Subject(s)
Frontal Sinusitis/diagnosis , Immunocompromised Host , Mycobacterium Infections, Nontuberculous/diagnosis , Mycobacterium chelonae/isolation & purification , Anti-Bacterial Agents/therapeutic use , Diagnosis, Differential , Drainage/methods , Frontal Sinusitis/microbiology , Frontal Sinusitis/therapy , Humans , Male , Middle Aged , Mycobacterium Infections, Nontuberculous/microbiology , Mycobacterium Infections, Nontuberculous/therapy , Natural Orifice Endoscopic Surgery/methods , Nose , Tomography, X-Ray ComputedABSTRACT
OBJECTIVE: To evaluate the complication rate in relation to the timing of surgical repair of midface fractures. STUDY DESIGN AND SUBJECTS: Retrospective chart review at a level 1 trauma center. RESULTS: Thirty-four patients were evaluated. Overall complication rate was 23.5% with no significant difference between the early repair (21.1%) and late repair (26.7%) groups. The scope of facial fracture repair was similar between the two groups as measured by the number of screws used and through an injury quantifying system. The only variable that tended toward significance was intraoperative blood loss, which was greater in the early repair group (P = 0.06). CONCLUSIONS: There is no clear consensus with respect to timing of midface trauma repair. Early repair may result in greater blood loss. Further study is needed to help establish a more precise recommendation for the timing of midface trauma repair.
Subject(s)
Facial Bones/injuries , Fractures, Bone/surgery , Blood Loss, Surgical/statistics & numerical data , Bone Screws , Female , Fracture Fixation, Internal , Humans , Male , Orthopedic Procedures/methods , Retrospective Studies , Time FactorsABSTRACT
OBJECTIVES/HYPOTHESIS: Nuclear factor (NF)-kappaB is an early response gene that has been associated with head and neck squamous cell cancer (HNSCC) progression. NF-kappaB activation is induced by some chemotherapy agents, including paclitaxel. The activation of this gene can be correlated with apoptosis resistance. Inositol hexaphosphate (IP6) is a naturally occurring polyphosphorylated carbohydrate. NF-kappaB levels were evaluated in oral cavity HNSCC lines after treatment with paclitaxel and IP6, alone and in combination. Resulting levels of cell death and apoptosis were assessed, and conclusions are drawn regarding a possible synergistic relationship between paclitaxel and IP6. METHODS: NF-kappaB activation in cancer cells treated with paclitaxel and IP6, alone and in combination, was measured by transient transfection, and results were interpreted by luminometry. Cell proliferation of treated cells was measured by MTT assay. Cell viability and apoptosis of cancer cells treated with paclitaxel and IP6 combinations were quantitated by trypan blue staining and Caspase-Glo 3/7 assay, respectively. RESULTS: IP6 was observed to significantly downregulate NF-kappaB activation in both NA and CA-9-22 oral cavity HNSCC cell lines. Paclitaxel treatments caused increased NF-kappaB activation in the same cell lines. IP6 was observed to mitigate paclitaxel-induced NF-kappaB activation in the CA-9-22 cell line. IP6, when combined with paclitaxel, reduces CA-9-22 cell proliferation, increases cell death, and increases apoptosis, when compared with treatment with paclitaxel alone. CONCLUSIONS: IP6 reduces paclitaxel induced NF-kappaB activation and increases paclitaxel-mediated cell killing and apoptosis. As a well-tolerated and safe supplement, IP6 deserves further study in the treatment of oral cavity squamous cell carcinoma.
