Actinomyces-like Organisms From A Vaginal Granuloma Following Intravaginal Slingplasty With Polypropylene Mesh

[No abstract available]1022172173Baessler, K., Hewson, A.D., Tunn, R., Schuessler, B., Maher, C.F., Severe mesh complications following intravaginal slingplasty (2005) Obstet Gynecol, 106, pp. 713-716Wai, C.Y., Nihira, M.A., Drewes, P.G., Chang, J.S., Siddiqui, M.T., Hemsell, D.L., Actinomyces associated with persistent vaginal granulation tissue (2005) Infect Dis Obstet Gynecol, 13, pp. 53-55Mali, B., Joshi, J.V., Wagle, U., Hazari, K., Shah, R., Chadha, U., Actinomyces in cervical smears of women using intrauterine contraceptive devices (1986) Acta Cytol, 30, pp. 367-37

Association Between High Risk Hpv Viral Load, P16ink4a Expression And Intra-epithelial Cervical Lesions [associação Entre A Carga Viral De Hpv De Alto Risco, Expressão De P16ink4a E Lesões Intra-epiteliais Escamosas Do Colo Uterino]

OBJECTIVE. To determine the (HR-HPV) high risk HPV viral load in squamous intra-epithelial lesions and association with p16INK4a expression. METHODS. A series of 109 cervical biopsies were studied (57 normal tissue, 26 low grade squamous intra-epithelial lesions [LSIL] and 26 high grade squamous intra-epithelial lesions [HSIL]). Detection of high risk HPV and viral load in cervical cells was made by molecular biology using hybrid capture 2nd generation collected before the biopsy. The p16INK4a was identified by immunohistochemistry using the p16INK4a kit (clone E6H4). RESULTS. High risk HPV was positive in 57.8% of all cases (29.8% in normal tissue, 80.8% in LSIL and 96.1% in HSIL). Protein p16INK4a was expressed in 23.8 % of squamous intraepithelial lesions (15.4% in LSIL and 84.6% in HSIL). In normal tissue all cases were negative to p16INK4a. The viral load was higher in p16 positive cases than in negative cases (positive p16 INK4a mean of 669.9 RLU/PCB [9.47 - 2814.9] and negative p16 INK4a mean of 253.94 RLU/PCB [1.07 - 1882.21] (p<0.05). However when studying just the HSIL cases differences were not significant. CONCLUSION. In this study although the HR-HPV viral load had shown a significant difference between p16 positive and negative cases, in HSIL cases this finding was not confirmed. New studies with a larger number of cases are necessary for consistent conclusions.536530534Schifman, M., Castle, P.E., Human papillomavirus: Epidemiology and public health (2003) Arch Pathol Lab Med, 127, pp. 930-934Wu, Y., Chen, Y., Li, L., Yu, G., Zhang, Y., He, Y., Associations of high risk HPV types and viral load with cervical cancer in China (2006) J Clin Virol, 35, pp. 264-269Andersson, S., Safari, H., Mints, M., Lewensohn-Fuchs, I., Gyllensten, U., Johansson, B., Type distribution, viral load and integration status of high risk human Papillomaviruses in pre-stages of cervical cancer (CIN) (2005) Br J Cancer, 91, pp. 2195-2200Eleutério Jr, J., Giraldo, P.C., Gonçalves, A.K., Cavalcante, D.I., de Almeida Ferreira, F.V., Mesquita, S.M., Morais, S.S., Prognostic markers of high-grade squamous intraepithelial lesions: The role of p16INK4a and high-risk human papillomavirus (2007) Acta Obstet Gynecol Scand, 86, pp. 94-98Castle, P.E., Schiffman, M., Wheeler, C.M., Hybrid capture 2 viral load and the 2-year cumulative risk of cervical intraepithelial neoplasia grade 3 or cancer (2004) Am J Obstet Gynecol, 191, pp. 1590-1597. , for the ALTS GroupSantos, A.L.F., Derchain, S.F.M., Martins, M.R., Sarian, L.O.Z., Martinez, E.Z., Syrjanen, K.J., Human Papillomavirus viral load in predicting high grade CIN in women with cervical smears showing only atypical squamous cells or low-grade squamous intraepithelial lesion (2003) São Paulo Med J, 121, pp. 238-243Sarian, L.O.Z., Santos, A.L.F., Derchain, S.F.M., Figueiredo, P.G., Morais, S.S., Carga viral do Papilomavirus humano na predição da gravidade de lesões cervicais em mulheres com atipias celulares na colpocitologia oncotica (2003) Rev Bras Ginecol Obstet, 25, pp. 365-370Flores, R., Papenfuss, Klimecki, W.T., Giuliano, A.R., Cross-sectional analysis of oncogenic HPV viral load and