Noriaki Fukatsu’s research while affiliated with Nagoya University and other places

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Publications (14)


Dorsomedial and preoptic hypothalamic circuits control torpor
  • Article

November 2023

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68 Reads

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2 Citations

Current Biology

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Noriaki Fukatsu

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[...]

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Endotherms can survive low temperatures and food shortage by actively entering a hypometabolic state known as torpor. Although the decrease in metabolic rate and body temperature (Tb) during torpor is controlled by the brain, the specific neural circuits underlying these processes have not been comprehen- sively elucidated. In this study, we identify the neural circuits involved in torpor regulation by combining whole-brain mapping of torpor-activated neurons, cell-type-specific manipulation of neural activity, and viral tracing-based circuit mapping. We find that Trpm2-positive neurons in the preoptic area and Vgat-positive neurons in the dorsal medial hypothalamus are activated during torpor. Genetic silencing shows that the ac- tivity of either cell type is necessary to enter the torpor state. Finally, we show that these cells receive pro- jections from the arcuate and suprachiasmatic nucleus and send projections to brain regions involved in ther- moregulation. Our results demonstrate an essential role of hypothalamic neurons in the regulation of Tb and metabolic rate during torpor and identify critical nodes of the torpor regulatory network.


Fig. 1. Activity recordings of orexin neurons across vigilance states in orexin-tTA mice as determined by fiber photometry. (A) Schematics illustrating the injection of AAV-TetO-GCaMP6s into the LH of orexin-tTA mice to induce expression of GCaMP6s in orexin neurons (Left) and combined fiber photometry with EEG/EMG recordings (Middle). Immunohistochemical confirmation of GCaMP6s expression in orexin neurons (Right). The dashed white lines at the top of each panel indicate the edge of the optic fiber. (B) Schematic of experimental procedures and data analysis. (C) Representative orexin neuronal activity across vigilance states measured by fiber photometry. (D) Summary of orexin neuron activity across vigilance states, expressed as Z-scores (all stages from N = 6 mice). (E) Orexin neuron activity for all 171 NREM to REM transitions (each stage > 1 min) determined from 24-h recordings in N = 6 mice. (F, Top) Mean Z-score of all NREM to REM transitions for each individual mouse (gray); mean Z-score of all the N = 6 mice (red). (F, Bottom) Summary of orexin neuron activity during NREM-REM state transitions for all six mice shown as Z-scores. Values are the mean ± SEM. *P < 0.05, **P < 0.01. Statistical analyses are shown in SI Appendix, Table S1. Vigilance state parameters of orexin-tTA mice (n = 6) in the fiber photometry experiments (24 h) and the 10-min episodes for Z-score (all stages) are described in SI Appendix, Tables S2 and S3, respectively. tNR, last 30 s during the transition from NREM to REM sleep; PMT, photomultiplier tube; W, wakefulness; NR, NREM; R, REM.
Fig. 2. Activity recordings of orexin neurons across vigilance states in orexin-tTA mice as determined by microendoscopy. (A) Schematics of GCaMP6s expression (Left) and nVista microendoscopy with EEG and EMG recordings (Right). (B) Representative identification of orexin neurons using nVista. Dashed white line indicates region of interest (ROI). (C) Representative traces of Ca 2+ activity during each vigilance state. (D) Activity of orexin neurons aligned by contribution to the three NREM clusters in G. (E) Activity during each vigilance state of orexin neurons determined to be active (n = 44 cells) or inactive (n = 93 cells) during REM sleep in N = 5 mice. (F) Venn diagram showing the number of orexin neurons (133 cells) exhibiting each activity pattern. A total of 137 cells were detected; four neurons were not classified. (G) Representation of the activity of orexin neurons within NREM clusters 1, 2, and 3. (H) Representative correlations of activity among orexin neuron pairs from NREM-active clusters 1 and 2 in G. Each dot reflects the location of the cells determined by the (x, y) position of the center of the neuron in the field of view. (I) Percentage of cells exhibiting activity synchronization, defined by the proportion of correlated (>0.2) pairs during each vigilance state. Values are the mean ± SEM. *P < 0.05, **P < 0.01. Statistical analyses are shown in SI Appendix, Table S1. W, wakefulness; NR, NREM; R, REM.
