The development of the biological soil crust regulates the fungal distribution and the stability of fungal networks.

The heterogeneous composition of fungi plays an indispensable role in the foundation of the multifunctionalities of ecosystems within drylands. The precise mechanisms that govern fluctuations in soil fungal assemblages in dryland ecosystems remain incompletely elucidated. In this study, biological soil crusts (biocrusts) at different successional stages in the Gurbantunggut Desert were used as substrates to examine the characteristics and driving factors that influence fungal abundance and community dynamics during biocrust development using qPCR and high-throughput sequencing of the ITS2 region. The findings showed that the physicochemical properties changed significantly with the development of biocrusts. In particular, total nitrogen increased 4.8 times, along with notable increases in ammonium, total phosphorus (2.1 times) and soil organic carbon (6.5 times). Initially, there was a rise in fungal abundance, which was subsequently followed by a decline as the biocrust developed, with the highest abundance detected in lichen crust (2.66 × 107 copies/g soil) and the lowest in bare sand (7.98 × 106 copies/g soil). Ascomycetes and Basidiomycetes emerged as dominant phyla, collectively forming 85% of the fungal community. As the biocrust developed, noticeable alterations occurred in fungal community compositions, resulting from changes in the relative proportions of Dothideomycetes, Lecanoromycetes and unclassified ascomycetes. Nitrogen, phosphorus, organic carbon content, and pH of biocrusts were identified as direct or indirect regulators of fungal abundance and community structure. The complexity of fungal networks increased as biocrusts developed as revealed by network analysis, but reduced in the stability of fungal communities within algal and lichen crusts. Keystone species within the fungal community also underwent changes as biocrust developed. These results suggested that shifts in interspecies relationships among fungi could further contribute to the variation in fungal communities during the development of biocrusts.

Effects of TNF-α on Behaviour and Inflammation in Rats with Rotator Cuff Injury through NGF.

OBJECTIVE: Rotator cuff injury is a common injury that includes inflammation, partial tearing, or complete tearing of the rotator cuff tendon. In cases of rotator cuff tears (RCTs), Tumor Necrosis Factor-alpha (TNF-α) can trigger the release of nerve growth factor (NGF). TNF-α is an important inflammatory mediator that affects rotator cuff activity and increased NGF expression is observed in RCTs. Therefore, this study aimed to investigate whether inhibition of TNF-α could reduce behavioural responses and inflammation levels in rats through NGF. METHODS: A rat RCT model was established, and the CatWalk gait analysis system was used for behavioural assessment. Immunohistochemistry was used to detect NGF protein levels in tendon tissue. Hematoxylin eosin (HE) staining was used to observe histopathological changes. The expressions of Interleukin-1beta (IL-1ß) and Cyclooxygenase-2 (COX2) were detected by western blotting (WB) and quantitative real-time polymerase chain reaction (qRT-PCR). The expression of apoptosis protein Bcl-2-associated X (Bax), B-cell lymphoma 2 (Bcl-2), and Cysteine-aspartic acid protease-3 (Caspase-3) were detected using WB. Oxidative stress markers, namely Reactive Oxygen Species (ROS), Malondialdehyde (MDA), and Superoxide Dismutase (SOD) were quantified in tissues using an ELISA kit. RESULTS: In the RCT model, elevated NGF protein expression, noticeable atrophy in the supraspinatus muscle tissue, and substantial fat infiltration were observed. The levels of IL-1ß, COX2, apoptosis, and oxidative stress were all increased. TNF-α inhibition resulted in decreased NFG expression, decreased tissue fibrosis, and improved tendon atrophy. Moreover, when TNF-α was inhibited, the expressions of IL-1ß and Cox2 were reduced and both apoptosis and oxidative stress were decreased. The results showed that inhibiting TNF-α had the potential to reduce inflammation levels and behavioural responses in rats. CONCLUSION: TNF-α can affect behaviour and inflammation in rats with RCTs through NGF, and TNF-α inhibition can improve rotator cuff injury.

Managing Post-Stroke Fatigue Using a Mobile Health Called iHealth After Intracerebral Hemorrhage.

