Investigation of the Status of Nurses Returning to Work After Recovering From COVID-19 and Influencing Factors.

BACKGROUND: More than 3000 medical personnel in China had been infected with coronavirus disease-2019 (COVID-19). We report on 75 previously infected nurses who returned to work. PURPOSE: The aim was to understand the adaptation status of nurses after recovering from COVID-19 and returning to work. METHODS: Data were collected online via the Work Adaptation Scale and the Psychological Capital Scale, and the related influencing factors were analyzed. RESULTS: The social integration and task mastery scores were highest, and the clear roles and cultural adaptation scores were low. The self-efficacy and hope scores were highest, but the resilience and optimism scores were not high. Psychological capital was positively correlated with work adaptation (P < .01). CONCLUSIONS: To ensure the quality and safety of nursing care, nurse managers should adopt effective intervention measures to address the physical and mental health of returning nurses and improve their levels of psychological capital and adaptability.

Histone demethylase UTX is a therapeutic target for diabetic kidney disease.

KEY POINTS: Diabetic kidney disease (DKD) is a major complication of diabetes. We found that UTX (ubiquitously transcribed tetratricopeptide repeat on chromosome X, also known as KDM6A), a histone demethylase, was upregulated in the renal mesangial and tubular cells of diabetic mice and DKD patients. In cultured renal mesangial and tubular cells, UTX overexpression promoted palmitic acid-induced elevation of inflammation and DNA damage, whereas UTX knockdown or GSK-J4 treatment showed the opposite effects. We found that UTX demethylase activity-dependently regulated the transcription of inflammatory genes and apoptosis; moreover, UTX bound with p53 and p53-dependently exacerbated DNA damage. Administration of GSK-J4, an H3K27 demethylase inhibitor, ameliorated the diabetes-induced renal abnormalities in db/db mice, an animal model of type 2 diabetes. These results revealed the possible mechanisms underlying the regulation of histone methylation in DKD and suggest UTX as a potential therapeutic target for DKD. ABSTRACT: Diabetic kidney disease (DKD) is a microvascular complication of diabetes and the leading cause of end-stage kidney disease worldwide without effective therapy available. UTX (ubiquitously transcribed tetratricopeptide repeat on chromosome X, also known as KDM6A), a histone demethylase that removes the di- and tri-methyl groups from histone H3K27, plays important biological roles in gene activation, cell fate control and life span regulation in Caenorhabditis elegans. In the present study, we report upregulated UTX in the kidneys of diabetic mice and DKD patients. Administration of GSK-J4, an H3K27 demethylase inhibitor, ameliorated the diabetes-induced renal dysfunction, abnormal morphology, inflammation, apoptosis and DNA damage in db/db mice, comprising an animal model of type 2 diabetes. In cultured renal mesanglial and tubular cells, UTX overexpression promoted palmitic acid induced elevation of inflammation and DNA damage, whereas UTX knockdown or GSK-J4 treatment showed the opposite effects. Mechanistically, we found that UTX demethylase activity-dependently regulated the transcription of inflammatory genes; moreover, UTX bound with p53 and p53-dependently exacerbated DNA damage. Collectively, our results suggest UTX as a potential therapeutic target for DKD.

Histone methyltransferase G9a modulates hepatic insulin signaling via regulating HMGA1.

Hepatic insulin sensitivity is critical for glucose homeostasis, and insulin resistance is a fundamental syndrome found in various metabolic disorders, including obesity and type 2 diabetes. Despite considerable studies on the mechanisms of hepatic insulin resistance, the link between epigenetic regulation and the development of insulin resistance remains elusive. Here, we reported that G9a/EHMT2, a histone methyltransferase, was markedly decreased in the liver of db/db mice and high-fat diet (HFD)-fed mice. In cultured hepatic cells, G9a knockdown resulted in downregulation of insulin receptor, p-AKT and p-GSK3ß; while upon upregulation, G9a prevented the palmitic acid- or glucosamine-induced insulin resistance by preserving the normal level of insulin receptor and integrity of insulin signaling. Further mechanistic study suggested that G9a regulated the expression level of high mobility group AT-hook 1 (HMGA1), a key regulator responsible for the transcription of insulin receptor (INSR) gene. Overexpression of HMGA1 normalized the impaired insulin signaling in G9a knockdown hepatic cells. Importantly, in db/db mice, restoring the expression level of G9a not only upregulated HMGA1 level and improved the impaired hepatic insulin signaling, but also alleviated hyperglycemia and hyperinsulinemia. Together, our results revealed a novel role for G9a in modulating insulin signaling, at least in part, depending on its regulatory function on HMGA1.

Hypoxic preconditioning protects microvascular endothelial cells against hypoxia/reoxygenation injury by attenuating endoplasmic reticulum stress.

