Cell viability and dopamine secretion of 6-hydroxydopamine-treated PC12 cells co-cultured with bone marrow-derived mesenchymal stem cells

In the present study, PC12 cells induced by 6-hydroxydopamine as a model of Parkinson＇s Disease, were used to investigate the protective effects of bone marrow-derived mesenchymal stem cells bone marrow-derived mesenchymal stem cells against 6-hydroxydopamine-induced neurotoxicity and to verify whether the mechanism of action relates to abnormal a-synuclein accumulation in cells Results showed that co-culture with bone marrow-derived mesenchymal stem cells enhanced PC12 cell viability and dopamine secretion in a cell dose-dependent manner. MitoLight staining was used to confirm that PC12 cells co-cultured with bone marrow-derived mesenchymal stem cells demonstrate reduced levels of cell apoptosis. Immunocytochemistry and western blot analysis found the quantity of α-synuclein accumulation was significantly reduced in PC12 cell and bone marrow-derived mesenchymal stem cell co-cultures. These results indicate that bone marrow-derived mesenchymal stem cells can attenuate 6-hydroxydopamine-induced cytotoxicity by reducing abnormal α-synuclein accumulation in PC12 cells.

Ghrelin alleviates 6-hydroxydopamine-induced neurotoxicity in SH-SY5Y cells

Ghrelin is a neuropeptide that has various physiological functions and has been demonstrated to be neuroprotective in a number of neurological disease models.However,the underlying mechanisms of ghrelin in Parkinson’s disease remain largely unexplored.The current study aimed to study the effects of ghrelin in a 6-hydroxydopamine(6-OHDA)-induced Parkinson’s disease model and evaluate the potential underlying mechanisms.In the present study,we treated an SH-SY5 Y cell model with 6-OHDA,and observed that pretreatment with different concentrations of ghrelin(1,10,and 100 nM)for 30 minutes relieved the neurotoxic effects of 6-OHDA,as revealed by Cell Counting Kit-8 and Annexin V/propidium iodide(PI)apoptosis assays.Reverse transcription quantitative polymerase chain reaction and western blot assay results demonstrated that 6-OHDA treatment upregulatedα-synuclein and lincRNA-p21 and downregulated TG-interacting factor 1(TGIF1),which was predicted as a potential transcription regulator of the gene encodingα-synuclein(SNCA).Ghrelin pretreatment was able to reverse the trends caused by 6-OHDA.The Annexin V/PI apoptosis assay results revealed that inhibiting eitherα-synuclein or lincRNA-p21 expression with small interfering RNA(siRNA)relieved 6-OHDA-induced cell apoptosis.Furthermore,inhibiting lincRNA-p21 also partially upregulated TGIF1.By retrieving information from a bioinformatics database and performing both double luciferase and RNA immunoprecipitation assays,we found that lincRNA-p21 and TGIF1 were able to form a double-stranded RNA-binding protein Staufen homolog 1(STAU1)binding site and further activate the STAU1-mediated mRNA decay pathway.In addition,TGIF1 was able to transcriptionally regulateα-synuclein expression by binding to the promoter of SNCA.The Annexin V/PI apoptosis assay results showed that either knockdown of TGIF1 or overexpression of lincRNA-p21 notably abolished the neuroprotective effects of ghrelin against 6-OHDA-induced neurotoxicity.Collectively,these findings suggest that ghrelin exerts neuroprotective effects against 6-OHDA-induced neurotoxicity via the lincRNA-p21/TGIF1/α-synuclein pathway.

