No abstract available.
Humans ; Infant, Newborn ; Infant, Premature* ; Nephroma, Mesoblastic* ; Ultrasonography, Prenatal*

To observe the role of oxygen free radical and enzymatic scavengers in cerebral ischemia, an infarction model was made using transorbital occlusion of the middle cerebral artery in cats. The changes of the superoxide radical production and the activities of superoxide dismutase and catalase were measured. The results were as follows ; 1) The infarction of the left middle cerebral artery(MCA) territory was identified with intracardiac perfusion of a TTC solution after transorbital occlusion. 2) The superoxide radical activities after occlusion of the left MCA were not changed in all groups except for the decrease in 6 hours group of the right side compared to the control group(p<0.05). 3) The Mn-superoxide dismutase activities of the left side in the 12 hours group were significantly higher than those of the right side(p<0.01) and those in the control group(p<0.05). 4) The Cu, Zn-superoxide dismutase activities of the left side in the 3 hours group after occlusion of the left MCA were significantly higher than those in the control group(p<0.05). 5) The catalase activities of the left side in the 3 hours, 6 hours and 12 hours groups after occlusion of the left MCA were significantly higher than those of the right side(p<0.05). 6) The catalase activities of the left side in the 12 hours group after occlusion of the left MCA were significantly higher than those in the control group(p<0.05). The authors suggest that the enzymatic scavangers such as Mn-SOD, Cu, Zn-SOD and catalase increased in the infarcted brain, which means an involvement of free radicals in cerebral infarction.
Animals ; Brain ; Brain Ischemia ; Catalase* ; Cats ; Cerebral Infarction* ; Free Radicals ; Infarction ; Middle Cerebral Artery ; Oxygen ; Perfusion ; Superoxide Dismutase* ; Superoxides*

Rectus sheath hematoma of the abdominal wall is a well-recognized, but uncommon condition, caused by a tear in an epigastric vessel and characterized by sudden onset of severe abdominal pain and palpable mass. In most cases, a precipitating cause can be demonstrated. Causes include external trauma, strenuous activities, coughing, lifting, sneezing, vomiting, straining while urinating or defecating, golfing, pregnancy and the puerperium, anticoagulation therapy, infection, chronic diesase, arteriosclerosis, hypertension, prior paracentesis or laparotomy, inadequate hemostasis or excessive retraction in surgery, and idiopathy. Unfortunately, the correct diagnosis often is missed, and the hematoma is found only during an exploratory laparotomy. Treatment should be conservative in most instances. Although the mortality rate for patients with rectus sheath hematoma is low, the condition may be fatal if the volume of the hemorrhage is large and if treatment is delayed. Hence, it should be included in the differential diagnosis of any patient who presents to the emergency department with acute onset of abdominal pain. Our purpose is to familiarlize emergency physicians with the pathophysiology, the diagnosis, and the treatment of rectus sheath hematoma. We describe a patient with fatal rectus sheath hematoma presenting to the emergency department and give a review of the literature.
Abdominal Pain ; Abdominal Wall ; Arteriosclerosis ; Cough ; Diagnosis ; Diagnosis, Differential ; Emergencies ; Emergency Service, Hospital ; Golf ; Hematoma* ; Hemorrhage ; Hemostasis ; Humans ; Hypertension ; Hypovolemia* ; Laparotomy ; Lifting ; Mortality ; Paracentesis ; Postpartum Period ; Pregnancy ; Shock* ; Sneezing ; Vomiting

BACKGROUND: Kerationcytes make up the vast majority of cells within the epidermis. Recent attention has focused on the role keratinocytes may play in the induction of T cell mediated inflammatory responses in skin, particularily because keratinocytes, when activated by immunologic stimuli, express MHC class llAg and secrete cytokines. But in experimentally induced lichenoid tissue reaction by interferon-nu, MHC class ll Ag was not essential for the enhanced T cell trafficking. There is growing evidence that keratinocyte intercellular adhesion molecule-1 (ICAM-1) expression is involved in the epidermal trafficking of T lymphocytes. OBJECT: To investigate the kinetics of expression of the HLA-DR and ICAM-1 on cultured human keratinocytes by recombinant-interferon-nu(IFN) and phorbol myristate acetate(PMA), and the influence of the HLA-DR and ICAM-1 and the stimulation of peripheral blood mononuclear leukocytes(PBML). RESULTS: 1. 1 U/ml of IFN can induce HLA-DR and ICAM-1 on keratinocytes. Expression of both antigens were increased in a dose and exporsure time dependent fashion. But expression of HLA-DR was less sensitive to IFN than ICAM-1 2. ICAM-1 induction was more rapid than HLA-DR. Keratinocytes expressed HLA-DR 6hours after IFN treatment amd increased rapidly after 12 hours. 3. HLA-DR positive keratinocytes were decreased more rapidly that ICAM-1 positive kerationcytes. 4. Proliferations of PBML were slightly inhibited when cultured with keratinocytes which were treated or not treated with IFN. But IFN treated keratinocytes stimulated the PBML more than untreated keratinocytes. Proliferaton of PBML by IFN treated keratinocytes were inhibited by anti-ICAM monoclonal antibody 5. PMA treated keratinocytes stimulated the PBML more than untreated keratinocytes. Proliferation of PBML by PMA treated keratinocytes was inhibited by anti-ICAM monoclonal antibodies and anti-LFA-1 monoclonal antibodies. CONCLUSION: These results suggest that keratinocytes can express not only HLA-DR but also ICAMP1 may play a important role in initiating immunologic response. Complete clarification of the function of HLA-DR and ICAM-1 positive keratinocytes requires furthe5r study
Antibodies, Monoclonal ; Cytokines ; Epidermis ; HLA-DR Antigens* ; Humans* ; Intercellular Adhesion Molecule-1* ; Keratinocytes* ; Kinetics* ; Myristic Acid ; Skin ; T-Lymphocytes

