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- Klionsky, Daniel J., et al.
(författare)
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Guidelines for the use and interpretation of assays for monitoring autophagy
- 2012
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Ingår i: Autophagy. - : Informa UK Limited. - 1554-8635 .- 1554-8627. ; 8:4, s. 445-544
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Forskningsöversikt (refereegranskat)abstract
- In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.
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- Zhang, Xuning, et al.
(författare)
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On the understanding of energy loss and device fill factor trade-offs in non-fullerene organic solar cells with varied energy levels
- 2020
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Ingår i: Nano Energy. - : ELSEVIER. - 2211-2855 .- 2211-3282. ; 75
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Tidskriftsartikel (refereegranskat)abstract
- Fill factor (FF) is an important parameter governing the power conversion efficiency (PCE) in non-fullerene organic solar cells (NF-OSCs), which however is less studied than the other two parameters (short-circuit current J(sc) and open-circuit voltage V-oc). To understand how energy offsets, exciton and charge carrier dynamics impact the FF, four groups of bulk heterojunctions (BHJs) NF-OSCs are investigated with FFs varying from 0.61 to 0.78 under progressive changes of HOMO-HOMO offsets (Delta(HOMOs), from 0.09 to 0.24 eV). By pump-probe optical spectroscopy, we find that the FF exhibits a positive dependence on Delta(HOMO) and charge-separated state lifetime (tau(CS)) in the blends, a result of inhibited back charge transfers and recombination at the donor-acceptor interface under higher Delta(HOMO)s. Moreover, we observe a fast charge extraction with decreased sensitivity to internal electric-fields in high-FF devices. Despite these merits, the gains of FF are at the expense of increasing the voltage loss to non-radiative recombination in our studied systems. The combined results suggest that remaining appropriate energetic offsets is essential for controlling the carrier dynamics with longer-lived CS-states, restraining charge back transfer and reducing charge recombination toward high FFs and photovoltaic efficiencies.
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- Zhu, Zhen-Long, et al.
(författare)
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Cytoplasmic expression of p33(ING1b) is correlated with tumorigenesis and progression of human esophageal squamous cell carcinoma.
- 2013
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Ingår i: Oncology letters. - : Spandidos Publications. - 1792-1074 .- 1792-1082. ; 5:1, s. 161-166
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Tidskriftsartikel (refereegranskat)abstract
- p33(ING1b), a newly discovered candidate tumor suppressor gene and a nuclear protein, belongs to the inhibitor of growth gene family. Previous studies have shown that p33(ING1b) is involved in the restriction of cell growth and proliferation, apoptosis, tumor anchorage-independent growth, cellular senescence, maintenance of genomic stability and modulation of cell cycle checkpoints. Loss of nuclear p33(ING1b) has been observed in melanoma, seminoma, papillary thyroid carcinoma, oral squamous cell carcinoma, breast ductal cancer and acute lymphoblastic leukemia. Inactivation and/or decreased expression of p33(ING1b) have been reported in various types of cancer, including head and neck squamous cell, breast, lung, stomach, blood and brain malignancies. Since little is known about the clinicopathological significance of p33(ING1b) in esophageal squamous cell carcinoma (ESCC), this study aimed to investigate the association of p33(ING1b) expression with clinicopathological variables and particularly interesting new cysteine-histidine rich protein (PINCH) in patients with ESCC. p33(ING1b) expression was examined by immunohistochemistry in 20 normal esophageal mucosa and in 64 ESCC specimens. The results revealed that the positive expression of p33(ING1b) protein in normal squamous cells was localized in the nucleus alone and the positive rate was 95%, while in ESCCs, the positive expression was mainly in the cytoplasm, together with nuclear expression, and the positive rate was 36% (P<0.0001). Furthermore, the cases with lymph node metastasis showed a higher frequency of positive cytoplasmic expression than those without metastasis (P=0.001). The cytoplasmic expression of p33(ING1b) was positively related to PINCH expression (P<0.0001) in ESCC, and the cases positive for both proteins had a high lymph node metastasis rate (P=0.001). In conclusion, p33(ING1b) cellular compartmental shift from the nucleus to the cytoplasm may cause loss of normal cellular function and play a central role in the tumorigenesis and metastasis of ESCC.
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- Zhu, Zhen-Long, et al.
