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Hydrogen peroxide is an aerobic metabolite playing a central role in redox signaling and oxidative stress. H

In this study, a hydrogen–air premixed flame in a partially tapered swirl burner in which a stable counterflow of unburned and burned gases is expected to be formed, was investigated. The experimental results indicate the formation of almost steady flames at equivalence ratios of as lean as 0.084, and the resulting ultra-lean flames in the swirling flow had a comet shape. Furthermore, the flame was numerically reproduced, and the mechanisms behind the phenomenon were identified by checking the balance among the chemical enthalpy through diffusion, heat flux by conduction, and transport of these parameters by convection. It was determined that the region around the tip of the flame head was almost dominated only by diffusion and heat conduction similar to a flame ball, but its formation mechanism was found to be essentially different from that of a flame ball because the comet-like flame can be numerically reproduced even without a radiative heat loss, in contrast to a flame ball.

Circadian clock genes regulate energy metabolism partly through neurotrophins in the body. The low affinity neurotrophin receptor p75NTR is a clock component directly regulated by the transcriptional factor Clock:Bmal1 complex. Brain-derived neurotrophic factor (BDNF) is expressed in the brain and plays a key role in coordinating metabolic interactions between neurons and astrocytes. BDNF transduces signals through TrkB and p75NTR receptors. This review highlights a novel molecular mechanism by which BDNF via circadian control of p75NTR leads to daily resetting of glucose and glycogen metabolism in brain astrocytes to accommodate their functional interaction with neurons. Astrocytes store glycogen as an energy reservoir to provide active neurons with the glycolytic metabolite lactate. Astrocytes predominantly express the truncated receptor TrkB.T1 which lacks an intracellular receptor tyrosine kinase domain. TrkB.T1 retains the capacity to regulate cell morphology through regulation of Rho GTPases. In contrast, p75NTR mediates generation of the bioactive lipid ceramide upon stimulation with BDNF and inhibits PKA activation. As ceramide directly activates PKCζ, we discuss the importance of the TrkB.T1-p75NTR-ceramide-PKCζ signaling axis in the stimulation of glycogen and lipid synthesis and activation of RhoA. Ceramide-PKCζ-casein kinase 2 signaling activates Nrf2 to support oxidative phosphorylation via upregulation of antioxidant enzymes. In the absence of p75NTR, TrkB.T1 functionally interacts with adenosine A2AR and dopamine D1R receptors to enhance cAMP-PKA signaling and activate Rac1 and NF-κB c-Rel, favoring glycogen hydrolysis, gluconeogenesis and aerobic glycolysis. Thus, diurnal changes in p75NTR levels in astrocytes resets energy metabolism via BDNF to accommodate their metabolic interaction with neurons.

Progressive damages in the open-hole compression (OHC) tests of composite laminates were experimentally and numerically studied. In the experiment, the failure mechanisms were investigated via in situ microscopy observation, digital image correlation, X-ray radiography, and X-ray computed tomography. Three layups were tested to examine the dependence of progressive damages on the layups. Additionally, numerical simulation was conducted to comprehensively examine the failure mechanisms. In the numerical studies, the simulation scheme, considering the plasticity, kink-band failure, multiple intra-laminar cracks, and delamination, was developed. From the experiment and simulation, it is clarified that the kink-band is initiated and propagated by the combined stress states consisting of longitudinal compression and in-plane shear around the intra-laminar cracks. Therefore, for the high-fidelity OHC simulation in various layups, it is necessary to capture the interaction between kink-band and intra-laminar cracks by considering the combined stress state in the kink-band failure criteria and modeling the multiple intra-laminar cracks.

