Chamomile (Matricaria chamomilla L.) is a popular herbal tea for the treatment of hepatitis and cholecystitis in traditional Uygur medicines.

To investigate the anti-inflammatory activity and chemical composition of M. chamomilla, and clarify its molecular mechanism.

M. chamomilla was extracted with 75% ethanol and then extracted with different solvents to obtain five fractions, namely petroleum ether fraction (EOPE), dichloromethane fraction (EOD), ethyl acetate fraction (EOEA), n-butanol fraction (EOB), and water fraction (EOW). Cytotoxicity and the effect on the nitric oxide (NO) production of RAW264.7cells induced by LPS of the five fractions were screened, and the most active one (EOD) was selected for further investigations. The components of EOD were identified by LC-MS/MS analysis in combination with comparison of retention time and UV absorption with authentic compounds by HPLC. In addition, five most abundant compounds of EOD were isolation by column chromatography and semi-preparative HPLC anthat EOD significantly decreased the protein expression levels of inflammatory factors (PGE

, MCP-1, IL-6, TNF-α), iNOS, COX-2, NF-κB (p-P65 and p-IκBα), MAPKs (p-p38, p-ERK and p-JNK), and increased the protein expression levels of Nrf2, HO-1 and CYP2E1. In addition, EOD blocked the p65 protein into the nucleus and promoted the nuclear translocation of Nrf2 in RAW264.7cells induced by LPS.

M. chamomilla exerted anti-inflammatory effect via NF-κB, MAPK and Nrf2/HO-1 pathways. It could be further applied as a safe anti-inflammatory agent from natural source.

M. chamomilla exerted anti-inflammatory effect via NF-κB, MAPK and Nrf2/HO-1 pathways. It could be further applied as a safe anti-inflammatory agent from natural source.Individuals with Down syndrome (DS), the result of trisomy of human chromosome Hsa21 (Ts21), present with an array of skeletal abnormalities typified by altered craniofacial features, short stature and low bone mineral density (BMD). While bone deficits progress with age in both sexes, low bone mass is more pronounced in DS men than women and osteopenia appears earlier. In the current study, the reproductive hormone status (FSH, LH, testosterone) of 17 DS patients (males, ages range 19-52 years) was measured. Although testosterone was consistently low, the hypothalamic-pituitary-gonadal axis was intact with corresponding rises in FSH and LH. To provide further insight into the heterogeneity of the bone mass in DS, the skeletal phenotypes of three of the most used murine DS models, Ts65Dn (Ts65), TC1, and Dp16(Yey1) (Dp16) were characterized and contrasted. Evaluation of the bone phenotype of both male and female 3-month-old Dp16 mice demonstrated sexual dimorphism, with low bone mass apparent in males, as it is in Ts65, but not in female Dp16. In contrast, male TC1 mice had no apparent bone phenotype. To determine whether low bone mass in DS impacted fracture healing, fractures of the middle phalanx (P2) digits were generated in both male and female Dp16 mice at 15 weeks of age, an age where the sexually dimorphic low BMD persisted. Fracture healing was assessed via in vivo microCT over (13 weeks) 93 days post fracture (DPF). At 93 DPF, 0 % of DS male (n = 12) or female (n = 8) fractures healed, compared to 50 % of the male (n = 28) or female (n = 8) WT littermate fractures. MicroCT revealed periosteal unbridged mineralized callus formation across the fracture gap in Dp16 mice, which was confirmed by subsequent histology. These studies provide the first direct evidence of significantly impaired fracture healing in the setting of DS.The pathological features of inflammatory bowel disease necessitate therapeutic strategies aimed at restoring intestinal mucosal barrier function in addition to controlling inflammation. Paeoniflorin, a bioactive herbal constituent isolated from the root of Paeonia albiflora Pall, has been reported to protect against acute colitis in mice. However, the direct molecular target of paeoniflorin in preventing colitis remains elusive. Here, we evaluated the therapeutical effects of Paeoniflorin using IL-10-/- chronic colitis model, and explored the precise mechanism of action involved. Our results demonstrated that intragastric administration of Paeoniflorin significantly ameliorated inflammatory response and restored the aberrant intestinal proliferation and differentiation in IL-10-/-colitis mice. By utilizing a chemical biology approach, we identified C1qa, a crucial component of C1q, is the direct target of Paeoniflorin. Binding of Paeoniflorin to C1qa prevented the cleavage of C1q on macrophages, resulting in the aggregation of surface membrane-anchored C1q and the diminished C1q secretion. The excessive surface membrane-anchored C1q significantly enhanced the phagocytic capability of macrophages and promoted the elimination of infiltrated bacteria and inflammatory cells in mouse colon. The reduced C1q secretion conferred by Paeoniflorin dampened Wnt/β-catenin signaling activation, thereby rectifying the aberrant proliferation and differentiation of intestinal stem cells (ISCs). In summary, our study demonstrates that Paeoniflorin can orchestrate mucosal healing and intestinal inflammation elimination through C1q-bridged macrophage-ISCs crosstalk, highlighting a novel strategy to treat chronic colitis by restoring mucosal homeostasis via targeting C1q.Epithelial-to-mesenchymal transition (EMT) mechanism is responsible for metastasis of tumor cells and their spread to various organs and tissues of body, providing undesirable prognosis. In addition to migration, EMT increases stemness and mediates therapy resistance. Hence, pathways involved in EMT regulation should be highlighted. STAT3 is an oncogenic pathway that can elevate growth rate and migratory ability of cancer cells and induce drug resistance. The inhibition of STAT3 signaling impairs cancer progression and promotes chemotherapy-mediated cell death. Present review focuses on STAT3 and EMT interaction in modulating cancer migration. First of all, STAT3 is an upstream mediator of EMT and is able to induce EMT-mediated metastasis in brain tumors, thoracic cancers and gastrointestinal cancers. Therefore, STAT3 inhibition significantly suppresses cancer metastasis and improves prognosis of patients. EMT regulators such as ZEB1/2 proteins, TGF-β, Twist, Snail and Slug are affected by STAT3 signaling to stimulate cancer migration and invasion. Different molecular pathways such as miRNAs, lncRNAs and circRNAs modulate STAT3/EMT axis. Furthermore, we discuss how STAT3 and EMT interaction affects therapy response of cancer cells. Finally, we demonstrate targeting STAT3/EMT axis by anti-tumor agents and clinical application of this axis for improving patient prognosis.

