Case report: A rare case of omental extrarenal rhabdoid tumor and review of the literature.

Extrarenal rhabdoid tumor of the greater omentum is extremely rare, with only sporadic reports and limited documentation of its ultrasonographic findings. Here, we report a case of an extrarenal rhabdoid tumor of the greater omentum in a 16-year-old girl and review the relevant literature. It was found that the disease mainly occurred in female children and adolescents, and mainly manifested as lower abdominal pain and a large abdominal cystic or solid hemorrhagic mass. The clinical characteristics include a high degree of malignancy and mortality. Ultrasound shows some malignant features, but it is not specific; thus, it is easy to be misdiagnosed in the clinic.

Carbon-reinforced Ni3S2/Ti3C2Tx MXene composite as an anode for superior-performance lithium-ion capacitors.

Lithium ion capacitors (LICs) are a new generation of energy storage devices that combine the super energy storage capability of lithium ion batteries with the satisfactory power density of supercapacitors. The development of high-performance LICs still faces great challenges due to the unbalanced reaction kinetics at the anode and cathode. Therefore, it is an inevitable need to enhance the electron/ion transfer capability of the anode materials. In this paper, to obtain a superior-rate and high-capacity Ni3S2-based anode, highly conductive Ti3C2Tx MXene sheets were introduced to sever as the carrier of Ni3S2 nanoparticles and simultaneously an amorphous carbon layer which coats onto the surface of Ni3S2 nanoparticles was in-situ generated by the carbonization of dopamine reactant. The as-synthesized Ni3S2/Ti3C2Tx/C composite exhibits a high specific surface area (112.6 m2/g) because of the addition of Ti3C2Tx that can reduce the aggregation of Ni3S2 nanoparticles and the in-situ generated amorphous carbon layer that can suppress the growth of Ni3S2 nanoparticles. The Ni3S2/Ti3C2Tx/C anode possesses a remarkable reversible discharge specific capacity (626.0 mAh/g under 0.2 A/g current density), which increases to 1150.8 mAh/g after 400-cycle charge/discharge measurement at the same measurement condition indicating eminent cyclability, along with superior rate capability. To construct a superior-performance LIC device, a sterculiae lychnophorae derived porous carbon (SLPC) cathode with an average discharge specific capacity of 73.4 mAh/g@0.1A/g was prepared. The Ni3S2/Ti3C2Tx/C//SLPC LIC device with optimal cathode/anode mass ratio has a satisfactory energy density ranging from 32.8 to 119.1 Wh kg-1 at the corresponding power density of 8799.4 to 157.5 W kg-1, together with a prominent capacity retention (95.5 %@1 A/g after 10,000 cycles).

ANXA1sp attenuates sepsis-induced myocardial injury by promoting mitochondrial biosynthesis and inhibiting oxidative stress and autophagy via SIRT3 upregulation.

Sepsis-induced myocardial injury is one of the most difficult complications of sepsis in intensive care units. Annexin A1 (ANXA1) short peptide (ANXA1sp) protects organs during the perioperative period. However, the protective effect of ANXA1sp against sepsis-induced myocardial injury remains unclear. We aimed to explore the protective effects and mechanisms of ANXA1sp against sepsis-induced myocardial injury both in vitro and in vivo. Cellular and animal models of myocardial injury in sepsis were established with lipopolysaccharide. The cardiac function of mice was assessed by high-frequency echocardiography. Elisa assay detected changes in inflammatory mediators and markers of myocardial injury. Western blotting detected autophagy and mitochondrial biosynthesis-related proteins. Autophagic flux changes were observed by confocal microscopy, and autophagosomes were evaluated by TEM. ATP, SOD, ROS, and MDA levels were also detected.ANXA1sp pretreatment enhanced the 7-day survival rate, improved cardiac function, and reduced TNF-α, IL-6, IL-1ß, CK-MB, cTnI, and LDH levels. ANXA1sp significantly increased the expression of sirtuin-3 (SIRT3), mitochondrial biosynthesis-related proteins peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α), and mitochondrial transcription factor A (TFAM). ANXA1sp increased mitochondrial membrane potential (△Ψm), ATP, and SOD, and decreased ROS, autophagy flux, the production of autophagosomes per unit area, and MDA levels. The protective effect of ANXA1sp decreased significantly after SIRT3 silencing in vitro and in vivo, indicating that the key factor in ANXA1sp's protective role is the upregulation of SIRT3. In summary, ANXA1sp attenuated sepsis-induced myocardial injury by upregulating SIRT3 to promote mitochondrial biosynthesis and inhibit oxidative stress and autophagy.

