Case report of anesthetic management for an infant with tricho-hepato-entric syndrome

Tricho-hepato-entric syndrome is a rare congenital disorder characterized by hair anomalies, neonatal hemochromatosis and intractable diarrhea. A three-year-old girl with this syndrome received general anesthesia for inguinal hernia repair. Anesthesia was induced with nitrous oxide and sevoflurane, and maintained with sevoflurane and fentanyl without muscle relaxant. Rectal acetaminophen was administered and ilioinguinal block was performed for postoperative analgesia. The anesthetic course was uneventful.     

Selective neuronal damage and chronic hemodynamic cerebral ischemia

OBJECTIVE: In atherothrombotic internal carotid artery or middle cerebral artery (MCA) occlusive disease, chronic hemodynamic compromise may increase the risk for cerebral ischemic damage. To determine whether selective neuronal damage demonstrated as a decrease in central benzodiazepine receptor (BZR) in the normal-appearing cerebral cortex is associated with increased oxygen extraction fraction (OEF) (misery perfusion). METHODS: We measured BZR and OEF using positron emission tomography in 105 nondisabled patients with atherothrombotic internal carotid artery or MCA occlusive disease and no cortical infarction. By using three-dimensional stereotactic surface projections and the stereotactic extraction estimation method, without correction for partial volume effects, the abnormally decreased BZR index [(the extent of the pixels with Z-score more than 2 compared with controls) x (average Z-score in those pixels)] in the cerebral cortex of the MCA distribution with arterial disease was calculated, and it was found to be correlated with the mean hemispheric value of OEF and several clinical variables. RESULTS: All patients had pixels with abnormally decreased BZR, with the extent varying from 0.04 to 60.91%. Multivariate analysis showed that the abnormally decreased BZR index was positively correlated with the value of OEF and the history of stroke, whereas it was negatively correlated with the presence of hypercholesterolemia with statin treatment. Follow-up examinations of 17 patients without ischemic episode showed that a decrease of BZR was associated with an increase of OEF. INTERPRETATION: In atherothrombotic internal carotid artery or MCA occlusive disease, misery perfusion may cause selective neuronal damage, and statins might have beneficial effects against neuronal damage.     

Novel G423S mutation of human alpha7 nicotinic receptor promotes agonist-induced desensitization by a protein kinase C-dependent mechanism

The alpha7 nicotinic acetylcholine receptor subunit (CHRNA7) gene harbors a high degree of polymorphism. In this study, we found a novel variant (1267 G to A) in exon 10 of the CHRNA7 gene in a Japanese population. This variant results in glycine-to-serine substitution at position 423 (G423S) located in the large cytoplasmic loop of the protein. To clarify the possibility that the G423S mutation alters the pharmacological properties of alpha7 receptors, acetylcholine (ACh)-elicited current through alpha7-G423S mutant receptors expressed in Xenopus laevis oocytes was measured using the two-electrode voltage-clamp technique. We found that the current elicited by ACh (1 mM, 5 s) through alpha7-G423S receptors, but not through alpha7 receptors, was significantly decreased by treatment with a protein kinase C activator, phorbol-12-myristate-13-acetate (PMA, 10-30 nM). In addition, PMA (10 nM) selectively promoted a progressive decrease in alpha7-G423S current induced by repetitive application of ACh pulses (1 mM, 0.1 s, 0.17-0.33 Hz) compared with alpha7 current. PMA also enhanced the inactivation of alpha7-G423S mutant receptors induced by a prolonged application of choline (30 microM) without affecting alpha7 receptor responses. Western blot analysis showed that the treatment with PMA (30 nM) increased the serine phosphorylation level of the alpha7-G423S mutant receptors but not that of the wild-type receptors. These findings demonstrate that the G423S mutation promotes receptor desensitization by a protein kinase C-dependent mechanism. Thus, we provide the first evidence that a variant in the human CHRNA7 gene alters the function of alpha7 nicotinic receptors.     

Anesthetic management of the ex-utero intrapartum treatment (EXIT) procedure for congenital high airway obstruction syndrome (CHAOS)

We report an experience of anesthetic management of the ex-utero intrapartum treatment (EXIT) procedure performed in a fetus with congenital high airway obstruction syndrome (CHAOS) due to laryngeal atresia at 30 weeks' gestation. Anesthesia of the mother was induced with rapid sequence, and maintained with 3.5% sevoflurane in 100% oxygen and fentanyl before delivery. Two minimum alveolar concentration (MAC) sevoflurane provided excellent uterine relaxation without maternal hypotension. After hysterotomy, a sterile pulse oxymeter was placed on the fetus hand for monitoring fetal SpO2 and pulse rate, and a Doppler ultrasound transducer was applied to monitor fetal heart rate. Fentanyl (5 microg x dl(-1)) and pancuronium (0.2 mg x dl(-1)) were injected into the fetal upper arm in addition to transplacental anesthetic agents. The fetal heart rate and SpO2 were stable throughout the fetal manipulations, but the rise in SpO2 after initiating ventilation via tracheostomy was very slow. The uterine tone improved soon after discontinuing sevoflurane and oxytocin infusion was started after delivery. Surfactant administration before first ventilation is recommended in preterm babies undergoing EXIT procedure, and capnometer may be useful to confirm the adequate ventilation before cutting the umbilical cord.     

