Subclinical cardiovascular disease (Sub-CVD) is an early stage of cardiovascular disease and is often asymptomatic. Risk factors, including hypertension, diabetes, obesity, and lifestyle, significantly affect Sub-CVD. Progress in imaging technology has facilitated the timely identification of disease phenotypes and risk categorization. The critical function of dual-energy x-ray absorptiometry (DXA) in predicting Sub-CVD was the subject of this research. Initially used to evaluate bone mineral density, DXA has now evolved into an indispensable tool for assessing body composition, which is a pivotal determinant in estimating cardiovascular risk. DXA offers precise measurements of body fat, lean muscle mass, bone density, and abdominal aortic calcification, rendering it an essential tool for Sub-CVD evaluation. This study examined the efficacy of DXA in integrating various risk factors into a comprehensive assessment and how the application of machine learning could enhance the early discovery and control of cardiovascular risks. DXA exhibits distinct advantages and constraints compared to alternative imaging modalities such as ultrasound, computed tomography, magnetic resonance imaging, and positron emission tomography. This review advocates DXA incorporation into cardiovascular health assessments, emphasizing its crucial role in the early identification and management of Sub-CVD.

BackgroundArterial stiffness, typically evaluated via estimated pulse wave velocity (ePWV), is believed to have a significant association with cardiovascular diseases. The objective of this study was to investigate the correlation between Life’s Essential 8 (LE8), a newly revised metric of cardiovascular health, and ePWV among adult population in the United States.MethodsThis research employed a cross-sectional methodology, drawing upon data from the National Health and Nutrition Examination Survey (NHANES) spanning from 2011 to 2018. To explore the relationship between LE8 and ePWV among adults in the US, both univariate and multivariate linear regression analyses were carried out. Additionally, the restricted cubic splines method was utilized to examine any non-linear correlation.ResultsThe study comprised 6,742 participants with an average age of 48.30 ± 0.35 years. Among these, 3,236 were males, representing a weighted percentage of 48%. The population’s weighted average LE8 score was 68.68 ± 0.37, while the average ePWV was 8.18 ± 0.04. An entirely adjusted model revealed a negative correlation between ePWV and LE8 scores [in the moderate LE8 group, coefficient − 0.17, 95% CI -0.28 to −0.06, p = 0.004; in the high LE8 group, coefficient − 0.44, 95% CI -0.56 to −0.32, p < 0.0001]. This negative correlation was consistent with the findings in demographic subgroup analysis, with the effect size being more pronounced among adults under the age of 60, and individuals without hypertension, cardiovascular disease, or diabetes.ConclusionOur study reveals a negative correlation between LE8 and ePWV in the adult population of the US, suggesting that LE8 could potentially serve as an indicative marker for evaluating the risk of vascular stiffness. This inverse relationship is markedly stronger in adults below 60 years and those without diagnosed vascular diseases. This implies that lifestyle upgrades and risk factor management could be especially advantageous in curbing arterial stiffness within these groups. These conclusions underscore the importance of primary prevention in mitigating the risk of vascular aging in a relatively healthy group, emphasizing the significance of early intervention and risk factor management in cardiovascular disease.

Rheumatoid arthritis (RA) is an autoimmune inflammatory disease, of which the leading cause of death is cardiovascular disease (CVD). The levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c), and high-density lipoprotein cholesterol (HDL-c) in RA decrease especially under hyperinflammatory conditions. It is conflictive with the increased risk of CVD in RA, which is called “lipid paradox”. The systemic inflammation may explain this apparent contradiction. The increased systemic proinflammatory cytokines in RA mainly include interleukin-6(IL-6)、interleukin-1(IL-1)and tumor necrosis factor alpha(TNF-α). The inflammation of RA cause changes in the subcomponents and structure of HDL particles, leading to a weakened anti-atherosclerosis function and promoting LDL oxidation and plaque formation. Dysfunctional HDL can further worsen the abnormalities of LDL metabolism, increasing the risk of cardiovascular disease. However, the specific mechanisms underlying lipid changes in RA and increased CVD risk remain unclear. Therefore, this article comprehensively integrates the latest existing literature to describe the unique lipid profile of RA, explore the mechanisms of lipid changes, and investigate the impact of lipid changes on cardiovascular disease.