Emphysematous thrombophlebitis caused by a misplaced central venous catheter: A case report.

BACKGROUND: Central venous catheters (CVCs) often cause life-threatening complications, especially CVC-related bloodstream infection (CVC-BSI) and catheter-related thrombosis (CRT). Here, we report an unusual case of misplaced CVC-induced emphysematous thrombophlebitis, a rare but potentially lethal form of CRT and CVC-BSI characterized by both thrombosis and gas formation. CASE SUMMARY: A 48-year-old male presented to the emergency room of a local hospital with sudden-onset headache and coma for 4 h. Computed tomography (CT) revealed right basal ganglia hemorrhage, so emergency decompressive craniotomy was performed and a CVC was inserted through the right subclavian vein for fluid resuscitation during anesthesia. Two days later, the patient was transferred to the intensive care unit of our hospital for further critical care. On day 9 after CVC insertion, the patient suddenly developed fever and hypotension. Point-of-care ultrasound (POCUS) demonstrated thrombosis and dilatation of the right internal jugular vein (IJV) filled with thrombosis. Ultrasonography also revealed that the CVC tip had been misplaced into the IJV and was surrounded by gas bubbles, which manifested as hyperechoic lines with dirty shadowing and comet-tail artifacts. Further CT scan confirmed air bubbles surrounding the CVC in the right neck. The final diagnosis was septic emphysematous thrombophlebitis induced by a misplaced CVC and ensuing septic shock. The responsible CVC was removed immediately. The patient received fluid resuscitation, intravenous noradrenaline, and a 10-d ultra-broad spectrum antibiotic treatment to combat septic shock. Both CVC and peripheral venous blood cultures yielded methicillin-resistant Staphylococcus cohnii. The patient was gradually weaned off vasopressors and the symptoms of redness and swelling in the right neck subsided within 7 d. CONCLUSION: Emphysematous thrombophlebitis is a fulminant and life-threatening CVC-BSI associated with thrombosis and gas formation in the vein. A misplaced CVC may facilitate the development of emphysematous thrombophlebitis. POCUS can easily identify the artifacts produced by gas and thrombosis, facilitating rapid diagnosis at the bedside.

Risk prediction model for distinguishing Gram-positive from Gram-negative bacteremia based on age and cytokine levels: A retrospective study.

BACKGROUND: Severe infection often results in bacteremia, which significantly increases mortality rate. Different therapeutic strategies are employed depending on whether the blood-borne infection is Gram-negative (G-) or Gram-positive (G+). However, there is no risk prediction model for assessing whether bacteremia patients are infected with G- or G+ pathogens. AIM: To establish a clinical prediction model to distinguish G- from G+ infection. METHODS: A total of 130 patients with positive blood culture admitted to a single intensive care unit were recruited, and Th1 and Th2 cytokine concentrations, routine blood test results, procalcitonin and C-reactive protein concentrations, liver and kidney function test results and coagulation function were compared between G+ and G- groups. Least absolute shrinkage and selection operator (LASSO) regression analysis was employed to optimize the selection of predictive variables by running cyclic coordinate descent and K-fold cross-validation (K = 10). The predictive variables selected by LASSO regression analysis were then included in multivariate logistic regression analysis to establish a prediction model. A nomogram was also constructed based on the prediction model. Calibration chart, receiver operating characteristic curve and decision curve analysis were adopted for validating the prediction model. RESULTS: Age, plasma interleukin 6 (IL-6) concentration and plasma aspartate aminotransferase concentration were identified from 57 measured variables as potential factors distinguishing G+ from G- infection by LASSO regression analysis. Inclusion of these three variables in a multivariate logistic regression model identified age and IL-6 as significant predictors. In receiver operating characteristic curve analysis, age and IL-6 yielded an area under the curve of 0.761 and distinguished G+ from G- infection with specificity of 0.756 and sensitivity of 0.692. Serum IL-6 and IL-10 levels were upregulated by more than 10-fold from baseline in the G- bacteremia group but by less than ten-fold in the G+ bacteremia group. The calibration curve of the model and Hosmer-Lemeshow test indicated good model fit (P > 0.05). When the decision curve analysis curve indicated a risk threshold probability between 0% and 68%, a nomogram could be applied in clinical settings. CONCLUSION: A simple prediction model distinguishing G- from G+ bacteremia can be constructed based on reciprocal association with age and IL-6 level.

Bow-and-arrow sign on point-of-care ultrasound for diagnosis of pacemaker lead-induced heart perforation: A case report and literature review.