Fig. 3. Activity recordings of orexin neurons across vigilance states in prepro-orexin knockout [orexin-Flp (KI/KI)] mice as determined by fiber photometry. (A) Schematics illustrating the injection of AAV-CMV-dFRT-GCaMP6s into homozygous orexin-Flp (KI/KI) mice to induce expression of GCaMP6s expression in orexin neurons (Left) and fiber photometry with EEG/EMG recordings (Middle). Histochemical confirmation of GCaMP6 expression in orexin neurons (Right). The dashed line at the top of the panel indicates the edge of the optic fiber. (B) Schematic of the experimental procedures and data analysis. (C) Representative orexin neural activity across vigilance states measured by fiber photometry. (D) Summary of orexin neuron activity across vigilance states, expressed as Z-scores (all stages from N = 5 mice). (E) Activity of orexin neurons from all 121 NREM to REM transitions recorded (each stage > 1 min) during 24-h recordings in N = 5 mice. (F, Top) Mean Z-score of all the transitions in each individual mouse (gray); mean Z-score of all the N = 5 mice (red). (F, Bottom) Summary of orexin neuron activity of all the mice during NREM-REM state transitions shown as Z-scores. Values are the mean ± SEM. *P < 0.05, **P < 0.01. Statistical analyses are shown in SI Appendix, Table S1. Vigilance state parameters of orexin-Flp (KI/KI) mice (n = 5) in the fiber photometry experiments (24 h) and the 10-min episodes for Z-score (all stages) are described in SI Appendix, Tables S2 and S3, respectively. tNR, the last 30 s during the transition from NREM to REM sleep; PMT, photomultiplier tube; W, wakefulness; NR, NREM; R, REM.
Fig. 5. Activity of orexin neurons during cataplexy in prepro-orexin knockout [orexin-Flp (KI/KI)] mice. (A) Representative trace of orexin neuron activity during cataplexy as measured by fiber photometry. (B) Activity of orexin neurons of all the state transitions (wake to cataplexy and cataplexy to wake, each stage > 40 s), measured from 24-h recordings in N = 5 mice. (C, Top) Mean Z-score of all the transitions in each individual mouse (gray); mean Z-score of all the N = 5 mice (red). (C, Bottom) Summary of orexin neuron activity of all the mice (wake to cataplexy and cataplexy to wake) shown as Z-scores. (D) Representative traces of the activity of 20 orexin neurons during cataplexy measured using nVista. (E) Summary of orexin neuron activity during transitions between wake and cataplexy for N = 50 orexin neurons from N = 3 mice. Values are the mean ± SEM. **P < 0.01. Statistical analyses are shown in SI Appendix, Table S1. C, cataplexy; W, wakefulness.
Fig. 6. Effects of optogenetic inhibition of orexin neurons on NREM-REM transitions in mice with or without orexin peptide expression. (A) Schematics of ArchT-EGFP expression in orexin neurons in orexin-tTA mice (Left) and implantation of bilateral optic fibers with EEG/EMG recordings (Right). (B) Immunohistochemical confirmation of ArchT-EGFP expression in orexin neurons in orexin-tTA mice (N = 6 mice). Dashed lines at the top of each image indicate the edge of the optic fiber. (C) Hypnogram (ZT7-8) during baseline (Upper) and optogenetic inhibition (Lower). (D) Representative EEG during REM sleep at baseline (Upper) and during optogenetic inhibition (Lower). Insets are EEG spectra of the indicated epochs. Note episodes of hypersynchronous paroxysmal theta (HSPT) in the EEG. (E) Total time in each vigilance state during baseline (gray) and optogenetic inhibition (green). (F) The number of HSPT bouts during baseline (gray) and optogenetic inhibition (green) in orexin neurons from orexin-tTA mice. (G) Optogenetic inhibition of orexin neurons decreases the transition ratio (Left) and cumulative probability (Right) for the NREM sleep to Wake transition in orexin-tTA mice. (H) Optogenetic inhibition of orexin neurons increases the transition ratio (Left) and cumulative probability (Right) for the NREM to REM sleep transition in mice expressing the orexin peptides (orexin-tTA mice). (I) Schematic summarizing the effect of optogenetic inhibition of orexin neurons in orexin-tTA mice. (J) Schematics of ArchT-EGFP expression in orexin neurons from orexin-Flp (KI/KI) mice which lack orexin peptides (N = 6 mice). (K) Histochemical confirmation of ArchT-EGFP expression in orexin-Flp (KI/KI) mice; dashed lines indicate the location of the optic fiber. (L) Hypnogram (ZT7-8) during baseline (Upper) and optogenetic inhibition (Lower). (M) Total time in each vigilance state during baseline (gray) and optogenetic inhibition (green) of orexin neurons in orexin-Flp (KI/KI) mice. (N) The number of HSPT bouts during baseline (gray) and optogenetic inhibition (green). (O) Transition ratio (Left) and cumulative probability (Right) for the transition from NREM sleep to Wake. (P) Transition ratio (Left) and cumulative probability (Right) for the transition from NREM to REM sleep. (Q) Schematic summarizing the absence of any effect of optogenetic inhibition of orexin neurons in orexin-Flp (KI/KI) mice. Values are the mean ± SEM. *P < 0.05, **P < 0.01. Statistical analyses are in SI Appendix, Table S1. HSPT, Hypersynchronous paroxysmal theta burst.

