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Automation in the food services industry is not as developed as in the automotive and electrical industries. This may be because (1) the tasks involve high-speed operations in unstructured environments and (2) the lack of effective robotic end-effectors. In this letter, we focus on the automation of dishwashing operations and propose a robotic hand capable of withdrawing and grasping a dish plate from a pile, even when there is water or oil left on the plate in a post-meal scenario. The robotic hand consists of withdrawing and grasping mechanisms. Each mechanism is actuated by two bellows actuators. Soft pads with special groove patterns were fabricated and used to provide sufficient friction when they come into contact with the plate. A theoretical analysis of the withdrawing and grasping operations was performed, and an analytical model of the bellows actuator was established by considering both the pressure thrust force and the elastic force. Bellows actuators were designed based on the analysis and fabricated using both 3D printing and casting methods. Characterization of bellows actuator was performed to validate the analytical model, and agreement was found on the thrust force, but discrepancy occurred in the elastic force due to the complex structure and deformation mode of bellows. Finally, handling experiments on different plates were conducted and results demonstrated that the proposed robotic hand can successfully withdraw and grasp a plate from a pile.

We previously reported in rats that preconditioning with hyperbaric oxygen (HBO; 100% O(2) 3.5-atomsphere absolute (ATA), 1 h/day for 5 days) provided neuroprotection against transient (8 min) forebrain ischemia possibly through protein synthesis relevant to neurotrophin receptor and inflammatory-immune system. A recent report suggested that HBO-induced neuroprotection is relevant to brain derived neurotrophic factor and its downstream event involving suppression of p38 mitogen activated protein kinase (p38) activation. In the present study, we first performed a dose comparison (1, 2, and 3.5 ATA) of HBO-induced neuroprotection and then investigated pharmacological modification by 10 mg/kg anisomycin (a protein synthesis inhibitor and potent activator for p38) and 200 microg/kg SB203580 (a p38 inhibitor), which were given intraperitoneally 60 and 30 min before every 3.5 ATA-HBO treatment, respectively. Most prominent protective effect on hippocampal CA1 neurons was observed with 3.5 ATA-HBO (survived neurons: 69% [62-73%] vs. untreated: 3.9% [2-8%], 1 ATA: 8.8% [0-26%], 2 ATA-HBO: 46% [22-62%] (median [range]) (7 days after ischemia). Anisomycin abolished a neuroprotective effect (survived neuron: 1.2% [0-7%]). SB203580, when given between administration of anisomycin and HBO treatment, resumed a neuroprotective effect (survived neuron: 52% [37-62%]). The level of phosphorylated p38 at 10-min reperfusion was significantly decreased in 3.5 ATA-HBO group (32% [12-53%] of sham). Single pretreatment with 100 and 200 microg/kg of SB203580 exerted a similar neuroprotective effect (39% [25-51%] and 59% [50-72%]) to 2 and 3.5 ATA-HBO preconditioning, respectively. It is concluded that suppression of p38 phosphorylation plays a key role in HBO-induced neuroprotection and that pretreatment with a p38 inhibitor (SB203580) can provide similar neuroprotection.

Inflammatory responses have been known to contribute to the development of neuronal damage after brain ischemia in experimental animals. Also, neutrophil elastase activity in the plasma has been elevated in the patients with acute cerebral infarction. In order to clarify whether neutrophil elastase distributes into the brain parenchyma and exacerbates neuronal damage following ischemia, we examined the effects of specific neutrophil elastase inhibitor, ONO-5046, on hippocampal CA1 neuronal death in relation to neutrophil elastase activity in the plasma and its distribution in the brain and to caspase-3/7 activity. ONO-5046 (5 and 10 mg/kg) or saline (control group) was administrated after 8 min of forebrain ischemia in rats. Ratio of surviving neurons (median, [range]) in hippocampal CA1 seven days after ischemia was significantly higher in the ONO-5046 5 mg/kg (31% [12-57%]), and 10 mg/kg groups (69% [39-76%]) than in the control group (3.2% [0-10%]). Plasma neutrophil elastase activity in the ONO-5046 10 mg/kg group was significantly lower than in the control group (14 [11-25] vs. 41 [35-68] nmol/ml). Neutrophil elastase distributed in the extracellular space in the hippocampal CA1 neuronal layer in the control group, while, in the ONO-5046 10 mg/kg group, trace of neutrophil elastase was detected only in the endothelium. Caspase-3/7 activity was elevated after ischemia over 8 h in the control group, while, in the ONO-5046 10 mg/kg group, no elevation was observed. The results suggest that neutrophil elastase may contribute to neuronal death in hippocampal CA1 following forebrain ischemia and that neutrophil elastase inhibitor attenuates neuronal death.