PURPOSE: The aim of this study was to evaluate the clinical manifestations, contact history, and status of tuberculosis contact investigations in school-age children and adolescents with pulmonary tuberculosis (TB) at two centers. METHODS: This study was conducted with 54 patients in the age ranging from 10 to 18 years, who were diagnosed with pulmonary TB at the Pusan National University Hospital and Pusan National University Children's Hospital, January 2008 to December 2012. We retrospectively reviewed the medical records of the patients. RESULTS: The median age of the patients was 16 years old; 11 patients were aged 10 to 14 and 43 patients were aged 15 to 18. Among 54 patients, 19 had history of contact with pulmonary TB, 10 had contact with house members (household), and remaining 9 had contact with classmates (non-household). One out of 10 patients who had household contacts and 6 out of 9 patients who had non-household contacts were evaluated with contact investigation after the exposure to pulmonary TB. Among 7 patients who were evaluated with contact investigation, 3 were diagnosed with active pulmonary TB, 1 had latent tuberculosis infection (LTBI), and 3 had no evidence of TB or LTBI. The median period of diagnosis after the exposure to active pulmonary TB was 2 years in patients with household contacts and 0.23 years in patients with non-household contacts. CONCLUSION: This study suggested that if the contact investigation conducted properly, it would be helpful for early diagnosis and prevention of pulmonary TB.
Adolescent* ; Busan ; Child* ; Diagnosis ; Early Diagnosis ; Family Characteristics ; Humans ; Latent Tuberculosis ; Medical Records ; Retrospective Studies ; Tuberculosis* ; Tuberculosis, Pulmonary*

The gene encoding the 66 kilodalton (kDa) protein of Borrelia hermsii HS1 was cloned and sequenced. Chromosomal DNA was prepared from purified B. hermsii and used in construction of genomic library. The library was screened for positive clones by 314 bp DIG-labeled probe synthesized on the basis of the part of the sequence of B. hermsii. Positive clone was subcloned into p2ErO vector and was designated as pBH11. pBH11 were subcloned into pBluscript vector and were designated as pBH11-1 (500 bp), pBH11-2 (800 bp), pBH11-3 (600 bp) and pBH11-4 (800 bp). The plasmids were sequenced and determined the nucleotide sequence of p66. The open reading frame of the p66 consisted of 1803 base pairs coding for 600 amino acid protein. The basic information on the p66 gene of B. hermsii HS1 obtained from this study will be useful for further analysis and experiment of pathogenesis of the borrelia.
Base Pairing ; Base Sequence ; Borrelia* ; Clinical Coding ; Clone Cells* ; Cloning, Organism* ; DNA ; Genomic Library ; Open Reading Frames ; Plasmids

