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"He, Ming"
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The woke salaryman crash course on capitalism & money : lessons from the world's most expensive city
\"The Woke Salaryman melds personal finance, economics, sociology and psychology to create a book that simply and succinctly explains money and capitalism. It's an antidote to rising discontentment and frustration about the society we live in, without being populist or pandering to the eat the rich ideology so commonly found on social media. The book will feature a collection of comics by The Woke Salaryman, including some of the most resonant comics they have done plus new ones that haven't yet been published. The comics will be accompanied by commentaries on the themes/topic the story will discuss. The commentaries will range from authors' notes, commentary on how their online readers reacted to the piece and what they take from it, to things such as further reading/references on the topic\"-- Provided by publisher.
Book
Towards an optimized paradigm: generative adversarial networks and 3D modeling in landscape design and generation
Virtual reality (VR) integrates technologies like computer graphics, artificial intelligence, and multi-sensor systems, creating transformative tools for designers and users. This study proposes a novel urban landscape design method using 3D laser scanning combined with frame reorganization and texture mapping. Despite the advancements in VR-based landscape design, existing methods often suffer from inefficiencies in rendering time and suboptimal visual fidelity, limiting their practical application in large-scale urban projects. In the initial phase, we acquire the central pixel point of the images via a meticulous 3D scanning process, thus facilitating a three-dimensional stereo reorganization of urban architectural landscapes. This stage is succeeded by the application of a terahertz wave image segmentation strategy, grounded in the sophisticated utilization of adversarial generative networks and a structured texture mapping procedure. This technique permits the virtual reconstruction of the architectural blueprint, wherein each image layer is systematically traversed, engendering a dynamic representation of the urban landscape. The final step generates realistic urban landscape simulations using integrated 3D laser scanning. To ascertain the efficacy of the proposed methodology, we embarked upon a series of performance assessments across four disparate simulation design scenarios, yielding verifiable outcomes. Our empirical findings demonstrate that the proposed method reduces rendering times by up to 90% compared to traditional tools like SketchUp and 3D Studio Max, while achieving a significant improvement in visual fidelity, as evidenced by standard image quality metrics. These results attest to the formidable potential of this avant-garde approach within the VR landscape design milieu, significantly diminishing the time imperative while augmenting visual fidelity and fortifying automatic display proficiencies. By virtue of its robust analytical underpinnings and innovative approach, this research furnishes a substantial theoretical scaffolding for the evolving discourse in landscape space design, prompting a reevaluation of conventional methodologies while propelling the field towards a more efficient and visually immersive future.
Journal Article
CPT1A-mediated fatty acid oxidation promotes colorectal cancer cell metastasis by inhibiting anoikis
Anoikis is a critical obstacle to cancer metastasis. Colorectal cancer (CRC) exhibits a high rate of metastasis, leading to death, and the mechanisms involved in anoikis resistance are still unclear. We identified that the fatty acid oxidation (FAO) pathway was activated in detached CRC cells. Multiple genes in the FAO pathway, specifically the rate-limiting enzyme CPT1A, were upregulated in CRC cells grown in suspension. Reactive oxygen species elimination mediated by CPT1A in CRC cells was vital to anoikis resistance. In vivo experiments showed that CPT1A-suppressed CRC cells colonized the lung at a much lower rate than normal CRC cells, suggesting that CPT1A-mediated FAO activation increased metastatic capacity. In clinical tissue specimens from CRC patients, elevated expression of CPT1A was observed in metastatic sites compared with primary sites. Our results demonstrate that CPT1A-mediated FAO activation induces CRC cells to resist anoikis, suggesting that CPT1A is an attractive target for treating metastatic CRC.
Journal Article
Long noncoding RNA AGPG regulates PFKFB3-mediated tumor glycolytic reprogramming
Tumor cells often reprogram their metabolism for rapid proliferation. The roles of long noncoding RNAs (lncRNAs) in metabolism remodeling and the underlying mechanisms remain elusive. Through screening, we found that the lncRNA Actin Gamma 1 Pseudogene (
AGPG
) is required for increased glycolysis activity and cell proliferation in esophageal squamous cell carcinoma (ESCC). Mechanistically,
AGPG
binds to and stabilizes 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3). By preventing APC/C-mediated ubiquitination,
AGPG
protects PFKFB3 from proteasomal degradation, leading to the accumulation of PFKFB3 in cancer cells, which subsequently activates glycolytic flux and promotes cell cycle progression.
