Meningocele in the Parapharyngeal Space: A Case Report and Review of the Literature.

The parapharyngeal space has been described as an inverted pyramid shape with the base of the skull and the great cornu of the hyoid bone at the top. Tumors of the parapharyngeal space account for 0.5% of head and neck tumors and a wide range of tumor types can occur in this area, 80% of which are benign, the most common being pleomorphic adenomas of the salivary glands and neurogenic tumors. We present a 39-year-old woman who was hospitalized due to left-sided neck pain with a feeling of blockage in the left ear and hearing loss for 10 months. Imaging showed that the mass was not connected to the cranium and the patient underwent surgical resection via a transoral approach, where the contents of the mass were found to be cerebrospinal fluid, and meningocele in the parapharyngeal space is a rare occurrence. The patient presented mainly with painful symptoms, which were eventually relieved by nerve block therapy.

Causal Relationship Between Body Mass Index and Risk of Otitis Media with Effusion in Children: A Mendelian Randomization Study.

Background: Body mass index(BMI) in children appears to be associated with Otitis media with effusion(OME) in observational studies, but the causal relationship is not clear. Methods: A two-sample Mendelian randomization (MR) study was used to explore the causal relationship between childhood BMI and OME in people of European ancestry. Genome-wide association studies (GWAS) of childhood BMI were used as exposures (n = 61,111), while GWAS of OME were used as outcomes (n = 429,290). The weighted inverse variance method (IVW) was used as a baseline method to test for causality. In addition, MR-Egger, simple mode analysis, weighted median, and weighted mode were used as complementary methods.MR-PRESSO analysis, MR-Egger intercept analysis, and Cochran's Q statistical analysis were also used to detect possible directional heterogeneity and polymorphism. To assess this association, we used ratios (OR) with 95% confidence intervals (ci). All statistical analyses were performed in R. Results: We selected 22 genome-wide significant single nucleotide polymorphisms (SNPs) from GWAS as instrumental variables (IVW). the IVW approach showed evidence supporting a causal relationship between BMI and OME in children (ß = 0.265, SE = 0.113, P = 0.018). MR-Egger regression showed that targeted polymorphisms were unlikely to bias the results bias (intercept=-0.022; P = 0.488), but there was no causal relationship between BMI and OME (ß = 0.584, SE = 0.465, P = 0.224). Although the results of the IVW and MR Egger analyses were not consistent, the IVW analysis maintained higher precision, and the Cochran Q test, heterogeneity and polymorphism tests showed no heterogeneity, no directionality and no polymorphism. Conclusions: MR studies suggest that genetically predicted body mass index in childhood is associated with an increased risk of OME. Notably, given the limitations of this study, the mechanism of association between body mass index and OME in childhood needs further investigation. These results support the importance of effective management of obesity, which may reduce OME occurrence and decrease OME recurrence.

Association of iron deficiency with chronic suppurative otitis media in adults.

BACKGROUND: Chronic suppurative otitis media (CSOM) is a prevalent chronic inflammatory disease globally. Current research suggests a possible association between anaemia and the development of CSOM. OBJECTIVES: The objective of this trial was to investigate the relationship between iron metabolism and chronic suppurative otitis media (CSOM) in adults aged 20-60 years. MATERIALS AND METHODS: A consecutive sampling case-control study was used. The study participants were divided into a case group (42 children diagnosed with CSOM) and a control group (42 children with normal ears). Haemoglobin (Hb), Hematocrit (Hct), mean corpuscular volume of erythrocytes (MCV), serum iron level (SI), unsaturated iron-binding capacity (UIBC), total iron-binding capacity (TIBC), transferrin (TF), ferritin (Fer) were tested in all the participants, and the results were compared with the normal ranges of the World Health Organization (WHO). The comparative analysis of cases and controls was performed using the Fisher extract test, independence t-test, or Mann-Whitney U test. p-value <.05 was considered statistically significant for correlation. RESULTS: There were 61 patients with CSOM and 61 controls included in the study. In the case group, 16 out of 61 patients (26.2%) had low ferritin levels and in the control group, 1 out of 61 patients (1.6%) had low ferritin levels (p < .001). In the case group, 6 (9.8%) of 61 patients had IDA, and in the control group, there were no patients with IDA among 61 patients (p = .027). There were significant differences in SI, UIBC, and Fer parameters between the groups. CONCLUSIONS: In adult patients, the incidence of iron deficiency was higher in CSOM patients than in controls. Iron deficiency may be considered a potential risk factor for chronic suppurative otitis media, and serum iron parameters should be evaluated in these CSOM patients and further studies should be conducted to better understand the potential link between iron deficiency and CSOM.