Further studies on specificity of red cell adherence test: nonmalignant bladder lesions

Specific red cell adherence test for blood group antigens was utilized in 32 nonmalignant bladder lesions, none of which was associated with bladder cancer, to determine the specificity of this test. All of the 14 lesions of cystitis cystica, cystitis glandularis, and chronic cystitis retained their antigens. Of the 18 lesions of squamous metaplasia, 13 (72%) were antigen positive. Testing for blood group antigens showed an overall 84 per cent specific rate in 27 of the 32 nonmalignant bladder lesions.     

The association between emergency clinic visits for asthmatic attacks and fluctuating environmental factors]

The number of nocturnal visits of asthmatic attack patients to the emergency room of Yokohama Medical Association's Clinic from January 1990 to December 1991 was compared to daily levels of air pollution (NO, NO2, SO2 and SPM) and weather (temperature and relative humidity) variables measured in Yokohama City. Trend-cycle components (Trend) that control for the weekly effects, other irregular variance for asthmatic attack incidence and environmental parameter measurements were estimated from the original data series using the method of Akaike and Ishiguro (1980). The rate of increase for each environmental parameter was then calculated from its trend-cycle components. We classified the data into four stages on the basis of rising and falling temperature and humidity. For each stage of temperature and humidity, fluctuation we estimated correlations between the number of asthmatic attack visits and original data series measurements, estimated trend-cycle components, and calculated rates of increase for each of the air pollutants. The daily number of asthmatic attack visits was negatively correlated to the daily mean values of all air pollutants, but positively correlated to the daily mean temperature and relative humidity. The trend-cycle components of the air pollutants were also negatively correlated to the frequencies of asthmatic attacks (p < 0.01 for all pollutants except NO2). In contrast, the number of asthmatic attack visits were in general positively correlated with increasing levels of pollutants. Furthermore, when both temperature and relative humidity decreased, significant correlations (r > 0.31, p < 0.001) between the number of asthmatic attacks and increased rates of all air pollutants were observed (r: NO2 > NO > SO2 > SPM).     

Pancreatic beta cell senescence contributes to the pathogenesis of type 2 diabetes in high-fat diet-induced diabetic mice

Aims/hypothesis During the pathogenesis of type 2 diabetes insulin resistance causes compensatory proliferation of beta cells. As beta cells have a limited replication potential, this compensatory proliferation might accelerate cellular senescence and lead to diabetes. We examined the cellular senescence of beta cells after proliferation during lipoglucotoxicity.Methods Senescence-associated markers in beta cells were examined in nutrient-induced diabetic C57BL/6J mice that were fed a high-fat diet. After 4 and 12 months of the high-fat diet, intraperitoneal glucose tolerance tests (IPGTTs) and histochemical analyses of Ki-67, p38, senescence-associated beta-galactosidase, and beta cell mass were performed.Results At 4 months, the AUC for plasma insulin levels during the IPGTT (AUC_insulin) was higher, beta cell mass was 3.1-fold greater, and the proliferation of beta cells was 2.2-fold higher than in the control group. However, at 12 months, AUC_insulin declined, the frequency of Ki-67-positive beta cells decreased to one-third that of the control group, and the senescence-associated, beta-galactosidase-positive area increased to 4.7-fold that of the control group. Moreover, small amounts of p38, which is induced by oxidative stress and mediates cellular senescence, were found in beta cells from the high-fat diet group, but not in beta cells from the control group. Furthermore, the senescence-associated, beta-galactosidase-positive area in the high-fat diet group had a highly significant negative correlation with AUC_insulin (r=–0.852, p<0.01).Conclusions/interpretation Beta cell senescence occurred in diet-induced type 2 diabetes and led to insufficient insulin release. These findings suggest that cellular senescence contributes to the pathogenesis of diet-induced diabetes.     

Development of a practicable non-contact bedside autonomic activation monitoring system using microwave radars and its clinical application in elderly people

We developed a practicable, non-contact, autonomic activation monitoring system using microwave radars without imposing any stress on monitored individuals. Recently, the rapid increase in the aging population has raised concerns in developed countries. Thus, hospitals and care facilities will need to perform long-term health monitoring of elderly patients. The system allows monitoring of geriatric autonomic dysfunctions caused by chronic diseases, such as diabetes or myocardial infarction (MI), while measuring vital signs in non-contact way. The system measures heart rate variability (HRV) of elderly people in bed using dual, 24-GHz, compact microwave radars attached beneath the bed mattress. HRV parameters (LF, HF, and LF/HF) were determined from the cardiac peak-to-peak intervals, which were detected by radars using the maximum entropy method. We tested the system on 15 elderly people with and without diabetes or MI (72–99 years old) from 7:00 p.m. to 6:00 a.m. at a special nursing home in Tokyo. LF/HF obtained by the system correlated significantly (R = 0.89; p < 0.01) with those obtained by Holter electrocardiography (ECG). Diabetic subjects showed significantly lower LF (radar) than non-diabetic (119.8 ± 57.8 for diabetic, 405.9 ± 112.6 for non-diabetic, p < 0.01). HF (radar) of post-MI subjects was significantly lower than that of non-MI (219.7 ± 131.7 for post-MI and 580.0 ± 654.6 for non-MI, p < 0.05). Previous studies using conventional ECG reveal that diabetic neuropathy decreases LF, and also MI causes parasympathetic attenuation which leads to HF reduction. Our study showed that average SDNN of post-MI patients is smaller than 50 ms which is known to have high mortality. The non-contact autonomic activation monitoring system allows a long-term health management especially during sleeping hours for elderly people at healthcare facilities.