Anti-E and anti-c is one of the clinical significant irregular antibodies developing a delayed hemolytic transfusion reaction and hemolytic disease of the newborn. Since anti-c occurs frequently with anti-E in immunized people whosoe cells are E-and c-, it has been recommended to select blood of the patient's own R1 phenotype for transfusion, even when the presence of anti-c cannot be demonstrated in his/her serum. To determine the utility of this approach, we reviewed the blood bank laboratory records of patients identified anti-E and anti-c in his/her serum in Severance hospital over a 12 year period (1985-1996). During the 12-year period of study, 53 patients were identified with anti-E and/or anti-c; 30(56.6%) patients had anti-E alone, 6(11.3%) had anti-c, and 17(32.1%) had both. Thirty eight of forty two patients whose Rh-hr phenotypes were tested were R1R1. Of these 38 R1R1 patients, 16 patients (42.1%) presented with anti-c concomitant with anti-E. Ouru study showed that the incidence of antni-c in R1R1 patients with anti-E is similar to that of studies reported in Caucasian groups. We highly suggest the transfusion protocol of prophylactic use of c negative blood for R1R1 patients with anti-E. Furthermore, because anti-c may be present in concentrations too low to be detected, the enzyme technique is recommended in parallel with standard serologic methods for the identification of irregular antibodies.
Antibodies ; Blood Banks ; Blood Group Incompatibility ; Humans ; Incidence ; Infant, Newborn ; Phenotype

No abstract available.
Intracranial Arteriovenous Malformations* ; Radiosurgery*

Background: Stroke is caused by disruption of blood supply and results in permanent disabilities as well as death. Chlorogenic acid is a phenolic compound found in various fruits and coffee and exerts antioxidant, anti-inflammatory, and anti-apoptotic effects. Objectives: The purpose of this study was to investigate whether chlorogenic acid regulates the PI3K-Akt-Bad signaling pathway in middle cerebral artery occlusion (MCAO)-induced damage. Methods: Chlorogenic acid (30 mg/kg) or vehicle was administered peritoneally to adult male rats 2 h after MCAO surgery, and animals were sacrificed 24 h after MCAO surgery.Neurobehavioral tests were performed, and brain tissues were isolated. The cerebral cortex was collected for Western blot and immunoprecipitation analyses. Results: MCAO damage caused severe neurobehavioral disorders and chlorogenic acid improved the neurological disorders. Chlorogenic acid alleviated the MCAO-induced histopathological changes and decreased the number of terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells. Furthermore, MCAO-induced damage reduced the expression of phospho-PDK1, phospho-Akt, and phospho-Bad, which was alleviated with administration of chlorogenic acid. The interaction between phospho-Bad and 14-3-3 levels was reduced in MCAO animals, which was attenuated by chlorogenic acid treatment. In addition, chlorogenic acid alleviated the increase of cytochrome c and caspase-3 expression caused by MCAO damage. Conclusions The results of the present study showed that chlorogenic acid activates phospho-Akt and phospho-Bad and promotes the interaction between phospho-Bad and 14-3-3 during MCAO damage. In conclusion, chlorogenic acid exerts neuroprotective effects by activating the Akt-Bad signaling pathway and maintaining the interaction between phosphoBad and 14-3-3 in ischemic stroke model.

PURPOSE: Interleukin (IL) -13 plays a pivotal role in the induction of immunoglobulin E (IgE) and in the pathogenesis of atopic dermatitis (AD). Recently, an association was reported between the polymorphism of the IL-13 promoter region (-1512A/C) and atopic asthma. We investigated the association between the IL-13 single nucleotide polymorphism (SNP) in the promoter region (-1512A/C) and atopic dermatitis in Korean children with AD. METHODS: We enrolled 204 allergic AD, 92 non-allergic AD, and 116 non-atopic healthy children. Evaluated phenotypes of atopic dermatitis included total IgE, total eosinophil count, and eosinophil fraction. We used a PCR-RFLP method to identify IL-13 genotypes. RESULTS: The allele frequencies of the IL-13 promoter polymorphism (-1512A/C) did not differ statistically among the three groups. Children with one or two copies of risk alleles in the promoter region (-1512C) did not show any significant association with the clinical phenotypes of atopic dermatitis including total IgE, eosinophil phenotypes and SCORAD score in the allergic or non-allergic atopic dermatitis. CONCLUSION: These data suggest that the -1512A/C polymorphism of IL-13 gene may not be associated with neither the development nor the clinical phenotypes of atopic dermatitis in Korean children.
Alleles ; Asthma ; Child* ; Dermatitis, Atopic* ; Eosinophils ; Gene Frequency ; Genotype ; Humans ; Immunoglobulin E ; Immunoglobulins ; Interleukin-13* ; Interleukins ; Phenotype ; Polymorphism, Single Nucleotide ; Promoter Regions, Genetic

