No abstract available.
Diskectomy*

No abstract available.
Humans* ; Interleukin-12* ; Mycobacterium tuberculosis* ; Mycobacterium* ; Tuberculosis, Pulmonary* ; Tumor Necrosis Factor-alpha*

Rippling muscle disease (RMD) is caused by dominant mutations of the caveolin-3 gene (CAV3), and presents with overlapping limb-girdle muscle weakness, elevated creatine kinase (hyper- CKemia), RMD, and distal myopathy. We report a patient with a CAV3 mutation who presented with myalgia, exercise-induced muscle stiffness, hyperCKemia, and percussion-induced rapid muscle contraction and muscle mounding. A familial genetic study revealed the same mutation in two family members, with physical examinations showing that both of them had rippling muscles.

Rippling muscle disease (RMD) is caused by dominant mutations of the caveolin-3 gene (CAV3), and presents with overlapping limb-girdle muscle weakness, elevated creatine kinase (hyper- CKemia), RMD, and distal myopathy. We report a patient with a CAV3 mutation who presented with myalgia, exercise-induced muscle stiffness, hyperCKemia, and percussion-induced rapid muscle contraction and muscle mounding. A familial genetic study revealed the same mutation in two family members, with physical examinations showing that both of them had rippling muscles.

Rippling muscle disease (RMD) is caused by dominant mutations of the caveolin-3 gene (CAV3), and presents with overlapping limb-girdle muscle weakness, elevated creatine kinase (hyper- CKemia), RMD, and distal myopathy. We report a patient with a CAV3 mutation who presented with myalgia, exercise-induced muscle stiffness, hyperCKemia, and percussion-induced rapid muscle contraction and muscle mounding. A familial genetic study revealed the same mutation in two family members, with physical examinations showing that both of them had rippling muscles.

Rippling muscle disease (RMD) is caused by dominant mutations of the caveolin-3 gene (CAV3), and presents with overlapping limb-girdle muscle weakness, elevated creatine kinase (hyper- CKemia), RMD, and distal myopathy. We report a patient with a CAV3 mutation who presented with myalgia, exercise-induced muscle stiffness, hyperCKemia, and percussion-induced rapid muscle contraction and muscle mounding. A familial genetic study revealed the same mutation in two family members, with physical examinations showing that both of them had rippling muscles.

PURPOSE: The purpose of this study is to report clinical and radiographic results over a period of two 2 years after cementless total hip arthroplasty (THA) with fourth generation ceramic-on-ceramic articulation. MATERIALS AND METHODS: We studied 22 patients, 23 cases which were followed up for two years among 25 patients, 26 patients who underwent cementless THA with the fourth generation ceramic between April 2009 and December 2009. The average age of the patients was 55.9 years old(22 to 72 years old), and the average follow-up duration was 28 months(24 to 32 months). A clinical evaluation was performed using the Harris hip score (HHS), and radiologic evaluation was based on acetabular cups and osteolysis of the femoral stems, instability, distance, angle, and so on. RESULTS: HHS showed an increase, from 54 for before-surgical treatment, to 91 at the last follow-up. Inguinal pain was observed in one case, and femoral pain was observed in two cases. Stable fixation was achieved in all cases, and no instability, osteolysis, or movement of acetabular cups and femoral stems was observed. CONCLUSION: Clinical and radiological short-term results for use ofthe fourth generation ceramic-on-ceramic cementless THA have favorable so far. Further follow-up study should be performed for evaluation of the long-term results.
Arthroplasty ; Ceramics ; Follow-Up Studies ; Hip ; Humans ; Osteolysis ; Tacrine

Extramedullary relapse of childhood acute lymphoblastic leukemia (ALL) occurs most commonly in the central nervous system or in the testes. Isolated relapse on chest wall as a soft tissue mass is extremely rare in children with ALL. We experenced a 12-year-old girl who developed an isolated relapse on chest wall during the treatment for ALL. She had a pain and protruding mass on right anterior chest wall 6 months after the initial diagnosis of ALL. Imaging study revealed an 5 7 cm sized soft tissue mass on the right chest wall. Histopathologic examination revealed infiltrates composed of immature lymphoblasts with morphology identical with that of previous bone marrow aspiration. Studies on bone marrow and cerebrospinal fluid were negative for disease at this time. The patient was treated with 3,000 cGy of local irradiation in 10 fractions and systemic chemotherapy with ifosfamide and etoposide. The mass size decreased markedly, but she has been suffering from development of multiple mass in other site and recurrent pleural effusion.
Bone Marrow ; Central Nervous System ; Cerebrospinal Fluid ; Child ; Diagnosis ; Drug Therapy ; Etoposide ; Female ; Humans ; Ifosfamide ; Pleural Effusion ; Precursor Cell Lymphoblastic Leukemia-Lymphoma* ; Recurrence* ; Testis ; Thoracic Wall* ; Thorax*

