Acute cerebral infarction: effect of JPEG compression on detection at CT

PURPOSE: To evaluate the effect of Joint Photographic Experts Group (JPEG) compression ratios of 10:1 and 20:1 on detection of acute cerebral infarction at computed tomography (CT). MATERIALS AND METHODS: CT images obtained in 25 patients with acute cerebral infarction and 25 patients with no lesions were compressed by means of a JPEG algorithm at ratios of 10:1 and 20:1. Normal and abnormal sections (on original and compressed images) were reviewed by using a color soft-copy computed monochrome cathode ray tube monitor. Five observers rated the presence or absence of a lesion with a 50-point scale (0, definitely absent; 25, equivocal; and 50, definitely present). Diagnostic accuracy was evaluated with receiver operating characteristic (ROC) curve analysis. Significant difference was defined as a P value less than.05 for the area tested with a two-tailed paired Student t test. RESULTS: At ROC analysis, no statistically significant difference was detected for all cases considered together (Az [area under the ROC curve] = 0.887 +/- 0.038 [mean +/- SD] on noncompressed images, Az = 0.897 +/- 0.038 on 10:1 compressed images, and Az = 0.842 +/- 0.073 on 20:1 compressed images; P >.05). CONCLUSION: JPEG compression at ratios of 10:1 and 20:1 was tolerated in the detection of acute cerebral infarction at CT.     

Pulmonary thromboendarterectomy for chronic pulmonary thromboembolism in protein C deficiency

Pulmonary thromboendarterectomy was performed on a patient with chronic pulmonary thromboembolism showing thrombophilia. The patient was a 56-year-old female with the above condition complicated by congenital protein C deficiency. She was admitted to our hospital with severe dyspnea accompanied by right ventricular failure. A pulmonary arteriogram showed occlusion and stenosis from lobar to segmental arteries Cardiac catheterization showed marked pulmonary hypertension. A lung perfusion scintigram revealed multiple defects in the right and left lungs. After the insertion of an inferior vena cava filter, she was operated on Following a median sternotomy, thromboendarterectomy of the bilateral pulmonary arteries was performed using deep hypothermia and intermittent circulatory arrest. Circulatory arrest was employed in three periods totaling up to 36 minutes. After surgery, she had improvements in pulmonary hypertension and pulmonary vascular resistance. She maintained improved lung functions, and remained in the New York Heart Association functional class I for more than two years and eight months after surgery.     

Surgical treatment for left ventricular false aneurysm caused by infective endocarditis; report of a case

A 24-year-old man who had left ventricular (LV) false aneurysm, which is caused by mitral valve infective endocarditis, underwent aneurysmectomy, direct closure of aneurysmal mouth and concomitant mitral valve replacement. Post-operative course was uneventful. It has been reported that the etiology of this false aneurysm was due to the vegetations' friction, which could have caused an initial endocardial ulceration that progressively expanded into the myocardium. The false aneurysmal wall should be completely removed in order to eliminate the possibility of recurrence of the infective endocarditis. We believe that the surgical treatment should be carried out as soon as possible after completion of diagnosis because the aneurysmal wall is usually quite thin and could rupture easily.     

Noradrenergic modulation of human pancreatic growth hormone-releasing factor (hpGHRF1-44)-induced growth hormone release in conscious male rabbits: involvement of endogenous somatostatin

To clarify the role of noradrenergic neurons in the regulation of GH secretion, the effects of iv administered noradrenergic antagonists were investigated in freely moving, conscious male rabbits. During a 6-h observation period (1030-1630 h), control rabbits manifested pulsatile GH secretion with surges between 1030-1200 and 1415-1630 h. Phenoxybenzamine, (POB), an alpha-adrenergic blocker (5 mg/kg, twice), abolished the episodic GH surges; propranolol, a beta-adrenergic blocker (2.5 mg/kg, twice), did not. The bolus injection (1 or 10 micrograms) of synthetic human pancreatic GH-releasing factor (hpGHRF) with 44 amino acid residues (hpGHRF1-44) resulted in significant rises in the plasma GH of control animals. The plasma GH responses to hpGHRF1-44 were significantly larger in propranolol-treated than control rabbits. In contrast, POB completely suppressed the hpGHRF1-44-induced GH release. The injection of antisomatostatin (SRIF) serum into POB-treated rabbits did not yield a disinhibition of the episodic GH surges but restored the plasma GH rises after hpGHRF1-44 injection. These results indicate that noradrenaline++ plays an important role in regulating GH secretion in the rabbit. We propose that alpha-noradrenergic blockade suppresses GH release not only by inhibiting the release of hypothalamic GHRF but also by stimulating the secretion of SRIF and that beta-noradrenergic blockade enhances GH release by inhibiting the release of SRIF from the hypothalamus.     

A case of pulmonary tuberculosis associated with adult respiratory distress syndrome during corticosteroid treatment of rheumatoid arthritis

We reported a case of 64 year-old female patient of pulmonary tuberculosis associated with ARDS during corticosteroid treatment of Rheumatoid Arthritis. On admission her chief complaints were fever, fatigue and dyspnea. A chest roentgenogram showed diffuse alveolar infiltration consistent with pulmonary edema. Arterial blood gas studies showed severe hypoxemia. We clinically diagnosed so-called ARDS. Smears of sputum for acid fast bacilli were negative, but transbronchial lung brushing by bronchofiberscope revealed many acid fast bacilli. Intensive therapy with anti-tuberculosis drugs (INH, RFP, SM), high dose corticosteroid (methylprednisolone) therapy and mechanical ventilation was started. During the following 2 weeks, the PaO2 rose gradually and the alveolar infiltration on the chest roentgenogram disappeared. The experience of this case to emphasized the importance of suspecting this condition because pulmonary tuberculosis is a potentially curable cause of ARDS and it should also be emphasized that the good treatment effect could be expected with combined use of high dose corticosteroid and mechanical ventilation.     

A case of Mycoplasma pneumoniae infection followed by Staphylococcus aureus bacteremia

A 19-year-old young man was admitted to our hospital complaining of fever and general fatigue. There were infiltrative shadows and pleural effusions in the both lung fields. Mycoplasma pneumoniae infection was diagnosed because of the elevation of mycoplasma antibody titers in the serum and pleural fluid. There was no recovery in clinical symptoms in spite of the administration of the EM (1200 mg) and CLDM (1200 mg) combination chemotherapy. Three week after admission, a cavity-like shadow appeared in the lt. middle lung field on the chest X-ray film, suprative arthritis and penicillin resistant S. aureus by blood culture test were found. Mycoplasma pneumoniae infection followed by S. aureus bacteremia was diagnosed. After the administration of antibiotics (CTT, FMOX) the clinical symptoms and laboratory findings improved 2 month after admission. Clinical and basic studies about the dual infection between M. pneumoniae and several bacteria were discussed.     

A case of inflammatory myofibroblastic tumor of the bladder

Here we report a rare case of inflammatory myofibroblastic tumor of the bladder. The patient was a 72-year-old man. We diagnosed this case preoperatively as urachal tumor from urine cytology, cystoscopy, and magnetic resonance imaging. We performed partial cystectomy. Histopathological examination revealed that the tumor was an inflammatory myofibroblastic tumor. To our knowledge, this is the 51st reported case of inflammatory myofibroblastic tumor of the bladder in Japan. He has been followed up for 13 months without any evidence of local recurrence.