Background: Post-stroke Fatigue (PSF) after Intracerebral Hemorrhage (ICH) is a long-term symptom in stroke survivors. However, the pathogenesis of PSF remains inadequately understood and sufficient evidence-based treatments are lacking. Mobile health (mHealth) technology offers a promising approach to expanding access to high-quality and culturally tailored evidence-based mental care. Aim: This study examined the role of mHealth called iHealth in the management of PSF after ICH. Methods: A total of 225 patients diagnosed with intracerebral hemorrhage (ICH) were included in the study and randomly assigned to either the Mobile Health Intervention Group (mHI Group) or the non-Mobile Health Intervention Group (non-mHI). The management involved the utilization of a digital healthcare application named iHealth, which incorporated digital questionnaires, fatigue scale tests, and online videos for the purpose of administering the Patient Fatigue Reporting Measurement Information System (PFRMIS) short form as part of the initial patient assessment following ICH. The study was conducted remotely via video conferencing over a 12-week period in mHI Group, with fatigue assessments being conducted 3 months post-ICH onset in two groups. Results: Following the administration of PSF by iHealth, Univariate Logistic analyses indicated a significant association between fatigue and the type of activity, with patients who were sedentary or did nothing experiencing higher levels of fatigue (ß=2.332, p<0.001; ß=2.517, p<0.001). Multivariate Logistic analyses demonstrated a positive association between the intensity of physical activity and decreased emotional well-being and family support, as well as increased fatigue. (p=0.001, p=0.002, p=0.001). The FSS results demonstrated a significantly reduced incidence of PSF in the MHI group in comparison to non-mHI group following the conclusion of the programme. (13.1% vs 40%, p<0.001). Conclusion: This study explored the effectiveness of the iHealth app for PSF following ICH, indicating that iHealth is a clinically valuable tool that warrants further dissemination.

Hypoxia-Challenged Pancreatic Adenocarcinoma Cell-Derived Exosomal circR3HCC1L Drives Tumor Growth Via Upregulating PKM2 Through Sequestering miR-873-5p.

Pancreatic adenocarcinoma (PAAD) is a fatal disease with poor survival. Increasing evidence show that hypoxia-induced exosomes are associated with cancer progression. Here, we aimed to investigate the function of hsa_circ_0007678 (circR3HCC1L) and hypoxic PAAD cell-derived exosomal circR3HCC1L in PAAD progression. Through the exoRBase 2.0 database, we screened for a circular RNA circR3HCC1L related to PAAD. Changes of circR3HCC1L in PAAD samples and cells were analyzed with real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferation, migration, invasion were analyzed by colony formation, cell counting, and transwell assays. Measurements of glucose uptake and lactate production were done using corresponding kits. Several protein levels were detected by western blotting. The regulation mechanism of circR3HCC1L was verified by dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays. Exosomes were separated by differential ultracentrifugation. Animal experiments were used to verify the function of hypoxia-derived exosomal circR3HCC1L. CircR3HCC1L was upregulated in PAAD samples and hypoxic PAAD cells. Knockdown of circR3HCC1L decreased hypoxia-driven PAAD cell proliferation, migration, invasion, and glycolysis. Hypoxic PAAD cell-derived exosomes had higher levels of circR3HCC1L, hypoxic PAAD cell-derived exosomal circR3HCC1L promoted normoxic cancer cell malignant transformation and glycolysis in vitro and xenograft tumor growth in mouse models in vivo. Mechanistically, circR3HCC1L regulated pyruvate kinase M2 (PKM2) expression via sponging miR-873-5p. Also, PKM2 overexpression or miR-873-5p silencing offset circR3HCC1L knockdown-mediated effects on hypoxia-challenged PAAD cell malignant transformation and glycolysis. Hypoxic PAAD cell-derived exosomal circR3HCC1L facilitated PAAD progression through the miR-873-5p/PKM2 axis, highlighting the contribution of hypoxic PAAD cell-derived exosomal circR3HCC1L in PAAD.

Investigation and analysis of magnetic resonance imaging experience and psychological status of patients.

OBJECTIVE: To analyze factors influencing the service experience of magnetic resonance imaging (MRI) examination and psychological status of patients admitted to a hospital and propose targeted solutions, and optimize the examination process and nursing by analyzing the MRI examination experience and psychological effect on patients. METHODS: The MRI examination rooms of two tertiary general hospitals in Haikou City were sampled at random, and 206 patients who met the study criteria were surveyed on site. RESULTS: (1) The item with the lowest mean score for patient examination services was whether earplugs were provided to the patient during the examination (B8 = 0.47). (2) Environmental logistics experience (16.83 ± 3.036) received the lowest score among the three service experience dimensions. (3) The average anxiety score of the patients was 5.38. (4) There was a positive correlation between the examination experience and the examination service experience of the patients. (5) Patients with higher monthly income had decreased anxiety (coefficient = -2.334), and MRI examination of the extremities relieved the anxiety (coefficient = -4.782). CONCLUSION: The environmental logistics factors, poor service attitude, examination site, and income were the most significant factors affecting the MRI examination experience and psychological status of patients, which can be improved by providing information, enhancing the waiting environment, providing targeted patient education, and evaluating the experience immediately.

