The glomus tumor is usually a benign solitary neoplasm that arises from modified smooth muscle cells of the glomus body, a type of neuromyoarterial receptor that plays a role in the regulation of arterial blood flow. We report a case of gastric glomus tumor diagnosed by endoscopic ultrasound-guided fine-needle aspiration. Smears exhibited groups of cohesive, uniform, small, round to polygonal cells with scant cytoplasm, indistinct cell borders, and round, hyperchromatic nuclei with homogeneous chromatin. The cell block contained fragments of cells with similar morphologic features and immunohistochemical staining exhibited positivity for smooth muscle actin and vimentin. The diagnosis was confirmed by the surgically resected specimen. Ultrastructural examination revealed prominent pinocytotic vesicles lining the plasmalemma. In this report, we discuss the differential diagnosis of gastric glomus tumor and compare the cytologic features of this case with two others reported in the literature.
We studied the use of immunocytochemical analysis with material procured by endoscopic ultrasound-guided fine-needle aspiration (EUS-guided FNA) for the diagnosis of subepithelial intramural gastrointestinal (GI) mesenchymal neoplasms (SIGIMNs). We identified all EUS-guided FNA specimens of SIGIMNs that had undergone immunocytochemical analysis. Results were compared with follow-up histologic diagnoses. There were 95 aspirates that were diagnosed as GI mesenchymal tumors (GI stromal tumors [GISTs], n = 46), leiomyomas (n = 38), peripheral nerve sheath tumors (n = 5), and other neoplasms by cytologic examination. Immunoreactivity with antibodies to CD117 always predicted GIST at follow-up; 15 of 16 cases immunoreactive with antibodies to CD34 were found to be GISTs at follow-up. Strong immunoreactivity with antibodies to smooth muscle actin or desmin usually predicted a leiomyoma at follow-up aside from a single glomus tumor and a case with apparent nonneoplastic smooth muscle contaminant. When sufficient material is present, immunocytochemical analysis used with material obtained by EUS-guided FNA is highly predictive of final pathologic diagnosis.
Group B streptococci (GBS) are among the most common causes of life-threatening neonatal infections.Vaccine development since the late 1970s has focused on the capsular polysaccharides, but a safe, effective product is still not available. Our quest for a vaccine turned to the streptococcal C5a peptidase (SCPB). This surface protein is antigenically conserved across most if not all serotypes. A murine model was used to assess the impact of SCPB on clearance of GBS from the lungs of intranasally infected animals. Mutational inactivation of SCPB resulted in more-rapid clearance of streptococci from the lung. Immunization with recombinant SCPB alone or SCPB conjugated to type III capsular polysaccharide produced serotype-independent protection, which was evidenced by more-rapid clearance of the serotype VI strain from the lungs. Immunization of mice with tetanus toxoid-type III polysaccharide conjugate did not produce protection, confirming that protection induced by SCPB conjugates was independent of type III polysaccharide antigen. Histological evaluation of lungs from infected mice revealed that pathology in animals immunized with SCPB or SCPB conjugates was significantly less than that in animals immunized with a tetanus toxoid-polysaccharide conjugate. These experiments suggest that inclusion of C5a peptidase in a vaccine will both add another level to and broaden the spectrum of the protection of a polysaccharide vaccine.
The dietary isoflavone genistein is the focus of much research involving its role as a potential therapeutic agent in a variety of diseases, including cancer and heart disease. However, there is recent evidence that dietary genistein may also have an inhibitory effect on extraintestinal invasion of enteric bacteria. To study the effects of genistein on bacterial adherence and internalization by confluent enterocytes, Caco-2 and HT-29 enterocytes (cultivated for 15-18 d and 21-24 d, respectively) were pretreated for 1 h with 0, 30, 100, or 300 micromol/L genistein, followed by 1-h incubation with pure cultures of Listeria monocytogenes, Salmonella typhimurium, Proteus mirabilis, or Escherichia coli. Pretreatment of Caco-2 and HT-29 enterocytes with genistein inhibited bacterial internalization in a dose-dependent manner (r = 0.60-0.79). Compared to untreated enterocytes, 1-h pretreatment with 300 micromol/L genistein was generally associated with decreased bacterial internalization (P < 0. 05) without a corresponding decrease in bacterial adherence. Using Caco-2 cell cultures, decreased bacterial internalization was associated with increased integrity of enterocyte tight junctions [measured by increased transepithelial electrical resistance (TEER)], with alterations in the distribution of enterocyte perijunctional actin filaments (visualized by fluorescein-labeled phalloidin), and with abrogation of the decreased TEER associated with S. typhimurium and E. coli incubation with the enterocytes (P < 0.01). Thus, genistein was associated with inhibition of enterocyte internalization of enteric bacteria by a mechanism that might be related to the integrity of the enterocyte tight junctions, suggesting that genistein might function as a barrier-sustaining agent, inhibiting extraintestinal invasion of enteric bacteria.
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