Creation of an artificial intelligence model for intubation difficulty classification by deep learning (convolutional neural network) using face images: an observational study.

BACKGROUND: Tracheal intubation is the gold standard for securing the airway, and it is not uncommon to encounter intubation difficulties in intensive care units and emergency rooms. Currently, there is a need for an objective measure to assess intubation difficulties in emergency situations by physicians, residents, and paramedics who are unfamiliar with tracheal intubation. Artificial intelligence (AI) is currently used in medical imaging owing to advanced performance. We aimed to create an AI model to classify intubation difficulties from the patient's facial image using a convolutional neural network (CNN), which links the facial image with the actual difficulty of intubation. METHODS: Patients scheduled for surgery at Yamagata University Hospital between April and August 2020 were enrolled. Patients who underwent surgery with altered facial appearance, surgery with altered range of motion in the neck, or intubation performed by a physician with less than 3 years of anesthesia experience were excluded. Sixteen different facial images were obtained from the patients since the day after surgery. All images were judged as "Easy"/"Difficult" by an anesthesiologist, and an AI classification model was created using deep learning by linking the patient's facial image and the intubation difficulty. Receiver operating characteristic curves of actual intubation difficulty and AI model were developed, and sensitivity, specificity, and area under the curve (AUC) were calculated; median AUC was used as the result. Class activation heat maps were used to visualize how the AI model classifies intubation difficulties. RESULTS: The best AI model for classifying intubation difficulties from 16 different images was generated in the supine-side-closed mouth-base position. The accuracy was 80.5%; sensitivity, 81.8%; specificity, 83.3%; AUC, 0.864; and 95% confidence interval, [0.731-0.969], indicating that the class activation heat map was concentrated around the neck regardless of the background; the AI model recognized facial contours and identified intubation difficulties. CONCLUSION: This is the first study to apply deep learning (CNN) to classify intubation difficulties using an AI model. We could create an AI model with an AUC of 0.864. Our AI model may be useful for tracheal intubation performed by inexperienced medical staff in emergency situations or under general anesthesia.

Growth Hormone Signaling Pathway Leading to the Induction of DNA Synthesis and Proliferation in Primary Cultured Hepatocytes of Adult Rats.

BACKGROUND: We investigated the signal transduction pathway associated with growth hormone (GH)-stimulated DNA synthesis and proliferation in primary cultured hepatocytes. METHODS: Adult rat hepatocytes were isolated from normal livers by two-step in situ collagenase perfusion to facilitate disaggregation of the adult rat liver. Then hepatocytes were cultured in serum-free Williams' medium E supplemented with GH (1-100 ng/ml) in the presence or absence of test reagents. GH-induced hepatocyte DNA synthesis and proliferation were determined, and the phosphorylation activities of Janus kinase (JAK) 2 (JAK2) (p125 kDa), p95-kDa RTK, and ERK1/2 were measured by western blotting. RESULTS: Hepatocytes grown in serum-free defined medium proliferated within 5 h of culture in the presence of GH (100 ng/ml) in a concentration- and time-dependent manner (EC50 75 ng/ml). These proliferative effects of GH were almost completely blocked by an anti-GH receptor monoclonal antibody (85 ng/ml) and an anti-insulin-like growth factor (IGF)-I receptor monoclonal antibody. In addition, the proliferative effects of GH were significantly blocked by a JAK2 inhibitor (TG101209, 10-6 M), as well as specific signal-transducing inhibitors of phospholipase C (PLC; U-73122, 10-6 M), RTK (AG538, 10-6 M), phosphoinositide 3-kinase (PI3K; LY294002, 10-6 M), mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (MEK/ERK; PD98059, 10-6 M), and mammalian target of rapamycin (mTOR; rapamycin, 10 ng/ml). GH significantly induced the phosphorylations of JAK2 (p125 kDa), p95-kDa IGF-I receptor tyrosine kinase (RTK), and ERK2 in this order according to western blotting analysis. CONCLUSIONS: The proliferative action of GH is mediated by two main signaling pathways. One includes activation of the GH receptor/JAK2/PLC/Ca2+ pathway, and the other involves activation of the p95-kDa IGF-I RTK/PI3K/ERK2/mTOR pathway in primary cultures of adult rat hepatocytes.

Autocrine secretion of insulin-like growth factor-I mediates growth hormone-stimulated DNA synthesis and proliferation in primary cultures of adult rat hepatocytes.

