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991.
Carmustine wafers improve the survival of patients with high-grade gliomas, but several adverse events have been reported. A 42-year-old man with left insulo-opercular anaplastic astrocytoma developed a massive intra-cavital hematoma with subarachnoid hemorrhage caused by ruptured pseudoaneurysm of the left middle cerebral artery (MCA) adjacent to the site of carmustine wafers implanted 6 months previously. Intraoperative finding demonstrated a dissection of the insular portion of the MCA, and pathological examination identified the resected pseudoaneurysm. This case demonstrates that carmustine wafers can cause changes in local vessels. Therefore, implantation of carmustine wafers near to important vessels passing close to the resection cavity should be considered with great caution.  相似文献   
992.
OBJECTIVE: The calcineurin pathway has been involved in the development of cardiac hypertrophy, yet it remains unknown whether calcineurin activity can be regulated in myocardium independently from hypertrophy and cardiac load. METHODS: To test that hypothesis, we measured calcineurin activity in a rat model of infrarenal aortic constriction (IR), which affects neurohormonal pathways without increasing cardiac afterload. RESULTS: In this model, there was no change in arterial pressure over the 4-week experimental period, and the left ventricle/body weight ratio did not increase. At 2 weeks after IR, calcineurin activity was increased 1.8-fold (P<0.05) and remained elevated at 4 weeks (1.7-fold, P<0.05). Similarly, the cardiac activity of calcium calmodulin kinase II (CaMKII) was increased significantly after IR, which confirms a regulation of Ca(2+)-dependent enzymes in this model. In cardiac myocytes, the increased activity of calcineurin was accompanied by a significant decrease in L-type Ca(2+) channel activity (I(Ca)) and contraction velocity (-dL/dt). Cardiac denervation prevented the activation of calcineurin after IR, which demonstrates that a neurohormonal mechanism is responsible for the changes in enzymatic activity. In addition, cardiac denervation suppressed the effects of IR on I(Ca) and -dL/dt, which shows that calcineurin activation is related to altered contractility. However, action potential duration, the densities of inward rectifier K(+) currents (I(K1)), and outward K(+) currents (I(to) and I(K)) were not altered in IR myocytes. CONCLUSIONS: Calcineurin can be activated in the heart through a neural stimulus, which induces alterations in Ca(2+) currents and contractility. These effects occur in the absence of myocyte hypertrophy, electrophysiological changes in action potential, and K(+) channel currents.  相似文献   
993.
A 27-year-old male visited the outpatient clinic of our hospital with the chief complaints of fever, right chest pain and shortness of breath. He was admitted to our hospital for detailed examination of the right hydrothorax. The pleural effusion obtained by thoracocentesis was exudative and negative for Mycobacterium tuberculosis. Since the titer of adenosine deaminase in the pleural effusion was abnormally high, antitubercular therapy was started under suspicion of tuberculous pleuritis. Thereafter, the patient's subjective symptoms and blood parameters improved. Necrotic tissues were obtained by pleural biopsy using the Cope needle. In order to make a definitive diagnosis, pleural biopsy was performed thoracoscopically. White tubercular lesions with a smooth surface were sparsely distributed on the pleura. Histopathologically, these lesions were characterized by central areas of caseous necrosis surrounded by epithelial cells and Langhans' giant cells. Therefore, they were considered to be granulomatous lesions. The patient was given a diagnosis of idiopathic tuberculous pleuritis, and was treated with four antitubercular drugs in combination. His clinical signs subsided, and he was discharged. This case indicates that the examination of the inside of the pleural cavity with a flexible bronchoscope, instead of thoracoscope, under local anesthesia is useful to diagnose patients having tuberculous pleuritis.  相似文献   
994.
To assist in making prognoses for patients with interstitial pneumonia (IP) who were treated with cyclosporin A (CsA), we conducted a review of forty-nine patients (32 men and 17 women with a mean age of 62 yrs) with progressive IP during the period from 1997 through 2001. All patients were steroid-resistant or acutely exacerbated cases. They received a low dosage of CsA (100-130 mg/day) combined with corticosteroids. Before and after the CsA therapy, blood gas analysis and HRCT scans were evaluated. Twenty-five patients underwent video-assisted thoracoscopic surgery (VATS) or autopsy for a histopathological evaluation. Among the 49 patients with IP, the documented underlying systemic diseases were of unknown etiology (IPF or IIP) in 26 and were collagen vascular diseases (CVD) in 23. The chest CT pattern and underlying systemic diseases of IP were classified as a usual interstitial pneumonia (UIP) pattern/IPF in 16 cases, a non-UIP pattern/IIP in 10 cases, a UIP pattern/CVD in 7 cases, and a non-UIP pattern/CVD in 16 cases. The prognoses after CsA treatment were improved or unchanged in 27% of cases with a UIP pattern/IPF, 78% of cases with a non-UIP pattern/IIP, 71% of cases with a UIP pattern/CVD and 75% of cases with a non-UIP pattern/CVD; deteriorated in 73%, 22%, 29% and 25% of cases, respectively, with these patterns and underlying diseases. At present, four out of thirteen (31%) patients with acute exacerbation of UIP pattern/IPF have survived for four to twelve months (mean: 7.5 months). Four patients revealed re-exacerbation of IP after the dose of CsA was tapered. Among the 25 patients with IP, the histopathological patterns of IP were classified as usual interstitial pneumonia (UIP) in 10 cases, nonspecific interstitial pneumonia (NSIP) in 14 cases (group I, 2; group II, 5; group III, 7) and diffuse alveolar damage (DAD) in 1 case. The prognoses were improved or unchanged in all cases of NSIP group I, in 80% of cases with NSIP group II, in 29% of cases of NSIP group III and in 20% of cases of UIP; and deteriorated in the case of DAD, in 80% of cases of UIP, in 71% of cases of NSIP group III, and in 20% of cases of NSIP group II. It should be emphasized that CsA combined with corticosteroids may be effective for the treatment of steroid-resistant or acute exacerbation cases of IP. Further studies are required to determine long-term outcome with this treatment.  相似文献   
995.

