Living Lab for Citizens' Wellness: A Case of Maintaining and Improving a Healthy Diet under the COVID-19 Pandemic.

The establishment and implementation of a healthy lifestyle is fundamental to public health and is an important issue for working-aged people, as it affects not only them but also the future generations. However, due to the COVID-19 pandemic and associated behavioural restrictions, lifestyles have altered, and, in certain environments, significantly worsened. In the present study, we conducted a project to improve the intestinal environment by focussing on the dietary habits of participants, utilising the living laboratory as a social technology to explore how to adapt to this drastic environmental change. We held eight workshops for voluntary participants and implemented a self-monitoring process of recording dietary behaviours (n = 78) and testing the intestinal environment (n = 14). Through this initiative, we developed a personalised wellness enhancement programme based on collaboration with multiple stakeholders and a framework for using personal data for research and practical purposes. These results provide an approach for promoting voluntary participation and behavioural changes among people, especially under the COVID-19 pandemic, as well as a practical basis for the government, academia, and industry to intervene effectively in raising people's awareness of health and wellness.

[A case of the transversus abdominis plane block in a super obese patient using a convex probe].

We report that the transversus abdominis plane block (TAP block) can be performed under ultrasound guidance using not a linear probe but a convex probe in a markedly obese patient undergoing laparoscopy-assisted distal gastrectomy. The TAP block is effective for providing perioperative analgesia. The common probe for the TAP block is a high-frequency linear probe, which can not depict the deeper tissues. We used a low-frequency convex probe for TAP block, which clearly showed the spread of local anesthetics in TAP block in a markedly obese patient. A convex probe is preferable for TAP block in markedly obese patients.

Intravenous anesthetic propofol suppresses prostaglandin E2 production in murine dendritic cells.

Propofol is an intravenous anesthetic that is widely used for anesthesia and sedation. Dendritic cells (DC) are one of the crucial immune cells that bridge innate and adaptive immunity, in which DC process antigens during innate immune responses to present them to naïve T-cells, leading to an establishment of adaptive immunity. Prostaglandin (PG)-E(2) may be secreted by DC into the microenvironment, considerably influencing DC phenotype and function, and thus determining the fate of adaptive immunity. Since propofol suppresses PGE(2) production in murine macrophages, the primary purpose of the present study was to determine whether propofol also suppresses PGE(2) production in DC. Assuming a positive finding of such suppression, we tested whether this also leads to alterations of interleukin (IL)-12 and IL-10 production and DC surface marker expression, both of which can be modulated by PGE(2). In bone marrow-derived DC, propofol significantly suppressed the PGE(2) production after lipopolysaccharide stimulation. Cyclo-oxygenase (COX) protein expression and arachidonic acid release were unaffected, while COX enzyme activity was significantly inhibited by propofol. The propofol-induced COX inhibition did not lead to the increased production of cysteinyl leukotrienes and leukotriene-B(4). Endogenous COX inhibition with propofol, as well as with the selective COX-2 inhibitor, NS-398, did not affect IL-12 and IL-10 production from DC. The surface expression of I-A(b) and CD40 on DC was not changed, while that of CD86 slightly increased, with both propofol and NS-398; expression of CD80 was not affected with propofol, but increased slightly with NS-398. Finally, endogenous COX inhibition with either propofol or NS-398 did not significantly affect the ability of DC to induce allogeneic T-cell proliferation. It is concluded that the intravenous anesthetic propofol suppresses COX enzyme activity in DC, with no consequences with respect to IL-12/IL-10 production and allogeneic T-cell proliferation, while minimal consequences were observed in surface molecule expression.

Possible link between cyclooxygenase-inhibiting and antitumor properties of propofol.

The intravenous anesthetic propofol has a number of well-known nonanesthetic effects, including anti-oxidation and anti-emesis. Another interesting nonanesthetic effect of propofol may be its cyclooxygenase (COX)-inhibiting activity. This activity may have important clinical implications, as propofol could have antitumor properties through COX inhibition. Propofol could counteract the activity of COX, which elicits, via its major product prostaglandin E(2), (1) tumor growth stimulation, (2) increased tumor survival, (3) enhanced tumor invasiveness, (4) stimulation of new vessel formation, and (5) tumor evasion of host immune surveillance through suppression of immune cell functions. Indeed, accumulated evidence indicates that propofol suppresses the proliferation, motility, and invasiveness of tumors in vitro and in vivo. Therefore, propofol could be a particularly suitable anesthetic for use during the perioperative period for cancer surgery. However, whether the COX-inhibiting activity of propofol is related to the reported antitumor properties of propofol is not known. Definitive evidence remains to be provided.

