Chronic atrophic gastritis （CAG）， a common digestive system disease， has an unclear pathogenesis. Currently， it is mostly believed to be related to Helicobacter pylori （Hp） infection， immune factors， dietary factors， bile reflux， long-term use of antibiotics and anti-inflammatory drugs， and other factors. Ferroptosis is a regulated cell death mechanism that is iron-dependent and characterized by disruption of iron metabolism and accumulation of lipid peroxides. More and more studies have found that ferroptosis is closely related to the onset of CAG. Professor LI Diangui， a master of traditional Chinese medicine， first proposed the turbid toxin theory， which holds that spleen deficiency and turbid toxin is the main pathogenic mechanism of CAG. Abnormal iron metabolism regulation is a prerequisite for the accumulation of turbid toxin in CAG， and ferroptosis is in accordance with the pathogenic mechanism （spleen deficiency and turbid toxin） of CAG. This article explores the pathological mechanism of spleen deficiency and turbid toxin in CAG from the perspectives of iron metabolism， oxidative stress， and lipid peroxidation， providing theoretical support of traditional Chinese medicine for the modern research on CAG. It enriches the modern scientific connotation of the turbid toxicity theory and provides new ideas and breakthrough points for the clinical treatment of CAG.

Chronic atrophic gastritis （CAG）， a common digestive system disease， has an unclear pathogenesis. Currently， it is mostly believed to be related to Helicobacter pylori （Hp） infection， immune factors， dietary factors， bile reflux， long-term use of antibiotics and anti-inflammatory drugs， and other factors. Ferroptosis is a regulated cell death mechanism that is iron-dependent and characterized by disruption of iron metabolism and accumulation of lipid peroxides. More and more studies have found that ferroptosis is closely related to the onset of CAG. Professor LI Diangui， a master of traditional Chinese medicine， first proposed the turbid toxin theory， which holds that spleen deficiency and turbid toxin is the main pathogenic mechanism of CAG. Abnormal iron metabolism regulation is a prerequisite for the accumulation of turbid toxin in CAG， and ferroptosis is in accordance with the pathogenic mechanism （spleen deficiency and turbid toxin） of CAG. This article explores the pathological mechanism of spleen deficiency and turbid toxin in CAG from the perspectives of iron metabolism， oxidative stress， and lipid peroxidation， providing theoretical support of traditional Chinese medicine for the modern research on CAG. It enriches the modern scientific connotation of the turbid toxicity theory and provides new ideas and breakthrough points for the clinical treatment of CAG.

ObjectiveTo explore the therapeutic effect and mechanism of Xianglian Huazhuo prescription on chronic atrophic gastritis （CAG） in rats based on the Hedgehog signaling pathway. MethodsThe CAG rat model was established by sodium salicylate， N-methyl-N′-nitro-N-nitroguanidine （MNNG）， and irregular feeding. The successfully modeled rats were randomly divided into a model group （180 mg·L^-1）， a moradan group （1.4 g·kg^-1）， and Xianglian Huazhuo Prescription groups with high， medium， and low doses （36， 9， 18 g·kg^-1）， followed by drug intervention. Hematoxylin-eosin （HE） staining was used to observe morphological changes in the gastric mucosa. Transmission electron microscopy was used to observe the ultrastructure of gastric mucosa cells. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression of Sonic Hedgehog （Shh）， Patched 1 （Ptch1）， and Glioma-associated oncogene homolog 1 （Gli1）. Western blot was used to detect the protein expression levels of Shh， Ptch1， and Gli1 in the gastric mucosa. Immunohistochemistry was used to observe the protein expression of the epithelial marker E-cadherin. ResultsCompared with the normal group， the CAG model group showed a reduction in gastric mucosal intrinsic glands and infiltration of inflammatory cells. The ultrastructure of gastric mucosal cells showed nuclear pyknosis， fewer mitochondria， and abnormal mitochondrial structure. The mRNA and protein expression of Shh， Ptch1， and Gli1 in the gastric mucosa were significantly decreased （P<0.05）， and E-cadherin protein expression was decreased. Compared with the model group， the intervention groups showed varying degrees of improvement in histopathological morphology and cellular ultrastructure. The mRNA and protein expression of Shh， Ptch1， Gli1， and E-cadherin increased to varying degrees. Xianglian Huazhuo Prescription upregulated the expression of key Hedgehog pathway factors and E-cadherin at both the mRNA and protein levels （P<0.05）. ConclusionXianglian Huazhuo prescription has a therapeutic effect on CAG in rats， and its mechanism may be related to activation of the Hedgehog signaling pathway and inhibition of epithelial-mesenchymal transition （EMT）.

