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Phospholipid-coated microbubbles are ultrasound contrast agents that, when functionalized, adhere to specific biomarkers on cells. In this concise review, we highlight recent developments in strategies for targeting the microbubbles and their use for ultrasound molecular imaging (UMI) and therapy. Recently developed novel targeting strategies include magnetic functionalization, triple targeting, and the use of several new ligands. UMI is a powerful technique for studying disease progression, diagnostic imaging, and monitoring of therapeutic responses. Targeted microbubbles (tMBs) have been used for the treatment of cardiovascular diseases and cancer, with therapeutics either coadministered or loaded onto the tMBs. Regardless of which disease was treated, the use of tMBs always resulted in a better therapeutic outcome than non-tMBs when compared in vitro or in vivo.

Primary malignancies arising in the external auditory canal (EAC) are rare and usually are treated surgically. We review techniques to reconstruct the EAC following ablative surgery, and introduce a rarely utilized tragal skin flap which has particular advantages for reconstruction of limited anterior EAC defects.

The terms "tragal flap", "external auditory canal", "preauricular tragal flap", "reconstructive techniques" were searched on PubMed and Google Scholar.

Our review identified one description of a tragal flap to reconstruct the EAC following resection of a malignancy. We add an additional case of a preauricular tragal flap to reconstruct the anterior EAC following resection of a recurrent basal cell carcinoma located in the EAC that led to a circumferential defect.

There are several surgical techniques that can be utilized to reconstruct the EAC. We describe a novel tragal flap used to reconstruct the anterior EAC following resection of a recurrent tumor.

There are several surgical techniques that can be utilized to reconstruct the EAC. We describe a novel tragal flap used to reconstruct the anterior EAC following resection of a recurrent tumor.

Residential airborne fungi may present obvious risk to human health. However, many countries do not recognize the necessarily need to control residential airborne culturable fungi (RAF). In China, few systemic investigations have been conducted to illustrate the distribution of residential airborne fungi and identify the association between indoor influencing variables and RAF under general living scenario in China.

This study aimed to investigate RAF with the on-site research of 12 typical cities in China, and provided the latest characteristics and potential influencing factors of RAF under general living scenario.

We measured RAF and investigated residential characteristics in 12 typical cities in China, 2018. At least 50 resident families were randomly selected both from downwind and upwind districts in each city with pre-proposed requirements. The RAF were sampled by the six-stage Anderson impactor. PM

