Unmanned Aerial Vehicle-Based Compressed Data Acquisition for Environmental Monitoring in WSNs.

With the increasing concerns for the environment, the amount of the data monitored by wireless sensor networks (WSNs) is becoming larger and the energy required for data transmission is greater. However, sensor nodes have limited storage capacity and battery power. The WSNs are faced with the challenge of handling larger data volumes while minimizing energy consumption for transmission. To address this issue, this paper employs data compression technology to eliminate redundant information in the environmental data, thereby reducing energy consumption of sensor nodes. Additionally, an unmanned aerial vehicle (UAV)-assisted compressed data acquisition algorithm is put forward. In this algorithm, compressive sensing (CS) is introduced to decrease the amount of data in the network and the UAV serves as a mobile aerial base station for efficient data gathering. Based on CS theory, the UAV selectively collects measurements from a subset of sensor nodes along a route planned using the optimized greedy algorithm with variation and insertion strategies. Once the UAV returns, the sink node reconstructs sensory data from these measurements using the reconstruction algorithms. Extensive experiments are conducted to verify the performance of this algorithm. Experimental results show that the proposed algorithm has lower energy consumption compared to other approaches. Furthermore, we employ different data reconstruction algorithms to recover data and discover that the data can be better reconstructed in a shorter time.

Point-wise spatial network for identifying carcinoma at the upper digestive and respiratory tract.

PROBLEM: Artificial intelligence has been widely investigated for diagnosis and treatment strategy design, with some models proposed for detecting oral pharyngeal, nasopharyngeal, or laryngeal carcinoma. However, no comprehensive model has been established for these regions. AIM: Our hypothesis was that a common pattern in the cancerous appearance of these regions could be recognized and integrated into a single model, thus improving the efficacy of deep learning models. METHODS: We utilized a point-wise spatial attention network model to perform semantic segmentation in these regions. RESULTS: Our study demonstrated an excellent outcome, with an average mIoU of 86.3%, and an average pixel accuracy of 96.3%. CONCLUSION: The research confirmed that the mucosa of oral pharyngeal, nasopharyngeal, and laryngeal regions may share a common appearance, including the appearance of tumors, which can be recognized by a single artificial intelligence model. Therefore, a deep learning model could be constructed to effectively recognize these tumors.

Synergistic Effects of Zanubrutinib Combined With CD19 CAR-T Cells in Raji Cells in Vitro and in Vivo.

Background and Objects: Bruton's tyrosine kinase inhibitors are commonly used and effective for lymphoma and chronic lymphocytic leukemia (CLL). Ibrutinib might improve the effect of anti-cluster of differentiation 19 (CD19) chimeric antigen receptor (CD19 CAR) T-cell therapy in lymphoma, but the effects of zanubrutinib combined with CAR-T cells is unclear. Methods: We selected a low effect-target ratio (E:T = 1:3) to study this synergistic effect in vitro. The programed cell death protein 1 (PD-1) expression in CD19 CAR-T cells and immune phenotype of T lymphocytes were analyzed by flow cytometry (FCM). We selected CD19 CAR-T cells of a patient with diffuse large B cell lymphoma (DLBCL) to study the synergistic effect of zanubrutinib with CAR-T cells by bioluminescence imaging monitoring. The CD19 CAR-T cells expansion in mice was compared by FCM. Results: Zanubrutinib and ibrutinib had dose-dependent toxicity on both CAR-T cells and lymphoma cells. But there was no significant synergistic effect of the CD19 CAR-T cells combined with zanubrutinib/ibrutinib in vitro. The PD-1 expression in CD19 CAR-T cells increased when the CD19 CAR-T cells were co-cultured with Raji cells and decreased when ibrutinib was added in culture, but zanubrutinib had no such effect. The extinction of luciferase expression was more obvious in the polytherapy group of ibrutinib and CD19 CAR-T cell than that in the other groups. Moreover, the proportion of CAR-T cells in the combination therapy group of CD19 CAR-T cells and ibrutinib was higher than that of the polytherapy group of CD19 CAR-T cells with zanubrutinib group. The synergistic effect could be observed obviously in mice receiving ibrutinib combined with CD19 CAR-T cells. But zanubrutinib cannot perform joint therapy effect either in vitro or in mice. Conclusion: Zanubrutinib might have no joint therapy effect with CD19 CAR-T cells neither in vitro nor in mice, but the mechanism of different curative effects requires our further research and exploration.

