cefoxitin and Inflammation

International studies could already prove a correlation between alexithymia and expressive suppression. This relationship has only been marginally considered in the German literature so far. The prioritized aim of the present study was to investigate a correlative and factorial relationship between alexithymia and expressive suppression.. A total of 317 persons participated in an online survey. Data on alexithymia and expressive suppression were collected using the German versions of the Toronto alexithymia scale (TAS-26) and the emotion regulation questionnaire (ERQ).. The results indicate that the TAS-26 scales in the components "difficulty in identifying feelings" and "difficulty in describing feelings" and the ERQ scale "suppression" in the component of "expressive suppression" have a common construct, which is referred to with the term speechlessness.. The online version contains supplementary material available at 10.1186/s40623-021-01518-w.. Even though the present study confirmed expected differences in complications and morbidity, it suggested that oncoplastic surgery is oncologically safe. Patients undergoing NSM/SSM should be followed closely to allow early detection and treatment of frequently associated complications and ensure timely start of adjuvant therapy.

Topics: Acacia; Acute Disease; Adaptive Immunity; Adolescent; Adult; Aged; Aged, 80 and over; Animals; Animals, Newborn; Anti-Bacterial Agents; Antibodies, Monoclonal; Antigens, Tumor-Associated, Carbohydrate; Biofilms; Biomarkers; Child; Child, Preschool; CRISPR-Cas Systems; Cytokines; Escherichia coli; Female; Gene Expression Profiling; Gene Knockout Techniques; Humans; Hypercalcemia; Hyperoxia; I-kappa B Kinase; Immunity, Cellular; Infant; Infant, Newborn; Inflammation; Interleukin-1 Receptor-Like 1 Protein; Interleukin-13; Kidney; Macrophage Activation; Macrophages; Male; Membrane Transport Modulators; Mice; Mice, Inbred BALB C; Microbial Sensitivity Tests; Middle Aged; Mutation; NF-kappa B p50 Subunit; Oxidative Stress; Pancreatitis; Phenotype; Plant Bark; Plant Extracts; Plant Stems; RNA-Seq; Severity of Illness Index; Sodium-Phosphate Cotransporter Proteins, Type IIa; Sodium-Phosphate Cotransporter Proteins, Type IIc; Staphylococcus aureus; THP-1 Cells; Toll-Like Receptors; Transcription Factor RelA; Transcriptome; Vitamin D3 24-Hydroxylase; Young Adult

Core 1-derived mucin-type O-glycans (O-glycans) are a major component of gastric mucus with an unclear role. To address this, we generated mice lacking gastric epithelial O-glycans (GEC C1galt1-/-). GEC C1galt1-/- mice exhibited spontaneous gastritis that progressed to adenocarcinoma with ∼80% penetrance by 1 yr. GEC C1galt1-/- gastric epithelium exhibited defective expression of a major mucus forming O-glycoprotein Muc5AC relative to WT controls, which was associated with impaired gastric acid homeostasis. Inflammation and tumorigenesis in GEC C1galt1-/- stomach were concurrent with activation of caspases 1 and 11 (Casp1/11)-dependent inflammasome. GEC C1galt1-/- mice genetically lacking Casp1/11 had reduced gastritis and gastric cancer progression. Notably, expression of Tn antigen, a truncated form of O-glycan, and CASP1 activation was associated with tumor progression in gastric cancer patients. These results reveal a critical role of O-glycosylation in gastric homeostasis and the protection of the gastric mucosa from Casp1-mediated gastric inflammation and cancer.

Topics: Animals; Antigens, Tumor-Associated, Carbohydrate; Carcinogenesis; Caspase 1; Female; Gastric Mucosa; Gastritis; Glycosylation; Homeostasis; Humans; Inflammation; Male; Mice; Mucins; Mucus; Neoplasms; Polysaccharides; Stomach Neoplasms

Hyperoxia therapy is often required to treat newborns with respiratory disorders. Prolonged hyperoxia exposure increases oxidative stress and arrests alveolar development in newborn rats. Tn antigen is N-acetylgalactosamine residue that is one of the most remarkable tumor-associated carbohydrate antigens. Tn immunization increases the serum anti-Tn antibody titers and attenuates hyperoxia-induced lung injury in adult mice. We hypothesized that maternal Tn immunizations would attenuate hyperoxia-induced lung injury through the suppression of oxidative stress in neonatal rats. Female Sprague-Dawley rats (6 weeks old) were intraperitoneally immunized five times with Tn (50 μg/dose) or carrier protein at biweekly intervals on 8, 6, 4, 2, and 0 weeks before the day of delivery. The pups were reared in room air (RA) or 2 weeks of 85% O

Topics: Animals; Animals, Newborn; Antibodies; Antigens, Tumor-Associated, Carbohydrate; Biomarkers; Cytokines; Disease Models, Animal; Female; Hyperoxia; Immunization; Immunohistochemistry; Inflammation; Lung Injury; Macrophages, Alveolar; Maternal Exposure; Oxidative Stress; Rats

Tn antigen (GalNAc-α-O-Ser/Thr), a mucin-type O-linked glycan, is a well-established cell surface marker for tumors and its elevated levels have been correlated with cancer progression and prognosis. There are also reports that Tn is elevated in inflammatory tissues. However, the molecular mechanism for its elevated levels in cancer and inflammation is unclear. In the current studies, we have explored the possibility that cytokines may be one of the common regulatory molecules for elevated Tn levels in both cancer and inflammation. We showed that the Tn level is elevated by the conditioned media of HrasG12V-transformed-BEAS-2B cells. Similarly, the conditioned media obtained from LPS-stimulated monocytes also elevated Tn levels in primary human gingival fibroblasts, suggesting the involvement of cytokines and/or other soluble factors. Indeed, purified inflammatory cytokines such as TNF-α and IL-6 up-regulated Tn levels in gingival fibroblasts. Furthermore, TNF-α was shown to down-regulate the COSMC gene as evidenced by reduced levels of the COSMC mRNA and protein, as well as hypermethylation of the CpG islands of the COSMC gene promoter. Since Cosmc, a chaperone for T-synthase, is known to negatively regulate Tn levels, our results suggest elevated Tn levels in cancer and inflammation may be commonly regulated by the cytokine-Cosmc signaling axis.