A Case Report of Concurrent Transplant Renal Artery Stenosis, Renal Cell Carcinoma, and Papillary Thyroid Cancer After Renal Transplantation: A Literature Review.

BACKGROUND: Kidney transplantation is the preferred treatment option for eligible patients with end-stage renal disease. With advanced transplantation technology and novel immunosuppressive agents, kidney transplant recipients survive significantly longer. However, the chance of developing malignant tumors has increased, posing a serious challenge to the survival of transplanted kidneys and patients. CASE PRESENTATION: We report a male patient (the patient's informed consent has been obtained) who underwent kidney transplantation 23 years ago. Subsequently, he developed transplant renal artery stenosis, primary renal clear cell carcinoma, and papillary thyroid cancer. The narrowed blood vessels were dilated through percutaneous transluminal angioplasty, and the malignant tumor was removed surgically. Currently, antirejection drugs are regularly taken, and the transplanted kidney function is good. The patient is satisfied with his living conditions. CONCLUSIONS: Hypertension that is difficult to control after kidney transplantation should be suspected as a possibility of graft vascular stenosis. When B-ultrasound cannot accurately diagnose it, magnetic resonance angiography should be used as early as possible to clarify the diagnosis and relieve the stenosis before graft dysfunction. Transplantation patients have a high incidence of malignant tumors after surgery, and the risk increases with the prolongation of the disease course. The focus should be on symptomatic treatment of related diseases, and antirejection drugs can be reduced or not reduced as appropriate.

Imaging, pathology, and diagnosis of solitary fibrous tumor of the pancreas: A case report and review of literature.

BACKGROUND: A solitary fibrous tumor (SFT) is often located in the pleura, while SFT of the pancreas is extremely rare. Here, we report a case of SFT of the pancreas and discuss imaging, histopathology, and immunohistochemistry for accurate diagnosis and treatment. CASE SUMMARY: A 54-year-old man presented to our hospital with pancreatic occupancy for over a month. There were no previous complaints of discomfort. His blood pressure was normal. Blood glucose, tumor markers, and enhanced computed tomography (CT) suggested a malignant tumor. Because the CT appearance of pancreatic cancer varies, we could not confirm the diagnosis; therefore, we performed endoscopic ultrasound-guided fine-needle biopsy (EUS-FNB). Pathology and immunohistochemistry were consistent with SFT of the pancreas. The postoperative pathology and immunohistochemistry were consistent with the puncture results. The patient presented for a follow-up examination one month after discharge with no adverse effects. CONCLUSION: Other diseases must be excluded in patients with a pancreatic mass that cannot be diagnosed. CT and pathological histology have diagnostic value for pancreatic tumors. Endoscopic puncture biopsy under ultrasound can help diagnose pancreatic masses that cannot be diagnosed preoperatively. Surgery is an effective treatment for SFT of the pancreas; however, long-term follow-up is strongly recommended because of the possibility of malignant transformation of the tumor.

EGFR mediates epithelial­mesenchymal transition through the Akt/GSK-3ß/Snail signaling pathway to promote liver cancer proliferation and migration.

Epidermal growth factor receptor (EGFR) is expressed in various types of cancer and is associated with the malignant biological behavior of cancer cells. In the present study, the expression of EGFR in hepatocellular carcinoma (HCC) tissues and liver cancer cells was detected by immunohistochemical staining, western blotting and immunofluorescence. Furthermore, a lentivirus was transduced into HepG2 liver cancer cells to knock down EGFR expression. Cell proliferation and migration, and the expression levels of epithelial-mesenchymal transition (EMT) markers were assessed by EdU staining, Cell Counting Kit-8, colony formation, wound healing and Transwell assays, and western blotting. The results revealed that EGF/EGFR can mediate EMT through the Akt/glycogen synthase kinase-3ß (GSK-3ß)/Snail signaling pathway to promote HepG2 cell proliferation and migration. Inhibition of the activation of the EGFR signaling pathway can help to partially reverse the EMT phenotype, and inhibit the proliferation and migration of HepG2 cells. In conclusion, the EGFR/Akt/GSK-3ß/Snail signaling pathway serves an important role in HCC progression, and inhibition of the activation of the EGFR signaling pathway may be a valuable strategy in liver cancer treatment.