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Deficiency of orexin signaling during sleep is involved in abnormal REM sleep architecture in narcolepsy
  • Article
  • Full-text available

October 2023

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216 Reads

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15 Citations

Proceedings of the National Academy of Sciences

Narcolepsy is a sleep disorder caused by deficiency of orexin signaling. However, the neural mechanisms by which deficient orexin signaling causes the abnormal rapid eye movement (REM) sleep characteristics of narcolepsy, such as cataplexy and frequent transitions to REM states, are not fully understood. Here, we determined the activity dynamics of orexin neurons during sleep that suppress the abnormal REM sleep architecture of narcolepsy. Orexin neurons were highly active during wakefulness, showed intermittent synchronous activity during non-REM (NREM) sleep, were quiescent prior to the transition from NREM to REM sleep, and a small subpopulation of these cells was active during REM sleep. Orexin neurons that lacked orexin peptides were less active during REM sleep and were mostly silent during cataplexy. Optogenetic inhibition of orexin neurons established that the activity dynamics of these cells during NREM sleep regulate NREM–REM sleep transitions. Inhibition of orexin neurons during REM sleep increased subsequent REM sleep in “orexin intact” mice and subsequent cataplexy in mice lacking orexin peptides, indicating that the activity of a subpopulation of orexin neurons during the preceding REM sleep suppresses subsequent REM sleep and cataplexy. Thus, these results identify how deficient orexin signaling during sleep results in the abnormal REM sleep architecture characteristic of narcolepsy.

