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Dynamics of phytoplankton in coastal waters is a function of nutrient influx and the present study investigated the trend in nutrient dynamics and phytoplankton abundance of Daya Bay (DB), South China Sea, from 1986 to 2020. Dissolved inorganic nitrogen (DIN), Dissolved inorganic phosphate (DIP) and Silicates were measured. DIN concentration exhibited an increasing trend over the last decades, and it was above the threshold for the phytoplankton growth. DIP level showed a significant decreasing trend throughout the studied period, falling below the threshold for phytoplankton growth in the last decade, where harmful algal blooms were dominated by the dinoflagellates. Long-term anthropogenic influences severely change influx of DIN, DIP, and silicates which in turn shape the architecture of phytoplankton communities. Thus, the understanding of the complex interaction between nutrient influx, anthropogenic activities and dynamics of both water quality and biological elements are particularly important to decide criteria to manage coastal ecosystems., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Objective: In this study we aimed to comprehensively evaluate the clinical features and treatment outcomes of Chinese patients with autoimmune pancreatitis (AIP) through a single-center real-world study., Methods: Patients diagnosed with AIP in Changhai Hospital, Naval Medical University from January 2014 to December 2021 were included. Baseline characteristics, laboratory test results, cross-sectional imaging and endoscopic ultrasound (EUS) findings, and long-term follow-up data were obtained. The differences in these characteristics between type 1 and type 2 AIP patients were analyzed., Results: Among all 320 patients, 271 (84.7%) and 49 (15.3%) had type 1 and type 2 AIP, respectively. The most common initial symptom was abdominal discomfort (58.1%), followed by obstructive jaundice (32.5%). Extrapancreatic organ involvement was identified in 126 (39.4%) patients, with the biliary system being the most commonly involved (36.6%). Elevated serum IgG4 level was rare in type 2 AIP patients. The diagnostic accuracy of computed tomography (CT), magnetic resonance imaging (MRI), and EUS for definitive and probable AIP were 78.0%, 68.7%, and 80.5%, respectively. EUS-guided tissue acquisition with immunohistochemical staining helped establish a final diagnosis in 39.7% of patients. During the follow-up period of 60 months, 18.6% of patients experienced relapse. The 1-, 3-, and 5-year relapse rates were higher in type 1 AIP patients, with an accumulated rate of 8.0%, 12.6%, and 15.1%, when compared with those with type 2 AIP., Conclusions: Type 2 AIP is not uncommon in Chinese population. The diagnostic accuracy of CT and EUS for AIP might be superior to that of MRI., (© 2024 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and John Wiley & Sons Australia, Ltd.)

Malic enzyme (ME) genes are key functional metabolic enzymes playing a crucial role in carcinogenesis. However, the detailed effects of ME gene expression on breast cancer progression remain unclear. Here, our results revealed ME1 expression was significantly upregulated in breast cancer, especially in patients with oestrogen receptor/progesterone receptor-negative and human epidermal growth factor receptor 2-positive breast cancer. Furthermore, upregulation of ME1 was significantly associated with more advanced pathological stages (p < 0.001), pT stage (p < 0.001) and tumour grade (p < 0.001). Kaplan-Meier analysis revealed ME1 upregulation was associated with poor disease-specific survival (DSS: p = 0.002) and disease-free survival (DFS: p = 0.003). Multivariate Cox regression analysis revealed ME1 upregulation was significantly correlated with poor DSS (adjusted hazard ratio [AHR] = 1.65; 95% CI: 1.08-2.52; p = 0.021) and DFS (AHR, 1.57; 95% CI: 1.03-2.41; p = 0.038). Stratification analysis indicated ME1 upregulation was significantly associated with poor DSS (p = 0.039) and DFS (p = 0.038) in patients with non-triple-negative breast cancer (TNBC). However, ME1 expression did not affect the DSS of patients with TNBC. Biological function analysis revealed ME1 knockdown could significantly suppress the growth of breast cancer cells and influence its migration ability. Furthermore, the infiltration of immune cells was significantly reduced when they were co-cultured with breast cancer cells with ME1 knockdown. In summary, ME1 plays an oncogenic role in the growth of breast cancer; it may serve as a potential biomarker of progression and constitute a therapeutic target in patients with breast cancer., (© 2024 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)

Current therapy for acute myeloid leukemia (AML) is largely hindered by the development of drug resistance of commonly used chemotherapy drugs, including cytarabine, daunorubicin, and idarubicin. In this study, we investigated the molecular mechanisms underlying the chemotherapy drug resistance and potential strategy to improve the efficacy of these drugs against AML. By analyzing data from ex vivo drug-response and multi-omics profiling public data for AML, we identified autophagy activation as a potential target in chemotherapy-resistant patients. In THP-1 and MV-4-11 cell lines, knockdown of autophagy-regulated genes ATG5 or MAP1LC3B significantly enhanced AML cell sensitivity to the chemotherapy drugs cytarabine, daunorubicin, and idarubicin. In silico screening, we found that chloroquine phosphate mimicked autophagy inactivation. We showed that chloroquine phosphate dose-dependently down-regulated the autophagy pathway in MV-4-11 cells. Furthermore, chloroquine phosphate exerted a synergistic antitumor effect with the chemotherapy drugs in vitro and in vivo. These results highlight autophagy activation as a drug resistance mechanism and the combination therapy of chloroquine phosphate and chemotherapy drugs can enhance anti-AML efficacy., (© 2023. The Author(s), under exclusive licence to Shanghai Institute of Materia Medica, Chinese Academy of Sciences and Chinese Pharmacological Society.)

