Low-dose radiotherapy (LDRT) has been explored as a treatment option for various inflammatory diseases; however, its application in the context of rheumatoid arthritis (RA) is lacking. This study aimed to elucidate the mechanism underlying LDRT-based treatment for RA and standardize it. LDRT reduced the total numbers of immune cells, but increased the apoptotic CD4+ T and B220+ B cells, in the draining lymph nodes of collagen induced arthritis and K/BxN models. In addition, it significantly reduced the severity of various pathological manifestations, including bone destruction, cartilage erosion, and swelling of hind limb ankle. Post-LDRT, the proportion of apoptotic CD4+ T and CD19 + B cells increased significantly in the PBMCs derived from human patients with RA. LDRT showed a similar effect in fibroblast-like synoviocytes as well. In conclusion, we report that LDRT induces apoptosis in immune cells and fibro-blast-like synoviocytes, contributing to attenuation of arthritis.

Low-dose radiotherapy (LDRT) has been explored as a treatment option for various inflammatory diseases; however, its application in the context of rheumatoid arthritis (RA) is lacking. This study aimed to elucidate the mechanism underlying LDRT-based treatment for RA and standardize it. LDRT reduced the total numbers of immune cells, but increased the apoptotic CD4+ T and B220+ B cells, in the draining lymph nodes of collagen induced arthritis and K/BxN models. In addition, it significantly reduced the severity of various pathological manifestations, including bone destruction, cartilage erosion, and swelling of hind limb ankle. Post-LDRT, the proportion of apoptotic CD4+ T and CD19 + B cells increased significantly in the PBMCs derived from human patients with RA. LDRT showed a similar effect in fibroblast-like synoviocytes as well. In conclusion, we report that LDRT induces apoptosis in immune cells and fibro-blast-like synoviocytes, contributing to attenuation of arthritis.

Low-dose radiotherapy (LDRT) has been explored as a treatment option for various inflammatory diseases; however, its application in the context of rheumatoid arthritis (RA) is lacking. This study aimed to elucidate the mechanism underlying LDRT-based treatment for RA and standardize it. LDRT reduced the total numbers of immune cells, but increased the apoptotic CD4+ T and B220+ B cells, in the draining lymph nodes of collagen induced arthritis and K/BxN models. In addition, it significantly reduced the severity of various pathological manifestations, including bone destruction, cartilage erosion, and swelling of hind limb ankle. Post-LDRT, the proportion of apoptotic CD4+ T and CD19 + B cells increased significantly in the PBMCs derived from human patients with RA. LDRT showed a similar effect in fibroblast-like synoviocytes as well. In conclusion, we report that LDRT induces apoptosis in immune cells and fibro-blast-like synoviocytes, contributing to attenuation of arthritis.

To investigate the adverse effects of clozapine on cardiovascular ion channels, we examined the inhibitory effect of clozapine on voltage-dependent K+(Kv) channels in rabbit coronary arterial smooth muscle cells. Clozapine-induced inhibition of Kv channels occurred in a concentration-dependent manner with an halfinhibitory concentration value of 7.84 ± 4.86 µM and a Hill coefficient of 0.47 ± 0.06.Clozapine did not shift the steady-state activation or inactivation curves, suggesting that it inhibited Kv channels regardless of gating properties. Application of train pulses (1 and 2 Hz) progressively augmented the clozapine-induced inhibition of Kv channels in the presence of the drug. Furthermore, the recovery time constant from inactivation was increased in the presence of clozapine, suggesting that clozapineinduced inhibition of Kv channels is use (state)-dependent. Pretreatment of a Kv1.5 subtype inhibitor decreased the Kv current amplitudes, but additional application of clozapine did not further inhibit the Kv current. Pretreatment with Kv2.1 or Kv7 subtype inhibitors partially blocked the inhibitory effect of clozapine. Based on these results, we conclude that clozapine inhibits arterial Kv channels in a concentrationand use (state)-dependent manner. Kv1.5 is the major subtype involved in clozapineinduced inhibition of Kv channels, and Kv2.1 and Kv7 subtypes are partially involved.