Neuroprotective effects of insulin-like growth factor-2 in 6-hydroxydopamine-induced cellular and mouse models of Parkinson’s disease

Skin-derived precursor Schwann cells have been reported to play a protective role in the central nervous system. The neuroprotective effects of skin-derived precursor Schwann cells may be attributable to the release of growth factors that nourish host cells. In this study, we first established a cellular model of Parkinson’s disease using 6-hydroxydopamine. When SH-SY5 Y cells were pretreated with conditioned medium from skin-derived precursor Schwann cells, their activity was greatly increased. The addition of insulin-like growth factor-2 neutralizing antibody markedly attenuated the neuroprotective effects of skin-derived precursor Schwann cells. We also found that insulin-like growth factor-2 levels in the peripheral blood were greatly increased in patients with Parkinson’s disease and in a mouse model of Parkinson’s disease. Next, we pretreated cell models of Parkinson’s disease with insulin-like growth factor-2 and administered insulin-like growth factor-2 intranasally to a mouse model of Parkinson’s disease induced by 6-hydroxydopamine and found that the level of tyrosine hydroxylase, a marker of dopamine neurons, was markedly restored, α-synuclein aggregation decreased, and insulin-like growth factor-2 receptor downregulation was alleviated. Finally, in vitro experiments showed that insulin-like growth factor-2 activated the phosphatidylinositol 3 kinase(PI3 K)/AKT pathway. These findings suggest that the neuroprotective effects of skin-derived precursor Schwann cells on the central nervous system were achieved through insulinlike growth factor-2, and that insulin-like growth factor-2 may play a neuroprotective role through the insulin-like growth factor-2 receptor/PI3 K/AKT pathway. Therefore, insulin-like growth factor-2 may be an useful target for Parkinson’s disease treatment.

Differences in brain pathological changes between rotenone and 6-hydroxydopamine Parkinson＇s disease models

Rotenone and 6-hydroxydopamine are two drugs commonly used to generate Parkinson＇s disease animal models.They not only achieve degenerative changes of dopaminergic neurons in the substantia nigra,but also satisfy the requirements for iron deposition.However,few studies have compared the characteristics of these two models by magnetic resonance imaging.In this study,rat models of Parkinson＇s disease were generated by injection of 3 μg rotenone or 10 μg 6-hydroxydopamine into the right substantia nigra.At 1,2,4,and 6 weeks after injection,coronal whole-brain T2-weighted imaging,transverse whole-brain T2-weighted imaging,and coronal diffusion tensor weighted imaging were conducted to measure fractional anisotropy and T2＊ values at the injury site.The fractional anisotropy value on the right side of the substantia nigra was remarkably lower at 6 weeks than at other time points in the rotenone group.In the 6-hydroxydopamine group,the fractional anisotropy value was decreased,but T2＊ values were increased on the right side of the substantia nigra at 1 week.Our findings confirm that the 6-hydroxydopamine-induced model is suitable for studying dopaminergic neurons over short periods,while the rotenone-induced model may be appropriate for studying the pathological and physiological processes of Parkinson＇s disease over long periods.

Reduced glutathione alleviates the toxic effect of 6-hydroxydopamine on bone marrow stromal cells

We studied the effect of reduced glutathione on bone marrow stromal cells （BMSCs） treated with 6-hydroxydopamine （6-OHDA）, which shows a toxic effect on dopaminergic neurons. The proliferation of BMSCs treated with 6-OHDA decreased, while that of BMSCs treated with reduced glutathione increased. The proliferation of BMSCs treated with both 6-OHDA and reduced glutathione was significantly higher compared with that treated with 6-OHDA alone. These findings indicate that reduced glutathione alleviates the toxic effect of 6-OHDA on BMSCs.

Dimethyl sulfide,a metabolite of the marine microorganism,protects SH-SY5Y cells against 6-hydroxydopamine and MPP~＋-induced apoptosis