Conventionally, efficiency is indirectly estimated through a respiratory gas analyser (oxygen, carbon dioxide), which is a complex and rather costly calculation method that is difficult to perform in many situations. Therefore, the present study proposed a modified definition of efficiency, called the efficiency factor (EF) (i.e., the ratio of work to the corresponding exercise intensity), and evaluated the relation between the EF and maximal oxygen uptake ([Formula: see text]), as well as compared the prediction models established based on the EF. The heart rate (maximal heart rate: 186 ± 6 beats min -1 ), rating of perceived exertion (19 ± 1), and [Formula: see text] (39.0 ± 7.1 mL kg -1  min -1 ) of 150 healthy men (age: 20 ± 2 years; height: 175.0 ± 6.0 cm; weight: 73.6 ± 10.7 kg; body mass index [BMI]: 24.0 ± 3.0 kg m -2 ; percent body fat [PBF]: 17.0 ± 5.7%) were measured during the cardiopulmonary exercise test (CPET). Through multiple linear regression analysis, we established the BMI model using age and BMI as parameters. Additionally, we created the PBF model HRR utilizing weight, PBF, and heart rate reserve (HRR) and developed PBF model EF6 and PBF model EF7 by incorporating EF6 from the exercise stage 6 and EF7 from the exercise stage 7 during the CPET, respectively. EF6 (r = 0.32, p = 0.001) and EF7 (r = 0.31, p = 0.002) were significantly related to [Formula: see text]. Among the models, the PBF model EF6 showed the highest accuracy, which could explain 62.6% of the variance in the [Formula: see text] at with a standard error of estimate (SEE) of 4.39 mL kg -1  min -1 (%SEE = 11.25%, p < 0.001). These results indicated that the EF is a significant predictor of [Formula: see text], and compared to the other models, the PBF model EF6 is the best model for estimating [Formula: see text]., (© 2023. Springer Nature Limited.)

Polymeric carbohydrates are abundant and their recycling by microbes is a key process of the ocean carbon cycle. A deeper analysis of carbohydrate-active enzymes (CAZymes) can offer a window into the mechanisms of microbial communities to degrade carbohydrates in the ocean. In this study, metagenomic genes encoding microbial CAZymes and sugar transporter systems were predicted to assess the microbial glycan niches and functional potentials of glycan utilization in the inner shelf of the Pearl River Estuary (PRE). The CAZymes gene compositions were significantly different between in free-living (0.2-3 μm, FL) and particle-associated (>3 μm, PA) bacteria of the water column and between water and surface sediments, reflecting glycan niche separation on size fraction and selective degradation in depth. Proteobacteria and Bacteroidota had the highest abundance and glycan niche width of CAZymes genes, respectively. At the genus level, Alteromonas (Gammaproteobacteria) exhibited the greatest abundance and glycan niche width of CAZymes genes and were marked by a high abundance of periplasmic transporter protein TonB and members of the major facilitator superfamily (MFS). The increasing contribution of genes encoding CAZymes and transporters for Alteromonas in bottom water contrasted to surface water and their metabolism are tightly related with particulate carbohydrates (pectin, alginate, starch, lignin-cellulose, chitin, and peptidoglycan) rather than on the utilization of ambient-water DOC. Candidatus Pelagibacter (Alphaproteobacteria) had a narrow glycan niche and was primarily preferred for nitrogen-containing carbohydrates, while their abundant sugar ABC (ATP binding cassette) transporter supported the scavenging mode for carbohydrate assimilation. Planctomycetota, Verrucomicrobiota, and Bacteroidota had similar potential glycan niches in the consumption of the main component of transparent exopolymer particles (sulfated fucose and rhamnose containing polysaccharide and sulfated-N-glycan), developing considerable niche overlap among these taxa. The most abundant CAZymes and transporter genes as well as the widest glycan niche in the abundant bacterial taxa implied their potential key roles on the organic carbon utilization, and the high degree of glycan niches separation and polysaccharide composition importantly influenced bacterial communities in the coastal waters of PRE. These findings expand the current understanding of the organic carbon biotransformation, underlying the size-fractionated glycan niche separation near the estuarine system., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Sun, Zhao, Yue, Cheng, Sun, Wang, Wu, Engel and Wang.)

