Quartet Superfluid in Two-Dimensional Mass-Imbalanced Fermi Mixtures.

Quartet superfluid (QSF) is a distinct type of fermion superfluidity that exhibits high-order correlation beyond the conventional BCS pairing paradigm. In this Letter, we report the emergent QSF in 2D mass-imbalanced Fermi mixtures with two-body contact interactions. This is facilitated by the formation of a quartet bound state in vacuum that consists of a light atom and three heavy fermions. For an optimized heavy-light number ratio 3:1, we identify QSF as the ground state in a considerable parameter regime of mass imbalance and 2D coupling strength. Its unique high-order correlation can be manifested in the momentum-space crystallization of a pairing field and density distribution of heavy fermions. Our results can be readily detected in Fermi-Fermi mixtures nowadays realized in cold atoms laboratories, and meanwhile shed light on exotic superfluidity in a broad context of mass-imbalanced fermion mixtures.

hIgD-Fc-Ig fusion protein regulates T cell functions by inhibiting TCR signaling pathway in adjuvant arthritis rats.

This study aimed to investigate the effect of hIgD-Fc-Ig on TCR-Lck-Erk activated by IgD in adjuvant arthritis (AA) rats. Wistar rats were divided into the normal, AA model, hIgD-Fc-Ig (1 mg/kg, 3 mg/kg and 9 mg/kg) and Etanercept (3 mg/kg) groups. The overall index of AA rats was measured every 3 days. The pathologic examination of knee joints and the proliferation of the spleen and thymus of AA rats were detected by H&E staining and CCK-8. The blood flow signal of knee joints of experimental rats was examined by US. The articular bone injury was detected by X-ray. The changes in PBMCs and spleen T cell subsets were detected by flow cytometry. The expression of CD3ε, p-Lck, p-Zap70, Ras, and p-Erk in rat spleens was detected by immunofluorescence and WB. Rat spleen T cells or Jurkat cells treated by IgD to observe the effect of hIgD-Fc-Ig on TCR and its downstream protein expression. The results showed that hIgD-Fc-Ig had a therapeutic effect on AA rats by reducing the secondary inflammation, improving pathological changes. hIgD-Fc-Ig can reduce the ratio of Th cells of PBMCs of AA rats, the ratio of Th, Th1, Th17 cells and increase the ratio of Th2, Treg cells of AA rat spleens. hIgD-Fc-Ig could down-regulate the expression of CD3ε, p-Lck, p-Zap70, Ras, p-Erk in vivo or in vitro. In conclusion, hIgD-Fc-Ig could alleviate the symptoms of AA rats and regulate T cells through TCR-Lck-Erk signaling pathway and maybe a new promising biological agent for RA.

BAFF Promotes FLS Activation Through BAFFR-Mediated Non-canonical NF-κB Pathway and the Effects of CP-25.

B cell activating factor (BAFF) has been shown to play a key role in regulating B cell function, but little is known about whether BAFF affects the function of fibroblast-like synoviocyte (FLS), an effector cell of rheumatoid arthritis (RA). CP-25, a new ester derivative of paeoniflorin, could alleviate the arthritis symptoms of collagen-induced arthritis (CIA) mice by inhibiting BAFF-mediated abnormal activation of B cells. In this study, we aimed to understand the mechanism by which BAFF activates FLS and the effect of CP-25 on FLS function. Therefore, the proliferation and migration abilities of FLS and key proteins on the non-canonical NF-κB pathway were examined. The results showed that compared with the FLS of normal rats/OA patients, the expression of BAFF-R, TRAF2, NIK, p-IKKα, P100, and P52 was higher in the FLS of AA rats/RA patients, while the expression of TRAF3 was lower. And, BAFF promotes FLS activation by activating the non-canonical NF-κB signaling pathway. Meanwhile, BAFFR-siRNA inhibited the proliferation of FLS and the activation of non-canonical NF-κB signaling in FLS induced by BAFF. Additionally, CP-25 could inhibit abnormal proliferation and migration of FLS by regulating non-canonical NF-κB signaling. We concluded that BAFF may act as an important role in facilitating the function of FLS through the BAFFR-mediated non-canonical NF-κB pathway, which would be useful for revealing the pathological mechanism of RA. And CP-25 may become a potential new drug for the treatment of RA, providing a scientific basis for the development of new drugs to treat RA.