Transplant recipients are highly susceptible to multidrug-resistant (MDR) related infections. The lack of early appropriate antimicrobial treatment may contribute to the high mortality due to MDR-related infections in transplant recipients especially in case of metallo-β-lactamases.

In this review, we present the current state of knowledge concerning multidrug-resistant Gram negative bacilli’s risk management in the care of solid-organ transplant recipients and suggest control strategies.

We searched for studies treating MDR g-negative bacilli related infections in the renal and hepatic transplant patient population. We included randomized and observational studies.

Solid-organ transplant is the best therapeutic option for patients diagnosed with end-stage organ disease. While the incidence of opportunistic infections is decreasing due to better prevention, the burden of „classical” infections related to MDR bacteria especially related to Gram-negative bacteria is constantly increasing. Over the last antibiotics.

Multidrug-resistant Gram-negative bacteria are associated with high morbidity and mortality in solid organ transplant recipients. It seems important to identify patients at risk of colonization/MDR bacteria to evaluate strategies to limit the risk of secondary infections and to minimize the inappropriate use of broad-spectrum antibiotics.The advent of transcatheter aortic valve implantation has revolutionized the treatment of calcific aortic valve stenosis. Elderly patients who were previously considered inoperable have currently an efficacious and safe therapy that provides better survival. In addition, current practice guidelines tend to recommend earlier intervention to avoid the irreversible consequences of long-lasting pressure overload caused by the stenotic aortic valve. Appropriate timing of the intervention relies significantly on imaging techniques that provide information on the severity of the aortic stenosis as well as on the hemodynamic consequences and cardiac remodeling. While left ventricular ejection fraction remains one of the main functional parameters for risk stratification in patients with severe aortic stenosis, advances in imaging techniques have provided new structural and functional parameters that allow the identification of patients who will benefit from intervention before the occurrence of symptoms or irreversible cardiac damage. Furthermore, ongoing research aiming to identify the medical therapies that can effectively halt the progression of aortic stenosis relies heavily on imaging endpoints, and new imaging techniques that characterize the metabolic activity of calcific aortic stenosis have been proposed to monitor the effects of these therapies. The present review provides an up-to-date overview of the imaging advances that characterizes the pathophysiology and that have changed the management paradigm of aortic stenosis.

Spontaneous coronary artery dissection (SCAD) is a rare cause of acute myocardial infarction (AMI). We sought to compare the results on in-hospital mortality and 30-day readmission rates among patients with AMI-SCAD vs AMI due to other causes (AMI-non-SCAD).

Risk-standardized in-hospital mortality (rIMR) and risk-standardized 30-day readmission ratios (rRAR) were calculated using the minimum dataset of the Spanish National Health System (2016-2019).

A total of 806 episodes of AMI-SCAD were compared with 119 425 episodes of AMI-non-SCAD. Patients with AMI-SCAD were younger and more frequently female than those with AMI-non-SCAD. Crude in-hospital mortality was lower (3% vs 7.6%; P<.001) and rIMR higher (7.6±1.7% vs 7.4±1.7%; P=.019) in AMI-SCAD. However, after propensity score adjustment (806 pairs), the mortality rate was similar in the 2 groups (AdjOR, 1.15; 95%CI, 0.61-2,2; P=.653). Crude 30-day readmission rates were also similar in the 2 groups (4.6% vs 5%, P=.67) whereas rRAR were lower (4.7±1% vs 4.8%±1%; P=.015) in patients with AMI-SCAD. Again, after propensity score adjustment (715 pairs) readmission rates were similar in the 2 groups (AdjOR, 1.14; 95%CI, 0.67-1.98; P=.603).

In-hospital mortality and readmission rates are similar in patients with AMI-SCAD and AMI-non-SCAD when adjusted for the differences in baseline characteristics. These findings underscore the need to optimize the management, treatment, and clinical follow-up of patients with SCAD.

In-hospital mortality and readmission rates are similar in patients with AMI-SCAD and AMI-non-SCAD when adjusted for the differences in baseline characteristics. These findings underscore the need to optimize the management, treatment, and clinical follow-up of patients with SCAD.