Identification of people who have a fever in public places during the occurrence of emerging infectious diseases is essential for controlling disease spread. The measurement of body temperature could identify infected persons. The environment affects body temperature, but little is known about the validity of measurements under different thermal environments. Therefore, the aim of this study was to determine the validity of measuring body temperature in cold and warm environments. We recruited 50 participants aged 18-69 years (26 males, 24 females) to measure body temperature using an axillary thermometer and an ear thermometer and by infrared thermal imaging (thermography). The body temperature obtained with an axillary thermometer was used as a reference; receiver operating characteristic (ROC) analysis was conducted to determine the validity of temperatures obtained by measurement with an ear thermometer and thermography at 36.7°C (median of the axillary body temperature). The area under the ROC curve (AUC) indicates the validity of measurements. The AUC for ear thermometers in a warm environment (mean temperature: 20.0°C) showed a fair accuracy (AUC: 0.74 [95% CI: 0.64-0.83]), while that (AUC: 0.62 [95% CI: 0.51-0.72]) in a cold environment (mean temperature: 12.6°C) and measurements with thermography used in both environments (AUC: 0.57 [95% CI: 0.45-0.68] in a warm environment and AUC: 0.65 [95% CI: 0.54-0.76] in a cold environment) showed a low accuracy. In conclusion, in a warm environment, measurement of body temperature with an ear thermometer is a valid procedure and effective for mass body temperature screening.
Blinking and opening/closing of the eyelid are considered to be different movements with independent control mechanisms. Apraxia of lid opening (ALO) is a clinical syndrome in which patients experience difficulty in opening their eyes voluntarily. Our previous study with fluorodeoxyglucose and positron emission tomography (PET) has suggested that functional impairments in the supplementary motor area (SMA) and the anterior cingulate gyrus may be involved in the pathophysiology of ALO. The aim of this study was to explore the physiological mechanisms for voluntary eyelid opening/closing and the difference between self-initiated and triggered movements, using [15O]H2O and PET. We measured the regional cerebral blood flow in 8 healthy subjects under 3 conditions: [A] at rest with eyes closed, [B] with self-paced lid opening/closing, and [C] with triggered lid opening/closing. All tasks were done with a blindfold to exclude the influence of visual input. The SMA proper and the angular gyrus were activated during self-paced and triggered lid opening/closing movements; however, the pre-SMA and the primary motor area (M1) were activated only during self-paced movements. The anterior cingulate gyrus and the cerebellum were activated during self-paced condition over triggered condition. The roles of SMA, M1 and cerebellum were assumed in eyelid opening/closing movements: the preparation and processing of movements in SMA, execution of movements in M1, and rhythmic generation in pre-SMA, M1 and cerebellum. We suggest that the activation in pre-SMA, anterior cingulate gyrus, and cerebellum may be responsible for the self-initiated eyelid opening/closing movements.
Acute lung injury and acute respiratory distress syndrome (ALI/ARDS) are severe forms of bilateral lung inflammation with poor clinical outcomes. However, the pathophysiology of ALI/ARDS remains largely obscure. Soluble receptor for advanced glycation endproducts (sRAGE) plays a key regulatory role during the acute phase of inflammation, and baseline plasma levels of sRAGE were recently found to be associated with severity of ALI/ARDS. We analyzed, in ALI/ARDS patients, plasma and alveolar levels of sRAGE over time and the association with severity of lung injury. We enrolled 21 ALI/ARDS patients admitted to our intensive care unit (ICU) and assayed plasma sRAGE on the first 2 days after diagnosis, every three days for the first month and then once a week, until ICU discharge or death. We also measured sRAGE levels in bronchoalveolar lavage fluids, obtained when clinically indicated. At each sampling time, we recorded physiological and clinical data of the patients. Plasma sRAGE levels peaked at day 1 and decreased over time. When all samples were considered, plasma and alveolar sRAGE levels were significantly higher in patients with worse oxygenation and higher need for ventilatory support (i.e., patients with more severe lung dysfunction). Moreover, the presence of lung infection yielded higher alveolar sRAGE levels. In conclusion, we show that the plasma and alveolar levels of sRAGE in ALI/ARDS patients are correlated to lung injury severity and to lung infection. Our findings may, in time, lead to the development of more effective therapies against ALI/ARDS.
