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M My yc co ob ba ac ct te er ri iu um m a av vi iu um m--i in nt tr ra ac ce el ll lu ul la ar re e p pl le eu ur ri it ti is s w wi it th h m ma as ss si iv ve e p pl le eu ur ra al l e ef ff fu us si io on n Although the clinical features of atypical mycobacterial infection (AMI) resemble those of tuberculosis, pleural effusion is rare in cases of AMI [1,2]. We report a case of Mycobacterium avium-intracellulare complex (MAC) pleuritis with massive pleural effusion. This has never been reported in non-immunocompromised patients. Case reportThe patient was a 35-year-old Japanese businessman. He was admitted to Keio University Hospital because of massive pleural effusion in the left thorax. Three months before admission he experienced general malaise, low grade fever, and discomfort in the left chest. One month before admission he noticed dull pain in the left lower chest.The patient was slightly ill-nourished. His temperature was 38.6°C, blood pressure was 120/80 mmHg, and the pulse was regular, 84 beats·min -1 . He breathed regularly, 16 breaths·min -1 , without difficulty. Respiratory sounds were remarkably diminished on the left side. On chest percussion, there was dullness on the left side below the frontal second intercostal space. No symptoms or signs suggesting immunodeficiency were noted.The erythrocyte sedimentation rate was 25 mm·h -1 . C reactive protein (CRP) was strongly positive. White blood cell count was 4.8×10 9 ·L -1 (4,800·cells·mm -3 ). Fibrinogen was increased, 477 mg·dL -1 . Total protein was 7.0 g·dL -1 , with decreased albumin (55%) and increased γ-globulin (22%) fractions. Human immunodeficiency virus (HIV) antibody was negative. A purified protein derivative (PPD) skin test was positive. Repeated microbiological examinations of sputum were negative.On chest roentgenogram, massive pleural effusion was observed in the left thorax ( fig. 1). The effusion was yellowish clear with specific gravity 1.021. Cytological examination of the effusion did not show malignant cells. Fig. 1. -Posteroanterior chest roentgenogram at the time of admission. There was massive pleural effusion in the left thorax. Apparent intrapulmonary lesion was not recognized. CASE STUDY

To elucidate the role of Ureaplasma urealyticum as a causative organism in chronic prostatitis we investigated its incidence in the urogenital tract in 131 chronic prostatitis patients and 120 prostatodynia patients; the presence of common bacteria or Chlamydia trachomatis was also recorded. According to the 4-glass localisation test, U. urealyticum (> or = 10(3) ccu/ml) was isolated from the prostates of 16 prostatitis patients and 2 prostatodynia patients; 5 of these prostatitis patients (but neither of the prostatodynia patients) had other bacteria in specimens after prostatic massage. Thus U. urealyticum was the sole organism isolated from the prostates of 11 prostatitis and 2 prostatodynia patients, which suggests that it is an aetiological agent in some cases of chronic non-bacterial prostatitis.

The injection of B16F10 melanoma cells with recombinant human tumor necrosis factor alpha (TNF-alpha) into the tail vein of C57BL/6 mice resulted in 2- to 25-fold more metastatic foci in the lungs than the injection of tumor cells alone. Clearly, TNF-alpha significantly enhanced experimental tumor metastasis. Furthermore, it enhanced the metastasis of Lewis lung carcinoma cells. In contrast, a mutein of TNF-alpha, designated as F4236, having the cell-adhesive sequence (Tyr-Ile-Gly-Ser-Arg) at the N-terminus of the TNF molecule did not enhance metastasis, but rather exhibited similar antitumor activity to wild-type TNF-alpha in fibrosarcoma-bearing mice.

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