Endothelial cells (ECs) are directly exposed to hypoxia and contribute to injury during myocardial ischemia/reperfusion. Hypoxic preconditioning (HPC) protects ECs against hypoxia injury. This study aimed to explore whether HPC attenuates hypoxia/reoxygenation (H/R) injury by suppressing excessive endoplasmic reticulum stress (ERS) in cultured microvascular ECs (MVECs) from rat heart. MVECs injury was measured by lactate dehydrogenase (LDH) leakage, cytoskeleton destruction, and apoptosis. Expression of glucose regulating protein 78 (GRP78) and C/EBP homologous protein (CHOP), activation of caspase-12 (pro-apoptosis factors) and phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) were detected by western blot analysis. HPC attenuated H/R-induced LDH leakage, cytoskeleton destruction, and cell apoptosis, as shown by flow cytometry, Bax/Bcl-2 ratio, caspase-3 activation and terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling. HPC suppressed H/R-induced ERS, as shown by a decrease in expression of GRP78 and CHOP, and caspase-12 activation. HPC enhanced p38 MAPK phosphorylation but decreased that of protein kinase R-like ER kinase (PERK, upstream regulator of CHOP). SB202190 (an inhibitor of p38 MAPK) abolished HPC-induced cytoprotection, downregulation of GRP78 and CHOP, and activation of caspase-12, as well as PERK phosphorylation. HPC may protect MVECs against H/R injury by suppressing CHOP-dependent apoptosis through p38 MAPK mediated downregulation of PERK activation.

Clinical pain management by a multidisciplinary palliative care team: Experience from a tertiary cancer center in China.

To investigate the effect of multidisciplinary interventions on pain management in cancer inpatients.Four hundred thirty eight patients with cancer pain, who performed the multidisciplinary intervention were recruited. Before and after intervention, the Brief Pain Inventory (BPI) and the MD Anderson Symptom Inventory (MDASI) score as the primary endpoints and QOL scores as the secondary endpoint were all evaluated. To investigate the factors that led to different responses to multidisciplinary interventions, patients were classified as non-responders or responders.Finally, 92 patients (63 male and 29 female) scheduled for cancer pain management by inter-professional team were studied. After individualized multidisciplinary therapy, both pain and symptom severity was improved, as demonstrated by lowered BPI worst and average pain scores, as well as symptom severity score measured by MDASI (P = .017, P = .003, and P = .011, respectively). The proportion of patients with mild pain increased regarding the BPI worst and average pain at baseline and after treatment (P < .05). The QOL analyses showed multidisciplinary interventions could significantly improve the function and symptom scores (P < .001). More patients in responder group received chemotherapy (58, 70.7%, P = .003), while fewer received mini-invasive therapy (6, 7.32%, P = .011).Multidisciplinary interventions had certain beneficial effect on cancer pain management, especially in patients with moderate or severe pain.

Histone methyltransferase G9a protects against acute liver injury through GSTP1.

Acute liver injury is commonly caused by bacterial endotoxin/lipopolysaccharide (LPS), and by drug overdose such as acetaminophen (APAP). The exact role of epigenetic modification in acute liver injury remains elusive. Here, we investigated the role of histone methyltransferase G9a in LPS- or APAP overdose-induced acute liver injury. Under D-galactosamine sensitization, liver-specific G9a-deficient mice (L-G9a-/-) exhibited 100% mortality after LPS injection, while the control and L-G9a+/- littermates showed very mild mortality. Moreover, abrogation of hepatic G9a or inhibiting the methyltransferase activity of G9a aggravated LPS-induced liver damage. Similarly, under sublethal APAP overdose, L-G9a-/- mice displayed more severe liver injury. Mechanistically, ablation of G9a inhibited H3K9me1 levels at the promoters of Gstp1/2, two liver detoxifying enzymes, and consequently suppressed their transcription. Notably, treating L-G9a-/- mice with recombinant mouse GSTP1 reversed the LPS- or APAP overdose-induced liver damage. Taken together, we identify a novel beneficial role of G9a-GSTP1 axis in protecting against acute liver injury.

[Primary research on arbuscular mycorrhizal fungi in rhizosphere of Chaenomeles speciosa in Xuancheng].

OBJECTIVE: To investigate the arbuscular mycorrhizal (AM) fungi resources in rhizosphere of Chaenomeles speciosa in Xuancheng, Anhui province. METHOD: Roots were stained with acid fuchsin and then mounted and observed under a microscope; Spores were extracted from the rhizosphere soil using wet-sieving method. RESULT: C. speciosa could be colonized and formed typical arbuscular mycorrhizas with AM fingi. 18 species of arbuscular mycorrhizal fungi were identified, belonging to four genera, 11 species of Glomus, 3 species of Acaulospora, 3 species of Scutellospora and 1 species of Entrophospora. Glomus were the dominant AM fungi in the rhizosphere. CONCLUSION: The resources of AM fungi in rhiszophere of C. speciosa were very abundant. Fungi from Glomus were possible the dominant AMF in the rhizosphere.

