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To explore the predictive value of combined detection of serum interleukin-6 (IL-6), chloride (ClFrom December 2020 to March 2022, 132 AP patients who met the criteria for inclusion were screened for retrospective analysis from 292 AP patients admitted in emergency surgery at the First Affiliated Hospital of Zhengzhou University and they were divided into severe acute pancreatitis (SAP) group and non-SAP group, with 63 in SAP group and 69 in non-SAP group, according to classification criteria. The data including lab results, abdominal doppler ultrasound and chest and abdominal CT, etc. The bedside index for severity in acute pancreatitis (BISAP) score was calculated. Multivariate Logistic regression analysis was carried out to find the risk factors for the severity of AP patients. The receiver operator characteristic curve (ROC) was drawn to judge the clinical predictive value of each factor.A total of 132 AP patients were enrolled. The serum IL-6, D-dimer, FDP levels and the BISAP score in SAP group were significantly higher than those in non-SAP group [serum IL-6 (ng/L): 62.73 (21.54, 187.47) vs. 8.22 (4.13, 14.70), D-dimer (mg/L): 5.36 (2.94, 8.25) vs. 0.94 (0.42, 2.21), FDP (mg/L): 13.54 (6.76, 22.45) vs. 3.20 (2.50, 6.10), BISAP score: 2.00 (1.00, 3.00) vs. 1.00 (0, 2.00), all P0.05], while the serum ClCompared with single index, the combined detection of serum IL-6, Cl

BACKGROUND Acute lung injury (ALI) is a common and life-threatening complication of severe acute pancreatitis (SAP). There are currently limited effective treatment options for SAP and associated ALI. Calycosin (Cal), a bioactive constituent extracted from the medicinal herb Radix Astragali exhibits potent anti-inflammatory properties, but its effect on SAP and associated ALI has yet to be determined. AIM To identify the roles of Cal in SAP-ALI and the underlying mechanism. METHODS SAP was induced via two intraperitoneal injections of L-arg (4 g/kg) and Cal (25 or 50 mg/kg) were injected 1 h prior to the first L-arg challenge. Mice were sacrificed 72 h after the induction of SAP and associated ALI was examined histologically and biochemically. An in vitro model of lipopolysaccharide (LPS)-induced ALI was established using A549 cells. Immunofluorescence analysis and western blot were evaluated in cells. Molecular docking analyses were conducted to examine the interaction of Cal with HMGB1. RESULTS Cal treatment substantially reduced the serum amylase levels and alleviated histopathological injury associated with SAP and ALI. Neutrophil infiltration and lung tissue levels of neutrophil mediator myeloperoxidase were reduced in line with protective effects of Cal against ALI in SAP. Cal treatment also attenuated the serum levels and mRNA expression of pro-inflammatory cytokines tumor necrosis factor-α, interleukin-6, IL-1β, HMGB1 and chemokine (CXC motif) ligand 1 in lung tissue. Immunofluorescence and western blot analyses showed that Cal treatment markedly suppressed the expression of HMGB1 and phosphorylated nuclear factor-kappa B (NF-κB) p65 in lung tissues and an in vitro model of LPS-induced ALI in A549 cells suggesting a role for HGMB1 in the pathogenesis of ALI. Furthermore, molecular docking analysis provided evidence for the direct interaction of Cal with HGMB1. CONCLUSION Cal protects mice against L-arg-induced SAP and associated ALI by attenuating local and systemic neutrophil infiltration and inflammatory response via inhibition of HGMB1 and the NF-κB signaling pathway.

Background Acute pancreatitis (AP) is an inflammatory disease in which the regulatory pathway is complex and not well understood. Soluble suppression of tumorigenicity 2 (sST2) protein receptor functions as a decoy receptor for interleukin (IL)-33 to prevent IL-33/suppression of tumorigenicity 2L (ST2L)-pathway-mediated T helper (Th)2 immune responses. Aim To investigate the role of sST2 in AP. Methods We assessed the association between sST2 and severity of AP in 123 patients enrolled in this study. The serum levels of sST2, C-reactive protein (CRP) and Th1- and Th2-related cytokines, including interferon (IFN)-γ, tumor necrosis factor (TNF)-α, IL-2, IL-4, IL-5 and IL-13, were measured by highly sensitive ELISA, and the severity of AP in patients was evaluated by the 2012 Atlanta Classification Criteria. Results Serum sST2 levels were significantly increased in AP patients, and further, these levels were significantly elevated in severe AP (SAP) patients compared to moderately severe AP (MSAP) and mild AP (MAP) patients. Logistic regression showed sST2 was a predictor of SAP [odds ratio (OR): 1.003 (1.001-1.006), P = 0.000]. sST2 cutoff point was 1190 pg/mL, and sST2 above this cutoff was associated with SAP. sST2 was also a predictor of any organ failure and mortality during AP [OR: 1.006 (1.003-1.009), P = 0.000, OR: 1.002 (1.001-1.004), P = 0.012, respectively]. Additionally, the Th1-related cytokines IFN-γ and TNF-α in the SAP group were higher and the Th2-related cytokine IL-4 in the SAP group was significantly lower than those in MSAP and MAP groups. Conclusion sST2 may be used as a novel inflammatory marker in predicting AP severity and may regulate the function and differentiation of IL-33/ST2-mediated Th1 and Th2 Lymphocytes in AP homeostasis.