The advent of stem cell therapy brings about the hope to restore the loss of cardiac pacemaker cells. However, it is largely unknown whether cardiac stem cells are able to differentiate into pacemaker cells. The purpose of this study was to determine whether the heart of large juvenile mammals contains cardiac stem cells (CSCs), which are suitable as seed cells for restoration of cardiac pacemaker cell. The c-kit+ CSCs were isolated from one-month-old mongrel dogs. CSCs that we sorted were self-renewing, and they could proliferate by clonal expansion. CSCs could differentiate into cardiac muscle, smooth muscle and endothelial cells at rates of 10.5 ± 4.2%, 13.5 ± 5.1% and 12.9 ± 3.5%, respectively, at week 4, as judged by the expression of respective differentiation markers: cardiac troponin I, smooth muscle actin, and CD31. At week 8, the differentiation rates were further increased to 23.2 ± 3.6%, 25.9 ± 6.6% and 28.3 ± 6.1% (P < 0.05 for each marker). Some of cells derived from CSCs could express cardiac transcription factor GATA-4 after week 2 and express pacing-related genes, including hyperpolarization-activated cyclic nucleotide-gated 2 (HCN2) and HCN4 after week 4. Importantly, a fraction of CSCs demonstrated the presence of inward currents that indicate the expression of inward current channels. In conclusion, c-kit+ CSCs may differentiate into cardiac muscle cell and sinus node-like cells, suggesting that CSCs would be useful as seed cells in treating sinus bradycardiac disorders or exploring the mechanism of pacemaker activity.
Bone morphogenetic proteins (BMPs), members of the transforming growth factor β cytokine superfamily, elicit various biological effects in different tissues. BMP receptor type II (BMPRII) contains a unique carboxyl-terminal region that interacts with multiple signaling molecules. However, expression of endogenous BMPRII is low in various mammalian cell lines, which hampers the analysis of BMP signaling. Therefore, we established a human cell line expressing BMPRII tagged with a Flag epitope (BMPRII-Flag) using the tetracycline-controlled Flp-In T-REx gene expression system. The BMPRII-Flag gene was introduced into the Flp-In T-REx 293 (FT293) cell line, a derivative of human 293 embryonic kidney fibroblasts. Then we analyzed the expression of key BMP target genes, inhibitors of DNA binding (Id) family members (Id1, Id2, and Id3) and the inhibitory Smads Smad6 and Smad7, in parental FT293 cells and an established cell line, FT293-BMPRII, by quantitative real-time PCR. Tetracycline treatment significantly increased the expression of BMPRII-Flag mRNA and protein in FT293-BMPRII cells, but induced no significant changes in expression of Id1, Id2, Id3, Smad6, or Smad7 mRNA. In contrast, treatment with a BMPRII ligand BMP2 induced the expression of Id1, Id2, Id3, and Smad6 in parental FT293 cells and FT293-BMPRII cells. Tetracycline-induced BMPRII-Flag expression significantly enhanced the induction of Id1, Id3, and Smad6 mRNA expression in FT293-BMPRII cells treated with BMP2. These findings provide evidence that although BMPRII has no obvious effect on the expression of representative BMP target genes, it differentially modulates the responsiveness of target genes to BMP2.
Flap prefabrication is started with transposition of a vascular pedicle into a donor area that lacks an axial blood supply. Adipose-derived stem cells (ASCs) have been proven beneficial for promoting neovascularization and tissue regeneration in several animal models. Here we investigated the feasibility of applying ASCs as a novel strategy to promote flap prefabrication, which involves the processes of neovascularization and regeneration. Prefabricated flaps were performed by two-stage procedure in a rat model. At stage one, the right femoral vascular pedicle was dissected and embedded underneath the abdominal flap to form a man-made axial flap. At stage two, the prefabricated abdominal flap was elevated as an island flap based on the implanted femoral vessel. Ninety rats were randomly divided into 3 groups and received allogeneic ASCs, chondrocytes and phosphate-buffered saline (PBS), respectively during the first operation. Eighteen flaps of each group were harvested for vascular endothelial growth factor-A (VEGF-A) protein assay after the first surgery. The other flaps were processed for flap viability measurements by flap survival rate and capillary density after the second surgery. Results demonstrated that the ASCs treated group had higher survival percentage and capillary density of flap as compared with either PBS group or chondrocyte group. Furthermore, the ASC group had the highest level of in vivo VEGF-A among three groups, while the chondrocyte group had the lowest. These results indicate that ASCs are capable of promoting flap prefabrication, and its therapeutic potential is correlated with the angiogenic cytokines such as VEGF-A.