A traumatic hepatic artery pseudoaneurysm and arterioportal fistula, with severe diarrhea as the first symptom: A case report and review of the literature.

RATIONALE: Hepaticarterioportal fistula (APF) is a rare cause of portal hypertension and gastrointestinal hemorrhage, and presents as abnormal communication between the hepatic artery and portal vein. Percutaneous liver biopsy is a main iatrogenic cause of AFP. However, non-iatrogenic, abdominal, trauma-related APF is rarely reported. PATIENT CONCERNS: A 29-year-old man presenting with severe, watery diarrhea was transferred to our hospital, and his condition was suspected to be acute gastroenteritis because he ate expired food and suffered a penetrating abdominal stab wound 5 years ago. After admission, the patient suffered from hematemesis, hematochezia, ascites, anuria, and kidney failure, and he developed shock. DIAGNOSES: The patient was finally diagnosed as a traumatic hepatic artery pseudoaneurysm and APF. INTERVENTIONS: This patient was treated with emergency transarterial embolization using coils. Since a secondary feeding vessel was exposed after the first embolization of the main feeding artery, a less-selective embolization was performed again. OUTCOMES: During the 6-month follow-up period, the patient remained asymptomatic. LESSONS: A penetrating abdominal stab wound is a rare cause of hepatic APFs, and occasionally leads to portal hypertension, the medical history and physical examination are the most important cornerstones of clinical diagnosis. Interventional radiology is essential for the diagnosis and treatment of an APF.

ANGPTL8 negatively regulates NF-κB activation by facilitating selective autophagic degradation of IKKγ.

Excessive nuclear factor-κB (NF-κB) activation mediated by tumor necrosis factor α (TNFα) plays a critical role in inflammation. Here we demonstrate that angiopoietin-like 8 (ANGPTL8) functions as a negative feedback regulator in TNFα-triggered NF-κB activation intracellularly. Inflammatory stimuli induce ANGPTL8 expression, and knockdown or knockout of ANGPTL8 potentiates TNFα-induced NF-κB activation in vitro. Mechanistically, upon TNFα stimulation, ANGPTL8 facilitates the interaction of IKKγ with p62 via forming a complex, thus promoting the selective autophagic degradation of IKKγ. Furthermore, the N-terminal domain mediated self-oligomerization of ANGPTL8 is essential for IKKγ degradation and NF-κB activation. In vivo, circulating ANGPTL8 level is high in patients diagnosed with infectious diseases, and the ANGPTL8/p62-IKKγ axis is responsive to inflammatory stimuli in the liver of LPS-injected mice. Altogether, our study suggests the ANGPTL8/p62-IKKγ axis as a negative feedback loop that regulates NF-κB activation, and extends the role of selective autophagy in fine-tuned inflammatory responses.

Intensive nursing care by an electronic followup system to promote secondary prevention after percutaneous coronary intervention: a randomized trial.

PURPOSE: To investigate the effectiveness of an intensive nursing care electronic followup system for cardiovascular risk management after percutaneous coronary intervention (PCI). METHODS: In total, 840 subjects who underwent PCI in a single hospital in Beijing between January 2010 and January 2012 were enrolled. All subjects were randomized into the control and intensive nursing care groups (n = 420 each group). Both groups received standard secondary prevention according to guidelines. The control group received regular followup while the intensive nursing care group was closely monitored and followed by specific nursing staff with the electronic followup system. RESULTS: In total, 807 subjects were followed up for 1 year. Compared with subjects in the control group, those in the intensive group had decreased levels of total cholesterol (3.99 ± 1.08 vs 3.76 ± 0.98; P < .05), systolic blood pressure (142.41 ± 11.53 vs 135.71 ± 14.57 mm Hg; P < .05), low-density lipoprotein cholesterol (LDL-C) (2.72 ± 1.01 vs 2.42 ± 0.81; P < .05), and body mass index (25.13 ± 5.12 vs 24.23 ± 6.22; P < .05); a higher percentage with target LDL-C < 2.6 mmol/L (66.99% vs 47.88%; P < .05); increased use of medication including aspirin (96.51% vs 99.26%; P < .05), clopidogrel (87.53% vs 98.77%; P < .05), statins (52.62% vs 93.10%; P < .05), ß-blockers (48.63% vs 61.33%; P < .05), and angiotensin-converting enzyme inhibitors (32.92% vs 61.82%; P < .05); and better dietary control and physical exercise (55.66% vs 26.18%, P < .05; 62.56% vs 38.65%, P < .05). CONCLUSIONS: Intensive nursing care by the electronic followup system may lead to an improvement in quality of secondary prevention after PCI, including risk factor control, the use of medication, and self-management abilities.