The " liver disease affecting to the spleen" theory first appeared in Nanjing and was further elaborated in Jingui Yaolue. This theory encapsulates the traditional Chinese medicine principles of the " unity of the five viscera" and the " preventive treatment of disease" . The theory emphasizes that the spleen is the pivotal point where depression may progress from a functional disorder to an organic disease. The liver governs the emotions and qi flow, whereas the spleen is responsible for qi, blood, and body. In the early stages of the disease, emotional disorders and qi flow disorders primarily affect the liver, manifesting as depression or low mood. As the condition progresses, the liver (Wood) overacts on the spleen (Earth), disrupting liver and spleen functions and causing qi and blood disharmony. This stage is marked by fatigue and psychomotor retardation. Prolonged illness depletes qi and blood, eventually involving all five viscera, disrupting the harmony of the five spirits, and affecting both body and spirit. At this advanced phase, intense emotional distress or agitation often arises, accompanied by a heightened risk of suicide. The disease progression follows a dynamic " qi-blood-spirit" pattern, in which depression begins in the liver, characterized by qi stagnation, then affects the spleen, involving blood disharmony. In later stages, the disease eventually affects all viscera, with profound effects on both physical and mental health. Treatment strategies should align with the disease stage. Early intervention should focus on regulating the flow of qi, treating the liver, and strengthening the spleen. In the middle stages, qi and blood should be harmonized while promoting the harmonized functions of the liver and spleen. In the later stages, treatment should harmonize the five viscera to restore balance between body and spirit. Guided by this theory, integrating modern medical understanding of the progression of depression from emotional to somatic symptoms and adopting a stage-based approach to treatment in clinical practice can yield effective therapeutic outcomes for managing depression and related disorders.

ObjectiveTo explore the mechanisms associated with Mahoniae Caulis alkaloids （MA） in ameliorating depression by network pharmacology， molecular docking， and animal experiments. MethodsThe component targets of MA were obtained through Swiss Target Prediction and TCMIP database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. Protein-protein interaction （PPI） network was constructed by protein interaction analysis （STRING） database. Gene ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） analyses were performed through Bioinformatics （DAVID） database. The docking of components and targets was performed by AGFR. The mouse model of depression was established by intraperitoneal injection of corticosterone （CORT） once a day for 35 consecutive days. Sixty mice were randomly allocated into control （0.9% normal saline）， model （CORT， 20 mg·kg^-1）， positive control （fluoxetine hydrochloride， 3.6 mg·kg^-1）， and MA （10， 5， and 2.5 mg·kg^-1） groups. Each group was administrated with corresponding medicine or normal saline once a day for 28 consecutive days. The depression-like behavior of mice was observed. The pathological changes of prefrontal cortex in mice were observed by hematoxylin-eosin staining. Terminal deoxynucleotidyl dUTP transferase nick end labeling （TUNEL） was employed to observe the apoptosis of neurons in the prefrontal cortex. Enzyme-linked immunosorbent assay was employed to assess the serum levels of brain-derived neurotrophic factor （BDNF）， dopamine （DA）， 5-hydroxytryptamine （5-HT）， and norepinephrine （NE） in mice. The mRNA levels of cyclic adenosine monophosphate （cAMP） pathway-related factors and inflammatory factors were determined by Real-time PCR. Western blot was employed to determine the expression of cAMP pathway-related factors and connexin 43 （Cx43）. ResultsA total of 434 component targets and 545 depression targets were obtained， including 84 common targets， among which 10 core targets were screened out. GO analysis predicted 34 biological processes， 15 cell components， and 11 molecular functions. The KEGG pathways were mainly related to gap junction and cAMP signaling pathway. The core components had good binding affinity with the core targets. The results of animal experiments showed that compared with the control group， CORT prolonged the immobility time of mice in forced swimming and tail suspension tests （P<0.01）， lowered the serum levels of NE， BDNF， and 5-HT （P<0.05）， up-regulated the mRNA levels of nuclear factor-κB （NF-κB） and interleukin-6 （IL-6） in the brain tissue （P<0.05）， and down-regulated the mRNA levels of cyclic adenosine monophosphate effector binding protein （CREB） and BDNF （P<0.05） and the protein levels of protein kinase （PRKACA）， phosphorylation （p）-CREB/CREB， BDNF， and Cx43 （P<0.05） in the brain tissue. Compared with the model group， high-dose MA reduced the immobility time of mice in forced swimming （P<0.05） and tail suspension （P<0.01） tests， raised the serum levels of NE， BDNF， and 5-HT （P<0.01）， down-regulated the mRNA level of NF-κB （P<0.01）， and up-regulated the mRNA level of BDNF （P<0.01） and protein levels of PRKACA， p-CREB/CREB， BDNF， and Cx43 （P<0.05）. ConclusionMA alleviates the CORT-induced depressive behavior of mice. It may play an antidepressant role by regulating cAMP signaling pathway and gap junction pathway， improving synaptic plasticity and gap junction function， and reducing neuroinflammation.