The intracellular signaling pathway of growth hormone (GH)-stimulated DNA synthesis and proliferation was investigated in primary cultures of adult rat hepatocytes. DNA synthesis and cell proliferation were detected in hepatocyte parenchymal cells grown in serum-free, defined medium containing GH (100 ng/ml). GH-stimulated hepatocyte DNA synthesis and proliferation were almost completely blocked by TG101209 (10-6 M), a selective Janus kinase (JAK)2 inhibitor, U-73122 (10-6 M), a selective phospholipase C (PLC) inhibitor, and a monoclonal antibody to insulin-like growth factor-I (IGF-I) receptor (100 ng/ml) or anti-secretion agents such as somatostatin (10-6 M) and BAPTA/AM (10-7 M). In addition, blocking monoclonal antibodies to IGF-I, but not transforming growth factor-α, completely inhibited GH-induced hepatocyte DNA synthesis and proliferation. IGF-I levels in the culture medium increased rapidly versus baseline levels within 5 min in response to GH (100 ng/ml), and the maximum IGF-I level (100 pg/ml) was reached 20 min after GH stimulation. Autocrine secretion of IGF-I into the culture medium was inhibited by a growth-inhibitory dose of TG101209, U-73122, somatostatin, or BAPTA/AM. These data indicate that the proliferative mechanism of action of GH is mediated mainly through a GH receptor/JAK2/PLC-stimulated increase in the autocrine secretion of IGF-I by primary cultured hepatocytes, followed by stimulation of the 95 kDa IGF-I receptor tyrosine kinase signaling pathway.

The Enhancing Effects of S-Allylcysteine on Liver Regeneration Are Associated with Increased Expression of mRNAs Encoding IGF-1 and Its Receptor in Two-Thirds Partially Hepatectomized Rats.

Two-thirds partial hepatectomy (PHx) was performed in rats, and the differences in effects between S-allylcysteine (SAC) and other sulfur-containing compounds on regeneration of the remaining liver and restoration of the injury were examined. Three days after two-thirds PHx, rats treated with 300 mg/kg/d, per os (p.o.) SAC showed a 1.2-fold increase in liver weight per 100 g body weight compared with saline-treated controls. In contrast, S-methylcysteine (SMC) (300 mg/kg/d, p.o.) or cysteine (Cys) (300 mg/kg/d, p.o.) did not have a regeneration-promoting effect. In the comparison with control rats, the regenerating liver of SAC-treated rats showed a significantly higher 5-bromo-2'-deoxyuridine labeling index on day 1. In contrast, serum alanine aminotransferase activity, which increases following PHx, was significantly inhibited by SAC and SMC (but not Cys) on day 1 after two-thirds PHx. In addition, SAC induced increases in insulin-like growth factor (IGF)-1 and its receptor mRNA expressions at 1 h after two-thirds PHx, and it increased phosphorylation of extracellular signal-regulated kinase (ERK)2 and Akt at 3 h after two-thirds PHx without affecting serum growth hormone levels. These results demonstrate that SAC is a mitogenic effector of normal remnant liver and promotes recuperation of liver function after two-thirds PHx. Moreover, SAC-induced proliferative effects are mediated via increased mRNA expressions of IGF-1 and its receptor and subsequent phosphorylation of ERK2 and Akt.

Ascorbic acid insufficiency impairs spatial memory formation in juvenile AKR1A-knockout mice.

AKR1A, an aldo-keto reductase, is involved in the synthesis of ascorbic acid as well as the reduction of a variety of aldehyde compounds. AKR1A-/- mice produce considerably less ascorbic acid (about 10%) compared to AKR1A+/+ mice and require ascorbic acid supplementation in order to breed. To elucidate the roles played by AKR1A in spatial memory, AKR1A-/- male mice were weaned at 4 weeks of age and groups that received ascorbic acid supplementation and no supplementation were subjected to a Morris water maze test. Juvenile AKR1A-/- mice that received no supplementation showed impaired spatial memory formation, even though about 70% of the ascorbic acid remained in the brains of the AKR1A-/- mice at day 7 after weaning. To the contrary, the young adult AKR1A-/- mice at 13-15 weeks of age maintained only 15% of ascorbic acid but showed no significant difference in the spatial memory compared with the AKR1A+/+ mice or ascorbic acid-supplemented AKR1A-/- mice. It is conceivable that juvenile mice require more ascorbic acid for the appropriate level of formation of spatial memory and that maturation of the neural system renders the memory forming process less sensitive to an ascorbic acid insufficiency.

Effect of Selective Serotonin (5-HT)2B Receptor Agonist BW723C86 on Epidermal Growth Factor/Transforming Growth Factor-α Receptor Tyrosine Kinase and Ribosomal p70 S6 Kinase Activities in Primary Cultures of Adult Rat Hepatocytes.