Background UVB radiation is the main source of sunburn and skin cancers. Apoptosis eliminates photodamaged cells, and is thus important for preventing epidermal carcinogenesis. The cytoplasmic regulatory protein p62/A170/sequestosome 1 (p62) molecule is involved in a variety of cellular and signaling pathways. p62 is known to be and important in autophagy, but its role in UVB-induced apoptosis remains to be clarified. Objective To investigate the role of p62 against UVB-induced apoptotic changes, using mouse embryonic fibroblasts (MEFs) derived from p62 homozygous knockout (p62 −/− ) mice. Methods p62 −/− and wild-type (p62 +/+ ) mice and MEFs were subjected to UVB irradiation, and the resultant apoptosis was analyzed using flow cytometry, quantitative real-time PCR, and western blots. Results Apoptosis was decreased in the p62 −/− MEFs compared to p62 +/+ MEFs in response to UVB treatment. Compared with p62 +/+ MEFs, p62 −/− MEFs expressed significantly more Bcl-2 and less Bax, and showed increased Src and Stat3 phosphorylation. Our results show that p62 regulates apoptotic pathways by modifying critical signaling intermediates such as Src and Stat3. Conclusion p62 reduces UVB-induced apoptosis by modulating intrinsic apoptotic signaling through Src phosphorylation.

This study conducts experimental and numerical studies on the progressive damage occurring during the drilling of composite laminates. In particular, this work focuses on push-out delamination, which occurs at the interface around the drill-exit and is the most critical damage suffered during the drilling process. To investigate the damage progression mechanisms, penetration and interruption drilling tests are performed on composite laminate consisting of quasi-isotropic CFRP plies and fabric GFRP ply (bottom side). After drilling tests, the damage evolution is evaluated using X-ray computed tomography and optical microscopy. Based on the experimental results, a simplified simulation model is established, and damage progression simulation is performed using an explicit dynamic finite element method. The results show that the bending deformation in the bottom two plies triggers the propagation of push-out delamination. Therefore, the extent of delamination is significantly affected by the thickness and the material properties of the bottom plies.

BDNF is the major neurotrophin in the brain playing a key role in the metabolic cooperation between astrocytes and neurons. BDNF transduce signals through high affinity TrkB receptors and the low affinity p75 receptor (p75NTR). Stimulation of p75NTR activates neutral sphingomyelinase to generate ceramide. As low levels of ceramide can activate atypical protein kinase C ζ (PKCζ), which phosphorylates and activates casein kinase 2 (CK2), we recently proposed that neurotrophins can activate p75NTR-ceramide-PKCζ-CK2 signaling pathway. Subsequently, CK2 directly phosphorylates and stabilizes/activates Nrf2. However, the receptor tyrosine kinase activity of full length TrkB (TrkB.FL) inhibits p75NTR-mediated ceramide generation. In contrast, the truncated form of TrkB (TrkB.T1), which lacks intracellular tyrosine kinase domain, supports p75NTR-mediated ceramide signaling. Astrocytes predominantly express TrkB.T1, but neurons express both TrkB.T1 and TrkB.FL. Notably, neurons increase the ratio of TrkB.T1 to TrkB.FL levels when they are stimulated. As p75NTR expression is controlled by the circadian rhythm, we discuss the significance of the time- and activity-dependent BDNF-TrkB.T1-p75NTR-Nrf2 signaling pathway for the metabolic interaction between astrocytes and neurons. [JSPS, BHF]

Sequestosome1/p62 (SQSTM1) is an oxidative stress-inducible protein regulated by the redox-sensitive transcription factor Nrf2. It is not an antioxidant but known as a multifunctional regulator of cell signaling with an ability to modulate targeted or selective degradation of proteins through autophagy. SQSTM1 implements these functions through physical interactions with different types of proteins including atypical PKCs, nonreceptor-type tyrosine kinase p56(Lck) (Lck), polyubiquitin, and autophagosomal factor LC3. One of the notable physiological functions of SQSTM1 is the regulation of redox-sensitive voltage-gated potassium (Kv) channels which are composed of α and β subunits: (Kvα)4 (Kvβ)4. Previous studies have established that SQSTM1 scaffolds PKCζ, enhancing phosphorylation of Kvβ which induces inhibition of pulmonary arterial Kv1.5 channels under acute hypoxia. Recent studies reveal that Lck indirectly interacts with Kv1.3 α subunits and plays a key role in acute hypoxia-induced Kv1.3 channel inhibition in T lymphocytes. Kv1.3 channels provide a signaling platform to modulate the migration and proliferation of arterial smooth muscle cells and activation of T lymphocytes, and hence have been recognized as a therapeutic target for treatment of restenosis and autoimmune diseases. In this review, we focus on the functional interactions of SQSTM1 with Kv channels through two key partners aPKCs and Lck. Furthermore, we provide molecular insights into the functions of SQSTM1 in suppression of proliferation of arterial smooth muscle cells and neointimal hyperplasia following carotid artery ligation, in T lymphocyte differentiation and activation, and in NGF-induced neurite outgrowth in PC12 cells.

