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Metabolic syndrome includes abdominal obesity, hyperlipidemia, diabetes, and hypertension. All, but hypertension, are obviously related to metabolism. However, hypertension might result from, at least in part, abdominal obesity, because adipose tissue produces bioactive mediators （adipocytokines）which increase blood pressure. In treatment of hypertension, we should concern insulin resistance, which is a major risk factor of cardiovascular events. Angiotensin converting enzyme inhibitor is known to improve insulin resistance, but results of angiotensin receptor blocker in animal studies are controversial. In clinical trial, there are many established data that ARBs prevent new onset of diabetes mellitus, suggesting that this agent also has a beneficial effect on glucose metabolism. Short acting Ca-antagonists, such as nifedipine, decrease insulin sensitivity, but long-acting Ca-antagonists increase it. βblockers decrease insulin sensitivity but those with α-blocking action improve insulin resistance. Recent study, ARB is more potent to reduce cardiovascular risk in those with obesity than in those with normal body weight, suggesting some drugs are more effective in metabolic syndrome. Thus, when we chose antihypertensive drugs in treating patients with metabolic syndrome, we have to choose proper drugs in addition to modify life-style

Bone microstructural characteristics or positional changes of condyle head affect short-term condyle head resorption after orthognathic surgery

Miyagawa K., Arikawa C., Hayashi K., et al. Bone microstructural characteristics or positional changes of condyle head affect short-term condyle head resorption after orthognathic surgery. Scientific Reports 14, 14269 (2024); https://doi.org/10.1038/s41598-024-65077-2.Condylar resorption occurs in some cases after orthognathic surgery, and the risk factors associated with postoperative condylar head resorption have been extensively described. Nevertheless, even in cases with a combination of risk factors, postoperative condylar resorption may not appear. This study analyzed the microstructure and three-dimensional positional change of the condylar bone via imaging in patients who have undergone bimaxillary orthognathic surgery to determine whether the microstructure or condylar position differs between patients with and without postoperative condylar resorption. Among asymptomatic patients who underwent bimaxillary surgery between April 2021 and March 2022 at our department, 17 patients were analyzed, limited to “female,” “skeletal Class II,” and “high-angle cases,” which are known risk factors for mandibular head resorption. Multidetector computed tomography was performed on these patients before and 6 months after surgery, and the bone microstructure of the condylar head and the three-dimensional positional changes of the condylar bone and the proximal bony fragments were compared with the presence of postoperative condyle resorption using the bone morphology software TRI/3D-BON. Patients with condylar bone abnormalities before surgery and those with high trabecular bone density can develop postoperative resorption if the condyle is misaligned by surgery

The phytoestrogen ginsensoside Re activates potassium channels of vascular smooth muscle cells through PI3K/Akt and nitric oxide pathways

In vascular smooth muscle cells, large-conductance Ca2+-activated K+ channels (KCa channels) play a pivotal role in determining membrane potential, and thereby the vascular tone. Ginsenoside Re, a phytochemical from ginseng, is reported to activate this channel, but its precise mechanism is unsolved. Patch clamp studies showed that ginsenoside Re activates KCa channels in the arterial smooth muscle cell line A10 in a dose-dependent manner. The channel-opening effect of ginsenoside Re was inhibited by 1 μM L-NIO, an inhibitor of eNOS, but not by 3 μM SMTC, an inhibitor of nNOS, indicating that ginsenoside Re activated KCa channels through activation of eNOS. SH-6 (10 μM), an Akt inhibitor, and wortmannin, a PI3-kinase inhibitor, completely blocked activation of KCa channels by ginsenoside Re, indicating that it activates eNOS via a c-Src/PI3-kinase/ Akt-dependent mechanism. In addition, the ginsenoside Re-induced activation of eNOS and KCa channel was blocked by 10 μM ICI 182,780, an inhibitor of membrane estrogen receptor-α, suggesting that eNOS activation occurs via a non-genomic pathway of this receptor. In conclusion, ginsenoside Re releases NO via a membrane sex steroid receptors, resulting in KCa channel activation in vascular smooth muscle cells, promoting vasodilation and preventing severe arterial contraction