ObjectiveTo explore the relationships between internet gaming disorder (IGD), interpersonal needs, loneliness, and depression in adolescents through the construction of a chain mediation model, to clarify the underlying mechanisms of these associations, and to provid a theoretical basis for depression prevention and intervention. MethodsBased on the data of the 7th Population Census, using convenient sampling method 1 106 adolescents aged between 10‒19 years in South China (176), North China (147), Central China (332), and East China (451) were selected to conduct a cross-sectional survey, with a ratio of 1∶1∶1.5∶2.5. The survey was conducted with a questionnaire consisting of general information (sex, age, grade, parents’ education level), the Chinese version of the IGDS9-SF, the INQ-15, the short-form of the ULS-8 and the PHQ-9 were used to evaluate the depression status of adolescents. Spearman correlation analysis was used to explore the correlation between the variables. A multiple-mediator model was constructed using IBM SPSS Statistics 22.0 PROCESS to examine the mediating effects of interpersonal needs and loneliness on the relationship between IGD and depression. The significance of the chain mediating effect was tested using the Bootstrap method. ResultsOverall, 39.06% (432/1 106) adolescents experienced depression. The incidence of depression among adolescents with smoking and without smoking was 62.50% and 38.36%, respectively. Similarly, the incidence of depression among adolescents with alcohol consuming and without alcohol consuming was 61.94% and 35.94%, respectively. There were statistically significant differences between IGD, interpersonal needs, loneliness, and depression (P<0.01). The chain mediation model demonstrated a good fit, and the bootstrap test showed that the 95%CI of each mediation path did not include 0, indicating significant mediation effects. The overall effect was 0.337. The direct effect of IGD on depression was significant (effect value=0.138, 95%CI:0.102-0.173, P<0.001). The mediation effects included three paths: ① IGD →interpersonal needs → depression (effect value=0.073, P<0.05), accounting for 21.47% of the total effect;② IGD→ loneliness → depression (effect value=0.093, P<0.05), accounting for 27.35%; and ③ IGD → interpersonal needs → loneliness → depression (effect value=0.036, P<0.05), accounting for 10.59%. ConclusionInterpersonal needs and loneliness independently and jointly mediate the relationship between IGD and depression among adolescents. To reduce depression and improve mental health in this population, measures should be taken to prevent and intervene in IGD, address adolescents’ social and emotional needs, enhance satisfaction of interpersonal needs, and reduce loneliness.

Objective:To investigate the genetic safety of allogeneic bone marrow mesenchymal stem cells (BMSCs) transplantation in traumatic brain injury (TBI).Methods:(1) In vivo experiment: BMSCs from male SD rats were isolated and cultured. Moderate TBI models were prepared by implanting and fixing micro-drug injection cannula into the left ventricle of 12 female SD rats, and 3 d after that, striking the right cerebral cortex of the rats with pneumatic precision percussion device was performed. Four h, and 3, 6, 9, and 12 d after modeling, TBI rats were given a single/multiple BMSCs infusion (2.5×10 5/time, total volume 10 μL) by cannula; 48 and 72 h, and 10 and 14 d after modeling, brain tissues of TBI rats (3 at each time point) were prepared into paraffin specimens. Immunofluorescent staining was used to detect the microglia activation, and RNAscope ? technology was used to detect the co-localization of astrocytes, neurons, microglia and transplanted BMSCs to observe whether the allogeneic BMSCs were integrated with the host brain cells after transplantation into TBI host. (2) In vitro experiment: the frozen and revived microglial cell line BV2 was transfected with green fluorescent protein (GFP)-positive lentiviral particles, and then, BMSCs prelabeled with pHrodo RED probe and BV2 cells pretreated with lipopolysaccharide were co-cultured in a certain ratio (BV2:BMSCs=1:1, 1:2, 2:1); after 36 and 72 h of co-culture, the phagocytosis between the 2 kinds of cells was observed under confocal fluorescence inverted microscope to observe the specific action forms of microglia on BMSCs. Results:(1) In vivo experiment: 48 and 72 h, and 10 and 14 d after modeling, no colocalization of transplanted BMSCs with astrocytes or neurons was found in paraffin sections of brain tissue in TBI rats; however, 10 and 14 d after modeling, microglia in TBI rats were obviously activated and migrated to the left lateral ventricle and choroid plexus, and co-localization of microglia with transplanted BMSCs was observed. (2) In vitro experiment: phagocytosis occurred after co-culture of BV2 cells at different proportions with BMSCs for 36 and 72 h. Conclusion:After transplantation, allogeneic BMSCs do not integrate with astrocytes or neurons of the TBI host, but they could be phagocytosed by microglia, indicating that allogeneic BMSCs transplantation for TBI is genetically safe.