Dimethyl sulfide(DMS)has been historically recognized as a metabolite of the marine microorganism or a disgusting component for the smell of halitosis patients.In our recent study,DMS has been identified as a cytoprotectant that protects against oxidative-stress induced cell death and aging.We found that at near-physiological concentrations,DMS reduced reactive oxygen species(ROS)in cultured PC12 cells and alleviated oxidative stress.The radical-scavenging capacity of DMS at near-physiological concentration was equivalent to endogenous methionine(Met)-centered antioxidant defense.Methionine sulfoxidereductase A(MsrA),the key antioxidant enzyme in Met-centered defense,bound to DMS and promoted its antioxidant capacity via facilitating the reaction of DMS with ROS through a sulfonium intermediate at residues Cys72,Tyr103,Glu115,followed by the release of dimethyl sulfoxide(DMSO).MTT assay and trypan blue test indicated that supplement of DMS exhibited cytoprotection against 6-hydroxydopamine and MPP+induced cell apoptosis.Furthermore,Msr A knockdown abolished the cytoprotective effect of DMS at near-physiological concentrations.The present study reveals new insight into the potential therapeutic value of DMS in Parkinson disease.

Protective Effect of Immaturue Bitter Orange(Citrus aurantium L.)Flavonoids Extracts on PC12 Cell Injury Induced by 6-Hydroxydopamine

To study the neuro protective effect of flavonoids extracts from immature bitter orange(Citrus aurantium L.),the PC12 cells treated with 6-hydroxydopamine(6-OHDA)were used as the Parkinson’s disease(PD)model.To determine the optimal dose of 6-OHDA for constructing a PD model,PC12 cells were incubated with different concentrations of 6-OHDA for 24 h.After 24 h incubation,PC12 cells of drug groups were added 6-OHDA and different concentrations of flavonoids extracts were measured cell viability by CCK8 for selecting effective concentration of flavonoids extracts;the ROS level was determined using flow cytometry;the levels of MDA,CAT,SOD and GSH-Px were assayed by Colorimetric kit for oxidative stress investigation.Compared with the model group,PC12 cell viability was significantly enhanced(P<0.05),the levels of ROS and MDA were reduced significantly(P<0.05),and the activities of SOD,CAT and GSH-Px were significantly enhanced(P<0.05)in drug groups.In conclusion,immature bitter orange flavonoids extracts could protect PC12 cells against 6-OHDA-induced oxidative stress.

Feasibility of establishing model of Parkinson disease by injecting 6-hydroxydopamine at different parts of the nigrostriatal pathway in the brain of rats

