Objective To transform hospital information service mode based on palm hospital based on WeChat.Methods Palm hospital based on WeChat was described from the aspects of background,execution and key points,whose effects and problems were analyzed.Results Palm hospital interfaced with hospital information system,changed the traditional medical service flow and doctor-patient communication,and posed a new mode for mobile medical service.Conclusion Palm hospital based on WeChat is one mode for embodiment of internet+ medical service,and may be of references and prospects for mobile medicine.

Objective : To investigate the impact of dexmedetomidine on the oncological behavior of hepatocellular carcinoma and explore the role of NF-E2-related factor 2 (Nrf2) at both in vitro and in vivo levels． Methods : In vivo experiment，Male C57BL/6J mice were randomly divided into a control group ( Ctrl group) ，a hepatocellular carcinoma group ( HCC group) ，and a hepatocellular carcinoma + dexmedetomidine group ( HCC + Dex group) . Hepatocellular carcinoma was induced in mice by combining N-Nitrosodiethylamine ( DEN) / carbon tetrachloride ( CCl4 ) ，followed by daily intraperitoneal injection of 10% dexmedetomidine for two weeks．After feeding the mice for one month，the mice were assessed for the quantity and size of liver tumors．The proliferation ability of liver cancer was evaluated using Ki67 immunohistochemistry．Additionally，the expression level of Nrf2 protein in tumor tissue was measured through immunofluorescence．In vitro experiment，Hepa1-6 cells were incubated with different concentrations of dexmedetomidine (0. 1，1，5 nmol /L) for 48 hours to examine their effects．The proliferation， migration and invasion abilities of Hepa1-6 cells were evaluated using the MTT and Transwell methods．The expres- sion level of Nrf2 protein in the Hepa1-6 cells was measured using Western blot and immunofluorescence．Addition- ally，the proliferation ，migration and invasion abilities of cells were assessed after Nrf2 knockdown via si-RNA transfection，in combination with incubation with 1 nmol /L dexmedetomidine for 48 hours. Results : ompared to the HCC group，the anatomical examination results revealed an increase in the number of liver tumors and the lon- gest diameter in the HCC + Dex group (P ＜0. 05) ． Ki67 immunohistochemistry results indicated the number of Ki67 positive cells in liver cancer tissue increased in the HCC + Dex group (P＜0. 01) ．The immunofluorescence assay demonstrated an upregulation of Nrf2 expression level in the HCC + Dex group (P ＜0. 05 ) ． MTT results showed that 1 nmol /L of dexmedetomidine increased the cell viability of Hepa1-6 cells (P＜0. 05) ．Transwell re- sults indicated that 0. 1 ，1 ，and 5 nmol /L of dexmedetomidine enhanced the invasive ability of Hepa1-6 cells， while 0. 1 and 1 nmol /L of dexmedetomidine enhanced the migration ability (P＜0. 05) ．Western blot and immu- nofluorescence results showed an upregulation of Nrf2 expression level in cells after treatment with 1 nmol /L dexme- detomidine (P＜0. 01) ．The Nrf2 expression level of cells was reduced using si-RNA，followed by treatment with 1 nmol /L dexmedetomidine．The results from MTT and Transwell assays revealed a decrease in the viability，invasion and migration ability of Hepa1-6 cells (P＜0. 01) ． Conclusion Dexmedetomidine may enhance the proliferation， invasion and migration capacity of hepatocellular carcinoma by upregulating the expression of Nrf2 .

OBJECTIVETo investigate the effects of drug-contained sera (DCS) of Naoluo Xintong (NLXT) and Zuogui Pill (ZGP) on the proliferation and differentiation of in vitro cultured embryonic neural stem cells (NSCs) in rats.

METHODSRat's embryonic NSCs were cultured in medium supplemented with 10% DCS with NLXT and ZGP separately, the effects of DCS in enhancing proliferation and inducing differentiation were observed and compared by phase contrast microscopy and immunofluorescence staining.