BACKGROUND: Weaning through noninvasive ventilation (NIV) after early extubation may facilitate invasive ventilation withdrawal and reduce related complications in patients with hypercapnic respiratory failure. However, the effects of NIV weaning are uncertain in patients with acute hypoxemic respiratory failure (AHRF). We aimed to investigate whether NIV weaning could reduce hospital mortality and other outcomes compared with invasive weaning in subjects with hypoxemic AHRF. METHODS: We searched medical literature databases for relevant articles published from inception to February 2019. Randomized controlled trials that adopted NIV as a weaning strategy compared with invasive weaning in hypoxemic AHRF were included. The primary outcome was hospital mortality. The secondary outcomes included ICU mortality, the ICU stay, weaning time, duration of ventilation, extubation failure, and adverse events. RESULTS: Six relevant studies, which involved 718 subjects, were included. There was no significant effect of NIV weaning on hospital mortality compared with invasive weaning (risk ratio 0.94, 95% CI 0.65–1.36; P = .74), whereas there was a significant effect of NIV weaning on shortening the ICU stay (mean difference −3.95, 95% CI −6.49 to −1.40, P = .002) and on decreasing adverse events without affecting the weaning time (standardized MD −0.04, 95% CI −0.21 to 0.14; P = .68). CONCLUSIONS: The strategy of NIV weaning did not decrease hospital mortality in subjects with hypoxemic AHRF, but it did shorten the ICU lengths of stay and reduce adverse events.

This study sought to investigate the biological effects of specific MIF inhibitor, ISO-1, on the proliferation, migration and invasion of PANC-1 human pancreatic cells in vitro, and on tumour growth in a xenograft tumour model in vivo. The effect of ISO-1 on PANC-1 cell proliferation was examined using CCK-8 cell proliferation assay. The effect of ISO-1 on collective cell migration and recolonization of PANC-1 cells was evaluated using the cell-wound closure migration assay. The effect of ISO-1 on the migration and invasion of individual PANC-1 cells in a 3-dimensional environment in response to a chemo-attractant was investigated through the use of Transwell migration/invasion assays. Quantitative real time PCR and western blot analyses were employed to investigate the effects of ISO-1 on MIF, NF-κB p65 and TNF-α mRNA and protein expression respectively. Finally, a xenograft tumor model in BALB/c nude mice were used to assess the in vivo effects of ISO-1 on PANC-1-induced tumor growth. We found high expression of MIF in pancreatic cancer tissues. We demonstrated that ISO-1 exerts anti-cancer effects on PANC-1 cell proliferation, migration and invasion in vitro, and inhibited PANC-1 cell-induced tumour growth in xenograft mice in vivo. Our data suggests that ISO-1 and its derivative may have potential therapeutic applications in pancreatic cancer.

Acute pancreatitis (AP) is a common serious acute condition of the digestive system that remains a clinical challenge. Severe acute pancreatitis (SAP) in particular is characterized by high morbidity and mortality. The present study was designed to investigate the protective effect of Galangin (Gal), a natural flavonol obtained from lesser galangal, on L-arginine-induced SAP in mice and in AR42J cells. Amylase and lipase activities were measured and the histopathology of the pancreas, lung, and kidney was evaluated. Inflammation and oxidative stress were assessed using ELISA, western blotting, RT-PCR, and immunohistochemistry. Gal was shown to reduce proinflammatory cytokine production and reactive oxygen species (ROS) generation in vivo and in vitro. L-arginine treatment reduced the expression of components of the nuclear factor E2-related factor 2 (Nrf2) signaling pathway and the downstream protein heme oxygenase-1 (HO-1) in mice, whereas Gal increased their expression. Furthermore, the Nrf2/HO-1 pathway inhibitor brusatol prevented the anti-inflammatory and antioxidant effects of Gal in mice with SAP. Taken together, our results imply that Gal has protective effects in L-arginine-induced SAP that are induced by the upregulation of the Nrf2/HO-1 pathway, which has anti-inflammatory and antioxidant effects. Thus, Gal may represent a promising treatment for SAP.