BACKGROUND： Previous researches found that animal models with Parkinson disease （PD） could be established by injecting 6-hydroxydopamine （6-OHDA） into medial forebrain bundle （MFB）, substantia nigra compacta （SNC） and caudate-putamen complex （CPU） of the nigrostriatal pathway. OBJECTIVE ： To compare behavioral, biochemica 6-OHDA injections in the areas of MFB, SNC and DESIGN： Controlled observational study and histological properties of these rats undergoing the CPU respectively. SEI-IING： Department of Neurology, First Affiliated Hospital of Guangxi Medical University MATERIALS： A total of 64 adult female SD rats weighing 180-230 g were provided by the Animal Experimental Center of Guangxi Medical University. 6-OHDA （Sigma Company, USA）; Brain solid positioner （Standard model 51600, Stoelting Co., IL, USA）; rotational monitoring of little animal （type QL-1, USA）; high liquid chromatography （HLC, Waters Company）. METHOOS： The experiment was carried out in the Medical Experimental Center of Guangxi Medical University from February to December 2005. ① According to digital table, 64 SD rats were divided into MFB group, SNC group, CPU group and control group with 16 in each group. On the basis of the brain atlas of Paxinos, rats in the first three groups were injected with 5 μL 6-OHDA into right MFB （0 mm of line of incisor tooth, A/P 4.4 mm, L/R 1.2 mm, ON -7.8 mm）, SNC （line of incisor tooth just equal to horizon, A/P -4.8 mm, L/R 1.6 mm, ON -7.8 mm） and CPU （0 mm of line of incisor tooth, A/P 1.2 mm, L/R 2.7 mm, ON -5.4 mm）, respectively. The rats in control group were injected with 5 μL ascorbic acid solution （2 g/L）. One week after operation, 0.1 g/L apomorphine （Apo, 0.05 mg/kg） was subcutaneously injected into neck and then rotational behavior induced by Apo was recorded once a week for 8 weeks. The PD models were considered successful only when rotational times more than or equal to 7 times per minute. Eight weeks after operation, micro-perfusion was used to obtain micro-perfusate in bilateral CPU and contents of 3,4-dihydroxyphenylacetic acid （3,4-DOPAC） and homovanillic acid （HVA） were also measured. In addition, amount of tyrosine hydroxylase positive cells （TH＊） in SNC was counted with immuno- histochemical staining. MAIN OUTCOME MEASURES ： ① Successful rate of PD models; ② contents of dopamine and its metabolite in MFB, SNC and CPU groups and TH＊ amount. RESULTS： All 64 SD rats were involved in the final analysis. ③ Successful rate and rotational behavior： One week after operation, there were 6 successful models both in SNC and MFB groups; in the 2^nd week, there were 6 both in SNC and MFB groups and 1 in CPU group; in the 3^nd week, there were 1 in MFB group and 3 in CPU group; in the 4^nd week, there were 3 in CPU group. Otherwise, no successful case was found out in the next 3 weeks. Abnormal rotational behavior was not observed in control group. Four weeks after operation, successful rates were 81% （13/16） in MFB group, 75% （12/16） in SNC group and 44% （7/16） in CPU group.② Contents of 3, 4-DOPAC and HVA： Eight weeks after operation, contents in the SNC area of the injured side were lower than those on non-lesion side （P 〈 0.01）.③Changes of TH＋ amount： Eight weeks after operation, TH＋ amount in the SNC area of the lesion side was lower than that on non-lesion side （P 〈 0.01 ）. CONCLUSION： Injecting 6-OHDA into MFB, SNC and CPU can damage dopaminergic cells and establish successful PD models.

Aged Garlic Extract Reduces ROS Production and Cell Death Induced by 6-Hydroxydopamine through Activation of the Nrf2-ARE Pathway in SH-SY5Y Cells

Many degenerative or pathological processes, such as aging, cancer and coronary heart disease, are related to reactive oxygen species (ROS) and radical-mediated reactions. We examined the effectiveness of aged garlic extract (AGE), a garlic preparation rich in water-soluble cysteinyl moieties, for protection of cells from ROS produced by 6-hydroxy-dopamine (6-OHDA) using human neuroblastoma SH-SY5Y cells. Concomitant treatment of cells with AGE (2 and 4 mg/ml) showed the dose-dependent protective effect on the cell death induced by 6-OHDA. In addition, the AGE treatment significantly suppressed the increase of ROS generation by 6-OHDA. Furthermore, the protective effect of AGE was accompanied by activation of the nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway and the increase of mRNAs of heme oxygenase-1 and NAD(P)H quinone oxidoreductase 1. These two enzymes are important in the cellular antioxidant system. These results indicated that AGE protected cells from ROS damage by not only capturing ROS directly but also activating the cellular antioxidant system by stimulating antioxidant gene expression via the Nrf2-ARE pathway. The present study suggested that AGE may be useful for prevention and treatment of cell damage caused by ROS.

Curcumin protects nigral dopaminergic neurons by iron-chelation in the 6-hydroxydopamine rat model of Parkinson's disease