Muc2 mucin O-glycosylation interacts with enteropathogenic Escherichia coli to influence the development of ulcerative colitis based on the NF-kB signaling pathway.

BACKGROUND: Ulcerative colitis (UC) is a chronic inflammatory disease of the intestine characterized by a compromised intestinal epithelial barrier. Mucin glycans are crucial in preserving barrier function during bacterial infections, although the underlying mechanisms remain largely unexplored. METHODS: A cohort comprising 15 patients diagnosed with UC and 15 healthy individuals was recruited. Stool samples were collected to perform 16S rRNA gene sequencing, while biopsy samples were subjected to nanocapillary liquid chromatography-tandem mass spectrometry (nanoLC-MS/MS) to assess O-glycosylation. Gene expression was evaluated through qPCR analysis and Western blotting. Furthermore, animal experiments were conducted to investigate the effects of Escherichia coli and/or O-glycan inhibitor benzyl-α-GalNAc on the development of colitis in mice. RESULTS: Our findings revealed that the mucus barrier was disrupted during the early stages of UC, while the MUC2 protein content remained unaltered. Additionally, a noteworthy reduction in the O-glycosylation of MUC2 was observed, along with significant changes in the intestinal microbiota during the early stages of UC. These changes included a decrease in intestinal species richness and an increase in the abundance of Escherichia coli (E. coli). Moreover, subsequent to the administration of galactose or O-glycan inhibitor to intestinal epithelial cells, it was observed that the cell culture supernatant had the ability to modify the proliferation and adhesive capacity of E. coli. Furthermore, when pathogenic E. coli or commensal E. coli were cocultured with intestinal epithelium, both strains elicited activation of the NF-KB signaling pathway in epithelial cells and facilitated the expression of serine protease in comparison to the untreated control. Consistently, the inhibition of O-glycans has been observed to enhance the pathogenicity of E. coli in vivo. Furthermore, a correlation has been established between the level of O-glycans and the development of ulcerative colitis. Specifically, a reduction in the O-glycan content of MUC2 cells has been found to increase the virulence of E. coli, thereby compromising the integrity of the intestinal epithelial barrier. CONCLUSIONS: Together, there exist complex interactions between the intestinal epithelium, O-glycans, and the intestinal microbiota, which may inform the development of novel therapeutic strategies for the treatment of ulcerative colitis.

Circ_103809 Aggravates the Malignant Phenotype of Pancreatic Cancer Through Modulating miR-197-3p/TSPAN3 Axis.

Pancreatic cancer (PC) is a malignant tumor with insidious clinical manifestations and dismal prognosis. Emerging reports have demonstrated that circRNAs exert pivotal biological function in PC. Here, we investigated the crucial biological role and underlying regulatory mechanisms of differentially expressed circ_103809 in PC. In this study, hsa_circ_103809 (hsa_circ_0072088) was identified as the research object via analyzing and screening the aberrantly expressed circRNAs in PC by GSE69362 dataset. The levels of circ_103809 in PC tissues and cells were assessed via qRT-PCR. Functional assays were conducted to monitor the impacts of circ_103809 on PC cells. Additionally, the downstream molecular targets and regulatory networks of circ_103809 were predicted by bioinformatics and validated using luciferase assays and rescue experiments. We found that circ_103809 was substantially upregulated in PC tissues and cells. Silencing circ_103809 restrained the growth viability, clonogenic rate, migration, and invasion capabilities of PC cells. Further mechanistic exploration disclosed that miR-197-3p was the downstream gene of circ_103809, while Tetraspanin-3 (TSPAN3) was a direct target of miR-197-3p. The suppressive effect of circ_103809 knockdown on malignant processes of PC cells was eliminated by miR-197-3p downregulation or TSPAN3 upregulation. Our study demonstrated that circ_103809 served as an innovative positive regulator in the growth and metastasis of PC cells. Furthermore, circ_103809 mediated the miR-197-3p/TSPAN3 axis to modulate the malignant progression of PC cells, which was prospected to be a probable biomarker and an efficient therapeutic target for PC.

Bacterial distribution and drug resistance in blood samples of children in Jiangxi Region, 2017-2021.

