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\"Information Fantasies focuses on the cultural practices and media imaginations around information technologies, cybernetics, and systems theory in late 1970s and 1980s China. Xiao Liu explores China's rise to prominence in the global economy through revisiting these earlier 'information fantasies' present in science fiction, modernist writing, films, scientific treatises, historical monographs, and key intellectual debates\"-- Provided by publisher.

Regulatory T cells (Tregs) and plasmacytoid dendritic cells (pDCs) play important roles in the immune escape of cancer. In this study, we investigated pDCs and pDC‐induced inducible costimulator (ICOS)+ Treg populations in peripheral blood from gastric cancer (GC) patients and healthy donors by flow cytometry. The distribution of these cells in carcinoma tissue, peritumor tissue, and normal gastric mucosa was detected by immunohistochemistry. Plasma and tissue concentration of the cytokines such as interleukin‐10 and transforming growth factor‐β1 were also measured. We found that the numbers of pDCs, Tregs, and ICOS+ Tregs in peripheral blood were increased in GC patients compared with healthy donors. In tissue, Tregs and ICOS+ Tregs were found distributing mainly in carcinoma tissue, whereas pDCs were mainly found in peritumor tissue. Moreover, the Foxp3+ICOS+/Foxp3+ cell ratio in carcinoma and peritumor tissue were higher than that in normal tissue. There were more ICOS+ Tregs in tumor and peritumor tissue of late‐stage GC patients. There was a positive correlation between pDCs and ICOS+ Tregs in peripheral blood and peritumor tissue from GC patients. In conclusion, pDCs may play a potential role in recruiting ICOS+ Tregs, and both participate in the immunosuppression microenvironment of GC. We found that numbers of pDCs, Tregs and ICOS+ Tregs in peripheral blood were increased in GC patients compared with healthy donors. In tissue, Tregs and ICOS+ Tregs were found distributing mainly in carcinoma tissue, while pDCs mainly in peritumor tissue. Both pDCs and ICOS+ Tregs participate in the immunosuppression microenviroment of gastric cancer together.

HighlightsRecent progress of active materials in supercapacitors synthesized by electrochemical techniques is reviewed.Electrochemically synthesized nanostructures of various dimensions, compositions, and electrochemical properties are discussed.The advantages and challenges of electrochemical technologies in preparing nano-/microstructured materials for electrochemical energy storage devices are summarized.The article reviews the recent progress of electrochemical techniques on synthesizing nano-/microstructures as supercapacitor electrodes. With a history of more than a century, electrochemical techniques have evolved from metal plating since their inception to versatile synthesis tools for electrochemically active materials of diverse morphologies, compositions, and functions. The review begins with tutorials on the operating mechanisms of five commonly used electrochemical techniques, including cyclic voltammetry, potentiostatic deposition, galvanostatic deposition, pulse deposition, and electrophoretic deposition, followed by thorough surveys of the nano-/microstructured materials synthesized electrochemically. Specifically, representative synthesis mechanisms and the state-of-the-art electrochemical performances of exfoliated graphene, conducting polymers, metal oxides, metal sulfides, and their composites are surveyed. The article concludes with summaries of the unique merits, potential challenges, and associated opportunities of electrochemical synthesis techniques for electrode materials in supercapacitors.

Dysregulated prefrontal control over amygdala is engaged in the pathogenesis of psychiatric diseases including depression and anxiety disorders. Here we show that, in a rodent anxiety model induced by chronic restraint stress (CRS), the dysregulation occurs in basolateral amygdala projection neurons receiving mono-directional inputs from dorsomedial prefrontal cortex (dmPFC→BLA PNs) rather than those reciprocally connected with dmPFC (dmPFC↔BLA PNs). Specifically, CRS shifts the dmPFC-driven excitatory-inhibitory balance towards excitation in the former, but not latter population. Such specificity is preferential to connections made by dmPFC, caused by enhanced presynaptic glutamate release, and highly correlated with the increased anxiety-like behavior in stressed mice. Importantly, low-frequency optogenetic stimulation of dmPFC afferents in BLA normalizes the enhanced prefrontal glutamate release onto dmPFC→BLA PNs and lastingly attenuates CRS-induced increase of anxiety-like behavior. Our findings thus reveal a target cell-based dysregulation of mPFC-to-amygdala transmission for stress-induced anxiety. Dysregulated prefrontal control over amygdala has been implicated in the etiology of stress-related psychiatric disorders. Here, the authors show that the dysregulation preferentially occurs in amygdala neurons that are mono- but not bi-directionally connected with dorsomedial prefrontal cortex.

