Mycobacterium fortuitum pulmonary infection in a healthy 17-year-old man]

A 17-year-old man was admitted with a 5-month history of intermittent dyspnea on exertion, 10 kg weight loss, cough, sputa and fever. He did not smoke, had no apparent underlying pulmonary disease, and was not immunocompromised. Mycobacterium fortuitum was cultured from sputa at admission. Chest radiograph showed many thin-walled cavities and infiltration in the bilateral middle and upper fields. Chest CT detected multiple cystic lesions that were not revealed in conventional X-ray. It was suggested that the formation of the cystic lesions was one of the predisposing factor of Mycobacterium fortuitum pulmonary infection in this patient. The pneumonic change improved after six-month treatment using isoniazid, rifampicin and streptomycin, despite in vitro resistance of the bacilli to all of these drugs.     

Isolation of MRSA from inpatients, staff and environment in the hospital]

The state of MRSA contamination of inpatients, hospital staff, and the hospital environment was evaluated. Nasal, pharyngeal, and digital samples from 182 patients admitted in September and October, 1990, and 288 hospital staff members and sputum, urine, and feces of the inpatients were cultured. Environmental contamination was examined in samples collected from the air by air sampling and from the floor by the wiping method. The MIC and the coagulase type of the MRSA obtained were determined, and their relationships were evaluated. MRSA was detected in 9.5% of nasal samples, 7% of pharyngeal samples, 10% of sputum samples, 0% of urine samples, and 2.6% of fecal samples from the 182 inpatients. It was detected in 4% of nasal samples, 0.7% of pharyngeal samples, and 1% of digital samples from the 288 hospital staff members. From the environment, MRSA was detected from hospital rooms of the surgery and neurosurgery wards, the nursing room and corridors of the obstetrics and gynecology ward, and the recovery room of the urology ward. The coagulase type of the MRSA obtained was the primarily type II regardless or whether the samples were obtained from the subjects or the environment. Concerning the drug sensitivity, many MRSA strains were highly resistant to DMPPC and FOM, but the sensitivity to RFP was 0.1 microgram/ml or less in all strains except for one highly resistant strain (200 micrograms/ml or above).(ABSTRACT TRUNCATED AT 250 WORDS)     

Valpha24+ natural killer T-cell responses against T-acute lymphoblastic leukaemia cells: implications for immunotherapy

Human Valpha24+ natural killer T (NKT) cells correspond to mouse Valpha14+ NKT cells, both cell types use an invariant T-cell receptor-alpha chain and are activated by glycolipids in a CD1d-dependent manner. Mouse Valpha14+ NKT cells have been reported to have an antitumour effect in vivo. Human Valpha24+ NKT cells can kill a proportion of tumour cells in a CD1d-dependent manner in vitro. We report here that many human leukaemic T-cell lines express CD1d and can be directly killed by Valpha24+ NKT cells. This killing activity was enhanced in the presence of alpha-galactosylceramide (alpha-GalCer), a ligand of Valpha24+ NKT cells. Moreover, primary leukaemic T cells from five of eight T-cell acute lymphoblastic leukaemia (T-ALL) patients expressed CD1d and were good targets of Valpha24+ NKT cells. This cytotoxicity was increased in the presence of alpha-GalCer. Our results suggest that T-ALL is a good candidate for Valpha24+ NKT-cell-based immuno-cell therapy.     

Hemodynamic effects of inhaled nitric oxide using pulse delivery and continuous delivery systems in pulmonary hypertension

OBJECTIVE: Inhaled nitric oxide (NO) has been used for pulmonary vasodilation therapy in patients with pulmonary hypertension. Inhaled NO for awake and ambulatory patients, however, is unusual because it requires intubation or a tightly fitting facemask, and a large-scale delivery system for the safe management of toxic nitrogen oxides. We undertook this study to investigate the possibility of using inhaled NO therapy for awake and ambulatory patients with pulmonary hypertension. METHODS: Patients with pulmonary hypertension underwent cardiac catheterization and hemodynamic variables were measured at the baseline, after inhaled NO using our pulse delivery system, which involved a nasal cannula and a pulse device, and after inhaled NO using a continuous delivery system. PATIENTS OR MATERIALS: We studied seventeen patients with precapillary pulmonary hypertension (4 men and 13 women; age, 41+/-3, ranging from 19 to 61). RESULTS: Cardiac output was increased significantly by each system. Pulmonary vascular resistance was decreased significantly by each system. There was no significant change in mean pulmonary artery pressure, mean systemic artery pressure, or systemic vascular resistance. The concentrations of NO and nitrogen dioxide (NO2) in the expiratory gas using the pulse delivery system were 0.0 ppm as long as the pulse device was synchronized with the patient's respiratory cycle. CONCLUSION: Inhaled NO using our pulse delivery system changed the hemodynamic variables similarly to those when using the continuous delivery system. The concentrations of NO and NO2 in the expiratory gas using the pulse delivery system were within safe limits.     