cervical intraepithelial neoplasia (2005) In J Cancer, 118, pp. 1187-1193Zerbini, M., Venturoli, S., Cricca, M., Gallinella, G., De Simone, P., Costa, S., Distribution and viral load of type specific HPVs in different cervical lesions as detected by PCR-ELISA (2001) J Clin Pathol, 54, pp. 377-380Schlecht, N.F., Trevisan, A., Duarte-Franco, E., Rohan, T.E., Ferenczy, A., Villa, L.L., Viral load as a predictor of the risk of cervical intraepithelial neoplasia (2003) In J Cancer, 103, pp. 519-524Sun, C.A., Lai, H.C., Chang, C.C., Neih, S., Yu, C.P., Chu, T.Y., The significance of human Papillomavirus viral load in prediction of histologic severity and size of squamous intraepithelial lesions of the uterine cervix (2001) Gynecol Oncol, 83, pp. 95-99Moberg, M., Gustavsson, I., Gyllensten, U., Type-specific associations of human Papillomavirus load with risk of developing cervical carcinoma in situ (2004) Int J Cancer, 112, pp. 824-829Moberg, M., Gustavsson, I., Wilander, E., Gyllensten, U., High viral loads of human Papillomavirus predict risk of invasive cervical carcinoma (2005) Br J Cancer, 92, pp. 891-894Abba, M.C., Mouron, S.A., Gomez, M.A., Dulout, F.N., Golijow, C.D., Association of human Papillomavirus viral load with HPV 16 and high-grade intraepithelial lesion (2003) Int J Gyencol Cancer, 13, pp. 154-158Dalstein, V., Riethmuller, D., Pretet, J.L., Carval, K.L.B., Sautiere, J.L., Carbillet, J.P., Persistence and load of high-risk HPV are predictors for development of high-grade cervical lesions: A longitudinal French cohort study (2003) Int J Cancer, 106, pp. 396-403Ylitlo, N., Sorensen, P., Josefsson, A.M., Magnusson, P.K., Andersen, P.K., Ponten, J., Consistent high viral load of human Papillomavirus 16 and risk of cervical carcinoma in situ: A nested case-control study (2000) Lancet, 355, pp. 2194-2198Josefsson, A.M., Magnusson, P.K., Ylitalo, N., Sorensen, P., Qwarforth-Tubbin, P., Andersen, P.K., Viral load of human Papillomavirus 16 as a determinant for development of cervical carcinoma in situ: A nested case-control study (2000) Lancet, 355, pp. 2189-2193Sun, C.A., Liu, J.F., Wu, D.M., Nieh, S., Yu, C.P., Chu, T.Y., Viral load of high risk human Papillomavirus in cervical squamous intraepithelial lesions (2002) Int J Gynecol Obstet, 76, pp. 41-47Pirog, E.C., Baergen, R.N., Soslow, R.A., Tam, D., DeMattia, A.E., Chen, Y.T., Diagnostic accuracy of cervical low-grade squamous intraepithelial lesions is improved with MIB-1 immunostaining (2002) Am J Surg Pathol, 26, pp. 70-75Keating, J.T., Cviko, A., Riethdorf, S., Quade, B.J., Sun, D., Duesing, S., Ki-67, Cyclin E and p16INK4a are complimentary surrogate biomarkers for Human papilloma virus-related cervical neoplasia (2001) Am J Surg Pathol, 25, pp. 884-891Guimaraes, M.C.M., Goncalves, M.A.G., Soares, C.P., Bettini, J.S., Duarte, R.A., Soares, E.G., Immunohistochemical expression of p16INK4a and bcl-2 according to HPV type and to the progression of cervical squamous intraepithelial lesions (2005) J Histochem Cytochem, 53, pp. 509-516Bigras, G., Marval, F., The probability for a Pap test to be abnormal is directly proportional to HPV viral load: Results from a Swiss study comparing HPV testing and liquid-based cytology to detect cervical cancer precursors in 13,842 women (2005) Br J Cancer, 93, pp. 575-581Wensveen CW, Kagie MJ, Nagelkerke RW, Veldhuizen RW, Trimbos JB. Can viral load, semi-quantitatively evaluated, of human Papillomavirus predict cytological or histological outcome in women with atypical squamous or glandular cells of undetermined significance cytology? Eu J Gynaecol Oncol. 2005;26:393-7Eleutério Jr, J., Cavalcante, D.I.M., Teixeira, F.M., Eleutério, R.M.N., Carga viral de HPV de alto risco por captura híbrida e lesões intra-epiteliais escamosas cervicais (2002) Rev Bras An Clin, 34, pp. 193-194Gravitt, P.E., Burk, R.D., Lorincz, A., Herrero, R., Hildesheim, A., Sherman, M.E., A comparison between real-time polymerase chain reaction and hybrid capture 2 for human Papillomavirus DNA quantification (2003) Can Epidemiol Biomarkers Prev, 12, pp. 477-48