Introduction: Patients with dyspnea and hypoxemia are common in emergency departments. However, it is unknown whether high-flow nasal cannula (HFNC) reduces the risk of requiring more advanced ventilation support and whether HFNC relieves dyspnea better than conventional oxygen therapy (COT). Areas covered: We searched the PubMed, Cochrane Library, Ovid, and Embase databases from inception to 1 September 2019 to identify relevant-randomized controlled trials comparing the effect of HFNC with COT in emergency departments regarding the severity of dyspnea, hospitalization rate, intubation rate, and hospital mortality. We identified four studies. HFNC was associated with a lower rate of requiring more advanced ventilation. HFNC reduced the rate of dyspnea, lowered the dyspnea scale score, and decreased patients’ respiratory rate significantly. However, there was insufficient evidence to show a significant effect on HFNC regarding patients’ oxygenation and hospital mortality. Expert opinion: For patients with dyspnea and hypoxemia before hospitalization, the short-term effect of HFNC was undeniable. HFNC reduced the risk of requiring more advanced ventilation and relived dyspnea better than COT. HFNC might be considered as a first-line therapy even before making a clear diagnosis for dyspnea. More studies are needed to explore the effect of HFNC on oxygenation and patients’ prognosis.

Aim Summarise the evidence regarding the safety of mechanical and manual chest compressions for cardiac arrest patients. Methods Two investigators separately screened the articles of EMBASE, PubMed, and Cochrane Central databases. Cohort studies and randomized clinical trials (RCTs) that evaluated the safety of mechanical (LUCAS or AutoPulse) and manual chest compressions in cardiac arrest patients were included. A meta-analysis was performed using a random effects model to calculate the pooled odds ratios (ORs) and their 95% confidence intervals (CIs). The primary outcome was the rate of overall compression-induced injuries. The secondary outcomes included the incidence of life-threatening injuries, skeletal fractures, visceral injuries, and other soft tissue injuries. Results The meta-analysis included 11 trials involving 2,818 patients. A significantly higher rate of overall compression-induced injuries was found for mechanical compressions than manual compressions (OR, 1.29; 95% CI, 1.19–1.41), while there was no significant difference between the two groups in respect of the rate of life-threatening injuries. Furthermore, both modalities shared similar incidences of sternal fractures, vertebral fractures, lung, spleen, and kidney injuries. However, compared to mechanical compressions, manual compressions were shown to present a reduced risk of posterior rib fractures, and heart and liver lesions. Conclusions The findings suggested that manual compressions could decrease the risk of compression-induced injuries compared to mechanical compressions in cardiac arrest patients. Interestingly, mechanical compressions have not increased the risk of life-threatening injuries, whereas additional high-quality RCTs are needed to further verify the safety of mechanical chest devices. Trial registry: INPLASY; Registration number: INPLASY2020110111; URL: https://inplasy.com/

The present study investigates whether paraquat (PQ) regulates polarization of alveolar macrophages through glycolysis and promotes the occurrence of acute lung injury in rats. In vivo, the PQ intraperitoneal injection was used to construct a model of acute lung injury in rats. In vitro, the study measured the effect of different concentrations of PQ on the viability of the alveolar macrophages, and explored the polarization and glycolysis metabolism of alveolar macrophages at different time points after PQ intervention. Compared with the normal control (NC) group, the lung pathological damage in rats increased gradually after PQ poisoning, reaching a significant degree at 48 h after poisoning. The PQ-poisoned rat serum showed increased expressions of interleukin-6 (IL-6), tumor necrosis factor- α (TNF-α), and M1 macrophage marker, iNOS, while the expression of interleukin-10 (IL-10) and M2 macrophage marker, Arg1, decreased. The toxic effect of PQ on alveolar macrophages was dose- and time-dependent. Compared with the NC group, IL-6 and TNF-α in the cell supernatant gradually increased after PQ intervention, while the IL-10 content gradually decreased. The PQ intervention in alveolar macrophages increased the expression of intracellular glycolysis rate-limiting enzyme pyruvate kinase isozymes M1/M2 (PKM1/M2), lactate, lactate/pyruvate ratio, and the polarization of alveolar macrophage towards M1. Inhibition of cellular glycolysis significantly reduced the PQ-induced alveolar macrophage polarization to M1 type. Thus, PQ induced increased polarization of lung macrophages toward M1 and decreased polarization toward M2, promoting acute lung injury. Therefore, it can be concluded that PQ regulates the polarization of alveolar macrophages through glycolysis.

