HPDE6-C7人正常胰腺导管上皮细胞、HPDE6-C7细胞

产品名称：HPDE6-C7人正常胰腺导管上皮细胞、HPDE6-C7人正常胰腺导管上皮细胞、HPDE6-C7人正常胰腺导管上皮细胞、HPDE6-C7人正常胰腺导管上皮细胞产品基本信息 细胞名称：HPDE6-C7，人正常胰腺导管上皮细胞 种属来源：人 组织来源：胰腺 细胞形态：上皮细胞样 生长特性：贴壁生长 培养基:：90%1640+10%FBS 生长条件：气相：95%空气+5%二氧化碳；温度：37℃ 传代方法：1:2至1:3，每周 3次 冻存条件：无血清冻存液，液氮储存 支原体检测：无 细胞培养操作 1）复苏细胞：将含有1 mL细胞悬液的冻存管在 37℃水浴中迅速摇晃解冻，加4 mL培养基混合均匀。在1000 rpm条件下离心3 min，弃去上清液，加1-2 mL培养基后吹匀。然后将所有细胞悬液加入含适量培养基的培养瓶中培养过夜（或将细胞悬液加入10 cm皿中，加入约8 mL培养基，培养过夜）。第二天换液并检查细胞密度。 2）细胞传代：如果细胞密度达80%-90%，即可进行传代培养。 a、弃去培养上清，用不含钙、镁离子的PBS润洗细胞1-2次。 b、加1 mL消化液（0.25%Trypsin-0.53mM EDTA）于培养瓶中，使消化液浸润所有细胞，弃去消化液，将培养瓶置于37℃培养箱中消化1 min，然后在显微镜下观察细胞消化情况，若细胞大部分变圆并脱落，迅速拿回操作台，轻敲几下培养瓶后加少量培养基终止消化。 c、按6-8 mL/瓶补加培养基，轻轻打匀后装入无菌离心管中，1000 rpm离心4 min，弃去上清液，补加1-2 mL培养液后吹匀。 d、将细胞悬液按1:2比例分到新的含8 mL培养基的新皿中或者瓶中，置于培养箱中培养。 3）细胞冻存：待细胞生长状态良好时，可进行细胞冻存。下面 T25 瓶为例； a、收集细胞及细胞培养液，装入无菌离心管中，1000 rpm条件下离心4 min，弃去上清液，用PBS清洗一遍，弃尽PBS，加 1 mL血清重悬细胞，进行细胞计数。 b、根据细胞数量加入无血清细胞冻存液，使细胞密度5×106~1×107/mL，轻轻混匀，每支冻存管冻存1mL细胞悬液，注意冻存管做好标识。 c、将冻存管放入-80℃冰箱，24 h后转入液氮灌储存。记录冻存管位置以便下次拿取。

Limited literature addresses the association between pollution, stress, and obesity, and knowledge synthesis on the associations between these three topics has yet to be made. Two reviewers independently conducted a systematic review of MEDLINE, Embase, and Web of Science Core Collection databases to identify studies dealing with the effects of semi-volatile organic compounds, pesticides, conservatives, and heavy metals on the psychosocial stress response and adiposity in humans, animals, and cells. The quality of papers and risk assessment were evaluated with ToxRTool, BEES-C instrument score, SYRCLEs risk of bias tool, and CAMARADES checklist. A protocol for the systematic review was registered on PROSPERO. Of 1869 identified references, 63 were eligible after title and abstract screening, 42 after full-text reading, and risk of bias and quality assessment. An important body of evidence shows a positive association between pollution, stress response, and obesity. Pollution stimulates the hypothalamic-pituitary-adrenal axis by activating the glucocorticoid receptor signaling and transcriptional factors responsible for adipocyte differentiation, hyperphagia, and obesity. Endocrine-disrupting chemicals also alter the Peroxisome Proliferator-activated Receptor gamma pathway to promote adipocyte hyperplasia and hypertrophy. However, these associations depend on sex, age, and pollutant type. Our findings evidence that pollution promotes stress, leading to obesity.

Background: Central synucleinopathies, including Parkinsons disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA), involve alpha-synuclein accumulation and dopaminergic cell loss in the substantia nigra (SN) and locus coeruleus (LC). Pure autonomic failure (PAF), a peripheral synucleinopathy, often precedes central synucleinopathies.

Objectives: To assess early brain involvement in PAF using neuromelanin-sensitive magnetic resonance imaging (NM-MRI) and fluorodopa-positron emission tomography (FDOPA-PET), and to determine whether PAF patients with a high likelihood ratio (LR) for conversion to a central synucleinopathy exhibit reduced NM-MRI contrast in the LC and SN compared with controls and low-LR patients.