Aging is an intricate process involving interactions among multiple factors, which is one of the main risks for chronic diseases, including Alzheimer's disease (AD). As a member of cysteine protease, cathepsin S (CTSS) has been implicated in inflammation across various diseases. Here, we investigated the role of neuronal CTSS in aging and AD started by examining CTSS expression in hippocampus neurons of aging mice and identified a significant increase, which was negatively correlated with recognition abilities. Concurrently, we observed an elevation of CTSS concentration in the serum of elderly people. Transcriptome and fluorescence‐activated cell sorting (FACS) results revealed that CTSS overexpression in neurons aggravated brain inflammatory milieu with microglia activation to M1 pro‐inflammatory phenotype, activation of chemokine C‐X3‐C‐motif ligand 1 (CX3CL1)—chemokine C‐X3‐C‐motif receptor 1 (CX3CR1) axis and janus kinase 2 (JAK2)—signal transducer and activator of transcription 3 (STAT3) pathway. As CX3CL1 is secreted by neurons and acts on the CX3CR1 in microglia, our results revealed for the first time the role of neuron CTSS in neuron–microglia “crosstalk.” Besides, we observed elevated CTSS expression in multiple brain regions of AD patients, including the hippocampus. Utilizing CTSS selective inhibitor, LY3000328, rescued AD‐related pathological features in APP/PS1 mice. We further noticed that neuronal CTSS overexpression increased cathepsin B (CTSB) activity, but decreased cathepsin L (CTSL) activity in microglia. Overall, we provide evidence that CTSS can be used as an aging biomarker and plays regulatory roles through modulating neuroinflammation and recognition in aging and AD process. Showing the roles of neuronal CTSS in the process of aging and Alzheimer's disease (AD). As a cysteine protease cathepsin family member, CTSS degrades proteins along the endocytic pathway in young and healthy mice. In aging and AD model mice, the expression level of neuronal CTSS is significantly elevated in neurons, which increases neuroinflammation and causes cognitive decline via CX3CL1‐CX3CR1 axis and JAK2‐STAT3 pathway. LY 3000328, the selective inhibitor of CTSS, LY3000328, significantly rescues AD‐related pathological features in APP/PS1 mice.

We study the Pcs(4459)0 recently observed by LHCb using the method of QCD sum rules. Our results support its interpretation as the D¯∗Ξc hadronic molecular state of either JP=1/2- or 3/2-. Within the hadronic molecular picture, the three LHCb experiments observing Pc and Pcs states (Aaij et al., Phys Rev Lett 115:072001, 2015; Aaij et al., Phys Rev Lett 122:222001, 2019; Aaij et al., arXiv:2012.10380 [hep-ex], 2012) can be well understood as a whole. This strongly supports the existence of hadronic molecules, whose studies can significantly improve our understanding on the construction of the subatomic world. To verify this picture, we propose to further investigate the Pcs(4459)0 to examine whether it can be separated into two states, and to search for the D¯Ξc molecular state of JP=1/2-.

Colorectal cancer (CRC) is among the most common malignant cancers worldwide, and its development is influenced by inflammation, nutrition, and the immune status. Therefore, we combined C-reactive protein (CRP), albumin, and lymphocyte, which could reflect above status, to be the CRP-albumin-lymphocyte (CALLY) index, and evaluated its association with overall survival (OS) in patients with CRC. The clinicopathological and laboratory characteristics of 1260 patients with CRC were collected from the Investigation on Nutrition Status and Clinical Outcome of Common Cancers (INSCOC) study. Cox regression analysis was performed to assess the association between the CALLY index and OS. A nomogram including sex, age, the CALLY index and TNM stage was constructed. The Concordance Index (C-index) was utilized to evaluate the prognostic value of the CALLY index and classical CRC prognostic factors, such as modified Glasgow prognostic score (mGPS), neutrocyte to lymphocyte ratio (NLR), systemic immune inflammation index (SII), and platelet to lymphocyte ratio (PLR), as well as to assess the prognostic value of the nomogram and TNM stage. Multivariate Cox regression analyses demonstrated that the CALLY index was independently associated with OS in patients with CRC [Hazard ratio (HR) = 0.91, 95% confidence interval (CI) = 0.87-0.95, <0.001]. The CALLY index showed the highest prognostic value (C-index = 0.666, 95% CI = 0.638-0.694, <0.001), followed by mGPS, NLR, SII, and PLR. The nomogram demonstrated higher prognostic value (C-index = 0.784, 95% CI = 0.762-0.807, <0.001) than the TNM stage. The CALLY index was independently associated with OS in patients with CRC and showed higher prognostic value than classical CRC prognostic factors. The nomogram could provide more accurate prognostic prediction than TNM stage.