The multitarget position-sensitivity security transmission scheme with orbital angular momentum (OAM) directional modulation (DM) waveform using the uniform circular frequency diverse array (FDA) is proposed. The transmitter employs FDA to generate dual-mode range-dependent OAM beam pattern, and the direction information of OAM beam is modulated into the signal. According to the modulation method, orthogonal carrier frequency can be designed to realize multitarget position-dependent OAM pattern. In the undesired position, the intensity pattern and the phase front of the radio beam vary randomly with the digital transmission sequence. Because modulation waveform is position-dependent, the technique offers security, as the signal can be purposely distorted in other positions. The composite dual-mode OAM signal makes it more difficult for eavesdroppers to demodulate correct messages. The receiver with a single antenna employs the phase compensation and helical phase factor to restore the correct digital signal in the desired position. Numerical results show that multitarget position-sensitivity OAM-DM technology based on FDA offers the security transmission scheme.

Background Acute kidney injury (AKI) is an important complication of severe acute pancreatitis (SAP) with a poor prognosis. The methyl ester of (S,R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid (ISO-1), an inhibitor of macrophage migration inhibitory factor (MIF), has protective effects against many diseases. Our previous study confirmed MIF inhibition alleviated SAP. Here, we explored the effects of ISO-1 in an experimental mouse model of SAP-associated AKI induced by l -arginine. Methods Mice were randomly divided into four treatment groups (n = 6 each): control (CON), SAP, SAP + ISO-1, and ISO-1. Histopathologic examination was used to observe damage in pancreatic and renal tissues. Biochemical and enzyme-linked immunosorbent assays (ELISA) kits were used to measure the serologic indicators amylase, lipase, creatinine, uric acid, interleukin (IL)-6, and tumor necrosis factor (TNF)-α. Immunohistochemistry was used to detect protein expression of NLRP3, ASC and caspase-1, and the infiltration of myeloperoxidase (MPO)-positive neutrophils in kidney tissue. Western blotting was used to detect NLRP3, ASC and caspase-1 and IL-1β protein expression, and real-time PCR was used to measure MIF, IL-6, TNF-α, IL-1β and IL-18 mRNA levels in kidney tissue. Results ISO-1 treatment alleviated pathological damage in pancreatic and renal tissues, and reduced the serum levels of amylase, lipase, creatinine, uric acid, IL-6 and TNF-α. ISO-1 also reduced protein expression of NLRP3, ASC, caspase-1 and IL-1β, mRNA expression of MIF, IL-6, TNF-α, IL-1β and IL-18, and the infiltration of MPO-positive neutrophils in kidney tissue. Conclusion ISO-1 has a protective effect against experimental SAP-associated AKI. And the mechanism may be associated with ISO-1 inhibiting NLRP3 inflammasome signaling pathway.

INTRODUCTION: Patients with cancer are more vulnerable to COVID-19 than the general population. Accordingly, it is necessary to identify the risk factors for death in patients with cancer and COVID-19. METHODS: PubMed, Cochrane Library, and Embase Ovid databases were searched for relevant articles published before July 31st, 2020. Studies that explored the risk factors for mortality were included. The effect size was relative risk (RR) and 95% confidence interval (CI). RESULTS: We included 17 observational studies involving 3268 patients. The pooled mortality was 24.8%. Male gender, age above 65 years, and comorbidities (especially hypertension and COPD) were risk factors for death (RR 1.16, 1.27, 1.12; 95% CI 0.7-1.95, 1.08-1.49, 1.04-1.2; P = 0.006, 0.004, and 0.002, respectively). Recent anti-cancer treatments did not increase mortality (P > 0.05). Dyspnea, cough, and sputum canused an elevated risk of death (P

Background Liver injury is one of the most common complications during sepsis. Macrophage migration inhibitory factor (MIF) is an important proinflammatory cytokine. This study explored the role of MIF in the lipopolysaccharide (LPS)-induced liver injury through genetically manipulated mouse strains. Methods The model of LPS-induced liver injury was established in wild-type and Mif-knockout C57/BL6 mice. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total bilirubin (TBil) were detected, and the expressions of MIF, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were measured. Liver histopathology was conducted to assess liver injury. Moreover, the inhibitions of MIF with (S,R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester (ISO-1) and 4-iodo-6-phenylpyrimidine (4-IPP) were used to evaluate their therapeutic potential of liver injury. Results Compared with wild-type mice, the liver function indices and inflammation factors presented no significant difference in the Mif−/− mice. After 72 h of the LPS-induced liver injury, serum levels of ALT, AST, and TBil as well as TNF-α and IL-1β were significantly increased, but the knockout of Mif attenuated liver injury and inflammatory response. In liver tissue, mRNA levels of TNF-α, IL-1β and NF-κB p65 were remarkably elevated in LPS-induced liver injury, while the knockout of Mif reduced these levels. Moreover, in LPS-induced liver injury, the inhibitions of MIF with ISO-1 and 4-IPP alleviated liver injury and slightly attenuated inflammatory response. Importantly, compared to mice with LPS-induced liver injury, Mif knockout or MIF inhibitions significantly prolonged the survival of the mice. Conclusions In LPS-induced liver injury, the knockout of Mif or MIF inhibitions alleviated liver injury and slightly attenuated inflammatory response, thereby prolonged the survival of the mice. Targeting MIF may be an important strategy to protect the liver from injury during sepsis.