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Fig. 1: Production of panitumumab-IR700 (pan-IR700) as an EGFR-targeting conjugate for NIR-PIT, and evaluation of in vitro NIR-PIT effect. (a) Quality control of panitumumab-IR700 with SDS-PAGE (upper: Colloidal Blue staining, lower: IR700-fluorescence). (b) Confirmation of binding of pan-IR700 on EGFR-expressing cells with a flow cytometer. pan-IR700 could bind on A431-luc-GFP cells, mdamb468-luc-GFP cells, or PC9-luc cells (EGFR overexpressing cancer cells), while did not bind on 3T3-luc cells (human EGFR negative mouse cells, negative control to see unspecific binding). Pan-IR700 was inhibited binding on the EGFR-expressing cells with excess panitumumab (panitumumab blocking). (c) Fluorescence microscopic evaluation of in vitro NIR-PIT (2 J/cm 2 ) targeting EGFR; A431-luc-GFP cells binding with pan-IR700 rapidly ruptured upon NIR-light-irradiation (2 J/cm 2 ), which were stained with PI (Propidium Iodide, necrotic cell staining). Bar = 50 μm. In vitro NIR-PIT targeting EGFR on mdamb469-luc-GFP or PC-9 cells were also evaluated in Supplementary Figs. S1a and S2a. (d) Fluorescence microscopic observation of in vitro NIR-PIT (2 J/cm 2 ) under co-culture of EGFR-positive (A431-luc-GFP) and EGFR-negative (3T3-RFP) cells; NIR-PIT (2 J/cm 2 ) did not cause toxicity to the adjacent 3T3-RFP and only destroyed A431-luc-GFP cells which was stained Sytox Blue dead cell staining. Bar = 50 μm. (e) Quantitative cytotoxicity evaluation of in vitro NIR-PIT varying NIR-light doses with luciferase activities (n = 4, p = 0.5 J: 0.034026436, 1 J: 0.020806296, 2 J: 0.010444204 < 0.05, student's t test).
Fig. 3: Histological analyses of SUPR effect with QD800 after in vivo NIR-PIT. (a) Fluorescence microscopic observation of the tumours. Immunostainings were performed on the frozen tumour specimen; blood vessels: red (PECAM-1), panitumumab-IR700: magenta, QD800: green. Bar = 200 μm. (b) Fluorescence intensity of PECAM-1 (red) and QD800 (green) over a cross-section of cells along the white lines in the frozen tumour specimen. (c) Quantification of QD800-fluorescence-signal along the intratumoral vessels. The QD800-fluorescence-signal besides the vascular was predominantly and significantly more increased in the NIR-PIT (100 J/cm 2 ) group (n = 6, p = 0.00000108 < 0.05, vs.
Fig. 5: Evaluation of micro-sized-SUPR effect after NIR-PIT using a micro-sized ultrasound contrast agent (micro-bubbles). (a) A representative image of the ultrasound contrast agent micro-bubbles, Sonazoid. The diameter of Sonazoid is around 2 μm. Bar = 25 μm. (b) Scheme of the study with an ultrasound contrast agent; Sonazoid. Pan-IR700 was intravenously injected at 1 day before NIR-light irradiation. To evaluate SUPR via micro-bubbles, intravenous injection of Sonazoid and harmonic ultrasound sonography was performed before and after the NIR-PIT with same mouse. At the next day of the NIR-PIT, the treated tumour was evaluated by BLIs and analyzed the correlation with micro-
Fig. 6: Micro-sized SUPR via CEUS imaging with micro-bubbles could be exploited for the monitoring of NIR-PIT therapeutic effect. Serial harmonic signal by Sonazoid persists in well-treated tumours and does not retain in poorly treated tumours. By assessing the increasing microbubbles' permeability and retention via the harmonic signals comparing the before NIR-light irradiation, the future efficacy of NIR-PIT can be predicted.
Contrast-enhanced ultrasound imaging for monitoring the efficacy of near-infrared photoimmunotherapy

August 2023

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36 Reads

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4 Citations

EBioMedicine

Background: Near-infrared photoimmunotherapy (NIR-PIT) is a promising cancer therapy combining NIR-light irradiation with an antibody and IR700DX, a light-sensitive substance, to destroy tumours. However, homogeneous irradiation is difficult because the light varies depending on the distance and tissue environment. Therefore, markers that indicate sufficient irradiation are necessary. Nanoparticles sized 10∼200 nm show enhanced permeation and retention within tumours, which is further enhanced via NIR-PIT (super enhanced permeability and retention, SUPR). We aimed to monitor the effectiveness of NIR-PIT by measuring SUPR. Methods: A xenograft mouse tumour model was established by inoculating human cancer cells in both buttocks of Balb/C-nu/nu mice, and NIR-PIT was performed on only one side. To evaluate SUPR, fluorescent signal examination was performed using QD800-fluorescent nanoparticles and NIR-fluorescent poly (d,l-lactide-co-glycolic acid) (NIR-PLGA) microparticles. Harmonic signals were evaluated using micro-bubbles of the contrast agent Sonazoid and contrast-enhanced ultrasound (CEUS) imaging. The correlation between SUPR immediately after treatment and NIR-PIT effectiveness on the day after treatment was evaluated. Findings: QD800 fluorescent signals persisted only in the treated tumours, and the intensity of remaining signals showed high positive correlation with the therapeutic effect. NIR-PLGA fluorescent signals and Sonazoid-derived harmonic signals remained for a longer time in the treated tumours than in the controls, and the kE value of the two-compartment model correlated with NIR-PIT effectiveness. Interpretation: SUPR measurement using Sonazoid and CEUS imaging could be easily adapted for clinical use as a therapeutic image-based biomarker for monitoring and confirming of NIR-PIT efficacy. Funding: This research was supported by ARIM JAPAN of MEXT, the Program for Developing Next-generation Researchers (Japan Science and Technology Agency), KAKEN (18K15923, 21K07217) (JSPS), CREST (JPMJCR19H2, JST), and FOREST-Souhatsu (JST). Mochida Memorial Foundation for Medical and Pharmaceutical Research; Takeda Science Foundation; The Japan Health Foundation; and Princess Takamatsu Cancer Research Fund. Funders only provided financial support and had no role in the study design, data collection, data analysis, interpretation, and writing of the report.