Objective Curcumin is a plant polyphenolic compound and a major component of spice turmeric （Curcuma longa）. It has been reported to possess free radical-scavenging, iron-chelating, and anti-inflammatory properties in dif- ferent tissues. Our previous study showed that curcumin protects MES23.5 dopaminergic cells from 6-hydroxydopamine （6-OHDA）-induced neurotoxicity in vitro. The present study aimed to explore this neuroprotective effect in the 6-OHDA-lesioned rat model of Parkinson＇s disease in vivo. Methods Rats were given intragastric curcumin for 24 days. 6-OHDA lesioning was conducted on day 4 of curcumin treatment. Dopamine content was assessed by high-performance liquid chromatography with electrochemical detection, tyrosine hydroxylase （TH）-containing neurons by immunohistochemistry, and iron-containing cells by Perls＇ iron staining. Results The dopamine content in the striatum and the number of TH-immunoreactive neurons decreased after 6-OHDA treatment. Curcumin pretreatment reversed these changes. Further studies demonstrated that 6-OHDA treatment increased the number of iron-staining cells, which was dramatically decreased by curcumin pretreatment. Conclusion The protective effects of curcumin against 6-OHDA may be attributable to the ironchelating activity of curcumin to suppress the iron-induced degeneration of nigral dopaminergic neurons.

Antagonistic effect of 6-hydroxydopamine (6-OHDA) on generation of immunosuppressive protein of stress in the rat

Neonatal rats were injected with 6-hydroxydopamine (6-OHDA) for chemical sympa-thectomy. The rats were treated with restraint stress when they grew up to 56 d. It has been found that the generation of immunosuppressive protein of stress (ISPS) is significantly reduced, suggesting that peripheral sympathetic nerve plays an important role in mediating the generation of ISPS.

Dopaminergic neurons show increased low-molecular-mass protein 7 activity induced by 6-hydroxydopamine in vitro and in vivo

Background:Abnormal expression of major histocompatibility complex class I(MHC-I)is increased in dopaminergic(DA)neurons in the substantia nigra(SN)in Parkinson’s disease(PD).Low-molecular-mass protein 7(β5i)is a proteolytic subunit of the immunoproteasome that regulates protein degradation and the MHC pathway in immune cells.Methods:In this study,we investigated the role of β5i in DA neurons using a 6-hydroxydopamine(6-OHDA)model in vitro and vivo.Results:We showed that 6-OHDA upregulatedβ5i expression in DA neurons in a concentration-and time-dependent manner.Inhibition and downregulation ofβ5i induced the expression of glucose-regulated protein(Bip)and exacerbated 6-OHDA neurotoxicity in DA neurons.The inhibition of β5i further promoted the activation of Caspase 3-related pathways induced by 6-OHDA.β5i also activated transporter associated with antigen processing 1(TAP1)and promoted MHC-I expression on DA neurons.Conclusion:Taken together,our data suggest that β5i is activated in DA neurons under 6-OHDA treatment and may play a neuroprotective role in PD.

隆德概念对重型颅脑损伤患者脑脊液IL-6、继发性脑水肿及预后影响的研究

目的观察运用隆德概念治疗重型颅脑损伤患者的临床效果。方法选取2022年8月—2023年10月柳州市人民医院重症医学科收治的50例重型颅脑损伤患者,采用随机数字表法分为对照组和观察组,每组25例。对照组采用常规治疗方法,观察组在常规治疗基础上运用隆德概念治疗。观察两组患者入ICU时及入ICU后24 h、3 d、7 d、14 d脑脊液白细胞介素-6(IL-6)水平、脑水肿CT评估量、颅内压(ICP)以及治疗前后格拉斯哥昏迷评分(GCS)、急性生理学和慢性健康状况评价Ⅱ(APACHEⅡ)评分、ICU停留时间及3个月后格拉斯哥预后评分(GOS)。结果与入ICU时相比,入ICU后24 h、3 d、7 d、14 d两组患者脑脊液IL-6水平、脑水肿CT评估量及ICP均不同程度升高;入ICU后24 h、3 d,观察组脑脊液IL-6水平、CT评估量低于对照组;入ICU后7 d,观察组脑脊液IL-6水平、脑水肿CT评估量及ICP低于对照组;入ICU后14 d,观察组ICP低于对照组,差异均有统计学意义(P<0.05)。治疗后,GCS评分高于对照组、APACHEⅡ评分低于对照组,ICU停留时间短于对照组,GOS预后良好率高于对照组,差异均有统计学意义(P<0.05)。结论隆德概念可以有效减少重型颅脑损伤患者脑脊液IL-6,控制伤后炎症反应,减轻继发性脑水肿,降低ICP,改善预后。