Circadian clock genes regulate energy metabolism partly through neurotrophins. The low affinity neurotrophin receptor p75NTR is a clock component directly regulated by the transcriptional factor Clock:Bmal1 complex. Brain-derived neurotrophic factor (BDNF) is expressed in brain and plays a key role in coordinating metabolic interactions between neurons and astrocytes. BDNF transduces signals through TrkB and p75NTR receptors, and the circadian control of p75NTR leads to daily resetting of glucose and glycogen metabolism in astrocytes to accommodate their functional interaction with neurons. Recent studies show that the circadian clock controls Nrf2-regulated antioxidant defense genes in mouse tissues. The protein level of Nrf2 in mouse lungs at early light phase is about 5-fold higher than that in the early dark phase. The Nrf2 gene has a E-box element and the Clock:Bmal1 complex stimulates transcription. However, the differences in the mRNA levels during the day are at most 1.7-fold, suggesting post-transcriptional regulation of Nrf2 protein may be much more important for the circadian control of Nrf2 activation. We propose a novel hypothesis that p75NTR-mediated signaling activates/stabilizes Nrf2 during light/rest phase in mouse brain astrocytes. Notably, stimulation of BDNF induces production of a lipid signal molecule ceramide through the p75NTR-neutral sphingomyelinase axis. Although high levels of ceramide are cytotoxic, physiological levels of ceramide activates PKCζ. An important target of PKCζ is casein kinase 2 (CK2), which plays a critical role in the regulation of circadian rhythm. As CK2 directly phosphorylates and stabilizes Nrf2, we propose that a p75NTR-ceramide-PKCζ-CK2 signaling pathway activates Nrf2, which in turn supports mitochondrial oxidative phosphorylation required for glycogenesis and lipogenesis in astrocytes.

This study evaluated the protective role of p38 mitogen-activated protein kinase (p38 MAPK) inhibitors and sequestosome 1 (Sqstm1/A170/p62), a stress-induced signal modulator, in acoustic injury of the cochlea in mice. Two weeks after the exposure of mice to acoustic stress, threshold shifts of the auditory brainstem response (ABR) from the pre-exposure level and hair cell loss were evaluated. The activation of p38 MAPK was observed in cochlea by immunostaining 4 h after acoustic stress. To examine the role of p38 MAPK in tissue injury, its inhibitors were i.p. injected into male wild-type C57BL mice before the acoustic overexposure. The inhibitors SB202190 and SB203580 but not the inactive analogue SB202474 dose-dependently decreased the auditory threshold shift and outer hair cell loss induced by acoustic overexposure, suggesting the involvement of p38 MAPK in ototoxicity. We found that acoustic overexposure induced the up-regulation of Sqstm1 mRNA expression in the cochlea of wild-type mice and that SQSTM1-deficient mice exhibited an enhanced ABR threshold shift and hair cell loss, suggesting a role of SQSTM1 in the protection of tissue from acoustic stress.

application/pdf, The anticancer agent cis-diamminedichloroplatinum (cisplatin) is a first-line chemotherapeutic agent for oral cancer. Cell exposure to cisplatin is associated with increased oxidative stress and post-translational changes in components of apoptosis pathways, including p38 Mitogen-activated protein kinase (MAPK), c-Jun-NH2-kinase (JNK), and extracellular signal-regulated kinase (ERK). Peroxiredoxin (Prx) I is an oxidative stress-inducible protein expressed in many tissues and important for reducing reactive oxygen species in vivo; however, whether Prx I helps protect cells from cisplatin injury is unknown. In this report, we examined the effects of Prx I on cell sensitivity to cisplatin-induced apoptosis. Mouse embryo fibroblasts (MEFs) derived from Prx I-deficient mice showed increased cisplatin-induced apoptosis compared with wild-type MEFs. Cisplatin treatment also led to increased activation of p38 MAPK and JNK, and reduced ERK phosphorylation in Prx I-deficient MEFs compared with wild-type MEFs. Furthermore, JNK- and ERK-specific inhibitors protected the Prx I-deficient MEFs from cisplatin-induced apoptosis, but Prx I-deficient MEFs remained more sensitive than wild-type MEFs when treated with a p38 MAPK-specific inhibitor. These findings indicate that Prx I modulates the cisplatin-evoked activation of MAPKs that lead to apoptosis, and Prx I may thus represent a useful target as a protective therapy against cisplatin cytotoxicity.

