In order to solve the problem of strong subjectivity and difficulty in quantification,clinical objectification mainly adopts the techniques of image processing,computer vision and machine learning.The acquisition and processing of prior knowledge is a key link in the objectification of inspection,as well as an important elaboration of the quantification of subjective judgment and macro performance in objectification research.However,there is still a lack of in-depth summary and parametric processing of prior knowledge.Based on the analysis of the current research status of objectification of inspection,this paper uses data mining technology to summarize the experience of TCM inspection.Moreover,the observation information can be transformed into quantifiable digital features through natural language processing and representation learning.Meanwhile,the application of deep learning can realize automatic diagnosis and analysis of observation images to improve accuracy and efficiency,and promote the process of TCM modernization.

Emerging research suggests a potential association of progression of Alzheimer's disease(AD)with al-terations in synaptic currents and mitochondrial dynamics.However,the specific associations between these pathological changes remain unclear.In this study,we utilized Aβ42-induced AD rats and primary neural cells as in vivo and in vitro models.The investigations included behavioural tests,brain magnetic resonance imaging(MRI),liquid chromatography-tandem mass spectrometry(UPLC-MS/MS)analysis,Nissl staining,thioflavin-S staining,enzyme-linked immunosorbent assay,Golgi-Cox staining,trans-mission electron microscopy(TEM),immunofluorescence staining,proteomics,adenosine triphosphate(ATP)detection,mitochondrial membrane potential(MMP)and reactive oxygen species(ROS)assess-ment,mitochondrial morphology analysis,electrophysiological studies,Western blotting,and molecular docking.The results revealed changes in synaptic currents,mitophagy,and mitochondrial dynamics in the AD models.Remarkably,intervention with Dengzhan Shengmai(DZSM)capsules emerged as a pivotal element in this investigation.Aβ42-induced synaptic dysfunction was significantly mitigated by DZSM intervention,which notably amplified the frequency and amplitude of synaptic transmission.The cognitive impairment observed in AD rats was ameliorated and accompanied by robust protection against structural damage in key brain regions,including the hippocampal CA3,primary cingular cortex,prelimbic system,and dysgranular insular cortex.DZSM intervention led to increased IDE levels,augmented long-term potential(LTP)amplitude,and enhanced dendritic spine density and length.Moreover,DZSM intervention led to favourable changes in mitochondrial parameters,including ROS expression,MMP and ATP contents,and mitochondrial morphology.In conclusion,our findings delved into the realm of altered synaptic currents,mitophagy,and mitochondrial dynamics in AD,concurrently highlighting the therapeutic potential of DZSM intervention.

Objective To investigate the effects of interlukin-22 (IL-22) on diabetic renal fibrosis and its possible mechanisms. Methods C57 BL/ 6 mice were randomized to normal control group ( NC group), diabetic nephropathy control group ( DN group), recombinant interlukin-22 ( rIL-22) group, and interlukin-22 antibody (Anti-IL-22) group. 8 weeks after successful establishment of diabetes model, mice were injected intraperitoneally with 200 ng/ g rIL-22, Anti-IL-22 or equal 0. 1% bovine serum albumin (BSA) twice a week for 4 weeks. After the intervention, blood glucose, kidney function and 24 h urine microalbumin creatinine ratio were measured. Renal pathological changes and collagen deposition were observed under the light microscope, and semiquantitative assessment of renal sclerosis and fibrosis were evaluated at the same time. The mRNA expression of transforming growth factor ( TGF)-β1 was determined by realtime PCR. The protein expressions of α-smooth muscle actin (α-SMA), E-cadherin, and fibronetin (FN) were examined by Western blotting. The protein expressions of collagenⅢ were examined by immunohistochemical analysis. Results After 4 weeks of intervention, the 24 h urine microalbumin creatinine ratio decreased significantly in the Anti-IL-22 group ( P<0. 05). Renal tubular epithelial cells vacuolar degeneration, protein cast formation, and glomerular mesangial expansion were observed under the light microscope. And the lesions were more severe in the rIL-22 group, whereas improved in the Anti-IL-22 group. Meanwhile, the collagen deposition was in accordance with the tubular injury score. Moreover, TGF-β1 gene expression increased significantly in the rIL-22 group (P<0. 01). α-SMA and E-cadherin, epithelial-mesenchymal transition (EMT) markers, increased or decreased significantly in the rIL-22 group respectively (P<0. 05). FN and collagen Ⅲ, extracellular matrix ( ECM ) proteins, increased significantly in the rIL-22 group as well ( P <0. 05). Conclusions IL-22 may induce renal tubular epithelial cells TGF-β1 high expression. As a consequence, this contributes to EMT occurance and ECM accumulation, eventually accelerating the progression of diabetic renal fibrosis.