虚血に伴う神経細胞傷害に蛋白を成熟させる細胞内小器官である小胞体 (ER) が関与する. 虚血によるアミノ酸やglucoseの低下, ER内Ca2+ 低下は異常蛋白蓄積を生じ, ERストレスとなる. 蓄積した異常蛋白のrefoldingにER chaperone GRP78が使われ, ER膜上のキナーゼ (PERK, ATF6, IRE1) を活性化する. いずれもERストレスを改善する遺伝子 (grp78など) を転写するが, PERKはeIF2αのリン酸化によりmRNAの翻訳を抑制し, 蛋白合成を阻害する. 虚血耐性では, GRP78の発現亢進と本虚血後のeIF2αのリン酸化が生じにくく, 異常蛋白の修復が速く, 蛋白合成抑制が生じにくい. バルプロ酸などによるGRP78の増強, ERの保護は神経細胞保護につながる.

Repeated hyperbaric oxygen (HBO) exposure prior to ischemia has been reported to provide neuroprotection against ischemic brain injury. The present study examined the time course of neuroprotection of HBO (3.5 atmosphere absolute, 100% oxygen, 1 h for 5 consecutive days) and the changes of gene/protein expression in rats. First, at 6 h, 12 h, 24 h, and 72 h after HBO sessions, rats were subjected to forebrain ischemia (8 min). Histopathological examination of hippocampal CA1 neurons was done 7 days after ischemia. Second, temporal genomic responses and protein expression were examined at the same time points after HBO sessions without subjecting animals to ischemia. HBO significantly reduced loss of hippocampal CA1 neurons that normally follows transient forebrain ischemia when the last HBO session was 6 h, 12 h, or 24 h before ischemia (survived neurons 55%, 75%, and 53%, respectively), whereas if there was a 72-h delay before the ischemic insult, HBO was not protective (survived neurons only 6%). Statistical analysis on microarray data showed significant upregulation in 60 probe sets including 7 annotated genes (p75NTR, C/EBPdelta, CD74, Edg2, Trip10, Nrp1, and Igf2), whose time course expressions corresponded to HBO-induced neuroprotection. The protein levels of p75NTR, C/EBPdelta, and CD74 were significantly increased (maximum fold changes 2.9, 2.0, and 7.9, respectively). The results suggest that HBO-induced neuroprotection against ischemic injury has time window, protective at 6 h, 12 h and 24 h but not protective at 72 h. Although the precise interaction is to be determined, the genes/proteins relevant to neurotrophin and inflammatory-immune system may be involved in HBO-induced neuroprotection.

Bispectral index (BIS) is the first scientifically validated and commercially supported monitor for anesthetic drug effect on CNS. BIS integrates four EEG parameters into a single variable. This enables tracking of the EEG change associated with the changes in depth of anesthesia from awake state to electrical silence. However, we should note some pitfalls in clinical use of BIS. BIS is not a magic number but a value calculated from EEG. Checking raw EEG is still important when using BIS monitor.

帝王切開時に用いる子宮収縮薬のオキシトシン(OX)とプロスタグランジンF2α(PGF2α)の体循環への影響と副作用について検討した.対象は脊椎麻酔下に帝王切開術を受けた基礎疾患のない妊婦68人で,OX群(n=34)では0×5単位を点滴静注し,PGF2α群(n=34)ではPGF2α500μgを子宮筋内に注入した.患者背景に群間差はなかった.子宮収縮薬投与直後,5分後の血圧はPGF2α群で有意に高かった.心拍数に有意差はなかった.副作用発生率(OX群=PGF2α群,32%=71%,p

抗不整脈薬ピルメノール(P)を内服している人工透析患者の術中心停止を経験した.症例は70歳の男性で,週3回の透析と心室性期外収縮(PVC)に対しPを服用.慢性動脈閉塞により壊死したI,II趾切断術を全身麻酔下に予定した.麻酔はチアミラール,フェンタニルで導入し,セボフルラン,亜酸化窒素で維持した.手術開始5分後にPVCが連発し,心室細動に移行した.低カリウム血症とP内服によりtriggered activityを誘発しやすい状態で,浅麻酔も加わり導入後のPVCが心室細動に移行したと考えられた.Pを内服している透析患者では,服用の減量および電解質の維持,また術前に脱水状態にしないことが重要である.