Aortitis syndrome with fatal acute aortic regurgitation due to aortic dilatation and aortic valve perforation--a case report.

This is a case report of a fifteen-year-old female with aortitis syndrome complicated by acute fatal aortic regurgitation due to the aortic valve perforation, as well as to aortic dilatation, which was confirmed by the autopsy. Aortic valve perforation was first recognized as the important cause of acute aortic regurgitation in the aortitis syndrome in this report.     

Bronchoesophageal fistula in a patient with untreated malignant lymphoma

Bronchoesophageal fistulae associated with lymphomas are generally associated with chemo-radiotherapy. We report here an unusual case of lymphoma with a therapy-unrelated bronchoesophageal fistula. Previously, only 10 similar cases have been reported. A 70-year-old male was diagnosed as having gastric diffuse large B-cell lymphoma in May 1998. In January 1999, he noted a cough after eating and drinking. Because of the presence of a febrile temperature, productive cough and dyspnea, he was referred to our hospital and diagnosed as having aspiration pneumonia. Antibiotics did not improve his symptoms. When tracheal intubation was performed with bronchoscopy, a bronchoesophageal fistula was revealed. Malignant lymphoma cells were found around the fistula in the biopsy specimen. The patient died of pneumonia after treatment with airway stenting and chemotherapy. Induction of necrosis by chemotherapy or low blood flow with stenting and dopamine probably caused enlargement of the fistula.     

Voxel-based analysis of age and gender effects on striatal [123I] FP-CIT binding in healthy Japanese adults

Annals of Nuclear Medicine - Although previous studies have investigated age and gender effects on striatal subregional dopamine transporter (DaT) binding, these studies were mostly based on a...     

Opening of the adenosine triphosphate-sensitive potassium channel attenuates cardiac remodeling induced by long-term inhibition of nitric oxide synthesis: role of 70-kDa S6 kinase and extracellular signal-regulated kinase

OBJECTIVES: We examined whether the adenosine triphosphate (ATP)-sensitive potassium (K(ATP)) channel openers (KCOs) block myocardial hypertrophy and whether the 70-kDa S6 kinase (p70S6K) or extracellular signal-regulated kinase (ERK)-dependent pathway is involved. BACKGROUND: Long-term inhibition of nitric oxide (NO) synthesis induces cardiac hypertrophy independent of blood pressure, by increasing protein synthesis in vivo. The KCOs attenuate calcium overload and confer cardioprotection against ischemic stress, thereby preventing myocardial remodeling. METHODS: Twelve Wistar-Kyoto rat groups underwent eight weeks of the drug treatment in combination with the NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME), the inactive isomer D(omega)-nitro-L-arginine methyl ester, KCOs (nicorandil, 3 and 10 mg/kg per day, or JTV-506, 0.3 mg/kg per day), or the K(ATP) channel blocker glibenclamide. The L-NAME was also used with hydralazine, the p70S6K inhibitor rapamycin, or the mitogen-activated protein kinase inhibitor PD98059. Finally, the left ventricular weight (LVW) to body weight (BW) ratio was quantified, followed by histologic examination and kinase assay. RESULTS: The L-NAME increased blood pressure and LVW/BW, as compared with the control agent. The KCOs and hydralazine equally cancelled the increase in blood pressure, whereas only KCOs blocked the increase in LVW/BW and myocardial hypertrophy induced by L-NAME. The L-NAME group showed both p70S6K and ERK activation in the myocardium (2.3-fold and 2.0-fold increases, respectively), as compared with the control group, which was not reversed by hydralazine. Selective inhibition of either p70S6K or ERK blocked myocardial hypertrophy. The KCOs prevented the increase in activity only of p70S6K. Glibenclamide reversed the effect of nicorandil in the presence of L-NAME. CONCLUSIONS: The KCOs modulate p70S6K, not ERK, to attenuate myocardial hypertrophy induced by long-term inhibition of NO synthesis in vivo.     

Japanese encephalitis virus in mosquito salivary glands.

Culex tritaeniorhynchus and C. pipiens mosquitoes were infected with Japanese encephalitis virus either by intrathoracic injection or by membrane feeding. The virus maturation sites and the process of virus particle concentration in salivary gland cells were studied by electron microscopy. Occurrence of mature virions was primarily associated with intracytoplasmic viral matrices which were extraordinarily large and had a perinuclear location in C. pipiens mosquitoes. The other sign of virus replication was the proliferation of small spherical vesicles throughout the cytoplasm. It appeared that mature virions were entrapped in intracellular vacuoles and later released into the apical cavity of salivary gland cells through the fusion of these vacuoles with the apical plasma membrane. This process seemed to be associated with primary resynthesis of saliva in mosquitoes following blood feeding activity. Another type of shedding involved virus particles either singly or in mass being released directly through the apical plasma membrane. All of these events occurred only in cells of the lateral lobes of the salivary glands, which fact was confirmed by immunofluorescent staining of infected glands. The median lobe of mosquito salivary glands may have a minor or no role in the transmission of Japanese encephalitis virus.