Variations in gastric emptying of liquid elicited by acute blood volume changes in awake rats

We have observed that acute blood volume expansion increases the gastroduodenal resistance to the flow of liquid in anesthetized dogs, while retraction decreases it (Santos et al. (1991) Acta Physiologica Scandinavica, 143: 261-269). This study evaluates the effect of blood volume expansion and retraction on the gastric emptying of liquid in awake rats using a modification of the technique of Scarpignato (1980) (Archives Internationales de Pharmacodynamie et de Therapie, 246: 286-294). Male Wistar rats (180-200 g) were fasted for 16 h with water ad libitum and 1.5 ml of the test meal (0.5 mg/ml phenol red solution in 5% glucose) was delivered to the stomach immediately after random submission to one of the following protocols: 1) normovolemic control (N = 22), 2) expansion (N = 72) by intravenous infusion (1 ml/min) of Ringer-bicarbonate solution, volumes of 1, 2, 3 or 5% body weight, or 3) retraction (N = 22) by controlled bleeding (1.5 ml/100 g). Gastric emptying of liquid was inhibited by 19-51.2% (P<0.05) after blood volume expansion (volumes of 1, 2, 3 or 5% body weight). Blood volume expansion produced a sustained increase in central venous pressure while mean arterial pressure was transiently increased during expansion (P<0.05). Blood volume retraction increased gastric emptying by 28.5-49.9% (P<0.05) and decreased central venous pressure and mean arterial pressure (P<0.05). Infusion of the shed blood 10 min after bleeding reversed the effect of retraction on gastric emptying. These findings suggest that gastric emptying of liquid is subject to modulation by the blood volume

Acute extracellular fluid volume changes increase ileocolonic resistance to saline flow in anesthetized dogs

We determined the effect of acute extracellular fluid volume changes on saline flow through 4 gut segments (ileocolonic, ileal, ileocolonic sphincter and proximal colon), perfused at constant pressure in anesthetized dogs. Two different experimental protocols were used: hypervolemia (iv saline infusion, 0.9% NaCl, 20 ml/min, volume up to 5% body weight) and controlled hemorrhage (up to a 50% drop in mean arterial pressure). Mean ileocolonic flow (N = 6) was gradually and significantly decreased during the expansion (17.1%, P<0.05) and expanded (44.9%, P<0.05) periods while mean ileal flow (N = 7) was significantly decreased only during the expanded period (38%, P<0.05). Mean colonic flow (N = 7) was decreased during expansion (12%, P<0.05) but returned to control levels during the expanded period. Mean ileocolonic sphincter flow (N = 6) was not significantly modified. Mean ileocolonic flow (N = 10) was also decreased after hemorrhage (retracted period) by 17% (P<0.05), but saline flow was not modified in the other separate circuits (N = 6, 5 and 4 for ileal, ileocolonic sphincter and colonic groups, respectively). The expansion effect was blocked by atropine (0.5 mg/kg, iv) both on the ileocolonic (N = 6) and ileal (N = 5) circuits. Acute extracellular fluid volume retraction and expansion increased the lower gastrointestinal resistances to saline flow. These effects, which could physiologically decrease the liquid volume being supplied to the colon, are possible mechanisms activated to acutely balance liquid volume deficit and excess

