A phenomenology of intercultural communication /

The present dissertation has two major purposes. The first is to examine the origin of intercultural communication as an independent academic field cultivated in the US. In order to carry out this task, this study employs Edmund Husserl's archaeology as a method. In short, this study unveils intercultural communication has developed as a manifestation of Western ideologies (e.g., individualism, pragmatism, etc.). The second objective, on the other hand, is to examine the necessary conditions which constitute the phenomenon of intercultural communication we experience in reality. Eidetic analysis is employed as an appropriate method for accomplishing this objective. The present eidetic analysis elucidates that differences in logics and styles are two necessary conditions which constitute a phenomenon of intercultural communication. This study suggests intercultural communication is not a pre-determined fixed phenomenon, but a unique place where different logics and different styles meet together. It is a manifestation of basic human similarities and meaningful human diversity. This dissertation also indicates latency (i.e., latent presuppositions, latent topics, latent methods, and latent theory, etc.) in the field of intercultural communication in the end

Reactive Mechanism of Cognitive Control System

The prefrontal cortex (PFC) is thought to modulate the neural network state in favor of the processing of task-relevant sensory information prior to the presentation of sensory stimuli. However, this proactive control mechanism cannot always optimize the network state because of intrinsic fluctuation of neural activity upon arrival of sensory information. In the present study, we have investigated an additional control mechanism, in which the control process to regulate the behavior is adjusted to the trial-by-trial fluctuation in neural representations of sensory information. We asked normal human subjects to perform a variant of the Stroop task. Using functional magnetic resonance imaging, we isolated cognitive conflict at a sensory processing stage on a single-trial basis by calculating the difference in activation between task-relevant and task-irrelevant sensory areas. Activation in the dorsolateral PFC (DLPFC) covaried with the neural estimate of sensory conflict only on incongruent trials. Also, the coupling between the DLPFC and anterior cingulate cortex (ACC) was tighter on high-sensory conflict trials with fast response. The results suggest that although detection of sensory conflict is achieved by the DLPFC, online behavioral adjustment is achieved by interactive mechanisms between the DLPFC and AC

Reactive Oxygen Species as Signaling Molecules in Neutrophil Chemotaxis

Neutrophil chemotaxis is a critical component in innate immunity. Recently, using a small-molecule functional screening, we identified NADPH-oxidase-dependent Reactive Oxygen Species (ROS) as key regulators of neutrophil chemotactic migration. Neutrophils depleted of ROS form more frequent multiple pseudopodia and lost their directionality as they migrate up a chemoattractant concentration gradient. Here, we further studied the role of ROS in neutrophil chemotaxis and found that multiple pseudopodia formation induced by NADPH inhibitor diphenyleneiodonium chloride (DPI) was more prominent in relatively shallow chemoattractant gradient. It was reported that, in shallow chemoattractant gradients, new pseudopods are usually generated when existing ones bifurcate. Directional sensing is mediated by maintaining the most accurate existing pseudopod, and destroying pseudopods facing the wrong direction by actin depolymerization. We propose that NADPH-mediated ROS production may be critical for disruption of misoriented pseudopods in chemotaxing neutrophils. Thus, inhibition of ROS production will lead to formation of multiple pseudopodia

Phosphoinositide Lipid Posphatase SHIP1 and PTEN Coordinate to Regulate Cell Migration and Adhesion

The second messenger phosphatidylinositol$(3,4,5)P_3 (PtdIns(3,4,5)P_3)$ is formed by stimulation of various receptors, including G protein–coupled receptors and integrins. The lipid phosphatases PTEN and SHIP1 are critical in regulating the level of PtdIns$(3,4,5)P_3$ during chemotaxis. Observations that loss of PTEN had minor and loss of SHIP1 resulted in a severe chemotaxis defect in neutrophils led to the belief that SHIP1 rather than PTEN acts as a predominant phospholipid phosphatase in establishing a PtdIns$(3,4,5)P_3$ compass. In this study, we show that SHIP1 regulates PtdIns$(3,4,5)P_3$ production in response to cell adhesion and plays a limited role when cells are in suspension. $SHIP1^{−/−}$ neutrophils lose their polarity upon cell adhesion and are extremely adherent, which impairs chemotaxis. However, chemo­taxis can be restored by reducing adhesion. Loss of SHIP1 elevates Akt activation following cell adhesion due to increased PtdIns$(3,4,5)P_3$ production. From our observations, we conclude that SHIP1 prevents formation of top-down PtdIns$(3,4,5)P_3$ polarity to facilitate proper cell attachment and detachment during chemotaxis

Criticality of plasma membrane lipids reflects activation state of macrophage cells.