It is noted that elevated serum amylase levels suggesting pancreatic damage has an association with prognosis in PQ patients. This study aimed to determine whether PQ can cause pancreatic damage. The two conventional models (intragastric infusion (iG) and intraperitoneal injection (iP)) may exhibit different effects on the pancreas depending on whether or not they pass through the digestive tract. In this study, the rats were divided into four groups: the intragastric infusion group (PQ-iG, n = 45), intraperitoneal injection group (PQ-iP, n = 53), normal control group 1 (NC-iG, n = 6) and normal control group 2 (NC-iP, n = 6). Pancreatic damage was compared between groups using serum amylase activity assay, hematoxylin and eosin (H&E) staining, TUNEL assay, and transmission electron microscopy (TEM). Serum amylase levels in group PQ-iG were significantly higher than in group PQ-iP (p < 0.05). Examination of the H&E sections showed damage to the pancreas. Both experimental groups were displayed inflammatory infiltration within 9 h of PQ treatment. After 9 h, patchy necrosis was observed in group PQ-iP, when inflammatory infiltration was still the dominant pathology. Necrosis appeared and gradually worsened in group PQ-iG, in which necrosis was the dominant pathology. The TUNEL assay showed significantly higher numbers of apoptotic cells in the pancreas of PQ-groups than in the control NC- groups (p < 0.05). TEM showed expansive endoplasmic reticulum lumens and mitochondria swelling in the pancreas of the PQ-groups. It is concluded that both methods of modeling could cause pancreatic damage and the type and degree of damage would change over time. Note that pancreatic damage in group PQ-iG was more severe than that in group PQ-iP. Therefore, clinical practitioners should pay close attention to pancreatic damage caused by PQ, especially when the route of PQ administration was oral.

Propofol is frequently used for anesthesia in cancer surgery. It has been suggested that treatment with propofol serves a tumor‑suppressing role in human gastric cancer (GC). Therefore, the present study aimed to explore the potential mechanism of propofol in GC. In the present study, GC cell lines (HGC‑27 and AGS) were treated with various concentrations of propofol, and an MTT assay was performed to detect the cell viability. In addition, flow cytometry and Transwell assays were used to evaluate the apoptosis and invasive ability of GC cells, respectively. Western blotting was performed to detect the protein levels of cyclin‑dependent kinase inhibitor P21 (P21), B‑cell lymphoma‑2 (Bcl‑2), matrix metalloproteinase 9 (MMP9) and E26 oncogene homolog 1 (ETS1). Furthermore, reverse transcription‑quantitative PCR was used to examine the expression levels of circular RNA‑PVT1 (circ‑PVT1), micoRNA‑195‑5p (miR‑195‑5p) and ETS1 in GC tissues and cells. The target interaction between miR‑195‑5p and circ‑PVT1 or ETS1 was predicted through bioinformatics analysis, and verified by dual‑luciferase reporter gene assay. In addition, a mouse xenograft model was established for in vivo experiments. It was identified that propofol inhibited the viability and invasion, but promoted apoptosis of HGC‑27 and AGS cells in a dose‑dependent manner. Propofol could inhibit Bcl‑2 and MMP9 expression, and increase P21 expression in GC cells. The expression levels of circ‑PVT1 and ETS1 were increased in GC tissues and cells, and miR‑195‑5p was decreased. Additionally, the treatment with propofol could lead to decreased circ‑PVT1 expression in GC cells. These results could be reversed by ETS1 upregulation or miR‑195‑5p‑knockdown in GC cells. Furthermore, circ‑PVT1 could act as a miR‑195‑5p sponge to modulate ETS1 expression. Additionally, the effects of transfection with circ‑PVT1 small interfering RNA (si‑circ‑PVT1) on HGC‑27 and AGS cells could be reversed by treatment with miR‑195‑5p inhibitor. Meanwhile, miR‑195‑5p inhibitor reversed the si‑circ‑PVT1‑induced low expression of ETS1. Downregulation of ETS1 induced by propofol in HGC‑27 and AGS cells could be restored by circ‑PVT1 upregulation or miR‑195‑5p silencing. Circ‑PVT1 silencing facilitated the propofol‑induced anti‑GC effect in vivo. In conclusion, the present study indicated that propofol inhibited the proliferation and invasion, but enhanced the apoptosis of GC cells by regulating the circ‑PVT1/miR‑195‑5p/ETS1 axis.