Serotonin (5-hydroxytryptamine; 5-HT) can induce hepatocyte DNA synthesis and proliferation by autocrine secretion of transforming growth factor (TGF)-α through 5-HT2B receptor/phospholipase C (PLC)/Ca2+ and a signaling pathway involving epidermal growth factor (EGF)/TGF-α receptor tyrosine kinase (RTK)/extracellular signal-regulated kinase 2 (ERK2)/mammalian target of rapamycin (mTOR). In the present study, we investigated whether 5-HT or a selective 5-HT2B receptor agonist BW723C86, would stimulate phosphorylation of TGF-α RTK and ribosomal p70 S6 kinase (p70S6K) in primary cultures of adult rat hepatocytes. Western blotting analysis was used to detect 5-HT- or BW723C86 (10-6 M)-induced phosphorylation of EGF/TGF-α RTK and p70S6K. Our results showed that 5-HT- or BW723C86 (10-6 M)-induced phosphorylation of EGF/TGF-α RTK peaked at between 5 and 10 min. On the other hand, 5-HT- or BW723C86 (10-6 M)-induced phosphorylation of p70S6K peaked at about 30 min. Furthermore, a selective 5-HT2B receptor antagonist LY272015, a specific PLC inhibitor U-73122, a membrane-permeable Ca2+ chelator BAPTA/AM, an L-type Ca2+ channel blocker verapamil, somatostatin, and a specific p70S6K inhibitor LY2584702 completely abolished the phosphorylation of p70S6K induced by both 5-HT and BW723C86. These results indicate that phosphorylation of p70S6K is dependent on the 5-HT2B-receptor-mediated autocrine secretion of TGF-α. In addition, these results demonstrate that the hepatocyte proliferating action of 5-HT and BW723C86 are mediated by phosphorylation of p70S6K, a downstream element of the EGF/TGF-α RTK signaling pathway.

Magnetic resonance imaging appropriate for construction of subject-specific head models for diffuse optical tomography.

Subject-specific head models of which their geometry is based on structural magnetic resonance images are essential to accurately estimate the spatial sensitivity profiles for image reconstruction in diffuse optical tomography. T1-weighted magnetic resonance images, which are commonly used for structural imaging, are not sufficient for the threshold-based segmentation of the superficial tissues. Two types of pulse sequences, which provide a high contrast among the superficial tissues, are introduced to complement the segmentation to construct the subject-specific head models. The magnetic resonance images acquired by the proposed pulse sequences are robust to the threshold level and adequate for the threshold-based segmentation of the superficial tissues compared to the T1- and T2-weighted images. The total scan time of the proposed pulse sequences is less than one-fourth of that for the T2-weighted pulse sequence.

Expeditious synthesis of 1-aminoindane derivatives achieved by [1,4]-hydride shift mediated C(sp3)-H bond functionalization.

Described herein is a [1,4]-hydride shift mediated expeditious synthesis of 1-aminoindane derivatives. A wide variety of substrates could be employed in this reaction to afford various indane derivatives in good to excellent chemical yields. Examination of the amine moiety revealed that the sterically hindered amine is the key to achieving both low catalyst loading and excellent chemical yields.

Double C(sp3)-H bond functionalization mediated by sequential hydride shift/cyclization process: diastereoselective construction of polyheterocycles.

Described herein are two novel types of double C(sp(3))-H bond functionalizations triggered by a sequential hydride shift/cyclization process: (1) construction of a bicyclo[3.2.2]nonane skeleton by a [1,6]- and [1,5]-hydride shift sequence and (2) sequential [1,4]- and [1,5]-hydride shift mediated construction of a linear tricyclic skeleton.

The influence of frontal sinus in brain activation measurements by near-infrared spectroscopy analyzed by realistic head models.

Adequate modeling of light propagation in the head is important to predict the sensitivity of NIRS signal and the spatial sensitivity profile of source-detector pairs. The 3D realistic head models of which the geometry is based upon the anatomical images acquired by magnetic resonance imaging and x-ray computed tomography are constructed to investigate the influence of the frontal sinus on the NIRS signal and spatial sensitivity. Light propagation in the head is strongly affected by the presence of the frontal sinus. The light tends to propagate around the frontal sinus. The influence of the frontal sinus on the sensitivity of the NIRS signal to the brain activation is not consistent and depends on the depth of the frontal sinus, the optical properties of the superficial tissues and the relative position between the source-detector pair and the frontal sinus. The frontal sinus located in the shallow region of the skull tends to reduce the sensitivity of the NIRS signal while the deep frontal sinus can increase the sensitivity of the NIRS signal.

Selective activation of enantiotopic C(sp3)-hydrogen by means of chiral phosphoric acid: asymmetric synthesis of tetrahydroquinoline derivatives.

Chiral phosphoric acid-catalyzed asymmetric C-H functionalization has been achieved. In this process, enantiotopic C(sp(3))-hydrogen is selectively activated by chiral phosphoric acid to afford tetrahydroquinoline derivatives with excellent enantioselectivities (up to 97% ee).