摘要：The GABAergic neurons in the parafacial zone（PZ） play an important role in sleep-wake regulation and have been identified as part of a sleep-promoting center in the brainstem, but the long-range connections mediating this function remain poorly characterized. Here, we performed whole-brain mapping of both the inputs and outputs of the GABAergic neurons in the PZ of the mouse brain. We used the modified rabies virus Env A-DG-Ds Red combined with a Cre/lox P gene-expression strategy to map the direct monosynaptic inputs to the GABAergic neurons in the PZ, and found that they receive inputs mainly from the hypothalamic area, zona incerta, and parasubthalamic nucleus in the hypothalamus; the substantia nigra, pars reticulata and deep mesencephalic nucleus in the midbrain;and the intermediate reticular nucleus and medial vestibular nucleus（parvocellular part） in the pons and *** also mapped the axonal projections of the PZ GABAergic neurons with adeno-associated virus, and defined the reciprocal connections of the PZ GABAergic neurons with their input and output nuclei. The newlyfound inputs and outputs of the PZ were also listed compared with the literature. This cell-type-specific neuronal whole-brain mapping of the PZ GABAergic neurons may reveal the circuits underlying various functions such as sleep-wake regulation.

摘要：In gamma camera and single-photon emission computerized tomography, the collimator removes most photons. Here, a gamma camera without collimator utilizes a specific arrangement of detectors. Instead of bending beams(like a lens) or directing beams(by parallel hole collimator), changes are created in detectors' field of view(FOV), so that each detector's FOV looks different from others. Simulation proved this theory, with 98 detectors(2 cm 9 1.41 cm) arranged in a zigzag manner for Monte Carlo simulation. A radioactive source with energy of140 ke V was situated on the detectors' faces. Sixty projections, each 3(0 –179) apart, were simulated by Monte Carlo N-Particle(MCNP) 4C code, rotating detectors around a radioactive point. The band containing the radioactive source is clearly visible in each *** obtained after simulation in different projections were reconstructed, and point source location emerged correctly. Simulation of gamma camera with zigzag arrangement of detectors and MCNP-4C code demonstrated that one could string the space and determine radioactive source by image reconstruction without using collimators, solely through these special detectors' distribution.

摘要：As we navigate the transition from the Fourth to the Fifth Industrial Revolution,the emerging fields of biomanufacturing and biofabrication are transforming life sciences and *** sectors are benefiting from a synergy of synthetic and engineering biology,sustainable manufacturing,and integrated design *** techniques such as 3D bioprinting,tissue engineering,directed assembly,and self-assembly are instrumental in creating biomimetic scaffolds,tissues,organoids,medical devices,and biohybrid *** field of biofabrication in the United Kingdom and Ireland is emerging as a pivotal force in bioscience and healthcare,propelled by cutting-edge research and *** on the production of biologically functional products for use in drug delivery,in vitro models,and tissue engineering,research institutions across these regions are dedicated to innovating healthcare solutions that adhere to ethical standards while prioritising sustainability,affordability,and healthcare system benefits.

摘要：背景:骨质疏松涉及破骨细胞分化成熟和成骨类细胞凋亡两方面,肿瘤坏死因子α能诱导多种细胞凋亡且效率差异很大,骨保护素能抑制破骨细胞成熟,但对成骨类细胞凋亡的作用未见报道。目的:探讨肿瘤坏死因子α能否诱导成骨类细胞凋亡及骨保护素能否抑制其凋亡。设计:以成骨细胞和MG63细胞作为实验对象、以鼠WEHI164细胞系用于阳性对照的观察对比分析。单位:解放军总医院全军口腔医学研究所、美国匹茨堡医学院退伍军人医疗中心。材料:本实验于2001-01/2003-12在***实验室和口腔研究所实验室完成。选择商品化细胞系,RPMI1640培养液和各种相关蛋白用于实验。方法:用人间充质干细胞在分化培养液中培养21d使之成为成骨细胞,与MG63一起用于凋亡实验。AnnexinV和原位末端标记法检测肿瘤坏死因子α诱导成骨类细胞凋亡。主要观察指标:全部细胞数及凋亡细胞数。结果:和FasL诱导细胞凋亡一样,肿瘤坏死因子α能引起MG63骨肉瘤细胞,间充质干细胞和成骨细胞的凋亡,并表现为明显的浓度依赖和时间依赖。低浓度肿瘤坏死因子α(170～500pmol/L)作用于细胞2～4h就显示了较明显的凋亡,而骨保护素在0.45～1.5nmol/L浓度时,几乎完全抑制了500pmol/L肿瘤坏死因子α诱导的凋亡。成骨细胞分泌骨保护素,而破骨细胞及破骨前体细胞产生肿瘤坏死因子α,它们相互作用降低成骨细胞的凋亡。结论:肿瘤坏死因子α能诱导成骨类细胞凋亡,骨保护素能够抑制肿瘤坏死因子α的凋亡诱导作用,从抑制破骨细胞成熟和成骨细胞凋亡两方面表现骨保护素防治骨质疏松的作用机制。