Cre-dependent ACR2-expressing reporter mouse strain for efficient long-lasting inhibition of neuronal activity

March 2023

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89 Reads

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1 Citation

Optogenetics is a powerful tool for manipulating neuronal activity by light illumination with high temporal and spatial resolution. Anion-channelrhodopsins (ACRs) are light-gated anion channels that allow researchers to efficiently inhibit neuronal activity. A blue light-sensitive ACR2 has recently been used in several in vivo studies; however, the reporter mouse strain expressing ACR2 has not yet been reported. Here, we generated a new reporter mouse strain, LSL-ACR2, in which ACR2 is expressed under the control of Cre recombinase. We crossed this strain with a noradrenergic neuron-specific driver mouse (NAT-Cre) to generate NAT-ACR2 mice. We confirmed Cre-dependent expression and function of ACR2 in the targeted neurons by immunohistochemistry and electrophysiological recordings in vitro, and confirmed physiological function using an in vivo behavioral experiment. Our results show that the LSL-ACR2 mouse strain can be applied for optogenetic inhibition of targeted neurons, particularly for long-lasting continuous inhibition, upon crossing with Cre-driver mouse strains. The LSL-ACR2 strain can be used to prepare transgenic mice with homogenous expression of ACR2 in targeted neurons with a high penetration ratio, good reproducibility, and no tissue invasion.


Brain-wide mapping of neuronal architecture controlling torpor

March 2023

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158 Reads

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3 Citations

Endotherms can survive low temperatures and food shortage by actively entering a hypometabolic state known as torpor. Although the decrease in metabolic rate and body temperature during torpor is controlled by the brain, the underlying neural circuits remain largely unknown. In this study, we identify the neural circuits involved in torpor regulation by combining whole-brain mapping of torpor-activated neurons, cell type-specific manipulation of neural activity, and viral tracing-based circuit mapping. We found that Trpm2-positive neurons in the preoptic area and Vgat-positive neurons in the dorsal medial hypothalamus are activated during torpor. Genetic silencing shows the activity of either cell type is necessary to enter the torpor state. Finally, we show that these cells receive projections from the arcuate and suprachiasmatic nucleus and send projections to brain regions involved in thermoregulation. Our results demonstrate an essential role of hypothalamic neurons in the regulation of body temperature and metabolic rate during torpor and identify critical nodes of the torpor-regulatory network.


Association of a third vaccination with antibody levels and side reactions in essential workers: A prospective cohort study

February 2023

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2 Reads

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1 Citation

Vaccine

Objective: To evaluate the relationship between the change of titer and adverse events after the third vaccination for COVID-19 among healthcare workers. Design and setting: This was a prospective cohort study, and the follow-up period was from December 2021 to November 2023. Participants: A total of 392 healthcare workers aged over 20 years who worked at the facility and wished to have vaccine antibody titers measured participated in this study. Exposures: A third dose of BNT162b2 COVID-19 vaccine was administered to healthcare workers working at the hospital, and we evaluated the changes in antibody titers before and after the vaccine, as well as adverse reactions after vaccination. Main outcomes and measures: The primary endpoints were adverse reactions within 7 days after the third dose of COVID-19 vaccine and the rate of increase in COVID-19 vaccine antibody titer at 4 weeks. Results: A total of 392 people participated in the study, of whom 358 participants had their antibody titers measured before and after the booster vaccination. The overall IgG geometric mean was 609 U/mL (561-663) before booster vaccination and increased to 18,735 U/mL (17,509-20,049) at 4 weeks after vaccination (p < 0.001). Multivariate analysis showed no statistically significant relationship between the primary endpoints, such as a change in antibody titer due to the presence of fever after vaccination or a change in antibody titer due to swelling at the vaccination site. Factors affecting the rate of increase in antibody titer, evaluated as secondary endpoints, were suggested to be age (1.02 (95 % confidence interval (CI): 1.01-1.03)) and hypertension (0.66 (95 % CI: 0.47-0.93)). Conclusions and relevance: In relation to the booster effect of the third dose of COVID-19 vaccination, there was no statistically significant difference in the presence of fever or use of antipyretic or other drugs.