ETHNOPHAMACOLOGICAL RELEVANCE:Simiao Pill (SM) as a classic prescription of traditional Chinese medicine treatment of damp-heat arthralgia, the earliest from 'Cheng Fan Bian Du ', written by the Qing Dynasty doctor Zhang Bingcheng. Previous studies have shown that SM has obvious curative effect on rheumatoid arthritis, which provides a basis for the application of SM in rheumatoid arthritis related complications. AIM OF THE STUDY:Interstitial lung disease (ILD), as the most severe complication of rheumatoid arthritis (RA), lacks effective clinical treatments and a corresponding animal model. Simiao pill (SM) is a traditional Chinese medicine prescription extensively used as a complementary and alternative treatment for RA. However, the effect and mechanism of SM on RA-ILD have not yet been reported. This study aimed to investigate an appropriate animal model that can simulate RA-ILD, and the efficacy, safety, and mechanism of SM on RA-ILD. METHODS:Collagen-induced arthritis (CIA) and bleomycin-induced pulmonary fibrosis model were combined to construct the CIA-BLM model. After the intervention of SM, the protective effects of SM on RA-ILD were determined by detecting the CIA mouse arthritis index (AI), Spleen index, and the extent of pulmonary fibrosis. The joint inflammation and pulmonary fibrosis were detected by immunohistochemistry, H&E staining, safranin- O fast green Sirius red staining, trap staining, and Masson staining. Finally, the mechanism was verified by Western blot and immunohistochemistry. RESULTS:Our work showed that SM significantly reduced joint swelling, arthritis index, pulmonary fibrosis score, and spleen index in CIA mice. The pathological examination results indicated Si-Miao Pill suppressed inflammation, pulmonary fibrosis, bone erosion, and cartilage degradation of the ankle joint. Besides, SM up-regulated expressions of E-cadherin, whereas down-regulated expressions of α-SMA. Further studies confirmed that SM regulated JAK2/STAT3 and TGF-β/SMAD2/3. CONCLUSION:SM can not only effectively improve joint inflammation by JAK2/STAT3 Pathway but also inhibit pulmonary fibrosis by TGF-β/SMAD2/3. The fibrosis induced by CIA-BLM model was more stable and obvious than that induced by CIA model alone.

目的 分析人体成分与不同年龄段人群骨密度(BMD)的相关性. 方法 纳入288例在我院体检的健康人群,应用人体成分分析仪检测并记录其体脂率、体脂含量、内脏脂肪面积、去脂体质量、肌肉量等人体成分指标.采用美国HOLOGIC discovery系列骨密度仪测量上述人群的BMD.将研究对象按照年龄分为青年组(30～44岁,n=70)、中年组(45～59岁,n=105)和老年组(60～75岁,n=113),采用Pearson相关系数描述不同年龄组人体成分与BMD的关系;采用多元线性回归分析BMD的独立影响因素. 结果 老年组的BMD值较青、中年组降低,骨质疏松症发生率明显高于青年组,差异均有统计学意义(P<0.05).3组人群的体质量、BMI、体脂率差异无统计学意义(P>0.05);与青年组相比,中、老年组内脏脂肪面积显著增加,老年组去脂体质量、肌肉量明显减少,差异均有统计学意义(P<0.05).Pearson相关分析显示,BMD与3组人群的年龄呈负相关,且随着年龄增长,该相关性逐渐增强(中、青、老年组分别为r=-0.22、-0.28、-0.37,均P<0.01);中、老年组BMD与去脂体质量及肌肉量均呈正相关,且老年组的相关性更加显著(中年组:r=0.27、0.27,老年组:r=0.49、0.49,均P<0.01).多元线性回归分析结果表明,年龄是BMD的独立危险因素,去脂体质量、肌肉量均是BMD的保护因素. 结论 老年人骨量减少与年龄及去脂体质量和肌肉量的增龄性改变相关.去脂体质量和肌肉量是BMD的保护因素.

