Surgical correction of cleft lip lower-lip deformity: a report of three cases

Cleft lip lower-lip deformity is a secondary deformity in patients who underwent primary cheiloplasty of the upper lip, characterized by an enlarged and anteriorly rotated lower lip. In these cases, soft-tissue imbalances remain even after skeletal correction with orthognathic surgery, and additional soft tissue treatment is required for lip harmony and esthetic facial balance in CLP (cleft lip palate) patients. This study describes three cases of transverse myomucosal excision of the lower lip for correction of cleft lip lower-lip deformity to restore facial esthetic balance. Each patient underwent orthognathic surgery, rhinoplasty, or upper lip revision cheiloplasty according to condition. Postoperatively, volume of the lower lip decreased and lip harmony was improved in all three patients. The surgeon should fully understand the anatomical structure around the lips and be able to evaluate overall harmony of the soft tissue. When a lower lip deformity is present, careful surgical planning and execution are important for each patient.

Treatment of severe pain in a patient with complex regional pain syndrome undergoing dental treatment under general anesthesia: A case report

Complex regional pain syndrome (CRPS) is rare, characterized by pain from diverse causes, and presents as extreme pain even with minor irritation. General anesthesia may be required for dental treatment because the pain may not be controlled with local anesthesia. However, treatment under general anesthesia is also challenging. A 38-year-old woman with CRPS arrived for outpatient dental treatment under general anesthesia. At the fourth general anesthesia induction, she experienced severe pain resulting from her right toe touching the dental chair. Anesthesia was induced to calm her and continue the treatment. After 55 minutes of general anesthesia, the patient still complained of extreme toe pain. Subsequently, two administrations for intravenous sedation were performed, and discharge was possible in the recovery room approximately 5 h after the pain onset. The pain was not located at the dental treatment site. Although the major factor causing pain relief was unknown, ketamine may have played a role.

Induction of apoptosis in colon cancer cells by nonsteroidal anti-inflammatory drugs

Epidemiological studies have demonstrated that nonsteroidal anti-inflammatory drugs (NSAIDs) decrease the incidence of colon cancer. In addition, NSAIDs reduce the number and size of polyps in patients with familial adenomatous polyposis. The mechanisms of the anti-neoplastic effect of NSAIDs are still far from complete understanding, but one possible mechanism is the induction of apoptosis. Several lines of evidence suggest that NSAIDs-induced apoptosis in colon cancer cells are mediated through the cyclooxygenase (COX)-independent pathway. In this study we explored the mechanism of NSAIDs-induced apoptosis in the colon cancer cell line, HT-29. We confirmed that NSAIDs induce apoptosis in HT-29 cells irrespective of their COX-selectivity. Indomethacin enhanced the expression of p21waf-1 in HT-29 cells. However the expression of apoptosis-related genes such as Fas, bcl-2 and bax was not affected by indomethacin. Intra- and extra-cellular calcium chelators, protein tyrosine kinase (PTK) inhibitor, protein kinase A (PKA) inhibitor and protein kinase C (PKC) inhibitors did not influence indomethacin-induced apoptosis in HT-29 cells. We concluded that NSAIDs-induced apoptosis in colon cancer cells may be independent from signals transducted through [Ca++]i, PTK, PKA, PKC or the expression of apoptosis-related genes. In contrast, our results demonstrating the induction of p21waf-1 transcription by NSAIDs suggest the possible association of NSAIDs-induced apoptosis and cell-cycle control in colon cancer cells.

Molecular Mechanism of Fas-mediated Apoptosis in Colon Cancer Cell Line

BACKGROUND/AIMS: Physiologic cell death occurs primarily through an evolutionary conserved form of cellular suicide termed apoptosis. Recent evidence suggests that alterations in regulation of apoptosis contribute to the pathogenesis of a number of human diseases, including cancer, viral infections, autoimmune diseases, degenerative diseases and inflammatory diseases. Fas antigen(APO-1, CD95) is a cell surface receptor protein that is broadly expressed in normal and neoplastic cells and can mediate apoptosis in susceptible cells. Fas is involved in immune-related apoptosis including T-cell selection in thymus, down regulation of immune response and cytotoxic T-cell mediated cytotoxicity. In contrast to immune system, little is known about the function of Fas antigen expressed on epithelial cells. Recently, however, it has been shown that Fas is also important for the pathogenesis of liver disease and inflammatory skin disease. We have recently reported that although colon cancer cells HT-29 express Fas antigen on their surface, Fas ligation using IgM anti-Fas monoclonal antibody(CH-11) is not sufficient to induce apoptosis. In addition, cellular activation by IFN-gamma not only enhances Fas expression but also sensitizes HT-29 to apoptosis induced by Fas ligation as well as treatment with cycloheximide and actinomycin D. However, molecular mechanisms of Fas-mediated apoptosis are yet far from complete understanding. We, therefore, studied the functional role of Fas and apoptosis-related gene expression in apoptosis of colon cancer cell line HT-29 and signal transduction pathways including protein kinase C as well as protein phosphatase I and 2A. METHODS: Fas, Fas ligand and apoptosis related gene mRNA expression was measured by RT-PCR. Cytotoxicity and cell survival were assessed by LDH assay and MTT assay, respectively. Apoptosis was detected by confocal microscopic observation of chromatin condensation after DAPI stain and confirmed by demonstration of DNA fragmentation in agarose gel electrophoresis as well as TUNEL assay. DNA content was deteunined by flow cytometry after staining with propidium iodide and sub-G1 peak was considered as apoptotic cells. Results: Fas ligation by IgM anti-Fas monoclonal antibody(CH-11) tailed to induce poptosis in control HT-29. However, Fas ligation in IFN- gamma pretreated HT-29 induced apoptosis dose-dependently. HT-29 expressed very low level of bcl-2 mRNA, which was not changed by IFN-gamma pretreatment. IFN-gamma pretreatment did not alter the mRNA expression levels of bax, c-myc, p53, and caspases such as ICE, hich and cpp32. Protein kinase C inhibitor such as staurosporine and H7 did not inhibit Fas-mediated apoptosis of IFN-gamma pretreated HT-29. Fas-mediated apoptosis of IFN-gamma pretreated HT-29 was not suppressed as well by protein phosphatase 1 and 2A inhibitor calyculin A. Conclusions: Colon cancer cell line HT-29 expresses Fas antigen on the surface which is not sufficient to induce apoptosis. IFN-gamma pretreatment sensitizes HT-29 to Fas-mediated apoptosis, but dose not alter the expression of apoptosis-related genes including bcl-2, bax, p53 and caspases. Fas-mediated apoptotic signal in IFN-gamma pretreated HT-29 maybe independent with protein kinase C as well as with protein phosphatase 1 and 2A.