(författare)
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PINCH expression and its clinicopathological significance in gastric adenocarcinoma
- 2012
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Ingår i: Disease Markers. - : IOS Press. - 0278-0240 .- 1875-8630. ; 33:4, s. 171-178
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Particularly interesting new cysteine-histidine rich protein (PINCH) is an important component of the local adhesion complexes and upregulated in several types of malignancies, and involved in the incidence and development of tumours. PINCH expression is also independently correlated with poorer survival in patients with colorectal cancer. However, there is no study of PINCH in gastric cancer, therefore, the aim of this project was to investigate PINCH expression and its clinicopathological significance in gastric adenocarcinoma. less thanbrgreater than less thanbrgreater thanPatients and methods: PINCH expression was immunohistochemically examined in normal gastric mucous (n = 30) and gastric adenocarcinoma (n = 73), from gastric cancer patients. less thanbrgreater than less thanbrgreater thanResults: PINCH expression in the associated-stroma of gastric cancers was heterogeneous, and its positive rate (75%) was higher than that of normal gastric mucosa (43%, X-2 = 9.711, p = 0.002). The stronger staining was observed at the invasive edge of tumour when compared to the inner area of tumour. The rate of positive PINCH (88%) in the cases with lymph node metastasis was higher than that (52%) in the cases without metastasis (X-2 = 11.151, p = 0.001). PINCH expression was not correlated with patients gender, age, tumour size, differentiation and invasion depth (p andgt; 0.05). less thanbrgreater than less thanbrgreater thanConclusion: PINCH protein might play an important role in the tumourigenesis and metastasis of gastric adenocarcinoma.
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- Kristan, Matej, et al.
(författare)
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The Visual Object Tracking VOT2015 challenge results
- 2015
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Ingår i: Proceedings 2015 IEEE International Conference on Computer Vision Workshops ICCVW 2015. - : IEEE. - 9780769557205 ; , s. 564-586
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Konferensbidrag (refereegranskat)abstract
- The Visual Object Tracking challenge 2015, VOT2015, aims at comparing short-term single-object visual trackers that do not apply pre-learned models of object appearance. Results of 62 trackers are presented. The number of tested trackers makes VOT 2015 the largest benchmark on short-term tracking to date. For each participating tracker, a short description is provided in the appendix. Features of the VOT2015 challenge that go beyond its VOT2014 predecessor are: (i) a new VOT2015 dataset twice as large as in VOT2014 with full annotation of targets by rotated bounding boxes and per-frame attribute, (ii) extensions of the VOT2014 evaluation methodology by introduction of a new performance measure. The dataset, the evaluation kit as well as the results are publicly available at the challenge website(1).
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| 9. |
- Wang, Hong, et al.
(författare)
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Real-time tracking of mitochondrial dynamics by a dual-sensitive probe
- 2020
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Ingår i: Sensors and actuators. B, Chemical. - : Elsevier. - 0925-4005 .- 1873-3077. ; 320
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Tidskriftsartikel (refereegranskat)abstract
- Tracking of mitochondrial dynamic processes including their morphology, biogenesis and elimination is of significance to deeply understand mitochondrial physiology and related diseases, which requires simultaneous and discriminative labeling of both mitochondria themselves and correlated downstream organelles. However, the combination of multiple fluorescent probes will bring the large invasive effect that seriously impacts the normal physiological processes of mitochondria within live cells. To address this issue, we herein construct a single molecular probe through the combination of two pH-sensitive fluorogens, hydroxyl-coumarin and rhodamine B, enabling the detection of intracellular microenvironmental pH variations. Importantly, the as-synthesized probe not only accumulates into mitochondria, indicated by cyan emission from hydroxyl-coumarin but also can be delivered to the downstream acidic autolysosomes upon the occurrence of mitophagy, indicated by red emission from rhodamine B. Taking advantage of a two-channel confocal microscopy strategy, we have achieved to real-time track the processes of mitochondrial replication, merge and autophagy.
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| 10. |
- Zhao, Zeng-Ren, et al.
(författare)
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Overexpression of Id-1 protein is a marker in colorectal cancer progression
- 2008
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Ingår i: Oncology Reports. - : Spandidos. - 1021-335X .- 1791-2431. ; 19:2, s. 419-424
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Tidskriftsartikel (refereegranskat)abstract
- Abstract: The inhibitor of differentiation/DNA binding 1 (Id-1), a negative regulator of basic helix-loop-helix transcription factors, plays an important role in the regulation of cell proliferation and differentiation. We examined the Id-1 expression by immunohistochemistry in 9 adenomas, 79 primary colorectal adenocarcinomas matched with 40 adjacent normal mucosa specimens and its relationship with clinicopathological factors. The Id-1 expression was increased in the carcinoma compared to the adjacent normal mucosa either in the unmatched and matched samples or to the adenoma. There was no significant difference in the Id-1 expression between normal mucosa and adenoma. The Id-1 expression of carcinoma was increased from Dukes' stages A to B, to C and to D. The cases with lymph node metastasis had a higher rate of a stronger Id-1 expression than those without lymph node metastasis. In conclusion, Id-1 overexpression plays an important role in colorectal cancer progression.
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