Background: Glycolysis is a glucose metabolism pathway that generates the high-energy compound adenosine triphosphate, which supports cancer cell growth. Phosphofructokinase platelet (PFKP) plays a crucial role in glycolysis regulation and is involved in human cancer progression. However, the biological function of PFKP remains unclear in colorectal cancer (CRC). Methods: We analyzed the expression levels of PFKF in colon cancer cells and clinical samples using real-time PCR and western blot techniques. To determine the clinical significance of PFKP expression in colorectal cancer (CRC), we analyzed public databases. In addition, we conducted in vitro assays to investigate the effects of PFKP on cell growth, cell cycle, and motility. Results: An analysis by the Cancer Genome Atlas database revealed that PFKP was significantly overexpressed in CRC. We examined the levels of PFKP mRNA and protein, revealing that PFKP expression was significantly increased in CRC. The results of the univariate Cox regression analysis showed that high PFKP expression was linked to worse disease-specific survival (DSS) and overall survival (OS) [DSS: crude hazard ratio (CHR) = 1.84, 95% confidence interval (CI): 1.01-3.36, p = 0.047; OS: CHR=1.91, 95% CI: 1.06-3.43, p = 0.031]. Multivariate Cox regression analysis revealed that high PFKP expression was an independent prognostic biomarker for the DSS and OS of patients with CRC (DSS: adjusted HR = 2.07, 95% CI: 1.13-3.79, p = 0.018; AHR = 2.34, 95% CI: 1.29-4.25, p = 0.005). PFKP knockdown reduced the proliferation, colony formation, and invasion of CRC cells. In addition, the knockdown induced cell cycle arrest at the G0/G1 phase by impairing cell cycle-related protein expression. Conclusion: Overexpression of PFKP contributes to the growth and invasion of CRC by regulating cell cycle progression. PFKP expression can serve as a valuable molecular biomarker for cancer prognosis and a potential therapeutic target for treating CRC., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

At present, tourism is counted among those industries which have gained global attention due to rapid growth. Hence, a constant diversification in terms of destination is needed in tourism development. The recent trends of industry highlight the demand of alternative tourism types, among which nature-related tourism appears to be an emerging concept. In this regard, the present article investigates the impact of economic conditions and sustainable rural development on the sustainability of tourism development in China. The current research has gathered secondary data from the World Bank from 1981 to 2020. The quartile autoregressive distributed lag model has been applied to test the association between the variables. The results revealed that GDP, inflation, FDI, exchange rate, energy use, gross savings, and sustainable rural development have a significant and positive association with the sustainability of tourism development in China. Findings offer managerial implications recommending the local government to focus on the sustainability of rural development and economic conditions that may lead to the implementation of tourism-related development projects. This study also guides the policymakers in establishing policies related to tourism development using different economic conditions and sustainable rural development., (© 2022. The Author(s).)

Economic growth is a global requirement that requires extensive energy consumption, and this phenomenon needs researchers' attention and regulators' focus. Thereby, the paper scrutinizes the determinants of energy consumption such as fossil fuel energy consumption (FFEC), energy use, nuclear energy consumption (NEC), energy import, and renewable energy consumption (REC) and sustainability-oriented eco-innovation and their effectiveness on the economic growth of Saudi Arabia. The study extracted data from the World Bank from 1989 to 2020. Stationarity was examined using augmented Dickey-Fuller (ADF) tests, and the associations among constructs were analyzed through QARDL model. The findings revealed that FFEC, EU, NEC, EI, REC, and sustainability-oriented eco-innovation are significantly correlated with the EG of Saudi Arabia. The study also provides insights to new researchers who will investigate this area in the future and guides regulators in developing regulations related to economic growth using an appropriate level of energy and adoption of sustainability-oriented eco-innovation., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Histone deacetylases (HDAs) regulate many aspects of plant development and responses to environmental changes. Previous studies have demonstrated that the Arabidopsis histone deacetylase HDA15 is a positive regulator in far-red (FR) light-mediated inhibition of hypocotyl elongation. Furthermore, HDA15 can be phosphorylated and its enzymatic activity is negatively regulated by phosphorylation. However, the kinases that can phosphorylate HDA15 are still unknown. Cyclin-dependent kinases (CDKs) are a large family of serine/threonine protein kinases and have been identified as major regulators of the cell cycle and transcription. In this study, we show that the cyclin-dependent kinase CDKC2 interacts with HDA15 both in vitro and in vivo. In vitro kinase assays show that CDKC2 phosphorylates HDA15. Genetic evidence suggests that HDA15 acts downstream of CDKC2 in hypocotyl elongation under FR light. Furthermore, HDA15 and CDKC2 function synergistically in the regulation of FR-mediated cell elongation. The expression of cell wall organization- and auxin signaling-related genes under FR light is increased in hda15 and cdkc2/hda15 mutants. Taken together, our study indicates that CDKC2 can phosphorylate HDA15 and plays an important role in FR light-regulated hypocotyl elongation., (© 2022 Society for Experimental Biology and John Wiley & Sons Ltd.)