ObjectiveTo explore the mechanisms associated with Mahoniae Caulis alkaloids （MA） in ameliorating depression by network pharmacology， molecular docking， and animal experiments. MethodsThe component targets of MA were obtained through Swiss Target Prediction and TCMIP database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. Protein-protein interaction （PPI） network was constructed by protein interaction analysis （STRING） database. Gene ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） analyses were performed through Bioinformatics （DAVID） database. The docking of components and targets was performed by AGFR. The mouse model of depression was established by intraperitoneal injection of corticosterone （CORT） once a day for 35 consecutive days. Sixty mice were randomly allocated into control （0.9% normal saline）， model （CORT， 20 mg·kg^-1）， positive control （fluoxetine hydrochloride， 3.6 mg·kg^-1）， and MA （10， 5， and 2.5 mg·kg^-1） groups. Each group was administrated with corresponding medicine or normal saline once a day for 28 consecutive days. The depression-like behavior of mice was observed. The pathological changes of prefrontal cortex in mice were observed by hematoxylin-eosin staining. Terminal deoxynucleotidyl dUTP transferase nick end labeling （TUNEL） was employed to observe the apoptosis of neurons in the prefrontal cortex. Enzyme-linked immunosorbent assay was employed to assess the serum levels of brain-derived neurotrophic factor （BDNF）， dopamine （DA）， 5-hydroxytryptamine （5-HT）， and norepinephrine （NE） in mice. The mRNA levels of cyclic adenosine monophosphate （cAMP） pathway-related factors and inflammatory factors were determined by Real-time PCR. Western blot was employed to determine the expression of cAMP pathway-related factors and connexin 43 （Cx43）. ResultsA total of 434 component targets and 545 depression targets were obtained， including 84 common targets， among which 10 core targets were screened out. GO analysis predicted 34 biological processes， 15 cell components， and 11 molecular functions. The KEGG pathways were mainly related to gap junction and cAMP signaling pathway. The core components had good binding affinity with the core targets. The results of animal experiments showed that compared with the control group， CORT prolonged the immobility time of mice in forced swimming and tail suspension tests （P<0.01）， lowered the serum levels of NE， BDNF， and 5-HT （P<0.05）， up-regulated the mRNA levels of nuclear factor-κB （NF-κB） and interleukin-6 （IL-6） in the brain tissue （P<0.05）， and down-regulated the mRNA levels of cyclic adenosine monophosphate effector binding protein （CREB） and BDNF （P<0.05） and the protein levels of protein kinase （PRKACA）， phosphorylation （p）-CREB/CREB， BDNF， and Cx43 （P<0.05） in the brain tissue. Compared with the model group， high-dose MA reduced the immobility time of mice in forced swimming （P<0.05） and tail suspension （P<0.01） tests， raised the serum levels of NE， BDNF， and 5-HT （P<0.01）， down-regulated the mRNA level of NF-κB （P<0.01）， and up-regulated the mRNA level of BDNF （P<0.01） and protein levels of PRKACA， p-CREB/CREB， BDNF， and Cx43 （P<0.05）. ConclusionMA alleviates the CORT-induced depressive behavior of mice. It may play an antidepressant role by regulating cAMP signaling pathway and gap junction pathway， improving synaptic plasticity and gap junction function， and reducing neuroinflammation.