We present a patient who complained of excessive daytime sleepiness (EDS), which started three years ago. She had no other medical, neurological, and psychiatric disorders. Nocturnal polysomnography did not indicate any sleep disorders, which might cause daytime EDS, such as obstructive sleep apnea. The following multiple sleep latency test was not compatible for narcolepsy. Her laboratory findings were remarkable for subclinical hypothyroidism, although free T4 and T3 were within reference rage, she had elevated thyroid stimulating hormone. After four weeks of levothyroxine treatment, her EDS resolved. The hypersomnolence, as a presenting symptom of subclinical hypothyroidism, was optimally treated after thyroid hormone replacement.
Disorders of Excessive Somnolence* ; Humans ; Hypothyroidism* ; Narcolepsy ; Polysomnography ; Rage ; Sleep Apnea, Obstructive ; Sleep Wake Disorders ; Thyroid Gland ; Thyrotropin ; Thyroxine*

BACKGROUND: The existing data indicate that obstructive sleep apnea syndrome contributes to the development of cardiovascular dysfunction such as systemic hypertension and cardiac arrhythmias, and the cardiovascular dysfunction has a major effect on high long-term mortality rate in obstructive sleep apnea syndrome patients. To a large extent the various studies have helped to clarify the pathophysiology of obstructive sleep apnea, but many basic questions still remain unanswered. METHOD: In this study, the influence of obstructive sleep apnea on systemic blood pressure, cardiac rhythm and urinary catecholamines concentration was evaluated. Over-night polysomnography, 24-hour ambulatory blood pressure and EGG monitoring, and measurement of urinary catecholamines, norepinephrine (UNE) and epinephrine (UEP), during waking and sleep were undertaken in obstructive sleep apnea syndrome patients group (OSAS, n=29) and control group (Gontrol, n=25). RESULTS: 1) In OSAS and Control, UNE and UEP concentrations during sleep were significantly lower than during waking (P<0.01). In UNE concentrations during sleep, OSAS showed higher levels compare to Control (P<0.05). 2) In OSAS, there was a increasing tendency of the number of non-dipper of nocturnal blood pressure compare to Control (P=0.089). 3) In both group (n=54), mean systolic blood pressure during waking and sleep showed significant correlation with polysomnographic data including apnea index (Al), apnea-hypopnea index (AHI), arterial oxygen saturation nadir (SaO2 nadir) and degree of oxygen desaturation (DOD). And UNE concentrations during sleep were correlated with Al, AHI, SaO2 nadir, DOD and mean diastolic blood pressure during sleep. 4) In OSAS with AI>20 (n=14), there was a significant difference of heart rates before, during and after apneic events (P<0.01), and these changes of heart rates were correlated with the duration of apnea (P<0.01). The difference of heart rates between apneic and postapneic period (deltaHR) was significantly correlated with the difference of arterial oxygen saturation between before and after apneic event (deltaSaO2) (r=0.223, P<0.001). 5) There was no significant difference in the incidence of cardiac arrhythmias between OSAS and Control. In Control, the incidence of ventricular ectopy during sleep was significantly lower than during waking. But in OSAS, there was no difference between during waking and sleep. CONCLUSION: These results suggested that recurrent hypoxia and arousals from sleep in patients with obstructive sleep apnea syndrome may increase sympathetic nervous system activity, and recurrent hypoxia and increased sympathetic nervous system activity could contribute to the development of cardiovascular dysfunction including the changes of systemic blood pressure and cardiac function.
Anoxia ; Apnea ; Arousal ; Arrhythmias, Cardiac ; Blood Pressure* ; Catecholamines* ; Epinephrine ; Heart Rate ; Humans ; Hypertension ; Incidence ; Mortality ; Norepinephrine ; Ovum ; Oxygen ; Polysomnography ; Sleep Apnea, Obstructive* ; Sympathetic Nervous System ; United Nations