PurA is the main target of aurodox, a type III secretion system inhibitor.

Anti-microbial resistance (AMR) is one of the greatest threats to global health. The continual battle between the emergence of AMR and the development of drugs will be extremely difficult to stop as long as traditional anti-biotic approaches are taken. In order to overcome this impasse, we here focused on the type III secretion system (T3SS), which is highly conserved in many Gram-negative pathogenic bacteria. The T3SS is known to be indispensable in establishing disease processes but not essential for pathogen survival. Therefore, T3SS inhibitors may be innovative anti-infective agents that could dramatically reduce the evolutionary selective pressure on strains resistant to treatment. Based on this concept, we previously identified a polyketide natural product, aurodox (AD), as a specific T3SS inhibitor using our original screening system. However, despite its promise as a unique anti-infective drug of AD, the molecular target of AD has remained unclear. In this paper, using an innovative chemistry and genetic biology-based approach, we show that AD binds to adenylosuccinate synthase (PurA), which suppresses the production of the secreted proteins from T3SS, resulting in the expression of bacterial virulence both in vitro and in vivo experiments. Our findings illuminate the potential of PurA as a target of anti-infective drugs and vaccination and could open a avenue for application of PurA in the regulation of T3SS.

The liver-brain-gut neural arc maintains the Treg cell niche in the gut.

Recent clinical and experimental evidence has evoked the concept of the gut-brain axis to explain mutual interactions between the central nervous system and gut microbiota that are closely associated with the bidirectional effects of inflammatory bowel disease and central nervous system disorders1-4. Despite recent advances in our understanding of neuroimmune interactions, it remains unclear how the gut and brain communicate to maintain gut immune homeostasis, including in the induction and maintenance of peripheral regulatory T cells (pTreg cells), and what environmental cues prompt the host to protect itself from development of inflammatory bowel diseases. Here we report a liver-brain-gut neural arc that ensures the proper differentiation and maintenance of pTreg cells in the gut. The hepatic vagal sensory afferent nerves are responsible for indirectly sensing the gut microenvironment and relaying the sensory inputs to the nucleus tractus solitarius of the brainstem, and ultimately to the vagal parasympathetic nerves and enteric neurons. Surgical and chemical perturbation of the vagal sensory afferents at the hepatic afferent level reduced the abundance of colonic pTreg cells; this was attributed to decreased aldehyde dehydrogenase (ALDH) expression and retinoic acid synthesis by intestinal antigen-presenting cells. Activation of muscarinic acetylcholine receptors directly induced ALDH gene expression in both human and mouse colonic antigen-presenting cells, whereas genetic ablation of these receptors abolished the stimulation of antigen-presenting cells in vitro. Disruption of left vagal sensory afferents from the liver to the brainstem in mouse models of colitis reduced the colonic pTreg cell pool, resulting in increased susceptibility to colitis. These results demonstrate that the novel vago-vagal liver-brain-gut reflex arc controls the number of pTreg cells and maintains gut homeostasis. Intervention in this autonomic feedback feedforward system could help in the development of therapeutic strategies to treat or prevent immunological disorders of the gut.

mTORC1 activity negatively regulates human hair follicle growth and pigmentation.

Dysregulation of the activity of the mechanistic target of rapamycin complex 1 (mTORC1) is commonly linked to aging, cancer, and genetic disorders such as tuberous sclerosis (TS), a rare neurodevelopmental multisystemic disease characterized by benign tumors, seizures, and intellectual disability. Although patches of white hair on the scalp (poliosis) are considered as early signs of TS, the underlying molecular mechanisms and potential involvement of mTORC1 in hair depigmentation remain unclear. Here, we have used healthy, organ-cultured human scalp hair follicles (HFs) to interrogate the role of mTORC1 in a prototypic human (mini-)organ. Gray/white HFs exhibit high mTORC1 activity, while mTORC1 inhibition by rapamycin stimulated HF growth and pigmentation, even in gray/white HFs that still contained some surviving melanocytes. Mechanistically, this occurred via increased intrafollicular production of the melanotropic hormone, α-MSH. In contrast, knockdown of intrafollicular TSC2, a negative regulator of mTORC1, significantly reduced HF pigmentation. Our findings introduce mTORC1 activity as an important negative regulator of human HF growth and pigmentation and suggest that pharmacological mTORC1 inhibition could become a novel strategy in the management of hair loss and depigmentation disorders.