The increasing worldwide automobile production and usage adversely impact the environmental, economic, and social well-being. Although the automobile companies are trying to solve this problem by adopting corporate sustainability, there is a gap in the extant literature on sustainable corporate practices that are the most important to empower better sustainability performance. This study highlights the impact of core corporate sustainable practices attributes, government initiative, technology usage, and organizational culture on the sustainable performance of the automobile industry in India. The study proposed six aspects and fifty-three criteria from the literature review. The current article has used survey questionnaires to collect the primary data. The present article also applied the smart-PLS to test the association among the variables. The results indicated that the corporate sustainable practices attributes, technology usage, and organizational culture have a positive and significant linkage with the sustainable performance of the automobile industry. The current article guides the regulators in developing the regulations to improve sustainable organizational performance using sustainable corporate practices., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Breast cancer is a heterogeneous disease, and the survival rate of patients with breast cancer strongly depends on their stage and clinicopathological features. Chemoradiation therapy is commonly employed to improve the survivability of patients with advanced breast cancer. However, the treatment process is often accompanied by the development of drug resistance, which eventually leads to treatment failure. Metabolism reprogramming has been recognized as a mechanism of breast cancer resistance. In this study, we established a doxorubicin-resistant MCF-7 (MCF-7-D500) cell line through a series of long-term doxorubicin in vitro treatments. Our data revealed that MCF-7-D500 cells exhibited increased multiple-drug resistance, cancer stemness, and invasiveness compared with parental cells. We analyzed the metabolic profiles of MCF-7 and MCF-7-D500 cells through liquid chromatography−mass spectrometry. We observed significant changes in 25 metabolites, of which, 21 exhibited increased levels (>1.5-fold change and p < 0.05) and 4 exhibited decreased levels (<0.75-fold change and p < 0.05) in MCF-7 cells with doxorubicin resistance. These results suggest the involvement of metabolism reprogramming in the development of drug resistance in breast cancer, especially the activation of glycolysis, the tricarboxylic acid (TCA) cycle, and the hexamine biosynthesis pathway (HBP). Furthermore, most of the enzymes involved in glycolysis, the HBP, and the TCA cycle were upregulated in MCF-7-D500 cells and contributed to the poor prognosis of patients with breast cancer. Our findings provide new insights into the regulation of drug resistance in breast cancer, and these drug resistance-related metabolic pathways can serve as targets for the treatment of chemoresistance in breast cancer.

The salesperson is a job that is prone to deviant behavior. Prior studies addressed that deviant behavior is a behavioral stress response. Although numerous studies have demonstrated the relationship between job stress and deviant behavior, the clarity of the job stress mechanism remains limited. Drawing from coping theory, we proposed that job stress acts as a critical mechanism in linking the association between work-family conflict and salesperson deviant behavior. The objectives of this study are threefold. First, this study investigates the relationship between work-family conflict and job stress. Second, this study examines how job stress determines the likelihood of a salesperson engaging in deviant behavior. Last, this study investigates the mediating mechanism of work-family conflict and job stress. Using an online survey of salespeople in Indonesia, we received 321 data and employed a partial least square to test our proposed hypotheses. The results of this study confirm all hypotheses. The implications for managers regarding the result of this study is encouraging managers to establish and implement family-friendly policies which can diminish the level of stress and will decrease the likelihood of salespeople engaging in deviant behavior. Our study offers a significant contribution to the body of knowledge by clarifying the mediating role of job stress., Competing Interests: The authors declare no conflict of interest., (© 2022 The Author(s).)

Histone deacetylases (HDAs) play an important role in transcriptional regulation of multiple biological processes. In this study, we investigated the function of HDA15 in abscisic acid (ABA) responses. We used immunopurification coupled with mass spectrometry-based proteomics to identify proteins interacting with HDA15 in Arabidopsis (Arabidopsis thaliana). HDA15 interacted with the core subunits of the MOS4-associated complex (MAC), MAC3A and MAC3B, with interaction between HDA15 and MAC3B enhanced by ABA. hda15 and mac3a/mac3b mutants were ABA-insensitive during seed germination and hyposensitive to salinity. RNA sequencing analysis demonstrated that HDA15 and MAC3A/MAC3B co-regulate ABA-responsive intron retention (IR). Furthermore, HDA15 reduced the histone acetylation level of genomic regions near ABA-responsive IR sites and the association of MAC3B with ABA-responsive pre-mRNA was dependent on HDA15. Our results indicate that HDA15 is involved in ABA responses by interacting with MAC3A/MAC3B to mediate splicing of introns., (© The Author(s) 2022. Published by Oxford University Press on behalf of American Society of Plant Biologists.)

Long noncoding RNAs play a key role in the progression of colorectal cancer (CRC). However, the role and mechanism of LOC550643 in CRC cell growth and metastasis remain largely unknown. In this study, we assessed the clinical impacts of LOC550643 on CRC through the analysis of The Cancer Genome Atlas database, which revealed the significant upregulation of LOC550643 in CRC. Moreover, the high expression of LOC550643 was associated with poor survival in patients with CRC ( p = 0.001). Multivariate Cox regression analysis indicated that LOC550643 overexpression was an independent prognostic factor for shorter overall survival in patients with CRC (adjusted hazard ratio, 1.90; 95% confidence interval, 1.21-3.00; p = 0.006). A biological function analysis revealed that LOC550643 knockdown reduced colon cancer cell growth by hindering cell cycle progression. In addition, LOC550643 knockdown significantly induced cell apoptosis through the inhibition of signaling activity in phosphoinositide 3-kinases. Moreover, LOC550643 knockdown contributed to the inhibition of migration and invasion ability in colon cancer cells. Furthermore, miR-29b-2-5p interacted with the LOC550643 sequence. Ectopic miR-29b-2-5p significantly suppressed colon cancer cell growth and motility and induced cell apoptosis. Our findings suggest that, LOC550643-miR-29b-2-5p axis was determined to participate in the growth and metastasis of colon cancer cells; this could serve as a useful molecular biomarker for cancer diagnosis and as a potential therapeutic target for CRC.