Microplastics induced inflammation and apoptosis via ferroptosis and the NF-κB pathway in carp.

Microplastics (MPs), a new class of pollutant that threatens aquatic biodiversity, are becoming increasingly prevalent around the world. Fish growth may be severely inhibited by microplastics, resulting in severe mortality. Exposure to microplastics increases the likelihood of intestinal injuries, but the underlying mechanisms remain equivocal. The objective of this study was to investigate the potential toxic mechanisms underlying microplastic-induced intestinal injury in fish and to assist researchers in identifying novel therapeutic targets. In this study, a model of carp exposed to microplastics was established successfully. Histological observation showed that exposure to polyethylene microplastics caused damage to the intestinal mucosal surface and a significant increase in goblet cells, which aggregated on the surface of the mucosa. The mucosal layer was observed to fall off. Lymphocytes in the intestinal wall proliferated and aggregated. TUNEL staining showed that apoptosis occurred in the group exposed to microplastics. The qPCR results showed that the expression of Ferroptosis apoptotic factors COX-2 and ACSL4 was upregulated, while the expression of TFRC, FIH1, SLC7A11, and GPX4 was downregulated. The NF-κB pathway (p-p65, IκBα), inflammatory cytokines (TNF-α, IL-8, IL-6) and apoptosis genes (Bax, Caspase3) were upregulated. Semi-quantitative detection of related proteins by Western blotting was consistent with the gene expression results. In addition, the ELISA assay showed that lipid peroxidation and inflammatory cytokines (TNF-α, IL-1ß, IL-6) were increased in the microplastic exposed group. To conclude, lipid peroxidation induced by microplastics activates the NF-κB pathway and causes ferroptosis, ultimately resulting in intestinal damage and cellular apoptosis.

Surface Properties of Fluorine-Functionalized Metal-Organic Frameworks Based on Inverse Gas Chromatography.

The introduction of the concept of surface properties can help us to better analyze the basic physicochemical property changes of metal-organic framework (MOF) materials before and after fluorine functional group treatment. In this study, several polar and nonpolar probes were selected to determine the surface properties, including surface-dispersive free energy, Lewis acid-base constants of Ni-MOF-74, and perfluoro carboxylic acid-modified Ni-MOF-74-Fn (n = 3, 5, and 7) in the range of 343.15-383.15 K by inverse gas chromatography (IGC). It was observed that the surface energy of the treated Ni-MOF-74-Fn showed a substantial decrease with the growth of the perfluorocarbon alkyl chains and the increase in surface roughness. In addition, Lewis acidic sites exposed by the Ni-MOF-74 material after adopting modification with fluorine functional groups increased with the increase of perfluorinated carboxylic acid chains, and their surface properties changed from amphiphilic acidic to strongly acidic. These results not only enrich the basic physical property data of Ni-MOF-74 but also provide more theoretical basis for the fluorinated functionalized custom-designed MOFs and enrich their applications in the fields of multiphase catalysis, gas adsorption, and chromatographic separation.

Exposure to polystyrene microplastics triggers lung injury via targeting toll-like receptor 2 and activation of the NF-κB signal in mice.