Periorbital dermatochalasis with upper eyelid hooding, brow ptosis, and sunken eyelids may appear with age. Because classic blepharoplasty is unable to correct all these issues, we developed a single operation, which we present herein, to correct dermatochalasis accompanied by sunken eyelids. This sub-brow approach is used with simultaneous browpexy by fixing the orbital portion of the orbicularis oculi muscle (OOM) to the periosteum immediately above the supraorbital rim using sutures with 3 or 4 points of fixation and correcting sunken eyelids by burying the elevated dermis, fat, and OOM after de-epithelization in the lower flap of the sunken upper eyelid along the submuscular plane. This method enables the correction of sunken eyelids during the same operation without requiring an additional procedure, and offers the advantages of a shortened operation time and decreased cost. The presence of sunken eyelids in patients with dermatochalasis and severe lateral hooding may be corrected by the procedure described herein, thereby achieving periorbital rejuvenation while maintaining the original shape of the eyes.
Blepharoplasty ; Dermis ; Eyelids ; Humans ; Methods ; Middle Aged ; Orbit ; Periosteum ; Rejuvenation ; Skin Aging ; Sutures

Hyperglycemia is one of the major risk factors for stroke. Hyperglycemia can lead to a more extensive infarct volume, aggravate neuronal damage after cerebral ischemia. α-Synuclein is especially abundant in neuronal tissue, where it underlies the etiopathology of several neurodegenerative diseases. This study investigated whether hyperglycemic conditions regulate the expression of α-synuclein in middle cerebral artery occlusion (MCAO)-induced cerebral ischemic injury. Male Sprague-Dawley rats were treated with streptozotocin (40 mg/kg) via intraperitoneal injection to induce hyperglycemic conditions. MCAO were performed four weeks after streptozotocin injection to induce focal cerebral ischemia, and cerebral cortex tissues were obtained 24 hours after MCAO. We confirmed that MCAO induced neurological functional deficits and cerebral infarction, and these changes were more extensive in diabetic animals compared to non-diabetic animals. Moreover, we identified a decrease in α-synuclein after MCAO injury. Diabetic animals showed a more serious decrease in α-synuclein than non-diabetic animals. Western blot and reverse-transcription PCR analyses confirmed more extensive decreases in α-synuclein expression in MCAO-injured animals with diabetic condition than these of non-diabetic animals. It is accepted that α-synuclein modulates neuronal cell death and exerts a neuroprotective effect. Thus, the results of this study suggest that hyperglycemic conditions cause more serious brain damage in ischemic brain injuries by decreasing α-synuclein expression.
alpha-Synuclein* ; Animals ; Blotting, Western ; Brain ; Brain Injuries ; Brain Ischemia ; Cell Death ; Cerebral Cortex ; Cerebral Infarction ; Humans ; Hyperglycemia* ; Infarction, Middle Cerebral Artery* ; Injections, Intraperitoneal ; Male ; Middle Cerebral Artery* ; Neurodegenerative Diseases ; Neurons ; Neuroprotective Agents ; Polymerase Chain Reaction ; Rats, Sprague-Dawley ; Risk Factors ; Streptozocin ; Stroke

Lipopolysaccharide (LPS) acts as an endotoxin, releases inflammatory cytokines, and promotes an inflammatory response in various tissues. This study investigated whether LPS modulates neuroglia activation and nuclear factor kappa B (NF-κB)-mediated inflammatory factors in the cerebral cortex. Adult male mice were divided into control animals and LPS-treated animals. The mice received LPS (250 µg/kg) or vehicle via an intraperitoneal injection for 5 days. We confirmed a reduction of body weight in LPS-treated animals and observed severe histopathological changes in the cerebral cortex. Moreover, we elucidated increases of reactive oxygen species and oxidative stress levels in LPS-treated animals. LPS administration led to increases of ionized calcium-binding adaptor molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) expression. Iba-1 and GFAP are well accepted as markers of activated microglia and astrocytes, respectively. Moreover, LPS exposure induced increases of NF-κB and pro-inflammatory factors, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Increases of these inflammatory mediators by LPS exposure indicate that LPS leads to inflammatory responses and tissue damage. These results demonstrated that LPS activates neuroglial cells and increases NF-κB-mediated inflammatory factors in the cerebral cortex. Thus, these findings suggest that LPS induces neurotoxicity by increasing oxidative stress and activating neuroglia and inflammatory factors in the cerebral cortex.
Adult ; Animals ; Astrocytes ; Body Weight ; Cerebral Cortex ; Cytokines ; Glial Fibrillary Acidic Protein ; Humans ; Injections, Intraperitoneal ; Male ; Mice ; Microglia ; Necrosis ; Neuroglia ; NF-kappa B ; Oxidative Stress ; Reactive Oxygen Species

