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Anti-aging treatments slow propagation of synucleinopathy by restoring lysosomal function

AUTOPHAGY 2016年第10期12卷 1849-1863页

作者： Kim, Dong-Kyu Lim, Hee-Sun Kawasaki, Ichiro Shim, Yhong-Hee Vaikath, Nishant N. El-Agnaf, Omar M. A. Lee, He-Jin Lee, Seung-Jae Seoul Natl Univ Coll Med Dept Biomed Sci 103 Daehak Ro Seoul 03080 South Korea Seoul Natl Univ Coll Med Neurosci Res Inst Seoul South Korea Konkuk Univ Dept Biomed Sci & Technol Seoul South Korea Konkuk Univ Dept Biosci & Biotechnoloy Seoul South Korea Konkuk Univ Inst KU Biotechnol Seoul South Korea United Arab Univ Coll Med & Hlth Sci Dept Biochem Al Ain U Arab Emirates QBRI Neurol Disorders Ctr Doha Qatar HBKU Qatar Fdn Coll Sci & Engn Doha Qatar Konkuk Univ Sch Med Dept Anat Seoul South Korea Celltrion Inc Inchon South Korea

Aging is the major risk factor for neurodegenerative diseases that are also associated with impaired proteostasis, resulting in abnormal accumulation of protein aggregates. However, the role of aging in development and progression of disease remains elusive. Here, we used caenorhabditis elegans models to show that aging-promoting genetic variations accelerated the rate of cell-to-cell transmission of SNcA/-synuclein aggregates, hallmarks of Parkinson disease, and the progression of disease phenotypes, such as nerve degeneration, behavioral deficits, and reduced life span. Genetic and pharmacological anti-aging manipulations slowed the spread of aggregates and the associated phenotypes. Lysosomal degradation was significantly impaired in aging models, while anti-aging treatments reduced the impairment. Transgenic expression of hlh-30p::hlh-30, the master controller of lysosomal biogenesis, alleviated intercellular transmission of aggregates in the aging model. Our results demonstrate that the rate of aging closely correlates with the rate of aggregate propagation and that general anti-aging treatments can slow aggregate propagation and associated disease progression by restoring lysosomal function.

关键词： aggregate propagation aging bimolecular fluorescence complementation c elegans lysosome Parkinson disease SNcA -synuclein

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Loss of the integral nuclear envelope protein SUN1 induces alteration of nucleoli

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NUcLEUS 2016年第1期7卷 68-83页

作者： Matsumoto, Ayaka Sakamoto, chiyomi Matsumori, Haruka Katahira, Jun Yasuda, Yoko Yoshidome, Katsuhide Tsujimoto, Masahiko Goldberg, Ilya G. Matsuura, Nariaki Nakao, Mitsuyoshi Saitoh, Noriko Hieda, Miki Osaka Univ Grad Sch Med & Hlth Sci Yamadaoka 1-7 Suita Osaka 5650871 Japan Kumamoto Univ Dept Med Cell Biol Inst Mol Embryol & Genet Kumamoto Japan Osaka Univ Grad Sch Frontier Biosci Suita Osaka Japan Osaka Police Hosp Dept Breast Surg Tennoji Ku Osaka Japan Osaka Police Hosp Dept Pathol Tennoji Ku Osaka Japan NIA Image Informat & Computat Biol Unit Genet Lab NIH Baltimore MD 21224 USA Japan Agcy Med Res & Dev CREST Tokyo Japan

A supervised machine learning algorithm, which is qualified for image classification and analyzing similarities, is based on multiple discriminative morphological features that are automatically assembled during the learning processes. The algorithm is suitable for population-based analysis of images of biological materials that are generally complex and heterogeneous. Here we used the algorithm wndchrm to quantify the effects on nucleolar morphology of the loss of the components of nuclear envelope in a human mammary epithelial cell line. The linker of nucleoskeleton and cytoskeleton (LINc) complex, an assembly of nuclear envelope proteins comprising mainly members of the SUN and nesprin families, connects the nuclear lamina and cytoskeletal filaments. The components of the LINc complex are markedly deficient in breast cancer tissues. We found that a reduction in the levels of SUN1, SUN2, and lamin A/c led to significant changes in morphologies that were computationally classified using wndchrm with approximately 100% accuracy. In particular, depletion of SUN1 caused nucleolar hypertrophy and reduced rRNA synthesis. Further, wndchrm revealed a consistent negative correlation between SUN1 expression and the size of nucleoli in human breast cancer tissues. Our unbiased morphological quantitation strategies using wndchrm revealed an unexpected link between the components of the LINc complex and the morphologies of nucleoli that serves as an indicator of the malignant phenotype of breast cancer cells.