Background

We have recently demonstrated that T cell-mediated nasal hyperresponsiveness (NHR) is a representative pathophysiological feature of allergic rhinitis (AR). Although several anti-allergic drugs are used for the treatment of AR, the efficacy of these drugs on T cell-mediated NHR have not been elucidated. In these studies we investigated the effects of dexamethasone (Dex), montelukast (Mk), and chlorpheniramine (Chl) on NHR in antigen-immunized and antigen-specific Th2 cell-transferred mice.

Methods

OVA-immunized BALB/c mice were treated with Dex, Mk, or Chl and challenged intranasally with OVA. We then assessed NHR, the number of inflammatory cells in the nasal lavage fluid (NALF), mRNA expression of Th2 cytokines in the nasal tissue, the population of CD3+CD4+ cells in the nasal lymphoid tissue (NALT), and antigen-specific serum IgE and IgG levels. Antigen-induced NHR and changes in antigen-specific T cells in the NALT were investigated in OVA-specific Th2 cell-transferred mice.

Results

Dex significantly suppressed antigen-induced NHR, inflammatory cell infiltration, and IL-4, IL-5, IL-6, and IL-13 expression in immunized mice. Chl was completely ineffective, and only IL-13 expression was suppressed by Mk. None of these drugs affected IgE and IgG production. Antigen-induced NHR and the increase in antigen-specific T cells in the NALT of Th2 cell-transferred mice were inhibited by Dex, but not by Mk or Chl.

Conclusions

Steroids are effective for the reduction of NHR in AR by suppressing the accumulation of inflammatory cells, especially antigen-specific T cells.  相似文献   
996.
997.
Summary The role of protein kinase C (PKC) system on CD3 expression on adult T-cell leukaemia (ATL) was examined. The down-regulation of CD3 on ATL cells is reportedly induced by CD3 down-regulating factor (CD3DF) contained in serum and culture supernatants of leukaemia cells from acute type ATL patients. After we cultured normal PBMC with a PKC inhibitor, H-7, CD3DF activity for PBMC was reduced significantly. Culture with H-7 of HTLV-1 transformed T cells, ATL-2 cells whose CD3 expression had been decreased, led to enhancement of CD3 expression in a time-dependent manner. These findings suggest that CD3DF may play an important role as a PKC system activator, resulting in CD3 down-regulation.  相似文献   
998.
999.
We retrospectively studied more than 1000 patients with type 2 diabetes attending 36 Japanese clinics to investigate the efficacy and safety of adding sitagliptin to various insulin regimens. We found that the treatment with add-on sitagliptin for 6-months was effective, irrespective of the type or dose of concomitant insulin.  相似文献   
1000.
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