Intraosseous hemangioma is a benign, rare neoplasm that accounts to 0.5 - 1% of all benign tumors of bones.1, 2 While most hemangiomas arise from soft tissues, it is uncommon for it to arise from bones.2 The most common sites of growth are in the vertebral body and the calvarium with frontal bone making up approximately 45% of calvarial cases.2,3 However, they are also encountered in the head and neck with sites such as the skull (53%), mandible (10.7%), nasal bones (9%), and cervical spine (6%).4 In the mandible, the body is mostly affected and 65% are found in the molar and premolar region.1 They are more common in adult females with peaks at the second and fifth decades of life.1-3 Hemangioma of the mandible is difficult to diagnose due to its nonspecific clinical presentation and radiographic features. It mimics various mass lesions in the mandible such as giant cell granuloma, fibrous dysplasia, multiple myeloma, osteosarcoma, ameloblastoma and keratocysts. Therefore, a comprehensive history taking and physical examination plus examination of the imaging studies available and tissue biopsy all play important roles in arriving at the final diagnosis.5 We present the case of an aggressive mandibular hemangioma in a young boy and our management involving a failed fibular free flap reconstruction.
Sirolimus ; Sirolimus

No abstract available.
Drug Monitoring ; Sirolimus ; Tacrolimus

Depression is a complicated psychiatric illness with severe consequences. Despite recent advanced achievements of molecular neurobiology, pathophysiology of depression has not been well elucidated. Among new findings of pathophysiology of depression, the possible fast antidepressant effect by N-methyl-D-asparate receptor antagonist, such as ketamine, is regarded as a promising treatment target of depression. Ketamine stimulates the mammalian target of rapamycin (mTOR) signaling pathway and activation of mTOR signaling pathway may be a key mechanism of the antidepressant effect of ketamine. Thus, this review describes the role of mTOR signaling in the pathophysiology of depression and developing a new treatment target of depression.
Depression* ; Ketamine ; Neurobiology ; Sirolimus*

Introduction: Cherry angiomas are a common type of acquired vascular proliferation of the skin which manifest as single or multiple bright red spots that usually appear on the trunk and arms. They are generally asymptomatic; patients may opt to remove the lesions for cosmetic reasons and prevention of bleeding. Conventionally, most cherry angiomas are treated with curettage, laser, and electrosurgery. Herein, we report a case of multiple cherry angiomas managed alternatively with oral sirolimus. Case: A 47-year-old Filipino female presented with a 10-month history of gradually enlarging multiple bright-red papules and pedunculated nodules with a propensity to spontaneously bleed on gentle manipulation involving the scalp and forehead. Clinicopathological correlation suggests a diagnosis of eruptive cherry angiomas. The patient was started on oral sirolimus, a mammalian target of rapamycin (mTOR) inhibitor. Conclusion We present a case of a patient with eruptive cherry angiomas who experienced significant decrease in size and bleeding with treatment of oral sirolimus with minimal adverse effects. For patients with eruptive cherry angiomas, especially with contraindicated comorbidities, first-line therapeutic option treatments with oral sirolimus can be beneficial.
sirolimus ; vascular malformation

PURPOSE: The purpose of this study was to determine whether immunosuppressant, rapamycin could inhibit corneal angiogenesis induced by angiogenin and to evalutate its role by micropocket assay. METHODS: The rabbit's eye was implanted intrastromally into the superior cornea with pellet for the control group, pellet containing of angiogenin for the angiogenin group, and pellet containing of angiogenin and rapamycin for the angiogenin+rapamycin group. Biomicrographically, corneal angiogenesis was evaluated for 14 days after pellet implantation, based on the number and the length of new vessels. The neovascularized cornea also was examined histologically. RESULTS: We could observe that the angiogenin inducing corneal angiogenesis was inhibited by rapamycin. The score of neovascularization was significantly decreased in the angiogenin+rapamycin group than in the angiogenin group at 3, 7 and 10 days after pellet implantation (p<0.05). Histologically, the cornea of angiogenin+rapamycin group also showed much less new vessels than that of angiogenin group, in which inflammatory cells and edema was observed. CONCLUSIONS: Rapamycin appears to inhibit angiogenin induced angiogenesis in a rabbit corneal micropocket assay and may have therapeutic potential as an antiangiogenic agent.
Cornea ; Corneal Neovascularization* ; Edema ; Rabbits* ; Sirolimus*

