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Decrease Morbidity (decrease + morbidity)
Selected AbstractsMohs Micrographic Surgery as an Alternative Treatment Method for Cutaneous MucormycosisDERMATOLOGIC SURGERY, Issue 8 2003F. Landon Clark BS Background. Mucormycosis is an invasive fungal disease that most commonly occurs in immunocompromised patients. Early angioinvasion and dissemination can lead to the rapid demise of the patient. The growing number of organ transplant patients on pharmacologic immunosuppression has increased the risk for this opportunistic mycosis. Traditional therapy has included aggressive debridement and resection as well as antifungal medications. Objective. To demonstrate that the margin control and tissue-sparing technique of Mohs micrographic surgery can effectively eradicate mucormycosis infection and decrease morbidity. Methods. Case presentation of a 64-year-old transplant patient presenting with biopsy-proven cutaneous mucormycosis treated with Mohs micrographic surgery. Margin control was confirmed by a rapid Gomori methenamine silver stain. Results. There has been no recurrence at 1-year follow-up with full preservation of extremity function. Conclusion. The use of the Mohs technique combined with rapid Gomori methenamine silver staining for mucormycosis can be an effective tissue-sparing method for local control of this fungal infection. Mohs micrographic surgery should be considered for the cutaneous manifestations of mucormycosis. [source] Noggin Inhibits Postoperative Resynostosis in Craniosynostotic Rabbits,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 7 2007Gregory M Cooper PhD Abstract Inhibition of bone formation after surgery to correct craniosynostosis would alleviate the need for secondary surgeries and decrease morbidity and mortality. This study used a single dose of Noggin protein to prevent resynostosis and improve postoperative outcomes in a rabbit model of craniosynostosis. Introduction: Craniosynostosis is defined as the premature fusion of one or more of the cranial sutures, which causes secondary deformations of the cranial vault, cranial base, and brain. Current surgical intervention involves extirpation of the fused suture to allow unrestricted brain growth. However, resynostosis of the extirpated regions often occurs. Several bone morphogenetic proteins (BMPs), well-described inducers of ossification, are involved in bone healing. This study tested the hypothesis that a postoperative treatment with Noggin, an extracellular BMP inhibitor, can inhibit resynostosis in a rabbit model of human familial nonsyndromic craniosynostosis. Materials and Methods: Thirty-one New Zealand white rabbits with bilateral coronal suture synostosis were divided into three groups: (1) suturectomy controls (n = 13); (2) suturectomy with BSA in a slow-resorbing collagen vehicle, (n = 8); and (3) suturectomy with Noggin in a slow-resorbing collagen vehicle (n = 10). At 10 days of age, a 3 × 15-mm coronal suturectomy was performed. The sites in groups 2 and 3 were immediately filled with BSA-loaded gel or Noggin-loaded gel, respectively. Serial 3D-CT scan reconstructions of the defects and standard radiographs were obtained at 10, 25, 42, and 84 days of age, and the sutures were harvested for histological analysis. Results: Radiographic analysis revealed that Noggin-treated animals had significantly greater coronal suture marker separation by 25 days and significantly greater craniofacial length at 84 days of age compared with controls. 3D-CT analysis revealed that Noggin treatment led to significantly greater defect areas through 84 days and to increased intracranial volumes at 84 days of age compared with other groups. Histological analysis supported CT data, showing that the untreated and BSA-treated groups had significant healing of the suturectomy site, whereas the Noggin-treated group had incomplete wound healing. Conclusions: These data support our hypothesis that inhibition of BMP activity using Noggin may prevent postoperative resynostosis in this rabbit model. These findings also suggest that Noggin therapy may have potential clinical use to prevent postoperative resynostosis in infants with craniosynostosis. [source] Clinical characteristics of perforated pyometra and impending perforation: Specific issues in gynecological emergencyJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 3 2010Yu-Che Ou Abstract Objective:, To evaluate the clinical characteristics of pyometra and the differences between perforated pyometra and early-drained pyometra in order to prevent morbidity. Material and Methods:, Retrospective study of 14 patients diagnosed between 1998 and 2008 with early-drainage pyometra and six patients with perforated pyometra were included. In addition, a review of the literature yielded another 30 perforated pyometra cases for comparison. Results:, Of 20 women with pyometra, the main presented symptoms at admission were abdominal pain (80%), fever (45%) and vaginal discharge (25%). The majority of organisms isolated were Bacteroides fragilis (seven cases), Streptococcus species (six cases) and Escherichia coli (five cases). Of the 36 cases with spontaneous uterine perforation to date, 35 cases (97%) had abdominal pain, 11 cases (31%) had fever, and 10 cases (27%) had vomiting. Hypoalbuminemia was found in seven patients (five cases in the perforation group and two cases in the drainage group). Conclusion:, Early diagnosis of pyometra before perforation can avoid surgical exploration and decrease morbidity and mortality. Perforated pyometra should be considered as a differential diagnosis in women with pneumoperitoneum and fever. Hypoalbuminemia should be considered as a predisposing factor for pyometra perforation. [source] Inhibition of Aurora Kinase A enhances chemosensitivity of medulloblastoma cell lines,PEDIATRIC BLOOD & CANCER, Issue 1 2010Ayman El-Sheikh MD Abstract Background Medulloblastoma comprises approximately 20% of all primary pediatric brain tumors. Despite recent advances, the survival rate for high-risk patients and the morbidity associated with these treatments remains suboptimal. To improve outcomes and decrease morbidity, more targeted therapy is required. One possible target is the Aurora Kinase family. The objective of this study was to evaluate the impact of Aurora Kinase A inhibition in medulloblastoma cell lines. Procedure Cell proliferation was measured using an MTS assay after adding an Aurora Kinase inhibitor (C1368) at different concentrations. Cell cycle analysis was carried out by Flow Cytometry using propidium iodide (PI). RNAi experiments were performed using siRNA oligonucleotides. Luciferase experiments were carried out using the Cignal Finder 10 Pathway Reporter Arrays. Results Inhibition of Aurora Kinase A induces cell death in medulloblastoma cells and lowers the IC50 of other chemotherapeutic agents (etoposide and cisplatin) used in medulloblastoma treatment. Cell arrest at G2/M phase was significantly increased in medulloblastoma cell lines treated with C1368 Sigma at IC30 or transfected siRNA. Inhibition of Aurora Kinase A resulted in decreased activity of pro-proliferative signaling pathways including Wnt, Myc, and RB as measured by luciferase reporter assays. Conclusions These data indicate that inhibition of Aurora Kinase A inhibits cell growth in medulloblastoma through inhibition of pro-proliferative signaling pathways Wnt, Myc, and RB. Additionally, combining Aurora Kinase A inhibition with other chemotherapeutic agents significantly lowers their IC50, which make it a promising small molecule target for medulloblastoma therapy. Pediatr Blood Cancer 2010;55:35,41. © 2010 Wiley-Liss, Inc. [source] | ||||||||||