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Pulmonary hernia is a rare disease caused mostly by chest trauma. Patients often present with non-specific signs and symptoms. Currently, there is no unified approach to treating it. For asymptomatic pulmonary hernias, conservative treatment has been chosen in the past. However, the increasing number of cases has shown that surgery has a more positive effect on some patients with asymptomatic pulmonary hernias. A 63-year-old female patient who accidentally fell from an agricultural vehicle while doing farm work presented with back pain and lower limb paralysis. Her vital signs were stable. A chest computed tomography (CT) scan showed the patient had a pulmonary hernia, thoracic vertebra Chance fracture, rib fractures, and right hydropneumothorax. The patient received an open reduction internal fixation (ORIF) of the thoracic vertebra at the trauma emergency center. The postoperative chest CT scan showed that the pulmonary hernia had reset to the chest cavity. Subsequently, the patient got a pulmonary hernia repair at the thoracic surgery department. The patient was discharged on the 19th day after the injury. Long-term follow-up showed good recovery from the thoracic trauma. The patient had a pulmonary hernia combined with thoracic Chance fracture and other injuries. Surgical repair achieved satisfactory results. We lack guidelines on whether to manage pulmonary hernias surgically. Patients with asymptomatic pulmonary hernias particularly should have their long-term prognoses fully evaluated. Surgery is needed if the patient has high-risk factors and severe intercostal muscle defects. • Pulmonary hernias that co-occur with Chance fractures are very rare. • Standardized guidelines for treating pulmonary hernias with varying degrees of injury do not exist. • Surgery reduces complications and improves quality of life for some patients. [ABSTRACT FROM AUTHOR]

Bio-based materials from Cardanol/cardol with episulfide group (CCES) and epoxy group (CCEO) were synthesized and further blended with commercial bisphenol-A diglycidyl ether type epoxy resin (DGEBA) for anti-corrosion coating application. The curing behavior of CCEO and CCES confirmed that episulfide exhibited a faster curing rate and higher curing conversion than epoxide. Anticorrosion properties of composite system CCEO/CCES and DGEBA were also carried out. Equilibrium water content of CCES-DGEBA blend was much lower than neat DGEBA and CCEO-DGEBA composite system in water absorption test, which met agreement with that CCES-DGEBA blend system revealed better adhesive to the metal compared with DGEBA and CCEO-DGEBA blend in lap sheer strength assessment. Further, CCES-DGEBA blend with 20 wt% of CCES exhibited optimized performance in corrosion resistance as it possessed the higher impedance modulus at low frequencies in EIS bode plots, lowest corrosion current and the highest corrosion voltage in Tafel test. [ABSTRACT FROM AUTHOR]

[Display omitted] • A novel method using metal-organic framework of NH2-MIL-101(Fe) for the enrichment and simultaneous determination of 12 nitrosamines (NAs) was firstly developed in antibody drug product analysis. • The proposed method has been successfully optimized and validated obtaining good analytical parameters especially for a better performance of LOD. • It exhibits relatively simple and convenient pretreatment and highly adsorption efficiency for NAs enrichment, as well as an environment friendly method. A highly efficient and convenient method for the simultaneous determination of 12 N-nitrosamines (NAs) has been developed using an amine-functionalized metal-organic framework (NH 2 -MIL-101(Fe)) as sorbent for dispersive micro-solid phase extraction (D-μSPE) coupled with LC-MS/MS in biopharmaceuticals. The experimental variables involved in the extraction process (i.e., amount of the sorbent, extraction time, desorption time, ionic strength, desorption solvent and volume) were optimized to achieve the best extraction efficiency of the target analytes. Under the optimum conditions, the method was successfully validated, showing good linearity in the range of 0.5–3.0 μg/L with determination coefficients (R 2) higher than 0.990, repeatability (RSD ≤ 10.0%, spiked level at 2.0 μg/L) and precision (RSD ≤ 8.2%). The limit of detection (LOD) and limit of quantitation (LOQ) were in the range of 0.005–0.025 μg/L and 0.010–0.250 μg/L, respectively. Satisfactory recoveries ranging from 82.4 to 116.8% were obtained by spiking standards at three different concentrations (0.5 μg/L, 2.0 μg/L and 3.0 μg/L). Other validation parameters, including specificity, stability, and robustness, met the validation criteria. More importantly, the plausible adsorption mechanism on NH 2 -MIL-101(Fe) was proposed by Fourier-transform infrared (FTIR) spectra technique. Finally, this method was successfully applied to detect trace nitrosamines in biopharmaceuticals. [ABSTRACT FROM AUTHOR]

