ObjectiveTo explore the recognition of oral breath odor map of chronic atrophic gastritis （CAG） patients with dampness-heat syndrome by electronic nose technique. MethodsPatients with chronic gastritis were recruited， including 60 cases in CAG group of dampness-heat syndrome， 50 cases in CAG group of non-dampness-heat syndrome， 60 cases in chronic non-atrophic gastritis （CNAG） group of dampness-heat syndrome， 50 cases in CNAG group of non-dampness-heat syndrome， and 30 cases of healthy volunteers were selected to set up the health control group. Ten cases in the CAG dampness-heat group and 50 cases in the CAG non-dampness-heat group were selected to form the CAG group， and 10 cases in CNAG dampness-heat group and 50 cases in CNAG non-dampness-heat group were selected to form the CNAG group. In addition to the health control group， the remaining patients were tested for Helicobacter pylori （Hp）； the electronic nose （GISXM-MQWA01） was used to collect the oral breath odor of all the participants to draw the mapping， and amplitudes and slopes of each curve （including curves A， B， C， D， E， F， G， H， I， J） of the oral odor mapping of health control group， CAG group， CNAG group， CAG dampness-heat group， CAG non-dampness-heat group， and CNAG dampness-heat group was compared. The modified transformer model was used to classify the odor mapping characteristics， and the confusion matrix method was used to evaluate the classification model， with metrics including accuracy and area under ROC curve （AUC）. ResultsThe Hp positivity rate in CAG dampness-heat group was 80.00% （48/60）， CAG non-dampness-heat group was 62.00% （31/50）， CNAG dampness-heat group was 46.67% （28/60）， and CNAG non-dampness-heat group was 42.00% （21/50）； the difference in Hp positivity rate between CAG dampness-heat group and CAG non-dampness-heat group was statistically significant （P＜0.05）. The amplitudes of response curves A， B， C， D， F， G， and I， and slopes of A and F in the odor mapping of the CAG group were lower than those in health control group， while the amplitude and slope of curve E were higher than those in the health control group and CNAG group （P＜0.05 or P＜0.01）； The amplitude of the response curves A， B， C， D， F， G， and I， and slopes of A， D， and F in the CNAG group were lower than those in the health control group （P＜0.05 or P＜0.01）. The amplitude of response curve D and slope of response curve J in the odor mapping of the CAG dampness-heat group were higher than those in CNAG dampness-heat group， the amplitude of curve F was lower than that in CAG non-dampness-heat group， and the amplitude of curve H and slopes of curve A， H， and J were higher than those in CAG non-dampness-heat group （P＜0.05）. The recognition accuracy of CAG group and health control group reached 77.78%， AUC = 0.88； the recognition accuracy of CAG group and CNAG group was 69.44%， AUC = 0.61； the recognition accuracy of CAG dampness-heat group and CAG non-dampness-heat group reached 75.8%， AUC=0.70. ConclusionElectronic nose technology can make a more accurate identification of the oral breath odor in CAG patients with dampness-heat syndrome， with a decrease in the amplitude of the curve F and an increase in the amplitude of the curve H and in the slopes of the curves A， H， and J may as the characteristics of their odor mapping.

Objective To investigate the inhibitory effect and elucidate the molecular mechanism of 6-gingerol on human multiple myeloma cells.Methods The human multiple myeloma cell lines RPMI 8226 and ARH77 were cultured in vitro,followed by treatment with varying concentrations(50,100,200,300,400 μmol/L)of 6-gingerol.The inhibitory effect on cell proliferation was assessed using the CCK-8 assay.Flow cytometry was employed to evaluate cell apoptosis and cycle distribution.Additionally,qRT-PCR and Western blotting techniques were utilized to analyze gene and protein expression levels.Results The proliferation of RPMI 8226 and ARH77 cells was dose-and time-dependently inhibited by 6-gingerol,leading to the induction of apoptosis with statistically significant differences(P＜0.05).Further mechanistic investigations revealed that treatment with 6-gingerol arrested RPMI 8226 cells in the G0/G1 phase,resulting in a significant increase in Bax levels and a decrease in Bcl-2 mRNA and c-Myc mRNA levels(P＜0.05).Additionally,it significantly upregulated the expression of Bax,Cleaved-PARP,Cleaved-caspase3,P53,and p-AKT proteins while down regulating the expression of Bcl-2 protein(P＜0.05).Conclusions The compound 6-Gingerol exhibits inhibitory effects on the proliferation and induction of apoptosis in MM cells,as well as cell cycle arrest at the G0/G1 phase.Its mechanism of action is likely associated with the suppression of the AKT signaling pathway,downregulation of Bcl-2 family protein expression,and inhibition of c-Myc expression.