To investigate the value of macrophage migration inhibitor factor (MIF) in early severe acute pancreatitis (SAP).(1) Animal experiment: according to the random number table method, 24 male Sprague-Dawley (SD) rats were divided into Sham group and SAP 3, 6 and 12 hours groups, with 6 rats in each group. SAP rat model was prepared by injecting 5% sodium taurocholate via the retrograde cholangiopancreatic duct. Liver, kidney, lung, pancreas and serum samples were harvested after 3, 6 and 12 hours. In the Sham group, tissue and serum were harvested immediately after pancreas was turned over. The histopathological changes of the pancreas were observed microscopically by hematoxylin-eosin (HE) staining. The MIF levels of serum, liver, kidney, lung and pancreas were measured by enzyme linked immunosorbent assay (ELISA). (2) Clinical study: an observational study was conducted. Seventy-two adult patients within 24 hours of the onset of abdominal pain (blood amylase was 3 times the normal level), and the clinical diagnosis met the criteria of acute pancreatitis (AP) admitted to the emergency department of the First Affiliated Hospital of Zhengzhou University from December 2018 to October 2019 were enrolled. Venous blood was extracted and serum MIF level was determined by ELISA. Acute physiology and chronic health evaluation II (APACHE II) was recorded for 24 hours. Patients were divided into SAP group (17 cases), moderate severe acute pancreatitis (MSAP) group (25 cases), and mild acute pancreatitis (MAP) group (30 cases) according to the revised Atlanta criteria for comparison between groups.(1) The results of animal experiments showed that the serum, liver, and pancreatic MIF levels of rats in the SAP group all reached the peak at 6 hours after modeling, and the differences were statistically significant compared with the Sham group [serum MIF (ng/L): 2 862.79±238.33 vs. 1 728.32±197.59, liver MIF (ng/L): 2 141.39±328.07 vs. 1 372.70±163.41, pancreas MIF (ng/L): 4 468.00±1 324.31 vs. 1 572.06±108.40, all P0.01]; although the levels of MIF in serum, liver and pancreas decreased at 12 hours after modeling, they were still significantly higher than Sham group. However, there was no statistically significant difference in MIF levels of lung and kidney in SAP rats compared with Sham group at 3, 6 and 12 hours after molding. (2) Clinical observation showed that early serum MIF levels of SAP, MSAP and MAP patients decreased in order, (14.83±2.99), (10.17±2.64), and (7.21±2.47) μg/L, respectively; APACHE II scores also decreased in order, 10.41±3.74, 7.60±3.18 and 4.00±2.41 respectively. Correlation analysis showed that serum MIF levels in patients with SAP, MSAP, and MAP had a good correlation with APACHE II scores of the respective groups, showing that MIF levels was positively correlated with disease severity (SAP: r = 0.51, P = 0.03; MSAP: r = 0.45, P = 0.02; MAP: r = 0.45, P = 0.01).MIF can predict the occurrence of early SAP, and it is related to the severity of early AP.

Background: SARS-CoV-2 is a newly discovered virus, leading COVID-19 a global threaten nowadays. Case Presentation: The first case of a patient with a thoracic aortic aneurysm (TAA) that became infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was reported here. The patient died suddenly from a ruptured aorta 19 h after hospital admission. Conclusion: COVID-19 patients with TAA should attract the highest vigilance as COVID-19 might expedite the process of TAA rupture through cytokine storm syndrome, leading to rapid death with little or no warning signs.

