Solid organ transplantation has significantly improved the survival rate of patients with terminal organ failure. However, its success is often compromised by allograft rejection, a process in which T helper 17 (Th17) cells play a crucial role. These cells facilitate rejection by enhancing neutrophil infiltration into the graft and by activating endothelial cells and fibroblasts. Additionally, Th17 cells can trigger the activation of other T cell types, including Th1, Th2, and CD8+ T cells, further contributing to rejection. An imbalance between Th17 and regulatory T cells (Tregs) is known to promote rejection. To counteract this, immunosuppressive drugs have been developed to inhibit T cell activity and foster transplant tolerance. Another approach involves the adoptive transfer of regulatory cells, such as Tregs and myeloid-derived suppressor cells, to dampen T cell functions. This review primarily focuses on the roles of Th17 cells in rejection and their interactions with other T cell subsets. We also explore various strategies aimed at suppressing T cells to induce tolerance.

Solid organ transplantation has significantly improved the survival rate of patients with terminal organ failure. However, its success is often compromised by allograft rejection, a process in which T helper 17 (Th17) cells play a crucial role. These cells facilitate rejection by enhancing neutrophil infiltration into the graft and by activating endothelial cells and fibroblasts. Additionally, Th17 cells can trigger the activation of other T cell types, including Th1, Th2, and CD8+ T cells, further contributing to rejection. An imbalance between Th17 and regulatory T cells (Tregs) is known to promote rejection. To counteract this, immunosuppressive drugs have been developed to inhibit T cell activity and foster transplant tolerance. Another approach involves the adoptive transfer of regulatory cells, such as Tregs and myeloid-derived suppressor cells, to dampen T cell functions. This review primarily focuses on the roles of Th17 cells in rejection and their interactions with other T cell subsets. We also explore various strategies aimed at suppressing T cells to induce tolerance.

Solid organ transplantation has significantly improved the survival rate of patients with terminal organ failure. However, its success is often compromised by allograft rejection, a process in which T helper 17 (Th17) cells play a crucial role. These cells facilitate rejection by enhancing neutrophil infiltration into the graft and by activating endothelial cells and fibroblasts. Additionally, Th17 cells can trigger the activation of other T cell types, including Th1, Th2, and CD8+ T cells, further contributing to rejection. An imbalance between Th17 and regulatory T cells (Tregs) is known to promote rejection. To counteract this, immunosuppressive drugs have been developed to inhibit T cell activity and foster transplant tolerance. Another approach involves the adoptive transfer of regulatory cells, such as Tregs and myeloid-derived suppressor cells, to dampen T cell functions. This review primarily focuses on the roles of Th17 cells in rejection and their interactions with other T cell subsets. We also explore various strategies aimed at suppressing T cells to induce tolerance.

Solid organ transplantation has significantly improved the survival rate of patients with terminal organ failure. However, its success is often compromised by allograft rejection, a process in which T helper 17 (Th17) cells play a crucial role. These cells facilitate rejection by enhancing neutrophil infiltration into the graft and by activating endothelial cells and fibroblasts. Additionally, Th17 cells can trigger the activation of other T cell types, including Th1, Th2, and CD8+ T cells, further contributing to rejection. An imbalance between Th17 and regulatory T cells (Tregs) is known to promote rejection. To counteract this, immunosuppressive drugs have been developed to inhibit T cell activity and foster transplant tolerance. Another approach involves the adoptive transfer of regulatory cells, such as Tregs and myeloid-derived suppressor cells, to dampen T cell functions. This review primarily focuses on the roles of Th17 cells in rejection and their interactions with other T cell subsets. We also explore various strategies aimed at suppressing T cells to induce tolerance.

Obstetrical hemorrhage is one of the deadly triad, along with hypertensive disorder in pregnancy and infection. Postpartum hemorrhage is the major cause of obstetrical hemorrhage. Uterine atony is the most common cause of postpartum hemorrhage, and resulted from poor uterine contraction after delivery of the fetus and placenta. Initial management to control postpartum uterine atonic bleeding is based on the use of uterotonics such as well known oxytocin and ergot preparations together with uterine massage. Prostaglandin E2 analogue, sulprostone can be used next when these agents are failed to produce uterine contraction. The woman unresponsive to non-surgical managements requires surgical interventions including emergency hysterectomy. Recently prostaglandin E1 analogue, misoprostol, has been known to elicit potent uterine contraction and cervical ripening after oral, vaginal or rectal administration. We have experienced two cases of postpartum uterine atonic bleedings which were unresponsive to oxytocin, ergot, or prostaglandin E2, but were successfully controlled by rectal administration of misoprostols.
Administration, Rectal ; Alprostadil ; Cervical Ripening ; Dinoprostone ; Emergencies ; Female ; Fetus ; Hemorrhage* ; Humans ; Hysterectomy ; Massage ; Misoprostol* ; Oxytocin ; Placenta ; Postpartum Hemorrhage ; Postpartum Period* ; Pregnancy ; Uterine Contraction ; Uterine Inertia

No abstract available.