Gastroduodenal resistance and neural mechanisms involved in saline flow decrease elicited by acute blood volume expansion in anesthetized rats

We have previously demonstrated that blood volume (BV) expansion decreases saline flow through the gastroduodenal (GD) segment in anesthetized rats (Xavier-Neto J, dos Santos AA & Rola FH (1990) Gut, 31: 1006-1010). The present study attempts to identify the site(s) of resistance and neural mechanisms involved in this phenomenon. Male Wistar rats (N = 97, 200-300 g) were surgically manipulated to create four gut circuits: GD, gastric, pyloric and duodenal. These circuits were perfused under barostatically controlled pressure (4 cmH2O). Steady-state changes in flow were taken to reflect modifications in circuit resistances during three periods of time: normovolemic control (20 min), expansion (10-15 min), and expanded (30 min). Perfusion flow rates did not change in normovolemic control animals over a period of 60 min. BV expansion (Ringer bicarbonate, 1 ml/min up to 5% body weight) significantly (P&lt;0.05) reduced perfusion flow in the GD (10.3 ± 0.5 to 7.6 ± 0.6 ml/min), pyloric (9.0 ± 0.6 to 5.6 ± 1.2 ml/min) and duodenal (10.8 ± 0.4 to 9.0 ± 0.6 ml/min) circuits, but not in the gastric circuit (11.9 ± 0.4 to 10.4 ± 0.6 ml/min). Prazosin (1 mg/kg) and yohimbine (3 mg/kg) prevented the expansion effect on the duodenal but not on the pyloric circuit. Bilateral cervical vagotomy prevented the expansion effect on the pylorus during the expansion but not during the expanded period and had no effect on the duodenum. Atropine (0.5 mg/kg), hexamethonium (10 mg/kg) and propranolol (2 mg/kg) were ineffective on both circuits. These results indicate that 1) BV expansion increases the GD resistance to liquid flow, 2) pylorus and duodenum are important sites of resistance, and 3) yohimbine and prazosin prevented the increase in duodenal resistance and vagotomy prevented it partially in the pyloru

Acute extracellular fluid volume changes increase ileocolonic resistance to saline flow in anesthetized dogs

We determined the effect of acute extracellular fluid volume changes on saline flow through 4 gut segments (ileocolonic, ileal, ileocolonic sphincter and proximal colon), perfused at constant pressure in anesthetized dogs. Two different experimental protocols were used: hypervolemia (iv saline infusion, 0.9% NaCl, 20 ml/min, volume up to 5% body weight) and controlled hemorrhage (up to a 50% drop in mean arterial pressure). Mean ileocolonic flow (N = 6) was gradually and significantly decreased during the expansion (17.1%, P<0.05) and expanded (44.9%, P<0.05) periods while mean ileal flow (N = 7) was significantly decreased only during the expanded period (38%, P<0.05). Mean colonic flow (N = 7) was decreased during expansion (12%, P<0.05) but returned to control levels during the expanded period. Mean ileocolonic sphincter flow (N = 6) was not significantly modified. Mean ileocolonic flow (N = 10) was also decreased after hemorrhage (retracted period) by 17% (P<0.05), but saline flow was not modified in the other separate circuits (N = 6, 5 and 4 for ileal, ileocolonic sphincter and colonic groups, respectively). The expansion effect was blocked by atropine (0.5 mg/kg, iv) both on the ileocolonic (N = 6) and ileal (N = 5) circuits. Acute extracellular fluid volume retraction and expansion increased the lower gastrointestinal resistances to saline flow. These effects, which could physiologically decrease the liquid volume being supplied to the colon, are possible mechanisms activated to acutely balance liquid volume deficit and excess