Objective. This study aimed to investigate whether berberine exerted anti-inflammatory and antiproliferative effects on the fibroblast-like synoviocytes of rheumatoid arthritis (FLS-RA) through regulating the lysophosphatidic acid (LPA) function. Methods. Firstly, the expression levels of LPA and lysophosphatidic acid receptor 1 (LPA1) in RA patients, osteoarthritis (OA) patients, and healthy controls were detected. Moreover, molecular docking was employed to characterize the binding sites of berberine in the predicted protein targets. Later, FLS-RA were stimulated using berberine, LPA, and the specific inhibitor (Ki16425) of LPA1, thereafter, the effects on the proliferation, apoptosis, the release of inflammatory mediators of FLS-RA, and the MAPK pathway were observed. Results. Compared with healthy controls (n = 25), the plasma LPA level (n = 28) and synovial fluid (n = 10) were markedly higher in RA patients. LPA1 was highly expressed in RA patients (n = 4) relative to that in OA patients (n = 4). Berberine remarkably inhibited the proliferation and the excessive production of IL-6 and TNF-α in FLS-RA, whereas suppressing the expression of K-ras, c-Raf, and p-38/ERK-phosphorylation. In addition, berberine inhibited the LPA-induced p-38/ERK-phosphorylation through binding to LPA1. Conclusions. LPA plays a certain role in promoting the proliferation and inflammation of FLS-RA. Berberine potentially modulates LPA function to suppress the proliferation and inflammation of FLS-RA through blocking the p38/ERK MAPK pathway mediated by LPA1. These findings suggest that, berberine possesses potential lipid-regulating, antiarthritis, and synovial hyperplasia inhibition activities against RA, which may provide a promising therapeutic target for the clinical drug development for RA patients with dyslipidemia and high CVD risk.

Objective To observe the expressions of leptin,insulin-like growth factor-1 (IGF-1),and insulin-like growth factorbinding protein-3 (IGFBP-3) in serum of postmenopausal women with osteoporosis,explore the clinical significance. Methods Sixty postmenopausal women with osteoporosis (observation group) were divided into non-fracture group (34 cases) and fracture group (26 cases) according to complicating with fracture or not. During the same period,40 postmenopausal women without osteoporosis were selected as control group. ELISA was used to detect the expression levels of serum leptin,IGF-1,ad IGFBP-3 in the three groups. Body mass density (BMD) detection equipment was used to detect BMD values of lumbar vertebra (L1-L4),femoral neck,and Wards triangle area in the three groups. The detection results were compared. The correlations between serum leptin,IGF-1,IGFBP-3 and BMD were analyzed. Results The expression levels of serum leptin,IGF-1,and IGFBP-3 in observation group were statistically significantly lower than those in control group (P＜0. 05). The expression levels of serum leptin,IGF-1,IGFBP-3 and BMD in fracture group were statistically significantly lower than those in non-fracture group (P＜0. 05). There were positive correlations among the four indexes (leptin,IGF-1, IGFBP-3,and BMD) (P＜0. 05). Conclusion Serum leptin,IGF-1,and IGFBP-3 can be used as sensitive laboratory indicators for early diagnosis of postmenopausal women with osteoporosis and assessment of the severity.

