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Purpose Postoperative delirium is one of the most common complications after cardiovascular surgery in older adults. Benzodiazepines are a reported risk factor for delirium; however, there are no studies investigating remimazolam, a novel anesthetic agent. Therefore, we prospectively investigated the effect of remimazolam on postoperative delirium. Methods We included elective cardiovascular surgery patients aged [greater than or equal to] 65 years at Hamamatsu University Hospital between August 2020 and February 2022. Patients who received general anesthesia with remimazolam were compared with those who received other anesthetics (control group). The primary outcome was delirium within 5 days after surgery. Secondary outcomes were delirium during intensive care unit stay and hospitalization, total duration of delirium, subsyndromal delirium, and differences in the Mini-Mental State Examination scores from preoperative to postoperative days 2 and 5. To adjust for differences in the groups' baseline covariates, we used stabilized inverse probability weighting as the primary analysis and propensity score matching as the sensitivity analysis. Results We enrolled 200 patients; 78 in the remimazolam group and 122 in the control group. After stabilized inverse probability weighting, 30.3% of the remimazolam group patients and 26.6% of the control group patients developed delirium within 5 days (risk difference, 3.8%; 95% confidence interval -11.5% to 19.1%; p = 0.63). The secondary outcomes did not differ significantly between the groups, and the sensitivity analysis results were similar to those for the primary analysis. Conclusion Remimazolam was not significantly associated with postoperative delirium when compared with other anesthetic agents., Author(s): Yoshitaka Aoki [sup.1], Tadayoshi Kurita [sup.1], Mikio Nakajima [sup.2] [sup.3], Ryo Imai [sup.1], Yuji Suzuki [sup.1], Hiroshi Makino [sup.1], Hiroyuki Kinoshita [sup.4], Matsuyuki Doi [sup.1], Yoshiki Nakajima [sup.1] Author [...]

Alternating‐rich copolymer of vinylboronic acid pinacol ester (VBpin) and maleic anhydride (MAH) was found to catalyze direct dehydrative esterification of carboxylic acid and alcohol. The key to the catalytic function is the activation of the MAH unit by the neighboring Lewis acidic boron directly connected to the backbone through the formation of five‐membered ring. The effects of the side‐chain cooperation were clarified through comparisons with the polymers having similar structures and a conventional titanium catalyst as well as the analyses of reactions with carboxylic acid or alcohol. The catalytic activity was enhanced as the molecular weight was higher, which is owing to the structural feature that boron is directly attached to the backbone. The cooperative catalysis is of interest because of its conceptual similarity with enzyme. [ABSTRACT FROM AUTHOR]

Purpose Hydrogen gas (H.sub.2) inhalation improved the survival rate of hemorrhagic shock. However, its mechanisms are unknown. We hypothesized that H.sub.2 protected the endothelial glycocalyx during hemorrhagic shock and prolonged survival time. Methods 83 Sprague-Dawley rats were anesthetized with isoflurane. The animals were randomly assigned to 5 groups: room air with no shock, 1.2% H.sub.2 with no shock, room air with shock (Control-S), 1.2% H.sub.2 with shock (H.sub.21.2%-S), and 3.0% H.sub.2 with shock (H.sub.23.0%-S). Shock groups were bled to a mean arterial pressure of 30-35 mmHg and held for 60 min, then resuscitated with normal saline at fourfold the amount of the shed blood volume. Results The syndecan-1 level was significantly lower in the H.sub.21.2%-S [8.3 ± 6.6 ng/ml; P = 0.01; 95% confidence interval (CI), 3.2-35.8] than in the Control-S (27.9 ± 17.0 ng/ml). The endothelial glycocalyx was significantly thicker in the H.sub.21.2%-S (0.15 ± 0.02 [micro]m; P = 0.007; 95% CI, 0.02-0.2) than in the Control-S (0.06 ± 0.02 [micro]m). The survival time was longer in the H.sub.21.2%-S (327 ± 67 min, P = 0.0160) than in the Control-S (246 ± 69 min). The hemoglobin level was significantly lower in the H.sub.21.2%-S (9.4 ± 0.5 g/dl; P = 0.0034; 95% CI, 0.6-2.9) than in the Control-S (11.1 ± 0.8 g/dl). However, the H.sub.23.0%-S was not significant. Conclusions Inhalation of 1.2% H.sub.2 gas protected the endothelial glycocalyx and prolonged survival time during hemorrhagic shock. Therapeutic efficacy might vary depending on the concentration., Author(s): Tsunehisa Sato [sup.1], Soichiro Mimuro [sup.1], Takasumi Katoh [sup.1], Tadayoshi Kurita [sup.1], Sang Kien Truong [sup.1], Kensuke Kobayashi [sup.1], Hiroshi Makino [sup.1], Matsuyuki Doi [sup.1], Yoshiki Nakajima [sup.1] Author [...]