Objective: This study aims to investigate the distribution and drug resistance of bacteria in clinical blood culture specimens from children in Jiangxi province in recent years and to provide a foundation for preventing and treating bloodstream infection diseases in children. Methods: The study involved a statistical analysis of the isolation and drug resistance of bacterial strains obtained from blood culture specimens of children in Jiangxi province between 2017 and 2021. The analysis was performed using the WHONET 5.6 software. Results: A total of 7,977 bacterial strains were isolated from the blood samples of children between 2017 and 2021. Of these, 2,334 strains (29.3%) were identified as Gram-negative bacteria, and 5,643 strains (70.7%) were identified as Gram-positive bacteria. The most commonly isolated pathogens were coagulase-negative Staphylococcus, Escherichia coli, and Staphylococcus aureus. Among the Gram-negative bacteria, Escherichia coli (840 strains, 36.0%), Klebsiella pneumoniae (385 strains), Salmonella (283 strains), Acinetobacter baumannii (137 strains), and Pseudomonas aeruginosa (109 strains) were the most prevalent. Among the Gram-positive bacteria, coagulase-negative Staphylococcus (3,424 strains, 60.7%), Staphylococcus aureus (679 strains), Streptococcus pneumoniae (432 strains), Enterococcus sp. (292 strains), and Streptococcus agalactiae (192 strains) were the most common. Resistance to third-generation cephalosporins (cefotaxime/ceftriaxone) was observed in 45.9% and 56.0% of Escherichia coli and Klebsiella pneumoniae strains, respectively, while resistance to carbapenems was observed in 4.6% and 20.3% of these strains, respectively. Resistance to third-generation cephalosporins (cefotaxime/ceftriaxone) was observed in 15.5% of Salmonella strains, while resistance to imipenem was absent. Carbapenem resistance was observed in 17.1% (20/117) and 13% (14/108) of Acinetobacter baumannii and Pseudomonas aeruginosa strains, respectively. Methicillin-resistant Staphylococcus aureus (MRSA) was detected in 32.7% of the strains, while methicillin-resistant coagulase-negative Staphylococcus was detected in 64.3% of the coagulase-negative Staphylococcus strains. No Staphylococcus bacteria resistant to vancomycin were detected. Four strains of vancomycin-resistant Enterococcus faecium were detected over the 5-year period, and one strain of linezolid-resistant Enterococcus faecalis was detected. Conclusion: Gram-positive cocci were the most commonly isolated clinical pathogens in blood specimens from children in Jiangxi province. The composition of the pathogen species showed a slight change over the years. The detection ratios of pathogens varied with age group and season. Although the isolation rate of common carbapenem-resistant Enterobacter bacteria has decreased, it remains high. It is necessary to monitor the antimicrobial resistance of pathogens causing bloodstream infections in children more closely, and antimicrobial agents should be used with caution.

CD83+ B cells alleviate uveitis through inhibiting DCs by sCD83.

Soluble CD83 (sCD83) exerts immunosuppressive functions in many autoimmune diseases, including experimental autoimmune uveitis (EAU), but the cells and mechanisms involved are unclear. This study showed that CD83+ B cells were the main sources of sCD83. They alleviated the symptoms of EAU and decreased the percentage of T cells and DCs in the eyes and lymph nodes. These CD83+ B cells decreased IL-1ß, IL-18 and IFN-γ secretion by DCs through sCD83. sCD83 interacted with GTPase Ras-related protein (Rab1a) in DCs to promote Rab1a accumulation in autolysosomes and inhibit mTORC1 phosphorylation and NLRP3 expression. Hence, CD83+ B cells play a regulatory role in EAU by secreting sCD83. The lack of regulation of CD83+ B cells might be an important factor leading to hyperimmune activation in patients with autoimmune uveitis. CD83+ B cells suppress activated DCs in uveitis, indicating the potential therapeutic role of CD83+ B cells in uveitis.

The transcription factor Foxp1 regulates aerobic glycolysis in adipocytes and myocytes.