关键词： breast cancer LINc complex lamin A c nuclear morphology nuclear envelope SUN1 SUN2 wndchrm

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Genomic change in hepatitis B virus associated with development of hepatocellular carcinoma

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World Journal of Gastroenterology 2016年第23期22卷 5393-5399页

作者： Danbi Lee Heather Lyu Young-Hwa chung Jeong A Kim Priya Mathews Elizabeth Jaffee Lei Zheng Eunsil Yu Young Joo Lee Soo Hyung Ryu Department of Internal Medicine University of Ulsan College of MedicineAsan Medical Center Sidney Kimmel Comprehensive Cancer Center Johns Hopkins University School of MedicineBaltimore Department of Pathology University of Ulsan College of MedicineAsan Medical Center Department of Hepatobiliary Surgery University of Ulsan College of MedicineAsan Medical Center Department of Internal Medicine Inje Uni-versity College of MedicineSeoul Paik Hospital

AIM: To determine the genomic changes in hepatitis B virus(HBV) and evaluate their role in the development of hepatocellular carcinoma(Hcc) in patients chronically infected with genotype c ***: Two hundred and forty chronic hepatitis B(cHB) patients were subjected and followed for a median of 105 mo. Hcc was diagnosed in accordance with AASLD guidelines. The whole X, S, basal core promoter(BcP), and precore regions of HBV were sequenced using the direct sequencing ***: All of the subjects were infected with genotype c HBV. Out of 240 cHB patients, 25(10%) had c1653 T and 33(14%) had T1753 V mutation in X region; 157(65%) had A1762T/G1764 A mutations in BcP region, 50(21%) had G1896 A mutation in precore region and 67(28%) had pre-S deletions. Hcc occurred in 6 patients(3%). The prevalence of T1753 V mutation was significantly higher in patients who developed Hcc than in those without Hcc. The cumulative occurrence rates of Hcc were 5% and 19% at 10 and 15 years, respectively, in patients with T1753 V mutant, which were significantly higher than 1% and 1% in those with wild type HBV(P < 0.001).cONcLUSION: The presence of T1753 V mutation in HBV X-gene significantly increases the risk of Hcc development in patients chronically infected with genotype c HBV.

关键词： Hepatocellular carcinoma chronic hepatitis B Genomic change Hepatitis B virus Genotype c

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The caenorhabditis elegans p38 MAPK Gene plays a key role in protection from mycobacteria

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MIcROBIOLOGYOPEN 2016年第3期5卷 436-452页

作者： Galbadage, Thushara Shepherd, Tonya F. cirillo, Suat L. G. Gumienny, Tina L. cirillo, Jeffrey D. Texas A&M Hlth Sci Ctr Dept Microbial Pathogenesis Bryan TX 77807 USA Texas A&M Hlth Sci Ctr Dept Immunol Bryan TX 77807 USA Texas Womans Univ Dept Biol Denton TX 76204 USA

Mitogen-activated protein kinases (MAPK) are critical mediators of cellular responses to pathogens and are activated in response to infection, but investigation is difficult in multi-cell hosts due to developmental lethality of mutations. Mycobacterium marinum (Mm) is an established model for tuberculosis, a disease afflicting nearly one-third of the world's population. We found that Mm-infected caenorhabditis elegans display >80% mortality, but nonpathogenic M. smegmatis cause <15% mortality. c. elegans display pathological changes when infected with Mm, whereas Mm mutants produce lower mortality, suggesting that *** is a promising virulence model for detailed genetic analysis. c. elegans MAPK mutants are hypersusceptible to mycobacterial infection;however, the c. elegans TOL-like, TGF- and insulin-like pathway genes do not play important roles in susceptibility. We show that pathogenic mycobacteria inhibit MAPK-mediated protection through the MAPK phosphatase gene and demonstrate that *** provide a genetically tractable pathogenicity model of both the host and pathogen.

关键词： c elegans innate immunity Mycobacterium

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cPViolation Sensitivity at the Belle II Experiment

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International Journal of Modern Physics: conference Series 2018年第46期ijmpcs卷

作者： Tao Luo Key Laboratory of Nuclear Physics and Ion-beam Application (MOE) and Institute of Modern Physics Fudan University Shanghai China 200443 Supported by Fudan University Grant No. JIH5913023 No. IDH5913011/003.