Although late stent thrombosis is a very rare complication after a drug-eluting stent implantation, this could induce significant sequelae. Several mechanisms for very late stent thrombosis have been suggested. We experienced a new possible mechanism of very late stent thrombosis after the implantation of a sirolimus-eluting stent. A sirolimus-eluting stent fracture might induce mechanical injury of the endothelium and then thrombotic occlusion at 24 months after the stent procedure.
Drug-Eluting Stents ; Endothelium ; Sirolimus ; Stents* ; Thrombosis*

The target of rapamycin (TOR) signaling pathway is a conserved pathway that regulates eukaryotic cell growth in response to environmental cues. Chemical genomic approaches that profile rapamycin sensitivity of yeast deletion strains have given insights into the function of TOR signaling pathway. In the present study, we analyzed the rapamycin sensitivity of yeast deletion library strains on synthetic medium. As a result, we identified 130 strains that are hypersensitive or resistant to rapamycin compared with wild-type cells. Among them, 36 genes are newly identified to be related to rapamycin sensitivity. Moreover, we found 16 strains that show alteration in rapamycin sensitivity between complex and synthetic media. We suggest that these genes may be involved in part of TOR signaling activities that is differentially regulated by media composition.
Cues ; Eukaryotic Cells ; Saccharomyces ; Saccharomyces cerevisiae ; Sirolimus ; Yeasts

No abstract available.
Angiofibroma* ; Carbon Dioxide* ; Carbon* ; Lasers, Gas* ; Sirolimus* ; Tuberous Sclerosis*

Depression is a common psychiatric illness with a high lifetime prevalence in the general population. Serious problem, such as suicide is commonly occurring in the patients with depression. Till now, the monoamine hypothesis has been the most popular theory of pathogenesis for depression. However, the more specific pathophysiology of depression and cellular molecular mechanism underlying action of commercial antidepressant has not been clearly defined. Several recent studies demonstrated that neural plasticity, epigenetic and mammalian target of rapamycin signaling are promising answers to the pathophysiology of depression. In this article, current understanding of biology and molecular mechanisms of depression and new research on the pathophysiology of depression will be discussed.
Biology ; Depression ; Epigenomics ; Humans ; Molecular Biology ; Plastics ; Prevalence ; Sirolimus ; Suicide

OBJECTIVEThe aim of this study was to explore whether rapamycin can induce the autophagy of HL-60 cells and UCH-L3 expression.

METHODSCell proliferation activity of HL-60 cells treated with rapamycin was measured by CCK-8 assay. After the cells were treated with rapamycin for different time, the fluorescent microscopy was used to detect the cells' modality, the morphology of autophagosomes was observed by transmission electron microscopy, the mRNA levels of autophagy-related genes LC3-II and UCH-L3 were detected by real-time PCR, and the Western blot was employed to detect the expression level of UCH-L3.

RESULTSDifferent concentrations of rapamycin could inhibit the proliferation of HL-60 cells. The inhititory levels in treatment groupall were statistically different from those in the control group (P<0.05). Under fluorescent microscopy, the fluorescence intensity in the control group was low, but in the treatment groups it strengthened along with the extension of process time. After treatmant with 2µmol/L rapamycin for different time (12、24 h), the number of autophagosomes in the control group was less , while in the treatment groups was more, the mRNA level of LC3-II was raised as compared with the control group, while the mRNA and protein level of UCH-L3 declined (P<0.05).

CONCLUSIONRapamycin can inhibit the proliferation of HL-60 cells and induce the autophagic death. UCH-L3 may play a role in the regulation of autophagic death of leukemia.