In recent years, lactate has been recognized as an important circulating energy substrate rather than only a dead-end metabolic waste product generated during glucose oxidation at low levels of oxygen. The term "aerobic glycolysis" has been coined to denote increased glucose uptake and lactate production despite normal oxygen levels and functional mitochondria. Hence, in "aerobic glycolysis," lactate production is a metabolic choice, whereas in "anaerobic glycolysis," it is a metabolic necessity based on inadequate levels of oxygen. Interestingly, lactate can be taken up by cells and oxidized to pyruvate and thus constitutes a source of pyruvate that is independent of insulin. Here, we show that the transcription factor Foxp1 regulates glucose uptake and lactate production in adipocytes and myocytes. Overexpression of Foxp1 leads to increased glucose uptake and lactate production. In addition, protein levels of several enzymes in the glycolytic pathway are upregulated, such as hexokinase 2, phosphofructokinase, aldolase, and lactate dehydrogenase. Using chromatin immunoprecipitation and real-time quantitative PCR assays, we demonstrate that Foxp1 directly interacts with promoter consensus cis-elements that regulate expression of several of these target genes. Conversely, knockdown of Foxp1 suppresses these enzyme levels and lowers glucose uptake and lactate production. Moreover, mice with a targeted deletion of Foxp1 in muscle display systemic glucose intolerance with decreased muscle glucose uptake. In primary human adipocytes with induced expression of Foxp1, we find increased glycolysis and glycolytic capacity. Our results indicate Foxp1 may play an important role as a regulator of aerobic glycolysis in adipose tissue and muscle.

IGF-1R down regulates the sensitivity of hepatocellular carcinoma to sorafenib through the PI3K / akt and RAS / raf / ERK signaling pathways.

BACKGROUND: Insulin-like growth factor-1 receptor (IGF-1R) promotes cell proliferation and migration and inhibitsapoptosis, all of which can contribute to the development of cancers. METHOD: This study investigated the effect and mechanism of IGF-1R in mediating the desensitization of hepatocellular carcinoma (HCC) to sorafenib. RESULTS: IGF-1R, highly expressed in the HCC cell lines SK-Hep1 and HepG2, promotes cell proliferation, migration, and anti-apoptosis through PI3K / Akt and RAS / Raf / ERK signaling pathways, resulting in HCC resistance to sorafenib. Knockdown of IGF-1R by RNA interference decreased proliferation and cell migration and upregulation of sorafenib-induced apoptosis of HCC cells. In vivo studies demonstrated that IGF-1R knockdown inhibited the growth of SK-Hep1 xenografts. CONCLUSION: These data are evidence that IGF-1R participates in regulating the survival and cell growth of HCC through the PI3K / Akt and RAS / Raf / ERK signaling pathways. Intervention in the expression of IGF-1R may increase the inhibitory effect of sorafenib on HCC.

A model of abusive supervision, self-efficacy, and work engagement among Chinese registered nurses: The mediating role of self-efficacy.

Abusive supervision could negatively influence individual work attitudes, behaviors, and work outcomes. Self-efficacy and work engagement can help to increase nursing performance. But few studies have attempted to determine the specific mechanism between them in China. The objective is to analyze the levels of abusive supervision, self-efficacy, and work engagement, and to explore the relationship between these three variables among Chinese clinical registered nurses. A predictive, cross-sectional quantitative survey was performed in a convenience sample of 923 Chinese clinical nurses. The instruments included the Demographic Data Questionnaire, Abusive Supervision Scale, Self-efficacy Scale and Work Engagement Scale. A total of 702 valid questionnaires were returned, yielding a favorable response rate of 76.1%. The level of abusive supervision was at the mid-low level, with a mean of 1.55. The nurses presented a relative high level of self-efficacy (M = 4.97) and work engagement (M = 5.01). A statistically significant negative correlation between abusive supervision and self-efficacy (r = -0.21, p < 0.01). A statistically significant negative correlation between abusive supervision and work engagement (r = -0.32, p < 0.01), and a statistically significant positive correlation between self-efficacy and work engagement (r = 0.43, p < 0.01). Abusive supervision had a directly negative effect on self-efficacy (ß = -0.23, p < 0.01) and work engagement (ß = -0.24, p < 0.01). Self-efficacy positively predicted work engagement (ß = 0.41, p < 0.01). The results indicated that abusive supervision could negatively predict nurses' work engagement directly and that abusive supervision could also indirectly influence work engagement partly through the mediation of self-efficacy. Nursing managers should take effective measures to prevent and control the abusive management and leadership behavior of head nurses, and improve nurses' self-efficacy, so that nurses can experience full respect, support, and self-confidence. They can devote themselves to work with the greatest enthusiasm.

Literature review of imaging, pathological diagnosis, and outcomes of metachronous lung and pancreatic metastasis of cecal cancer.