Objective To assess the association of subclinical thyroid dysfunction with fractures. Methods Medline, Embase, Pubmed, Cochrane Library, CBM, CNKI, Wan Fang, and VIP databases were systematically searched from January 1990 to August 2015 to identify prospective cohort studies which have studied the risk of fracture in patients with subclinical thyroid dysfunction. The relative risks ( RR) of cohort studies were pooled respectively, depending on the result of heterogeneity test among the individual studies search. The Stata (version 13. 0) software was used for meta-analysis. Results Nine prospective cohort studies including 292460 participants were identified as eligible for the meta-analysis. RR of subclinical hyperthyroidism for fracture was 1. 39(95%CI 1. 24-1. 55);for hip fracture, RR was 1. 24(95%CI 1. 10-1. 40);for nonspine fracture, RR was 1. 32 (95%CI 1. 09-1. 60). Different gender for subclinical hyperthyroid was associated with higher fracture rates:for females, RR was 1. 15(95%CI 1. 04-1. 27); for males, RR was 1. 31 (95% CI 1. 08-1. 59). The incidence of fracture in patients with subclinical hyperthyroidism was higher during the follow-up. For subclinical hypothyroidism, the RR was 1. 21(95% CI 1. 03-1. 42). Subgroup analysis indicated that there were significant differences between endogenous/exogenous subclinical hyperthyroidism and euthyroid, but no differences between endogenous/exogenous subclinical hypothyroidism and euthyroid were found. Conclusion Subclinical hyperthyroidism is associated with an increased risk of fracture in the population, especially hip fracture and nonspine fracture. During the course of subclinical hyperthyroidism, the incidences of fracture should be noticed both in females and males. However, there is no evidence which could prove a definite association between subclinical hypothyroidism and the risk of fracture.

Objective To investigate the protective effects of aerobic exercise and miR-222 expression in myocardium of diabetic mice. Methods C57BL/ 6 mice were divided into 4 groups: normal non-exercise group (SC), normal exercise group(EC), non-exercise diabetic group(SD), and exercise diabetic group(ED). After the diabetic model was established successfully, EC and ED underwent a swimming training for 5 weeks. By the end of the experiment, light microscope was used to observe the pathological changes of heart, RT-PCR for myocardial miR-222 expression, and Western blot for phosphatase and tensin homolog deleted on chromosome ten ( PTEN ), phosphatidylinositol 3-kinase (PI3K), and protein kinase B (Akt) protein expressions in myocardial tissue. Results (1) Under the light microscope, the diabetic mice had a significant change in myocardial structure, with great disorder in the cell arrangement. After exercise intervention, the lesion was alleviated. (2) MiR-222 expression was increased in the myocardium of normal mice and DM mice after exercise (all P<0. 05); (3) Compared with SC group, PTEN expression was increased and PI3K/ Akt expressions were inhibited in myocardium of diabetic mice(all P <0. 05). After exercise intervention, the expression of PTEN reduced( P < 0. 05) and PI3K/ Akt pathway was reactivated in myocardium of diabetic mice (all P<0. 05). Conclusion Exercise intervention may protect the myocardium under high glucose via inducing miR-222 and activating PI3K/ Akt signaling pathway.

AIM: To study the protective effect of aerobic exercise on cardiac dysfunction in mice and its mechanism, and to provide theoretical and practical basis for the exercise therapy of diabetic cardiac dysfunction .METH-ODS:The mice were divided into normal control non-exercise (NNC) group, normal control exercise (ENC) group, dia-betic non-exercise (NDM) group and diabetic exercise (EDM) group.At the end of the experiment , the cardiac function was evaluated by echocardiography .The pathological changes of the myocardial tissues and the development of fibrosis were observed.The mRNA expression of ANP, and the protein levels of PI3K (p110α) and Akt were determined.RESULTS:The decrease in cardiac function of diabetic mice was observed , and the cardiac function recovered after exercise interven-tion (P<0.05).Under light microscope with HE and Masson staining , the myocardial structure in NDM group was in ex-treme disorder , cell arrangement was not neat , and the degree of fibrosis increased , but the myocardial damage was im-proved in ENC group .Compared with NNC group , the mRNA expression of ANP in the myocardium of diabetic mice was up-regulated (P<0.05).The protein levels of PI3K (p110α) and Akt were decreased (P<0.05), and the cascade was inactivated.Compared with NDM group , the mRNA expression of ANP was down-regulated and the protein levels of PI 3K (p110α) and Akt were up-regulated in EDM group (P<0.05).CONCLUSION:Diabetes results in myocardial damage in mice, and reduces cardiac function .Exercise intervention alleviates the heart dysfunction induced by high glucose via activating PI3K( p110α)/Akt signaling pathway to protect the structure and function of the myocardium .