No abstract available.
Calcium* ; Child* ; Humans

No abstract available.
Biopsy, Fine-Needle* ; Salivary Glands*

Objective: We evaluated the protective effect of dexamethasone (DX) administration on brain damage produced in a perinatal model of cerebral hypoxia-ischemia in the rat. Since hyperglycemia has been shown to reduce hypoxic-ischemic brain injury (HI) in immature tar, we investigated the role of glucocorticoid-induced hyperglycemia in the neuroprotective mechanism of DX. Methods: Hypoxic-ischemic brain injury in 7-day-old rats was induced by right common carotid artery occlusion and 2 hours of 8% oxygen. Pups received 3 doses of DX (0.5mg/kg/d intraperitoneally) 48 hours, 24 hours and immediately before HI (Dx1)(n=12), a single dose of DX 24 hours(DX2)(n=16), 3 hours (DX3)(N=10)or immediately before HI (DX4)(n=14), a single dose of DX immediately after HI (DX5) (n=9), 3 doses of DX immediately, 24 hours and 48 hours after HI (DX6) (n=14) and a single dose of DX 24 hours before HI with insulin (0.5U/kg, subcutaneously, 1.5 hours before HI)(IN)(n=8). Control pups (n=15) received a single dose of normal saline 24 hours before HI. Blood glucose was estimated before hypoxia, 1 hour and 2 hours after hypoxia using glucometer in DX 1~4. IN and control rats. Pups were killed at 14 days of age for determination of mortality during HI, gross cerebral infarction and right cerebral hemisphere atrophy. We measured the diameter of each cerebral hemisphere and cortical thickness from a coronal section at the dorsal hippocampus level, and expressed the % atrophy from the change in the right vs left hemisphere diameter. Results: The mortality that occurred during and after HI was similar in all groups. The incidence of gross cerebral infarction was 0.0%, 0.0%, 75.0%, 83.3%, 87.5%, and 90.0% in DX 1~6, respectively, 0.0%in IN, and 100.0% in control group. There was a significant difference (p<0.001)in the incidence of gross cerebral infarction of DX1, DX2, IN vs control group. The mean % atrophy was 5.4 +/- 2.2, 4.9 +/- 1.8, 21.7 +/- 8.1, 29.7 +/- 5.0, 37.4 +/- 5.5, 33.4 +/- 9.3 in DX 1~6, respectively, 1.5 +/- 1.1 in IN, and 29.1 +/- 3.4 (mean+/-SEM) in control group. There was a significant difference in % atrophy of DX1, DX2, IN vs control group. Before hypoxia, there was no significant difference in blood glucose between saline, all DX, and DX with insulin treated groups. But after hypoxia, pups in DX1 and Dx2 were more hyperglycemic compared to DX 3~4, IN, or saline treated groups. Conclusions: Dexamethasone administration in the neonatal period protects the brain during the subsequent periods of hypoxia-ischemia in rats and glucocorticoid-induced hyperglycemia does not explain the neuroprotective effects dexamethasone.
Animals ; Anoxia ; Atrophy ; Blood Glucose ; Brain Injuries ; Brain* ; Carotid Artery, Common ; Cerebral Infarction ; Cerebrum ; Dexamethasone* ; Hippocampus ; Hyperglycemia* ; Hypoxia-Ischemia, Brain ; Incidence ; Insulin ; Mortality ; Neuroprotective Agents ; Oxygen ; Rats*

Injury to specific areas of the immature brain, in both the human and animals, can result in compensatory reorganization in undamaged adjacent or contralateral areas. The functional plasticity of such compensatory hypertrophy is not well known, but in some cases may be responsible for recovery of function. In order to investigate the effect of unilateral ischemic injury on the contralateral cerebral hemisphere in neonatal rats, early and late changes in various areas of both cerebral hemispheres were assessed. Seventy-seven seven-day-old Sprague-Dawley rats underwent unilateral carotid artery ligation and were then exposed to hypoxia(8% oxygen) for 3 hours. The animals were killed one week(Group I, 58 rats) and three months(Group II, 19 rats) later. Twelve rats, comprising Group III, were exposed to hypoxia for 3 hours without carotid artery ligation. The control group, consisting of 19 rats, did not undergo any of the above procedures. In each slice of brain tissue(4mm posterior to the bregma), the area of the whole brain, each hemisphere, and the frontoparietal, temporal and hippocampal regions in each hemisphere were measured, using the image analysis program(Optimas 5.2), and to assess which regions were affected, proportions of each hemisphere occupied by each region were compared. In Group II, the proportional areas of the frontoparietal(p<0.05) and temporal(p<0.01) regions in the contralateral hemisphere increased significantly, compared with the control group, but the hippocampal region showed no significant change. In Group I, there was no contralateral hypertrophy. The ipsilateral hemisphere showed significant atrophy and there was weight reduction in Groups I(p<0.001) and II(p<0.001). This study suggests that unilateral hypoxia-ischemia results in ipsilateral hemispheric atrophy and contralateral hypertrophy, especially in the frontoparietal and temporal areas, may contribute to some functional recovery and compensation in addition to uncrossed corticospinal or other descending motor systems.
Animals ; Anoxia ; Atrophy ; Brain* ; Carotid Arteries ; Cerebrum* ; Compensation and Redress ; Humans ; Hypertrophy ; Hypoxia-Ischemia, Brain* ; Ligation ; Plastics ; Rats* ; Rats, Sprague-Dawley ; Recovery of Function ; Weight Loss