Pioglitazone may have potential benefits as an alternative therapeutic treatment for patients with Alzheimer's disease (AD), particularly in individuals that also have comorbid diabetes; however, the mechanisms of action remain unclear. The present study aimed to explore the effects of pioglitazone on amyloid β, isoform 42 (Aβ42) deposition in rats with diet‑induced insulin resistance (IR). Diet‑induced IR model rats were established in the presence or absence of pioglitazone. Plasma glucose and insulin levels, and cerebrospinal fluid insulin levels were measured; in addition, hippocampal tissues were collected for immunohistochemical analysis of Aβ42 expression. The levels of insulin‑degrading enzyme (IDE) and peroxisome proliferator‑activated receptor γ (PPARγ) mRNA and protein expression were analyzed by reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. In addition, the activation of glycogen synthase kinase 3β (GSK3β) induced by phosphatidylinositol 3‑kinase (PI3K) /protein kinase B (AKT) signaling was detected by western blotting. Results from the present study demonstrated that pioglitazone may enhance peripheral and brain insulin sensitivity in diet‑induced IR model rats. Treatment with pioglitazone ameliorated Aβ42 deposition in the hippocampus by increasing IDE and PPARγ expression. Notably, activation of the PI3K/AKT/GSK3β pathway was also demonstrated to serve a role in pioglitazone‑induced Aβ42 degradation, which was abrogated by the PPARγ antagonist GW9662. Results from the present study indicated that pioglitazone may improve insulin sensitivity and ameliorate Aβ42 accumulation in rats with diet‑induced IR by regulating AKT/GSK3β activation, suggesting that pioglitazone may be a promising drug for AD treatment.

目的:通过比较四妙丸配方颗粒对胶原诱导关节炎(CIA)大鼠关节的影响,明确四妙丸对关节炎和溶血磷脂酸(LPA)的作用.方法:选用Wistar大鼠建立关节炎模型,以正常组(15只)、关节炎模型组(21只)和四妙丸治疗组(21只)作为对照,观察四妙丸配方颗粒治疗6周后大鼠关节炎指数积分、足部体积、滑膜病理切片中CD34和vWF以及检测血清中LPA和炎性因子的浓度.结果:CIA大鼠经四妙丸配方颗粒治疗后足部体积、关节炎指数积分均明显下降,病理切片的滑膜增生层次和炎症细胞浸润均明显改善,关节滑膜病理切片中抗CⅡ型胶原抗体、CD34和vWF蛋白表达明显下降(P＜o.01).与模型组比较,四妙丸治疗组大鼠血清中肿瘤坏死因子-α和白介素-1β浓度下降(P＜0.05),而LPX、自体素水平明显降低(P＜0.01).结论:四妙丸配方颗粒能够缓解CIA大鼠关节炎症状,抑制关节滑膜增生和降低血清炎性因子水平,其机制可能与降低血脂LPA进而抑制滑模炎症相关通路的作用相关.

Objective. Interleukin 34 (IL-34) and microRNA 21 (miR-21) were found to be involved in the pathological process of rheumatoid arthritis (RA), but the details were unclear. In this study, we aimed to clarify the relationship between IL-34 and miR-21 in RA. Methods. IL-34 concentrations in serum and synovial fluid (SF) of patients with RA were measured by ELISA. Fibroblast-like synovial cells (FLS) were cultured for evaluation of STAT3 activation, miR-21, and Bax/Bcl-2 expression by Western blot and real-time PCR. Correlations were analyzed between clinical features and detectable variables including SF IL-34 levels and miR-21 expression. Results. SF IL-34 levels were significantly higher in patients with RA who had a high 28-joint Disease Activity Score (DAS28 ≥ 3.2) than in those with a lower DAS28 (DAS28 < 3.2). DAS28 scores and miR-21 expression in FLS had a significant positive correlation with the SF IL-34 levels. In addition, IL-34 stimulation strengthened the activation of p-STAT3, resulting in the increment of miR-21 expression. Inhibiting of miR-21 expression contributed to decreased Bcl-2/Bax ratio, suggesting that miR-21 was involved in the resistance to apoptosis. With the blocking of the colony-stimulating factor-1 receptor (CSF1R), decreased protein expressions including CSF1R, p-STAT3/STAT3, and Bcl-2/Bax were shown, suggesting that CSF1R participated in the biological functions of IL-34 in RA. Conclusion. The IL-34/STAT3/miR-21 pathway is crucial for the survival of synovial fibroblasts in RA, which might be candidate therapeutic targets for RA treatment.