Universal Tetramer and Pentamer Bound States in Two-Dimensional Fermionic Mixtures.

We study the emergence of universal tetramer and pentamer bound states in the two-dimensional (N+1) system, which consists of N identical heavy fermions interacting with a light atom. We show that the critical heavy-light mass ratio to support a (3+1) tetramer below the trimer threshold is 3.38, and to support a (4+1) pentamer below the tetramer threshold is 5.14. While the ground state tetramer and pentamer are both with zero total angular momentum, they exhibit very different density distributions and correlations in momentum space, due to their distinct angular momentum decompositions in the dimer-fermion frame. These universal bound states can be accessible by a number of Fermi-Fermi mixtures now realized in cold atoms laboratories, which also suggest novel few-body correlations dominant in their corresponding many-body systems.

Advance in bone destruction participated by JAK/STAT in rheumatoid arthritis and therapeutic effect of JAK/STAT inhibitors.

Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic joint inflammation and bone erosion. The bones in the human body are constantly undergoing bone remodeling throughout their lives, which is the process of bone resorption by osteoclasts to damaged bone tissue and new bone formation by osteoblasts. Osteoblasts (OBs) are the main functional cells in bone formation, responsible for the synthesis, secretion and mineralization of the bone matrix. On the contrary, osteoclasts (OCs) mediate bone breakdown during natural bone turnover, but excessive breakdown occurs in RA. Under the condition of RA inflammation, many molecules, such as IL-1ß, IL-6, TNF-α, IL-17 and hypoxia-inducible factor-1α (HIF-1α) are produced that could mediate bone loss. Studies have shown that cytokines mainly promote the formation of OCs and play a role in bone resorption by stimulating OBs to express receptor activator of NF-κB ligand (RANKL). JAK/STAT plays a crucial role in the process of bone destruction. And JAK/STAT pathway mediates the RANKL/receptor activator of NF-κB (RANK)/osteoprotegerin (OPG) axis. Tofacitinib, Baricitinib, Peficitinib and Filgotinib are now being used in patients with moderate to severe RA, as well as in patients with RA who have an inadequate response to methotrexate therapy and bone destruction. Currently, Tofacitiniband Baritinib areapprovedfor thetreatmentof moderate-to-severely active RA. JAK inhibitors have been reported to have better efficacy and lower adverse effects compared with methotrexate and adalimumab. In addition, two JAK inhibitors are currently in development: the JAK1 selective Upadacitinib, and the JAK3 selective inhibitor Decernotinib. In addition to the above JAK inhibitors, some small molecular compounds inhibit bone destruction by inhibiting the Phosphorylation of STAT3. In this paper, the research progress of bone destruction participated by JAK/ STAT in rheumatoid arthritis and therapeutic effect of JAK/STAT inhibitors were reviewed.

The ROS/GRK2/HIF-1α/NLRP3 Pathway Mediates Pyroptosis of Fibroblast-Like Synoviocytes and the Regulation of Monomer Derivatives of Paeoniflorin.

Hypoxia is an important factor in the development of synovitis in rheumatoid arthritis (RA). The previous study of the research group found that monomeric derivatives of paeoniflorin (MDP) can alleviate joint inflammation in adjuvant-induced arthritis (AA) rats by inhibiting macrophage pyroptosis. This study revealed increased levels of hypoxia-inducible factor- (HIF-) 1α and N-terminal p30 fragment of GSDMD (GSDMD-N) in fibroblast-like synoviocytes (FLS) of RA patients and AA rats, while MDP significantly inhibited their expression. Subsequently, FLS were exposed to a hypoxic environment or treated with cobalt ion in vitro. Western blot and immunofluorescence analysis showed increased expression of G protein-coupled receptor kinase 2 (GRK2), HIF-1α, nucleotide-binding oligomerization segment-like receptor family 3 (NLRP3), ASC, caspase-1, cleaved-caspase-1, and GSDMD-N. Electron microscopy revealed FLS pyroptosis after exposure in hypoxia. Next, corresponding shRNAs were transferred into FLS to knock down hypoxia-inducible factor- (HIF-) 1α, and in turn, NLRP3 and western blot results confirmed the same. The enhanced level of GSDMD was reversed under hypoxia by inhibiting NLRP3 expression. Knockdown and overexpression of GRK2 in FLS revealed GRK2 to be a positive regulator of HIF-1α. Levels of GRK2 and HIF-1α were inhibited by eliminating excess reactive oxygen species (ROS). Furthermore, MDP reduced FLS pyroptosis through targeted inhibition of GRK2 phosphorylation. According to these findings, hypoxia induces FLS pyroptosis through the ROS/GRK2/HIF-1α/NLRP3 pathway, while MDP regulates this pathway to reduce FLS pyroptosis.