Acute cadmium (Cd) exposure is a significant risk factor for renal injury and lacks effective treatment strategies. Ferroptosis is a recently identified iron-dependent form of nonapoptotic cell death mediated by membrane damage resulting from lipid peroxidation, and it is implicated in many diseases. However, whether ferroptosis is involved in Cd-induced renal injury and, if so, how it operates. Here, we show that Cd can induce ferroptosis in kidney and renal tubular epithelial cells, as demonstrated by elevation of intracellular iron levels and lipid peroxidation, as well as impaired antioxidant production. Treatment with a ferroptosis inhibitor alleviated Cd-induced cell death. Intriguingly, we established that Cd-induced ferroptosis depended on endoplasmic reticulum (ER) stress, by demonstrating that Cd activated the PERK-eIF2α-ATF4-CHOP pathway and that inhibition of ER stress reduced ferroptosis caused by Cd. We further found that autophagy was required for Cd-induced ferroptosis because the inhibition of autophagy by chloroquine mitigated Cd-induced ferroptosis. Furthermore, we showed that iron dysregulation by ferritinophagy contributed to Cd-induced ferroptosis, by showing that the iron chelator desferrioxamine alleviated Cd-induced cell death and lipid peroxidation. In addition, ER stress is likely activated by MitoROS which trigger autophagy and ferroptosis. Collectively, our results indicate that ferroptosis is involved in Cd-induced renal toxicity and regulated by the MitoROS-ER stress-ferritinophagy axis. [Display omitted] • Cadmium (Cd) exposure induces ferroptosis in mice and renal tubular epithelial cells. • ER stress is required for Cd-induced ferroptosis in renal tubular epithelial cells. • ER stress-mediated ferritinophagy promotes ferroptosis by the degradation of ferritin. • Mitochondrial ROS manipulates the ER stress-autophagy triggered ferroptosis caused by Cd. [ABSTRACT FROM AUTHOR]

• Kynurenic acid (KYNA) alleviates LPS-induced mastitis in mice. • KYNA improves the integrity of blood-milk barrier and limits pro-inflammatory cytokines expression in vivo and in vitro. • KYNA inhibits NF-κB and activates of Nrf2/Ho-1 signaling pathways. • The inhibition of KYNA on LPS-induced inflammation is mediated by GPR35. • KYNA ameliorates S. aureus and E. coli induced mastitis in mice. Mastitis is one of the most serious diseases in humans and animals, especially in the modern dairy industry. Seeking safe and effective mastitis prevention strategies is urgent since food safety and drug residues in milk remain an enormous concern, despite the contribution of antibiotics to control mastitis. Kynurenic acid (KYNA), derived from the kynurenine pathway of tryptophan metabolism, has been shown to exhibit anti-inflammatory and immunomodulatory effects in many diseases. Recently, it was reported that impaired KYNA levels were associated with mastitis. However, the physiological role of KYNA in mastitis has not yet been elucidated. Therefore, the aim of this study was to investigate the protective role of KYNA in pathogen-induced mastitis in mice, as well as the underlying mechanism of this effect. We first evaluated the effects of KYNA on LPS-induced mastitis in mice. Additionally, the underlying anti-inflammatory mechanism of KYNA was investigated in mammary epithelial cells (MMECs). Furthermore, we examined the effects of KYNA on S. aureus and E. coli induced mastitis in mice. Our results demonstrated that KYNA alleviated LPS-induced mastitis by reducing inflammatory responses and enhancing blood-milk barrier integrity. The fundamental mechanisms involved the inhibition of NF-κB and activation of Nrf2/Ho-1, which is probably mediated by G protein-coupled receptor 35 but not aryl hydrocarbon receptor. Notably, KYNA also protected against S. aureus and E. coli induced mastitis in mice. In conclusion, our results highlight the role of KYNA in mastitis and serve as a basis for using endogenous metabolite as a novel preventative or therapeutic strategy for disease intervention. [ABSTRACT FROM AUTHOR]

3-Hydroxy-3-methylglutaryl coenzyme-A reductase (HMGR) is generally regarded as targets for the treatment of hypercholesterolemia. HMGR inhibitors (more commonly known as statins) are discovered as plasma cholesterol lowering molecules. In this work, 120 atorvastatin analogues were studied using a combination of molecular modeling techniques including three-dimensional quantitative structure-activity relationship (3D-QSAR), molecular docking and molecular dynamics (MD) simulation. The results show that the best CoMFA (comparative molecular field analysis) model has q2=0.558 and r2=0.977, and the best CoMSIA (comparative molecular similarity indices analysis) model has q2=0.582 and r2=0.919. Molecular docking and MD simulation explored the binding relationship of the ligand and the receptor protein. The calculation results indicated that the hydrophobic and electrostatic fields play key roles in QSAR model. After MD simulation, we found four vital residues (Lys735, Arg590, Asp690 and Asn686) and three hydrophobic regions in HMGR binding site. The calculation results show that atorvastatin analogues obtained by introduction of F atoms or gem-difluoro groups could obviously improve the inhibitory activity. The new HMGR inhibitor analogues design in this Letter had been submitted which is being currently synthesized by our laboratories. [ABSTRACT FROM AUTHOR]