目的 比较四妙丸和甲氨蝶呤对高脂饲料胶原诱导关节炎(CIA)大鼠的影响,明确四妙丸对关节炎和血脂的影响.方法 选用Wistar大鼠建立高脂饲料的关节炎模型,观察四妙丸和甲氨蝶呤两种治疗4周后大鼠关节炎指数积分、滑膜HE染色以及检测血清中血脂和炎症因子的浓度.结果 CIA大鼠经甲氨蝶呤和四妙丸治疗后关节炎指数积分均明显下降,病理切片的滑膜增生层次和炎症细胞浸润均明显改善.与甲氨蝶呤组比较,四妙丸组血清中总胆固醇、低密度脂蛋白胆固醇水平明显降低(P＜0.01),而高密度脂蛋白胆固醇则明显升高(P＜0.01);前炎症因子肿瘤坏死因子-α浓度下降(P＜0.05),而白介素-17浓度则明显升高(P＜0.05).结论 四妙丸可能兼具有抑制免疫和降低血脂的作用来阻止CIA的进展.

Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by inflammation and joint destruction. In this study, we explored the effect of berberine on rats with bovine type II collagen-induced arthritis (CIA), an animal model for RA. Following treatment, berberine attenuates arthritic scores and suppresses collagen–specific immune responses in CIA rats. Compared with the un-treated CIA group, berberine reversed pathological changes, which showed a significant improvement in synovial hyperplasia and inflammatory infiltration. The expression levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-17 and vascular endothelial growth factor (VEGF) were obviously reduced in the sera of berberine-treated rats (all P < 0.05). Moreover, berberine showed marked inhibition of the expression of VEGF and CD34 (all P < 0.05). Interestingly, berberine significantly suppresses p-ERK, p-p38 and p-JNK activation (all P < 0.05), which may partially explain the anti-RA activity of berberine. These results suggest that berberine ameliorates CIA in rats associated with anti-inflammatory and anti-angiogenic effects, which might be of great therapeutic value for RA.

Objective To study the effects of high fat diet on the joints of rat models of collagen-induced arthritis( CIA). Methods Sixty healthy,4-5-week old female Wistar rats were used in this study. Subcutaneous injection of bovine type II collagen and incomplete Freund's adjuvant were used to establish the CIA models. Normal diet was fed to the rats of control group and high fat diet was fed to the experimental rats. The arthritis index scores were measured and the synovial biopsies were examined by histopathology with HE staining, and the concentrations of serum lipids and inflammatory factors were detected. Results Compared with those of the normal group,the arthritis index scores,synovial proliferation,pannus formation and inflammatory cell infiltration in the synovium were increased in the CIA rats with high fat diet. Serum TC and LDL-C levels were also significantly increased in the high fat diet CIA rat group( P < 0. 01) apart from HDL-C,which was decreased obviously( P < 0. 05). Serum levels of pro-inflammatory cytokines TNF-α,IL-1β and IL-17 were also significantly increased in the high fat diet CIA rats( P < 0. 05). Conclusions High fat diet may promote the progress of arthritis in CIA rats by enhancing synovial hyperplasia and inflammatory cytokines.

