Agerskovfuttrup1010

Cyclin B1 (CCNB1) is regarded as an oncogene in multiple tumors. This work aims to investigate the expression, function, and related mechanisms of CCNB1 in ovarian carcinoma (OC). Three microarray datasets (GSE14407, GSE18520, and GSE54388) were obtained from the Gene Expression Omnibus (GEO) database and screened for differentially expressed genes (DEGs) of OC tissues and normal ovarian tissues. CCNB1 expression in OC tissues and paracancerous tissues was detected by immunohistochemistry. Kaplan-Meier plotter database was utilized to analyze the correlation between CCNB1 expression and the prognosis of OC patients. After the loss-of-function and gain-of-function cell models were established, cell counting kit-8 (CCK-8), bromo-deoxyuridine (BrdU), and transwell experiments were employed to examine the proliferation, migration, and invasion of OC cells, respectively. The targeting relationship between miR-559 and CCNB1 was verified using the dual-luciferase reporter gene experiment. The expressions of CCNB1 mRd by miR-559, facilitates proliferation, migration, and invasion of OC cells, therefore, working as a potential therapeutic target of OC. This work provides new insights into the clinical diagnosis and treatment of OC.This study discovered a novel chitosanase from Penicillium oxalicum M2 based on a new screening strategy. An extracellular chitosanase was isolated and purified from the fermentation broth of Penicillium oxalicum M2. A 19.34-fold purification was achieved on a cation exchange column. Using sodium dodecylsulfate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis, chitosanase was determined at approximately 42 kDa without any subunits. The sequence of peptide in the protein was identified as SALNKNYITNFSTLR by MALTI-TOF/TOF MS. The maximum catalytic activity of the purified enzyme was 60.45 U/mg at the optimum pH and temperature of 5.5 and 60 °C. The enzyme activity held stability in the range of 35-50 °C and pH 3-4.5. Ca2+, Mn2+, non-ionic surfactants (Tween 20/40/60/80 and Trition X-100) and some common reducing agents (DTT and β-ME) could significantly activate chitosanase. The purified enzyme showed rigorous specificity to chitosan as a substrate. The hydrolysate in the final stage of hydrolysis consisted of chitooligosaccharides with a degree of polymerization ranging from 2 to 5 and without glucosamine or acetylglucosamine. The monomeric enzyme obtained by one-step purification reveal applications potential in sugar industry, and expanded our understanding of the GH75 family chitosanases simultaneously.Patients with coronary artery disease (CAD) often experience anger events before cardiovascular events. Anger is a psychological risk factor and causes underlying psychophysiological mechanisms to lose balance of the autonomic nervous system (ANS). The heart rate variability (HRV) was the common index for ANS regulation. It has been confirmed that heart rate variability biofeedback (HRV-BF) restored ANS balance in patients with CAD during the resting state. However, the effects of HRV-BF during and after the anger event remain unknown. This study aimed to examine the effects of HRV-BF on ANS reactivity and recovery during the anger recall task in patients with CAD. This study was a randomized control trial with a wait-list control group design, with forty patients in the HRV-BF group (for six sessions) and 44 patients in the control group. CompK in vivo All patients received five stages of an anger recall task, including baseline, neutral recall task, neutral recovery, anger recall task, and anger recovery. HRV reactivity in the HRV-BF group at the post-test was lower than that in the control group. HRV recovery at the post-test in the HRV-BF group was higher than that in the control group. The HRV-BF reduced ANS reactivity during anger events and increased ANS recovery after anger events for CAD patients. The possible mechanisms of HRV-BF may increase total HRV, ANS regulation, and baroreflex activation at anger events for patients with CAD, and may be a suitable program for cardiac rehabilitation.

To outline sex-specific features of coronary artery disease (CAD) that should be considered in the assessment of women, including those from ethnic minority populations with suspected stable ischemic heart disease (IHD). Second, to determine the latest nuclear imaging tools available to assess microvascular CAD.

Latest studies indicate that women are more likely to have ischemia with no obstructive coronary arteries (INOCA) and paradoxically have worse outcomes. Therefore, the evaluation of women with suspected IHD should include assessing microvascular and epicardial coronary circulation. The prevalence of CAD is increasing in younger women due to the increased cardiovascular disease (CVD) risk burden. CAD is often underrecognized in these patients. There is increasing recognition that INOCA is not benign and should be accurately diagnosed and managed. Nuclear imaging assesses the full spectrum of CAD from microvascular CAD to multivessel obstructive epicardial CAD. Further research on myocardial blood flow (MBF) assessment with PET MPI is needed.