BACKGROUND: Pancreatic metastasis from colorectal cancer is extremely rare. Here, we report a case of colorectal cancer with lung and pancreatic metastasis and analyze the histopathology, immunohistochemistry, and next-generation sequencing (NGS) to generate a differential diagnosis and treatment of metastatic colon cancer. CASE PRESENTATION: AC1 A 78-year-old man was admitted because of a recently elevated carcinoembryonic antigen. This patient had undergone laparoscopic right hemicolectomy for cecal cancer IIA (T3N0M0) 5 years before admission, and thoracoscopic left upper lung wedge resection for primary colon cancer lung metastasis 2 years before admission. At that time, the patient was thought to have pancreatic metastasis from colon cancer. He underwent laparoscopic distal pancreatectomy (combined with splenectomy). Postoperative pathology revealed colon cancer metastasis. We performed NGS on tumor samples at three loci and found colon cancer's most common oncogenic driver genes (KRAS, APC, and TP53). One month after surgery, the patient was given capecitabine for six cycles of chemotherapy. At present, no high adverse reactions have been reported. DISCUSSION: For patients with pancreatic space-occupying, such as a previous history of colorectal cancer, and recent carcinoembryonic antigen elevation, we should highly suspect pancreatic metastatic colorectal cancer. NGS is an essential auxiliary for identifying metastatic tumors. Surgery combined with postoperative chemotherapy is an effective treatment.

CircLMTK2 Silencing Attenuates Gemcitabine Resistance in Pancreatic Cancer by Sponging miR-485-5p and to Target PAK1.

Pancreatic cancer (PC) has a high degree of malignancy and poor prognosis, and countless patients have distant metastasis when diagnosed. Gemcitabine (GEM) chemotherapy is one of the main ways of treatment. However, PC cells have been displayed chemoresistance to GEM during treatment. Circular RNAs (circRNAs) have been demonstrated to be the most popular diagnostic and prognostic biomarkers in PC with GEM resistance. Here, we assessed the potential of circLMTK2 in the GEM resistance of PC cells. Functional assays were implemented to measure the impacts of circLMTK2 on the proliferation, migration/invasion, and apoptosis of GEM-resistant PC cells. Bioinformatics analysis and mechanical experiments displayed the underlying mechanism of circLMTK2 in GEM-resistant PC cells. We found that circLMTK2 was upregulated in PC and GEM-resistant PC tissues and cells. CircLMTK2 knockdown suppressed proliferation, invasion, migration, and enhanced apoptosis in GEM-resistant PC cells. Moreover, circLMTK2 silencing could decrease GEM resistance-associated tumor size in vivo. In terms of mechanism, circLMTK2 served as a sponge for miR-485-5p, and miR-485-5p bound to p21 (RAC1) activated kinase 1 (PAK1), which were clarified via the dual-luciferase assay in PC cell lines. We confirmed that circLMTK2 knockdown attenuated GEM-resistant PC cells by regulating PAK1 via miR-485-5p. Our study demonstrated that circLMTK2 may be a novel diagnostic and prognostic biomarker in GEM-resistant PC cells.

Differences in the characteristics and pulmonary toxicity of nano- and micron-sized respirable coal dust.

BACKGROUND: The characteristics of coal dust (CD) particles affect the inhalation of CD, which causes coal worker's pneumoconiosis (CWP). CD nanoparticles (CD-NPs, < 500 nm) and micron particles (CD-MPs, < 5 µm) are components of the respirable CD. However, the differences in physicochemical properties and pulmonary toxicity between CD-NPs and CD-MPs remain unclear. METHODS: CD was analyzed by scanning electron microscopy, Malvern nanoparticle size potentiometer, energy dispersive spectroscopy, infrared spectroscopy, and electron paramagnetic resonance spectroscopy. CCK-8 assay, ELISA, transmission electron microscope, JC-1 staining, reactive oxygen species activity probe, calcium ion fluorescent probe, AO/EB staining, flow cytometry, and western blot were used to determine the differences between CD-NPs and CD-MPs on acute pulmonary toxicity. CCK-8, scratch healing and Transwell assay, hematoxylin-eosin and Masson staining, immunohistochemistry, immunofluorescence, and western blot were applied to examine the effects of CD-NPs and CD-MPs on pneumoconiosis. RESULTS: Analysis of the size distribution of CD revealed that the samples had been size segregated. The carbon content of CD-NPs was greater than that of CD-MPs, and the oxygen, aluminum, and silicon contents were less. In in vitro experiments with A549 and BEAS-2B cells, CD-NPs, compared with CD-MPs, had more inflammatory vacuoles, release of pro-inflammatory cytokines (IL-6, IL-1ß, TNFα) and profibrotic cytokines (CXCL2, TGFß1), mitochondrial damage (reactive oxygen species and Ca2+ levels and decreased mitochondrial membrane potential), and cell death (apoptosis, pyroptosis, and necrosis). CD-NPs-induced fibrosis model cells had stronger proliferation, migration, and invasion than did CD-MPs. In in vivo experiments, lung coefficient, alveolar inflammation score, and lung tissue fibrosis score (mean: 1.1%, 1.33, 1.33) of CD-NPs were higher than those of CD-MPs (mean: 1.3%, 2.67, 2.67). CD-NPs accelerated the progression of pulmonary fibrosis by upregulating the expression of pro-fibrotic proteins and promoting epithelial-mesenchymal transition. The regulatory molecules involved were E-cadherin, N-cadherin, COL-1, COL-3, ZO-1, ZEB1, Slug, α-SMA, TGFß1, and Vimentin. CONCLUSIONS: Stimulation with CD-NPs resulted in more pronounced acute and chronic lung toxicity than did stimulation with CD-MPs. These effects included acute inflammatory response, mitochondrial damage, pyroptosis, and necrosis, and more pulmonary fibrosis induced by epithelial-mesenchymal transition.