Clinical impact and characteristics of erythroid dysplasia in adult aplastic anaemia: Results from a multicentre registry.

Morphological dysplasia in haematopoietic cells, defined by a 10% threshold in each lineage, is one of the diagnostic criteria for myelodysplastic neoplasms. Dysplasia limited to the erythroid lineage has also been reported in some cases of aplastic anaemia (AA); however, its significance remains unclear. We herein examined the impact of erythroid dysplasia on immunosuppressive therapy responses and survival in AA patients. The present study included 100 eligible AA patients without ring sideroblasts. Among them, 32 had dysplasia in the erythroid lineage (AA with minimal dysplasia [mini-D]). No significant sex or age differences were observed between AA groups with and without erythroid dysplasia. In severe/very severe AA and non-severe AA patients, a response to anti-thymocyte globulin + ciclosporin within 12 months was observed in 80.0% and 60.0% of AA with mini-D and 42.9% and 90.0% of those without dysplasia, with no significant difference (p = 0.29 and p = 0.24 respectively). Overall survival and leukaemia-free survival did not significantly differ between the groups. Collectively, the present results indicate that the presence of erythroid dysplasia did not significantly affect clinical characteristics or outcomes in AA patients, suggesting that its presence in AA is acceptable. Therefore, erythroid dysplasia should not exclude an AA diagnosis.

Quality assessment of enzymatic methyl-seq library constructed using crude cell lysate.

Enzymatic methyl-seq (EM-seq), an enzyme-based method, identifies genome-wide DNA methylation, which enables us to obtain reliable methylome data from purified genomic DNA by avoiding bisulfite-induced DNA damage. However, the loss of DNA during purification hinders the methylome analysis of limited samples. The crude DNA extraction method is the quickest and minimal sample loss approach for obtaining useable DNA without requiring additional dissolution and purification. However, it remains unclear whether crude DNA can be used directly for EM-seq library construction. In this study, we aimed to assess the quality of EM-seq libraries prepared directly using crude DNA. The crude DNA-derived libraries provided appropriate fragment sizes and concentrations for sequencing similar to those of the purified DNA-derived libraries. However, the sequencing results of crude samples exhibited lower reference sequence mapping efficiencies than those of the purified samples. Additionally, the lower-input crude DNA-derived sample exhibited a marginally lower cytosine-to-thymine conversion efficiency and hypermethylated pattern around gene regulatory elements than the higher-input crude DNA- or purified DNA-derived samples. In contrast, the methylation profiles of the crude and purified samples exhibited a significant correlation. Our findings indicate that crude DNA can be used as a raw material for EM-seq library construction.

Conversion of dehydrocoelenterazine to coelenterazine in mammalian cells: Identification using cultured cells stably expressing coelenterazine-utilizing luciferase.

Dehydrocoelenterazine (dCTZ) is a dehydrogenated form of coelenterazine (CTZ), which is well-known as the luciferin responsible for the bioluminescence reaction in marine organisms. In this report, we demonstrate for the first time that dCTZ is readily reduced to CTZ in mammalian cells. Using an FDSS®/µCell functional drug screening system, the conversion of dCTZ to CTZ in cells was identified through the luciferin (CTZ)-luciferase reaction in Chinese hamster ovary K1 (CHO-K1) cell lines, which stably expressed CTZ-utilizing luciferases of Renilla luciferase (RLase) or QL-nanoKAZ (a mutant of the 19 kDa protein of Oplophorus luciferase). After loading dCTZ into CHO-K1 cells expressing RLase or QL-nanoKAZ, the luminescence from both cells was detected within 10 s and continued for over 30 min. Thus, dCTZ permeates mammalian cells and is immediately converted to CTZ. This suggests that dCTZ could potentially be used as a substitute for CTZ in in vivo assays of the CTZ-dependent luminescence systems.