IgD promotes pannus formation by activating Wnt5A-Fzd5-CTHRC1-NF-κB signaling pathway in FLS of CIA rats and the regulation of IgD-Fc-Ig fusion protein.

Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by joint inflammation, synovial hyperplasia, cartilage degeneration, bone erosion, and pannus. Immunoglobulin D (IgD) plays an important role in autoimmune diseases although the content of it in vivo is low. Increased concentrations of anti-IgD autoantibodies have been detected in many RA patients. IgD-Fc-Ig fusion protein is constructed by connecting human IgD Fc domain and IgG1 Fc domain, which specifically block the IgD/ IgDR pathway and regulate the function of cells expressing IgDR to treat RA. The expression levels of Wnt5A and Frizzled 5 are higher in RA synovial tissue specimens. The complex of Wnt5A-Fzd5-LRP5/6-CTHRC1 promotes the expression of hypoxia inducible factor-1α by activating nuclear factor kappa-B (NF-κB), leading to high expression of VEGF and participating in angiogenesis. VEGF is the strongest angiogenic factor found so far. Here, we aimed to explore whether IgD participates in synovitis by binding to IgDR and regulating the activation of Wnt5A-Fzd5-CTHRC1-NF-κB signaling pathway in fibroblast synovial cells (FLSs), whether IgD-Fc-Ig fusion protein inhibits VEGF production in FLS of CIA and explore mechanism. We found that IgDR is expressed on MH7A and FLS. IgD promotes VEGF expression by activating Wnt5A-Fzd5-CTHRC1-NF-κB signaling pathway in MH7A and FLS. After activation of Fzd5 with Wnt5A, IgD-Fc-Ig reduced VEGF-A level in the culture supernatant of MH7A stimulation by IgD. The expressions of CTHRC1, Fzd5, p-P65 and VEGF in MH7A and FLSs were down-regulated after IgD-Fc-Ig treatment. IgD-Fc-Ig suppressed the combination of CTHRC1 and Fzd5 as well. By using the animal model, we demonstrated that IgD-Fc-Ig suppress ankle CTHRC1 and Fzd5 production resulted in inhibition of index of joint inflammation of CIA rats, which were consistent with vitro results. Conclusively, IgD-Fc-Ig inhibits IgD and Wnt5A-induced angiogenesis and joint inflammation by suppressing the combination of CTHRC1 and Fzd5. Our results show that IgD-Fc-Ig exerts its suppressive effect on IgD and Wnt5A by Wnt5A-Fzd5-CTHRC1-NF-κB signaling pathway.

Lactate up-regulates the expression of PD-L1 in kidney and causes immunosuppression in septic Acute Renal Injury.

BACKGROUND: This study aims to explore the mechanism of immunosuppression in septic Acute Renal Injury (AKI) and the role of programmed death-1 (PD-1/PD-L1) pathway in septic AKI. METHODS: This study established a septic AKI model by Cecal ligation and puncture (CLP) in C57/B6 mice, ELISA was used to test the level of lactate and creatinine in serum, blood was collected for flow cytometry and kidney samples for Western blot analyses. This study further analyzed the expression of PD-L1 in kidney and the expression of PD-1 in CD4+, CD8+ T cell, and the number of CD3+ T cells to identify apoptosis in T cells in the blood. RESULTS: The CLP sepsis model induced AKI in C57/B6 mice; The expression of PD-1 and PD-L1 were increased in septic AKI mice; PD-1/PD-L1 induced apoptosis in T cells: the number of lymphocytes decreased by 64%, while the number of CD3+ T cells decreased by 27% compared with the sham group; Results also indicated that lactate up-regulates expression of PD-L1 in the kidney. CONCLUSIONS: Lactate activated PD-1/PD-L1 pathway can induce immunosuppression by inducing apoptosis in lymphocytes in septic AKI. Moreover, blocking the receptor of lactate or PD-1/PD-L1 might be a new therapy for septic AKI.