Topics: Antigens, Tumor-Associated, Carbohydrate; Breast Neoplasms; Bronchi; Cell Line; CpG Islands; Culture Media, Conditioned; Disease Progression; DNA Methylation; Female; Fibroblasts; Gene Expression Regulation, Neoplastic; Genes, ras; Gingiva; Humans; Inflammation; Interleukin-6; Male; Molecular Chaperones; Prognosis; Promoter Regions, Genetic; Prostatic Neoplasms; Signal Transduction; Tumor Necrosis Factor-alpha; Uterine Cervical Neoplasms

Immunoglobulin A nephropathy (IgAN) is the most common form of glomerulonephritis worldwide and is histologically characterized by the deposition of IgA1 and consequent inflammation in the glomerular mesangium. Prior studies suggested that serum IgA1 from IgAN patients contains aberrant, undergalactosylated O-glycans, for example, Tn antigen and its sialylated version, SialylTn (STn), but the mechanisms underlying aberrant O-glycosylation are not well understood. Here we have used serial lectin separation technologies, Western blot, enzymatic modifications, and mass spectrometry to explore whether there are different glycoforms of IgA1 in plasma from patients with IgAN and healthy individuals. Although total plasma IgA in IgAN patients was elevated ∼ 1.6-fold compared with that in healthy donors, IgA1 in all samples was unexpectedly separable into two distinct glycoforms: one with core 1 based O-glycans, and the other exclusively containing Tn/STn structures. Importantly, Tn antigen present on IgA1 from IgAN patients and controls was convertible into the core 1 structure in vitro by recombinant T-synthase. Our results demonstrate that undergalactosylation of O-glycans in IgA1 is not restricted to IgAN and suggest that in vivo inefficiency of T-synthase toward IgA1 in a subpopulation of B or plasma cells, as well as overall elevation of IgA, may contribute to IgAN pathogenesis.

Topics: Adult; Antigens, Tumor-Associated, Carbohydrate; B-Lymphocytes; Female; Galactose; Galactosyltransferases; Glomerular Mesangium; Glomerulonephritis, IGA; Glycosylation; Humans; Immunoglobulin A; Inflammation; Lectins; Male; Peanut Agglutinin; Polysaccharides; Sialyltransferases; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization

Several factors, including uncontrolled inflammation, gut barrier failure, and sepsis, have been implicated in the development of multiple organ failure. To investigate the relative importance and interrelationships among some of these factors, increasing doses of the inflammatory agent zymosan were used to induce a systemic inflammatory state in mice. At nonlethal doses (0.1 and 0.5 mg/g body weight), zymosan caused injury to the intestinal mucosa, increased intestinal xanthine oxidase activity, and promoted bacterial translocation in a dose-dependent fashion. Inhibition or inactivation of xanthine oxidase activity was effective in reducing mucosal injury and bacterial translocation when zymosan was injected at 0.1 mg/g but not at 0.5 mg/g body weight. At a dose of 1 mg/g, the lethal effects of zymosan appeared to be related to gut-origin sepsis, since cefoxitin (1 mg/g) reduced the seven-day mortality rate from 100% to 20% (p less than 0.01). However, at a zymosan dose of 2 mg/g, antibiotics did not improve survival. Zymosan thus induced gut barrier failure and systemic infection in a dose-dependent fashion. Additionally, the mechanism of zymosan-induced bacterial translocation and the relationship of gut-origin sepsis to survival appeared to be related to the magnitude of the inflammatory insult (the dose of zymosan).

Topics: Allopurinol; Animals; Bacteria; Bacterial Infections; Bacterial Physiological Phenomena; Cefoxitin; Colony Count, Microbial; Dose-Response Relationship, Drug; Female; Inflammation; Intestines; Liver; Male; Mice; Tungsten; Xanthine Oxidase; Zymosan

We have noted that prairie dogs given cefoxitin develop diarrhea and lose weight yet survive for periods of up to 4 weeks. Therefore, we tested the hypothesis that cefoxitin causes Clostridium difficile cecitis in prairie dogs. Six prairie dogs were given a single intramuscular dose of 100 mg of cefoxitin per kg of body weight, and six control animals received saline; both groups were sacrificed 1 week later. Controls had no diarrhea and lost 2% of their body weight, whereas cefoxitin-treated animals had diarrhea (P less than 0.001) and lost 16% of their body weight (P less than 0.001); one animals died 6 days after cefoxitin challenge. None of the controls yielded C. difficile or had cecal cytotoxin or pseudomembranes detected. Cecal contents from all cefoxitin-treated animals, however, yielded C. difficile (P less than 0.01) and had cecal cytotoxin present (P less than 0.01). Four of five surviving animals also had cecal pseudomembranes present (P less than 0.01). These results demonstrate that in prairie dogs cefoxitin induces C. difficile cecitis. We conclude that the prairie dog is another model for the study of antibiotic-induced diarrhea. The disease in prairie dogs may have a more chronic course than in other animal models of C. difficile-induced diarrhea and may be useful as a model for studying certain aspects of C. difficile-induced diarrhea.

Topics: Animals; Bacterial Toxins; Cecal Diseases; Cecum; Cefoxitin; Clostridium; Diarrhea; Disease Models, Animal; Inflammation; Sciuridae