Objective: The patient with electrically injured myelopathy showed mild motor weakness without somatosensory pathway abnormalities. Few reports have been reported on the pathophysiological mechanisms of electrically injured myelopathy, and there is controversy about the exact pathological causes. This study aimed to investigate the ultrastructural changes in the electron microscopic findings of electrical spinal cord injury. Methods: Nine rats were used in this study. We performed 7 electrical shocks (frequency, 120 Hz; pulse width, 0.9 ms; duration, 3 seconds; current, 99 mA) using an electroconvulsive therapy (ECT) apparatus (57800 ECT unit; UGO BASILE). We used one ear and one contralateral hind limb as entry and exit sites, respectively. We only enrolled rats with hind limb weakness and performed electron microscopy evaluations of the spinal cord on the first day and 4 weeks after injury. Results: On the first day after injury, an electron microscopic examination showed a directly damaged area that appeared to be torn as physical damage, damaged myelin sheath, vacuolated axons in the myelin sheath, swollen Golgi apparatus, and injured mitochondria.Looking at changes in motor and sensory nerves, the sensory neurons showed recovered mitochondria and Golgi apparatus 4 weeks after injury; however, motor neurons still showed injured mitochondria, swollen Golgi apparatus, and endoplasmic reticulum. Conclusion This study showed that recovery from ultrastructural injury was more rapid in sensory neurons than in motor neurons.

This rare venous congenital anomaly has been diagnosed preoperatively in a 35-year-old female with complaint of the right flank pain. Herein a case of retrocaval ureter is presented with brief review of literatures.
Adult ; Female ; Flank Pain ; Humans ; Retrocaval Ureter*

No abstract available.
Thumb*

No abstract available.
Female ; Nifedipine* ; Obstetric Labor, Premature* ; Pregnancy ; Ritodrine*

No abstract available.
Lymph Nodes* ; Tuberculosis*

No abstract available.
Teratoma*

OBJECTIVE: This study aimed to test the possible association between Cholecystokinin B receptor (CCKBR) promoter gene and panic disorder. METHODS: 262 patients with panic disorder and 76 healthy controls participated in this study. Genotyping was performed by polymerase chain reaction-based method. RESULTS: Allele distribution of CT repeat polymorphism in patients with panic disorder was not different from those of the controls. However, after excluding the patients with panic disorder comorbid with major depressive disorder and other anxiety disorder, we found out the significant association of CCKBR (CT)n repeat with the panic disorder without comorbidities. And we analysed the data as a di-allelic polymorphism with a short (140-162 bp) and a long (164-180 bp) allele. In the di-allelic analysis, there was an excess of the shorter allele in patients with panic disorder. CONCLUSION: The present study suggested that the CCKBR promoter dinucleotide polymorphism may have a potential role for susceptibility to panic disorder in the Korean population and thus calls for consecutive studies in order to pile up the data with larger different ethnic background.
Alleles ; Anxiety Disorders ; Cholecystokinin* ; Comorbidity ; Depressive Disorder, Major ; Diagnosis* ; Drug Therapy* ; Humans ; Panic Disorder* ; Panic* ; Receptor, Cholecystokinin B*

No abstract available.
Adenoma* ; Kidney*

No abstract available.
Adenoma* ; Kidney*

Myotonic dystrophy is a multisystemic disorder inherited as an autosomal dominant trait. The characteristic clinical features include the presence of myotonia, atrophy of the muscles of the face and the sternocleidomastoids and numerous nonmusclar manifestations such as cataracts, frontal baldness, gonadal dysfunctions and cardiac abnormalities. We experienced one case of myotonic dystrophy with prolonged atrial flutter in 30-year-old male who was admitted because of palpitation. We present this case with reviewing literatures.
Adult ; Alopecia ; Atrial Flutter* ; Atrophy ; Cataract ; Gonads ; Humans ; Male ; Muscles ; Myotonia ; Myotonic Dystrophy*