Microplastics are ubiquitous pollutants with a wide range of plastic applications. More recently, microplastics are in the air and can be inhaled into the lungs, causing respiratory diseases. Knowledge of the underlying mechanisms by which microplastics may induce respiratory disease is still limited. This study used intranasal instillation to develop a model of lung injury. The histopathology result showed that the mouse lung had severe inflammatory responses, apoptosis and collagen deposition with chronic exposure to different sizes (Small: 1-5 µm and Large: 10-20 µm) of polystyrene microplastics (PS-MPS), and the damage of smaller sizes was obvious. The expression levels of the Toll-like receptors (TLRs) family, evolutionarily conserved pattern recognition receptors, were detected, and the levels of TLR2 mRNA was significantly increased. In transfection experiments, PS-MPS increased the inflammatory response in HEK293 cells with TLR2 expression. Furthermore, exposure to small polystyrene microplastics promoted oxidative stress and apoptosis, and accelerated the process of fibrosis. Interestingly, inhibition of the NF-κB signal relieves inflammation and oxidative stress, reduces apoptosis, and thus controls the fibrosis process. These results suggested that PS-MPS targeted binding to TLR2 and further exacerbated fibrosis by facilitating inflammation, oxidative stress, and apoptosis with the activation of NF-κB signal.

Tea Polyphenols Protect the Mammary Gland of Dairy Cows by Enhancing Antioxidant Capacity and Regulating the TGF-ß1/p38/JNK Pathway.

Tea polyphenols (TPs) are the main active substances in tea and they have many beneficial effects, such as anti-inflammation, antioxidant, anti-cancer and metabolic regulation effects. The quality of milk is affected by mammary gland diseases and there are substantial economic losses resulting from reduced milk production as a consequence of inflammatory injury of the mammary gland. In this study, transcriptome analysis and molecular biology techniques were used to study the effects of TPs on inflammatory injury of the mammary gland. After intervention with TPs, a total of 2085 differentially expressed genes were identified, including 1189 up-regulated genes and 896 down-regulated genes. GO analysis showed that differentially expressed genes played an important role in proton transmembrane transport, oxidation-reduction reactions and inflammatory response. KEGG enrichment suggested that differential genes were concentrated in the TGF-ß pathway and active oxygen metabolism process. Experiments were performed to confirm that TPs increased SOD, CAT, T-AOC and GSH-Px content along with a reduction in MDA. Meanwhile, TPs inhibited the expression of TGF-ß1 and reduced the phosphorylation of p38 and JNK. The expression of inflammatory cytokines IL-1ß, IL-6 and TNF-α were significantly decreased after intervention with TPs. In summary, all the data indicated that TPs protected the mammary gland by enhancing the antioxidant capacity and down-regulating the TGF-ß1/p38/JNK pathway.

Therapeutic Mechanisms of Berberine to Improve the Intestinal Barrier Function via Modulating Gut Microbiota, TLR4/NF-κ B/MTORC Pathway and Autophagy in Cats.

Background: Inflammatory bowel disease (IBD), a disease that seriously harms human and animal health, has attracted many researchers' attention because of its complexity and difficulty in treatment. Most research has involved rats and dogs, and very little was cats. We should know that gut microbiota varies significantly from animal to animal. Traditional Chinese Medicine and its monomer component have many advantages compared with antibiotics used in pet clinics. Numerous studies have shown berberine (berberine hydrochloride) therapeutic value for IBD. However, the specific mechanism remains to consider. Results: We assessed gut pathology and analyzed fecal bacterial composition using Histological staining and 16S rRNA sequence. Dioctyl sodium sulfosuccinate (DSS) administration destroyed intestinal mucosal structure and changed the diversity of intestinal flora relative to control. RT-PCR and western blot confirmed specific molecular mechanisms that trigger acute inflammation and intestinal mucosal barrier function disruption after DSS treatment. And autophagy inhibition is typical pathogenesis of IBD. Interestingly, berberine ameliorates inflammation during the development of the intestinal by modulating the toll-like receptors 4 (TLR4)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway and activating autophagy. Berberine significantly reduces tumor necrosis factor α (TNF-α), interleukin (IL)-6, and IL-1ß expression in cats' serum. Enhancing the antioxidant effect of IBD cats is one of the protective mechanisms of berberine. We demonstrated that berberine repairs intestinal barrier function by activating the mammalian target of rapamycin (mTOR) complex (MTORC), which inhibits autophagy. Conclusion: Berberine can restore intestinal microbiota homeostasis and regulate the TLR4/NF-κB pathway, thereby controlling inflammatory responses. We propose a novel mechanism of berberine therapy for IBD, namely, berberine therapy can simultaneously activate MTORC and autophagy to restore intestinal mucosal barrier function in cats, which should be further studied to shed light on berberine to IBD.