A limited delivery of oxygen and metabolic substrate to the heart caused by myocardial infarction (MI) impairs the cardiac function, and often results in heart failure. Here, we identified a circRNA (circ-SNRK) from SNRK (sucrose nonfermenting 1-related kinase, which can increase the cardiac mitochondrial efficiency) in cardiomyocytes (CMs). Circ-SNRK can sponge the miR-33 and in turn improved the ATP synthesis via SNRK, proving the existence of circ-SNRK - miR-33 - SNRK axis. Furthermore, we found that protein NOVA1 (NOVA alternative splicing regulator 1) could accelerate the circ-SNRK formation; a cleaved peptide (~55 kDa) from SNRK enters the nucleus and blocks the cyclization of circ-SNRK via binding to NOVA1. The aforementioned negative feedback of SNRK to circ-SNRK limited the SNRK at a proper level, and inhibited the protective role of circ-SNRK in ischemic heart. In addition, our in vivo experiment indicated that the overexpression of exogenic circ-SNRK could break this loop and improves the cardiac function post-MI in rats. Together, our results demonstrated that the negative loop of circ-SNRK with SNRK regulates the energy metabolism in CMs, thus might be a potential therapeutic target for heart failure.

Papillary thyroid carcinoma (PTC) represents a malignant epithelial tumor characterized with a preference for younger individuals. Despite its generally favorable prognosis, PTC still poses considerable challenges, particularly in regards to the propensity for distant metastasis. As a key enzyme in the glycolytic pathway, phosphoglycerate kinase 1 (PGK1) has been linked to the progression of various cancer types. However, its role in PTC remains to be elucidated. This study aimed to investigate the association between PGK1 expression in thyroid cancer tissues and clinicopathological features, postoperative recurrence, and prognosis to provide clinical assessment and intervention reference. We investigated the correlation between PGK1 expression and the clinicopathological characteristics, recurrence, and prognosis in 97 PTC patients who underwent surgical treatments between 1 January 2020, and 31 December 2020 in Zhengzhou University First Affiliated Hospital. Besides, we also analysed the correlation of PGK1 expression with the 10-year survival rate of patients with thyroid carcinoma (THCA) in UALCAN database. PGK1 expression was higher in cancerous tissues than that in adjacent non-cancerous tissues. Further analysis of PGK1 expression across clinicopathological characteristics revealed that patients with poorly differentiated tumors, TNM stages III-IV, lymph node metastasis, and tumor diameter ≥1.0 cm exhibited higher PGK1 expression levels in cancerous tissues. A subsequent 3-year postoperative follow-up was conducted to evaluate the correlation between PGK1 expression and recurrence. During this period, 31.96% of patients experienced recurrence, with higher PGK1 expression correlating with increased recurrence rates. Moreover, patients with higher PGK1 expression in cancerous tissue exhibited a significantly lower survival rate of 79.20% compared to the PGK1-low/medium group. Lastly, age, lymph node metastasis, differentiation degree, TNM stage, and tumor diameter were identified as risk factors for poor prognosis in patients with PTC analyzed by Cox regression. Our study demonstrated that PGK1 expression may serve as a potential prognostic biomarker of PTC.

The incorporation of defects, such as vacancies, into functional materials could substantially tailor their intrinsic properties. Progress in vacancy chemistry has enabled advances in many technological applications, but creating new type of vacancies in existing material system remains a big challenge. We show here that ionized nitrogen plasma can break bonds of iron-carbon-nitrogen-nickel units in nickel-iron Prussian blue analogues, forming unconventional carbon-nitrogen vacancies. We study oxygen evolution reaction on the carbon-nitrogen vacancy-mediated Prussian blue analogues, which exhibit a low overpotential of 283 millivolts at 10 milliamperes per square centimeter in alkali, far exceeding that of original Prussian blue analogues and previously reported oxygen evolution catalysts with vacancies. We ascribe this enhancement to the in-situ generated nickel-iron oxy(hydroxide) active layer during oxygen evolution reaction, where the Fe leaching was significantly suppressed by the unconventional carbon-nitrogen vacancies. This work opens up opportunities for producing vacancy defects in nanomaterials for broad applications. Defect-engineering offers a promising route to vary material properties and reactivities, although the achievable defect types are limited. Here, the authors introduced unusual CN-vacancies in Prussian blue analogue pre-catalysts that can limit Fe leaching and improve oxygen evolution performances.