Search

Most patients with liver cysts are asymptomatic and require no treatment. In this patient with symptoms and restrictive ventilatory impairment, percutaneous needle aspiration with injection of minocycline hydrochloride was effective.

The pulmonary toxicity of multi-wall carbon nanotubes (MWCNT) were examined by intratracheal instillation. We prepared a well-dispersed MWCNT dispersion including MWCNTs of 3.71 µm geometric average length. The fiber length of most of the MWCNTs in the dispersion was 10 µm or less. The MWCNT dispersion was administered to rat lung by single intratracheal instillation at doses of 0.2 mg and 0.6 mg/rat. Bronchoalveolar lavage fluid (BALF) was collected at 3 days, 1 week, 1 month, 3 months, and 6 months after instillation. The influences of the longer MWCNTs on the induction of inflammation and oxidative stress were examined by the number of neutrophils, cytokine induced neutrophil chemoattractant-1 (CINC-1), CINC-2, CINC-3 and HO-1 in the BALF. Additionally, ho-1 gene expression in the lung was examined. The intratracheal instillation of MWCNT induced transient inflammation dose dependently in the lung. The number of neutrophils was highest at 3 days after instillation and then decreased. However, the neutrophils in the MWCNT administered animals tended to be higher than in the control group until 3 months after instillation. The CINC-1 and CINC-2 concentrations in the BALF increased at 1 month after instillation. There were no significant differences in CINC-3 and HO-1 between the MWCNT administered animals and the control animals. These results revealed that the MWCNTs of 1–10 µm in length induced persistent inflammation in rat lung. There were no remarkable differences between the MWCNTs in the present study and previously reported, shorter MWCNTs prepared from “the same” raw MWCNT material.

We newly developed a histamine-triggered electrochemical switching aptazyme by utilizing a hemin molecule and a hemin-targeting aptamer (AptDNA) complex (hemin/AptDNA). We spectroscopically and electrochemically found that the electroactivity of hemin/AptDNA is suppressed or restored in the presence or absence of histamine, respectively. The observed hyperchromicity of the Soret band of hemin at 404 nm showed the interaction of hemin with the G-quadruplex structure of AptDNA. The absorbance at 418 nm for the hemin/AptDNA solution increased in the presence of dihydrogen peroxide (H2O2) and 2,2'-azinobis(3- ethylbenzothiozoline)-6-sulfonic acid (ABTS), where the colorless ABTS2- was oxidized to the green ABTS•-. These results led us to conclude that hemin/AptDNA worked as a redox aptazyme for the redox reaction of H2O2 and ABTS. The presence of histamine inhibited this reaction. This was also electrochemically ascertained. Electrochemical investigation demonstrated that the reduction reaction of H2O2 was facilitated by hemin/AptDNA compared with the case of AptDNA and that the reaction was restrained by the addition of histamine to the solution. These spectroscopic and electrochemical investigations revealed that the electroactivity of hemin/AptDNA is switched on/off in the presence/absence of histamine as a redox aptazyme, respectively. [ABSTRACT FROM AUTHOR]

We fabricated a novel sensor array chip that enables simple, rapid, and sequence-specific DNA detection without any process to label DNAs or any external electrochemical indicators. We found the conditions for the cleaning of electrode surfaces and the preparation of DNA sensor array chips. A long-term storage for several weeks inactivated photolithographically fabricated 384-ch microelectrode array chips before surface modification. We revealed that the treatments with O2 plasma and acidic solutions reactivated the long-term stored chips, and demonstrated that the DNA sensor arrays prepared from the reactivated chips detected DNAs sequence-specifically, similarly to freshly fabricated sensors. We found that feasible DNA sensor array chips can be prepared from the electrode array chips stored even for a long period, as long as the stored chips are treated before use with O2 plasma and acid solutions under optimized conditions. [ABSTRACT FROM AUTHOR]

Objective: It is not known whether autonomic neuropathy is a feature of Sjögren's syndrome (SS) or whether it is related to circulating antiganglionic acetylcholine receptor (gAChR) antibodies. The goal of the present study was to investigate the autonomic dysfunction in patients with SS and the associations between autonomic dysfunction, anti-gAChR antibodies, and clinical features of SS. Methods: (1) The first observational study tested for the presence of gAChR antibodies in the serum samples from 39 patients with SS (absent information regarding autonomic symptoms) and healthy volunteers. (2) In the second study, serological and clinical data from 10 Japanese patients diagnosed with SS were reviewed. These patients showed autonomic dysfunction, and luciferase immunoprecipitation systems (LIPS) test was conducted to detect anti-a3 and anti-b4 gAChR antibodies. (3) In the final analysis, we combined the data of seropositive SS patients with autonomic symptom from the first study with all of the patients from the second study, and analyzed the clinical features. Results: (1) The LIPS assay revealed that anti-gAChRa3 and anti-gAChRb4 antibodies were detected in the sera from patients with SS (23.1%, 9/39). Five of nine SS patients had autonomic symptoms. (2) Anti-a3 and anti-b4 gAChR antibodies were also detected in 80.0% (8/10) of patients with SS with autonomic symptoms. Six of the ten patients were diagnosed as having SS after neurological symptoms developed. These seropositive patients had predominant and severe autonomic symptoms and were diagnosed with autonomic neuropathy. (3) Thirteen of fifteen SS patients with autonomic symptoms (86.7%) were seropositive for anti-gAChR antibodies, and we confirmed sicca complex, orthostatic hypotension, upper and lower gastrointestinal (GI) symptoms, and bladder dysfunction at high rates. Conclusion: The present results suggest the possibility of anti-gAChR antibodies aiding the diagnostics of SS with autonomic dysfunction. [ABSTRACT FROM AUTHOR]