Possible role of propofol's cyclooxygenase-inhibiting property in alleviating dopaminergic neuronal loss in the substantia nigra in an MPTP-induced murine model of Parkinson's disease.

Propofol is an intravenous anesthetic widely used for sedation and general anesthesia. We investigated the effect of propofol on prostanoid production by activated microglia. Primary microglial culture was obtained from the brains of neonatal C57BL/6 mice. The microglia were stimulated with lipopolysaccharide (LPS) in the presence of propofol. Propofol suppressed the LPS-induced production of prostaglandin E(2) and thromboxane B(2). Cyclooxygenase (COX) protein expression and arachidonic acid release were not affected by propofol, while COX enzyme activity was significantly inhibited by propofol. The COX-inhibiting activity was also observed with purified enzymes, with COX-2 inhibition being significantly greater than COX-1 inhibition. Next, we studied whether the COX-inhibiting activity of propofol resulted in dopaminergic neuroprotection in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) murine model of Parkinson's disease, in which COX inhibitors, such as non-steroidal anti-inflammatory drugs, are reported to be neuroprotective. C57BL/6 mice received intraperitoneal injections of MPTP with or without propofol treatment, and the dopaminergic neurons in the substantia nigra pars compacta (SNpc) were examined immunohistochemically by observing the tyrosine hydroxylase-positive cells. The number of dopaminergic neurons in the SNpc was significantly reduced by MPTP treatment, while the MPTP-induced neuronal loss was minimal upon treatment with propofol or the selective COX-2 inhibitor, NS-398. These results indicate that propofol might be beneficial in mitigating MPTP-induced dopaminergic neurons, possibly via its COX-inhibiting activity.

Promotion of interferon-gamma production by natural killer cells via suppression of murine peritoneal macrophage prostaglandin E2 production using intravenous anesthetic propofol.

Propofol is an intravenous anesthetic, widely used for general anesthesia during surgery, which inevitably involves tissue trauma with inflammation. At sites of inflammation, prostanoids, especially prostaglandin E2 (PGE2), are abundant. This study addresses the effect of propofol on macrophage PGE2 production. Using thioglycollate-elicited murine peritoneal macrophages, propofol (7.5-30 µM) suppressed lipopolysaccharide-induced PGE2 production. The suppression was via the direct inhibition of cyclooxygenase (COX) enzyme activity and due neither to the downregulation of COX expression nor the inhibition of arachidonic acid release from plasma membranes. In macrophage:natural killer (NK) cell co-culture, propofol dramatically increased interferon-gamma (IFN-γ) production, and the actions of propofol were mimicked by a selective COX-2 inhibitor, NS-398, as well as the selective EP4 receptor antagonist L-161,982, suggesting a role of PGE2 suppression in the upregulation of IFN-γ production. Furthermore, in purified NK cell culture, PGE2 directly suppressed the production of IFN-γ by activated NK cells, which was reversed by selective inhibition of EP4 activity. Taken together, our results show that, in macrophage:NK cell co-culture, propofol, through the suppression of macrophage PGE2 production, upregulates NK cell IFN-γ production by alleviating EP4 receptor-mediated suppression of IFN-γ production. Propofol may potentially exert considerable influence on inflammation and immunity by suppressing PGE2 synthesis.

Propofol suppresses prostaglandin E(2) production in human peripheral monocytes.

Prostaglandin E(2) secreted from monocytes/macrophages plays important roles in immunity and in inflammation. Currently, propofol, an intravenous anesthetic, is the most widely used drug for the anesthesia and sedation of patients, including those who are vulnerable to infection and/or immunosuppression. Here we report that propofol suppressed prostaglandin E(2) production in lipopolysaccharide-activated human peripheral monocytes. The suppressive effects of propofol were ascribed to its inhibition of cyclooxygenase-2 activity rather than to effects on cyclooxygenase protein expression or substrate availability. Thus, propofol seems to have a prominent effect on immunity and inflammation.

Vaccines using dendritic cells, differentiated with propofol, enhance antitumor immunity in mice.