“6T”实务管理在高校学生公寓现场管理中的应用——以云南省某高校为例

随着高等学校的改革发展,学生公寓管理工作值得关注。结合云南省某高校学生公寓管理现状分析可知,目前我国高等学校学生公寓工作存在一些问题,如员工流动性大、整体素质不高,学生安全意识淡薄,安全事件时有发生,缺乏有效的管理措施,学生公寓的服务与学生对美好生活的需求有差距。实施学生公寓6T实务管理后,员工队伍稳定、素质普遍提高,有效防范和化解各类风险,实现学生公寓由单一公寓向综合社区转变,提升学生公寓的管理水平和服务质量,满足学生多样化、个性化校园生活需求。

白蜡树FcF6′H1基因的密码子偏好性分析

利用CodonW、EMBOSS在线程序分析白蜡树FcF6'H1基因的密码子偏好性,对芸香科、豆科、伞形科、木犀科以及模式植物拟南芥、烟草和番茄中F6'H1的基因密码子进行聚类分析、中性绘图、ENC-plot分析和PR2-plot偏倚分析,研究影响白蜡树FcF6'H1基因密码子偏好性形成的因素,通过FcF6'H1与模式生物的密码子使用频率比较获得最佳受体。结果表明,白蜡树FcF6'H1的GC、GC1、GC2、GC3和GC12含量分别为0.4312、0.5125、0.3490、0.4321和0.4308,CAI值为0.216,ENC值为57.84,表明白蜡树FcF6'H1基因的偏好性较弱;中性绘图、ENC-plot和PR2-plot偏倚分析结果表明,碱基突变和自然选择均会影响FcF6'H1密码子的偏好性;CDS进化树和RSCU值聚类分析结果不完全一致,但是均表明白蜡树FcF6'H1与木樨榄XM_023028611.1、XM_023036788.1、XM_023034893.1聚为一类,确定了F6'H1基因的6个最优密码子,分别是CUC、AUC、AAG、GAG、UCG和ACA;密码子使用频率分析表明,模式生物中番茄和烟草适合作为遗传转化受体,大肠杆菌表达系统适合作为FcF6'H1的异源表达载体。文章初步阐明了白蜡树FcF6'H1基因密码子的使用规律。

肺腺癌中PTEN和6KDMB的表达与临床病理特征的关系

目的观察PTEN和6KDMB在肺浸润性腺癌中的表达,分析两者与多个临床病理参数的关系及相关性,加深对肺腺癌发病机制的认识。方法利用生物信息学分析手段评估PTEN和6KDMB mRNA在肺腺癌及正常肺组织中的表达情况。用免疫组织化学SP法检测74例肺浸润性腺癌组织及相应的正常肺组织中PTEN和6KDMB蛋白的表达情况,分析其与肺浸润性腺癌多个临床病理参数的关系,用Spearman法分析两者的相关性。结果PTEN和6KDMB mRNA在肺浸润性腺癌组织中的表达水平均较正常肺组织下调;59例配对肺腺癌及正常肺组织分析结果显示6KDMB mRNA在肺腺癌组织中表达水平较正常肺组织下调(P<0.05)。免疫组化结果显示浸润性肺腺癌中PTEN蛋白表达率(33.78%,25/74)显著低于正常肺组织(54.05%,40/74),6KDMB蛋白的表达率(72.97%,54/74)显著高于正常肺组织(21.62%,16/74)(P<0.05)。在74例浸润性肺腺癌中,PTEN在高分化、无气道播撒及TNM分期Ⅰ+Ⅱ表达率较高(均P<0.05)。6KDMB在淋巴结有转移和TNM分期Ⅲ+Ⅳ表达率较高(P<0.05)。74例肺浸润性腺癌中PTEN表达越低,6KDMB的表达越高,Spearman相关分析结果显示两者呈显著负相关(R_(s)=0.53,P<0.001)。结论肺浸润性腺癌中PTEN和6KDMB蛋白与侵袭和转移相关,两者呈显著负相关性,对PTEN和6KDMB在肺浸润性腺癌中的表达规律及相关性的研究,将为分子生物机制进一步研究提供一定的理论依据。