重症破傷風2症例にイソフルラン(ISO)とダントロレン(DNT)を使用し,筋強直と循環変動に対し良好な結果を得たので報告する。症例1は,最初の6病日間に血管作動薬投与と硬膜外麻酔を行ったが収縮期血圧は153±29mmHg(mean±SD)とばらつきが大きく,循環変動を制御できなかった。第7病日よりISO吸入を行い,収縮期血圧を135±15mmHgに維持できた。DNTを第41病日より投与した結果,筋強直が軽減し,第51病日にICUを退室した。症例2はISO吸入を初期より行い,循環変動を制御したが,ISO離脱を図るごとに著明な循環変動と筋強直が再現した。第18病日からDNTを投与した結果,筋強直の改善に伴い第37病日にISO吸入から離脱ができ,第41病日にICUを退室した。ISOは初期の重症破傷風管理に極めて有効で,DNTは筋強直を改善し,ISOからの離脱を促進したと示唆される。

Protein kinase C zeta (PKC zeta), a member of the atypical PKC subgroup, is insensitive to Ca2+, diacylglycerol, and phorbol esters, but is activated by phospholipids such as phosphatidylinositol-3,4,5-triphosphate, a product of phosphatidylinositol 3-kinase (PI3-kinase). Here we show that PKC zeta translocates from the cytosol to the 1000 x g pellet (nuclear-myofibrillar) fraction during ischemia for 40 min in Langendorff-perfused rat hearts. In addition, immunohistochemical observation shows that ischemia induces the translocation of PKC zeta to the nucleus. The nuclear translocation during ischemia is inhibited in a dose-dependent manner by wortmannin (10(-9)-10(-7) M), an inhibitor of PI3-kinase.

We present a patient with myotonic dystrophy (MD) who was anesthetized with propofol using a target-controlled technique for electrophysiologic examination and cardiac catheter ablation. The patient became apneic unexpectedly at the same time when he fell asleep, with effect-site propofol concentration of 1.6 microg ml(-1). We had to insert a laryngeal mask airway (LMA), and mechanical ventilation was performed. The patient opened his eyes on verbal command at an effect-site concentration of 1.2 microg ml(-1) after the procedure. This concentration (1.2 microg ml(-1)) was slightly lower than our institutional average for adult male patients (1.5 +/- 0.2 microg ml(-1)). However, the time from the end of anesthesia to the patient's awakening was about 10 min. We considered that emergence from anesthesia was not delayed in this case. Careful titration of propofol by target-controlled infusion (TCI) enabled to evaluate the patient's sensitivity to propofol. We conclude that TCI of propofol was a useful anesthetic technique in the MD patient. Respiratory depression might occur in MD patients at low propofol concentrations. Precise control and titration over target propofol concentration is important in anesthetic management for MD patients.

To explore the spatial and temporal localization of PKC isoforms during ischemia, we quantified PKC isoforms in the subcellular fractions in perfused rat heart by immunoblotting using specific antibodies against PKC isoforms. PKCs-alpha and epsilon translocated from the 100000 x g supernatant (S, cytosolic) fraction to the 1000 x g pellet (PI, nucleus-myofibril) and the 1000-100000 x g pellet (P2, membrane) fractions during 5-40 min of ischemia. PKC-delta redistributed from the P2 to the S fraction. A 50-kDa fragment of PKC-alpha appeared during ischemia possibly through calpain action. Immunohistochemical observations showed the different localizations of PKC-alpha, delta, and epsilon in the myocytes. The PKC assay displayed high basal levels of Ca(2+)-independent PKC, the activation of Ca(2+)-dependent PKC in the P1 and P2 fractions, and the activation of Ca(2+)-independent PKC in the P1 fraction after 20 min of ischemia. These observations show that ischemia induces different patterns of translocation of the three PKC isoforms, suggesting differences in their roles.

We report three patients with a history of neuroleptic malignant syndrome for whom modified electroconvulsive therapy (m-ECT) was scheduled. Two patients suffered from schizophrenia, and one suffered from depression. Their symptoms, such as hyperthermia, consciousness disturbance, myotonus, tremor, sweating, and tachycardia, improved gradually with administration of dantrolene and fluid infusion. However, their psychotic state was exacerbated. Therefore, m-ECT was scheduled. When patients were restless at the hospital ward, they were sedated with propofol and transferred to the operating room. General anesthesia was induced with thiopental 2.5-5 mg x kg(-1). After loss of consciousness, vecuronium bromide 0.01 mg x kg(-1) followed by a dose of 0.1 mg x kg(-1) was administered and ventilation was assisted using a face mask and 100% oxygen. After the ECT stimulus, the patients were sedated with propofol until full recovery from muscle relaxation. Although anesthesia time (mean 38 min) was slightly longer (19 min) than in those anesthetized with thiopental and suxamethonium chloride, m-ECT was performed safely and effectively.