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Cre-dependent ACR2-expressing reporter mouse strain for efficient long-lasting inhibition of neuronal activity

December 2022

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59 Reads

Optogenetics is a powerful tool for manipulating neuronal activity by light illumination with high temporal and spatial resolution. Anion-channelrhodopsins (ACRs) are light-gated anion channels that allow researchers to efficiently inhibit neuronal activity. A blue light-sensitive ACR2 has recently been used in several in vivo studies; however, the reporter mouse strain expressing ACR2 has not yet been reported. Here, we generated a new reporter mouse strain, LSL-ACR2 , in which ACR2 is expressed under the control of Cre recombinase. We crossed this strain with a noradrenergic neuron-specific driver mouse ( NAT-Cre ) to generate NAT-ACR2 mice. We confirmed Cre-dependent expression and function of ACR2 in the targeted neurons by immunohistochemistry and electrophysiological recordings in vitro , and confirmed physiological function using an in vivo behavioral experiment. Our results show that the LSL-ACR2 mouse strain can be applied for optogenetic inhibition of targeted neurons, particularly for long-lasting continuous inhibition, upon crossing with Cre-driver mouse strains. The LSL-ACR2 strain can be used to prepare transgenic mice with homogenous expression of ACR2 in targeted neurons with a high penetration ratio, good reproducibility, and no tissue invasion.


An analysis modality for vascular structures combining tissue-clearing technology and topological data analysis

September 2022

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447 Reads

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23 Citations

The blood and lymphatic vasculature networks are not yet fully understood even in mouse because of the inherent limitations of imaging systems and quantification methods. This study aims to evaluate the usefulness of the tissue-clearing technology for visualizing blood and lymphatic vessels in adult mouse. Clear, unobstructed brain/body imaging cocktails and computational analysis (CUBIC) enables us to capture the high-resolution 3D images of organ- or area-specific vascular structures. To evaluate these 3D structural images, signals are first classified from the original captured images by machine learning at pixel base. Then, these classified target signals are subjected to topological data analysis and non-homogeneous Poisson process model to extract geometric features. Consequently, the structural difference of vasculatures is successfully evaluated in mouse disease models. In conclusion, this study demonstrates the utility of CUBIC for analysis of vascular structures and presents its feasibility as an analysis modality in combination with 3D images and mathematical frameworks.


Prevention of droplet dispersal with ‘e‐mask’: A new daily use endoscopic mask during bronchoscopy

June 2022

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8 Reads

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2 Citations

Respirology

Background and objective: Bronchoscopy is an airborne particle-generating procedure. However, few methods for safe bronchoscopy have been developed. To reduce airborne particles during bronchoscopy, we created an 'e-mask', which is a simple, disposable mask for patients. Our objective was to evaluate the e-mask's protective ability against airborne particles and to assess respiratory adverse events and complications. Methods: Patients with stage 2-4 chronic obstructive pulmonary disease were excluded. We performed visualization and quantifying experiments on airborne particles with and without the e-mask. We prospectively evaluated whether wearing the e-mask during bronchoscopy was associated with the incidence of patients requiring >5 L/min oxygen to maintain >90% oxygen saturation, and patients with >45 mm Hg end-tidal carbon dioxide (EtCO2 ) elevation, in addition to complications, compared to historical controls. Results: In the visualization experiment, more than ten thousand times of airborne particles were generated without the e-mask than with the e-mask. The volume of airborne particles was significantly reduced with the e-mask, compared to that without the e-mask (p = 0.011). Multivariate logistic regression analysis revealed that wearing the e-mask had no significant effect on the incidence of patients requiring >5 L/min oxygen to maintain >90% oxygen saturation, (p = 0.959); however, wearing the e-mask was a significant factor in >45 mm Hg EtCO2 elevation (p = 0.026). No significant differences in complications were observed between the e-mask and control groups (5.8% vs. 2.5%, p = 0.395). Conclusion: Wearing the e-mask during bronchoscopy significantly reduced the generation of airborne particles during bronchoscopy without increasing complications.



