Background: Toxoplasma gondii infection causes intestinal inflammation and diarrhea indicating possible intestinal motor dysfunction. Anatomical studies have shown alterations in the colonic myenteric plexus, but it is unknown whether this impacts motility and therefore whether motility is a target for treatment. We determined whether colonic coordinated movements are compromised by toxoplasmic infection and how it is associated with anatomical changes. Methods: Male Wistar rats were evaluated at 6, 12, 24, 48, and 72 hours and 30 days postinfection (dpi) and controls. Infected rats received orally 5 × 10 3 sporulated oocysts of strain ME-49 (genotype II) of T gondii. The colon was collected for anatomical analysis (including the myenteric plexus immunolabeled with HuC/D, nNOS, and ChAT) and motility analysis in vitro (conventional manometry). Fecal output was measured daily. Key Results: At 12 hours postinfection, T gondii caused hypertrophy of the muscularis externa layer of the distal colon. There was loss of total, nitrergic, and cholinergic myenteric neurons in the proximal colon at 30 day postinfection (dpi); however, only loss of cholinergic neurons was found in the distal colon. Contractile complexes in the middle and distal colon were longer in duration in infected animals, which was associated with slower migration of the colonic motor complex. However, gastrointestinal transit time and fecal pellet output remained unchanged during the T gondii infection. Conclusions and Inferences: Toxoplasma gondii caused myenteric neuronal loss in the proximal and distal colon and altered the motility pattern in the middle and distal colon to a more propulsive phenotype.

These findings highlight some important changes in diabetic animal responses to C. albicans infection that may be important to the pathophysiological processes underpinning cutaneous candidiasis in diabetic patients.

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Purpose Metastasis represents the major cause of deaths in cancer patients, and the tumor surrounding extracellular matrix (ECM) passes through changes in its organization during the evolution of this process. Therefore, the aim of the present study was to quantify the deposition of proteins that constitute the ECM, namely total collagen, collagen I (Col I) and collagen III (Col III) in samples from patients with metastatic (mPCa) and non-metastatic prostate cancer (PCa), in addition of evaluating the basement membrane integrity. Methods Tissue samples from 60 patients were divided into three groups according to parameters ISUP grade, TNM staging and PSA concentration: better prognosis (n = 20), worse prognosis (n = 23) and metastatic (n = 17). To quantify collagen, the Picrosirius Red technique was used with further analysis under a polarization microscope, and to basement membrane analysis the Periodic Acid Schiff (PAS) technique was employed, where the coloring was classified in G1, G2 and G3. Results It was observed that the Col I/ Col III ratio was higher in the metastatic group in relation to better prognosis (p = 0.012) and worse prognosis (p = 0.018) groups. About the basement integrity, it was observed that its constitution in the malignant tumor tissue differed from the adjacent non-tumor tissue (p = 0.000). Also, the worsening in the tumor tissue integrity was positively correlated with worse prognosis parameters (advanced ISUP grade, extraprostatic extension and perineural invasion). Conclusion Our study indicates that the absence of Col III can constitute a marker for potential metastatic tumors. The basement membrane integrity also seems to be an indicator of poor prognosis in malignant prostatic tumors.