Objective:To improve recognition of the clinical phenotype and genotype of achondroplasia(ACH).Methods:The clinical data and genetic test results of 2 children with ACH were analyzed retrospectively, and the related literature was reviewed.Results:Case 1 was a 1-year-old girl whose mother was short in stature.She was admitted to the hospital due to knee reflexes of both lower limbs for more than 9 months.Physical examination showed that her head circumference was 45 cm and she had short stature, short limbs, low muscle tension of both lower limbs, the developmental quotient was 65 scores.Bilateral ilium and hip joint lesions by X-ray were considered as ACH.According to the submitted gene results, FGFR3 gene c. 1138G >A (p.Gly380Arg) of the girl showed the heterozygous variation, and that gene of her mother showed the heterozygous variation.Case 2 was a 10-month-old girl, who was admitted to the hospital due to limb weakness for over 5 months.Physical examination showed head circumference of 46 cm, short stature, short limbs, reduced muscle tension of limbs, grade 4 muscle strength of limbs, and the developmental quotient was 41 scores.X-ray showed that both lower limbs were in accordance with ACH.The gene results suggested the heterozygous variation of FGFR3 gene c. 1138G >A (p.Gly380Arg) in the girl(a novel mutation), and a wild-type gene in her parents. Conclusions:The clinical features of achondroplasia are diverse.The bone changes and nerve development also need to be recognized and discriminated.

A great number of studies have demonstrated functional abnormalities in children with attention-deficit/hyperactivity disorder (ADHD), although conflicting results have also been reported. And few studies analyzed homotopic functional connectivity between hemispheres. In this study, resting-state functional magnetic resonance imaging (MRI) data were recorded from 45 medication-naïve ADHD children and 26 healthy controls. The regional homogeneity (ReHo), degree centrality (DC) and voxel-mirrored homotopic connectivity (VMHC) values were compared between the two groups to depict the intrinsic brain activities. We found that ADHD children exhibited significantly lower ReHo and DC values in the right middle frontal gyrus and the two values correlated with each other; moreover, lower VMHC values were found in the bilateral occipital lobes of ADHD children, which was negatively related with anxiety scores of Conners' Parent Rating Scale (CPRS-R) and positively related with completed categories of Wisconsin Card Sorting Test (WCST). Our results might suggest that less spontaneous neuronal activities of the right middle frontal gyrus and the bilateral occipital lobes in ADHD children.

Objective: To investigate low intensity pulsed ultrasound (LIPUS) on the expression of L-type calcium ion channels(cav1. 2) and Na +-Ca2 + exchangers(NCX1) during dentin-pulp complex injury and repair in rats. Methods: Cavity preparation was made on the upper right first molar of 40 male adult SD rats,20 of them and the upper left first molar of the other 20 were randomly chosen for LIPUS irradiation(frequency: 1. 5 MHz,200 μs pulses,pulse repetition frequency: 1 KHz,ISATA 30 mW/cm2,20 min /d),so the animals were randomly allocated into 4 groups(n = 10): Control group,LIPUS group,cavity preparation group and cavity preparation + LIPUS group. At 1,3,7,14 d post-irradiation the rats were sacrificed respectively for HE stain and immunohistochemical analysis. Results: Reparative dentin formation was observed at 14 days after cavity preparation and LIPUS irradiation,the expression of Cav1. 2(L-type) and NCX1 in this group were increased significantly at day 1 and day 3. Compared with the control group, the expression of Cav1. 2 in LIPUS group increased at day 1 post-irradiation. Conclusion: LIPUS may enhance tertiary dentin formation and up-regulate the expression of Cav1. 2 and NCX1 at the early period of dentin injury.

Objective To investigate the clinical significance and changes of neuron-specific enolase (NSE) and S100 protein in blood serum in patients with enterovirus 71 infection.Methods A total of 176 children with enterovirus 71 infection admitted from March 1,2012 through October 31,2012 were enrolled for a prospective and control study.According to diagnostic criteria of the enterovirus 71 (EV71) infection instituted by expert consensus for treatment of severe patients sets in 2011,the patients were divided into three groups:mild group (n =62),severe group (n =65) and critically care group (n =49),and another 30 healthy children served as control group.The demographics of patients including age and sex were comparable between control group and the sick children groups.Four milliliter of peripheral blood were taken from ill children on the first day before treatment and on the first,second,third day after treatment.The blood samples of healthy children were taken on the first day after physical examination.At the same time,the clinical data of blood routine,blood biochemistry,myocardial enzymes and C-reactive protein during the first 24 hours were collected.Immunohistochemical technique was used to study the change of NSE and S100 levels in serum.Data were expressed in mean ± standard deviation ((x) ± s) and were statistically analyzed by using SPSS 13.0 statistical software.Comparisons were carried out among different groups with one way analysis of variance (ANOVA) and between groups were performed with the Student t test.Changes were considered as statistically significant if P values was less than 0.05.Results ①Compared with mild group and control group,the levels of NSE and S100 protein were significantly higher in severe group and critically care group (P ＜0.05).②The serum levels of NSE and S100 protein in severe group were higher than in those in mild group with better outcomes (P ＜ 0.05).Conclusion The serum levels of NSE and S100 protein as biomarkers can be used to evaluate the severity of EV71 infection,and can also be used to determine the efficacy of treatment.