Theories have proposed that, in sensory cortices, learning can enhance top-down modulation by higher brain areas while reducing bottom-up sensory drives. To address circuit mechanisms underlying this process, we examined the activity of layer 2/3 (L2/3) excitatory neurons in the mouse primary visual cortex (V1) as well as L4 excitatory neurons, the main bottom-up source, and long-range top-down projections from the retrosplenial cortex (RSC) during associative learning over days using chronic two-photon calcium imaging. During learning, L4 responses gradually weakened, whereas RSC inputs became stronger. Furthermore, L2/3 acquired a ramp-up response temporal profile, potentially encoding the timing of the associated event, which coincided with a similar change in RSC inputs. Learning also reduced the activity of somatostatin-expressing inhibitory neurons (SOM-INs) in V1 that could potentially gate top-down inputs. Finally, RSC inactivation or SOM-IN activation was sufficient to partially reverse the learning-induced changes in L2/3. Together, these results reveal a learning-dependent dynamic shift in the balance between bottom-up and top-down information streams and uncover a role of SOM-INs in controlling this process.

Introduction: Iron accumulation in vessel walls induces oxidative stress and inflammation, which can cause cerebrovascular damage, vascular wall degeneration, and intracranial aneurysmal formation, growth, and rupture. Subarachnoid hemorrhage from intracranial aneurysm rupture results in significant morbidity and mortality. This study used a mouse model of intracranial aneurysm to evaluate the effect of dietary iron restriction on aneurysm formation and rupture. Methods: Intracranial aneurysms were induced using deoxycorticosterone acetate-salt-induced hypertension and a single injection of elastase into the cerebrospinal fluid of the basal cistern. Mice were fed an iron-restricted diet (n = 23) or a normal diet (n = 25). Aneurysm rupture was detected by neurological symptoms, while the presence of intracranial aneurysm with subarachnoid hemorrhage was confirmed by post-mortem examination. Results: The aneurysmal rupture rate was significantly lower in iron-restricted diet mice (37%) compared with normal diet mice (76%; p < 0.05). Serum oxidative stress, iron accumulation, macrophage infiltration, and 8-hydroxy-2′-deoxyguanosine in the vascular wall were lower in iron-restricted diet mice (p < 0.01). The areas of iron positivity were similar to the areas of CD68 positivity and 8-hydroxy-2′-deoxyguanosine in both normal diet and iron-restricted diet mouse aneurysms. Conclusions: These findings suggest that iron is involved in intracranial aneurysm rupture via vascular inflammation and oxidative stress. Dietary iron restriction may have a promising role in preventing intracranial aneurysm rupture. [ABSTRACT FROM AUTHOR]

Purpose Heatstroke causes systemic inflammation, followed by vascular endothelial damage. The normal vascular endothelium is coated by endothelial glycocalyx (EGCX). Dexmedetomidine (DEX) has an anti-inflammatory effect, but there has been little investigation on the influence of heatstroke on EGCX and the effect of DEX on this condition. Therefore, we examined whether EGCX was disrupted in heatstroke and if DEX improved survival and preserves EGCX. Methods Anesthetized Wistar rats were randomly assigned to three groups: a DEX group treated with DEX (5 [micro]g/kg/h) and 0.9% saline infused continuously at 10 ml/kg/h during heat exposure; a NSS group given 0.9% saline during heat exposure; and a SHAM group given 0.9% saline alone without heat exposure. Heatstroke was induced by exposure to an ambient temperature of 40 °C with relative humidity of 60%. The survival rate was assessed up to 2 h after the start of heat exposure. Plasma levels of syndecan-1 and the thickness of EGCX using electron microscopy were measured when the systolic blood pressure fell to less than 80 mmHg. Results The survival rate after 2 h of heat exposure was significantly higher in the DEX group compared to the NSS group (89% vs. 22%, P = 0.004). Plasma levels of syndecan-1 were 0.6 ± 1.3, 9.7 ± 5.9, and 2.1 ± 3.4 ng/ml in the SHAM, NSS and DEX groups, respectively (P = 0.013). The thickness of EGCX was significantly higher in the DEX group compared with the NSS group (P = 0.001). Conclusions EGCX was disrupted in heatstroke, and DEX improved survival and preserved EGCX., Author(s): Kensuke Kobayashi [sup.1] , Soichiro Mimuro [sup.1] , Tsunehisa Sato [sup.1] , Atsushi Kobayashi [sup.1] , Shingo Kawashima [sup.1] , Hiroshi Makino [sup.1] , Matsuyuki Doi [sup.1] , Takasumi [...]