Assessment of patient-centered outcomes (PROs) in inflammatory bowel disease (IBD): a multicenter survey preceding a cross-disciplinary (functional) consensus.

BACKGROUND: With a shift in the healthcare paradigm towards a more patient-centered approach, data on inflammatory bowel disease (IBD) needs to be further explored. This study aimed to determine patient perspectives on the effect of IBD and features of patients with lower satisfaction level and compare patient and physician perception of IBD-related Quality of Care (QoC). METHODS: A previously developed pre-standardised set of questions regarding patient-centered outcome (PRO) measures for IBD, comprising 36 items, was administered in five centers, and a concomitant questionnaire for specialised physicians was adapted and administered. RESULTS: Overall, 1005 patients with IBD met the inclusion criteria. Sixty-five questionnaires were administered to specialised physicians. Both patients and physicians perceived the IBD-related QoC as being satisfactory. Furthermore, this study revealed areas of shortcomings where it comes to patient perceptions. Female sex and the presence of negatively impacting disease characteristics (presence of significant pain or discomfort, lack of energy, feeling fatigued most of the time, experiencing anxiety or depression in the last 2 weeks) were associated with lower satisfaction levels. CONCLUSIONS: Our findings can be used in establishing strategies aimed at improving patient QoC and defining strategic priorities. These data can aid in improving the communication of the pressing needs of IBD patients, to both the public payers and health authorities.

Arsenic removal from alkaline leaching solution using Fe (III) precipitation.

The alkaline leaching solution from arsenic-containing gold concentrate contains a large amount of arsenate ions, which should be removed because it is harmful to the production process and to the environment. In this study, conventional Fe (III) precipitation was used to remove arsenic from the leaching solution. The precipitation reaction was carried out at the normal temperature, and the effects of pH value and Fe/As ratio on the arsenic removal were investigated. The results show that the removal rate of arsenic is distinctive at different pH values, and the effect is best within the pH range of 5.25-5.96. The removal rate can be further increased by increasing the ratio of Fe/As. When the pH = 5.25-5.96 and Fe/As > 1.8, the arsenic in the solution can be reduced to below 5 mg/L. However, the crystallinity of ferric arsenate is poor, and the particle size is small, most of which is about 1 µm. The leaching toxicity test shows the leaching toxicity of precipitates gradually decreased by the increase of Fe/As. The precipitates can be stored safely as the ratio of Fe/As exceeded 2.5.

Boosted activity of graphene encapsulated CoFe alloys by blending with activated carbon for oxygen reduction reaction.

The slow oxygen reduction reaction (ORR) hampers the efficiency of microbial fuel cells (MFCs) to a large extent, which usually requires catalysts to facilitate the electron transfer. The major challenge of the existed non-precious metals in place of the noble metal catalysts (Pt, Pd, Au et al.) for ORR is their low efficiency, which urgently needs special route to tackle this issue. Herein, we report a simple and convenient technique using prussian blue analogues as precursor to directly synthesize the N-doped graphene encapsulated CoFe alloy which is present in "Core-Shell" structure via calcination of Co2Fe(CN)6 in inert condition. The encapsulation of metal alloy within graphene shell immensely promotes the electron transfer from the encapsulated metals to the graphene surface. It efficiently optimizes the electronic structure of the as-synthesized catalyst and thereby triggers high ORR activity. The surrounding activated carbon (AC) contributes to the large pore structure and further offers a commodious route for the oxygen to gain electron. Therefore, the total resistance of air cathodes is significantly reduced from 17.300â€¯Ω to 9.551â€¯Ω and the electrochemical activity is greatly improved. The power performances of MFCs indicate that CoFe/C-10% presents the highest maximum power density (MPD) of 1616 mW m-2, which is 5 times larger than that of the bare AC. It is well concluded that the graphene encapsulated CoFe alloy can be recognized as potential ORR catalyst for MFCs.