It has been speculated that the nerve root entry zone in the spinal cord, known as the Obersteiner-Redlich zone, may be more sensitive to large concentrations of local anesthetics administered intrathecally. However, there has been no morphological evidence for this. In the present study, we examined morphological changes of nerve fibers at the nerve root entry zone after administration of intrathecal tetracaine in rabbits. Rabbits were assigned to 4 groups (n = 6 in each) and received intrathecal 0.3 mL saline (control), or 1%, 2%, or 4% tetracaine. Neurological and histopathological assessments were performed 1 wk after the administration. Tetracaine 1% selectively injured the myelin sheaths made by oligodendrocytes at the nerve root entry zones of both ventral and dorsal roots, although neurological dysfunction could not be detected. With tetracaine 2% and 4%, histopathological damage extended to the dorsal funiculus, distal part of roots, and cauda equina and neurological dysfunction became apparent. These results demonstrate that the myelin sheaths made by oligodendrocytes at the nerve root entry zone are highly vulnerable to large concentrations of tetracaine given intrathecally.

We are developing an adjustment method of real-time computer graphics, to obtain effective ones which give audience various senses intended by producer, utilizing human sensibility technologically. Generally, production of real-time computer graphics needs much adjustment of various parameters, such as 3D object models/their motions/attributes/view angle/parallax etc., in order that the graphics gives audience superior effects as reality of materials, sense of experience and so on. And it is also known it costs much to adjust such various parameters by trial and error. A graphics producer often evaluates his graphics to improve it. For example, it may lack 'sense of speed' or be necessary to be given more 'sense of settle down,' to improve it. On the other hand, we can know how the parameters in computer graphics affect such senses by means of statistically analyzing several samples of computer graphics which provide different senses. We paid attention to these two facts, so that we designed an adjustment method of the parameters by inputting phases of sense into a computer. By the way of using this method, it becomes possible to adjust real-time computer graphics more effectively than by conventional way of trial and error.© (1997) COPYRIGHT SPIE--The International Society for Optical Engineering. Downloading of the abstract is permitted for personal use only.

In this paper, we describe an implementation method that enables users to real time control their avatars that is real and complex shaped in a 3D virtual world. We realized an avatar using quasi 3D models and moving picture, enabling movement and actions to be performed in real time according to user operations. This avatar has the following characteristics. 1) The avatar is highly precise. 2) Avatar actions can be controlled in real time. 3) The avatar has smooth actions. We also describe an evaluation of our implementation method. A prototype system consisting of avatars capable of performing walking action using a quasi 3D model comprised of five polygons and a virtual 3D shared space containing these avatars was created, and the effectiveness of this system was confirmed.

The serum levels of CA 125 and CA 19-9 were determined by an immunoradiometric assay employing the monoclonal antibody OC 125 and anti-CA 19-9 antibody in 88 patients with ovarian carcinoma. When a cut-off value of CA 125 was set below 35 U/ml in the control group, serum elevated levels of CA 125 were found in 86.7% of the patients with surgically demonstrable ovarian serous cystadenocarcinoma, in 100% (4/4 cases) of clear-cell carcinoma, in 50% (2/4 cases) of endometrioid carcinoma, in 100% (5/5 cases) of undifferentiated carcinoma, and in 80% of the recurrent cases. Using a cut-off value of 37 U/ml, serum elevated levels of CA 19-9 were detected in 68.2% of mucinous cystadenocarcinoma, in 28.9% of serous cystadenocarcinoma, in 75% (3/4 cases) of metastatic ovarian carcinoma, and in 37.5% of the recurrent cases. A statistical analysis of the combination assay using CA 125, CA 19–9, tissue polypeptide antigen (TPA), immunosuppressive acidic protein (IAP), ferritin and CEA was carried out by multivariate method (discriminatory analysis) in 45 patients with ovarian carcinoma and 50 healthy subjects. As a result before treatment, positive rates of a single tumor marker were 79.7% with CA 125, 42.7% with CA-19-9, 73.1% with IAP, 61.7% with TPA, 64.3% with ferritin and 25.4% with CEA, respectively. A combination assay of these markers was useful for detecting identification of ovarian carcinoma, by which it gave a higher accuracy of ovarian cancer detection.