To investigate the effect and tolerance of non-invasive ventilation (NIV) with helmet in patients with respiratory failure caused by acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and the effect on improving blood gas, alleviating dyspnea and the occurrence of complications.Patients with AECOPD and respiratory failure admitted to emergency intensive care unit (EICU) and respiratory intensive care unit (RICU) of the First Affiliated Hospital of Zhengzhou University from January 1st, 2018 to May 31st, 2019 were enrolled. After obtaining the informed consent of the patients or their authorized family members, the patients were divided into two groups: the helmet group and the facial mask group by random number table. NIV was carried out by using helmet or facial mask, respectively. During the course of NIV (immediately, 1 hour, 4 hours and at the end of NIV), the tolerance score, blood gas analysis, heart rate (HR), respiratory rate (RR) of patients were monitored, and the incidence of tracheal intubation, in-hospital mortality and complications were observed. Kaplan-Meier survival curve was plotted to analyze the 30-day cumulative survival of the two groups.A total of 82 patients with AECOPD and respiratory failure were included during the study period. After excluding patients with the oxygenation index (PaONIV with helmet has better comfort for patients with AECOPD combined with respiratory failure, and better effect on improving oxygenation and relieving dyspnea, and its effect on carbon dioxide emissions is not inferior to that of traditional mask NIV.

This paper theoretically explores photocontrolled terahertz amplified modulator in electron plasma wave optically switched resonant tunneling diode (ORTD) gate high-electron mobility transistor. We present a developed distributed circuit model based on the Khmyrova model. Photoexcitation causes ORTD operating state between negative differential conductivity and positive differential conductivity, which power gain of the device can be control by photoexcitation. Numerical and analytical results show that photoexcitation enabling amplified modulator can realize much larger modulation depth (>95%) than what has been reported in photocontrolled modulator. Our results show the potential of this device in several fields of terahertz technology, such as photocontrolled modulator, mixer, and other two port networks.

Background Patients with cervical spinal cord injuries (CSCIs) may be required to undergo tracheostomy. However, in patients undergoing anterior cervical fusion (ACF), percutaneous dilational tracheostomy (PDT) may be delayed given the risk of cross-contamination. We aimed to evaluate the risk of surgical site infection (SSI) in early PDT in patients with traumatic CSCI after ACF. Methods All trauma patients admitted to the intensive care unit from 2008 to 2018 were retrospectively analyzed. Patients with CSCIs who underwent both ACF and PDT were identified, with or without posterior cervical fusion. Cases were classified as having undergone early PDT (≤4 days after ACF) versus late PDT (>4 days after ACF). Propensity scores were matched, and outcomes were compared between matched groups to reduce confounding by indication. Results From a total of 133 enrolled patients, a well-balanced propensity-matched cohort of 68 patients was defined. On the basis of the comparison of outcomes after matching, no significant difference in SSI was observed between both groups. There was no patient with SSI in the early PDT group (0%), whereas there were 2 SSI patients (5.9%) in the late PDT group (P = 0.493): The tracheostomy site was involved in 1, and the posterior approach site was involved in the other. Early PDT was associated with a shorter duration of mechanical ventilation (P = 0.042). There were no significant differences in the length of intensive care unit stay and hospital mortality between groups. Conclusions Early PDT within 4 days after ACF did not increase the risk of SSI compared with late PDT in patients with traumatic CSCIs.

Background: Chinese emergency medical staff have great mental and work pressure in fighting the coronavirus disease 2019 (COVID-19) pandemic, and it is necessary to understand the prevalenece and influencing factors for depression. Methods: A cross-sectional national survey of general emergency medical staff who were on duty and participated in COVID-19 anti-pandemic from November 2019 to April 2020 was conducted and we used the scale of Patient Health Questionnaire-9 (PHQ-9) to assess depression symptom. Univariate analysis and multivariable logistic-regression models assessed for the associations of influencing PHQ-9 scores. Results: 6588 emergncy medical staff from 1060 hospitals responded to the survey. The average PHQ-9 score of all medical staff was 10.94±5.1. We use PHQ-9≥10 as the cut-off value to define major depression, the prevalence of major depression was 57.60%.The results of univariate analysis showed that demographic factors (gender, age, occupation, relationship status, living with childen ≤16 years-old or adults≥70 years- old), work factors (direct contact with confirmed COVID-19 patients or working in an isolation unit with COVID-19 patients), and forced isolation in the hospital all had an increased risk of major depression. In addition, multivariate logistic regression analysis indicated that main factors associated with major depression symptom were direct contact with confirmed COVID-19 patient (OR 1.153), working in a COVID-19 isolation ward (OR 1.366), age between 31-45 years old (OR 1.139), and living with children ≤16 years old (OR 1.126) or adults≥70 years old (OR 1.325). Working in Hubei province (the epicenter of the outbreak) during COVID-19 had no correlation with depression. Conclusion: Chinese emergency medical staff experienced depression burden during COVID-19 period, particularly, those aged 31-45,those working in isolation unit COVID-19, those living with children or older people These results reinforce the value of effective, targeted staff support during the COVID-19 or future outbreaks. Funding Statement: None. Declaration of Interests: The authors declare no competing interests. Ethics Approval Statement: The study has been approved by the Ethics Committee of Peking Union Medical College Hospital, and all the participants provided informed consent.