Objective To study the effects and possible mechanisms of Olmensartan,an AT1R blocker on the inflammation response,in a mouse model of nonalcoholic fatty liver disease(NAFLD).Methods 24 male C57BL/6 mice of 8 weeks were randomly divided into a normal diet group and a high fat diet(HFD) group.Mice in the HFD group were given high fat diet for 12 weeks and further divided into a high fat diet control group and a high fat diet treatment group.For 8 weeks,along with the same access to high fat diet,the treatment group received 0.75mg/kg/d Olmesartan by gavage.All animals were killed after gavage was over.Serum was obtained to evaluate ALT,AST and TG levels.Livers were obtained for morphology(HE,Oil red O),immunohistochemistry(F4/80),Real-time PCR and Western blot analysis.Results Olmesartan had benefitical effects on high fat diet-induced hepatic steatosis and inflammation,and dramatically improved liver function.Increased expression levels of TNF-α and IL-6 mRNA were reduced and the NF-κB pathway activation was inhibited in liver by Olmesartan.Conclusion Olmesartan reduce hepatic lipid accumulation and inflammation in NAFLD.The mechanisms may be related with inhibiting NF-κB activation and reducing liver TNF-α and IL-6 expression.

Metformin was commonly used in patients with obesity and insulin resistance.Several studies indicated that metformin increased the risk of Alzheimer's disease,but the molecular mechanism remained unclear.Extracellular deposits of the amyloid β-peptide as the originating pathophysiology of Alzheimer's disease,may be the key point.This study was designed to determine the effects of metformin on β-amyloid(Aβ) and related factors in hippocampus of diet-induced obese rat model.The SD rats were fed with high glucose,high fat and high protein for 12 weeks to establish the OB models.Metformin was administered intragastrically for 4 weeks and the MET group was made.The expression of TNF-α,peroxisome proliferator-activated receptor γ(PPARγ) and insulin degrading enzyme(IDE) gene in hippocampus were analyzed by real time-PCR and the protein level of TNF-α,Aβ42,PPARγ,IDE were determined by Western blotting and immunohistochemistry.The plasma insulin and insulin resistance calculated by HOMA-IR were significantly higher in OB group(P<0.01) than that in CTL group(P<0.05).The level of TNF-α and Aβ42 was up-regulation in OB group(P<0.05),while PPARγ and IDE were descent(P<0.05).In MET group,the level of TNF-α and Aβ42 was highest while PPARγ and IDE were lowest(P<0.01).These findings suggest that metformin could reduce the level of plasma insulin and IR in obese rat models.At the same time,the drug could increase the degree of TNF-α in hippocampus,then down-regulate the level of PPARγ and IDE,which induces the deposition of Aβ42.

To identify the major serum biomarkers predicting the response to methotrexate (MTX) treatment in patients with early rheumatoid arthritis (RA), we evaluated the relationships between the individual response to MTX and various associated factors utilizing the (1)H nuclear magnetic resonance ((1)H NMR)-based metabolomic method. Thirty-eight early RA patients were enrolled in this cohort study, and they received MTX (10 mg/week) orally as monotherapy for 24 weeks. According to the American College of Rheumatology criteria for improvement, clinical evaluation following MTX treatment was carried out at baseline and at the end of 24 weeks. Furthermore, collected serum samples were analyzed using 600 M (1)H NMR for spectral binning. The obtained data were processed by both the unsupervised principal component analysis (PCA) and the supervised partial least squares discriminant analysis (PLS-DA). Lastly, multivariate analyses were performed to recognize the spectral pattern of endogenous metabolites related to MTX treatment. Differential clustering of (1)H NMR spectra identified by PCA was found between the effective (n=25) and non-effective (n=13) group of RA patients receiving MTX treatment. Multivariate statistical analysis showed a difference in metabolic profiles between the two groups using PLS-DA (R(2)=0.802, Q(2)=0.643). In targeted profiling, 11 endogenous metabolites of the effective group showed a significant difference when compared with those of the non-effective group (p<0.05). Serum metabolites correlated with MTX treatment in patients with early RA were identified, which may be the major predictive factors for evaluating the response to MTX treatment in patients with early RA. Furthermore, our results highlight the usefulness of (1)H NMR-based metabolomics as a feasible and efficient prognostic tool for predicting therapeutic efficacy to MTX treatment.