17~45岁肥胖门诊患者的6分钟步行试验距离参考方程研究

背景 目前6分钟步行试验(6MWT)已经被广泛用于评估肥胖人群的运动能力,并为制订干预措施提供了参考依据。国外已有研究提出了其他人群的6MWT距离参考方程,但中国17~45岁且BMI≥30 kg/m^(2)肥胖受试者的6MWT距离参考方程研究较少。目的 为17~45岁门诊肥胖受试者制订6MWT距离参考方程,并评估其影响因素。方法 根据美国胸科学会指南,前瞻性选取2022年6月—2023年9月于江苏省苏北人民医院内分泌科肥胖门诊部就诊的143名年龄17~45岁且BMI≥30 kg/m^(2)的成年人(71名男性和72名女性),进行人体测量和6MWT。采用逐步多元回归模型建立6MWT距离参考方程,将新建立的6MWT距离参考方程与现有的预测方程进行比较。结果 143名受试者的平均6MWT距离为(506.1±49.8)m,其中男性平均6MWT距离为(515.7±50.1)m,大于女性的平均6MWT距离(496.6±47.9)m(P<0.05)。在年龄段17~23岁、24~30岁、31~37岁以及38~45岁中,男性与女性6MWT距离比较,差异均有统计学意义(P<0.05)。男性受试者的体质量、BMI、最大心率(HR_(max))、心率差(ΔHR)、腰围、舒张压差(ΔDBP)、Borg量表评分差(ΔBorg)与6MWT距离相关(P<0.05),女性受试者的体质量、BMI、腰围与6MWT距离相关(P<0.05)。以步进的方法将潜在的影响因素纳入多元线性回归方程中,最终建立6MWT距离参考公式:男性y=494.463+1.414×ΔHR-3.903×BMI+0.874×HR_(max),R^(2)=0.429,女性y=670.448+0.299×ΔHR-4.342×BMI-0.195×HR_(max),R^(2)=0.312。结论 17~45岁门诊肥胖受试者中,男性的平均6MWT距离长于女性,且在不同年龄段均有显著差异。男性的体质量、BMI、HR_(max)、ΔHR、腰围、ΔDBP、ΔBorg与6MWT距离相关,女性的体质量、BMI、腰围、ΔSBP与6MWT距离相关。通过多元线性回归分析,为男性和女性分别建立了预测6MWT距离的参考方程,这些公式可能为评估个体的体能水平提供有价值的参考。

N6-甲基腺苷甲基化相关基因IGF2BP3在肾透明细胞癌的作用研究

目的筛选肾透明细胞癌(ccRCC)中的关键N6-甲基腺苷(m^(6)A)甲基化相关基因,并研究其与ccRCC预后、ccRCC细胞的迁移和侵袭的关系。方法从癌症基因组图谱(TCGA)和基因型组织表达(GTEx)数据库中下载ccRCC和癌旁组织的RNA测序数据和临床数据,采用R4.1.1分析表达谱和预后,并筛选关键基因。收集10例ccRCC手术临床标本,采用定量PCR(qPCR)和免疫组织化学法分别检测基因mRNA和蛋白表达。在人ccRCC细胞系RCC23中,通过SiRNA敲减关键基因,并用CCK-8检测细胞的存活率,采用划痕试验和Transwell试验分别检测细胞的迁移和侵袭。结果19个m^(6)A甲基化相关基因中仅有胰岛素样生长因子ⅡmRNA结合蛋白3(IGF2BP3)在ccRCC组织中高表达,且IGF2BP3高表达与ccRCC患者预后不良呈正相关。通过qPCR和免疫组织化学法在临床标本中验证了IGF2BP3的高表达。通过小干扰RNA(siRNA)将IGF2BP3敲减后发现,RCC23细胞的存活率明显下降,且细胞的迁移和侵袭能力下降。结论IGF2BP3可能是预测ccRCC患者预后的生物标志物和潜在的药物治疗靶点。