Mechanisms of Renal-Splenic Axis Involvement in Acute Kidney Injury Mediated by the α7nAChR-NF-κB Signaling Pathway.

This study aimed to investigate the effect of splenectomy on dexmedetomidine-activated cholinergic anti-inflammatory pathway-mediated alleviation of LPS-induced AKI. A mouse model of septic kidney injury was established in C57BL/6 mice. A total of 30 C57BL/6 mice were randomly divided into the control group, LPS group, dexmedetomidine + LPS group, splenectomy group, splenectomy + LPS group, and splenectomy + dexmedetomidine + LPS group. The pathological effects in kidney tissues in each group were analyzed by HE staining. Apoptosis in each group was examined by the TUNEL method. Cr and Cys-C levels in each group were measured by ELISA. The expression levels of IL-6, NF-κB p65, Caspase-3, the antiapoptotic protein Bcl-2, the proapoptotic protein Bax, and α7nAChR in each group were measured by qRT-PCR and Western blotting. Dexmedetomidine alone reduced apoptosis in kidney tissue; however, apoptosis was increased after splenectomy in mice treated with dexmedetomidine. Splenectomy reduced the production of proinflammatory cytokines in circulation and had a protective effect on the kidney. Splenectomy inhibited dexmedetomidine-mediated activation of the α7nAChR pathway. Dexmedetomidine effectively alleviated LPS-induced kidney injury, and splenectomy inhibited the anti-inflammatory, antiapoptotic, and renoprotective effects of dexmedetomidine. The kidney-spleen axis is mediated by the α7nAChR-NF-κB signaling pathway and is involved in the development of AKI.

Effect of initiation of renal replacement therapy on mortality in acute pancreatitis patients.

This study aims to explore effect of initiation of renal replacement therapy (RRT) on mortality in acute pancreatitis (AP) patients. In this study, a total of 92 patients from the surgical intensive care unit (SICU) of the Second Affiliated Hospital of Harbin Medical University who were diagnosed with AP and underwent RRT or not between January 2014 and December 2018 were included in this retrospective study. Demographic and clinical data were obtained on admission to SICU. Patients were divided into early initiation of RRT group (n = 44) and delayed initiation of RRT group (n = 48). Duration of mechanical ventilation (MV), intra-peritoneal pressure, vasopressors infusion, body temperature, procalcitonin, creatinine, platelet counts, length of hospital stay and prognosis were recorded during hospitalization, and then compared between groups. Patients with delayed initiation of RRT exhibited significantly higher APACHE II score, SOFA score and lower GCS score than those with early initiation of RRT (P < 0.001, <0.001,  = 0.04, respectively). No difference in the rest of the baseline data and vasopressors infusion was found. Dose of Norepinephrine, maximum and mean PCT, maximum and mean creatinine, maximum and mean intra-peritoneal pressure, length of hospital stay, prognosis of ICU and hospitalization showed significant difference between groups. Early initiation of RRT may be beneficial for AP patients, which can provide some insight and support for patients' treatment in clinic.

Erratum to "An Inhibitor of DRP1 (Mdivi-1) Alleviates LPS-Induced Septic AKI by Inhibiting NLRP3 Inflammasome Activation".

[This corrects the article DOI: 10.1155/2020/2398420.].

An Inhibitor of DRP1 (Mdivi-1) Alleviates LPS-Induced Septic AKI by Inhibiting NLRP3 Inflammasome Activation.