Citations (8)


... Transcranial ultrasound stimulation at the preoptic area induces torpor-like hypothermia via activation of Trpm2positive neurons [49]. Also, Yamaguchi et al. demonstrated that fasting-induced daily torpor was not observed in mice where Trpm2-positive neurons in the MPA were hyperpolarized and their neural activity inhibited by overexpressing the inwardly rectifying cation channel Kir2.1 [50]. The authors also showed that optogenetic activation of Trpm2-positive cells localized in the MPA induces a body temperature decrease, and mice swiftly recover their body temperature upon cessation of light stimulation [50]. ...

Reference:

The Art of Chilling Out: How Neurons Regulate Torpor
Dorsomedial and preoptic hypothalamic circuits control torpor
  • Citing Article
  • November 2023

Current Biology

... Orexin neurons release two homologous neuropeptides orexin A and B, which target two G-protein coupled receptors OX1R and OX2R (5,6). Dysfunction of the orexin circuit is linked to narcolepsy with cataplexy, characterized by disrupted sleep-wake patterns and sudden loss of muscle tone (11,12). Studies have shown that OX2R knockout mice exhibit symptoms of narcolepsy, while OX1R knockout mice have been grossly normal, highlighting the critical role of OX2R in sleep-wake control (13). ...

Deficiency of orexin signaling during sleep is involved in abnormal REM sleep architecture in narcolepsy

Proceedings of the National Academy of Sciences

... Notably, they have democratized experimental access to spatially integrated intact whole-brain anatomy, at the resolution of single-cells and within computationally feasible datasets that are compatible with brain atlas mapping. For example, in combination with genetic fluorescent labeling, these techniques have facilitated the mapping of cellular activity [4][5][6][7][8][9][10][11][12][13][14][15][16] , cell-type distributions [17][18][19][20] , and endogenous genetic 21 and connectivity patterns 22 . ...

Brain-wide mapping of neuronal architecture controlling torpor

... There is limited research on AE after booster COVID-19 vaccination and the relationship with antibody levels. A study from September 2022 on the Comirnaty first booster reported a trend for higher antibodies in the month after vaccination in participants who experienced fever, but this association was not significant [33]. ...

Association of a third vaccination with antibody levels and side reactions in essential workers: A prospective cohort study
  • Citing Article
  • February 2023

Vaccine

... 14 Growing awareness of vascularity and immunity has raised demand for understanding their spatial heterogeneity. 15 However, traditional spatial studies predominantly rely on tissue sections, limiting 3D characteristics analysis. 16 Advances in tissue clearing have revolutionized this field, enabling easy and effective 3D visualization of whole organs and organisms. ...

An analysis modality for vascular structures combining tissue-clearing technology and topological data analysis

... Precautions were taken to prevent the spread of droplets and aerosols from the patients. Various reports exist regarding patients using masks or modified face masks while undergoing bronchoscopy to prevent the spread of droplets [8][9][10] . ...

Prevention of droplet dispersal with ‘e‐mask’: A new daily use endoscopic mask during bronchoscopy
  • Citing Article
  • June 2022

Respirology

... Performing hand hygiene is essential before donning and after doffing PPE. Furthermore, several reports exist regarding patients wearing masks to prevent droplet and aerosol dispersion, in addition to healthcare workers wearing PPE to protect themselves 9,10,17) . The study by Yasui and Ito demonstrated significant effectiveness in preventing dispersion using a surgical mask with holes, supported by video evidence captured with a high-speed camera 9,17) . ...

Development of a Mask for Bronchoscopy to Prevent Infection Under COVID-19 Pandemic: Image Evaluation
  • Citing Article
  • June 2021

American Journal of Respiratory and Critical Care Medicine

... It has been found that VTA glutamatergic neurons and dopaminergic neurons promote wake from sleep [26][27][28], while GABAergic neurons promote sleep [14,29]. We showed that VTA dopaminergic neuronal firing did not significantly change during the sleep-wake, glutamatergic and GABAergic neuronal firing were higher in wake and REM sleep than in NREM sleep. ...

GABA neurons in the ventral tegmental area regulate non-rapid eye movement sleep in mice

eLife