The transcription factor Nrf2 is a key regulator for hepatic induction of detoxifying enzymes, antioxidative stress genes and Mrp efflux transporters. We aimed to investigate whether Nrf2 activation counteracts liver injury associated with cholestasis. The role of Nrf2 activation in counteracting cholestatic liver injury was studied using a bile duct-ligation (BDL) model of Keap1 gene-knockdown (Keap1-kd) mice that represent the sustained activation of Nrf2 in the liver. Upon Nrf2 activation, Keap1-kd mice showed large increases in Mrp efflux transporters, detoxifying enzymes and antioxidative stress genes in the livers. After BDL, the number of hepatic parenchymal necrosis and the reactive oxygen species content were significantly smaller in the livers of the Keap1-kd mice than in those of the WT mice. Moreover, the increase in serum bilirubin levels was attenuated in the Keap1-kd mice. In conclusion, the results suggest a hepatoprotective role of sustained Nrf2 activation against liver injury associated with cholestasis.

Peroxiredoxin (Prx) I, a ubiquitous antioxidant enzyme, is known to protect against inflammation; however, its role in the allergic inflammation remains unidentified. We determined whether intristic Prx I protects against allergic asthma traits using Prx-I knockout (-/-) mice. Prx I (-/-) and wild-type (WT) mice were immunized with ovalbumin (OVA) plus aluminum potassium sulfate (Alum: Th2 adjuvant) and subsequently challenged with OVA. Twenty-four hours after the last OVA challenge, leukocyte influx including eosinophils into bronchoalveolar lavage fluid was significantly greater in Prx I (-/-) mice compared to that in WT mice. On the other hand, when these mice were immunized with OVA+complete Freund's adjuvant (Th1 adjuvant), opposite phenomenon was observed. In the presence of OVA/Alum, peribronchial inflammatory leukocyte infiltration, cholinergic airway resistance, and the lung expression of interleukin (IL)-2 were significantly greater and that of interferon-gamma was significantly lesser in Prx I (-/-) than in WT mice. In vitro, OVA/Alum-sensitized Prx I (-/-) T cells proliferated more profoundly than WT T cells when they were cocultured with syngeneic bone marrow-generated dendritic cells. These results indicate that endogenous Prx I protects against allergen-related Th2-type airway inflammation and hyperresponsiveness, at least partly, via the suppression of the lung expression of IL-2 and regulation of the Th1/Th2 balance in addition to its antioxidative properties. Furthermore, Prx I can inhibit allergen-specific T-cell proliferation through immunological synapse. Our findings implicate an alternative therapeutic value of Prx I in the treatment of Th2-skewed allergic airway inflammatory diseases such as atopic asthma.

We adopted antibiotic (Ab) protocols for managing surgical site infections in children and assessed their effectiveness.We used our protocols on 1313 children between 2004 and 2005. All wounds were monitored for 30 days and classified as clean, clean-contaminated, contaminated, or dirty-infected. Infections were defined as superficial, deep, or organ/space. A retrospective study involving 721 children who had surgery in 2003 was also performed. Chi2 statistical analysis was performed.Postprotocol, all Abs were administered accurately by anesthesiologists and infections developed in only 22 cases (1.7%): 0.2% (clean), 2.6% (clean-contaminated), 5.8% (contaminated), and 20.8% (dirty-infected), respectively; 21 were superficial or deep and 1 was organ/space. Age at surgery and sex did not influence incidence, neither did length of surgery for clean-contaminated, contaminated, and dirty-infected wounds; clean wounds were excluded because all surgery was minor. Overall, incidence of infections was 1.2% for elective surgery and 4.5% for emergency surgery (P.01). Preprotocol, only 67% had Ab and infections developed in 27 cases (3.7%), which is significantly higher than in postprotocol (P.01).Accurate administration of Ab and careful supervision by an infection control team appear to be effective for preventing wound infections in children.