Dendritic cell-based vaccines are useful for enhancing antitumor immunity. It has been suggested that propofol, an intravenous anesthetic, can enhance antitumor immunity in mice. We tested vaccine efficacy for eliciting antitumor immunity, using dendritic cells differentiated from bone marrow cells in the presence of propofol. Propofol-differentiated (but not control vehicle-differentiated) dendritic cells significantly delayed the growth of B16 melanoma in vivo. In vitro cytotoxic T cell activity was not affected by propofol. However, natural killer cell activity in mice vaccinated with dendritic cells differentiated in propofol was significantly upregulated, compared to unvaccinated mice.

Edaravone, a free radical scavenger, mitigates both gray and white matter damages after global cerebral ischemia in rats.

Recent studies have shown that similar to cerebral gray matter (mainly composed of neuronal perikarya), white matter (composed of axons and glias) is vulnerable to ischemia. Edaravone, a free radical scavenger, has neuroprotective effects against focal cerebral ischemia even in humans. In this study, we investigated the time course and the severity of both gray and white matter damage following global cerebral ischemia by cardiac arrest, and examined whether edaravone protected the gray and the white matter. Male Sprague-Dawley rats were used. Global cerebral ischemia was induced by 5 min of cardiac arrest and resuscitation (CAR). Edaravone, 3 mg/kg, was administered intravenously either immediately or 60 min after CAR. The morphological damage was assessed by cresyl violet staining. The microtubule-associated protein 2 (a maker of neuronal perikarya and dendrites), the beta amyloid precursor protein (the accumulation of which is a maker of axonal damage), and the ionized calcium binding adaptor molecule 1 (a marker of microglia) were stained for immunohistochemical analysis. Significant neuronal perikaryal damage and marked microglial activation were observed in the hippocampal CA1 region with little axonal damage one week after CAR. Two weeks after CAR, the perikaryal damage and microglial activation were unchanged, but obvious axonal damage occurred. Administration of edaravone 60 min after CAR significantly mitigated the perikaryal damage, the axonal damage, and the microglial activation. Our results show that axonal damage develops slower than perikaryal damage and that edaravone can protect both gray and white matter after CAR in rats.

Propofol inhibits cyclo-oxygenase activity in human monocytic THP-1 cells.

PURPOSE: Monocytes/macrophages are key players in innate and adaptive immunity. Upon stimulation, they secrete prostanoids, which are produced by cyclooxygenase from arachidonic acid. Prostanoids influence inflammation and immune responses. We investigated the effect of propofol on prostaglandin E(2) and thromboxane B(2) production by the human monocytic cell line THP-1. METHODS: The THP-1 cells were cultured with lipopolysaccharide (1 microg ml(-1)) in the presence of clinically relevant sedative/anesthetic concentrations of propofol (0-30 microM) for 18 h, and the concentration of prostaglandin E(2) and thromboxane B(2) in culture supernatants was measured using an enzyme immunoassay. Intracellular cyclooxygenase protein expression was measured by flow cytometry. Cyclooxygenase activity was assessed by measuring production of prostaglandin E(2) and thromboxane B(2) by THP-1 cells after arachidonic acid (10 microM) substrate provision. RESULTS: Propofol decreased the production of prostaglandin E(2) (75.4 +/- 6.4 pg ml(-1) at 0 microM vs. 28.5 +/- 11.2 pg ml(-1) at 30 microM; P < 0.001) and thromboxane B(2) (282.4 +/- 79.2 pg ml(-1) at 0 microM vs. 40.4 +/- 21.7 pg ml(-1) at 30 microM; P < 0.001). The inhibition was not due to the decreased cyclooxygenase protein expression because intracellular staining of this enzyme was not affected by propofol. After arachidonic acid provision, prostaglandin E(2) and thromboxane B(2) production from activated THP-1 cells was significantly (P < 0.001) decreased with propofol, indicating direct suppression of cyclooxygenase activity with propofol. CONCLUSIONS: Propofol may modulate inflammation via the suppression of cyclooxygenase activity. Through the inhibition of prostanoid production, propofol may enhance immune responses.

An unusual case of airway obstruction at the tip of an endotracheal tube caused by insertion of a nasogastric tube.