Mitochondria play an essential role in energy metabolism. Oxygen deprivation can poison cells and generate a chain reaction due to the free radical release. In patients with sepsis, the kidneys tend to be the organ primarily affected and the proximal renal tubules are highly susceptible to energy metabolism imbalances. Dynamin-related protein 1 (DRP1) is an essential regulator of mitochondrial fission. Few studies have confirmed the role and mechanism of DRP1 in acute kidney injury (AKI) caused by sepsis. We established animal and cell sepsis-induced AKI (S-AKI) models to keep DRP1 expression high. We found that Mdivi-1, a DRP1 inhibitor, can reduce the activation of the NOD-like receptor pyrin domain-3 (NLRP3) inflammasome-mediated pyroptosis pathway and improve mitochondrial function. Both S-AKI models showed that Mdivi-1 was able to prevent the mitochondrial content release and decrease the expression of NLRP3 inflammasome-related proteins. In addition, silencing NLRP3 gene expression further emphasized the pyroptosis importance in S-AKI occurrence. Our results indicate that the possible mechanism of action of Mdivi-1 is to inhibit mitochondrial fission and protect mitochondrial function, thereby reducing pyroptosis. These data can provide a potential theoretical basis for Mdivi-1 potential use in the S-AKI prevention.

Uncoupling Protein 2 Drives Myocardial Dysfunction in Murine Models of Septic Shock.

Cardiac dysfunction is a major component of sepsis-induced multiorgan failure in critical care units. Uncoupling protein 2 (UCP2) involves immune response, regulation of oxidative stress, and maintenance of mitochondrial membrane potential as well as energy production. However, whether and how UCP2 plays roles in the development of septic cardiac dysfunction are largely unknown. Here, intraperitoneal injection of LPS significantly activated UCP2 expression accompanied by a significant decrease of cardiac function and caused a significantly lower survival rate in mice. Of note, knockdown of UCP2 through a cardiotropic adenoassociated viral vector carrying a short hairpin RNA (shRNA) specifically targeting the UCP2 evoked resistance to LPS-triggered septic cardiac dysfunction and lethality in vivo. Moreover, UCP2 deficiency ameliorated the reduced levels of intracellular ATP in the LPS-challenged heart tissues and preserved mitochondrial membrane potential loss in primary adult mouse cardiomyocytes in LPS-challenged animals. Mechanistically, we confirmed that the inhibition of UCP2 promoted autophagy in response to LPS, as shown by an increase in LC3II and a decrease in p62. At last, the autophagy inhibitor 3-MA abolished UCP2 knockdown-afforded cardioprotective effects. Those results indicate that UCP2 drives septic cardiac dysfunction and that the targeted induction of UCP2-mediated autophagy may have important therapeutic potential.

Effect of splenectomy on attenuation of LPS-induced AKI through GTS-21-induced cholinergic anti-inflammatory pathway.

This work was undertaken to explore the role of splenectomy on attenuation of lipopolysaccharide (LPS)-induced acute kidney injury (AKI) through GTS-21-induced cholinergic anti-inflammatory pathway. C57BL/6 mice were used to construct models of sepsis-induced renal injury. HE, Tunel and blood assays were used to determine the success of the model. The animals were examined after splenectomy with or without LPS and GTS-21+LPS treatments. The pathological changes and apoptosis in the renal tissue were detected using HE and Tunel assays. The contents of creatinine (Cr) and cystatin-C (Cys-C) were measured using ELISA. The expression of IL-6, NF-kB p65, Caspase-3, anti-apoptotic protein Bcl-2, apoptotic protein Bax and α7nAChR was quantified using qRT-PCR. The expression of Bcl-2, Bax, Caspase-3, IL-6, NF-kB p65, α7nAChR and p-STAT3 was using assessed using Western blot analysis. HE, Tunel, BUN and serum creatinine (SC) assay showed that renal injury models were successfully established. Compared with the control, the apoptosis in the LPS group was significantly increased and decreased after GTS-21 treatment. However, splenectomy combined with GTS-21 increased the apoptosis, indicating that splenectomy could partially offset the anti-apoptosis effect of GTS-21. In animals treated with LPS, the contents of Cr and Cys-C increased significantly. These contents reduced following GTS-21 treatment, but increased after splenectomy. After LPS treatment, the expression of IL-6, NF-kB p65, p-STAT3, Caspase-3 and Bax was significantly up-regulated, while the expression of α7nAChR and Bcl-2 significantly down-regulated. Compared with LPS treated mice, splenectomy reduced the expression of IL-6, NF-kB p65 and p-STAT3, suggesting that splenectomy inhibits the activation of α7nAChR pathway by the GTS-21. It is clear that GTS-21 effectively attenuates LPS-induced renal injury; splenectomy suppresses the anti-inflammatory and anti-apoptosis activity and renal protective effect of GTS-21. On other hand, splenectomy reduces the production of inflammatory cytokines in the circulation, and has certain protective effect on the kidney. Therefore, the impact of splenectomy on LPS-induced AKI depends on the strength of the two aspects.