According to studies using animal models of multiple sclerosis (MS), the pathogenesis of Interleukin-1 (IL-1) and the effects of the IL-1 inhibition therapy for MS have been clarified. In both MS and neuromyelitis optica, systemic IL-1 inhibition will be a therapeutic target. However, studies to clarify whether maintenance therapy for MS with IL-1 inhibitor will prevent the next relapse will be needed, because IL-1ra gene therapy after disease onset was not effective in the animal study.

We have previously reported that antioxidant response element (ARE)-regulated genes, such as heme oxygenase 1 (HO-1), sequestosome 1 (SQSTM1), and NAD(P)H quinone oxidoreductase 1 (NQO1), are induced in human umbilical vein endothelial cells (HUVEC) upon exposure to laminar shear stress. In the present study, we have confirmed a critical role for NF-E2-related factor 2 (Nrf2) in the induction of gene expression in HUVEC exposed to laminar shear stress. Although the mRNA levels of Nrf2 were unchanged during exposure to shear stress, the protein levels of Nrf2 were markedly increased. Small interfering RNA (SiRNA) against Nrf2 significantly attenuated the expression of Nrf2-regulated genes such as HO-1, SQSTM1, NQO1, glutamate-cysteine ligase modifier subunit (GCLM), and ferritin heavy chain. Nrf2 was rapidly degraded in cells treated with cycloheximide under static conditions, but shear stress decreased the rate of Nrf2 degradation. Incubation with the thiol antioxidant N-acetylcysteine strongly inhibited both the Nrf2 accumulation and the expression of Nrf2-regulated genes such as HO-1, GCLM, and SQSTM1. Nitric oxide (NO) production was increased with the strength of shear stress but neither the inhibitor of endothelial NO synthase (eNOS) nor the siRNA against eNOS affected the expression of Nrf2-regulated genes. A xanthine oxidase inhibitor oxypurinol and the flavoprotein inhibitor diphenyleneiodonium, which inhibits NAD(P)H oxidase and mitochondrial respiratory chain, markedly suppressed the expression of these genes. Moreover, diphenylpyrenlphosphine, a reducing compound of lipid hydroperoxides, also significantly suppressed Nrf2-regulated gene expression. Taken together, these findings suggest that shear stress stabilizes Nrf2 protein via the lipid peroxidation elicited by xanthine oxidase and flavoprotein mediated generation of superoxide, resulting in gene induction by the Nrf2-ARE signaling pathway.

Posterior-anterior body weight shift during stance phase of human overground locomotion was investigated by recording sole-floor reaction force from five anatomically discrete points with strain gauge transducers of 14 mm diameter attached firmly to the sole of bare foot. At first the subject was asked to walk straight on the laboratory floor at his/her preferred velocity. Then the subject was asked to walk curved path of about 1 m radius. For kicking off the body at the end of stance phase, sole-floor reaction force from 3rd metatarsal was stronger than 1st metatarsal or 5th metatarsal during the straight walking, thus body weight shift is represented from heel to 3rd metatarsal line. When walking along a curved path, two types of strategies were recognized; a group of subjects walked leaning to inner leading foot during stance period as judged by stronger forces recorded from 5th metatarsal combined with stronger force from 1st metatarsal of outer trailing foot. Another group of subjects showed almost the same patterns either in the straight and curved walking, suggesting the subjects changed direction of the foot during the immediately previous swing phase to the tangent direction of the curve and placed the foot without leaning the body weight to either direction. Hemiplegic patients showed strikingly different distribution of sole-floor reaction forces from the five points; strongest forces were recorded from 3rd and 5th metatarsals combined with reduced reaction force from heel, therefore characteristic y-vector patterns were observed.

Right and left balance during human locomotion has been estimated by the distance between locations of the sequential right and left heel-strikes, or step width. During the stance phase of human locomotion one leg maintains medial-lateral balance for the progression. We focused our attention on this point, and medial-lateral balance during straight-ahead and circular walking was investigated by recording sole-floor reaction force from five anatomically discrete points of human sole; calcaneus, 1st, 3rd, 5th metatarsals and great toe. Forces from these points were recorded during straight walking and circular walking. Medial-lateral balance was obtained by subtracting force at 5th metatarsal from force at 1st metatarsal (x-axis vector). The foot takes off the floor from medial balance in most steps, although in some steps the foot takes off from lateral balance at slower walking speed at 2 km/h or 4 km/h, showing variable patterns of x-axis vector. At faster walking speed at 6 km/h or 8 km/h body weight shifted to 1st metatarsal before taking off the floor. During circular walking body weight shift to 1st metatarsal in the outer foot, and to 5th metatarsal in the inner foot in most cases.

