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Purpose: Studies on the effect of diabetes mellitus (DM) on the radiologic findings of pulmonary tuberculosis (PTB) have reported inconsistent results. These findings may have been influenced by the glycemic control status of the patients studied. To our knowledge, no recent data have described the effect of the DM control status on CT findings in PTB in terms of medium-sized airway involvement that is visualized as bronchial erosion on CT. The aim of this present study was to determine whether the DM control status influenced radiological manifestations in patients with PTB, with an emphasis on bronchial erosive changes. Methods: We conducted a retrospective single-center study on patients who were newly diagnosed with PTB. A total of 426 consecutive patients with PTB who underwent CT scans at the time of diagnosis from 1 January 2017 to 31 March 2020 were included in this study. The included patients were categorized as having no DM (non-DM), controlled DM, or uncontrolled DM. The patient medical charts, microbiology study results, and pulmonary changes on the CT scans were analyzed. Results: Among 426 patients with PTB who underwent CT scans at the time of diagnosis, 91 were excluded either due to undetermined hemoglobin A1C (HbA1C) levels (n = 25) or concomitant pulmonary diseases (n = 66) that would make the analysis of the pulmonary changes on CT scans difficult. Finally, 335 patients were included in this study (224 men and 111 women; mean age, 59 years; range, 16–95 years). Among the 335 patients, 82 (24.5%) had DM and 52 of those (63.4%) had an uncontrolled status. The frequency of cavitation (43% vs. 23% vs. 79%, p < 0.001) and bronchial erosion (44% vs. 30% vs. 73%, p < 0.001) was significantly different between the three groups. The uncontrolled DM group showed a high frequency of cavitation and bronchial erosion compared to the non-DM (cavitation, p < 0.001 and bronchial erosion, p < 0.001) and controlled DM groups (p < 0.001 and p < 0.001). However, the frequency of cavitation and bronchial erosion in the controlled DM group was not different compared to the non-DM group. Conclusion: The glycemic status (HbA1C ≥ 7.0), not the presence of DM, influenced the radiologic manifestations of PTB, especially in terms of medium-sized bronchial involvement, appearing as bronchial erosive changes and the feeding bronchus sign on chest CT scans. This difference in the uncontrolled DM group was likely to contribute to the higher frequency of cavitation. [ABSTRACT FROM AUTHOR]

It has been stated that bronchial anthracofibrosis (BAF) has an important relationship with pulmonary tuberculosis (TB), and the coexistence of TB and BAF is high. The purpose of this study was to compare the differences in computed tomography (CT) characteristics of pulmonary TB according to the presence of underlying BAF. Total of 202 consecutive patients who were diagnosed with pulmonary TB and underwent bronchoscopy and CT in our institution were retrospectively reviewed. We classified the patients into two groups according to the presence of BAF and compared the clinicoradiological findings between the two groups (anthracofibrosis group vs. nonanthracofibrosis group). Elderly and female patients were significantly higher in anthracofibrosis group (mean age 79 ± 7 (64–94) vs. 56 ± 17 (16–95), p < 0.001; female 89% vs. 29%, p < 0.001). The frequency of internal low-density area or focal contour bulge within atelectasis (64% vs. 1%, p < 0.001), lower lobe predominance (43% vs. 9%, p < 0.001), endobronchial involvement (46% vs. 15%, p < 0.001), and lymphadenopathy (57% vs. 28%, p = 0.002) were significantly higher in anthracofibrosis group. In contrast, the anthracofibrosis group showed lower frequency of upper lobe predominance (32% vs. 81%, p < 0.001) and cavitation (14% vs. 51%, p = 0.001). In conclusion, being aware of these atypical manifestations of pulmonary TB in the presence of BAF will be of great help in early detection of TB. [ABSTRACT FROM AUTHOR]

