Metabolic reprogramming is an emerging hallmark of cancer cells, in which cancer cells exhibit distinct metabolic phenotypes to fuel their proliferation and progression. The significant advancements made in the area of metabolic reprogramming make possible new strategies for overcoming malignant cancer, including triple-negative breast cancer. Triple-negative breast cancer (TNBC) is associated with high histologic grade, aggressive phenotype, and poor prognosis. Even though triple-negative breast cancer patients benefit from standard chemotherapy, they still face high recurrence rates and are more likely to develop resistance to chemotherapeutic drugs. Therefore, there is an urgent need to explore vulnerabilities of triple-negative breast cancer and develop novel therapeutic drugs to improve clinical outcomes for triple-negative breast cancer patients. Metabolic reprogramming may provide promising therapeutic targets for the treatment of triple-negative breast cancer. In this paper, we primarily discuss how triple-negative breast cancer cells reprogram their metabolic phenotype and that of stromal cells in the microenvironment to survive under nutrient-poor conditions. Considering that metastasis and chemoresistance are the main contributors to mortality in triple-negative breast cancer patients, we also focus on the role of metabolic adaption in mediating metastasis and chemoresistance of triple-negative breast cancer tumors.

Periodontal pathogens such as Porphyromonas gingivalis and Fusobacterium nucleatum produce five different short-chain fatty acids (SCFAs) as metabolic by-products. We detect significantly higher levels of SCFAs in the saliva of patients with severe periodontal disease. The different SCFAs stimulate lytic gene expression of Kaposi's sarcoma-associated herpesvirus (KSHV) dose dependently and synergistically. SCFAs inhibit class-1/2 histone deacetylases (HDACs) and downregulate expression of silent information regulator-1 (SIRT1). SCFAs also downregulate expression of enhancer of zeste homolog2 (EZH2) and suppressor of variegation 3-9 homolog1 (SUV39H1), which are two histone N-lysine methyltransferases (HLMTs). By suppressing the different components of host epigenetic regulatory machinery, SCFAs increase histone acetylation and decrease repressive histone trimethylations to transactivate the viral chromatin. These new findings provide mechanistic support that SCFAs from periodontal pathogens stimulate KSHV replication and infection in the oral cavity and are potential risk factors for development of oral Kaposi's sarcoma (KS). IMPORTANCE About 20% of KS patients develop KS lesions first in the oral cavity, while other patients never develop oral KS. It is not known ifthe oral microenvironment plays a role in oral KS tumor development. In this work, we demonstrate that a group of metabolic by-products, namely, short-chain fatty acids, from bacteria that cause periodontal disease promote lytic replication of KSHV, the etiological agent associated with KS. These new findings provide mechanistic support that periodontal pathogens create a unique microenvironment in the oral cavity that contributes to KSHV replication and development of oral KS.

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These AIV subtypes could spark a human pandemic once adapted through mutation. Why have they persisted in China? How have they been circulating in China? What strategies have been implemented in China to control the spread of AIV? How scientific and effective are these strategies? What lessons can we learn from the experience in China for the control of AIV? We attempted to answer these questions in this review based on relevant studies in the literature and our unpublished surveillance data collected over a 12-year period from 2007 to 2018 (Tables 1 and 2), with the aim to provide insights to improve guidelines for the control of AIV, both in China and globally. 2 | ROOTS OF THE PROB LEMS The prevalence of AIV in China is rooted in its ingrained ecosystem and socioeconomic features. First, billions of wild birds come into contact with domestic birds, either directly or indirectly,

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Introduction: Given the ongoing coronavirus disease 2019 (COVID-19) pandemic and the consequent global healthcare crisis, there is an urgent need to better understand risk factors for symptom deterioration and mortality among patients with COVID-19. This systematic review aimed to meet the need by determining the predictive value of chronic diseases for COVID-19 severity and mortality.Methods: We searched PubMed, Embase, Web of Science, and Cumulative Index to Nursing and Allied Health Complete to identify studies published between December 1, 2019, and December 31, 2020. Two hundred and seventeen observational studies from 26 countries involving 624,986 patients were included. We assessed the risk of bias of the included studies and performed a cumulative meta-analysis.Results: We found that among COVID-19 patients, hypertension was a very common condition and was associated with higher severity, intensive care unit (ICU) admission, acute respiratory distress syndrome, and mortality. Chronic obstructive pulmonary disease was the strongest predictor for COVID-19 severity, admission to ICU, and mortality, while asthma was associated with a reduced risk of COVID-19 mortality. Patients with obesity were at a higher risk of experiencing severe symptoms of COVID-19 rather than mortality. Patients with cerebrovascular disease, chronic liver disease, chronic renal disease, or cancer were more likely to become severe COVID-19 cases and had a greater probability of mortality.Conclusions: COVID-19 patients with chronic diseases were more likely to experience severe symptoms and ICU admission and faced a higher risk of mortality. Aggressive strategies to combat the COVID-19 pandemic should target patients with chronic diseases as a priority.

The basic helix-loop-helix (bHLH) proteins are a large family of transcription factors that control various developmental processes in eukaryotes, but the biological roles of most bHLH proteins are not very clear, especially in tomato. In this study, a PRE-like atypical bHLH gene was isolated and designated as SlPRE2 in tomato. SlPRE2 was highly expressed in immature-green fruits, moderately in young leaves, flowers, and mature-green fruits. To further research the function of SlPRE2, a 35 S:PRE2 binary vector was constructed and transformed into wild type tomato. The transgenic plants showed increased leaf angle and stem internode length, rolling leaves with decreased chlorophyll content. The water loss rate of detached leaves was increased in young transgenic lines but depressed in mature leaves. Besides, overexpression of SlPRE2 promoted morphogenesis in seedling development, producing light-green unripening fruits and yellowing ripen fruits with reduced chlorophyll and carotenoid accumulation in pericarps, respectively. Quantitative RT-PCR analysis showed that expression of the chlorophyll related genes, such as GOLDEN 2-LIKE and RbcS, were decreased in unripening 35  S:PRE2 fruit, and carotenoid biosynthesis-related genes PHYTOENE SYNTHASE1A and ζ-CAROTENE DESATURASE in ripening fruit were also down-regulated. These results suggest that SlPRE2 affects plant morphology and is a negative regulator of fruit pigment accumulation.