Characterization of a hybrid polyacrylamide and its flocculation properties in cyanide tailing suspensions.

An inorganic-organic hybrid flocculant Al(OH)3-polyacrylamide (Al-PAM) with narrow molecular weight distribution was synthesized using inverse microemulsion polymerization. The hybrid polymer Al-PAM was characterized by Infrared spectroscopy, thermogravimetric analysis, transmission electron microscopy and scanning electron microscopy, and it was found that it had a 'star-like' structure in which Al(OH)3 colloidal particles acted as cores linking PAM chains. The properties of Al-PAM were investigated in flocculating 10 wt% cyanide tailing suspensions. It was found that as the amount of Al-PAMM1 with high molecular weight and aluminum content increased, the initial settling rate of particles accelerated, achieving the maximum 6.6 m/h, 17.3 times the rate of the control without flocculants. The turbidity of the supernatant decreased to 35 ± 2 NTU accordingly, compared to 353 ± 2 NTU of that in the control, which meant that 90.0% of turbidity was removed from the cyanide tailing suspensions. The flocculation mechanism was further explored by floccule size and ζ potential measurements. The superior performance of cationic Al-PAM in flocculating negatively charged particles compared to commercial non-ionic GG indicated that electrostatic repulsion between tailing particles was a crucial factor in deciding the flocculation performance of the polymer. The study demonstrated that both charge neutralization and bridge adsorption were conductive to the particle flocculation.

FOXQ1 regulates senescence-associated inflammation via activation of SIRT1 expression.

Cellular senescence is an initial barrier to tumor development that prevents the proliferation of premalignant cells. However, some of the features of senescent cells seem to promote tumor progression via senescence-associated secretory phenotype (SASP). Here, we demonstrated that the protein level of forkhead box Q1 (FOXQ1), which highly overexpresses in several kinds of tumors, was significantly downregulated during both replicative and oncogene-induced senescence. Moreover, overexpression of FOXQ1 delayed senescence, whereas FOXQ1 silence led to premature senescence in human fibroblasts. Furthermore, we identified that FOXQ1 upregulated SIRT1 expression through transcriptional regulation via directly binding to the SIRT1 promoter. Finally, we showed that FOXQ1 remarkably inhibited the replicative senescence through depressing the expression of the inflammatory cytokines interleukin-6 (IL-6) and IL-8 via modulation of SIRT1-NF-κB pathway. In addition, FOXQ1 overexpressed in human esophageal cancer cells and ablation of FOXQ1 restrained the tumourigenic ability of the esophageal cancer cells (EC109 and EC9706) in a mouse xenograft model in vivo. Taken together, these findings uncover a previously unidentified role of FOXQ1 regulating SASP and tumor development at same time.

Regulation of the MDM2-p53 pathway by the nucleolar protein CSIG in response to nucleolar stress.

Nucleolar proteins play an important role in the regulation of the MDM2-p53 pathway, which coordinates cellular response to stress. However, the mechanism underlying this regulation remains poorly understood. Here, we report that the nucleolar protein CSIG is a novel and crucial regulator of the MDM2-p53 pathway. We demonstrate that CSIG translocates from the nucleolus to the nucleoplasm in response to nucleolar stress. Moreover, knockdown of CSIG attenuates the induction of p53 and abrogates G1 phase arrest in response to nucleolar stress. CSIG interacts directly with the MDM2 RING finger domain and inhibits MDM2 E3 ubiquitin ligase activity, thus resulting in a decrease in MDM2-mediated p53 ubiquitination and degradation. Our results suggest that the CSIG-MDM2-p53 regulatory pathway plays an important role in the cellular response to nucleolar stress.