Circulating α-Klotho Counteracts Transforming Growth Factor-ß-Induced Sarcopenia.

α-Klotho is a longevity-related protein. Its deficiency shortens lifespan with prominent senescent phenotypes, including muscle atrophy and weakness in mice. α-Klotho has two forms: membrane α-Klotho and circulating α-Klotho (c-α-Klotho). Loss of membrane α-Klotho impairs a phosphaturic effect, thereby accelerating phosphate-induced aging. However, the mechanisms of senescence on c-α-Klotho loss remain largely unknown. Herein, with the aging of wild-type mice, c-α-Klotho declined, whereas Smad2, an intracellular transforming growth factor (TGF)-ß effector, became activated in skeletal muscle. Moreover, c-α-Klotho suppressed muscle-wasting TGF-ß molecules, including myostatin, growth and differentiation factor 11, activin, and TGF-ß1, through binding to ligands as well as type I and type II serine/threonine kinase receptors. Indeed, c-α-Klotho reversed impaired in vitro myogenesis caused by these TGF-ßs. Oral administration of Ki26894, a small-molecule inhibitor of type I receptors for these TGF-ßs, restored muscle atrophy and weakness in α-Klotho (-/-) mice and in elderly wild-type mice by suppression of activated Smad2 and up-regulated Cdkn1a (p21) transcript, a target of phosphorylated Smad2. Ki26894 also induced the slow to fast myofiber switch. These findings show c-α-Klotho's potential as a circulating inhibitor counteracting TGF-ß-induced sarcopenia. These data highlight the potential of a novel therapy involving TGF-ß blockade to prevent sarcopenia.

C-C motif chemokine ligand 2 regulates prostaglandin synthesis and embryo attachment of the bovine endometrium during implantation.

C-C motif chemokine ligand 2 (CCL2) has been reported to be expressed in the bovine endometrium during pregnancy. However, the details of its functions involved in the implantation mechanism are still not clear. The purpose of this study is to analyze the functional properties of CCL2 in the bovine endometrium and embryos. The expression of CCR2 was not different between the luteal phase and implantation phase of their endometrial tissues, but was significantly high in IFNa treated bovine endometrial stromal (BES) cells in vitro. The expressions of PGES1, PGES2, AKR1C4, and AKR1C4 were high at the implantation stage compared with the luteal stage. On the other hand, PGES2 and AKR1B1 in BEE and PGES3 and AKR1A1 in BES were significantly increased by CCL2 treatment, respectively. The expressions of PCNA and IFNt were found significantly high in the bovine trophoblastic cells (BT) treated with CCL2 compared to the control. CCL2 significantly increased the attachment rate of BT vesicles to BEE in in vitro co-culture system. The expression of OPN and ICAM-1 increased in BEE, and ICAM-1 increased in BT by CCL2 treatment, respectively. The present results indicate that CCL2 has the potential to regulate the synthesis of PGs in the endometrium and the embryo growth. In addition, CCL2 has the possibility to regulate the process of bovine embryo attachment to the endometrium by modulation of binding molecules expression.

Interleukin-15 is a hair follicle immune privilege guardian.

