ABSTRACT Objective: To evaluate the efficacy of endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) in the diagnosis of thoracic sarcoidosis. Methods: A retrospective dataset of 35 patients who receive d EBUS-TBNA was analysed. These patients underwent EBUS-TBNA due to suspected sarcoidosis (radiographic stages I and II) with enlarged hilar or mediastinal lymph nodes (≥ 1.0 cm) revealed by computed tomography. When EBUS-TBNA was considered to be nondiagnostic, surgical biopsy and clinical and radiological follow-up was performed. Results: Twenty-eight of 35 (80%) patients had a final diagnosis of sarcoidosis. Among them, 25 (89.3%) were diagnosed by EBUS-TBNA. Conclusion: Endobronchial ultrasound-guided transbronchial needle aspiration is a safe and effective procedure for the diagnosis of stages I and II of thoracic sarcoidosis.

RESUMEN Objetivo: Evaluar la eficacia de la aspiración con aguja transbronquial guiada por ultrasonido endo-bronquial (EBUS-TBNA, por sus siglas en inglés) en el diagnóstico de la sarcoidosis torácica. Métodos: Se analizó un conjunto de datos retrospectivos de 35 pacientes que recibieron EBUS-TBNA. Estos pacientes experimentaron EBUS-TBNA debido a sospecha de sarcoidosis (etapas radiográficas I y II) con agrandamiento de los ganglios linfáticos o hiliares (≥ 1,0 cm) revelados por tomografía com-putarizada. Cuando se consideraba que el EBUS-TBNA no conducía a un diagnóstico, se realizaba una biopsia quirúrgica y un seguimiento clínico y radiológico. Resultados: Veintiocho de 35 (80%) pacientes tuvieron un diagnóstico final de sarcoidosis. De ellos, 25 (89.3%) fueron diagnosticados mediante EBUS-TBNA. Conclusión: La aspiración mediante aguja transbronquial guiada por ecografía endobronquial es un procedimiento seguro y eficaz para el diagnóstico de la sarcoidosis torácica en las etapas I y II.

B7 homolog 1 (B7-H1) is the most potent immunoinhibitory molecule in the B7 family. In this study, we examined the effects of tumor-associated B7-H1 on T-cell proliferation in lung cancer. The expression of B7-H1 in human adenocarcinoma A549 and mouse Lewis lung carcinoma (LLC) cells were examined by flow cytometry. To assess the in vitro effect of tumor-associated B7-H1 on T-cell proliferation, we isolated T cells from peripheral blood mononuclear cells (PBMCs) of healthy individuals, labeled them with carboxyfluorescein succinimidyl ester, and co-cultured them with A549 cells in the absence or presence of anti-B7-H1 antibody. For in vivo analysis, LLC cells were subcutaneously injected into mice treated or not with anti-B7-H1 antibody. T-cell proliferation in both in vitro and in vivo assays was analyzed by flow cytometry. In vitro, co-culturing T cells with A549 cells significantly inhibited the proliferation of the former compared with the proliferation of T cells alone (P<0.01), and the addition of B7-H1 blocking antibody dramatically reversed the inhibition of T-cell proliferation by A549 cells. Similarly, in mice bearing LLC-derived xenograft tumors, in vivo administration of anti-B7-H1 antibody significantly increased the total number of spleen and tumor T cells compared to levels in control mice that did not receive anti-B7-H1 antibody. Functionally, in vivo administration of anti-B7-H1 antibody markedly reduced tumor growth. Tumor-associated B7-H1 may facilitate immune evasion by inhibiting T-cell proliferation. Targeting of this mechanism offers a promising therapy for cancer immunotherapy.

β-arrestins are expressed proteins that were first described, and are well-known, as negative regulators of G protein-coupled receptor signaling. Penehyclidine hydrochloride (PHC) is a new anti-cholinergic drug that can inhibit biomembrane lipid peroxidation, and decrease cytokines and oxyradicals. However, to date, no reports on the effects of PHC on β-arrestin-1 in cells have been published. The aim of this study was to investigate the effect of PHC on β-arrestin-1 expression in lipopolysaccharide (LPS)-induced human pulmonary microvascular endothelial cells (HPMEC). Cultured HPMEC were pretreated with PHC, followed by LPS treatment. Muscarinic receptor mRNAs were assayed by real-time quantitative PCR. Cell viability was assayed by the methyl thiazolyl tetrazolium (MTT) conversion test. The dose and time effects of PHC on β-arrestin-1 expression in LPS-induced HPMEC were determined by Western blot analysis. Cell malondialdehyde (MDA) level and superoxide dismutase (SOD) activity were measured. It was found that the M3 receptor was the one most highly expressed, and was activated 5 min after LPS challenge. Furthermore, 2 μg/mL PHC significantly upregulated expression of β-arrestin-1 within 10 to 15 min. Compared with the control group, MDA levels in cells were remarkably increased and SOD activities were significantly decreased in LPS pretreated cells, while PHC markedly decreased MDA levels and increased SOD activities. We conclude that PHC attenuated ROS injury by upregulating β-arrestin-1 expression, thereby implicating a mechanism by which PHC may exert its protective effects against LPS-induced pulmonary microvascular endothelial cell injury.

A conventional approach for solving an economic production quantity (EPQ) model with multi-delivery policy and quality assurance is to use mathematical modeling for deriving the system cost function and to employ differential calculus for proving convexity of the cost function before determining the optimal operating policy. This paper presents a simplified solution procedure to reexamine a specific EPQ model [1] and demonstrates that both, the optimal manufacturing lot size and the long-run cost function can be derived without derivatives. The proposed approach may enable practitioners-with little knowledge of calculus-to understand such a real life vendor-buyer integrated system with ease.