Objective: Attentional biases toward emotional scenes may represent vulnerability and maintenance factors in depression. Antidepressant therapy may improve cognitive function and reduce depression, and is considered as the mechanism of action of antidepressants. Therefore, we conducted an eye-tracking test to examine whether selective serotonin re-uptake inhibitor (SSRI) antidepressants can reduce negative attentional biases and elicit clinical responses in depression. Methods: Twenty first-episode depressive patients freely viewed three types of pictures that depicted different emotional scenes (i.e., positive-control, neutral-control, and negative-control) for 4,000 ms while their eye movements were monitored. The attentional bias to different emotional scenes was assessed before and after eight weeks of SSRI treatment using the eye-tracking method. The control group included a group of healthy individuals. Results: The results revealed that first-episode depressive patients oriented their gaze more frequently to negative images and less to happy images, compared to controls. Importantly, the attentional bias in depressive patients was regulated after eight weeks of SSRI treatment. Patients showed an increased tendency to fixate on positive images and a decreased tendency to focus on negative images. Conclusion This suggests that SSRI antidepressants decrease vulnerability to negative images, while having an effect on attention in respect to positive images.

Objective To investigate the expression profile of cancer-related genes in human bone marrow-derived neural stem cells (Md-NSCs) to determine whether there are any characteristics that could help the evaluation of their tumorigenic potentials.Methods Md-NSCs were cultured in vitro and identified (experimental group);fresh human adult bone marrow cells were used as control group (sifting erythrocytes).The expression profiles of 440 cancer-related genes in cells from the two groups were analyzed by Oligo GEArray Human Cancer Microarray OHS-802;real-time quantitative PCR was performed to detect the expressions of oncogene MYC,matrix metalloproteinase 2 (MMP2),Notch congener 2 (Notch2),stanniocalcin 1 (STC1),integrin α3 (ITGA 3),signal transduction and transcriptional activation factor 5b (STA T5b),Ras congene gene family C (RhoC),and wingless-type MMTV integration site family member 1 (Wnt1).Results As compared with those in the control group,the Md-NSCs from experimental group had 66 tumor-related genes with high expressions (＞3 folds).MYC,MMP2,Notch2,STCI,ITGA3,STA T5b,RhoC and Wnt1 expressions in the Md-NSCs from experimental group were significantly higher than those in the control group (P＜0.05),whose results were accorded with genechip detection results,enjoying the folds of 4.35×100,2.84×100,2.87×100,3.41 ×102,2.22×102,6.99× 100,4.92 × 100 and 3.64 ×100,respectively.Conclusion A number of cancer-related genes are over-expressed in Md-NSCs,and the activations of some of these important oncogenes have been proved to promote human tumorigenesis.

Objective To investigate the effect of celastrol on space learning capability and expressions of beta-amyloid (Aβ) 40 and Aβ42 in hippocampus in APPswe/PS1dE9 double transgenic mouse after partial hepatolobectomy.Methods The 3-month-old APPswe/PS1dE9 double transgenic mice (n =96) were randomly divided into three groups according to the random number table method.Surgery group (group S, partial hepatolobectomy;n =32), celastrol group (group C, injections of dimethyl sulphoxide/DMSO and celastrol for 3 days before undergoing partial hepatectomy, on the surgery day, and for a further 4 days after surgery;n =32), and DMSO group (group D, injections of DMSO for 3 days before undergoing partial hepatectomy, on the surgery day, and for a further 4 days after surgery;n =32).Eight mice were selected randomly in each group and were Morris-water maze trained for continuous 5 days.Theirs learning and memory abilities were evaluated at 1,3, 7 and 14 d after surgery, respectively.Hippocampus was collected and the changes of β40 and Aβ42 were measured by enzyme-linked immunosorbent assay (ELISA) at the time set in advance in each group.Results The average escape latency of group C was significantly shorter than groups S and D at 3, 7 and 14 d after partial hepatectomy (P ＜ 0.05).Times of passing through the platform groups S and D were significantly less than group C (P ＜ 0.05).The expressions of Aβ40/Aβ42 in group C were lower than group S and group D at 1, 3, 7 and 14 d after partial hepatectomy (P ＜ 0.05).Conclusions Through decreasing the expressions of Aβ40 and Aβ42 in hippocampus,celastrol improves the space learning capability in APPswe/PS1dE9, the double transgenic mouse after partial hepatolobectomy.