The autoimmunity-promoting cytokine, Interleukin-15 (IL-15), is often claimed to be a key pathogenic cytokine in alopecia areata (AA). Yet, rhIL-15 promotes human hair follicle (HF) growth ex vivo. We have asked whether the expression of IL-15 and its receptor (IL-15R) isoforms is altered in human AA and how IL-15 impacts on human HF immune privilege (HF-IP) in the presence/absence of interferon-γ (IFNγ), the well-documented key AA-pathogenic cytokine, as well as on hair regrowth after experimental AA induction in vivo. Quantitative immunohistomorphometry showed the number of perifollicular IL-15+ T cells in AA skin biopsies to be significantly increased compared to healthy control skin, while IL-15, IL-15Rα, and IL-15Rγ protein expression within the hair bulb were significantly down-regulated in AA HFs. In organ-cultured human scalp HFs, rhIL-15 significantly reduced hair bulb expression of MICA, the key "danger" signal in AA pathogenesis, and increased production of the HF-IP guardian, α-MSH. Crucially, ex vivo, rhIL-15 prevented IFNγ-induced HF-IP collapse, restored a collapsed HF-IP by IL-15Rα-dependent signaling (as documented by IL-15Rα-silencing), and protected AA-preventive immunoinhibitory iNKT10 cells from IFNγ-induced apoptosis. rhIL-15 even promoted hair regrowth after experimental AA induction in human scalp skin xenotransplants on SCID/beige mice in vivo. Our data introduce IL-15 as a novel, functionally important HF-IP guardian whose signaling is constitutively defective in scalp HFs of AA patients. Our data suggest that selective stimulation of intrafollicular IL-15Rα signaling could become a novel therapeutic approach in AA management, while blocking it pharmacologically may hinder both HF-IP restoration and hair re-growth and may thus make HFs more vulnerable to AA relapse.

Unique Reactivity of the 1,4-Bis(silyloxy)-1,3-cyclopentadiene Moiety: Application to the Synthesis of 7-Norbornanone Derivatives.

We describe a method for the synthesis of various 2-silyloxy-2-norbornen-7-ones by exploiting the specific reactivity of the 1,4-bis(silyloxy)-1,3-cyclopentadiene framework, which is generated by the silylation of a 2,2-disubstituted-1,3-cyclopentanedione bearing a picolinoyloxy group at the 2' position of its C-2 side chain. The release of the acyloxy group during the reaction generates carbocations that are then attacked by silyloxy-substituted carbons in the 1,4-bis(silyloxy)-1,3-cyclopentadiene moiety skeleton, forming a 4,5-cis-fused ring skeleton. Skeletal rearrangement of the bicyclic core results in the formation of the corresponding 2-silyloxy-2-norbornen-7-one. This novel transformation of 1,3-cyclopentanedione moieties can be used to synthesise other cyclopentenone-fused bicyclic frameworks.

Alcohol synthesis based on the SN2 reactions of alkyl halides with the squarate dianion.

A convenient method has been developed for transforming alkyl halides into the corresponding alcohols via an SN2 reaction. Treatment of an alkyl halide with the squarate dianion at high temperature produces mono-alkyl squarate, and a one-pot basic hydrolysis of the intermediate affords the alcohol in good yield.

Total synthesis of jamaicamide B.

Jamaicamide B was isolated from the cyanobacterium Moorea producens in Jamaica and shows neurotoxicity. This unique mixed peptide-polyketide structure contains a pyrrolinone ring, a ß-methoxy enone, an (E)-olefin, an undetermined stereocenter at C9, an (E)-chloroolefin, and a terminal alkyne. We report herein the first total synthesis and structural confirmation of the marine natural product (9R)-jamaicamide B.

Scoping Review of Screening and Assessment Tools for Social Determinants of Health in the Field of Cardiovascular Disease.