RESULTSMajority of NSCs were induced to neurons, astrocytes or oligodendrocytes in medium supplemented with either DCS-NLXT or DCS-ZGP, with the growth of them promoted to some extent. However, DCS-NLXT induced the differentiation rather slowly but with the differentiated neurons more resemble to the mature neuron in morphology, while DCS-ZGP promoted the stem cell growth more effectively.

CONCLUSIONBoth NLXT and ZGP could promote the differentiation and growth of in vitro cultured NSCs, but with exiguous difference. It is feasible to induce the proliferation and differentiation of NSCs by way of using Chinese medicine drug-therapy for supplementing qi and activating blood circulation as well as that for tonifying Shen to generate marrow.

Animals ; Cell Differentiation ; drug effects ; Cell Proliferation ; drug effects ; Cells, Cultured ; Drugs, Chinese Herbal ; pharmacology ; Female ; Male ; Neural Stem Cells ; drug effects ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Serum ; chemistry

OBJECTIVETo observe the expression levels of hippocampal vascular endothelial growth factor (VEGF), fms-like tyrosine kinase-1 (flt-1), basic fibroblast growth factor (bFGF), and basic fibroblast growth factor receptor (bFGF-r) in vascular dementia (VD) rats, thus studying the angiogenesis mechanism of moxibustion in VD.

METHODSSixty male elderly Wistar rats were selected. The VD rat model was prepared by bilateral carotid artery occlusion and reperfusion of sodium nitroprusside injection. The model rats were divided into 3 groups by the random digit table, i. e., the moxibustion group, the Western medicine group, and the model group. A sham-operation control group was also set up. In the moxibustion group rats was acupunctured at Baihui (GV20), Shenting (GV14), and Dazhui (GV24). Aniracetam was given to rats in the Western medicine group by gastrogavage for 2 therapeutic courses, 15 days as one course. The learning and memory results were observed by the neuroethological score in combination of step-down avoidance test before treatment and by the end of the 2nd course respectively. The expression levels of hippocampal VEGF, flt-1, bFGF, and bFGF-r of all rats were detected using immunohistochemical assay.

RESULTSAfter 2 courses of treatment, statistical difference existed in the latent period, the error times, and the neuroethological score in the moxibustion group and the Western medicine group when compared with the model group (P < 0.01, P < 0.05). Statistical difference existed in the latent period and the neuroethological score between the moxibustion group and the Western medicine group (P < 0.05), which indicated that moxibustion and Western medicine showed significant effects in improving the latent period, decreasing the error times and the neuroethological score. Better results were obtained in the moxibustion group than in the Western medicine group (P < 0.01, P < 0.05). Statistical difference of the average grey level (AGL) of hippocampal VEGF, flt-1, and bFGF existed in the moxibustion group and the Western medicine group when compared with the model group. Statistical difference of the bFGF-r expression existed only between the moxibustion group and the model group. Statistical difference of the VEGF and flt-1 expressions existed between the moxibustion group and the Western medicine group (P < 0.05).

CONCLUSIONSMoxibustion showed confirmative effects in improving the behavioral score and memory performance in VD rats. Its mechanisms might lie in that moxibustion regulated and controlled the expression levels of hippocampal VEGF, flt-1, bFGF, and bFGF-r in VD rats. Particularly it up-regulated the expression levels of key factors VEGF and flt-1, promoted the angiogenesis in the vital parts, and ultimately stimulated the repairing mechanisms of cerebral nerve injury.