AGPG
is also a transcriptional target of p53; loss or mutation of
TP53
triggers the marked upregulation of
AGPG
. Notably, inhibiting
AGPG
dramatically impaired tumor growth in patient-derived xenograft (PDX) models. Clinically,
AGPG
is highly expressed in many cancers, and high
AGPG
expression levels are correlated with poor prognosis, suggesting that
AGPG
is a potential biomarker and cancer therapeutic target.
PFKFB3 enhances glycolysis to promote cancer cell proliferation. Here, the authors identify a long noncoding RNA in esophageal squamous cell carcinoma,
AGPG
, which interacts with PFKFB3 and promotes its stability, leading to increased glycolysis and proliferation.
Journal Article
Targeting cancer stem cells for reversing therapy resistance: mechanism, signaling, and prospective agents
Cancer stem cells (CSCs) show a self-renewal capacity and differentiation potential that contribute to tumor progression and therapy resistance. However, the underlying processes are still unclear. Elucidation of the key hallmarks and resistance mechanisms of CSCs may help improve patient outcomes and reduce relapse by altering therapeutic regimens. Here, we reviewed the identification of CSCs, the intrinsic and extrinsic mechanisms of therapy resistance in CSCs, the signaling pathways of CSCs that mediate treatment failure, and potential CSC-targeting agents in various tumors from the clinical perspective. Targeting the mechanisms and pathways described here might contribute to further drug discovery and therapy.
Journal Article
Lipid metabolism alteration contributes to and maintains the properties of cancer stem cells
Lipids, the basic components of the cell membrane, execute fundamental roles in almost all the cell activities including cell-cell recognition, signalling transduction and energy supplies. Lipid metabolism is elementary for life sustentation that balances activity between synthesis and degradation. An accumulating amount of data has indicated abnormal lipid metabolism in cancer stem cells (CSCs), and that the alteration of lipid metabolism exerts a great impact on CSCs' properties such as the capability of self-renewal, differentiation, invasion, metastasis, and drug sensitivity and resistance. CSCs' formation and maintenance cannot do without the regulation of fatty acids and cholesterol. In normal cells and embryonic development, fatty acids and cholesterol metabolism are regulated by some important signalling pathways (such as Hedgehog, Notch, Wnt signalling pathways); these signalling pathways also play crucial roles in initiating and/or maintaining CSCs' properties, and such signalling is shown to be commonly modulated by the abnormal lipid metabolism in CSCs; on the other hand, the altered lipid metabolism in turn modifies the cell signalling and generates additional impacts on CSCs. Metabolic rewiring is considered as an ideal hallmark of CSCs, and metabolic alterations would be promising therapeutic targets of CSCs for aggressive tumors. In this review, we summarize the most updated findings of lipid metabolic abnormalities in CSCs and prospect the potential applications of targeting lipid metabolism for anticancer treatment.
Journal Article
Risk of colorectal neoplasia after removal of conventional adenomas and serrated polyps: a comprehensive evaluation of risk factors and surveillance use
BackgroundSurveillance colonoscopy after polyp removal is recommended to prevent subsequent colorectal cancer (CRC). It is known that advanced adenomas have a substantially higher risk than non-advanced ones, but optimal intervals for surveillance remain unclear.DesignWe prospectively followed 156 699 participants who had undergone a colonoscopy from 2007 to 2017 in a large integrated healthcare system. Using multivariable Cox proportional hazards regression we estimated the subsequent risk of CRC and high-risk polyps, respectively, according to index colonoscopy polyps, colonoscopy quality measures, patient characteristics and the use of surveillance colonoscopy.ResultsAfter a median follow-up of 5.3 years, we documented 309 CRC and 3053 high-risk polyp cases. Compared with participants with no polyps at index colonoscopy, those with high-risk adenomas and high-risk serrated polyps had a consistently higher risk of CRC during follow-up, with the highest risk observed at 3 years after polypectomy (multivariable HR 5.44 (95% CI 3.56 to 8.29) and 8.35 (95% CI 4.20 to 16.59), respectively). Recurrence of high-risk polyps showed a similar risk distribution. The use of surveillance colonoscopy was associated with lower risk of CRC, with an HR of 0.61 (95% CI 0.39 to 0.98) among patients with high-risk polyps and 0.57 (95% CI 0.35 to 0.92) among low-risk polyps. Among 1548 patients who had high-risk polyps at both index and surveillance colonoscopies, 65% had their index polyps in the proximal colon and 30% had index and interval polyps in the same segments.ConclusionPatients with high-risk polyp findings were at higher risk of subsequent CRC and high-risk polyps and may benefit from early surveillance within 3 years. The subsite distribution of the index and recurrent high-risk polyps suggests the contribution of incomplete resection and missed lesions to the development of interval neoplasia.
