DESIGN: Saliva samples were collected after the morning meal by placing a sterile cotton swab in the vestibule of the oral cavity from cleft lip and palate patients immediately preoperative and 12 weeks postoperative. Normal children were examined as a control group. Samples were cultured; Staphylococcus and Streptococcus isolates were identified and quantified.
PATIENTS: Fifteen cleft lip and palate patients and 22 normal children, aged 3 to 39 months were examined.
RESULTS: Streptococcus mitis biovar 1, Streptococcus salivarius and Streptococcus oralis of the viridans group of streptococci were the most commonly found in normal children, as well as in cleft lip and palate children. In the cleft lip and palate group, mean streptococcal count was 32.41 (29.80) and 46.46 (42.80) in the pre- and postoperative periods, respectively; in the normal group, the count was 20.93 (27.93) and 49.92 (34.72) at 0 week and 12 weeks, respectively. Staphylococcus aureus was the most common Staphylococcus species found in CLP patients, representing 47.4% postoperatively. In the cleft lip and palate children, mean staphylococcal count was 5.34 (8.13) and 0.56 (0.92) in the pre- and postoperative periods, respectively; in normal children, the count was 0.82 (1.98) and 0.60 (2.55) at 0 and 12 weeks, respectively. The differences were statistically significant only for the staphylococcal count between pre- and postoperative periods in children with cleft lip and palate as tested by analysis of variance (p < .05).
CONCLUSIONS: Cleft lip and palate patients had more colonization by S. aureus compared with normal children, and the colony count decreased significantly following surgical repair of the cleft lip and palate.
(: MVD) is the quantification method of various aspects of tumor vasculature that indicates angiogenic activity. This study aims to analyze the correlation between MVD to the expression of VEGFRs on breast cancer tissue.
Materials and Method: A total of 60 N-methyl-N-nitrosourea (MNU)-induced breast carcinomas in rats were suppressed by using antiangiogenic drugs. The rats were then sacrificed, and the tumor was fixed in 10% formalin, paraffin embedded, and immunohistochemistry stained using VEGFRs and CD34.
Result: One-way ANOVA test showed a significant difference in all markers that have been used (P < 0.05) on MNU-breast tumor treated with rapamycin (M= 90.1664, SD= 7.4487), PF4 (M= 93.7946, SD= 7.1303) and rapamycin + PF4 (M= 93.6990, SD= 1.8432). We obtained a significant reduction of MVD count on breast carcinoma for rapamycin group (M= 25.6786, SD= 9.7075) and rapamycin + PF4 group (M= 30.5250, SD= 13.6928) while PF4 group (M=47.7985, SD=4.8892) showed slightly increase compared to control (M= 45.1875, SD= 4.4786). There was a moderately strong, positive correlation between angiogenic markers; Flt-1 (r= 0.544, n=60, P < 0.005) and Flt-4 (r= 0.555, n= 60, P < 0.005) while Flk-1 (r= 0.797, n= 60, P < 0.005) showed a strong, positive correlation with MVD.
Conclusion: MVD was strongly correlated to the VEGFRs expression on breast carcinoma.
MATERIALS AND METHODS: Thirty five female Sprague Dawley rats at age 21-day old were divided into 4 groups; Group 1 (control, n=10), Group 2 (PF4, n=5), Group 3 (rapamycin, n=10) and Group 4 (rapamycin+PF4, n=10). MNU was administered intraperitionally, dosed at 70 mg/kg body weight. The rats were treated when the tumors reached the size of 14.5 ± 0.5 mm and subsequently sacrificed after 5 days. Rapamycin and PF4 were administered as focal intralesional injections at the dose of 20 μg/lesion. The tumor tissue was then subjected to histopathological examinations for morphological appraisal and immunohistochemical assessment of the pro-apoptotic marker, Bax and anti-apoptotic markers, Bcl-2 and survivin.
RESULTS: The histopathological pattern of the untreated control cohort showed that the severity of the malignancy augments with mammary tumor growth. Tumors developing in untreated groups were more aggressive whilst those in treated groups demonstrated a transformation to a less aggressive subtype. Combined treatment resulted in a significant reduction of tumor size without phenotypic changes. Bax, the pro-apoptotic marker, was significantly expressed at higher levels in the rapamycin-treated and rapamycin+PF4-treated groups compared to controls (p<0.05). Consequently, survivin was also significantly downregulated in the rapamycin-treated and rapamycin+PF4-treated group and this was significantly different when compared to controls (p).
CONCLUSIONS: In our rat model, it could be clearly shown that rapamycin specifically affects Bax and survivin signaling pathways in activation of apoptosis. We conclude that rapamycin plays a critical role in the induction of apoptosis in MNU-induced mammary carcinoma.