We report an unusual case of ventilatory impediment caused by the obstruction of an endotracheal tube (ETT) by a nasogastric (NG) tube. A 72-year-old woman with bronchial asthma was scheduled for colostomy closure. An ETT of 7.5-mm internal diameter (ID) could not be advanced, and finally a 5.0-mm ID ETT was placed, because she had post-intubation tracheal stenosis. When an NG tube was inserted after endotracheal intubation, ventilation suddenly became nearly impossible. She was treated for an asthmatic attack, but her respiratory condition did not recover. We then exchanged the ETT for a laryngeal mask airway (LMA) and removed the NG tube. It was suspected that the cause of the airway obstruction was that the NG tube in the esophagus compressed the membranous portion of the stenotic trachea and the tip of the ETT was obstructed.

[Bronchial blocking with a balloon wedge pressure Catheter in a small infant].

The need for one-lung ventilation has been increasing even in pediatric patients. However, the trachea is so narrow in pediatric patients that ordinary double-lumen tubes can not be used and there have been many reports on devices or measures to block one lung. We report our experience with a female infant weighing 2 kg who had severe chronic lung disease under mechanical ventilation, and underwent left lung lower lobectomy with one-lung ventilation technique. We chose a balloon wedge pressure catheter to block the left main bronchus, because it has a central lumen through which a guide wire can be passed and sucking is available. The infant was in need of continuous ventilation and the catheter was too soft to be inserted directly. We first inserted an 18G catheter of a needle-catheter assemble outside the tracheal tube through which a guide wire was inserted into the left main bronchus with the aid of direct vision of a 2-mm fiberoptic bronchoscope through the tracheal tube, and then inserted the balloon wedge pressure catheter placing it in an appropriate position. One-lung ventilation was successfully achieved and the operative and postoperative course was uneventful.

Successful management of cesarean section in a patient with Romano-Ward syndrome using landiolol, a selective and short-acting beta1 receptor antagonist.

Romano-Ward (R-W) syndrome is an autosomal dominant hereditary disorder and is characterized by a prolonged QT interval on the electrocardiogram (ECG), syncope, and sudden death. We report here a case of cesarian section in a patient with R-W syndrome whose QT prolongation was successfully managed with landiolol, a selective beta1 receptor blocker. A 25-year-old woman with R-W syndrome was scheduled for cesarean section. In the operating room, the patient's ECG showed tachycardia (102 beats x min(-1)) and marked QT prolongation (QTc = 0.56 s). After spinal anesthesia, the patient's heart rate (HR) increased to 130 beats/min accompanied by a slight decrease in arterial blood pressure to 97/57 mmHg and the QTc was prolonged to 0.57 s. Landiolol was continuously infused at a rate of 0.04 mg.kg(-1) x min(-1) and the HR gradually decreased to 80-90 beats x min(-1) accompanied by the normalization of QTc to 0.48 s. We thought that the use of landiolol was more rational and was preferable to a nonselective beta receptor blocker for a term-pregnant woman because blockade of the beta2 receptor might cause uterine contraction. After the use of landiolol, intraoperative and postoperative courses in both the patient and the baby were uneventful.

[Airway obstruction during one-lung ventilation using a bronchial blocker and a tracheostomy tube].

We describe our experience with a 60-year-old man who had severe airway obstruction during one-lung ventilation with the tracheostomy tube using a bronchial blocker. The blocker, deriving from Univent tube, was passed through the tracheostomy tube and placed in the right main bronchus. We checked that the blocker was in appropriate place with a bronchofiberscope and obtained good one-lung ventilation with the patient in the left lateral position. However, just after the start of operation, when the skin was incised, sever hypoxia and resultant bradycardia and hypotension occurred, probably because of not only malposition of blocker but also atelectasis in the upper lobe of the dependent lung by secretion.

[Propofol anesthesia for fetal sedation].

We were requested to reduce neonatal respiratory effort at delivery in anesthetic management for Cesarean section. A 26-year-old pregnant woman was suspected through abdominal ultrasound examination and amniotic fluid test, of her baby having immature lungs associated with remarkable pleural effusion. Lungs could be damaged by respiratory effort after delivery, and respiratory management immediately after delivery was planned. Anesthesia was induced with propofol and fentanyl 300 micrograms. Propofol was administered with a target controlled infusion setting with the target blood concentration of 10 micrograms.ml-1. Fetal electrocardiogram was monitored for detecting fetal sedation. The concentrations of propofol at delivery were 10.7 and 4.1 micrograms.ml-1 in maternal arterial and umbilical venous blood, respectively, and the baby was apneic. Respiration of the baby was managed with a high frequency jet ventilation mode, and 160 ml of pleural effusion was aspirated immediately after the delivery. The baby was discharged from the hospital 5 weeks afterward.