The ATPase Family AAA Domain Containing 3A (ATAD3A), is a mitochondrial inner membrane protein conserved in metazoans. ATAD3A has been associated with several mitochondrial functions, including nucleoid organization, cholesterol metabolism, and mitochondrial translation. To address its primary role, we generated a neuronal-specific conditional knockout (Atad3 nKO) mouse model, which developed a severe encephalopathy by 5 months of age. Pre-symptomatic mice showed aberrant mitochondrial cristae morphogenesis in the cortex as early as 2 months. Using a multi-omics approach in the CNS of 2-to-3-month-old mice, we found early alterations in the organelle membrane structure. We also show that human ATAD3A associates with different components of the inner membrane, including OXPHOS complex I, Letm1, and prohibitin complexes. Stochastic Optical Reconstruction Microscopy (STORM) shows that ATAD3A is regularly distributed along the inner mitochondrial membrane, suggesting a critical structural role in inner mitochondrial membrane and its organization, most likely in an ATPase-dependent manner., Competing Interests: Declaration of interests The authors declare no conflict of interests., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

Long noncoding RNAs (lncRNAs) are a group of nonprotein coding transcripts that play a critical role in cancer progression. However, the role of lncRNA in metformin-induced inhibition of cell growth and its biological function in gastric cancer remain largely unknown. In this study, we identified an oncogenic lncRNA, Loc100506691, the expression of which was decreased in gastric cancer cells with metformin treatment. Moreover, Loc100506691 was significantly overexpressed in gastric cancer compared with adjacent normal tissues (p < 0.001), and high Loc100506691 expression was significantly correlated with poor survival of patients with gastric cancer. Additionally, Loc100506691 knockdown could significantly suppress gastric cancer cell growth in vitro , and ectopic Loc100506691 expression accelerated tumor growth in an in vivo mouse model. Analysis of the cell cycle revealed that Loc100506691 knockdown induced cell cycle arrest at the G2/M phase by impairing cell entry from the G2/M to G1 phase. Loc100506691 negatively regulated CHAC1 expression by modulating miR-26a-5p/miR-330-5p expression, and CHAC1 knockdown markedly attenuated Loc100506691 knockdown-induced gastric cancer cell growth and motility suppression. We concluded that anti-proliferative effects of metformin in gastric cancer may be partially caused by suppression of the Loc100506691-miR-26a-5p/miR-330-5p-CHAC1 axis., Competing Interests: The authors declare no competing interests., (© 2021 The Authors.)

Metastatic disease is responsible for over 90% of death in patients with breast cancer. Therefore, identifying the molecular mechanisms that regulate metastasis and developing useful therapies are crucial tasks. Long non-coding RNAs (lncRNAs), which are non-coding transcripts with >200 nucleotides, have recently been identified as critical molecules for monitoring cancer progression. This study examined the novel lncRNAs involved in the regulation of tumor progression in breast cancer. This study identified 73 metastasis-related lncRNA candidates from comparison of paired isogenic high and low human metastatic breast cancer cell lines, and their expression levels were verified in clinical tumor samples by using The Cancer Genome Atlas. Among the cell lines, a novel lncRNA, LOC550643 , was highly expressed in breast cancer cells. Furthermore, the high expression of LOC550643 was significantly correlated with the poor prognosis of breast cancer patients, especially those with triple-negative breast cancer. Knockdown of LOC550643 inhibited cell proliferation of breast cancer cells by blocking cell cycle progression at S phase. LOC550643 promoted important in vitro metastatic traits such as cell migration and invasion. Furthermore, LOC550643 could inhibit miR-125b-2-3p expression to promote breast cancer cell growth and invasiveness. In addition, by using a xenograft mouse model, we demonstrated that depletion of LOC550643 suppressed the lung metastatic potential of breast cancer cells. Overall, our study shows that LOC550643 plays an important role in breast cancer cell metastasis and growth, and LOC550643 could be a potential diagnosis biomarker and therapeutic target for breast cancer., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Tsai, Chong, Li, Tu, Chen, Lee, Chan, Wang and Chang.)

Sarcopenia is a condition in which there is a loss of muscle caused by aging and it is one of the most significant factors that affects physical fragility. In recent years, the role of the gut-muscle axis has garnered attention as, along with the gut microbiota, it potentially plays a significant role in muscle regeneration, in addition to nutritional supplements and exercise training. Past studies have found that supplementation with Lactobacillus plantarum TWK10 could effectively increase the muscle mass of animals or adult humans. Therefore, in this study, we investigated whether the supplementation of L. plantarum TWK10 produces increased muscle mass and improves the functional performance of elderly persons with mild fragility. A total of 68 elderly subjects were recruited, of which 13 subjects were excluded or withdrew from the study. We adopted a double-blind design, and the 55 subjects were randomly divided into three groups: the placebo group, the TWK10 low-dose group (2 × 10 10 CFU/day) (TWK10-L), and the TWK10 high-dose group (6 × 10 10 colony-forming unit (CFU)/day) (TWK10-H). For 18 weeks, all subjects were required to regularly take experimental samples, perform functional activity testing, and have their body composition analyzed before the study and every six weeks after the intervention. Finally, 17 subjects in the placebo group, 12 subjects in the TWK10-L group, and 13 subjects in the TWK10-H group finished the study. It was found that supplementation with TWK10 had a tendency to increase and improve muscle mass, left hand grip strength, lower limb muscle strength, and gait speed and balance after the sixth week, especially in the TWK10-H group, and, as the supplement time was longer up to the 18th week, it had an even greater effect ( p < 0.05). In conclusion, consecutive supplementation of L. plantarum TWK10 for more than six weeks could effectively improve the muscle strength and endurance of the elderly, reducing sarcopenia and physical fragility. This trial was registered as NCT04893746.