No abstract available.
Female ; Hysterectomy, Vaginal* ; Uterine Prolapse*

OBJECTIVES: The aim of this study is to evaluate the effect of light intensity variation on the polymerization rate of composite resin using IB system (the experimental equipment designed by Dr. IB Lee) by which real-time volumetric change of composite can be measured. METHODS: Three commercial composite resins [Z100(Z1), AeliteFil(AF), SureFil(SF)] were photopolymerized with Variable Intensity Polymerizer unit (Bisco, U.S.A.) under the variable light intensity (75/150/225/300/375/450mW2) during 20 sec. Polymerization shrinkage of samples was detected continuously by IB system during 110 sec and the rate of polymerization shrinkage was obtained by its shrinkage data. Peak time(P.T.) showing the maximum rate of polymerization shrinkage was used to compare the polymerization rate. RESULTS: Peak time decreased with increasing light intensity(p<0.05). Maximum rate of polymerization shrinkage increased with increasing light intensity(p<0.05). Statistical analysis revealed a significant positive correlation between peak time and inverse square root of the light intensity (AF:R=0.965, Z1:R=0.974, SF:R=0.927). Statistical analysis revealed a significant negative correlation between the maximum rate of polymerization shrinkage and peak time(AF:R=-0.933, Z1:R=-0.892, SF:R=-0.883), and a significant positive correlation between the maximum rate of polymerization shrinkage and square root of the light intensity (AF:R=0.988, Z1:R=0.974, SF:R=0.946). DISCUSSION AND CONCLUSIONS: The polymerization rate of composite resins used in this study was proportional to the square root of light intensity. Maximum rate of polymerization shrinkage as well as peak time can be used to compare the polymerization rate. Real-time volume method using IB system can be a simple, alternative method to obtain the polymerization rate of composite resins.
Composite Resins ; Equipment Design ; Light ; Polymerization ; Polymers

PURPOSE: A variety of biodegradable polymers have been utilized to fabricate matrices for engineering genitourinary tissues, Chitosan is a biosynthetic polysaccharide that is the deacetylated derivative of chitin. The aims were to investigate the characteristics of the newly developed porous chitosan-based biodegradable scaffolds and to reconstruct cavernosal smooth muscle structure in vivo. MATERIALS AND METHODS: To study the cytotoxicity of the newly developed scaffolds, cultured L929 murine fibroblasts were stained with PKH-26 and then cultured on culture plate or loaded in chitosan/hyaluronic acid polymers. For in vivo study, human corpus cavernosal smooth muscle cells were seeded on the scaffolds at concentration of 20*106 cells per cm3 .A total of 24 polymer scaffolds were implanted subcutaneously with cells in one side and without cells in the other side, respectively, in 12 athymic mice, Mice were scarificed 7, 14, 28 days after implantation, respectively. H-E stain and monoclonal anti-alpha smooth muscle actin stain were performed. RESULTS: Scanning electron micrographs of chitosan and 0.03% hyaluronic acid based scaffolds showed sheet-like porous structure. The cell division numbers of L929 murine fibroblasts sere significantly increased in scaffolds by chitosan/hyaluronic acid compared with chitosan alone, Histologically the retrieved polymers seeded with cavernosal smooth muscle cells showed organized smooth muscle structure 28 days after implantation. immunohistochemical analysis confirmed the smooth muscle phenotype. CONCLUSION: These results show that porous chitosan-based biodegradable scaffolds are new biomaterials for the reconstruction of cavernosal smooth muscle structure. However, further studies are needed to make cavernosal sinusoidal structure using this new scaffolds.
Actins ; Animals ; Biocompatible Materials ; Cell Division ; Chitin ; Chitosan ; Fibroblasts ; Humans ; Hyaluronic Acid ; Male ; Mice ; Mice, Nude ; Muscle, Smooth* ; Myocytes, Smooth Muscle ; Penis ; Phenotype ; Polymers ; Tissue Engineering

PURPOSE: To report a case of corneal failure after implantation of the Ahmed glaucoma valve occurring in a patient diagnosed with Fuchs' heterochromic iridocyclitis. CASE SUMMARY: A 53-year-old male who complained of ocular pain and suddenly decreased visual acuity in his right eye visited our clinic. His visual acuity was 0.15 and intraocular pressure (IOP) was 55 mm Hg. The slit-lamp examination revealed edematous cornea, fine round or stellate keratic precipitates connected with fine filaments on the endothelium and depigmentation of the iris. The corneal endothelial cell density was 2,958 cells/mm2. There was no specific finding in his left eye. The IOP did not improve with medical treatment, therefore, an Ahmed glaucoma valve was implanted in his right eye. At every follow-up exam the tube was well positioned and the IOP was maintained between 8 and 13 mm Hg. Eight months postoperatively, the patient complained of decreased visual acuity and the cell density was decreased to 1,408 cells/mm2. Posterior subcapsular cataract opacity was observed as well as progression of depigmentation and distortion of the iris. Seventeen months after the surgery, the cell density was 700 cells/mm2. On follow-up examination, his visual acuity was decreased to FC10 cm with the cataract progressing, therefore cataract surgery was performed. One month postoperatively, his vision improved to 0.1. However, the visual acuity deteriorated due to progression of the corneal edema and penetrating keratoplasty was performed. CONCLUSIONS: Aggravation of the corneal complication after Ahmed glaucoma valve implantation should be considered in patients with Fuchs' heterochromic iridocyclitis-induced glaucoma.
Cataract ; Cell Count ; Cornea ; Corneal Edema ; Corneal Endothelial Cell Loss* ; Endothelial Cells ; Endothelium ; Follow-Up Studies ; Glaucoma ; Humans ; Intraocular Pressure ; Iridocyclitis* ; Iris ; Keratoplasty, Penetrating ; Male ; Middle Aged ; Visual Acuity