Recently, bioactive glass nanoparticles (BGns) have been acknowledged for their ability to promote interactions with the periapical tissue and enhance tissue regeneration by releasing therapeutic ions. However, there have been no studies on calcium silicate sealers with bioactive glass nanoparticle (BGn) additives. In the present study, a premixed calcium silicate root canal sealer reinforced with BGn (pre-mixed-RCS@BGn) was developed and its physicochemical features and biological effects were analyzed. Three specimens were in the trial: 0%, 0.5%, and 1% bioactive glass nanoparticles (BGns) were gradually added to the premixed type of calcium silicate-based sealer (pre-mixed-RCS). To elucidate the surface properties, scanning electron microscopy, X-ray diffraction, and energy-dispersive spectroscopy were used and flowability, setting time, solubility, and radiopacity were analyzed to evaluate the physical properties. Chemical properties were investigated by water contact angle, pH change, and ion release measurements. The antibacterial effects of the bioactive set sealers were tested with Enterococcus faecalis and the viability of human bone marrow-derived mesenchymal stem cells (hMSCs) with this biomaterial was examined. In addition, osteogenic differentiation was highly stimulated, which was confirmed by ALP (Alkaline phosphatase) activity and the ARS (Alizarin red S) staining of hMSCs. The pre-mixed-RCS@BGn satisfied the ISO standards for root canal sealers and maintained antimicrobial activity. Moreover, pre-mixed-RCS@BGn with more BGns turned out to have less cytotoxicity than pre-mixed-RCS without BGns while promoting osteogenic differentiation, mainly due to calcium and silicon ion release. Our results suggest that BGns enhance the biological properties of this calcium silicate-based sealer and that the newly introduced pre-mixed-RCS@BGn has the capability to be applied in dental procedures as a root canal sealer. Further studies focusing more on the biocompatibility of pre-mixed-RCS@BGn should be performed to investigate in vivo systems, including pulp tissue. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) is a common autoimmune disease characterized by immune cell infiltration of the synovium, leading to the loss of cartilage, bone, and joint function. Although regulatory T (Treg) cells are thought to modulate the initiation and progression of RA, a consensus has yet to be reached regarding the function and composition of Treg cells in RA patients. To address these discrepancies, we analyzed not only the total Treg frequency but also that of Treg subpopulations in the peripheral blood of RA patients and healthy controls by flow cytometry. We found that the total Treg population was not significantly different between RA and control subjects. However, the effector Treg cell subgroup, defined as CD45RA−CD25hi, showed markedly decreased frequency in RA patients. In addition, the total Treg population from RA patients showed a significant decline in the expression of CD25. Both the naïve and effector Treg subgroups also showed marked reduction of CD25 expression in RA patients compared to controls. These data suggest that the decreased frequency of effector Treg cells and overall reduction of CD25 expression in Treg cells in the peripheral blood may be evidence of altered Treg homeostasis associated with RA pathogenesis. [ABSTRACT FROM AUTHOR]

Rheumatoid arthritis (RA) is a chronic autoimmune disease that is associated with systemic inflammation and results in the destruction of joints and cartilage. The pathogenesis of RA involves a complex inflammatory process resulting from the action of various proinflammatory cytokines and, therefore, many novel therapeutic agents to block cytokines or cytokine-mediated signaling have been developed. Here, we tested the preventive effects of a small peptide, AESIS-1, in a mouse model of collagen-induced arthritis (CIA) with the aim of identifying a novel safe and effective biological for treating RA. This novel peptide significantly suppressed the induction and development of CIA, resulting in the suppression of synovial inflammation and cartilage degradation in vivo. Moreover, AESIS-1 regulated JAK/STAT3-mediated gene expression in vitro. In particular, the gene with the most significant change in expression was suppressor of cytokine signaling 3 ( Socs3 ), which was enhanced 8-fold. Expression of the STAT3-specific inhibitor, Socs3 , was obviously enhanced dose-dependently by AESIS-1 at both the mRNA and protein levels, resulting in a significant reduction of STAT3 phosphorylation in splenocytes from severe CIA mice. This indicated that AESIS-1 regulated STAT3 activity by upregulation of SOCS3 expression. Furthermore, IL-17 expression and the frequency of Th17 cells were considerably decreased by AESIS-1 in vivo and in vitro. Collectively, our data suggest that the novel synthetic peptide AESIS-1 could be an effective therapeutic for treating RA via the downregulation of STAT3 signaling.

Melanoma, one of the aggressive cancers, is known to be resistant to chemotherapy. Because of its aggressive nature, effectively inducing apoptosis is necessary to treat melanoma. Erythroid differentiation regulator 1 (Erdr1) is known to be a stress-related survival factor exhibiting anti-cancer effects in several cancers. However, little is known about the functions and underlying mechanisms of Erdr1 so far. To demonstrate the effect of Erdr1 in melanoma apoptosis, recombinant murine Erdr1 was injected into mice implanted with B16F10 melanoma cells. In vivo tumor growth was significantly inhibited in mice injected with Erdr1 compared to the control. In addition, the tumor from Erdr1-injected mice showed an increased level of apoptosis. Accordingly, apoptosis-regulating factors including anti-apoptotic marker Bcl-2 and pro-apoptotic marker Bax in the tumor tissues were examined. As expected, the decreased level of Bcl-2 and increased level of Bax were detected in tumors within the mice injected with Erdr1. Based on the in vivo study, the role of Erdr1 in tumor apoptosis was further tested by incubating it with cells of the murine melanoma cell line B16F10. Erdr1-induced apoptosis in B16F10 cells was observed. Additionally, Erdr1 downregulated STAT3 activity, inhibiting apoptosis via regulation of the Bcl-2 family. Overall, data demonstrate that Erdr1 induced murine melanoma apoptosis through the regulation of Bcl-2 and Bax. These findings suggest that Erdr1 is a novel regulator of apoptosis in melanoma.