The pressure-state-response (PSR) model was applied to establish a mangrove ecosystem health evaluation system combined with analytical hierarchy process (AHP) in this paper. The mangrove wetlands are divided into five ecological levels: excellent health, good health, health, sub-health and morbidity, which is based on the comprehensive health index (CHI) value. Twelve representative sites were selected for sampling to assess the ecological health condition of mangroves. As a result, the ecological health level of Gaoqiao mangrove area is excellent health; the ecological health level of Taiping mangrove area is good health; the ecological health level of Huguang and Qi'ao mangrove area is health; the ecological health level of Techeng and He'an mangrove area is sub-health; the ecological health level of Huidong mangrove area is morbidity. These results will give some advises for ecological protection and biological resource sustainable development of mangrove ecosystem in China.

Over the past decade, the rise of cancer immunotherapy has coincided with a remarkable breakthrough in cancer therapy, which attracted increased interests in public. The scientific community clearly showed that the emergence of immunotherapy is an inevitable outcome of a holistic approach for cancer treatment. It is well established that traditional Chinese medicine (TCM) utilizes the principle of homeostasis and balance to adjust the healthy status of body. TCM treatment toward cancer has a long history, and the diagnosis and treatment of tumors were discussed in the ancient and classical literatures of Chinese medicine, such as the Yellow Emperor's Inner Canon. Precious heritage has laid the foundation for the innovation and development of cancer treatment with TCM. The modern study indicated that TCM facilitates the treatment of cancer and enhances the survival rate and life expectancy of patients. However, the pharmacological mechanisms underlying these effects are not yet completely understood. In addition, physicians cannot always explain why the TCM treatment is effective and the mechanism of action cannot be explained in scientific terms. Here, we attempted to provide insights into the development of TCM in the treatment and interpret how TCM practitioners treat cancer through six general principles of TCM by using modern scientific language and terms based on newly discovered evidence., Competing Interests: S-HL is a chief technology officer of Celgen Biotech whose nutraceutical products contain β-glucan, sulforaphane, and bovine tracheal cartilage (BTC) components. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Lee, Liu, Chen, Huang, Hung, Lee, Lin and Lin.)

Background: Form deprivation myopia is a type of ametropia, with identifiable causes in humans, that has been induced in many animals. The age of onset of myopia induced by monocular form deprivation coincides with the period of visual development in guinea pigs. However, visual acuity of form-deprived eyes in guinea pigs is not understood yet. In this study, we investigated whether monocular form deprivation would affect visual acuity in infant guinea pigs by evaluating the development of myopia and amblyopia after monocular form deprivation, and whether form deprivation myopia and amblyopia occurred simultaneously or successively., Methods: Twenty pigmented guinea pigs (2 weeks old) were randomly assigned to two groups: monocularly form-deprived (n=10), in which facemasks modified from latex balloons covered the right eye, and normal controls (n=10). Refraction, axial length, and visual acuity were measured at 4 intervals (after 0, 1, 4, and 8 weeks of form deprivation), using cycloplegic streak retinoscopy, A-scan ultrasonography (with an oscillation frequency of 10 MHz), and sweep visual evoked potentials (sweep VEPs), respectively. Sweep VEPs were performed with correction of the induced myopic refractive error., Results: Longer deprivation periods resulted in significant refractive errors in form-deprived eyes compared with those in contralateral and normal control eyes; the axial lengths of form-deprived eyes increased significantly after 4 and 8 weeks of form deprivation. These results revealed that myopia was established at 4 weeks. The acuity of form-deprived eyes was unchanged compared to that at the pretreatment time point, while that of contralateral eyes and eyes in normal control guinea pigs improved; there were significant differences between the deprived eyes and the other two open eyes from 1 to 8 weeks of form deprivation, showing that amblyopia was possibly established during 1 week of form deprivation., Conclusions: This study demonstrated the feasibility of using sweep VEPs to estimate the visual acuity of guinea pigs. Further, our results revealed that amblyopia likely occurred earlier than myopia; amblyopia and myopia coexisted after a long duration of monocular form deprivation in guinea pigs. Understanding this relationship may help provide insights into failures of treatment of amblyopia associated with myopic anisometropia., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at http://dx.doi.org/10.21037/atm-20-5433). The authors have no conflicts of interest to declare., (2021 Annals of Translational Medicine. All rights reserved.)