The sensitivity on the measurements of the angles of the cKM unitarity triangle, i.e. ϕ 1 , ϕ 2 and ϕ 3 , for Belle II experiment is presented in this letter, the cKM mechanism is expected to be tested at 1% level on ... 详细信息

关键词： c P Violation the angles of the cKM unitarity triangle the Belle II experiment

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An Investigation of Wood and Wood Packaging Waste in the United States

An Investigation of Wood and Wood Packaging Waste in the Uni...

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作者： Shiner, Zachary Philip Virginia Tech | University

Each year a large number of wooden pallets are manufactured, recycled, and disposed of during the transportation of goods throughout the United States. The production of these pallets consumes a significant amount of wood and a large number of pallets also end up in landfills at the end of their useful life cycle. However, these pallets can be recovered through repair, broken apart into components, ground into mulch, fuel, animal bedding, or used by landfills for day to day operations. The purpose of this research was to investigate the total number of pallets and crates reaching landfills in the United States as well as to gain a better understanding of the overall waste stream. This was done by surveying all licensed Municipal Solid Waste (MSW) and construction and Demolition (candD) landfills in the continental United States. A questionnaire was sent to these landfills, and this entire study was intended to build upon previous Virginia Tech landfill surveys conducted in 1995 and 1998 with some changes made after careful review. Overall, it was found the average MSW facility in the United States received 185,077 tons of waste and the average candD facility received 74,911 tons. This results in a total national estimate of 253 million tons of MSW and 76.9 million tons of candD waste. Approximately 18.3 million pallets were landfilled and an additional 13.8 million were recovered, repurposed, or reused at MSW facilities. At candD facilities, approximately 19.2 million pallets were landfilled while 38.3 million were recovered.

关键词： Wood Pallets MSW Waste c Waste Management Thesis

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Paradoxical delay of senescence upon depletion of BRcA2 in telomerase-deficient worms

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FEBS OPEN BIO 2016年第10期6卷 1016-1024页

作者： Kwon, Mi-Sun Min, Jaewon Jeon, Hee-Yeon Hwang, Kwangwoo Kim, chuna Lee, Junho Joung, Je-Gun Park, Woong-Yang Lee, Hyunsook Seoul Natl Univ Dept Biol Sci 1 Gwanak Ro Seoul 151742 South Korea Seoul Natl Univ Inst Mol Biol & Genet 1 Gwanak Ro Seoul 151742 South Korea Samsung Med Ctr Samsung Genome Inst Seoul South Korea

BRcA2 is a multifunctional tumor suppressor involved in homologous recombination (HR), mitotic checkpoint regulation, and telomere homeostasis. Absence of Brca2 in mice results in progressive shortening of telomeres and senescence, yet cells are prone to neoplastic transformation with elongated telomeres, suggesting that BRcA2 has positive and negative effects on telomere length regulation along the path to tumorigenesis. Using caenorhabditis elegans as a model, we show here that depletion of BRc-2, an ortholog of BRcA2, paradoxically delays senescence in telomerase-deficient mutant worms. Telomerase-deficient worms (trt-1) exhibit early replication senescence due to short telomeres. It should be noted that worms mutated in brc-2 are not viable as well due to massive genotoxic insults. However, when BRc-2 is depleted by RNA interference in trt-1 mutant worms, the number of generations is unexpectedly increased with telomere length maintained, compared to telomerase mutants. Interestingly, depletion of other HR genes such as rad-51 and rad-54 exhibited similar effects. In worms doubly deficient of telomerase and brc-2, rad-51, or rad-54, extra telomeric c-circles were generated, suggesting that abrogation of HR induces an alteration in telomere environment favorable to illegitimate telomere maintenance when telomerase is absent. collectively, absence of BRc-2 in telomerase-deficient background first leads to telomere shortening, followed by an induction of an as-yet-unknown telomere maintenance pathway, resulting in delay of senescence. The results have implications in the understanding of dysfunctional BRcA2-associated tumorigenesis.

关键词： breast cancer susceptibility gene 2 c elegans homologous recombination senescence telomere length trt-1

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Aberrant hnRNP K expression: All roads lead to cancer

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cELL cYcLE 2016年第12期15卷 1552-1557页

作者： Gallardo, Miguel Hornbaker, Marisa J. Zhang, Xiaorui Hu, Peter Bueso-Ramos, carlos Post, Sean M. Univ Texas MD Anderson Canc Ctr Dept Leukemia 1515 Holcombe Blvd Houston TX 77030 USA Univ Texas Grad Sch Biomed Sci Houston Houston TX USA Univ Texas MD Anderson Canc Ctr Sch Hlth Profess Houston TX 77030 USA Univ Texas MD Anderson Canc Ctr Dept Hematopathol Houston TX 77030 USA

