Ureaplasma parvum meningitis following atypical choroid plexus papilloma resection in an adult patient: a case report and literature review.

BACKGROUND: While Ureaplasma parvum has previously been linked to the incidence of chorioamnionitis, abortion, premature birth, and perinatal complications, there have only been rare reports of invasive infections of the central nervous system (CNS) in adults. Owing to its atypical presentation and the fact that it will yield sterile cultures using conventional techniques, diagnosing U. parvum meningitis can be challenging. CASE PRESENTATION: We describe a case of U. parvum meningitis detected in an adult patient following surgical brain tumor ablation. After operation, the patient experienced epilepsy, meningeal irritation, and fever with unconsciousness. Cerebrospinal fluid (CSF) analysis showed leukocytosis (484 * 106 /L), elevated protein levels (1.92 g/L), and decreased glucose concentrations (0.02 mmol/L). Evidence suggested that the patient was suffering from bacterial meningitis. However, no bacterial pathogens in either CSF or blood were detected by routine culture or serology. The symptoms did not improve with empirical antibiotics. Therefore, we performed metagenomic next-generation sequencing (mNGS) to identify the etiology of the meningitis. Ureaplasma parvum was detected by mNGS in CSF samples. To the best of our knowledge, this case is the first reported instance of U. parvum meningitis in an adult patient in Asian. After diagnosis, the patient underwent successful moxifloxacin treatment and recovered without complications. CONCLUSIONS: As mNGS strategies can enable the simultaneous detection of a diverse array of microbes in a single analysis, they may represent a valuable means of diagnosing the pathogens responsible for CNS infections and other clinical conditions with atypical presentations.

Clinical significance of sHER2­ECD and calpain­10 expression in tumor tissues of patients with breast cancer.

Human epidermal growth factor receptor 2 (HER2) is composed of an extracellular domain (ECD), a lipophilic transmembrane region and an intracellular domain (ICD). The most commonly used method to determine the status of HER2 is immunohistochemistry. However, false­negative results are sometimes given, which causes some patients to lose the opportunity for anti­HER2 therapy. We found that calpain­10 may prohibit HER2­ECD into peripheral blood resulting in a HER2­negative result by the immunohistochemical method. We enrolled 289 patients into our experiment to assess the relationship between sHER2­ECD and calpain­10. The results showed that there was a positive correlation between sHER2­ECD and calpain­10. Moreover, we also investigated the prognostic values of sHER2­ECD and calpain­10 in breast cancer patients. According to the follow­up results, positive sHER2­ECD and tissue calpain­10 were indicative of a poor prognosis in breast cancer patients. Subsequently, we further validated the relationship between the two molecules in in vitro experiments. In the in vitro experiments, the level of HER2­ECD in the culture medium was increased or decreased with a decrease or increase in calpain­10 by transfection technology, showing an inverse association. The results indicated that sHER2­ECD and tissue calpain­10 levels were powerful factors to assess the status of HER2. In combination with tissue HER2 detection, the occurrence of false­negative HER2 was reduced, providing patients with additional treatment opportunities. In conclusion, sHER2­ECD and tissue calpain­10 may be used as new prognostic indices for breast cancer.

Mechanism analysis of colorectal cancer according to the microRNA expression profile.

The present study aimed to identify specific microRNAs (miRs) and their predicted target genes to clarify the molecular mechanisms of colorectal cancer (CRC). An miR expression profile (array ID, GSE39833), which consisted of 88 CRC samples with various tumor-necrosis-metastasis stages and 11 healthy controls, was downloaded from the Gene Expression Omnibus database. Subsequently, the differentially expressed miRs and their target genes were screened. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathways of target genes were analyzed using the Database for Annotation Visualization and Integrated Discovery. A protein-protein interaction (PPI) network of the target genes was constructed using the Search Tool for the Retrieval of Interacting Genes database. The present study identified a total of 18 differentially expressed miRs (upregulated, 8; downregulated, 10) in the sera of the CRC patients compared with the healthy controls. Of these, 3 upregulated (let-7b, miR-1290 and miR-126) and 2 downregulated (miR-16 and miR-760) differentially expressed miRs and their target genes, including cyclin D1 (CCND1), v-myc avian myelocytomatosis viral oncogene homolog (MYC), phosphoinositide-3-kinase, regulatory subunit 2 (beta) (PIK3R2) and SMAD family member 3 (SMAD3), were significantly enriched in the CRC developmental pathway. All these target genes had higher node degrees in the PPI network. In conclusion, let-7b, miR-1290, miR-126, miR-16 and miR-760 and their target genes, CCND1, MYC, PIK3R2 and SMAD3, may be important in the molecular mechanisms for the progression of CRC.

Prevalence of Th17 and Treg cells in gastric cancer patients and its correlation with clinical parameters.

Th17 cells and CD4+CD25+ regulatory T (Treg) cells have been reported to share reciprocal developmental pathways but exhibit opposite effects, and the balance between them controls inflammation and autoimmune diseases. However, information regarding Th17/Treg cells in cancer-bearing hosts is still limited. In the present study, we investigated the distribution of Th17 cells in relation to Treg cells in gastric cancer patients, and evaluated how the imbalance in Th17/Treg cells in gastric cancer correlates with clinical and pathological parameters. We observed that the accumulation of Th17 and Treg cells in the tumor microenvironment was gradually increased according to disease progression, leading to an imbalance in Th17/Treg cells in gastric cancer patients. TGF-ß and interleukin (IL)­6 present in the gastric cancer microenvironment promoted the differentiation and expansion of Th17 cells, and increased numbers of Th17 cells promoted tumor progression through promotion of inflammation by secretion of IL-17. Treg cells promoted tumor progression by helping cancer cells escape from host immunosurveillance by secreting TGF-ß, and a high level of TGF-ß in the tumor microenvironment promoted differentiation and expansion of Treg cells. In conclusion, the imbalance in Th17/Treg cells was involved in the development and progression of gastric cancer. A better understanding of the nature, regulation, and function of Th17 and Treg cells in tumor immunity may aid in the development of novel and effective immunotherapy for gastric cancer.