Acetylation of FOXM1 is essential for its transactivation and tumor growth stimulation.

Forkhead box transcription factor M1 (FOXM1) plays crucial roles in a wide array of biological processes, including cell proliferation and differentiation, the cell cycle, and tumorigenesis by regulating the expression of its target genes. Elevated expression of FOXM1 is frequently observed in a multitude of malignancies. Here we show that FOXM1 can be acetylated by p300/CBP at lysines K63, K422, K440, K603 and K614 in vivo. This modification is essential for its transactivation on the target genes. Acetylation of FOXM1 increases during the S phase and remains high throughout the G2 and M phases, when FOXM1 transcriptional activity is required. We find that the acetylation-deficient FOXM1 mutant is less active and exhibits significantly weaker tumorigenic activities compared to wild-type FOXM1. Mechanistically, the acetylation of FOXM1 enhances its transcriptional activity by increasing its DNA binding affinity, protein stability, and phosphorylation sensitivity. In addition, we demonstrate that NAD-dependent histone deacetylase SIRT1 physically binds to and deacetylates FOXM1 in vivo. The deacetylation of FOXM1 by SIRT1 attenuates its transcriptional activity and decreases its protein stability. Together, our findings demonstrate that the reversible acetylation of FOXM1 by p300/CBP and SIRT1 modulates its transactivation function.

The Effect of Danazol in Primary Immune Thrombocytopenia: An Analysis of a Large Cohort From a Single Center in China.

AIM: This study assessed the long-term benefits and side effects of low-to-medium dose of danazol therapy in primary immune thrombocytopenia (ITP). METHODS: The retrospective analysis included 319 patients with ITP who accepted danazol therapy. Patients accepted danazol alone or in combination with glucocorticoids. Clinical outcome and tolerance were assessed in all patients. RESULTS: Among patients with persistent or chronic ITP, the overall response rate of danazol therapy was 65.0%. Sixty-five (63.1%) of the 103 patients reached remission with danazol alone, and 93 (48.7%) of the 191 patients who accepted combination therapies acquired remission and discontinued glucocorticoids successfully. Age and previous treatments were 2 risk factors for response rate. In newly diagnosed patients with ITP, the response rate and median response time did not differ significantly with or without danazol. However, the relapse rate was significantly lower in patients administered danazol combined with glucocorticoids than those accepted glucocorticoids alone. Totally, 21.1% of the patients experienced mild or moderate side effects, and 1.2% of the patients discontinued treatment due to intolerable side effects. CONCLUSION: Low-to-medium dosage of danazol is better tolerated and effective in patients with ITP, even in those refractory to other treatments. Combination of danazol and glucocorticoids for initial treatment may decrease relapse rates to achieve well-tolerated long-term remission.

Interleukin 35 may contribute to the loss of immunological self-tolerance in patients with primary immune thrombocytopenia.

Primary immune thrombocytopenia (ITP) is an autoimmune disorder. Interleukin-35 (IL35) can suppress T cell proliferation and elicit the development of inducible regulatory T cells (Tregs). Previous studies have shown decreased plasma IL35 levels and dysfunctional T cells in patients with ITP. In this study, we determined whether decreased IL35 levels correlate with T cell dysfunction in ITP patients. Plasma IL35 levels were found to be lower in ITP patients than in healthy controls, were positively correlated with platelet levels and the percentage of peripheral circulating Tregs, and negatively correlated with the levels of T helper-1 cells in ITP patients. We also evaluated the effects of IL35 on cytokines contributing to T cell proliferation. IL35 promoted the secretion of interleukin 10 (IL10) and transforming growth factor-ß1 but reduced the levels of interferon-γ and IL17A (also termed IL17). Moreover, IL35 inhibited the proliferation of CD4+ and CD8+ T cells but induced the differentiation and proliferation of Tregs in ITP. In summary, IL35 appears to contribute to the loss of immunological self-tolerance in ITP patients by modulating T cells and immunoregulatory cytokines.

Protein kinase D1 is essential for Ras-induced senescence and tumor suppression by regulating senescence-associated inflammation.