Objective To explore the relationship between PAH-DNA adducts and CYP1A1,GSTM1 gene polymorphisms and lymphoma.Methods PAH-DNA adducts from bone marrow of lymphoma patients and control cases were determined by competitive ELISA.The genotypes of both CYP1A1 and GSTM1 were detected by PCR-based restriction fragment length polymorphisms (PCR-RELP).Results The level of PAH-DNA adducts in lymphoma patients [(2 498±1 250) pg/ml] was significantly higher than that in control [(1 882±797) pg/ml] (t =0.006,P ＜ 0.05).CYP1A1 mutant genotype and GSTM1 null genotype had increased risk of lymphoma,with OR being 1.36 (95 ％ CI 0.56-3.31,P ＞ 0.05),4.03 (95 ％ CI 1.51-10.76,P ＜ 0.05),respectively.GSTM1 null genotype individuals with PAH-DNA level higher (or equal) than 2 200 pg/ml had increased risk of lymphoma.Conclusions The content of PAH-DNA adducts and the occurrence of lymphoma may have a certain correlation.GSTM1 null genotype may be linked to lymphoma and increase the risk.

This article uses methods such as professional research,critical analysis,literature research,professional consultation etc to create and construct the basic structure of 5-year higher vocational school medical laboratory integrated project courses,aiming to qualify and instruct the professional medical laboratory teachers,to promote the revolution of medical laboratory education,and to form a reference for improving the professional medical laboratory teachers'practical abilities of developing and carrying out project courses.

BACKGROUND: Methamphetamine (MA) has neurotoxic effects to central nervous system. However, as the 5-hydroxytryplamine reuptake enhancer, it is uncertain that if there are protective effects of tianeptine to the damages of 5-hydroxytryp-taminergic neurons caused by MA.OBJECTIVE: To investigate the neurotoxicity of MA and the neuroprotective effects of tianeptine as well as the acting mechanism.DESIGN: Randomized case control study based on animals.SETTING: Animal research room and pathology research room of a university.MATERIALS: The experiment was completed in the Experimental Animal Centre of Sichuan University and Molecular Pathology Laboratory of West China Hospital during June to August 2003. Totally 25 male Wistar rats were injected MA through abdominal cavity to build model. Methamphetamine was provided by National Institute for the Control of Pharmaceutical and Biological Products(NICPBP) while tianeptine was given by French Servier Company (Batch No. OE3086). The TUNEL testing kit was purchased from Boehringer Mannheim Company.INTERVENTIONS: There were one control group and four experimental groups(A, B, C, D). A group was used intraperitoneal injection of MA while B, C, D, groups were administered tianeptine 7 days, 4 days before and the same day of MA administration. Normal saline with same volume was injected into rats of control group. HE stain and silver stain were conducted after experiment to observe the morphologic changes of neurons. And TUNEL method was used to detect apoptotic cells.MAIN OUTCOME MEASURES: The HE stain and silver stain of brain tissue sections and counts of TUNEL positive neurons.RESULTS: MA could damage the axon and dendrite of neurons and the absorbance of silver positive cell was(50.74 ± 1.86) . It could also induce cell apoptosis while the apoptotic cell count every high power field was 29.26 ±4. 14. There were less apoptotic cells in the group with 7 days usage of tianeptine with the cell count of( 18.90 ± 1.60) per high power field.CONCLUSION: MA can cause neurotoxicity by inducing cell apoptosis.And giving tianeptine in advance can protect neurons.