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207 results on '"Deng, Guangtong"'

11. The prevalence, complications, and risk factors for infantile hemangioma: a systematic review and meta‐analysis.

Author

Sun, Yuming, Zhao, Jinhong, Meng, Yu, Luo, Xiangyue, Jiang, Chufeng, Deng, Guangtong, and Lei, Shaorong

Subjects
HEMANGIOMAS, PREGNANCY complications, PREGNANT women, SOCIOECONOMIC factors, GLOBAL studies
Abstract

The epidemiological landscape of infantile hemangioma (IH) has been extensively explored through diverse data sources; however, a scarcity of systematically pooled and quantified evidence from comprehensive global studies persists. In this meta‐analysis, we systematically review available literature to elucidate the prevalence, distribution of lesions, complications, and risk factors associated with IH. A meticulous search encompassing the Cochrane Library, PubMed, Embase, and Web of Science identified 3206 records, of which 55 studies met the inclusion criteria. We found that the overall prevalence of IH is 2.8% [95% confidence interval (CI): 1.5–4.4%] (31,274,396 infants), and IH was located more frequently in the head and neck with a prevalence of 47.4% (95% CI: 39.5–55.4%). The overall prevalence of complications of IH is 24.3% (95% CI: 18.6–30.5%), ulceration is 16.0% (95% CI: 10.4–21.2%), bleeding is 5.6% (95% CI: 3.3–8.5%), visual impairment is 5.6% (95% CI: 3.0–8.9%), infection is 2.8% (95% CI: 1.5–4.8%), subglottic obstruction is 1.5% (95% CI: 0.5–3.0%), respectively. Through 27 studies, we have evaluated 35 factors encompassing perinatal factors, socioeconomic factors, maternal complications, drug factors, and antepartum procedures, and identified 18 risk factors that increase the prevalence of IH. These findings can greatly assist clinicians and family members in effectively evaluating the risk of IH, and determining whether pregnant women should undergo intensified monitoring or preventive measures. [ABSTRACT FROM AUTHOR]

Published
2024
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16. Beclin 2 negatively regulates innate immune signaling and tumor development

Author

Zhu, Motao, Deng, Guangtong, Tan, Peng, Xing, Changsheng, Guan, Cuiping, Jiang, Chongming, Zhang, Yinlong, Ning, Bo, Li, Chaoran, Yin, Bingnan, Chen, Kaifu, Zhao, Yuliang, Wang, Helen Y., Levine, Beth, Nie, Guangjun, and Wang, Rong-Fu

Subjects
Cytokines, Obesity -- Development and progression, Inflammation -- Development and progression, Non-Hodgkin's lymphomas -- Development and progression, B cells, Health care industry
Abstract

Beclin 2 plays a critical role in metabolic regulation and obesity, but its functions in innate immune signaling and cancer development remain largely unknown. Here, we identified Beclin 2 as a critical negative regulator of inflammation and lymphoma development. Mice with homozygous ablation of BCL2-interacting protein 2 (Becn2) developed splenomegaly and lymphadenopathy and markedly increased ERK1/2 and NF-[kappa]B signaling for proinflammatory cytokine production. Beclin 2 targeted the key signaling kinases MEKK3 and TAK1 for degradation through an ATG9A-dependent, but ATG16L/ Beclin 1/LC3-independent, autophagic pathway. Mechanistically, Beclin 2 recruited MEKK3 or TAK1 through ATG9A to form a complex (Beclin 2-ATG9A-MEKK3) on [ATG9A.sup.+] vesicles upon ULK1 activation. Beclin 2 further interacted with STX5 and STX6 to promote the fusion of MEKK3- or TAK1-associated [ATG9A.sup.+] vesicles to phagophores for subsequent degradation. Importantly, Becn2-deficient mice had a markedly increased incidence of lymphoma development, with persistent STAT3 activation. Myeloid-specific ablation of MEKK3 (Map3k3) completely rescued the phenotypes (splenomegaly, higher amounts of proinflammatory cytokines, and cancer incidence) of Becn2-deficient mice. Hence, our findings have identified an important role of Beclin 2 in the negative regulation of innate immune signaling and tumor development through an ATG9Adependent, but ATG16L/Beclin 1/LC3-independent, autophagic pathway, thus providing a potential target for the treatment of inflammatory diseases and cancer., Introduction Autophagy is an essential cellular process for maintaining cell homeostasis and attenuating cell stresses through a 'self-eating' mechanism. Many autophagy-related (ATG) proteins have been identified as functioning in autophagy [...]

Published
2020
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24. Real‐world effectiveness of Azvudine versus nirmatrelvir–ritonavir in hospitalized patients with COVID‐19: A retrospective cohort study

Author

Deng, Guangtong, primary, Li, Daishi, additional, Sun, Yuming, additional, Jin, Liping, additional, Zhou, Qian, additional, Xiao, Chenggen, additional, Wu, Qingrong, additional, Sun, Huiyan, additional, Dian, Yating, additional, Zeng, Furong, additional, Pan, Pinhua, additional, and Shen, Minxue, additional

Published
2023
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26. Cover Image, Volume 95, Number 2, February 2023

Author

Pan, Jie, primary, Yang, Songchun, additional, Chen, Xiaozhen, additional, Che, Xuanlin, additional, Lin, Wenrui, additional, Chen, Mingliang, additional, Chen, Xiang, additional, Deng, Guangtong, additional, and Su, Juan, additional

Published
2023
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47. Disulfidptosis: a new form of regulated cell death for cancer treatment.

Author

Meng, Yu, Chen, Xiang, and Deng, Guangtong

Subjects
CELL death, CANCER cells, CANCER treatment, CYTOSKELETON, PENTOSE phosphate pathway
Abstract

The supplementation of cystine also induced disulfidptosis in cancer cells with SLC7A11 low expression, accompanied by intracellular NADPH depletion, aberrant disulfide frormation in actin cytoskeleton and F-actin contraction. A recent study published in I Nature Cell Biology i demonstrated a novel type of regulated cell death (RCD) termed disulfidptosis that is caused by excessive disulfide formation in actin cytoskeleton and actin filament (F-actin) collapse, highlighting a promising anticancer strategy to target disulfidptosis [[1]]. Inhibiting NADPH depletion with cystine starvation, increasing NADPH supply with 2-deoxyglucose (2-DG), or treatment with disulfide-reducing agent 2-ME prevented the retarded migration of these actin cytoskeleton-associated proteins and disulfidptosis. [Extracted from the article]

Published
2023
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