A 59-year-old Japanese woman was referred to our hospital due to upper abdominal pain. At the age of 44, she was diagnosed with a congenital choledochal cyst, Todani's type Ic. She then underwent bypass operation with end-to-side choledochojejunostomy with Roux-en-Y technique as well as cholecystectomy. Magnetic resonance cholangiopancreatography revealed an ‘oval’ shaped cystic lesion with a maximal diameter of 25 mm, which had been ‘spindle’ shaped with a maximal diameter of 18 mm, 15 years ago. It also showed an anomalous pancreaticobiliary ductal union. In addition, a complete absence of the dorsal primordia of pancreas was revealed by magnetic resonance image and computed tomography scan. The patient underwent the surgical exploration for the resection of the ‘oval’ shaped cystic lesion. Haematoxylin and eosin staining of the thin section of the resected cyst showed a compact spindle cell pattern which was compatible with schwannoma, Antoni type A, which was confirmed by immunocytochemical technique. We present a very interesting case showing choledochal cyst, anomalous pancreaticobiliary ductal union, total agenesis of the dorsal pancreas and late-development of bile duct schwannoma in the remnant choledochal cyst.

Expression of mRNA protein tyrosine phosphatases (PTPs) was surveyed in an esophageal cancer cell line by RT-PCR using degenerate primers. The mRNAs for eight kinds of PTPs were expressed in the cell line. We examined mRNA expression of these PTPs in 12 cases of esophageal cancer by Northern analysis. Significant signals were obtained for three kinds of PTPs, PTP1B, PTPH1, and PTPD1. The magnitude of expression of each PTP was measured as the ratio of the signal intensity of each PTP to that of a control gene (NADPH), and the ratio was then compared to normal mucosa around the cancer lesion. Among the three kinds of PTPs, the expression of PTP1B mRNA was significantly depressed in cancer lesions compared with that in the surrounding normal mucosa. In contrast, the expression of PTPH1 mRNA was significantly increased in cancer lesions compared with that in normal mucosa. PTPD1 did not show any significant trend in comparisons of cancer and surrounding normal mucosa. The results suggest that PTP1B and PTPH1 are engaged in opposing signaling pathways, the tumor-suppressive and tumor-promoting pathways, respectively, in esophageal carcinogenesis.

Summary We immunohistologically investigated 76 cases of primary colorectal cancer and 13 cases of adenoma to clarify the relationship of MHC class 11 expression with the grade of differentiation, the density of tumor-infiltrating lymphocytes, and the incidence of metastasis to lymph nodes. MHC class II expression was mostly negative in normal colonic epithelium. In contrast, 32 out of 76 cases (42%) of cancer and five out of 13 cases (38%) of adenoma were positive for MHC class II. MHC class II expression was higher in well-differentiated than in poorly differentiated adenocarcinoma. The density of infiltrating lymphocytes was higher in cancer than in the normal mucosa, and higher in MHC class II-positive tissues than in negative lesions. The incidences of lymphatic invasion and cancer metastasis to lymph nodes were definitely higher in MHC class IInegative cancers than in MHC class II-positive cancers. MHC class II was rarely expressed in metastatic cancer cells of lymph nodes. These results indicated that the loss of MHC class II is correlated with the incidence of metastasis to regional lymph nodes.

Koshikamide A1, a new cytotoxic linear peptide, was isolated from a marine sponge, Theonella sp. Its structure was elucidated by spectroscopic and chemical methods.