BACKGROUND: Despite the importance of implementing the concept of social determinants of health (SDOH) in the clinical practice of cardiovascular disease (CVD), the tools available to assess SDOH have not been systematically investigated. We conducted a scoping review for tools to assess SDOH and comprehensively evaluated how these tools could be applied in the field of CVD.Methods and Results: We conducted a systematic literature search of PubMed and Embase databases on July 25, 2023. Studies that evaluated an SDOH screening tool with CVD as an outcome or those that explicitly sampled or included participants based on their having CVD were eligible for inclusion. In addition, studies had to have focused on at least one SDOH domain defined by Healthy People 2030. After screening 1984 articles, 58 articles that evaluated 41 distinct screening tools were selected. Of the 58 articles, 39 (67.2%) targeted populations with CVD, whereas 16 (27.6%) evaluated CVD outcome in non-CVD populations. Three (5.2%) compared SDOH differences between CVD and non-CVD populations. Of 41 screening tools, 24 evaluated multiple SDOH domains and 17 evaluated only 1 domain. CONCLUSIONS: Our review revealed recent interest in SDOH in the field of CVD, with many useful screening tools that can evaluate SDOH. Future studies are needed to clarify the importance of the intervention in SDOH regarding CVD.

Effects of 1-kestose on microbiome changes caused by vonoprazan: a randomized, double-blind, placebo-controlled pilot study.

BACKGROUND AND AIM: Potassium-competitive acid blockers more strongly suppress the gastric acid barrier than proton pump inhibitors and cause dysbiosis. However, preventive measures in this regard have not been established. We aimed to evaluate whether 1-kestose, a known prebiotic, was effective at alleviating dysbiosis caused by potassium-competitive acid blockers. METHODS: Patients scheduled to undergo endoscopic resection for superficial gastroduodenal tumors were enrolled and randomized 1:1 to receive either 1-kestose or placebo. All patients were started on potassium-competitive acid blocker (vonoprazan 20 mg/day) and took 1-kestose 10 g/day or placebo (maltose) 5 g/day for 8 weeks. The primary outcome was the effect of 1-kestose on potassium-competitive acid blocker-induced alterations in the microbiome. The fecal microbiome was analyzed before and after potassium-competitive acid blocker treatment via MiSeq (16S rRNA gene V3-V4 region). RESULTS: Forty patients were enrolled, and 16 in each group were analyzed. In the placebo group, the Simpson index, an alpha diversity, was significantly decreased and relative abundance of Streptococcus was significantly increased by 1.9-fold. In the kestose group, the Simpson index did not change significantly and relative abundance of Streptococcus increased 1.3-fold, but this was not a significant change. In both groups, no adverse events occurred, ulcers were well healed, and pretreatment and posttreatment short-chain fatty acid levels did not differ. CONCLUSIONS: The potassium-competitive acid blocker caused dysbiosis in the placebo group; this effect was prevented by 1-kestose. Thus, 1-kestose may be useful in dysbiosis treatment.

Netrin-4 synthesized in satellite cell-derived myoblasts stimulates autonomous fusion.

Satellite cells are indispensable for skeletal muscle regeneration and hypertrophy by forming nascent myofibers (myotubes). They synthesize multi-potent modulator netrins (secreted subtypes: netrin-1, -3, and -4), originally found as classical neural axon guidance molecules. While netrin-1 and -3 have key roles in myogenic differentiation, the physiological significance of netrin-4 is still unclear. This study examined whether netrin-4 regulates myofiber type commitment and myotube formation. Initially, the expression profiles indicated that satellite cells isolated from the extensor digitorum longus muscle (EDL muscle: fast-twitch myofiber-abundant) expressed slightly more netrin-4 than the soleus muscle (slow-type abundant) cells. As netrin-4 knockdown inhibited both slow- and fast-type myotube formation, netrin-4 may not directly regulate myofiber type commitment. However, netrin-4 knockdown in satellite cell-derived myoblasts reduced the myotube fusion index, while exogenous netrin-4 promoted myotube formation, even though netrin-4 expression level was maximum during the initiation stage of myogenic differentiation. Furthermore, netrin-4 knockdown also inhibited MyoD (a master transcriptional factor of myogenesis) and Myomixer (a myoblast fusogenic molecule) expression. These data suggest that satellite cells synthesize netrin-4 during myogenic differentiation initiation to promote their own fusion, stimulating the MyoD-Myomixer signaling axis.