Risk factors for outcomes of acute respiratory distress syndrome patients: a retrospective study.

BACKGROUND: The determination of risk factors for acute respiratory distress syndrome (ARDS) patients remains a challenge. Our study aims to explore the epidemiology and risk factors affecting outcomes of ARDS patients and provide a theoretical basis for patients' prognosis. METHODS: This retrospective study included 207 ARDS patients admitted to the general intensive care unit (ICU) in the Second Affiliated Hospital of Harbin Medical University from Jan 1st, 2016 to Jan 1st, 2017. The criteria were defined according to the Berlin Definition, and clinical data were collected from the medical record system. The mortality rate and duration of mechanical ventilation were compared in ARDS patients. Furthermore, logistic regression analysis was applied to screen clinically accessible risk factors for survival and duration of mechanical ventilation. RESULTS: The total mortality in ARDS patients was 39.13% (81/207) compared to 13.57% (151/1,113) in the whole ICU population. The period prevalence of mild, moderate and severe ARDS was 39.61% (82/207), 37.20% (77/207) and 23.19% (48/207), respectively. Logistic regression analysis showed that acute physiology and chronic health evaluation II (APACHE II) score (OR 3.4316; 95% CI: 1.3130-8.9686; P=0.0119), number of organ failure (OR 3.4928; 95% CI: 1.9775-6.1693; P<0.0001), mean arterial pressure (MAP) (OR 5.1049; 95% CI: 1.8317-14.2274; P=0.0018), driving pressure (OR 6.0017; 95% CI: 2.1746-16.5641; P=0.0005) and lactate level (OR 4.0754; 95% CI: 1.6114-10.3068; P=0.0030) were influence factors for survival; severity of ARDS (OR 1.6715; 95% CI: 1.0307-2.7108; P=0.0373), ventilator-associated pneumonia (VAP) (OR 7.3746; 95% CI: 2.9799-18.2505; P<0.0001) and transfusion history (OR 2.2822; 95% CI: 1.0462-4.9783; P=0.0381) were influence factors for duration of mechanical ventilation. CONCLUSIONS: Higher APACHE II score, more organ failures, lower MAP, higher driving pressure and higher lactate level are risk factors for survival. Higher severity of ARDS, VAP and transfusion history are risk factors for prolonged duration of mechanical ventilation. Application of these parameters would enable intensivists to treat their patients more precisely and comprehensively.

A multi-center cross-sectional study on blood purification among adult patients in intensive care unit in China: a study protocol.

BACKGROUND: Blood purification (BP) is one of the most important rescue measures for patients with critical illness in the intensive care unit (ICU), especially for those with acute kidney injury. The purpose of this nationwide survey was to reveal the real world of current BP practice in different ICUs all over China. This study was designed to be a multi-center cross-sectional study. METHODS: All adult patients (over 18 years of age), who were admitted to ICU and required BP in 35 sub-centers across China were included during 30-day survey period in 2018. Demographic characteristics and clinical data were recorded including the timing of treatment initiation, indications, modality, relative contraindication, establishment of vascular access, selection of filter/membrane, settings, anti-coagulation, executive department, complication, intake, and output. DISCUSSION: This nationwide survey may contribute to reveal the real world of current BP practice in different ICUs all over China. TRIAL REGISTRATION: Chinese Clinical Trial Registry, ChiCTR-EOC-17013119; http://www.chictr.org.cn/showproj.aspx?proj=22487.