ASIC1α up-regulates MMP-2/9 expression to enhance mobility and proliferation of liver cancer cells via the PI3K/AKT/mTOR pathway.

A major challenge in the treatment of liver cancer is that a large proportion of patients fail to achieve long-term disease control, with death from liver cancer cell migration and invasion. Acid-sensitive ion channel 1α (ASIC1α) is involved in the migration, invasion, and proliferation of liver cancer cells. Therefore, we explored the mechanism of ASIC1α-mediated liver cancer cell migration and invasion. We determined the levels of ASIC1α by western blotting and immunofluorescence in HepG2 and SK-Hep1 cells cultured in various acidic conditions. In addition, wound healing assay, transwell invasion assay, and MTT assay were conducted to assess the migration, invasion, and proliferation abilities of liver cancer cells. Western blotting was conducted to determine the levels of MMP2, MMP9, ASIC1α, p-PI3Kp85, t-PI3Kp85, p-AKT(Ser473), t-AKT, p-mTOR (Ser2448), t-mTOR. We first found that the levels of ASIC1α in the HepG2 and SK-Hep1 cells in acidic conditions (pH 6.5) were significantly increased. Inhibition and knockdown of ASIC1α down-regulated MMP-2/9 expression and inhibited the migration, invasion, and proliferation of HepG2 and SK-Hep1 cells; overexpression of ASIC1α had the opposite effect. We further demonstrated that ASIC1α up-regulates MMP-2/9 via activation of the PI3K/AKT/mTOR pathway, thereby promoting migration, invasion, and proliferation of liver cancer cells. Overexpression of MMP-2/9 and activation of AKT reversed these effects on liver cancer cells caused by inhibition of ASIC1α. We conclude that ASIC1α can regulate migration, invasion, and proliferation of liver cancer cells through the MMP-2/9/PI3K/AKT/mTOR pathway. These observations may provide a new reference for liver cancer chemotherapy.

Nanoparticles Loaded with GSK1059615 Combined with Sorafenib Inhibited Programmed Cell Death 1 Ligand 1 Expression by Negatively Regulating the PI3K/Akt/NF-κB Pathway, Thereby Reversing the Drug Resistance of Hepatocellular Carcinoma to Sorafenib.

Activation of the cellular signaling pathways can induce sorafenib-resistant hepatocellular carcinoma (HCCR). In this work, the PI3K/mTOR inhibitor GSK1059615 inhibited the proliferation and invasion of HCCR cells. PLGA-PEG-mal diblock copolymer was used to load GSK1059615 and sorafenib, and the vector was further modified with GPC3 antibody (hGC33) to obtain hGC33-modified GSK1059615 and sorafenib-loaded nanoparticles (Ab-G/S-NP). Ab-G/S-NP regulated the activation of cellular signaling pathways in HCCR cells by inhibiting the expression and activation of NF-κB and downregulating the level of programmed cell death 1 ligand 1(PD-L1) to reverse drug resistance of HCCR cells to sorafenib. These findings deserve further study in the combined treatment of HCCR cells with GSK1059615 in vivo to develop a more effective treatment of sorafenib-resistant cancers.