Oncogene-induced senescence (OIS) is an initial barrier to tumor development. Reactive oxygen species (ROS) is critical for oncogenic Ras OIS, but the downstream effectors to mediate ROS signaling are still relatively elusive. Senescent cells develop a senescence-associated secretory phenotype (SASP). However, the mechanisms underlying the regulation of the SASP are largely unknown. Here, we identify protein kinase D1 (PKD1) as a downstream effector of ROS signaling to mediate Ras OIS and SASP. PKD1 is activated by oncogenic Ras expression and PKD1 promotes Ras OIS by mediating inflammatory cytokines interleukin-6 (IL-6) and interleukin-8 (IL-8) via modulation of NF-κB activity. We demonstrate that ROS-protein kinase Cδ (PKCδ)-PKD1 axis is essential for the establishment and maintenance of IL-6/IL8 induction. In addition, ablation of PKD1 causes the bypass of Ras OIS, and promotes cell transformation and tumorigenesis. Together, these findings uncover a previously unidentified role of ROS-PKCδ-PKD1 pathway in Ras OIS and SASP regulation.

External validation and clinical evaluation of the International Prognostic Score of Thrombosis for Essential Thrombocythemia (IPSET-thrombosis) in a large cohort of Chinese patients.

OBJECTIVES: In patients with essential thrombocythemia (ET), vascular complications contribute to both morbidity and mortality. To better predict the occurrence of thrombotic events, an International Prognostic Score of thrombosis for ET (IPSET-thrombosis) was recently developed. We hereby presented an external validation and analysis of this model in a large Cohort of Chinese Patients. METHODS: We retrospectively evaluated the characteristics and risk factors for thrombosis in 970 Chinese patients with ET and estimated the clinical implications of the IPSET-thrombosis model. RESULTS: The median follow-up was 49 months (range, 0-360). Chinese ET patients had similar clinical characteristics as Caucasian patients. Similar to the IPSET-thrombosis study, our multivariate analysis revealed age >60 (HR = 1.949), previous thrombosis (HR = 2.484), JAK2V617F mutation (HR = 1.719), and cardiovascular risk factors (HR = 1.877) as independent risk factors for thrombosis. We confirmed that the above risk factors in IPSET-thrombosis, when compared with traditional risk factors (e.g., age ≥60 and previous thrombotic events), were more predictive of thrombotic events (C-index 0.714 vs. 0.647). Classification by IPSET-thrombosis risk groups revealed different cumulative thrombosis-free survival (P < 0.001). For treatment, patients in the intermediate- and high-risk group derived clinical benefit from cytoreductive agents (P < 0.05), but those in the low-risk group did not (P = 0.446). The lower risk of thrombosis on cytoreductive therapy was related to decrease in leukocyte count during the disease course. CONCLUSIONS: We validate the reproducibility of IPSET-thrombosis in Chinese ET patients and provide key clinical implications.

FOXA1 mediates p16(INK4a) activation during cellular senescence.

Mechanisms governing the transcription of p16(INK4a), one of the master regulators of cellular senescence, have been extensively studied. However, little is known about chromatin dynamics taking place at its promoter and distal enhancer. Here, we report that Forkhead box A1 protein (FOXA1) is significantly upregulated in both replicative and oncogene-induced senescence, and in turn activates transcription of p16(INK4a) through multiple mechanisms. In addition to acting as a classic sequence-specific transcriptional activator, FOXA1 binding leads to a decrease in nucleosome density at the p16(INK4a) promoter in senescent fibroblasts. Moreover, FOXA1, itself a direct target of Polycomb-mediated repression, antagonizes Polycomb function at the p16(INK4a) locus. Finally, a systematic survey of putative FOXA1 binding sites in the p16(INK4a) genomic region revealed an ∼150 kb distal element that could loop back to the promoter and potentiate p16(INK4a) expression. Overall, our findings establish several mechanisms by which FOXA1 controls p16(INK4a) expression during cellular senescence.