No abstract available.
Abdomen, Acute*

No abstract available.
Anxiety Disorders* ; Anxiety*

No abstract available.
Emergencies* ; Emergency Medicine* ; Internship and Residency*

Neurofibromatosis, or von Recklinghausen's disease, is a hereditary, harmartomatous disorder that primarilyinvolves neuroectoderm and mesoderm. The estimated incidence is 1 in 2,500 to 3,000 births. The clinical featuresare skin manifestations such as cafe-au-lait spots, skeletal manifestations primarily in volving vertebrae,central and peripheral nervous manifestations, and other associated abnormalities with increased risk ofmalignancy. The authors analysed the radiologic findings of 18 cases of patients with neurofibromatosis whovisited Pusan Kosin Medical Center and Taegu Dongsan Medical Center during the last five years. All were proven bysurgery, biopsy and other diagnostic criteria. The results obtained were as follows: 1. The male ot female ratiowas 11:7 and the age ranged from 11 months to 51 years. 2. All the cases fulfilled the diagnotic criteria of Croweand associates. 3. Bone manifestations were present in 44% of the cases. The other radiologic findings wereintrathoracic meningocele, bilateral acoustic neurinomas, mediastinal or chest wall mass shadows, and peripheralsoft tissue masses. 4. One of the soft tissue masses was proved to be malignant.
Biopsy ; Busan ; Cafe-au-Lait Spots ; Daegu ; Female ; Humans ; Incidence ; Male ; Meningocele ; Mesoderm ; Neural Plate ; Neurofibromatoses ; Neurofibromatosis 1 ; Neurofibromatosis 2 ; Parturition ; Skin Manifestations ; Thoracic Wall

No abstract available.
Child* ; Humans ; Plasma* ; Renal Veins* ; Renin* ; Veins*

No abstract available.
Humans ; Infant, Newborn*

No abstract available.
Arrhythmias, Cardiac*

OBJECTIVE: Brain-derived neurotrophic factor (BDNF), one of the most abundant and important neurotrophins, is known to be involved in the development, survival, maintenance, and plasticity of neurons in the nervous system. Some studies have suggested that BDNF may play a role in the pathophysiology of several psychiatric illnesses such as depression and schizophrenia. Similarly, it is likely that the alteration of BDNF may be associated with the neuro-modulation that contributes to the development of somatization disorder. METHODS: The purpose of this study was to determine whether there is an abnormality of plasma BDNF levels in patients with somatization disorder, and to analyze the nature of the alteration after pharmacotherapy using an enzyme-linked immunosorbent assay (ELISA). RESULTS: The plasma BDNF levels of the patients with a somatization disorder were significantly lower compared with those of the control volunteers (83.61±89.97 pg/mL vs. 771.36±562.14 pg/mL); moreover, the plasma BDNF levels of those patients who received an antidepressant were significantly increased after the treatment (118.13±91.45 pg/mL vs. 72.92±88.21 pg/mL). CONCLUSION: These results suggest that BDNF may play a role in the pathophysiology of somatization disorder.
Brain-Derived Neurotrophic Factor* ; Depression ; Drug Therapy ; Enzyme-Linked Immunosorbent Assay ; Humans ; Nerve Growth Factors ; Nervous System ; Neurons ; Plasma* ; Plastics ; Schizophrenia ; Somatoform Disorders* ; Volunteers

BACKGROUND: While a significant genetic predisposition to schizophrenia has been proposed, the mode of inheritance or nature of etiological factors is unknown. Previous reports of a genome-wide survey for schizophrenia susceptibility genes have indicated a possible region of linkage on chromosome 22. In order to test the possibility that the interleukin-2 recepto beta chain(IL-2R beta ) gene on chromosome 22 is of etiological importance in schizophrenia, a case-control association study was conducted. METHODS: Subjects were ninety-three schizophrenic patients with a diagnosis of schizophrenia by DSM- III -R criteria and ninety-seven normal controls. Schizophrenic patients were divided by clinical phenotypes such as DSM- III -R diagnostic subtypes, positive and negative symptoms, and family history so as to increase the homogeneity of schizophrenics. Genomic DNA was extracted from whole blood lymphocytes according to standard procedures. The DNA was used to study a dinucleotide repeat in the IL-2R beta gene. To reveal the dinucleotide polymorphism, genomic DNA of subjects was amplified by polymerase chain reactions(PCR). RESULTS: At the IL-2R beta gene locus, all the previously reported alleles (eight different alleles) of a dinucleotide polymorphism were identified. There was no significant difference between number of heterozygosity in schizophrenic patients and in normal controls. There was no significant difference in the distribution of frequencies of alleles between schizophrenics and normal controls. In addition, there was no significant difrfrence in the allele frequencies among subtypes of schizophrenic patients according to DSM- III -R diagnostic subtypes, positive and negative symptoms, and family history. CONCLUSIONS: The present study did not detect a difference in frequencies of alleles of a dinucleotide polymorphism at the IL-2R beta gene locus between schizophrenic patients and normal controls. These results do not support an evidence that IL-2R beta gene plays, a major role in the etiology of schizophrenia.
Alleles ; Case-Control Studies ; Chromosomes, Human, Pair 22* ; Diagnosis ; Dinucleotide Repeats ; DNA ; Gene Frequency ; Genetic Predisposition to Disease ; Humans ; Interleukin-2 Receptor beta Subunit ; Interleukin-2* ; Lymphocytes ; Phenotype ; Schizophrenia ; Wills

A study of effect of local hypothermia upon the spinal cord was performed in cats. With a cuff, a cooler, to which was attached connecting tubes to a refrigerator, the experimental technique was deviced to cool the spinal cord locally at midthoracic level. Cold liquid, saline at a temperature of +/-1.1 degrees C, was circulated in closed system through the tubing into the cuff which was snugly rested on the dorsal surface of the spinal cord as a heat exchanger. The temperatures were measured with thermocouples at various sites in the spinal cord before, during, and after the cooling every two minutes upto twenty minutes. In the cord underneath the cuff, the mean precooling temperature of 35.4 degrees C in normal control group was lowered to 11.0 degrees C during the first two minutes of cooling. After this in initial rapid drop in temperature, there was a further gradual reduction of 4.5 degrees C upto 20 minutes cooling to be 6.5 degrees C. The lowest mean temperatures recorded throughout cooling were 4.3 degrees C at dorsal surface and 6.9 degrees C at center of the cord. And the temperature lowering was nearly not noted beyond the cord 1 cm apart from an edge of cuff in rostral and caudal directions. For comparison, the temperature in the cord that had not been injured was also measured. The rate of cooling in the cord underneath the cuff seemed to be faster than in the control group of animal in which the cord was not injured. Another design of this experiment was an evaluation of the protective effect of local hypothermia with respect to cord edema and injury associated cord hemorrhage. Immediately after intravenous administrations of fluorescin the spinal cords were contused with impaction injury. These injured cords were removed ar different time intervals after trauma, and spread or distribution of fluorescin in frozen sectioned specimens was observed under ultraviolet illumination with fluorescence microscope. In all cooling groups, pathological pictures were reduced in its degree and extent more than those in the control group, and that, earlier the cooling after the injury to the cord, better the result was outcome. It would be well to say that local hypothermia might be within the margin of safety and beneficial in the management of spinal cord injury in this experiment.
Administration, Intravenous ; Animals ; Cats ; Edema ; Fluorescence ; Hemorrhage ; Hot Temperature ; Hypothermia* ; Lighting ; Spinal Cord Injuries ; Spinal Cord*