Animals ; Dementia, Vascular ; metabolism ; therapy ; Fibroblast Growth Factor 2 ; metabolism ; Hippocampus ; metabolism ; Male ; Moxibustion ; Rats ; Rats, Wistar ; Receptor, Fibroblast Growth Factor, Type 2 ; metabolism ; Vascular Endothelial Growth Factor A ; metabolism ; Vascular Endothelial Growth Factor Receptor-1 ; metabolism

Objective To investigate the relationship between MRI rating of white matter hyperintensities (WMH) within cholinergic pathway and vascular dementia in Binswanger's disease.Methods 41 patients with Binswanger's disease undergone inspection of MRI. On 4 selected axial images, the severity of WMH in the cholinergic pathways was rated on a 3-point scale for ten regions identified with major anatomical landmarks. The cholinergic pathways hyperintensities scale (CHIPS) were developed by Bocti based immunohistochemical tracings of the cholinergic pathways. Subjects underwent neuropsychological testing with the Mattis Dementia Rating Scale (DRS) to assess cognitive domains of interest (attention, episodic memory, executive functions). Spearman correlation coefficients were used to compute association between CHIPS score and DRS score.Results The total score of DRS, the scores of DRS attention subscale and memory subscale were 105.6±18.2, 29.5±4.2 and 11.3±3.2 respectively. The score of CHIPS was 35.6±13.7. After accounting for age and education in a multiple linear regression model, the CHIP ratings were associated with impaired performance on the DRS ( r=-0.43, P<0.05).Conclusion The MRI rating of WMH within cholinergic pathway has strong correlations with cognitive performance in patients with Binswanger's disease.

Objective : To study the effect of crisaborole on imiquimod (IMQ) Ⅳinduced psoriasis in mice. Methods: Forty eight Balb/c mice were randomly divided into crisaborole group (7. 5 , 15 , 30 mg/cm2），halometasone group ( 15 mg/cm2 ) , model group and normal group. IMQ was applied to the back of mice to establish the psoriasis model. Psoriasis area and severity index ( PASI) score was calculated , pathological changes , skin epidermal thickness and inflammatory cell infiltration in the dermis were observed by HE staining. The expressions of keratin (K) 1 , K10 , K6 , K16 and K17 in skin lesions were detected by Western blot and immunohistochemistry. The levels of cyclic adenosine monophosphate ( cAMP) , protein kinase A ( PKA) and phospho⁃cAMP response element binding protein (p⁃CREB) were detected. Results : Compared with the model group , the PASI score of the crisaborole group decreased , the expression levels of proliferative keratin ( K6 , K16 and K17 ) decreased( F = 12. 62、19. 41、28. 39 ,P < 0. 01) , and the expression levels of differentiation keratin (K1 and K10) increased(F = 27. 95、9. 64 , P < 0. 01) . Conclusion Crisaborole plays a therapeutic role in IMQ⁃induced psoriasis in mice by regulating the abnormal proliferation and differentiation of keratinocytes.

Objective: To investigate the effect of berberine (BBR) on the proliferation and autophagy of mesangial cells in high glucose (HG) environment and the specific molecular mechanism． Methods: Mesangium cells at exponential growth stage were divided into the following groups : normal group，high glucose group，high glucose + BBR treatment group (30，60 and 90 μmol / L) ，high glucose + BBR (90 μmol / L) + AMPK inhibitor Compound C group ( CC group) ; the number of mesangial cells was calculated by high content cell imager．The expressions of type Ⅳ collagen ( Col-Ⅳ) ，fibronectin (FN) and microtubule-associated protein 1 light chain 3B (LC3B) in mesangial cells were detected by immunofluorescence assay．The protein expression levels of LC3B，Beclin-1， p62，Col-Ⅳ , FN and silencing regulatory factor 1 (SIRT1) / adenylate activated protein kinase (AMPK) signaling pathway were detected by Western blot. Results: Compared with the normal group ，high content cell imaging showed abnormal proliferation of mesangial cells in the hyperglycemic group．The results of immunofluorescence and Western blot showed that the expression levels of Col-Ⅳ and FN deposited in mesangial extracellular matrix increased in the high glucose group．The results of Western blot showed that the protein expressions of SIRT1，p- AMPK，LC3B and Beclin-1 decreased，while the protein expressions of p-p65 and p62 increased．BBR inhibited the abnormal proliferation of mesangial cells induced by high glucose．BBR could reduce the expression levels of Col-Ⅳ and FN deposited in mesangial extracellular matrix． BBR could increase the expressions of SIRT1 ，p- AMPK，LC3B and Beclin-1 proteins in mesangial cells，while decrease the expressions of p-p65 and p62 proteins. CC group weakened the inhibition of mesangial cell proliferation and autophagy by high dose BBR. Conclusion Berberine can effectively inhibit the proliferation of mesangial cells induced by high glucose and increase the level of autophagy，which may be related to SIRT1 / AMPK signaling pathway.