Objective: This study analyzed the relationship between the timing of vasopressin treatment and the prognosis ofpatients with septic shock. Methods: Patients who were admitted to a university hospital for one year using vasopressin were studied retrospectively.All records were collected through the medical records; several factors were studied to determine the prognosis of thepatient. The 24-hour, 48-hour mortality, and hospital mortality were examined. The difference in the timing of vasopressinadministration between death and survival patients was analyzed to determine the effect of the vasopressor on the survivalrate using the receiver operating characteristic (ROC) curve. Results: The general characteristics of the patients in the hospital and survivors were similar. Vasopressin infusion wasfaster in the surviving patients than in the death patients, but there was no significant difference (survival, 187.0 minutes;interquartile range [IQR], 95.0-548.0 minutes vs. death, 285.5 minutes; IQR, 92.7-739.2). To determine the effect of vasopressorinjection on the survival rate, the ROC curve was drawn, and the area under curve was not affected significantlyby norepinephrine (NE) 0.416 and vasopressin 0.529. In addition, the duration of the ventilator application was found toincrease with increasing NE injection period in survivors (period of application of ventilator: NE injection time, r=0.460,P=0.048; vasopressin, r=0.369, P=0.120). Conclusion The prognosis was similar regardless of the timing of vasopressin in patients with septic shock.

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OBJECTIVE: The current guidelines for the treatment of ST-segment elevation myocardial infarction (STEMI) recommends early reperfusion with a door to balloon (DTB) time of 90 minutes or less in patients undergoing primary percutaneous coronary intervention (PPCI). Therefore, the focus of most studies has been the DTB time. On the other hand, the ischemic time is related to the symptom to balloon (STB) time rather than the DTB time. This study examined the clinical effects of the STB time as well as the social and clinical factors affecting the STB time in STEMI patients. METHODS: This study analyzed 286 patients diagnosed with STEMI from December 2008 to December 2016. The STB time (≤4 hours and>4 hours, ≤12 hours, and >12 hours) in the groups was compared. The mortality and ejection fraction were investigated. In addition, the characteristics of patients and socioeconomic factors affecting STB were analyzed. RESULTS: The SBT time is inversely associated with the ejection fraction (R=−0.126, P=0.033), and the ejection fraction of the ≤12 hours group was higher than that of the >12 hours group (54% vs. 50%, P=0.047). On the other hand, there was no significant difference in mortality between the two groups (3.26% vs. 4.84%, P=0.506). In multivariate analysis, the variable related to SBT was only typical chest pain (adjusted odd ratio, 1.931; 95% confidential interval, 1.014-3.792; P=0.045). CONCLUSION The results of the study support the prognostic value of SBT in STEMI undergoing PPCI. Therefore, efforts should be made to shorten the STB time.

BACKGROUND: Mesenchymal stromal cells (MSCs) are multipotent stem cells that can differentiate into several cell types. In addition, many studies have shown that MSCs modulate the immune response. However, little information is currently available regarding the maintenance of immunomodulatory characteristics of MSCs through passages. Therefore, we investigated and compared cytokine and gene expression levels from adipose (AD) and bone marrow (BM)-derived MSCs relevant to immune modulation from early to late passages. METHODS: MSC immunophenotype, growth characteristics, cytokine expressions, and gene expressions were analyzed. RESULTS: AD-MSCs and BM-MSCs had similar cell morphologies and surface marker expressions from passage 4 to passage 10. Cytokines secreted by AD-MSCs and BM-MSCs were similar from early to late passages. AD-MSCs and BM-MSCs showed similar immunomodulatory properties in terms of cytokine secretion levels. However, the gene expressions of tumor necrosis factor-stimulated gene (TSG)-6 and human leukocyte antigen (HLA)-G were decreased and gene expressions of galectin-1 and -3 were increased in both AD- and BM-MSCs with repeated passages. CONCLUSION: Our study showed that the immunophenotype and expression of immunomodulation-related cytokines of AD-MSCs and BM-MSCs immunomodulation through the passages were not significantly different, even though the gene expressions of both MSCs were different.
Bone Marrow ; Cytokines* ; Galectin 1 ; Gene Expression ; Humans* ; Immunomodulation ; Leukocytes ; Mesenchymal Stromal Cells* ; Multipotent Stem Cells ; Necrosis