摘要：β-Glucuronidase(GUS)plays a key role in tumor initiation,metastasis,and progression,and thus,has been proposed as a promising cancer *** this study,we designed an enzyme-activatable near-infrared(NIR)fluorescent probe(DCM-βGlcA)for the rapid and accurate detection of GUS activity in vitro,in vivo and ex *** DCM-βGlcA was prepared by linking a glucuronic acid residue to dicyanomethylene-4 H-pyran(DCM).This probe exhibited significant light-up NIR fluorescent signals at 680 nm after reacting with GUS and the Stokes shift could reach 150 *** DCM-βGlcA showed a high sensitivity toward GUS and an excellent linear relationship at concentrations ranging between 0 and 4 U L^(-1)(R^(2)=0.9974)with the limit of detection as low as 0.19 U L^(-1).We used the DCM-βGlcA to identify GUS serum levels in both cancer patients and healthy individuals with a similar accuracy as that of an enzyme-linked immunosorbent assay(ELISA)while being easier and faster to ***,the DCM-βGlcA was used for tracking endogenous GUS in living cells,thereby discriminating GUSoverexpressed liver cancer from normal ***,the DCM-βGlcA was able to detect and image endogenous GUS in liver cancer tissue and tumor-bearing mouse *** findings demonstrate the potential of the DCM-βGlcA as a promising tool for detecting and monitoring GUS activity in preclinical applications.

摘要：目的 :观察原发性急性闭角型青光眼 (PAACG)患者房水的一氧化氮 (NO)、脂质过氧化产物丙二醛 (MDA)和超氧化物歧化酶(SOD)水平及其临床意义。方法 :采用配对设计进行分组 ,2 7例患者的急性发作眼为发作组 ,同一患者的另外一只未发作眼为对照组。用分光光度计检测两组房水 NO、MDA的含量和 SOD的活性。结果 :两组比较 ,PAACG组的 NO与 MDA非常显著高于对照组 (Ρ<0 .0 1 ) ,而SOD显著下降 (Ρ <0 .0 1 )。结论 :眼压升高可能导致 PAACG患者房水 NO与 MDA明显升高 ,而 SOD非常显著下降 ,导致损伤小梁网及邻近的葡萄膜和视网膜 ,促进了青光眼的高眼压及视神经病变的发展。

摘要：随着下丘中与调节能量稳态有关的脑星形胶质细胞信号传导的发现,星形胶质细胞在控制摄食的脑回路中的作用正逐渐被认识。脑干背侧迷走神经复合体(DVC)内的孤束核(NTS)整合了来自内脏的迷走神经传入信息,并起调节摄食的作用。我们假定该核团中的星形胶质细胞对食物摄入做出反应并影响食物摄入。在黑暗期喂食高脂食物12 h的小鼠出现NTS星形胶质细胞活化,表现为与对照饲料喂养的小鼠相比,极后区(AP)邻近的神经胶质纤维酸性蛋白(GFAP)免疫反应性细胞数量增加(65%)和形态复杂性增高。为了检测星形胶质细胞活化对食物摄入的影响,我们使用腺相关病毒(AAV)载体(AAV-GFAPh M3Dq-m Cherry)将设计药物激活的设计受体(DREADDs)导入DVC星形胶质细胞(包括孤束核、极后区和迷走神经背运动核)。使用氯氮平-N-氧化物(0.3 mg/kg)进行化学遗传激活星形胶质细胞使其产生了比平行处理组星形细胞更复杂的形态,并在注射后4 h使动物在黑暗期进食减少84%。与表达AAV-GFAPm Cherry的对照小鼠相比,DVC星形胶质细胞的h M3Dq激活在禁食过夜后仍然减少黑暗期摄食(注射后4 h降低71%)。DREADD介导的星形胶质细胞激活不影响运动功能。DVC中星形胶质细胞的h M3Dq激活引起邻近的摄食神经回路(包括臂旁核)中c-FOS的表达。这表明NTS星形胶质细胞能对急性营养过剩做出反应,参与外周饱腹感信号的整合,并且在其激活后可以减少食物摄入。