Huperzine A (Hup-A) is a poorly water-soluble drug with low oral bioavailability. A self-microemulsifying drug delivery system (SMEDDS) was used to enhance the oral bioavailability and lymphatic uptake and transport of Hup-A. A single-pass intestinal perfusion (SPIP) technique and a chylomicron flow-blocking approach were used to study its intestinal absorption, mesenteric lymph node distribution and intestinal lymphatic uptake. The value of the area under the plasma concentration-time curve (AUC) of Hup-A SMEDDS was significantly higher than that of a Hup-A suspension (<0.01). The absorption rate constant () and the apparent permeability coefficient () for Hup-A in different parts of the intestine suggested a passive transport mechanism, and the values ofandof Hup-A SMEDDS in the ileum were much higher than those in other intestinal segments. The determination of Hup-A concentration in mesenteric lymph nodes can be used to explain the intestinal lymphatic absorption of Hup-A SMEDDS. For Hup-A SMEDDS, the values of AUC and maximum plasma concentration () of the blocking model were significantly lower than those of the control model (<0.05). The proportion of lymphatic transport of Hup-A SMEDDS and Hup-A suspension were about 40% and 5%, respectively, suggesting that SMEDDS can significantly improve the intestinal lymphatic uptake and transport of Hup-A.

ObjectiveTo observe the inhibitory effect of modified Xiao Xianxiongtang on epithelial-mesenchymal transition （EMT） of human gastric cancer MGC803 cells and its relationship with secretory glycoprotein Wnt/β-catenin pathway. MethodThe BALB/c nude mice were implanted with human gastric cancer MGC803 cell suspension in the heterotopic subcutaneous position for inducing tumor. After successful modeling， they were randomly divided into the model group， low-， medium-， and high-dose （16.0，32.0，and 64.0 g·kg^-1） groups of modified Xiao Xianxiongtang， and capecitabine （400 mg·kg^-1） group， with eight mice in each group， and gavaged with the corresponding drugs， once per day， for 28 consecutive days. Those in the capecitabine group received one-week discontinuation after every two weeks of treatment. The general state and body weight of the nude mice were observed， and the transplanted tumor volume was measured. After being killed， they were weighed and the tumor inhibition rate was calculated. Hematoxylin-eosin （HE） staining was carried out for observing the pathological changes in transplanted tumor tissues. The gene and protein expression levels of Wnt1 and β-catenin were detected by real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot， followed by the determination of matrix metalloproteinase-9 （MMP-9）， vascular endothelial growth factor （VEGF）， N-cadherin， E-cadherin， Vimentin， and Snail protein expression by Western blot. The expression levels of cyclooxygenase 2 （COX2） and prostaglandin E₂ （PGE₂） were detected by enzyme-linked immunosorbent assay （ELISA）. ResultIt was found that the transplanted tumor in each group showed different growth trends with time， with the most obvious growth observed in the model group. Compared with the model group， the low-， medium-， and high-dose modified Xiao Xianxiongtang groups exhibited reduced tumor volume and slowed growth to varying degrees over time. After medication for days 7，14，21，and 28， the tumor volumes in the low- and high-dose modified Xiao Xianxiongtang groups and capecitabine group declined （P<0.05， P<0.01）， and that in the medium-dose Xiao Xianxiongtang group was also remarkably reduced after medication for days 14，21，and 28 （P<0.01）. Compared with the model group， the high-dose modified Xiao Xianxiongtang group and capecitabine group showed a significant reduction in the relative tumor volume after treatment for days 7，14，21，28 （P<0.01）， and the low- and medium-dose modified Xiao Xianxiongtang groups also presented with decreased relative tumor volume after treatment for days 14，21，28 （P<0.05， P<0.01）. Compared with the model group， the modified Xiao Xianxiongtang at low， medium， and high doses and capecitabine all increased the tumor inhibition rate to varying degrees （P<0.01）， down-regulated the mRNA and protein expression levels of Wnt1 and β-catenin in tumor tissue （P<0.05， P<0.01） and protein expression levels of MMP-9， VEGF， N-cadherin， Vimentin， and Snail （P<0.05， P<0.01）， up-regulated E-cadherin protein expression （P<0.05， P<0.01）， and reduced COX2 and PGE₂ contents （P<0.05， P<0.01）. ConclusionModified Xiao Xianxiongtang inhibits the EMT of human gastric cancer MGC803 cell-transplanted tumor， which may be related to Wnt/β-catenin pathway.