Journal Article
The increased frequency of combined El Niño and positive IOD events since 1965s and its impacts on maritime continent hydroclimates
The Indian and Pacific Oceans surround the Maritime Continent (MC). Major modes of sea surface temperature variability in both oceans, including the Indian Ocean Dipole (IOD) and El Niño–Southern Oscillation (ENSO), can strongly affect precipitation on the MC. The prevalence of fires in the MC is closely associated with precipitation amount and terrestrial water storage in September and October. Precipitation and terrestrial water storage, which is a measurement of hydrological drought conditions, are significantly modulated by Indian Ocean Dipole (IOD) and El Niño events. We utilize long-term datasets to study the combined effects of ENSO and the IOD on MC precipitation during the past 100 years (1900–2019) and find that the reductions in MC precipitation and terrestrial water storage are more pronounced during years when El Niño and a positive phase of the IOD (pIOD) coincided. The combined negative effects are produced mainly through an enhanced reduction of upward motion over the MC. Coincident El Niño-pIOD events have occurred more frequently after 1965. However, climate models do not project a higher occurrence of coincident El Niño-pIOD events in a severely warming condition, implying that not the global warming but the natural variability might be the leading cause of this phenomenon.
Journal Article
Molecular mechanisms of chemo‐ and radiotherapy resistance and the potential implications for cancer treatment
Cancer is a leading cause of death worldwide. Surgery is the primary treatment approach for cancer, but the survival rate is very low due to the rapid progression of the disease and presence of local and distant metastasis at diagnosis. Adjuvant chemotherapy and radiotherapy are important components of the multidisciplinary approaches for cancer treatment. However, resistance to radiotherapy and chemotherapy may result in treatment failure or even cancer recurrence. Radioresistance in cancer is often caused by the repair response to radiation‐induced DNA damage, cell cycle dysregulation, cancer stem cells (CSCs) resilience, and epithelial‐mesenchymal transition (EMT). Understanding the molecular alterations that lead to radioresistance may provide new diagnostic markers and therapeutic targets to improve radiotherapy efficacy. Patients who develop resistance to chemotherapy drugs cannot benefit from the cytotoxicity induced by the prescribed drug and will likely have a poor outcome with these treatments. Chemotherapy often shows a low response rate due to various drug resistance mechanisms. This review focuses on the molecular mechanisms of radioresistance and chemoresistance in cancer and discusses recent developments in therapeutic strategies targeting chemoradiotherapy resistance to improve treatment outcomes. This review discussed the molecular mechanisms of cancer resistance to radiotherapy and chemotherapy including enhanced DNA damage repair, reduced intracellular accumulation of drugs, drug inactivation, changes in drug targets, apoptosis‐growth balance disruption. We also focused on the roles of oncogenes and tumor suppressor genes in therapeutic resistance. Some anticancer drugs targeting oncogenes associated with therapeutic resistance were summarized.
Journal Article
Towards optimal single-photon sources from polarized microcavities
An optimal single-photon source should deterministically deliver one, and only one, photon at a time, with no trade-off between the source’s efficiency and the photon indistinguishability. However, all reported solid-state sources of indistinguishable single photons had to rely on polarization filtering, which reduced the efficiency by 50%, fundamentally limiting the scaling of photonic quantum technologies. Here, we overcome this long-standing challenge by coherently driving quantum dots deterministically coupled to polarization-selective Purcell microcavities. We present two examples: narrowband, elliptical micropillars and broadband, elliptical Bragg gratings. A polarization-orthogonal excitation–collection scheme is designed to minimize the polarization filtering loss under resonant excitation. We demonstrate a polarized single-photon efficiency of 0.60 ± 0.02 (0.56 ± 0.02), a single-photon purity of 0.975 ± 0.005 (0.991 ± 0.003) and an indistinguishability of 0.975 ± 0.006 (0.951 ± 0.005) for the micropillar (Bragg grating) device. Our work provides promising solutions for truly optimal single-photon sources combining near-unity indistinguishability and near-unity system efficiency simultaneously.
Journal Article