Background: Chinese emergency medical staff have great mental and work pressure in fighting the coronavirus disease 2019 (COVID-19) pandemic, and it is necessary to understand the prevalenece and influencing factors for depression. Methods: A cross-sectional national survey of general emergency medical staff who were on duty and participated in COVID-19 anti-pandemic from November 2019 to April 2020 was conducted and we used the scale of Patient Health Questionnaire-9 (PHQ-9) to assess depression symptom. Univariate analysis and multivariable logistic-regression models assessed for the associations of influencing PHQ-9 scores. Results: 6588 emergncy medical staff from 1060 hospitals responded to the survey. The average PHQ-9 score of all medical staff was 10.94±5.1. We use PHQ-9≥10 as the cut-off value to define major depression, the prevalence of major depression was 57.60%.The results of univariate analysis showed that demographic factors(gender, age, occupation, relationship status, living with childen ≤16 years-old or adults≥70 years- old), work factors (direct contact with confirmed COVID-19 patients or working in an isolation unit with COVID-19 patients), and forced isolation in the hospital all had an increased risk of major depression. In addition, multivariate logistic regression analysis indicated that main factors associated with major depression symptom were direct contact with confirmed COVID-19 patient (OR 1.153), working in a COVID-19 isolation ward (OR 1.366), age between 31-45 years old (OR 1.139), and living with children ≤16 years old(OR 1.126) or adults≥70 years old (OR 1.325). Working in Hubei province (the epicenter of the outbreak) during COVID-19 had no correlation with depression. Conclusion: Chinese emergency medical staff experienced depression burden during COVID-19 period, particularly, those aged 31-45,those working in isolation unit COVID-19, those living with children or older people These results reinforce the value of effective, targeted staff support during the COVID-19 or future outbreaks. Funding Statement: The authors state that there is no funding for this article. Declaration of Interests: The authors declare no competing interests. Ethics Approval Statement: The study has been approved by the Ethics Committee of Peking Union Medical College Hospital, and all the participants provided informed consent.

This study describes the design of a resonant tunneling diode (RTD) oscillator (RTD oscillator) with a RTD-gated-graphene-2DEF (two dimensional electron fluid) and demonstrates the functioning of this RTD oscillator through a transmission line simulation model. Impedance of the RTD oscillator changes periodically when physical dimension of the device is of considerable fraction of the electrical wavelength. As long as impedance matching is achieved, the oscillation frequency is not limited by the size of the device. An RTD oscillator with a graphene film and negative differential resistance (NDR) will produce power amplification. The positive electrode of the DC power supply is modified and designed as an antenna. So, the reflected power can also be radiated to increase RTD oscillator output power. The output analysis shows that through the optimization of the antenna structure, it is possible to increase the RTD oscillator output to 22 mW at 1.9 THz and 20 mW at 6.1 THz respectively. Furthermore, the RTD oscillator has the potential to oscillate at 50 THz with a matching antenna.

Background Macrophage migration inhibitory factor (MIF) is an important pro-inflammatory cytokine implicated in sepsis, rheumatoid arthritis and other diseases. However, the role of MIF in acute pancreatitis (AP) remains unclear. This study aims to explore the role of MIF in the pathogenesis of AP using MIF−/− mice (referred to as KO) and the biological effects of pharmacological inhibition of MIF in l -arginine induced AP. Methods AP was induced in C57BL/6 wild-type (referred to as WT) and KO mice by administration of l -arginine. The severity of AP was assessed by serum analysis of amylase and lipase, and of these pro-inflammatory cytokines TNF-α and IL-1β. Histological hematoxylin and eosin (H&E) and immunohistochemical staining of pancreatic tissues were examined for inflammation and expression of pro-inflammatory mediators. We also investigated the biological effects of pharmacological inhibition of MIF activity using ISO-1((S,R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester). Results At 72 h after the induction of AP with l -arginine, significantly lower levels of serum amylase, lipase, TNF-α, and IL-1β were observed in KO mice when compared with WT controls. Histological examination further showed protective effects against pancreatic tissue damage and inflammation, with pancreatic expression of TNF-α, IL-1β and NF-κB p65 markedly reduced. Pharmacological inhibition of MIF activity with ISO-1 markedly mirrored the protective effect seen in the KO AP model providing further evidence that MIF is involved in the pathogenesis of AP. Conclusion Our data provided strong evidence for the participation of MIF in the pathogenesis of AP and subsequent inflammatory response. The genetic ablation of MIF or its inhibition with pharmacological agents significantly ameliorated the severity of AP.