Development of a method for the simultaneous determination of ionic nutrients in hydroponic solutions using cation-/anion-exchange chromatography with a neutral eluent.

Nutrient availability in hydroponic solutions must be accurately monitored to maintain crop productivity; however, few cost-effective, accurate, real-time, and long-term monitoring technologies have been developed. In this study, we describe the development and application of cation-/anion-exchange chromatography with a neutral eluent (20-mmol/L sodium formate, pH 7.87) for the simultaneous separation (within 50 min) of ionic nutrients, including K+, NH4+, NO2-, NO3-, and phosphate ion, in a hydroponic fertilizer solution. Using the neutral eluent avoided degradation of the separation column during precipitation of metal ion species, such as hydroxides, with an alkaline eluent and oxidation of NO2- to NO3- with an acidic eluent. The suitability of the current method for monitoring ionic components in a hydroponic fertilizer solution was confirmed. Based on our data, we propose a controlled fertilizer strategy to optimize fertilizer consumption and reduce the chemical load of drained fertilizer solutions.

Remodeling of the Proximal Sealing Zone and Sac Shrinkage after Endovascular Aortic Repair or Fenestrated Endovascular Aortic Repair.

BACKGROUND: Variations in sac shrinkage (SS) are noted between endovascular aneurysm repair for abdominal aortic aneurysm (AAA) and fenestrated endovascular aneurysm repair for short neck AAA. These variations may originate from difference in the geometry and length of proximal sealing, which influences the quality and durability of the seal. This study aimed to explore the disparities in aneurysm exclusion and sac remodeling across these 2 scenarios. METHODS: This study involved a retrospective analysis of prospectively collected data from 2014 to 2021. Of 486 endovascular abdominal aortic repair cases, 33 that exclusively used a low permeability expanded polytetrafluoroethylene infrarenal device, strictly adhering to the instructions for use (IFUs), were selected. Concurrently, 30 cases of fenestrated repair that utilized modified polyester woven fabric devices proximally with consistent use of the aforementioned low-permeability devices infrarenally were examined. The quality of both proximal and distal sealing zones in fenestrated repairs was maintained within the range specified in the expanded polytetrafluoroethylene infrarenal device's IFUs, ensuring consistent sealing integrity for reliable group comparisons. Key metrics used for analysis were the detection of endoleaks and measurements of sac dimensions. Additional analyses included comparisons of demographic data and postoperative diameter changes in the proximal sealing zone (PZ) (encompassing 0, 5, 10, 15, and 20 mm below the most proximal sealing stent). RESULTS: The demographic data and preoperative maximum-minimum diameter of the aneurysms did not differ between the groups. Proximal neck dilatation was similarly observed after both procedures. Immediately after the procedure, the incidence of lumbar arterial type II endoleaks was significantly lower after fenestrated repair than that after endovascular aortic repair (EVAR, 10% vs. 39.4%, P = 0.0094). At the final observation, EVAR substantially reduced the PZ length (-4.73 ± 15.30%), while fenestrated repair maintained the length (21.98 ± 24.34%; P < 0.0001). The preservation of the sealing length in fenestrated repairs was attributable to dilation occurring within the sealing range of the proximal device, oversized to accommodate the larger diameters in the more proximal sections of the aorta. The cumulative occurrence of SS (>5 mm) following fenestrated repair increased faster than that after endovascular repair (P = 0.002). CONCLUSIONS: Although aortic neck dilatation progressed similarly in both groups, fenestrated repair maintained the sealing length and demonstrated a greater extent of SS, even under the challenging circumstances in PZ. The superior postoperative results were linked to both the durability of proximal sealing and a lower occurrence of lumbar arterial type II endoleaks, stemming from the effective shuttering of the collateral sources in the proximal lumbar or intercostal arteries.

