The purpose of the study is to minimize the incidence of glaucoma and ocular hypertension caused by using corticosteroids during induction chemotherapy for acute lymphoblastic leukemia in children. We have periodically observed the intraocular pressure and the variation of C / D ratio of two 7 years old boys with chemotherapy in our pediatric department. We observed the increase in intraocular pressure using applanation tonometer, and we managed by beta- blockers, carbonic anhydrase inhibitor and etc. Increased intraocular pressure has been normalized after chemotherapy. The frequency of occurrence of the ocular hypertension and glaucoma can be controlled with the quantity of corticosteroids used.
Adrenal Cortex Hormones ; Carbonic Anhydrases ; Child ; Drug Therapy ; Glaucoma* ; Humans ; Incidence ; Induction Chemotherapy* ; Intraocular Pressure ; Leukemia ; Ocular Hypertension ; Precursor Cell Lymphoblastic Leukemia-Lymphoma*

OBJECTIVES: Lipocortin-1 (LC-1), a member of annexin family of calcium-binding proteins induced by corticosteroid, originally evoked interest as one of the secondary messengers in the antiinflammatory action of corticosteroid, But the exact mechanism of LC-1 responsible for antiinflammatory effect is still unclear. We investigated the potential role of LC-1 in the effect of corticosteroid on amelioration of collagen induced arthritis (CIA) in mice. METHODS: Four groups of DBA/1j mice were immunized by intradermal injection of 5mg/kg of type 2 collagen with complete Freunds adjuvant which was boostered on day 21 and 42. Group 1 received no treatment and group 2 received 1mg/kg dexamethasone intraperitoneally twice weekly from day 21. Group 3 and 4 were treated with 50 and 0.5microgram/kg of anti LC-1 monoclonal antibody subcutaneously and dexamethasone from day 21 twice weekly, respectively. The prevalence of arthritis and arthritis score were assessed twice weekly. At week 10, we measured serum anticollagen antibody levels and splenic mononuclear cell stimulation indices (SI) to collagen. RESULT: CIA started to develop after 4 weeks of collagen treatment in all groups. All mice of group 1 developed arthritis by the 9 week. Treatment with dexamethasone markedly inhibited arthritis development (P<0.05). Cotreatment of anti LC-1 monoclonal antibody and dexamethasone abolished the antiinflammatory effect of dexamethasone (P<0.05). But there was no significant difference in the serum levels of anticollagen antibody or splenic mononuclear cell SI among the groups. CONCLUSION: These findings support the hypothesis that LC-1 is involved, at least in part, in the antiinflammatory actions of corticosteroid in chronic inflammation, although the mechanism of which is unclear.
Animals ; Arthritis* ; Calcium-Binding Proteins ; Collagen* ; Dexamethasone ; Freund's Adjuvant ; Humans ; Inflammation ; Injections, Intradermal ; Mice ; Prevalence

OBJECTIVE: To evaluate the effect of IL-10 on development of collagen-induced arthritis, on humoral and cellular immunity and on the endogenous production of IL-10 in DBA/1J mice. METHODS: DBA/1J mice were immunized with chicken type II collagen in Freund s complete adjuvant. Murine recombinant IL-10 was given intraperitoneally twice a week from the day of second immunization (week 3) in doses of 0.002ug, 0. 02ug and 0. 2ug for 3 different groups, respectively. Dexamethasone was injected in one group to suppress the arthritis development and this group was used as negative control group. Levels of anti-collagen antibodies, serum IL-10 and stimulation indices of splenic monocytes to collagen were measured at the end of study. RESULTS: The 0. 02ug IL-10 and 0. 2ug IL-10 treated groups developed earlier and more severe arthritis (week 6 and 8) compared to that of the control group while the 0. 002ug IL-10 group has shown similar course to the control group in terms of incidence and severity of arthritis, At week 10, all groups with or without IL-10 injections developed arthritis with similar degree of severity while dexamethasone group showed far less incidence and severity of arthritis. The serum levels of anti-collagen antibody, IL-10 and spleen monocyte stimulation indices to collagen antigen showed no difference among control group, IL-10 injected groups and dexamethasone injected group. CONCLUSION: This study shows IL-10 could worsen the arthritis in CIA with the dosage used in this study without significant influence on the level of anti-collagen antibodies or stimulation indices of spenic monocyte to collagen.
Animals ; Antibodies ; Arthritis ; Arthritis, Experimental* ; Chickens ; Collagen ; Collagen Type II ; Dexamethasone ; Immunity, Cellular ; Immunization ; Incidence ; Interleukin-10* ; Mice ; Monocytes ; Spleen

No abstract available.

No abstract available.