and PM

were monitored by calibrated light-scattering dust meters. CO and CO

were monitored turable in China.The mammalian target of rapamycin (mTOR) is a conserved serine/threonine-protein kinase, comprising two subunit protein complexes mTORC1 and mTORC2. In response to insult and cancer, the mTOR pathway plays a crucial role in regulating growth, metabolism, cell survival, and protein synthesis. Key subunits of mTORC1/2 catalyze the phosphorylation of various molecules, including eukaryotic translation initiation factor 4E binding protein 1 (4E-BP1), ribosomal protein S6 kinase β-1 (S6K1). The DNA damage response (DDR) maintains genomic stability and provides an opportunity for treating tumors with defects caused by DNA damaging agents. Many mTOR inhibitors are utilized for the treatment of cancers. However, several clinical trials are still assessing the efficacy of mTOR inhibitors. This paper discusses the role of the mTOR signaling pathway and its regulators in developing cancer. In the following, we will review the interaction between DDR and mTOR signaling and the innovative therapies applied in preclinical and clinical trials for treating cancers.The objective of this study was to provide a biomechanical comparison of two different types of active chairs (AC1 & AC2) versus a static chair (NAC). Thirty healthy participants were recruited fifteen healthy females and fifteen healthy males. Participants worked at a computer workstation (1-h per chair). Equipment included Pressure pads, Electromyography, Near-Infrared Spectroscopy, and Questionnaires (rate of perceived discomfort, seating discomfort questionnaire and exit survey). A significant increase in anterior-posterior postural sway was found on the seat pan with the use of the AC1. An increase in neuromuscular activity of the external obliques and an increase change in total oxygen index (%TOI) values in the gastrocnemius were also found using the AC1, however the difference was not much higher than the NAC and AC2. Lower discomfort scores in the gluteal area were found with the use of active chair AC1 compared to the NAC. Preliminary findings suggest that having an office chair with a split seat pan design shows potential to yield biomechanical and physiological benefits for the sitter, however further research is needed to better understand the ergonomic benefits of active sitting.Work-Related Musculoskeletal Disorders of the Upper Limbs (WRMSDs-ULs) are one of the most common occupational diseases worldwide. Repetitive motion is one of the main risk factors associated with these conditions. Several efforts have been made within the scientific community in order to develop specific methods to assess the risk that repetitive work represents. Furthermore, internationally coordinated work has resulted in the generation of a series of ISO standards to address issues around ergonomics in the workplace. In 2012, Chile adopted the ISO11228-3 standard checklist in its regulatory process, creating the first technical standard of risk management for repetitive motion. The aim of this study is to present the results of a nation-wide online survey of Chilean Health and Safety Practitioners and Ergonomists, which was conducted in order to identify their level of application experience, most commonly adopted practices, and opinions on the first Chilean Standard for WRMSDs-ULs risk assessment. A secoate and public-public organizations contribute to poor consultation, validation, and adaptation processes. Suggestions to improve the current Chilean standard, as well as considerations for developing countries, are presented.The resistance of Rhipicephalus microplus to acaricides is a serious control problem, so its early diagnosis by a molecular technique is important. This study aims to develop a multiplex allele-specific polymerase chain reaction (PCR) for single-nucleotide polymorphisms (SNPs) in the para-sodium channel gene and in the GABA-Cl gene, associated with pyrethroids (cypermethrin and flumethrin) and fipronil resistance, respectively. We used 22 tick field isolates from farms with tick control problems (sampling convenience). These farms are located in departments of northern Uruguay. Three mutations in the sodium channel gene (Domain II S4-5 C190A and G215T; domain III S6 T2134A) and one in the GABA-Cl gene (A286S/L CG856CC/TG) were studied. Mutations G215T and T213A were not detected. In all field isolates, the resistant allele (R) for C190A mutation (knockdown resistance, kdr) was detected, mainly in heterozygous individuals (SR) (11.1% to 86.7%). The highest incidence of the kdr mutant allele occurred in the Taceir frequency varied between 0.06% and 60%. Genotypic analysis shows that tick resistance to both acaricides, especially pyrethroids, is a serious problem. It is important to monitor the resistance using molecular techniques to plan efficient control measures. AZD9291 This is the first report describing kdr and rdl detection in R. microplus in Uruguay.Ferroptosis is a programmed iron-dependent cell death associated with peroxidation of lipids particularly, phospholipids. Several studies suggested a possible contribution of mitochondria to ferroptosis although the mechanisms underlying mitochondria-mediated ferroptotic pathways remain elusive. Reduced glutathione (GSH) is a central player in ferroptosis that is required for glutathione peroxidase 4 to eliminate oxidized phospholipids. Mitochondria do not produce GSH, and although the transport of GSH to mitochondria is not fully understood, two carrier proteins, the dicarboxylate carrier (DIC, SLC25A10) and the oxoglutarate carrier (OGC, SLC25A11) have been suggested to participate in GSH transport. Here, we elucidated the role of DIC and OGC as well as mitochondrial bioenergetics in ferroptosis in H9c2 cardioblasts. Results showed that mitochondria are highly sensitive to ferroptotic stimuli displaying fragmentation, and lipid peroxidation shortly after the onset of ferroptotic stimulus. Inhibition of electron transport chain complexes and oxidative phosphorylation worsened RSL3-induced ferroptosis. LC-MS/MS analysis revealed a dramatic increase in the levels of pro-ferroptotic oxygenated phosphatidylethanolamine species in mitochondria in response to RSL3 (ferroptosis inducer) and cardiac ischemia-reperfusion. Inhibition of DIC and OGC aggravated ferroptosis and increased mitochondrial ROS, membrane depolarization, and GSH depletion. Dihydrolipoic acid, an essential cofactor for several mitochondrial multienzyme complexes, attenuated ferroptosis and induced direct reduction of pro-ferroptotic peroxidized phospholipids to hydroxy-phospholipids in vitro. In conclusion, we suggest that ferroptotic stimuli diminishes mitochondrial bioenergetics and stimulates GSH depletion and glutathione peroxidase 4 inactivation leading to ferroptosis.Exposure to toxic levels of fatty acids (lipotoxicity) leads to cell damage and death and is involved in the pathogenesis of the metabolic syndrome. Since the metabolic consequences of lipotoxicity are still poorly understood, we studied the bioenergetic effects of the saturated fatty acid palmitate, quantifying changes in mitochondrial morphology, real-time oxygen consumption, ATP production sources, and extracellular acidification in hepatoma cells. Surprisingly, glycolysis was enhanced by the presence of palmitate as soon as 1 h after stimulus, while oxygen consumption and oxidative phosphorylation were unchanged, despite overt mitochondrial fragmentation. Palmitate only induced mitochondrial fragmentation if glucose and glutamine were available, while glycolytic enhancement did not require glutamine, showing it is independent of mitochondrial morphological changes. Redox state was altered by palmitate, as indicated by NAD(P)H quantification. Furthermore, the mitochondrial antioxidant mitoquinone, or a selective inhibitor of complex I electron leakage (S1QEL) further enhanced palmitate-induced glycolysis. Our results demonstrate that palmitate overload and lipotoxicity involves an unexpected and early increase in glycolytic flux, while, surprisingly, no changes in oxidative phosphorylation are observed. Interestingly, enhanced glycolysis involves signaling by mitochondrially-generated oxidants, uncovering a novel regulatory mechanism for this pathway.