目的:检测肥胖大鼠海马内肿瘤坏死因子α（tumor necrosis factorα,TNF-α）、胰岛素降解酶（in-sulin-degrading enzyme,IDE）、过氧化物酶体增殖物激活受体γ（peroxisome proliferator-activated receptorγ,PPARγ）和淀粉样β肽（amyloidβ-peptide,Aβ）水平,探讨TNF-α对肥胖大鼠海马内IDE和Aβ的影响,观察TNF-α、Aβ与PPARγ的关系。方法:建立肥胖（obesity,OB）大鼠模型;葡萄糖氧化酶法检测大鼠血糖水平,放射免疫法测血浆胰岛素水平;实时荧光定量PCR检测大鼠海马内TNF-α、淀粉样β蛋白前体（amyloidβ-protein precur-sor,APP）、PPARγ及IDE的mRNA水平;蛋白免疫印记技术及免疫组织化学染色法检测大鼠海马内TNF-α、Aβ42（由APP降解产生）、PPARγ及IDE的蛋白表达。结果:OB组大鼠血糖较正常组无明显差别,胰岛素明显升高并存在胰岛素抵抗（P＜0.05）;实时荧光定量PCR结果显示肥胖大鼠海马内TNF-α和APP mRNA水平较正常组升高（P＜0.01）,而PPARγ和IDE mRNA表达减少（P＜0.01）;蛋白免疫印记技术及免疫组织化学法检测与实时荧光定量PCR结果一致。结论:肥胖时大鼠海马内存在炎性改变,TNF-α表达升高,IDE和PPARγ表达减少,Aβ沉积增加。IDE作为Aβ的重要降解酶,其表达减少是Aβ沉积的关键因素;PPARγ作为调控IDE转录的核转录因子,在本实验肥胖大鼠海马内表达下降,提示IDE生成减少可能与PPARγ作用下降有关。

AIM: To investigate the relationship between classical Wnt pathway with β-amyloid peptide(Aβ) deposition in hippocampus of insulin resistance(IR) rat model and to observe the above-mentioned proteins and the correlation with peroxisome proliferator-activated receptor γ(PPARγ) by treating the IR rats with rosiglitazone. METHODS: The rat models of IR and TZD were made.The plasma insulin and the plasma glucose levels were tested by RIA and glucose-oxidase methods,respectively.The indexes of insulin resistance were calculated by HOMA-IR.The proteins of Aβ,Wnt3a,β-catenin and PPARγ were analyzed by Western blotting. RESULTS: The plasma insulin in IR group was significantly higher than that in control group.Insulin resistance,which was calculated by HOMA-IR,was significantly higher in IR group than that in control group.The levels of Aβ and β-catenin in IR group were higher than those in control group,while the levels of Wnt3a and PPARγ were decreased.After treatment with rosiglitazone,Aβ was reduced but Wnt3a,β-catenin and PPARγ were increased. CONCLUSION: In hippocampus of IR rats,Aβ is deposited and the levels of Wnt3a and Wnt are reduced.Rosiglitazone,as a PPARγ agonist,can upregulate the activity of Wnt pathway and reduce Aβ deposition in rat hippocampus.

Objective To analyze the clinical data, including clinical features, treatment, and prognosis,in patients with different kinds of pituitary adenomas. Methods In this retrospective study, 746 cases were included. The characteristics of general epidemiology, clinical symptoms, pathology, imaging, treatment, and prognosis were analyzed. Results Clinical features were different among various pituitary adenomas. Symptoms caused by mass effect and hormone abnormality were expresssed in varying degrees. Serum prolactin>121.28 μg/L can differentiate the prolactin adenoma from the other huge tumor causing hyperprolactinemia due to the mass effect. There is significant relationship between the size and the various types of pituitary adenomas ( P<0.01 ),also between the size and the invasive capability ( P<0.01 ). Conclusions The pituitary adenomas may have their specific epidemiological, clinical, pathological, and imaging features, due to the distinct biological behavior. It is necessary to do the diagnosis, treatment, and prognosis evaluation individually.