Pilot Analysis of Asbestos-induced Diffuse Pleural Thickening with Respiratory Compromise

We investigated the clinical features of asbestos-induced diffuse pleural thickening (DPT) with severe respiratory compromise. We conducted a retrospective study of consecutive subjects with asbestos-induced DPT. Medical data such as initial symptoms, radiological findings, respiratory function test results, and clinical course were collected and analyzed. There were 24 patients between 2003 and 2012. All were men, and the median age at the development of DPT was 74 years. The top occupational category associated with asbestos exposure was dockyard workers. The median duration of asbestos exposure was 35.0 years, and the median latency from first exposure to the onset of DPT was 49.0 years. There were no significant differences in respiratory function test results between the higher and lower Brinkman index groups or between unilateral and bilateral DPT. Thirteen patients had a history of benign asbestos pleural effusion (BAPE), and the median duration from pleural fluid accumulation to DPT with severe respiratory compromise was 28.4 months. DPT with severe respiratory compromise can develop after a long latency following occupational asbestos exposure and a history of BAPE

Early diagnosis of acute renal allograft rejection: efficacy of macrophage migration inhibition test as an immunological diagnosis

1. Three cases of acute rejection were detected by macrophage migration inhibition tests (MIT) conducted directly on seven patients who had received renal allografts. The macrophage migration inhibitory factor (MIF) activity was positive in all cases 1-2 days before the appearance of acute rejection. 2. After the administration of a high dose of Solu-Medrol (1g/day for 3 days) to suppress the acute rejection, MIF activity recovered to its normal level 3 days later. These findings seem to indicate that MIT yields immunologically useful criteria for the early detection of an acute rejection.</p

Inhibition of neutrophil elastase attenuates airway hyperresponsiveness and inflammation in a mouse model of secondary allergen challenge: neutrophil elastase inhibition attenuates allergic airway responses

Background: Chronic asthma is often associated with neutrophilic infiltration in the airways. Neutrophils contain elastase, a potent secretagogue in the airways, nonetheless the role for neutrophil elastase as well as neutrophilic inflammation in allergen-induced airway responses is not well defined. In this study, we have investigated the impact of neutrophil elastase inhibition on the development of allergic airway inflammation and airway hyperresponsiveness (AHR) in previously sensitized and challenged mice. Methods: BALB/c mice were sensitized and challenged (primary) with ovalbumin (OVA). Six weeks later, a single OVA aerosol (secondary challenge) was delivered and airway inflammation and airway responses were monitored 6 and 48 hrs later. An inhibitor of neutrophil elastase was administered prior to secondary challenge. Results: Mice developed a two-phase airway inflammatory response after secondary allergen challenge, one neutrophilic at 6 hr and the other eosinophilic, at 48 hr. PAR-2 expression in the lung tissues was enhanced following secondary challenge, and that PAR-2 intracellular expression on peribronchial lymph node (PBLN) T cells was also increased following allergen challenge of sensitized mice. Inhibition of neutrophil elastase significantly attenuated AHR, goblet cell metaplasia, and inflammatory cell accumulation in the airways following secondary OVA challenge. Levels of IL-4, IL-5 and IL-13, and eotaxin in BAL fluid 6 hr after secondary allergen challenge were significantly suppressed by the treatment. At 48 hr, treatment with the neutrophil elastase inhibitor significantly reduced the levels of IL-13 and TGF-beta 1 in the BAL fluid. In parallel, in vitro IL-13 production was significantly inhibited in spleen cells from sensitized mice. Conclusion: These data indicate that neutrophil elastase plays an important role in the development of allergic airway inflammation and hyperresponsiveness, and would suggest that the neutrophil elastase inhibitor reduced AHR to inhaled methacholine indicating the potential for its use as a modulator of the immune/inflammatory response in both the neutrophil-and eosinophil-dominant phases of the response to secondary allergen challenge

Automated parallel test form assembly based on discrete algorithms

電気通信大学博士（工学）2024doctoral thesi

The Synergistic Antitumor Effect of Natural-Human TNF and Anticancer Drugs

In the present report, we compared and discussed synergistic antitumor effects of natural-human tumor necrosis factor (n-TNF) which was derived from human acute lymphoblastic leukemia BALL-I cells and conventional anticancer drugs by using Lewis lung carcinoma which was transplanted on BDF1 mice. n-TNF and anticancer drugs were administered daily for 10 days. n-TNF showed antitumor effects which were equivalent to or stronger than MMC (1 mg/kg/day, i.v.), 5FU (5 mg/kg/day, i.v.), Adriamycin (1 mg/kg/day, i.v.), Actinomycin D (0.05 mg/kg/day, i.v.), Cyclophosphamide (10 mg/kg/day, i.v.) and OK-432 (0.5 KE/mouse/day, s.c.). And synergistic antitumor effects were observed when n-TNF was administered with anticancer drugs, and the strong enforcement was obtained especially when it was combined with 5FU

Antitumor Effects of Natural-Human TNF on BDFI Mice Bearing Lewis Lung Carcinoma

Natural-human tumor necrosis factor (n-TNF) was obtained by isolating and refining lymphokines which were extracted from human acute lymphoblastic leukemia BALL-I cells. Antitumor effects of this n-TNF were studied by using Lewis lung carcinoma (3LL) which was transplanted on BDFI mice. n-TNF showed inhibitory effects of the proliferation of metastatic tumors dose-dependently through i.v. injection daily for 10 days. And the study of the dose schedule of the administration and the route of the administration showed that routes of i.v., i.m. and i.t. injections were effective respectively through daily administration. Histological study showed effects which were ranked Grade Ilb (and partially III) of Shimosato and Ohboshi's histological criteria

Synergistic Antitumor Effects of Natural Human Tumor Necrosis Factor and Mouse Interferon Beta and Gamma

Referring to synergistic antitumor effects of natural human tumor necrosis factor (n-TNF) derived from human acute lymphoblastic leukemia BALL-I cell as well as mouse interferon beta (mIFNbeta) and mouse interferon gamma (mIFNgamma), a series of the study was made using Lewis lung carcinoma grafted on BDF1 mice. With a combination dose of n-TNF (1 x 10^2 U/kg/day) and mIFNbeta (1 x 10^2 IU/kg/day) as well as that of n-TNF (1 x 10^2 U/kg/day) and mIFNgamma (1 x 10^2 IU/kg/day), a significant enhancement of antitumor effect was observed. Furthermore, with a triple combination dose of n-TNF (1 x 10^2 U/kg/day), mIFNbeta (I x 10^2 IU/kg/day) and mIFNgamma (I x 10^2 IU/kg/day), too, a strong synergistic effect was noted. The concentration of n-TNF required for concomitant use with mIFNbeta and mIFNgamma was 1 over 5 x 10^3 of that required for single dose of n-TNF, to obtain the same level of effect