Common chickweed ( Stellaria media Vill.) is one of the major weeds in upland and orchard in Japan and has been known to be a species poorly controlled by diphenyl ether herbicides. Laboratory experiments were conducted to determine the physiological basis of the plant's tolerance to the diphenyl ether herbicide oxyfluorfen (2-chloro-4-trifluoromethylphenyl 3-ethoxy-4-nitrophenyl ether). Uptake, translocation, and metabolism of the herbicide, sensitivity of the action site, porphyrin accumulation, and tolerance to singlet oxygen in common chickweed were compared with slender amaranth ( Amaranthus viridis ) and large crabgrass ( Digitaria adscendens ), oxyfluorfen-sensitive species. Common chickweed showed a little visible herbicide injury to 10 μM of sprayed oxyfluorfen, while the herbicide significantly reduced the fresh weight of large crabgrass and slender amaranth at 1 μM. Uptake of 14 C following [ 14 C]oxyfluorfen application to the adaxial surface of the second leaf for 2 h was similar for common chickweed and large crabgrass, although the initial rate was greater in large crabgrass. No translocation of the herbicide out of the treated leaf was observed in either species. The major part of absorbed 14 C was identified as unmetabolized oxyfluorfen in common chickweed and large crabgrass 24 h after application. The herbicide caused protoporphyrin IX accumulation in slender amaranth and large crabgrass. In contrast, no accumulation of the photosensitizing tetrapyrrole was observed in common chickweed. When excised leaf disks of slender amaranth and large crabgrass were treated with the herbicide, the porphyrin accumulation occurred faster than in intact plants. However, no accumulation was detected in leaf disks of common chickweed. Furthermore, vacuum infiltration of oxyfluorfen solution into the leaf disks of common chickweed did not promote the porphyrin accumulation. Protoporphyrinogen oxidase, the target enzyme of the herbicide, in common chickweed was inhibited by oxyfluorfen in vitro . The plant was also more tolerant to the singlet oxygen generating agent, rose bengal, than the susceptible species. However, tolerance of common chickweed to oxyfluorfen is considered to be due mainly to the mechanism which prevents protoporphyrin IX accumulation.

Osteolysis associated with artificial joint arthroplasty seems to be the result of particles of wear debris (from ultra-high molecular weight polyethylene (UHMWPE), polymethylmethacrylate (PMMA), and metals), causing a macrophage response, Silicon particles, as residual contaminants embedded in the surface of both textured metal implants and polyethylene sockets, may be a factor in osteolysis. We present the case of a 57-year-old woman who had massive and aggressive osteolysis. The osteolytic lesion was isolated in the greater trochanter region 5 years after she had had primary cementless total hip arthroplasty (Cobalt-chromium alloy). There were no signs of mechanical loosening, but she experienced moderate pain. Under a polarized microscope and scanning electron micrography, a biopsied specimen from the osteolytic lesion revealed conglomerates of UHMWPE particles of various sizes between proliferated synovium-like cells. Quantative energy-dispersive X-ray analysis focused on the conglomerates of UHMPWE particles demonstrated a marked presence of silicon. Although the definitive causative factor for a the osteolysis was regarded as a foreign-body reaction induced by UHMWPE particles, the presence of silicon was interesting in terms of the pathogenesis of osteolysis associated with artificial joint surgery.

Strain gauge transducers were firmly attached to five points of the human sole: calcaneus, 1st, 3rd, and 5th metatarsals and great toe. Forces from these five points were recorded during treadmill walking at different speeds. With this method it is possible to obtain data of several dozen steps successively. Lateral-medial force change (x-vector) during progression was obtained from the 5th and 1st metatarsals and posterior-anterior force change (y-vector) was obtained from the calcaneus and 3rd metatarsal. Lateral balance and medial balance were differentiated in x-vector and rearfoot phase and forefoot phase were distinguished in y-vector. The percentage of the forefoot phase among the stance period shows a linear increase with speed of progression. It was concluded that the phase of body sway forward is regulated by walking speeds.

Stimulation of the dorsal part of the fastigial nucleus in macaques is known to evoke ipsilateral saccades, while those of the ventral part produce contralateral saccades. It was found that stimulation of the transitional zone moved the visual axis (eyes) to converge at an area (focus) in the oculomotor range, regardless of the initial eye position. These saccades were designated as ‘converging saccades’. Converging saccades were directed to the focus, but the eyes did not attain the focus in one motion. Only the repetition of stimuli brought the eyes near the focus. When stimulation is applied to the transitional zone at progressively more ventral sites, the focus gradually shifted, starting from the ipsilateral hemifield to the contralateral hemifield by taking various routes.