林培政教授从“暑湿”论治成人风疹病毒性脑炎验案

成人风疹病毒性脑炎是风疹病毒感染的少见并发症,是一种累及神经系统的罕见病,目前发病机制尚未明确,尚无特异治疗,西医以抗病毒、抗炎、增强免疫力等治疗为主。林培政教授以温病理论为指导,结合患者发病特点,辨病为暑湿病,辨证先后属暑湿弥漫三焦、困阻中下焦、暑湿伤气,分别以清暑化湿、宣通三焦,清暑化湿、健脾化湿消积,清暑化湿、培元和中为法,完全治愈1例成人风疹病毒性脑炎患者,无任何后遗症,疗效确切。     

林国华针灸治疗难治性突发性耳聋经验撷要

总结林国华教授针灸治疗难治性突发性耳聋经验,并对典型医案进行介绍.林国华教授认为本病多因少阳经气厥塞所致,提倡尽早针灸干预,治病求本,谨守"少阳暴厥"之病机,谨遵"疏解少阳,通耳开窍"之法,临证必用听宫,主取少阳经穴,辅予辨经取穴,巧施发蒙针法与气流灌耳法,妙用岭南火针疗法,必要时调气调神、加取募穴,共奏通耳复聪之效.     

DCIS and LCIS are confusing and outdated terms. They should be abandoned in favor of ductal intraepithelial neoplasia (DIN) and lobular intraepithelial neoplasia (LIN)

The terms ductal and lobular intraepithelial neoplasia (DIN and LIN) were introduced by Tavossoli 15 years ago, who proposed they should replace, respectively, ductal and lobular carcinoma in situ (DCIS and LCIS). This proposal has been slowly gaining ground. We argue that DCIS and LCIS should now be definitively abandoned. Bringing together ‘in situ’ and other entities into the simpler and more logical DIN/LIN framework–as has been done with intraepithelial neoplasias of cervix, vagina, vulva, prostate, and pancreas–would eliminate the artificial and illogical distinctions between ‘not cancers’ (e.g. flat epithelial atypia, atypical ductal hyperplasia–now classified as low grade DIN) and ‘cancers’ (e.g. DCIS–now considered medium–high grade DIN). Elimination of the term ‘carcinoma’ from entities that cannot metastasize will reduce confusion among health professionals and patients, and contribute to reducing the risk of overtreatment, as well as reducing adverse psychological reactions in patients.     

HACE1和LIN28B基因单核苷酸多态性与中国汉族儿童神经母细胞瘤易感性的关联研究

目的 探讨HACE1和LIN28B基因多态与中国汉族儿童神经母细胞瘤的相关性。方法 采用病例对照研究,收集246例中国汉族神经母细胞瘤患儿和328例中国汉族健康儿重标本,提取外周血DNA,通过PCR扩增目的基因片段,随后应用Sequenommassarray对目的片段进行测序分型。并采用卡方检验、校验后Logistic回归分析等统计学方法,比较各SNP位点与NB肿瘤发生发展相关性。结果 HACE1基因rs45521835位点携带AA基因型的患儿以及rs6927608位点携带CC基因型的患儿其NB肿瘤始发于肾上腺较多,OR值分别为5.20(95%CI:1.06~25.56,P:0.047)和5.00(95%CI:1.02~24.55,P=0.052)。LIN28B基因SNP位点rs7759938(CC基因型)、rs314280(TTT基因型)、rs314276(AA基因型)和rs314263(CC基因型)主要与GNB密切相关,OR值分别2.94(95%CI:1.06~8.20,P=0.047)、2.94(95%CI:1.06~8.20,P=0.047)、2.95(95%CI:1.06~8.24,P=0.047)和3.02(95%CI:1.08~8.41,P=0.042)。结论 在中国汉族儿童中,HACE1基因(rs45521835,rs6927608)和LIN28B基因(rs7759938,rs314280,rs314276,rs314263)SNPs与原发于肾上腺的神经母细胞瘤或者节细胞性神经母细胞瘤(GNB)密切相关。     

LIN28A和LAMP1在膀胱癌细胞系中的表达及意义

目的:探讨LIN28A和LAMP1在膀胱癌细胞系中表达情况,以及两者之间的关系,推测其可能临床意义及对肿瘤进展的影响。方法:采用RT-PCR检测膀胱癌细胞系LIN28A、LIN28B和LAMP1表达,免疫荧光检测LIN28A和LAMP1二者蛋白表达定位;LIN28A敲减后通过qRT-PCR检测LAMP1的mRNA表达变化。结果:5个癌细胞系T24、UM-UC3、J82、5637和SW780和正常移行上皮细胞系SV-HUC-1均表达LIN28A,其中J82也表达LIN28B;5个癌细胞系均表达LAMP1,SV-HUC-1不表达LAMP1;LIN28A和LAMP1蛋白均定位在胞浆;LIN28A敲减后对LAMP1的mRNA表达变化无明显影响,相应蛋白变化需要进一步验证。结论:4个膀胱癌细胞系T24、5637、UM-UC3和SW780可以用于LIN28A与肿瘤相关的机制研究,而J82可用于LIN28B的机制研究。LIN28A对肿瘤细胞和干细胞的调控方面可能具有相似性,敲减后对其靶点mRNA表达量无明显影响,LAMP1蛋白可能对肿瘤细胞侵袭转移具有抑制作用。     