The diameter of the inferior vena cava (IVC) measured with echocardiography is clinically used as a parameter to estimate right atrial pressure, which reflects dehydration or overhydration. Because elderly patients fall easily into dehydration, normal values for IVC diameters in elderly patients may be helpful for geriatric medicine. However, normal values of IVC diameter in relation to age have not been investigated. The purpose of this study was to elucidate age-related changes in IVC diameter using echocardiography. Enrolled in the study were 200 patients (67 ± 15 yrs: range 17-94 yrs) with cardiovascular risk factors but no overt cardiac diseases. IVC diameters throughout the respiratory cycle were measured as maximum and minimum IVC diameters (IVCmax, IVCmin) using M-mode echocardiography. To assess IVC collapsibility, the respirophasic variation of IVC diameter was calculated as (IVCmax − IVCmin)/(IVCmax) ×100. Maximum IVC diameter was decreased with advancing age (r = −0.221, p = 0.002). The respirophasic variation of the IVC diameter was increased with advancing age (r = 0.244, p = 0.001). Stepwise multiple regression analysis showed that age was an independent determinant for both maximum IVC diameter (ß coefficient = −0.249, p < 0.001) and respirophasic variation of the IVC diameter (ß coefficient = 0.268, p < 0.001). Age-related decrease in maximum IVC diameter and increase in the respirophasic IVC collapsibility may indicate the decrease in right atrial pressure in some elderly patients. Therefore, elderly patients with decreased maximum IVC and increased respirophasic IVC collapsibility may need prevention for dehydration.
Duchenne muscular dystrophy (DMD) is a severe recessive X-linked form of muscular dystrophy caused by mutations in the dystrophin gene and it affects males predominantly. Here we report a 4-year-old girl with DMD from a healthy family, in which her parents and sister have no DMD genotype. A PCR-based method of multiple ligation-dependent probe amplification (MLPA) analysis showed the deletion of exons 46 and 47 in the dystrophin gene, which led to loss of dystrophin function. No obvious phenotype of Turner syndrome was observed in this patient and cytogenetic analysis revealed that her karyotype is 46,X,i(X)(q10). In conclusion, we describe the first female patient with DMD who carries a de novo mutation of the dystrophin gene in one chromosome and isochromosome Xq, i(Xq), in another chromosome.
It has been shown that mild to moderate exercise can accelerate gastric emptying in humans. However, understanding of the underlying mechanism is hampered by the lack of appropriate animal models. To investigate the effects of mild exercise on gastric motility, we developed an animal model, in which strain gauge transducers were surgically planted on the antral surfaces of female Sprague−Dawley rats. We continuously recorded the contractions of gastric circular muscle in unrestrained conscious rats, divided into four groups: sham-operated exercise, sham-operated sedentary, vagotomized exercise, and vagotomized sedentary. The rats were trained for 3 weeks, and gastric motility was monitored before and after exercise. Although exercise accelerates gastric antral contraction in sham-operated rats, this effect was absent in the vagotomized exercise group, indicating the involvement of the vagal nerve in the exercise-mediated increase in gastric motility. Among the four groups, daily food intake was highest in the sham-operated exercise group. In contrast, the vagotomized exercise group exhibited the smallest body weight gain. Severe gastric retention was observed in vagotomized rats, suggesting a role of the vagal nerve in facilitating food movement and digestion in the stomach. Moreover, at the end of the 3-week exercise, there were no differences in plasma levels of growth hormone, peptid YY, and ghrelin among the four groups. These results indicate that in response to a mild physical exercise challenge, the vagal nerve stimulates gastric motility and enhances the ability of the stomach to process food. Our findings highlight the significance of neuronal control of stomach function.
Tohoku J. Exp. Med., 221: 287-298, 2010. In the version of this article published in the August issue, 2010, the affiliation number of the tenth author (Shigeru Tsuchiya) was mistyped (page 287). The correct affiliation is shown above. In addition, the lettering of ‘ZT’ is a misprint for ‘CT’ in panels A, B and C of Figures 6 and 7 (pages 294 and 295).