but it required long period, multiple procedures and body fixation for three weeks.

CONCLUSIONSMidline forehead flap with bilateral frontotemporal flaps for repairing the donor site may be good for small nose reconstruction while expanded forehead flap could reconstruct a big nose. Tubed flap of arm may be used to the patients who do not wish to leave any scar on the forehead. Forehead flap with skin graft to repair the donor sit- should generally be avoided for nose reconstruction.

Adolescent ; Adult ; Female ; Humans ; Male ; Middle Aged ; Nose ; surgery ; transplantation ; Nose Deformities, Acquired ; surgery ; Reconstructive Surgical Procedures ; methods ; Reproducibility of Results ; Retrospective Studies ; Skin Transplantation ; methods ; Surgical Flaps ; Treatment Outcome

OBJECTIVE Regulating P2x7R- NLRP3 inflammasome activation might be a potentialtherapeutic strategy to treat alcoholic hepatosteatosis. We investigated whether this process would be modulated by gentiopicroside (GPS), which is attributed to the bitterness of gentian root extract. METHODSAn in vivo model was established by intragastrically treating mice with ethanol, and an in vitro modelwas created by treating HepG2 cells with ethanol or treating RAW 264.7 macrophages and murinebone marrow- derived macrophages (BMDMs) with lipopolysaccharides (LPS) plus adenosine triphos-phate (ATP). RESULTS In alcoholic hepatosteatotic mice model, GPS decreased serum aminotrans-ferase and triglyceride accumulation. GPS regulated sterol regulatory element-binding protein-1 (Srebp1),peroxisome proliferators- actived receptors α (PPARα) and acetyl CoA carboxylase (ACC) expressionvia elevating liver kinase B1 (LKB1)/AMP-activated Kinase (AMPK). Suppression of nucleotide-bindingoligomerization domain-like receptor protein 3 (NLRP3), caspase-1 and expression by GPS resulted inthe inhibition of interleukin-1β (IL-1β) production. In ethanol-exposed HepG2 cells, GPS reduced lipo-genesis and promoted lipid oxidation via P2x7R- NLRP3 inflammasome activation. P2x7R silencingenhanced AMPK activity, and reduced Srebp1 expression in ethanol-treated hepatocytes. GPS down-regulated P2x7R-mediated inflammatory response to extracellular ATP in LPS-primed RAW 264.7 macro-phages and BMDMs. Additionally, P2x7R deficiency attenuated IL- 1β cleavage in RAW 264.7 macro-phages, and GPS further suppressed IL-1β cleavage. CONCLUSION Activation of LKB1/AMPK signalingby GPS might be mediated by P2x7R-NLRP3 inflammasome, suggesting a therapeutic utility of P2x7Rblockade in alcoholic hepatosteatosis treatment.

OBJECTIVE The current study was designed to investigate the anti-steatosis effect of Pleurotus citrinopileatus extract (PC) and the underlying mechanism in vivo and in vitro. METHODS Acute and chronic alcoholic hepatosteatosis murine models and ethanol-treated HepG2 cells were applied. RESULTS In vitro,the anti-steatosis effect of PC was further confirmed via Nile red staining in HepG2 cells treated with ethanol.Both of acute and chronic alcohol-induced mice hepatosteatosis model,PC decreased serum aminotransferase and triglyceride accumulation. Upregulated sterol-regulatory element binding protein1(Srebp1),purinergic ligand-gated ion channel 7receptor(P2X7R)and downregulated sirtuin1 (SIRT1), adenosine 5′-monophosphate (AMP)-activated protein kinase α (AMPKα) caused by acute and chronic alcohol intake were modulated by PC.In ethanol-exposed HepG2 cells,PC reduced lipid accumulation in a concentration-dependent manner and exhibited superior ability in controlling lipid accumulation compared with metformin. CONCLUSION PC could abolish hepatic lipid accumulation through regulating SIRT1-AMPKα signaling in acute and chronic alcohol-induced hepatic steatosis.

OBJECTIVE To investigate toll-like receptor 4(TLR4)-related the regulation of Ornithog-alum caudatum extract(OCE)on inflammatory responses in lipopolysaccharide(LPS)activated macro-phages.METHODS Primary peritoneal macrophage,Raw 264.7,and THP-1 were incubated in 96-well plate for 24 h and treated with OCE of the concentration of 0-400 μg/ml for 4h.The viability of cells was measured by MTT assay.Specific concentrations of OCE were added into the medium of primary peri-toneal macrophage, Raw 264.7, and THP-1, respectively, then following with lipopolysaccharides (LPS). Cells were harvested and the total cellular protein and nuclear protein were extracted, and the protein content was determined using BCA protein assay Kit.The expressions of TLR4,inducible nitric oxide synthase(iNOS),cyclooxygenase 2(COX-2),α-inhibitor of NF-κB(IκB-α)and nuclear factor-κB (NF-κB)were assayed by Western blot.The expressions of interleukin-1α(IL-1α),interleukin-1β(IL-1β), interleukin-18(IL-18),and tumor necrosis factor-α(TNF-α)were measured by RT-PCR.RESULTS The results of MTT showed that OCE has no cytotoxicity in Raw 264.7 cells between 1.56 μg/ml and 400 μg/ml. Compared with normal group,the expressions of TLR4,iNOS,COX-2,NF-κB and IL-1α,IL-1β,IL-18, TNF-α,the level of nitric oxide(NO)were significantly increased by LPS stimulation,while OCE pretreat-ment reduced these increase induced by LPS. However, OCE pretreatment reversed the reduction of IκB-α after LPS stimulation.CONCLUSION OCE might suppress TLR4 expression and block the inflamma-tion process of NF-κB and iNOS,further decrease the expression of COX-2 and inhibit the release of inflammatory factors.