PURPOSE: This study was performed to examine the serial alteration of the optic nerve in chronic ischemia-induced brain injury of albino rat, which might be an experimental model of ischemia-induced optic nerve disease and vasogenic glaucoma in human. METHODS: We ligated bilateral common carotid arteries so that the brain and optic nerve had permanent ischemic injuries. Serial alteration of the optic nerve was studied on postoperative 1 day, 3 day, 5 day, 1 week, 2 week, 4 week and 9 week. After fixing the brain by perfusing formaline through the left ventiricle, we dissected the brain and optic nerve and then made specimen for Hematoxilin-Eosin (HE) stain to observe the histopathology of the optic nerve. Kluiver-Barrera (KB) stain was performed to qualify the myelin injury and optic nerve injury status. RESULTS: The HE stain specimen showed increased spaces in the nerve fiber layer and increased number of vacuoles three days after the operation. The optic neve injury became augmented with time. The KB stain showed better-defined configuration of HE stain. CONCLUSIONS: We were able to notice that optic nerve injury was induced by the bilateral common carotid ligation in this chronic ischemic experimental model, which might be an help to the studies of ischemic optic nerve disease, neurodefensive mechanism, and the hemodynamic mechanism of glaucoma in human.
Animals ; Brain ; Brain Injuries ; Carotid Arteries* ; Carotid Artery, Common ; Formaldehyde ; Glaucoma ; Hemodynamics ; Humans ; Ligation ; Models, Theoretical* ; Myelin Sheath ; Nerve Fibers ; Optic Nerve Diseases ; Optic Nerve Injuries ; Optic Nerve* ; Rats* ; Vacuoles

PURPOSE: The effect of 0.2% cyclosporin A (CsA) as an adjuvant therapy after glaucoma-filtering surgery was the focus of this study. METHODS: A posterior lip sclerotomy was performed in 16 eyes of 8 rabbits, and 0.2% CsA was administered into the right eyes. The left eyes served as controls. The intraocular pressure (IOP) was measured 1, 3, 5, 7, 14, and 28 days after surgery. Hematoxylin-eosin (HE) and anti-bromodeoxyuridine (BrdU) immunocytochemical staining were performed at 1, 2, 4, and 8 weeks. RESULTS: The IOP at 7 and 14 days after surgery was lower in the 0.2% CsA group and statistically significant (P=0.047, P=0.48; respectively). HE staining did not show any difference between experimental and control eyes, but anti-BrdU staining showed a lower number of positive cells in the experimental eyes at 1 week. The fibroblast proliferation rate was significantly lower 1 week after surgery in the 0.2% CsA group (P=0.003). CONCLUSIONS: An effect of 0.2% CsA on early wound healing was observed. The data suggest that a low concentration of CsA can be useful when employed as adjuvant therapy in glaucoma filtering surgery.
Cyclosporine ; Eye ; Fibroblasts ; Filtering Surgery ; Glaucoma ; Intraocular Pressure ; Lip ; Pilot Projects ; Rabbits ; Wound Healing

No abstract available.
Niemann-Pick Disease, Type A*

Human cardiomyocytes (CMs) cease to proliferate and remain terminally differentiated thereafter, when humans reach the mid-20s. Thus, any damages sustained by myocardium tissue are irreversible, and they require medical interventions to regain functionality. To date, new surgical procedures and drugs have been developed, albeit with limited success, to treat various heart diseases including myocardial infarction. Hence, there is a pressing need to develop more effective treatment methods to address the increasing mortality rate of the heart diseases. Functional CMs are not only an important in vitro cellular tool to model various types of heart diseases for drug development, but they are also a promising therapeutic agent for cell therapy. However, the limited proliferative capacity entails difficulties in acquiring functional CMs in the scale that is required for pathological studies and cell therapy development. Stem cells, human pluripotent stem cells (hPSCs) in particular, have been considered as an unlimited cellular source for providing functional CMs for various applications. Notable progress has already been made: the first clinical trials of hPSCs derived CMs (hPSC-CMs) for treating myocardial infarction was approved in 2015, and their potential use in disease modeling and drug discovery is being fully explored. This concise review gives an account of current development of differentiation, purification and maturation techniques for hPSC-CMs, and their application in cell therapy development and pharmaceutical industries will be discussed with the latest experimental evidence.
Cell- and Tissue-Based Therapy ; Drug Discovery ; Drug Industry ; Heart Diseases ; Humans* ; In Vitro Techniques ; Mortality ; Myocardial Infarction ; Myocardium ; Myocytes, Cardiac* ; Pluripotent Stem Cells* ; Stem Cells

Background: Psoriasis is a chronic T17 cell-driven immune-mediated inflammatory disease. However, patients with psoriasis may have elevated total serum immunoglobulin E (IgE) levels, which is a hallmark of Th2 inflammation.In previous case reports, psoriasis patients with elevated total serum IgE levels did not respond well to treatment or had exacerbated eczema lesions. Objective: We sought to investigate the clinical characteristics of psoriasis patients with elevated total serum IgE levels. Methods: This is a retrospective chart review of 130 patients with psoriasis who were tested for total serum IgE levels from November 1, 2009, to October 31, 2019. We compared the demographics, clinical characteristics, disease severity, and treatment regimen for each elevated IgE group (＞214 U/mL) and normal IgE group (≤214 U/mL). Results: Among 130 patients with psoriasis, 41 (31.5%) had elevated total serum IgE levels. Elevated total serum IgE levels were positively associated with the severity of disease; psoriasis lesions including those on the scalp, hands, feet, and flexures, which are difficult to treat, were observed to be significantly higher in patients with elevated total serum IgE levels. There was no correlation between age, sex, disease duration, or presence of pruritus and total serum IgE levels. Conclusion This study identified the clinical characteristics of psoriasis patients with elevated total serum IgE levels in Korea.