Schizophrenia is linked with abnormal neurodevelopment, on which growth differentiation factor 11 (GDF-11) has a great impact. However, a direct evidence linking GDF-11 to the pathophysiology of schizophrenia is still lacking. The current study aimed to investigate the relationship between plasma GDF-11 levels and both psychopathological symptoms and cognitive function in schizophrenia. Eighty-seven schizophrenia patients and 76 healthy controls were enrolled in the present study. The symptomatology of schizophrenia was evaluated using the Positive and Negative Syndrome Scale (PANSS). Cognitive function was assessed by Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) including twelve neurocognitive tests in five aspects of cognitive function. Plasma GDF-11 levels were determined by enzyme-linked immunosorbent assay (ELISA). We found that plasma levels of GDF-11 were significantly lower in schizophrenia patients relative to healthy controls. Correlation analysis showed significant negative correlations between the GDF-11 levels and the PANSS total score, the positive symptoms score, the negative symptoms score or the general score. Additionally, positive associations were observed between plasma GDF-11 levels and the visuospatial/constructional, attention, immediate memory, or delayed memory in patients. Partial correlation analysis showed that these correlations were still significant after adjusting for age, gender, education years, body mass index, duration of illness, and age of onset except for the visuospatial/constructional and attention index. Multiple regression analysis revealed that GDF-11 was an independent contributor to the immediate memory, delayed memory and RBANS total score in patients. Collectively, the correlations between plasma GDF-11 and psychopathological and cognitive symptoms suggest that abnormal GDF-11 signaling might contribute to schizophrenic psychopathology and cognitive impairments and GDF-11 could be a potential and promising biomarker for schizophrenia., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2020 Yang, Zhan, Xiong, Wei, Fu, Liu, Tu, Yang and Wan.)

Lung cancer is the most prevalent types of cancer and the leading cause of cancer-related deaths worldwide. Among all cancers, lung cancer has the highest incidence, accompanied by a high mortality rate at the advanced stage. Favorable prognostic biomarkers can effectively increase the survival rate in lung cancer. Our results revealed FAM83A (Family with sequence similarity 83, member A) overexpression in lung cancer tissues compared with adjacent normal tissues. Furthermore, high FAM83A expression was closely associated with poor lung cancer survival. Here, through siRNA transfection, we effectively inhibited FAM83A expression in the lung cancer cell lines H1355 and A549. FAM83A knockdown significantly suppressed the proliferation, migration, and invasion ability of these cells. Furthermore, FAM83A knockdown could suppress Epidermal growth factor receptor (EGFR)/Mitogen-activated protein kinase (MAPK)/Choline kinase alpha (CHKA) signaling activation in A549 and H1355. By using a bioinformatics approach, we found that FAM83A overexpression in lung cancer may result from miR-1-3p downregulation. In summary, we identified a novel miR-1-FAM83A axis could partially modulate the EGFR/choline phospholipid metabolism signaling pathway, which suppressed lung cancer growth and motility. Our findings provide new insights for the development of lung cancer therapeutics.

Background: Benvitimod cream, a novel synthetic small molecule, was effective in treating mild-to-moderate plaque psoriasis. We conducted a phase III clinical trial to assess the efficacy and safety of benvitimod cream in patients with mild-to-moderate plaque psoriasis., Methods: We randomly assigned 686 patients (2:1:1) to receive 1% benvitimod cream, 0.005% calcipotriol ointment or placebo twice a day for 12 weeks. The primary efficacy end points were the percentage of patients with a 75% or greater reduction from baseline in the psoriasis area and severity index (PASI 75) score and with a score of 0 or 1 in static physician's global assessment (sPGA) at week 12., Results: The results showed that 50.4% of patients in the benvitimod group achieved PASI 75, which was significantly higher than that in the calcipotriol (38.5%, P < 0.05) and placebo (13.9%, P < 0.05) groups. The proportion of patients achieving an sPGA score 0 or 1 was 66.3% in the benvitimod group and 63.9% in the calcipotriol group, which were both significantly higher than that in the placebo group (34%, P < 0.05). In the long-term follow-up study, 50.8% of patients experienced recurrence. After retreatment with 1% benvitimod, 73.3% of patients achieved an sPGA score of 0 or 1 again at week 52. Adverse events included application site irritation, follicular papules, and contact dermatitis. No systemic adverse reactions were reported., Conclusion: During this 12-week study, benvitimod cream was demonstrated with high effectiveness and safety in patients with mild-to-moderate plaque psoriasis., Trial Registration: Chinese Clinical Trial Registry (ChiCTR), ChiCTR-TRC-13003259; http://www.chictr.org.cn/showprojen.aspx?proj=6300., (Copyright © 2020 The Chinese Medical Association, produced by Wolters Kluwer, Inc. under the CC-BY-NC-ND license.)

