Transperineal ultrasound guided prostate seed brachytherapy (PSI) is a common procedure performed for the long-term control of prostate cancer. After the completion of the procedure, a cystoscopy is often performed to ensure that no seeds were inadvertently introduced into the bladder. After the patient recovers, he is generally given a trial of voiding. If the patient cannot urinate or has significant urinary retention, a Foley catheter is generally replaced, and the patient is sent home with the catheter for 1-2 weeks to allow for a decrease in prostatic edema. Published studies have shown differences in urinary symptoms for patients who underwent rigid versus flexible cystoscopy outside of the setting of PSI. Here, we investigate possible factors including cystoscopy that may contribute to urinary toxicity, the most common form of toxicity in patients receiving PSI. A retrospective chart review was performed for 62 consecutive patients who received PSI at our institution from 12/2006 to 9/2009. Possible contributing factors were collected: whether or not cystoscopy was performed and type of cystoscopy, prostate volume, isotope type, and the number of seeds and needles used. Possible outcomes were collected: Foley catheter requirement immediately after PSI and International Prostate Symptom Score (IPSS) at the time of first follow-up (if in the first 3 months) as well as the change from the pre-procedure IPSS. There was a large and significant difference (p = 0.0000454) between rates if Foley catheter requirement after rigid cystoscopy (75.0%) versus flexible cystoscopy (17.2%) and no cystoscopy (12.5%) by Chi-square analysis. There was no statistical difference between flexible and no cystoscopy. Foley catheter requirement was not associated with prostate volume, isotope, or the number of seeds and needles. No factors were associated with post-implant IPSS. We report a strong singular association between rigid cystoscopy and Foley catheter requirement after PSI in our institutional experience. Although rigid cystoscopy is often favored by urologists for better visualization, flexible cystoscopy should be performed instead whenever possible to reduce the risk of urinary retention and Foley catheter requirement after PSI.

RATIONALE: Airway eosinophilia is a predictor of asthma exacerbations and a marker of asthma severity. Viral infections, including rhinovirus, account for the majority of asthma exacerbations. The role of eosinophils (EOS) in virus-induced inflammation remains to be defined. We chose to study human EOS regulatory activity in altering host responses to virus stimulation through interactions with peripheral blood mononuclear cells (PBMCs), monocytes, and epithelial cells (ECs). We have previously shown significant increases in IL-13 and IFN-gamma in co-culture experiments of EOS with CD4 + T-cells. The synthetic double-stranded RNA polyinosinic: polycytidylic acid (poly I: C) was used as a virus analogue for the co-culture of eosinophils with PBMCs and monocytes. METHODS: Using an in vitro co-culture system, purified human peripheral blood EOS were incubated with primary human PBMCs or monocytes and stimulated by poly I: C at 25 mcg/ml for 48 hours. EOS were also incubated with primary ECs and BEAS-2B cells for 24 hours. Supernatants from the co-cultures were collected and analyses of cytokine production were performed by ELISA. RESULTS: Co-culture of EOS with PBMCs stimulated with poly I: C in vitro significantly increased IL-13 expression (p = 0.010.) Co-culture of EOS with monocytes stimulated by poly I: C significantly increased IL-1beta expression (p = 0.008). Preliminary experiments suggest that incubation of EOS with primary ECs decreases IL-8 expression. CONCLUSIONS: The presence of EOS alters in vitro cytokine expression of PBMCs, monocytes and ECs. Thus, EOS may affect host response to viral infection in asthma by altering cytokine production of inflammatory cells as well as epithelial cells.

Maintenance of eosinophils on the conjunctival epithelium is an important feature of ocular allergic inflammation, yet the specific receptors involved have not been identified. The purpose of this study was to examine eosinophil adhesion to junctional adhesion molecules (JAM) A, B and C; and the potential role of JAM in eosinophil adhesion to conjunctival epithelial cells. Peripheral blood eosinophil adhesion to recombinant JAM-A, JAM-B or JAM-C coated plates and a human conjunctival epithelial cell line (IOBA-NHC, Valladolid, Spain) were evaluated using an eosinophil peroxidase assay of adherent eosinophils. Eosinophil adhesion was stimulated with fMLP or PAF. IOBA-NHC cells were pre-treated with pro-inflammatory cytokines and/or blocking antibody to JAM-A. IOBA-NHC cells were also examined for surface expression of JAM-A and JAM-C using flow cytometry. Unstimulated eosinophil adhesion to recombinant JAM-A, B, or C was increased compared to uncoated wells (p < 0.05). Moreover, eosinophils stimulated with fMLP or PAF were more adherent to JAM-A, B, and C than to uncoated wells (p < 0.05). IOBA-NHC cells expressed JAM-A and JAM-C. Pro-inflammatory cytokine stimulation of IOBA-NHC cells enhanced eosinophil adhesion, while a blocking JAM-A antibody inhibited eosinophil adhesion to levels below that of unstimulated IOBA-NHC cells. Eosinophil adhesion to junctional adhesion molecules is a novel finding and may provide a therapeutic target in ocular and other types of allergic inflammation.

In vivo cell culture has been known for several years. The earliest attempts were made by Rezzesi (18) and Bisceglie (6). These investigators reported that Ehrlich carcinoma of mice survived for 12 days in the peritoneal cavity of guinea pigs when cultured in collodion dialysis sacs. More recently Prehn, Weaver, and Algire (16, 17) introduced the diffusion chamber technic using Millipore Filters for the porous membranes of the chamber. These diffusion chambers separate the cell culture from host cells but provide free diffusion of all nutrient materials, including protein, needed for growth. In such a system the cells in culture should be subject to all the noncellular growth-controlling influences of the host. Since 1954 many reports have appeared on the use of these technics to culture cells in vivo (1-5, 12, 15, 21, 2s The methods used by these investigators (except [5]),: although useful, did not permit quantitative measurement of cell growth; growth was demonstrated by the presence of mitotic indices in stained preparations and by gross appearance. In general, the inoculum sizes were large (perhaps exceeding the capacity of the chamber to support growth) or consisted of small bits of tissue containing unknown numbers of cells. This report is intended to present methods for quantitative measurement of cell growth in vivo and to demonstrate the type of growth curves obtained by such a method. The cell lines chosen for the initial experiments were the L-fibroblast (originally derived from normal connective tissue of the CSH mouse) and the Sarcoma 180, a malignant cell line of mesodermal origin.