MicroRNAs (miRNAs) are a class of endogenous;non-coding small RNA molecules;which can degradate target mRNA;or negatively regulate the expression of the corresponding target genes in the post transcriptional level through inhibiting target gene translation;inducing degradation and so on.MiRNAs exert important parts in the process of metabolism;cell growth;and development.MicroRNA 222 (miR-222) is an important member of microRNAs;which plays an important role in cell proliferation;differentiation;apoptosis and the development of a variety of biological tissues.Recent studies found that miR-222 could mediate a variety of physiological and pathological processes;and significantly influence the development of cardiovascular disease.MiR-222 has an important role in inflammatory response and apoptosis.Here;we reviewed the relationship between miR-222 and cardiovascular disease.

Objective To study the effect and mechanisms of berberine (BBR) on the proliferation of papillary thyroid cancer K1 cells induced by high glucose.Methods K1 cells were cultured under 5.5 mmol/L or 25 mmol/L glucose condition with or without different concentration of BBR (0,10,40 and 80 μmol/L) for 24 hours.The proliferations of K1 cells in each condition were detected by MTT.Western blot was used to measure the expression of nuclear factor erythroid 2-related factor 2 (Nrt2),phosphoinositide 3-kinase (PI3K),protein kinase B (Akt) and phosphorylated-Akt (p-Akt).The distribution pattern of Nrf2 in K1 cells was determined using immunofluorescent staining.Results Compared with 5.5 mmol/L condition,the proliferation rate [(126.64 ± 5.41) ％ vs (87.31 ± 3.67) ％],expression levels of PI3K (0.425 ±0.019 vs 0.272 ±0.039),p-Akt/Akt (0.446 ±0.021 vs 0.168 ±0.035) and Nrf2 (0.597 ± 0.014 vs 0.308 ± 0.026),and Nrf2 distribution (93.0％ vs 23.1％) in nuclear of K 1 cells under 25 mmol/L condition were significantly elevated,respectively (all P ＜0.01).Addition of BBR in 25 mmol/L condition dose dependently (10,40,80 μmol/L) lowered the proliferation rate of K1 cells [(111.76 ± 4.10)％,(70.03 ±2.18)％,(32.41 ±3.76)％ vs (126.64 ±5.41)％,all P＜0.05],and suppressed the expression of PI3K,p-Akt/Akt,Nrf2,and Nrf2 nuclear distribution (P ＜ 0.05).Conclusions BBR dose dependently inhibited the proliferation of high glucose-induced K1 cells.This effect was associated with the suppression on of PI3K/Akt signaling activation,Nrf2 expression and its nuclear translocation.

Humanumbilicalveinendothelialcells(HUVECs)weretreatedwith3nmol/Lliraglutidefor10, 15, 30, 45, 60, 90, 120, 150, 180, 210, 240, and 270 minutes at the concentrations of 5. 5 or 30 mmol/L glucose. Western blot analysis was used to detected protein expression and phosphorylation of insulin receptor substrates-1 ( IRS-1 ) and endothelial nitric oxide synthase ( eNOS ) . The results showed that the baseline level of phosphorylated-eNOS/eNOS was lower in high glucose group than that in normal group(0. 239 ± 0. 016 vs 0. 400 ± 0. 02,P<0. 05). Liraglutide time-dependently increased phosphorylated-eNOS/eNOS and phosphorylated-IRS-1/IRS-1 levels at 5. 5 or 30 mmol/L glucose.

Objective To investigate the role of AT1 receptor autoantibody (AT1-AA) in the inhibitory action of irbesartan on endoplasmic reticulum stress (ERS)-related apoptotic signals in rat kidney with diabetic nephropathy (DN).Methods DN model rats were induced by high-sugar and high-fat diet plus intraperitoneal injection of streptozotocin,and the serum level of AT1-AA was detected by ELISA.These DN rats with positive or negative AT1-AA were divided into DN group and irbesartan treated group.After 4 weeks of irbesartan treatment,TUNEL staining was used to detect renal cell apoptosis.The protein and mRNA expressions of ERS chaperone protein glucose-regulated protein 78 (GRP78) and ERS-associated apoptosis proteins were determined by Western blot and RT-PCR.Results Compared with NC group,the apoptosis rate of renal cells in DN group was obviously increased,along with the increased expressions of GRP78,C/EBP homology protein (CHOP),phosphorylated c-Jun N-terminal kinase (JNK),and Caspase12 protein and mRNA (all P＜0.01).The cell apoptosis and protein and mRNA levels of these genes were significantly decreased after irbesartan treatment (all P＜ 0.01),especially in AT1-AA positive DN rats(all P＜0.05).The renal cell apoptosis rate,and protein and mRNA levels of these four genes in AT1-AA positive DN group were much greater than those in AT1-AA negative DN group (all P＜0.05).Conclusions AT1-AA may be involved in ERS-related cell apoptosis in the kidney of DN rats,and play a role in irbesartan-improved renal function via inhibiting ERS-associated CHOP-JNK-Caspase12 apoptotic signals and renal cell apoptosis.