The classification of a gene as an oncogene or a tumor suppressor has been a staple of cancer biology for decades. However, as we delve deeper into the biology of these genes, this simple classification has become increasingly difficult for some. In the case of heterogeneous nuclear ribonuclear protein K (hnRNP K), its role as a tumor suppressor has recently been described in acute myeloid leukemia and demonstrated in a haploinsufficient mouse model. In contrast, data from other clinical correlation studies suggest that hnRNP K may be more fittingly described as an oncogene, due to its increased levels in a variety of malignancies. hnRNP K is a multifunctional protein that can regulate both oncogenic and tumor suppressive pathways through a bevy of chromatin-, DNA-, RNA-, and protein-mediated activates, suggesting its aberrant expression may have broad-reaching cellular impacts. In this review, we highlight our current understanding of hnRNP K, with particular emphasis on its apparently dichotomous roles in tumorigenesis.

关键词： 9q21 32 acute myeloid leukemia c-Myc c EBP hnRNP K haploinsufficiency mouse models p53 p21

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PKc- activation in neutrophils promotes fungal clearance

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JOURNAL OF LEUKOcYTE BIOLOGY 2016年第3期100卷 581-588页

作者： Li, Xun cullere, Xavier Nishi, Hiroshi Saggu, Gurpanna Durand, Enrique Mansour, Michael K. Tam, Jenny M. Song, Xiu-yu Lin, Xin Vyas, Jatin M. Mayadas, Tanya Brigham & Womens Hosp Dept Pathol Ctr Excellence Vasc Biol 75 Francis St Boston MA 02115 USA Harvard Med Sch 77 Ave Louis PasteurNRB Rm 752O Boston MA 02115 USA Xiamen Univ Coll Med Affiliated Hosp 1 Dept Lab Med Xiamen Fujian Peoples R China Harvard Med Sch Massachusetts Gen Hosp Div Infect Dis Dept Med Boston MA USA Univ Texas MD Anderson Canc Ctr Dept Mol & Cellular Oncol Houston TX 77030 USA

PKc is essential for neutrophil, but not macrophage functions required for host defense against fungal pathogens. The c-type lectin receptor dectin-1 and the integrin Mac-1 have key roles in controlling fungal infection. Here, we demonstrate that dectin-1- and Mac-1-induced activation of protein kinase c in neutrophils, independent of the card9 adaptor, is required for reactive oxygen species production and for intracellular killing upon candida albicans uptake. Protein kinase c was also required for zymosan-induced cytokine generation in neutrophils. In macrophages, protein kinase c deficiency prevented fungi-induced reactive oxygen species generation but had no effect on activation of TGF--activated kinase-1, an effector of card9, or nuclear factor B activation, nor did it affect phagolysosomal maturation, autophagy, or intracellular c. albicans killing. In vivo, protein kinase c-deficient mice were highly susceptible to c. albicans and Aspergillus fumigatus infection, which was partially rescued with adoptively transferred wild-type neutrophils. Thus, protein kinase c activation downstream of dectin-1 and Mac-1 has an important role in neutrophil, but not macrophage, functions required for host defense against fungal pathogens.

关键词： dectin-1 Mac-1 c albicans reactive oxygen species host defense signaling

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Research on the large-scale application of nitrogen removal for the treatment of synthetic ammonia wastewater

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DESALINATION AND WATER TREATMENT 2016年第27期57卷 12763-12769页

作者： Bao, Yufei Li, Meng Zhang, Qian Wuhan Univ Technol Sch Civil Engn & Architecture Wuhan 430070 Peoples R China

The capability of anoxic-aerobic (A/O) process treatment and influencing factors of high concentration ammonia industrial wastewater were studied in this paper. Results showed that the A/O process system had achieved favorable performance and the quality of effluent could meet the direct emission standard of Discharge standard of water pollutants for ammonia industry (GB13458-2013) under the optimal conditions as follows: the perfect inflow loading of ammonia 0.12kg/(m(3)d), the mixed liquid recycle ratio (R) 200%, and sludge return ratio 80%, the carbon-to-nitrogen ratio (c/N ratio) 4.5-5.5. Besides, the results also confirmed that the activity of nitrifying bacteria in activated sludge was greatly inhibited due to the high concentration of free ammonia (FA). In addition, carbon shortage had a marked effect on the denitrification efficiency of the system.

关键词： High-content ammonia nitrogen Synthetic ammonia wastewater Nitrogen removal c N ratio Ammonia loading

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