Effect of Combined Oxygen Therapy and Use of a Surgical Mask or N95 Mask on Inspired Oxygen Fraction and Expired Carbon Dioxide Fraction.

Combined use of a surgical mask and oxygen mask might decrease the inspired oxygen concentration and increase the risk of hypercapnia. We investigated the fraction of inspired oxygen (FiO2) and end-tidal carbon dioxide (ETCO2) under different combinations of masks and oxygen flows. Five healthy volunteers were administered oxygen using the following methods: oxygen mask alone (O group), oxygen mask over a surgical mask (S group), and oxygen mask over an N95 mask (N group). FiO2 and ETCO2 were measured at oxygen flow rates of 0, 5, and 8 L/min under each mask condition. At oxygen flow rates of 5 and 8 L/min, FiO2 was lower in the order of N group (0.32 at 5 L/min, 0.36 at 8 L/min), S group (0.45 at 5 L/min, 0.52 at 8 L/min), and O group (0.61 at 5 L/min, 0.73 at 8 L/min). ETCO2 was higher in the order of N, S, and O groups. In conclusion, wearing the oxygen mask over the surgical mask or N95 mask reduces FiO2 and increases ETCO2 in healthy volunteers. Since patients who have emerged from general anaesthesia are more likely to have worse respiratory conditions, they need close observation to avoid hypoxemia and hypercapnia.

Changes in Blood Volume and Oxygenation in Lower Limb Tissue in Patients Maintaining the Lithotomy Position Under General Anaesthesia.

To investigate the effect of the lithotomy position on lower limb circulation under general anaesthesia, near-infrared spectroscopy (NIRS) was used to measure changes in blood volume and oxygenation in thigh tissue in patients (n = 35) under general anaesthesia in the lithotomy position. The NIRS measurement items, including total haemoglobin concentration (total-Hb), tissue haemoglobin index (nTHI), and tissue oxygenation index (TOI) in the thigh, were recorded for 60 min, while the patients were in the lithotomy position. The correlation between changes in each measurement item and patient characteristics, elevation of the lower extremities, and cardiorespiratory indices were evaluated. Data obtained from 24 patients were analysed. The median values (quartile deviation) of changes in total-Hb, nTHI, and TOI during the 60-min period from baseline were + 3.09 (1.99) µmol/L, +0.08 (0.03) a.u., and + 2.25 (1.75) %, respectively, all of which were significantly increased (p < 0.05). Regression analysis showed that no factor was significantly associated with the increase in any measurement item. The present results suggest that circulation in thigh tissue tends to shift towards hyperaemia during 60 min of general anaesthesia in the lithotomy position, regardless of patient background factors or changes in cardiorespiratory conditions.

A Case Report of Changes in Regional Cortical Blood Volume and Oxygenation During Induction of General Anaesthesia with Sevoflurane Versus Propofol in a Paediatric Moyamoya Disease, Evaluated by Near-Infrared Spectroscopy.

A safe induction method of general anaesthesia for paediatric moyamoya disease patients has not been fully established. We had the opportunity to administer general anaesthesia twice to a two-year-old girl diagnosed with moyamoya disease. We used different induction methods for general anaesthesia at each session, i.e. slow induction with sevoflurane and rapid induction with propofol, and were able to evaluate changes in her left regional cortical blood volume (rCBV) and oxygenation (rCBO) during both anaesthesia inductions using near-infrared spectroscopy (NIRS). The mean change value of total-Hb (rCBV) (mean ± SD; µmol/L) in the rapid induction was lower than that in the slow induction (-0.54 ± 1.43 vs. 1.82 ± 1.74). However, the TOI (rCBO) levels during both anaesthesia inductions were constantly higher than these respective baseline values (64% in the slow induction, 71% in the rapid induction), and these mean change values in each of the anaesthesia induction were about the same. The present results suggested that both the slow induction method with sevoflurane and the rapid induction method with propofol might be safe and effective for anaesthesia induction in paediatric patients with moyamoya disease.