BACKGROUND: Pacemaker lead-induced heart perforation is a rare but life-threatening complication of pacemaker implantation, and timely diagnosis remains a challenge for clinicians. Here, we report a case of pacemaker lead-induced cardiac perforation rapidly diagnosed by a "bow-and-arrow" sign on point-of-care ultrasound (POCUS). CASE SUMMARY: A 74-year-old Chinese woman who had undergone permanent pacemaker implantation 26 d before suddenly developed severe dyspnea, chest pain, and hypotension. The patient had received emergency laparotomy for an incarcerated groin hernia and was transferred to the intensive care unit 6 d before. Computed tomography was not available due to unstable hemodynamic status, so POCUS was performed at the bedside and revealed severe pericardial effusion and cardiac tamponade. Subsequent pericardiocentesis yielded a large volume of bloody pericardial fluid. Further POCUS by an ultrasonographist revealed a unique "bow-and-arrow" sign indicating right ventricular (RV) apex perforation by the pacemaker lead, which facilitated the rapid diagnosis of lead perforation. Given the persistent drainage of pericardial bleeding, urgent off-pump open chest surgery was performed to repair the perforation. However, the patient died of shock and multiple organ dysfunction syndrome within 24 h post-surgery. In addition, we also performed a literature review on the sonographic features of RV apex perforation by lead. CONCLUSION: POCUS enables the early diagnosis of pacemaker lead perforation at the bedside. A step-wise ultrasonographic approach and the "bow-and-arrow" sign on POCUS are helpful for rapid diagnosis of lead perforation.

Synthesis and antitumor activities of novel hybrid molecules containing 1,3,4-oxadiazole and 1,3,4-thiadiazole bearing Schiff base moiety.

A series of novel hybrid molecules containing 1,3,4-oxadiazole and 1,3,4-thiadiazole bearing Schiff base moiety were designed, synthesized and evaluated for their in vitro antitumor activities against SMMC-7721, MCF-7 and A549 human tumor cell lines by CCK-8 assay. The bioassay results demonstrated that most of the tested compounds showed potent antitumor activities, and some compounds exhibited stronger effects than positive control 5-fluorouracil (5-FU) against various cell lines. Among these compounds, compound 8d showed the best inhibitory effect against SMMC-7721 cells, with IC50 value of 2.84 µM. Compounds 8k and 8 n displayed highly effective antitumor activities against MCF-7 cells, with IC50 values of 4.56 and 4.25 µM, respectively. Compounds 8a and 8 n exhibited significant antiproliferative activity against A549 cells, with IC50 values of 4.11 and 4.13 µM, respectively. The pharmacological results suggest that the substituents of phenyl ring on the 1,3,4-oxadiazole are vital for modulating antiproliferative activities against various tumor cell lines.

Altered thalamocortical functional connectivity by propofol anesthesia in rats.

Anesthesia, a state of profound central nervous system suppression, involves a sequence of events that is still not well understood. In the present study, we examined the action of propofol (a sedative-hypnotic drug commonly used as anesthetic) on thalamocortical functional connectivity in rats by using functional connectivity magnetic resonance imaging (fcMRI) with a 3.0-tesla MR scanner. Intraperitoneal injections of propofol (80 or 160 mg/kg) were administered to Sprague-Dawley rats. Synchronized low-frequency fluctuations (LFF) of blood oxygen level-dependent (BOLD) signals were found between the thalamic and somatosensory cortices (S1/S2) after administration of 80 mg/kg propofol. However, after application of 160 mg/kg propofol, synchronized LFF of BOLD signals disappeared. These observations indicate that thalamocortical connectivity may play an important role in propofol anesthesia. We also observed that regionally specific long-range correlations of spontaneous low-frequency physiological fluctuations in BOLD signals may be present across somatosensory networks of the brain in the absence of external stimulation. However, our experiment suggests that fcMRI can be used to investigate brain networks that exhibit correlated fluctuations.

[The role of heme oxygenase 1 in hydrogen peroxide induced apoptosis and mitochondrial trans membrane potential change in rat primary type II alveolar epithelium cells].