Background/aim: Lipopolysaccharide-induced tumor necrosis factor alpha factor (LITAF) has been identified as a tumor suppressor in human cancers. Present study, we assessed biological role of LITAF in human gastric cancer., Materials and Methods: The clinical impacts of LITAF expression were assessed in gastric cancer using public databases. The biological role of LITAF was assessed in gastric cancer cells using siLITAF transfection., Results: High LITAF expression was correlated well with worse prognosis, including pathological stage (p=0.034) and pathological T stage (p=0.047), as well as with shorter survival. Herein, we present a novel finding that miR-1-3p could inhibit LITAF expression by directly binding to the 3'-untranslated region of LITAF mRNA. Cell functional assays revealed that LITAF knockdown could significantly suppress gastric cancer growth and motility., Conclusion: High LITAF expression resulting from low miR-1-3p expression is a biomarker for poor prognosis or therapeutic targets in gastric cancer., (Copyright© 2020, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)

Mammalian histone deacetylases (HDACs) undergo phosphorylation to regulate their localization, activity, and function. However, little is known about the regulation of plant HDAC function and activity by phosphorylation. Here, we report the crystal structure of the Reduced Potassium Dependency3/Histone Deacetylase1 (RPD3/HDA1) type class II histone deacetylase HDA15 in Arabidopsis ( Arabidopsis thaliana ). The histone deacetylase domain of HDA15 (HDA15HD) assembles as tetrameric forms with each monomer composed of 12 α-helices and 9 β-sheets. The L1 loop and β2 sheet of HDA15HD are the essential interfaces for the tetramer formation. The N-terminal zinc finger domain enhances HDA15HD dimerization and increases its enzymatic activity. Furthermore, HDA15 can also be phosphorylated at Ser-448 and Ser-452 in etiolated seedlings. The HDA15 phosphorylation status determines its subnuclear localization and oligomerization. Phosphomimetics of HDA15 partially disrupt its oligomerization and cause loss of enzymatic activity and translocation from the nucleolus into nucleoplasm. Together, these data indicate that phosphorylation plays a critical role in regulating the structure and function of HDA15., (© 2020 American Society of Plant Biologists. All Rights Reserved.)

Colorectal carcinoma (CRC) is one of the most prevalent cancers worldwide and has a high mortality rate. Long noncoding RNAs (lncRNAs) have been noted to play critical roles in cell growth; cell apoptosis; and metastasis in CRC. This study determined that LOC441461 expression was significantly higher in CRC tissues than in adjacent normal mucosa. Pathway enrichment analysis of LOC441461-coexpressed genes revealed that LOC441461 was involved in biological functions related to cancer cell growth and motility. Knockdown of the LOC441461 expression significantly suppressed colon cancer cell growth by impairing cell cycle progression and inducing cell apoptosis. Furthermore, significantly higher LOC441461 expression was discovered in primary colon tumors and metastatic liver tumors than in the corresponding normal mucosa, and LOC441461 knockdown was noted to suppress colon cancer cell motility. Knockdown of LOC441461 expression suppressed the phosphorylation of MLC and LIMK1 through the inhibition of RhoA/ROCK signaling. Overall, LOC441461 was discovered to play an oncogenic role in CRC cell growth and motility through RhoA/ROCK signaling. Our findings provide new insights into the regulation of lncRNAs and their application in the treatment of colon cancer.

Background: Inertial sensors, such as accelerometers, serve as convenient devices to predict the energy expenditures (EEs) during physical activities by a predictive equation. Although the accuracy of estimate EEs especially matter to athletes receive physical training, most EE predictive equations adopted in accelerometers are based on the general population, not athletes. This study included the heart rate reserve (HRR) as a compensatory parameter for physical intensity and derived new equations customized for sedentary, regularly exercising, non-endurance athlete, and endurance athlete adults., Methods: With indirect calorimetry as the criterion measure (CM), the EEs of participants on a treadmill were measured, and vector magnitudes (VM), as well as HRR, were simultaneously recorded by a waist-worn accelerometer with a heart rate monitor. Participants comprised a sedentary group (SG), an exercise-habit group (EHG), a non-endurance group (NEG), and an endurance group (EG), with 30 adults in each group., Results: EE predictive equations were revised using linear regression with cross-validation on VM, HRR, and body mass (BM). The modified model demonstrates valid and reliable predictions across four populations (Pearson correlation coefficient, r : 0.922 to 0.932; intraclass correlation coefficient, ICC: 0.919 to 0.930)., Conclusion: Using accelerometers with a heart rate monitorcan accurately predict EEs of athletes and non-athletes with an optimized predictive equation integrating the VM, HRR, and BM parameters., Competing Interests: The authors declare there are no competing interests., (©2020 Chang et al.)

Daya Bay is facing the influence of human activities and nature changes, which result in phytoplankton adjusting to the changing environment. The data about environmental changes and phytoplankton were obtained from four seasonal cruises in 2013 in the bay. It is helpful to explore seasonal succession of phytoplankton driven by the determining environmental factors in this bay. Temperature is a significant indicator of season change. The limiting factor of phytoplankton growth totally changed from P (PO 4 -P) limiting during the southwest monsoon to Si (SiO 3 -Si) limiting during northeast monsoon. The order of diatoms and dinoflagellates was the dominant phytoplankton groups in Daya Bay. The dominant species included chain-forming diatoms (Skeletonema, Pseudo-nitzschia, Thalassionema, Chaetoceros and Rhizosolenia) were found all the year round and filamentous cyanobacteria (Trichodesmium) in spring and autumn. Partial least square regression (PLS) found that salinity, temperature and nutrients were important driving force for phytoplankton seasonal succession.