Flat-band ferromagnetism of SU(N) Hubbard model on Tasaki lattices.

We investigate the para-ferro magnetic transition of the repulsive SU(N) Hubbard model on a type of one- and two-dimensional decorated cubic lattices, referred as Tasaki lattices, which feature massive single-particle ground state degeneracy. Under certain restrictions for constructing localized many-particle ground states of flat-band ferromagnetism, the quantum model of strongly correlated electrons is mapped to a classical statistical geometric site-percolation problem, where the nontrivial weights of different configurations must be considered. We prove rigorously the existence of para-ferro transition for the SU(N) Hubbard model on one-dimensional Tasaki lattice and determine the critical density by the transfer-matrix method. In two dimensions, we numerically investigate the phase transition of SU(3), SU(4) and SU(10) Hubbard models by Metropolis Monte Carlo simulation. We find that the critical density exceeds that of standard percolation, and increases with spin degrees of freedom, implying that the effective repulsive interaction becomes stronger for larger N. We further rigorously prove the existence of flat-band ferromagnetism of the SU(N) Hubbard model when the number of particles equals to the degeneracy of the lowest band in the single-particle energy spectrum.

Dexmedetomidine protects against lipopolysaccharide-induced sepsis-associated acute kidney injury via an α7 nAChR-dependent pathway.

Acute kidney injury (AKI) is a clinical syndrome that results in severe tubular damage with high morbidity and mortality. However, there is a lack of effective therapy strategies. Therefore, it is critical to develop effective drugs for AKI. Dexmedetomidine (DEX), a highly selective α2-adrenoreceptor agonist, has neuroprotective, anti-inflammatory and sympatholytic properties. The present study aimed to investigate the effect DEX on attenuating the inflammatory reaction and apoptosis in the kidney tissues of septic mice and to explore its underlying mechanisms. Sepsis-induced AKI mice models were generated via intraperitoneal injection of lipopolysaccaride (LPS). DEX reduced LPS-induced local inflammation and tubular apoptosis, which was aggravated in the pathogenesis of renal dysfunction. Reverse transcription-quantitative polymerase chain reaction and western blot analysis results revealed that the expression of pro-apoptotic genes and inflammatory factors were markedly reduced by DEX pretreatment. Furthermore, the protective role of DEX was markedly inhibited by the α7 nicotinic acetylcholine receptor (nAChR) antagonist α-bungarotoxin. These findings provided novel evidence for the anti-apoptotic and anti-inflammatory effects of DEX in LPS-induced AKI mice through an α7 nAChR-dependent signaling pathway.

Cross-sectional survey on adult acute kidney injury in Chinese ICU: the study protocol (CARE-AKI).

INTRODUCTION: Acute kidney injury (AKI) is one of the most serious syndromes in intensive care unit (ICU) patients, and is a mysterious problem in clinical practice worldwide. Due to unknown aetiology and mechanism, awareness of AKI diagnosis and treatment in China varies, resulting in underestimated incidence and poor prognosis. To solve this problem, we design this national survey of AKI in adult ICUs. Various indexes are included and analysed to classify the epidemiology of adult AKI in Chinese ICUs, including AKI aetiology, risk factors, mortality, prognosis, therapeutic strategies and cognition of ICU medical staff. METHODS: A multicentre, cross-sectional survey, which will involve about 35 hospitals and 6147 patients from 23 provinces, 4 municipalities and 5 autonomous regions, is planned. All patients who meet the inclusion criteria are eligible to apply for enrolment in the study, which cover baseline demographics, clinical performance, and follow-up related to diagnosis and treatment. CONCLUSION: The study is expected to fill the gap between China and developed countries, and to provide a theoretical foundation for developing more scientific and standardised approaches to AKI diagnosis and treatment. ETHICS AND DISSEMINATION: Ethical approval was obtained from the ethics committee of Harbin Medical University Cancer Hospital (registration number KY2017-21). The findings of this review will be communicated through peer-reviewed publications and scientific presentations. TRIAL REGISTRATION NUMBER: ChiCTR-EOC-17013133; Pre-results.