Latest studies indicate that women are more likely to have ischemia with no obstructive coronary arteries (INOCA) and paradoxically have worse outcomes. Therefore, the evaluation of women with suspected IHD should include assessing microvascular and epicardial coronary circulation. The prevalence of CAD is increasing in younger women due to the increased cardiovascular disease (CVD) risk burden. CAD is often underrecognized in these patients. There is increasing recognition that INOCA is not benign and should be accurately diagnosed and managed. Nuclear imaging assesses the full spectrum of CAD from microvascular CAD to multivessel obstructive epicardial CAD. Further research on myocardial blood flow (MBF) assessment with PET MPI is needed.Psoas abscess is a rare pathology that usually presents with non-specific signs and rare clinical features. These characteristics can delay the diagnosis leading to complications and death. We report a forensic autopsy case of a 65-year-old male, alcoholic, smoker, with a history of hypertension, and urinary infection, who presented to the emergency room for anorexia and consciousness disorder. On physical examination, the patient was febrile and confused. Laboratory exams revealed leukocytosis and elevated C-reactive protein (CRP). Two days later, he died despite extensive resuscitation. Forensic autopsy revealed a large amount of green pus in the left psoas muscle extending to the muscles of the thigh of the same side with multiple cavities. The pus extended to the left kidney with destructive parenchyma and coralliform lithiasis. Histological examination showed destroyed renal tissue by lesions of chronic and acute pyelonephritis with dilatation of the pyelocaliceal cavities. Bacteriological analysis of the pus showed the presence of Escherichia coli. The psoas abscess was secondary to pyonephrosis favored by the immunodeficiency. Thus, death was attributed to a septic shock secondary to a psoas abscess complicating pyonephrosis.A 47-year-old woman with a long-term history of intravenous heroin use was found dead lying on the couch in a pool of blood with the wound in her right groin, 15 × 4 mm in diameter. The autopsy revealed the thickened superficial right femoral artery wall and the tract communication between the artery lumen and the skin surface, with pseudoaneurysm formation, confirmed by microscopic examination. Toxicological findings were negative for heroin and its metabolites. The cause of death was fatal blood loss from ruptured chronic femoral pseudoaneurysm. Persons with a long-term history of intravenous drug use experience injection-related problems prominent vein scarring, lumps, and swelling. The risk of injecting the groin is substantially greater than in typical areas such as the cubital fossa. The proximity of the femoral vein to the femoral artery and nerve poses the risk of accidental trauma to these sites. Accidental groin arterial injections can cause a tear in the arterial wall, on which a pseudoaneurysm can develop. A false or pseudoaneurysm is a breach in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space. In the presented case, the autopsy findings pointed out that the fatal blood loss from femoral pseudoaneurysm rupture occurred probably after trivial trauma (shortly after sexual intercourse) or even spontaneously, and not immediately or shortly after arterial drug injection.We aim to investigate the mechanisms underlying the beneficial effects of exercise rehabilitation (ER) and/or astragaloside (AST) in counteracting amyloid-beta (Aβ) pathology. Aβ oligomers were microinjected into the bilateral ventricles to induce Aβ neuropathology in rats. Neurobehavioral functions were evaluated. Cortical and hippocampal expressions of both BDNF/TrkB and cathepsin D were determined by the western blotting method. The rat primary cultured cortical neurons were incubated with BDNF and/or AST and ANA12 followed by exposure to aggregated Aβ for 24 h. In vivo results showed that ER and/or AST reversed neurobehavioral disorders, downregulation of cortical and hippocampal expression of both BDNF/TrkB and cathepsin D, neural pathology, Aβ accumulation, and altered microglial polarization caused by Aβ. In vitro studies also confirmed that topical application of BDNF and/or AST reversed the Aβ-induced cytotoxicity, apoptosis, mitochondrial distress, and synaptotoxicity and decreased expression of p-TrkB, p-Akt, p-GSK3β, and β-catenin in rat cortical neurons. The beneficial effects of combined ER (or BDNF) and AST therapy in vivo and in vitro were superior to ER (or BDNF) or AST alone. Furthermore, we observed that any gains from ER (or BDNF) and/or AST could be significantly eliminated by ANA-12, a potent BDNF/TrkB antagonist. These results indicate that whereas ER (or BDNF) and/or AST attenuate Aβ pathology by reversing BDNF/TrkB signaling deficits and mitochondrial dysfunction, combining these two potentiates each other's therapeutic effects. In particular, AST can be an alternative therapy to replace ER.Numerous studies have demonstrated the role of neuroinflammation in mediating acute pathophysiological events of early brain injury after subarachnoid hemorrhage (SAH). However, it is not clear how to target this inflammatory cascade after SAH. M1 activation of microglia is an important pathological mechanism driving neuroinflammation in SAH, which is considered aggressive, leading to cytotoxicity and robust inflammation related to the release of proinflammatory cytokines and chemokines after SAH. Thus, reducing the number of M1 microglia represents a potential target for therapies to improve outcomes after SAH. Previous studies have found that inducible nitric oxide synthase (iNOS/NO•) plays an essential role in promoting the survival of M1 microglia by blocking ferroptosis. Ferroptosis is a new type of iron-dependent cellular procedural death associated with pathological cell death related to mammalian degenerative diseases, cerebral hemorrhage, and traumatic brain injury. Here, we investigated the effect of L-NIL, an inhibitor of iNOS, on M1 microglia, neuroinflammation, neuronal cell death, brain edema, and neurological function in an experimental SAH model in vivo and in vitro.