Objective To investigate the effects of different doses of dexmedetomidine and propofol on electrocorticography (ECoG)during epileptic resection.Methods One hundred cases of epileptic patients undergoing epileptic resection were randomized into five groups (n=20 cases).Af-ter exposure of the cortex,patients were allocated to propofol group or dexmedetomidine group,the propofol were injected intravenously with different target-controlled-infusion (TCI)concentrations at 1.5 μg/ml (group C1),5.0 μg/ml (group C2)respectively.The dexmedetomidine were injected with a loading dose of 0.5 μg/kg within 1 5 min,then followed by a speed of 0.25 μg·kg-1 ·h-1 (group D1 ),0.5 μg·kg-1 ·h-1 (group D2),and 1.0 μg·kg-1 ·h-1 (group D3)respectively.After 1 5 min of steady infusion,the characteristics of ECoG were recorded.Results Compared with the other four groups,the epileptic spike-wave,αandβwaves were significantly decreased,whileδwave was significantly increased in group C2 (P < 0.05 ).Sometimes burst-suppression-patterns were recorded under propofol. With the dose of dexemedetomidine increasing in groups D1,D2,D3,the epileptic spike-wave,αwave andβwave gradually decreased,while δwave gradually increased (P <0.05).Conclusion Propofol produces dose-dependent inhibition on ECoG,but the epileptic spike-wave still can be differentiated if the plasma con-centration lower than 1.5 μg/ml.Compared with propofol,dexmedetomidine injected with 0.25-0.5 μg· kg-1 ·h-1 ,has few disturbance on epileptic spike-wave differentiation and location during ECoG monito-ring,and is more eligible for epileptic resection anesthesia.

Objective To study the influences of hepatolobectomy on space learning capability and the expressions of Drebrin and PSD95 in the hippocampus in APP/PS1 transgenic mouse model of Alzheimer's disease.Methods A total of fifty-four 3-month-old APP/PS1 transgenic mouse were randomly divided into 3 groups:3-month-old control group,sham surgery group,hepatolobectomy group,3-month-old littermates control group and 6-month-old control group.Morris water maze test was used to observe space learning capability on the 1st,3rd,7th,14th day after surgery,meanwhile the expressions of Drebrin and PSD95 in hippocampus were measured by Western blotting.Results Compared with the sham surgery group,the results of the Morris water maze test were decreased in hepatolobectomy group at day 3,7,14 after surgery [(62.9±6.9) s vs.(35.7±12.2) s,(66.3± 9.5) s vs.(39.3±8.3) s,(67.1±7.5) s vs.(32.6±14.1) s],and 6-month-old control group [(75.9±12.1) s] (all P＜0.05).The escape latency were (62.9±6.9)s,(66.3±9.5)s,(67.1± 7.5)s and (75.9±12.1)s,the probe trials were (2.1±0.7) times,(1.83±1.5) times,(2.5±1.9) times and (1.8±0.8) times respectively in hepatolobectomy group at day 3,7,14 after surgery and 6-month old control group.No significant differences in the results of the Morris water maze test were found among 3-month-old control group,3-month-old littermates control group,and sham surgery group.Compared with 3-month-old control group and sham surgery group atday 1,3,7,14 after surgery the expressions of Drebrin were decreased in 6-month-old control group and the hepatolobectomy group at the same time points.Meanwhile,the expression of Drebrin in hepatolobectomy group was increasedat day 14 versus day 7 after surgery.Compared with 3 month-old control group,the expression of Drebrin was increased at day 7 after sham surgery.Compared with 3-month-old control group and sham surgery group at day 3,7 and 14,the expressions of PSD95 were decreased in hepatolobectomy group at the same time points.Compared with 3-month-old control group,the expression of PSD95 was increased in sham surgery group at 7th day (P＜0.05).Between 3 month-old control group and 3-month-old littermates control group,the expressions of Drebrin and PSD95 had no significant differences.Concltsions Hepatolobectomy can impair the capabilities of space learning and memory in 3-month-old APP/PS1 transgenic mice,which may be associated with the decreased expressions of Drebrin and PSD95 in hippocampus.