Baicalin is a natural flavonoid that exerts a variety of pharmaceutical effects such as anti-inflammatory and antioxidant. Lipopolysaccharide (LPS) is an endotoxin that releases inflammatory cytokines and induces inflammatory response. This study was investigated the anti-inflammatory mechanism of baicalin against LPS-induced inflammatory response in the hippocampus. Adult mice were randomly grouped into control, LPS-treated, and LPS and baicalin co-treated animals. LPS (250 μg/kg/day) and baicalin (10 mg/kg/day) were administered intraperitoneally for 7 consecutive days. We measured neuroglia cells activation and inflammatory factors activation using Western blot analysis and immunofluorescence staining techniques. Ionized calcium binding adaptor molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) are widely used as microglia and astrocyte markers, respectively. LPS treatment increased Iba-1 and GFAP expression, while baicalin co-treatment attenuated this overexpression. Nuclear factor-kappa B (NF-κB) is a key mediator of inflammation. Baicalin co-treatment alleviated LPS-induced increase of NF-κB in the hippocampus. In addition, LPS treatment upregulated pro-inflammatory cytokines including interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). However, baicalin co-treatment prevented LPS-induced increases of IL-1β and TNF-α in the hippocampus. Results from the present study showed that baicalin suppresses LPS-induced neuroinflammation by regulating microglia and astrocyte activation and modulating inflammatory factors in the hippocampus. Thus, these results demonstrate that baicalin has neuroprotective effect by alleviates microglia and astrocyte activation and modulates inflammatory response by suppressing NF-κB expression in hippocampus with neuroinflammation caused by LPS.

Purpose: Preimplantation genetic testing for monogenic disorders (PGT-M) has been successfully used to prevent couples with monogenic disorders from passing them on to their child. Charcot–Marie–Tooth Disease (CMT) is a genetic disorder characterized by progressive extremity muscle degeneration and loss of sensory function. For the first time in Korea, we report our experience of applying single nucleotide polymorphism genotyping and karyomapping for PGT-M of CMT disease. Materials and Methods: Prior to clinical PGT-M, preclinical tests were performed using genotypes of affected families to identify informative single-nucleotide polymorphisms associated with mutant alleles. We performed five cycles of in vitro fertilization PGT-M in four couples with CMT1A, CMT2A, and CMT2S in CHA Fertility Center, Seoul Station. Results: From July 2020 through August 2021, five cycles of PGT-M with karyomapping in four cases with CMT1 and CMT2 were analyzed retrospectively. A total of 17 blastocysts were biopsied and 15 embryos were successfully diagnosed (88.2%).Ten out of 15 embryos were diagnosed as unaffected (66.7%). Five cycles of PGT-M resulted in four transfer cycles, in which four embryos were transferred. Three clinical pregnancies were achieved (75%) and the prenatal diagnosis by amniocentesis for all three women confirmed PGT-M of karyomapping. One woman delivered a healthy baby uneventfully and two pregnancies are currently ongoing. Conclusion This is the first report in Korea on the application of karyomapping in PGT-M for CMT patients. This study shows that karyomapping is an efficient, reliable and accurate diagnostic method for PGT-M in various types of CMT diseases.

PURPOSE: This correlational study was to examine the relationships between dementia knowledge, attitude, self-efficacy and preventive behavior of low income middled-aged women. METHODS: The subjects for this study were 125 low income middle aged women living in I city. The data were collected using the questionnaires for dementia knowledge, attitude, self-efficacy and preventive behavior. The data analysis was done by descriptive statistics, t-test, ANOVA, Pearson product moment correlation and stepwise multiple regression analysis. RESULTS: The mean of dementia knowledge was 13.96 out of 20, attitude was 43.98 out of 60, self-efficacy was 54.07 out of 75 and preventive behavior was 25.98 out of 36. The positive correlations were revealed between dementia knowledge (r=.458, p=.000), attitude (r=.498, p=.000), self-efficacy (r=.573, p=.000) and preventive behavior. The influencing factors for dementia preventive behavior were self-efficacy, belief in Buddhism and attitude which accounted for 42.5% of the total variance. CONCLUSION: Dementia knowledge, attitude and self-efficacy were identified as variables that correlate dementia preventive behavior. Also, self-efficacy is the most influential factor affecting dementia preventive behavior. On the basis of these results, it is necessary for nurses to consider using dementia knowledge and mode of efficacy expectation in order to improve dementia preventive behavior.
Buddhism ; Dementia ; Female ; Humans ; Middle Aged ; Statistics as Topic ; Surveys and Questionnaires