OBJECTIVE: To understand the role of heme oxygenase-1 (HO-1) in hydrogen peroxide [H(2)O(2)] induced apoptosis and mitochondrial trans-membrane potential (MTMP) change in primary alveolar epithelial cell type II(AEC II). METHODS: Primary AEC II collected from healthy Sprague Dawley (SD) rats were cultured for 24 hours, then divided into four groups to be treated with: (1) saline; (2) H(2)O(2) (0.5 mmol/L); (3) H(2)O(2) +HO-1 (0.2 mmol/L); (4) H(2)O(2) +zinc original porphyrin IX (HO-1 inhibitor, 20 µmol/L). The morphology of cells in the cultures was examined by fluorescent microscopy 2.5 hours later, and the number of apoptotic cells / the MTMP determined by flow-cytometry 0.5, 1.0, 1.5, 2.0 and 2.5 hours later. RESULTS: Large number of cells in with green (early apoptotic) or red (later apoptotic) fluorescence were observed by microscope in cultures treated with H(2)O(2) , and H(2)O(2) + HO-1 inhibitor, but such cells were obviously fewer in HO-1 treated cultures. Compared with saline treated cells, H(2)O(2) treated cells had significantly higher apoptosis rate, that increased with time, reaching peak value 2.5 hours into the treatment [0.5 hour: (30.27 ± 0.74)% vs. (3.76 ± 0.81)%, 2.5 hours: (40.46 ± 0.91)% vs. (22.74 ± 0.60)%, both P < 0.05], while the rate of MTMP depolarization was significantly lower (0.99 ± 0.21 vs. 1.91 ± 0.16, P < 0.05) in these cells. Compared with H(2)O(2) treated cells, the apoptosis rate in HO-1 treated cells was significantly lower [0.5 hour: (5.99 ± 0.60)% vs. (30.27 ± 0.74)%, 2.5 hours: (22.69 ± 1.69)% vs. (40.46 ± 0.91)%, both P < 0.05], and their rate of MTMP depolarization higher (2.02 ± 0.12 vs. 0.99 ± 0.21, P < 0.05). Compared with HO-1 treated cells, HO-1 inhibitor treated cells had significantly higher apoptosis rate which reached peak value 2.5 hours into the treatment [0.5 hour: (30.73 ± 1.08)% vs. (5.99 ± 0.60)%, 2.5 hours: (41.38 ± 0.57)% vs. (22.69 ± 1.69)%, both P < 0.05], while rate of MTMP depolarization in these cells was significantly lower (0.98 ± 0.09 vs. 2.02 ± 0.12, P < 0.05). CONCLUSION: HO-1 could maintain the integrity of AEC II and stabilize their mitochondria membrane potential, protecting the cells from H(2)O(2) induced damage.

Protective effects of pinacidil hyperpolarizing cardioplegia on myocardial ischemia reperfusion injury by mitochondrial KATP channels.

BACKGROUND: Many studies have indicated that hyperpolarizing cardioplegia is responsible for myocardial preservation and researchers have suggested that the adenosine triphosphate-sensitive potassium channels (K(ATP)) were the end effectors of cardio-protection. But whether mitochondrial K(ATP) plays an important role in hyperpolarizing cardioplegia is not apparent. The present study investigated the effect of hyperpolarizing cardioplegia containing pinacidil (a nonselective K(ATP) opener) on ischemia/reperfusion injury in rat hearts, especially the role of mitochondrial K(ATP) in pinacidil hyperpolarizing cardioplegia. METHODS: Sprague-Dawley rat hearts were Langendorff-perfused for 20 minutes with Krebs-Henseleit buffer at 37°C before equilibration. Cardiac arrest was then induced in different treatments: there was no arrest and ischemia in the normal group, the control group were arrested by clamping the aorta, depolarizing caidioplegia (St. Thomas solution containing 16 mmol/L KCl) and hyperpolarizing cardioplegia groups used St. Thomas solution containing 0.05 mmol/L pinacidil and 5 mmol/L KCl to induce cardiac arrest in group hyperkalemic and group pinacidil, in group hyperkalemic + 5-hydroxydecanote (5HD) and Pinacidil + 5HD, 5HD (0.1 mmol/L) was added to the above two solutions to block mitochondria K(ATP) channels. Global ischemia was then administrated for 40 minutes at 37°C, followed by 30 minutes of reperfusion. At the end of equilibration and reperfusion, hemodynamics, ultrastructure, and mitochondrial function were measured. RESULTS: In the control group, ischemia/reperfusion decreased the left ventricular developed pressure, heart rate, coronary flow, mitochondrial membrane potential, impaired mitochondrial respiratory function, increased reactive oxygen species and left ventricular end diastolic pressure. Damage to myocardial ultrastructure was also evident. Both depolarized arrest and especially hyperpolarized cardioplegia significantly reduced these lesions. 5HD partially blocked the beneficial effects of pinacidil cardioplegia but showing no effects on hyperkalemic arrest. CONCLUSIONS: Pinacidil cardioplegia provides better cardioprotection with preservation of hemodynamics, ultrastructure, and mitochondrial function than traditional cardioplegia. The mitochondria K(ATP) channels may play an important role in the protection mechanism.