诱导多能干细胞建系过程中关键转录因子的作用

通过添加OCT4、SOX2等转录因子,体外诱导细胞重编程获得诱导多能干细胞是近年干细胞领域的一大突破.OCT4、SOX2和NANOG等转录因子在启动细胞重编程、维持诱导多能干细胞多能性和决定其是否走向分化方面起了关键作用.对这些转录因子作用机制的了解,有助于细胞莺编程分子机制的进一步阐明.     

林胜友主任中医师治疗化疗相关性呕吐经验

[目的]分析讨论林胜友主任中医师治疗化疗相关性呕吐的临证经验。[方法]通过跟师学习,归纳整理病案,结合林师平日指导,分析化疗相关性呕吐的病因病机,总结林师治疗该疾病的临床经验,并附验案加以佐证。[结果]林师认为化疗相关性呕吐的病因病机为中焦土虚,胃气失和;腑实不通,浊气犯胃;肝胆不利,气机失转,治疗上主要从健脾土、通肠腑、畅气机着手。所举验案,患者辨证为脾虚腑实,兼有肝郁,采取健脾通腑,辅以疏肝解郁治疗化疗相关性呕吐,疗效明显,顺利帮助患者度过化疗阶段。[结论]林师治疗化疗相关性呕吐采用健脾、通腑、疏肝治法,通补并用,可以取得较好的疗效。     

LIN28A attenuates high glucose-induced retinal pigmented epithelium injury through activating SIRT1-dependent autophagy

AIM: To evaluate the effects of LIN28A (human) on high glucose-induced retinal pigmented epithelium (RPE) cell injury and its possible mechanism. METHODS: Diabetic retinopathy model was generated following 48h of exposure to 30 mmol/L high glucose (HG) in ARPE-19 cells. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot tested the expression of the corresponding genes and proteins. Cell viability as well as apoptosis was determined through cell counting kit-8 (CCK-8) and flow cytometry assays. Immunofluorescence assay was adopted to evaluate autophagy activity. Caspase 3 activity, oxidative stress markers, and cytokines were appraised adopting their commercial kits, respectively. Finally, ARPE-19 cells were preincubated with EX527, a Sirtuin 1 (SIRT1) inhibitor, prior to HG stimulation to validate the regulatory mechanism. RESULTS: LIN28A was downregulated in HG-challenged ARPE-19 cells. LIN28A overexpression greatly inhibited HG-induced ARPE-19 cell viability loss, apoptosis, oxidative damage as well as inflammatory response. Meanwhile, the repressed autophagy and SIRT1 in ARPE-19 cells challenged with HG were elevated after LIN28A overexpression. In addition, treatment of EX527 greatly inhibited the activated autophagy following LIN28A overexpression and partly abolished the protective role of LIN28A against HG-elicited apoptosis, oxidative damage as well as inflammation in ARPE-19 cells. CONCLUSION: LIN28A exerts a protective role against HG-elicited RPE oxidative damage, inflammation, as well as apoptosis via regulating SIRT1/autophagy.     

Disrupting LIN28 in atypical teratoid rhabdoid tumors reveals the importance of the mitogen activated protein kinase pathway as a therapeutic target

Atypical teratoid rhabdoid tumor (AT/RT) is among the most fatal of all pediatric brain tumors. Aside from loss of function mutations in the SMARCB1 (BAF47/INI1/SNF5) chromatin remodeling gene, little is known of other molecular drivers of AT/RT. LIN28A and LIN28B are stem cell factors that regulate thousands of RNAs and are expressed in aggressive cancers. We identified high-levels of LIN28A and LIN28B in AT/RT primary tumors and cell lines, with corresponding low levels of the LIN28-regulated microRNAs of the let-7 family. Knockdown of LIN28A by lentiviral shRNA in the AT/RT cell lines CHLA-06-ATRT and BT37 inhibited growth, cell proliferation and colony formation and induced apoptosis. Suppression of LIN28A in orthotopic xenograft models led to a more than doubling of median survival compared to empty vector controls (48 vs 115 days). LIN28A knockdown led to increased expression of let-7b and let-7g microRNAs and a down-regulation of KRAS mRNA. AT/RT primary tumors expressed increased mitogen activated protein (MAP) kinase pathway activity, and the MEK inhibitor selumetinib (AZD6244) decreased AT/RT growth and increased apoptosis. These data implicate LIN28/RAS/MAP kinase as key drivers of AT/RT tumorigenesis and indicate that targeting this pathway may be a therapeutic option in this aggressive pediatric malignancy.