Objective To investigate the inhibitory effect and elucidate the molecular mechanism of 6-gingerol on human multiple myeloma cells.Methods The human multiple myeloma cell lines RPMI 8226 and ARH77 were cultured in vitro,followed by treatment with varying concentrations(50,100,200,300,400 μmol/L)of 6-gingerol.The inhibitory effect on cell proliferation was assessed using the CCK-8 assay.Flow cytometry was employed to evaluate cell apoptosis and cycle distribution.Additionally,qRT-PCR and Western blotting techniques were utilized to analyze gene and protein expression levels.Results The proliferation of RPMI 8226 and ARH77 cells was dose-and time-dependently inhibited by 6-gingerol,leading to the induction of apoptosis with statistically significant differences(P＜0.05).Further mechanistic investigations revealed that treatment with 6-gingerol arrested RPMI 8226 cells in the G0/G1 phase,resulting in a significant increase in Bax levels and a decrease in Bcl-2 mRNA and c-Myc mRNA levels(P＜0.05).Additionally,it significantly upregulated the expression of Bax,Cleaved-PARP,Cleaved-caspase3,P53,and p-AKT proteins while down regulating the expression of Bcl-2 protein(P＜0.05).Conclusions The compound 6-Gingerol exhibits inhibitory effects on the proliferation and induction of apoptosis in MM cells,as well as cell cycle arrest at the G0/G1 phase.Its mechanism of action is likely associated with the suppression of the AKT signaling pathway,downregulation of Bcl-2 family protein expression,and inhibition of c-Myc expression.

Objective To evaluate the risk factors and sonographic findings of pregnancies complicated by placenta increta or placenta percreta. Methods Totally, 2219 cases were retrospectively analyzed from 20 tertiary hospitals in China from January 2011 to December 2015. The data were collected based on the original case records. All cases were divided into two groups, the placenta increta (PI) group (79.1％, 1755/2219) and the placenta percreta (PP) group (20.9％, 464/2219), according to the degree of placental implantation. The risk factors and sonographic findings of placenta increta or percreta were analyzed by uni-factor and logistic regression statistic methods. Results The risk factors associated with the degree of placental implantation were age, gravida, previous abortion or miscarriage, previous cesarean sections, and placenta previa (all P<0.05), especially, previous cesarean sections (χ2=157.961) and placenta previa (χ2=91.759). Sonographic findings could be used to predict the degree of placental invasion especially the boundaries between placenta and uterine serosa, the boundary between placenta and myometrium, the disruption of the placental-uterine wall interface and loss of the normal retroplacental hypoechoic zone(all P<0.01). Conclusions Previous cesarean sections and placenta previa are the main independent risk factors associated with the degree of placenta implantation. Ultrasound could be used to make a prenatal suggestive diagnosis of placenta accreta spectrum disorders.

Objective To explore the effect of atorvastatin on the proliferation and apoptosis of K562 cells andto investigate its mechanisms.Methods The cells were treated by different concentrations of atorvastatin.The CCK-8 assay was employed to detect the cell proliferation.The cell apoptosis was detected by AnnexinV-FITC/PI dual staining;the flow cytometry was used to detect the cellular cycle;the activities of caspase-3,-8,-9 were detected by the colorimetric method;qRT-PCR was employed to measure the mRNA expression levels of Bcl-2 and PDCD5 in K562 cells.Results Atorvastatin could inhibit the proliferation of K562 cells in a time-and dose-dependent manner(P＜0.05);and induced the apoptosis of K562 cells,the percentage of G0/G1 phase cells was increased after atorvastatin treating k562 cells(P＜0.01),while the percentage of S phase cells was decreased(P＜0.01),moreover which showing the concentration dependence(P＜0.01);atorvastatin activated the caspase-3,-8,-9 (P＜0.01);down-regulated Bcl-2 mRNA expression and up-regulated PDCD5 mRNA expressionin a concentration dependence(P＜0.01).Conclusion Atorvastatin can inhibit the proliferation and induce apoptosis in K562 cells.

Portable electrocardiogram monitor is an important equipment in the clinical diagnosis of cardiovascular diseases due to its portable, real-time features. It has a broad application and development prospects in China. In the present review, previous researches on the portable electrocardiogram monitors have been arranged, analyzed and summarized. According to the characteristics of the electrocardiogram (ECG), this paper discusses the ergonomic design of the portable electrocardiogram monitor, including hardware and software. The circuit components and software modules were parsed from the ECG features and system functions. Finally, the development trend and reference are provided for the portable electrocardiogram monitors and for the subsequent research and product design.
China ; Electrocardiography ; instrumentation ; Equipment Design ; Humans ; Monitoring, Physiologic ; instrumentation ; Software

Objective To explore the differentiation of human bone marrow measenchymal stem cells (hMSCs) into neuron-like and dopaminergic neuron-like cells in vitro.Methods The hMSCs were isolated from adult human bone marrow and expanded on the flask undifferentiated state for 2 passages. After pretreatment with WHI-P131 for 48 h, the hMSCs were cultured at the medium containing 10 ng/ml basic fibroblast growth factor for 24 h, then incubated with all-trans-retinoic acid and glial-derived neurotrophic factor in serum-free media for 5 h. The surface markers of differentiated neuron were detected by immunocytochemical method and the transdifferentiation process was observed under light microscope.Results Under induction conditions, hMSCs progressively resumed typical neuronal morphological characteristics. After hMSCs were incubated in induction medium for 5 h, the percentage of NSE, nestin, GFAP, TH and DAT positive cells were (77.0?5.7)%, (54.2?3.7)%,(8.8?2.4)%, (36.5?15.8)% and (26.0?14.2)%, respectively. There were no positive expressions in the control group.Conclusion The hMSCs are able to differentiate into neuron-like and dopaminergic neuron-like cells in vitro.