Superstructured α-Fe2O3 nanorods as novel binder-free anodes for high-performing fiber-shaped Ni/Fe battery.

Fiber-shaped energy storage devices areindispensableparts of wearable and portable electronics. Aqueous rechargeable Ni/Fe battery is a very appropriate energy storage device due to their good safety without organic electrolytes, high ionic conductivity, and low cost. Unfortunately, the low energy density, poor power density and cycling performance hinder its further practical applications. In this study, in order to obtain high performance negative iron-based material, we first synthesized α-iron oxide (α-Fe2O3) nanorods (NRs) with superstructures on the surface of highly conductive carbon nanotube fibers (CNTFs), then electrically conductive polypyrrole (PPy) was coated to enhance the electron, ion diffusion and cycle stability. Theas-prepared α-Fe2O3@PPy NRs/CNTF electrode shows a high specific capacity of 0.62 Ah cm-3 at the current density of 1 A cm-3. Furthermore, the Ni/Fe battery that was assembled by the above negative electrode shows a maximum volumetric energy density of 15.47 mWh cm-3 with 228.2 mW cm-3 at a current density of 1 A cm-3. The cycling durability and mechanical flexibility of the Ni/Fe battery were tested, which show good prospect for practical application. In summary, these merits make it possible for our Ni/Fe battery to have practical applications in next generation flexible energy storage devices.

Two faces of Hippo: activate or suppress the Hippo pathway in cancer.

The Hippo pathway has generated considerable interest in recent years because of its involvement in several key hallmarks of cancer progression and metastasis. Research on the Hippo signaling pathway in cancer has been used to determine the activity of yes-associated protein (YAP) in tumorigenesis and disease progression. Previous studies have shown that the Hippo pathway can be used as a target to inhibit YAP activity and is a viable treatment for cancer. However, more studies are required to further advance our understanding of the Hippo signaling pathway in cancer. It has been shown that knockout of serine/threonine-kinases LATS1/2 in the Hippo pathway suppresses cancer immunity in mice. In addition, suppression of the oncogene YAP could contribute toward cancer immune therapy. Therefore, regulation of Hippo signaling can be an attractive alternative strategy for cancer treatment. This review will provide a summary of currently known compounds that activate or suppress the Hippo pathway.

Trends and Prospects of Stem Cell Research in China.

Great progresses have been made in fundamental and clinical stem cell research in China in recent years. The official policy on stem cells, which was announced in 2015, seems as the spring of stem cell therapy in China. However, the regulation, governance, and management of clinical expectations are still challenging. This review summarized the current stem cell research and development in the field, as well as its rapidly evolving commercial, regulatory and ethical environment in China. As expected, the prospects of stem cells in China look prospective.

Compensatory Increase of Transglutaminase 2 Is Responsible for Resistance to mTOR Inhibitor Treatment.

The mechanistic target of rapamycin complex 1 (mTORC1) plays a crucial role in controlling cell growth and homeostasis. Deregulation of mTOR signaling is frequently observed in some cancers, making it an attractive drug target for cancer therapy. Although mTORC1 inhibitor rapalog-based therapy has shown positive results in various pre-clinical animal cancer studies, tumors rebound upon treatment discontinuation. Moreover, several recent clinical trials showed that the mTORC1 inhibitors rapamycin and rapalog only reduce the capacity for cell proliferation without promoting cell death, consistent with the concept that rapamycin is cytostatic and reduces disease progression but is not cytotoxic. It is imperative that rapamycin-regulated events and additional targets for more effective drug combinations be identified. Here, we report that rapamycin treatment promotes a compensatory increase in transglutaminase 2 (TGM2) levels in mTORC1-driven tumors. TGM2 inhibition potently sensitizes mTORC1-hyperactive cancer cells to rapamycin treatment, and a rapamycin-induced autophagy blockade inhibits the compensatory TGM2 upregulation. More importantly, tumor regression was observed in MCF-7-xenograft tumor-bearing mice treated with both mTORC1 and TGM2 inhibitors compared with those treated with either a single inhibitor or the vehicle control. These results demonstrate a critical role for the compensatory increase in transglutaminase 2 levels in promoting mTORC1 inhibitor resistance and suggest that rational combination therapy may potentially suppress cancer therapy resistance.