ObjectiveTo explore the effect of Xiao Xianxiongtang （XXXT） on the transforming growth factor （TGF）-β₁-induced invasion， metastasis， and epithelial-mesenchymal transition （EMT） of gastric cancer MGC-803 cells and the underlying mechanism. MethodThe molecular docking between XXXT and nuclear factor of activated T cells （NFAT） was performed by CB-DOCK （http：//clab.labshare.cn/cb-dock/）. The invasion and metastasis model of MGC-803 cells was established with 10 μg·L^-1 TGF-β₁. MGC-803 cells were classified into blank group， model group， 0.1 g·L^-1 XXXT group， 0.2 g·L^-1 XXXT group， and 0.4 g·L^-1 XXXT group. For further clarifying the key role of Wnt5a/Ca²⁺/NFAT signaling pathway in the inhibition of XXXT on gastric cancer， MGC-803 cells were transfected with Wnt5a overexpression plasmid， and then the cells were classified into blank plasmid group， Wnt5a-OE group， blank plasmid + XXXT （0.4 g·L^-1） group， and Wnt5a-OE + XXXT （0.4 g·L^-1） group. Cell viability was determined by cell counting kit-8 （CCK-8） assay， cell invasion and migration ability by Transwell invasion assay and wound healing assay， expression of EMT-related proteins （E-cadherin， N-cadherin， Vimentin， Snail） and Wnt5a/Ca²⁺/NFAT signaling pathway-related key proteins ［Wnt5a， calcineurin （CaN）， NFAT1， and p-NFAT1］ by Western blot， and changes in intracellular Ca²⁺ concentration by immunofluorescence assay. ResultMolecular docking suggested that XXXT acted on Wnt5a/Ca²⁺/NFAT signaling pathway. XXXT （0.1， 0.2， 0.4 g·L^-1） significantly promoted the loss of MGC-803 cell viability （P<0.05，P<0.01）. It inhibited cells from invading the transwell lower chamber and slowed down the healing of cell wounds in a dose-dependent manner （P<0.05， P<0.01）. Moreover， it promoted the expression of E-cadherin while suppressed the expression of N-cadherin， Vimentin， and Snail （P<0.05， P<0.01）. Further experiments showed that XXXT could inhibit the expression of Wnt5a， CaN， NFAT1， and p-NFAT1， and reduce the nuclear expression of NFAT1 and the transcription activity mediated by NFAT1， so as to reduce the cellular Ca²⁺ concentration （P<0.05， P<0.01）. XXXT can reverse the effect of Wnt5a （P<0.05， P<0.01）. ConclusionXXXT can attenuate the invasion， metastasis， and EMT of MGC-803 cells via the Wnt5a/Ca²⁺/NFAT pathway， thereby weakening the tumor-promoting effect of TGF-β₁. In summary， XXXT may exert therapeutic effect on gastric cancer by regulating the invasion， metastasis， and EMT of gastric cancer cells.