血清神经元特异性烯醇化酶、白细胞介素-6、肿瘤坏死因子-α水平评估肺癌患者预后不良的价值

目的探讨血清神经元特异性烯醇化酶(NSE)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)水平评估肺癌患者预后不良的价值,为临床提供参考。方法回顾性分析2021年7月至2023年8月仙桃市第一人民医院收治的94例肺癌患者的临床资料。根据随访1年预后情况的不同分为预后不良组(25例,复发、转移、癌症死亡)与预后良好组(69例)。比较两组患者临床资料;分析影响肺癌患者预后不良的独立危险因素;分析NSE、IL-6、TNF-α水平单独及联合检测预测肺癌患者预后不良的价值。结果预后不良组患者肿瘤TNM分期为Ⅲ~Ⅳ期占比、Karnofsky评分<80分占比、NSE、IL-6、TNF-α水平均高于预后良好组,整体分化程度低于预后良好组(均P<0.05)。多因素Logistic分析结果显示,肿瘤TNM分期为Ⅲ~Ⅳ期、低分化、Karnofsky评分<80分、NSE、IL-6、TNF-α水平升高均是影响肺癌患者预后不良的独立危险因素(均P<0.05)。受试者操作特征(ROC)曲线分析结果显示,NSE、IL-6、TNF-α水平单独及联合预测肺癌患者预后不良的曲线下面积(AUC)分别为0.819、0.887、0.852、0.953,灵敏度分别为0.760、0.880、0.840、0.920,特异度分别为0.768、0.913、0.696、0.942(均P<0.05)。结论肿瘤TNM分期为Ⅲ~Ⅳ期、低分化、Karnofsky评分<80分、NSE、IL-6、TNF-α水平升高均是影响肺癌患者预后不良的独立危险因素,联合检测NSE、IL-6、TNF-α在肺癌患者预后不良评估中效能较高。

基于柔性苯二乙酸CM6@Zn-MOF纳米材料的构筑和光电性能研究

金属有机框架(Metal-organic frameworks,简称MOFs)作为有效能量转移的供体,在人工光采集材料领域中已引起许多专家的关注。特别是二维MOFs纳米片,因每个活性位点暴露在外易靠近受体,可以有效地将内部能量转移给外部受体,具有更为非凡的光电性能。通过选用柔性的1,2-苯二乙酸(H_(2)opda)和刚性的3,5-二(三氮唑)吡啶(btyp)作为有机配体,合成了一种新型的二维配位聚合物[Zn_(3)(btyp)_(2)(opda)_(3)(H_(2)O)_(3)]·(btyp)(H_(2)O)_(3)(Zn-MOF),晶体属于三斜晶系、P-1空间群。在该晶体结构中,反式opda配体的2个羧基均以双齿螯合模式与Zn(Ⅱ)离子配位,形成一维无限链;btyp配体桥链支撑相邻一维链,构成二维网面;通过opda羧基O与结晶H_(2)O之间多个O—H…O的相互作用形成三维超分子网络结构。Zn-MOF且具有完整的循环伏安曲线(还原、氧化电位分别为-0.22、0.05 V),良好的扫描速率。使用超声粉碎法将Zn-MOF层状结构剥离形成二维纳米片,再与香豆素6(CM6)掺杂形成CM6@Zn-MOF纳米材料,荧光从蓝光向绿光移动,将光收集范围从紫外光扩展到可见光,加之良好的电化学循环伏安性能(还原、氧化电位分别为-0.21、0.08 V),有望成为光电应用新材料。