Signalling is of particular importance in immune cells, and upstream in the signalling pathway many membrane receptors are functional only as complexes, co-locating with particular lipid species. Work over the last 15 years has shown that plasma membrane lipid composition is close to a critical point of phase separation, with evidence that cells adapt their composition in ways that alter the proximity to this thermodynamic point. Macrophage cells are a key component of the innate immune system, are responsive to infections and regulate the local state of inflammation. We investigate changes in the plasma membrane's proximity to the critical point as a response to stimulation by various pro- and anti-inflammatory agents. Pro-inflammatory (interferon γ, Kdo 2-Lipid A, lipopolysaccharide) perturbations induce an increase in the transition temperature of giant plasma membrane vesicles; anti-inflammatory interleukin 4 has the opposite effect. These changes recapitulate complex plasma membrane composition changes, and are consistent with lipid criticality playing a master regulatory role: being closer to critical conditions increases membrane protein activity.Research was funded by EUMarie Curie action ITN TransPol (EC), NIH-R01GM110052 and NSF10 MCB1552439 (SLV), Cambridge University Commonwealth, European and International Trust 11 (JS) ITN BioPol (PC), and Wellcome Trust Investigator grant 08045/Z/15/Z (CEB)

Activation of Toll-like receptors nucleates assembly of the MyDDosome signaling hub.

Infection and tissue damage induces assembly of supramolecular organizing centres (SMOCs)), such as the Toll-like receptor (TLR) MyDDosome, to co-ordinate inflammatory signaling. SMOC assembly is thought to drive digital all-or-none responses, yet TLR activation by diverse microbes induces anything from mild to severe inflammation. Using single-molecule imaging of TLR4-MyDDosome signaling in living macrophages, we find that MyDDosomes assemble within minutes of TLR4 stimulation. TLR4/MD2 activation leads only to formation of TLR4/MD2 heterotetramers, but not oligomers, suggesting a stoichiometric mismatch between activated receptors and MyDDosomes. The strength of TLR4 signalling depends not only on the number and size of MyDDosomes formed but also how quickly these structures assemble. Activated TLR4, therefore, acts transiently nucleating assembly of MyDDosomes, a process that is uncoupled from receptor activation. These data explain how the oncogenic mutation of MyD88 (L265P) assembles MyDDosomes in the absence of receptor activation to cause constitutive activation of pro-survival NF-κB signalling

Effects of continuous passive motion on the expression of membrane type 1-matrix metalloproteinase in rat immobilized muscles

We examined the effects of continuous passive motion（ CPM） on membrane type 1-matrix metalloproteinase（ MT1-MMP） expression in rat immobilized muscles. Eight-week-old male Wister rats were used for each of two trials, one with 2 weeks, and another one with 4 weeks of immobilization with/without CPM. In each trial, rats were immobilized（ immobilization group）, and immobilized and simultaneously given CPM （CPM group）. The soleus muscle of each rat was evaluated by gelatin zymography, western blotting and reverse transcription-polymerase chain reaction（ RT-PCR）. Gelatin zymography revealed a greater level of gelatinase activity in the extract of the muscles of the immobilization group than in those of the control and CPM group. The expressions of matrix metalloproteinase 2 （MMP-2） and MT1-MMP mRNA in the muscle extract of the immobilization group were also greater than those in the control and CPM group. Our results suggested that joint immobilization induces expression of MT1-MMP, a cleavage enzyme of MMP-2 in muscles, resulting in muscular degeneration, and that CPM can prevent these changes

IL-6 Impairs Vaccine Responses in Neonatal Mice

The inability of infants to mount proper follicular helper T (TFH) cell response renders this age group susceptible to infectious diseases. Initial instruction of T cells by antigen presenting cells and subsequent differentiation into TFH cells are controlled by T cell receptor signal strength, co-stimulatory molecules and cytokines such as IL-6 and IL-21. In immunized adults, IL-6 promotes TFH development by increasing the expression of CXCR5 and the TFH master transcription factor, B cell lymphoma 6. Underscoring the importance of IL-6 in TFH generation, we found improved antibody responses accompanied by increased TFH cells and decreased follicular regulatory helper T (TFR) cells, a Foxp3 expressing inhibitory CD4+ T cell occupying the germinal center (GC), when a tetanus toxoid conjugated pneumococcal polysaccharide type 14 vaccine was injected in adult mice together with IL-6. Paradoxically, in neonates IL-6 containing PPS14-TT vaccine suppressed the already impaired TFH development and antibody responses in addition to increasing TFR cell population. Supporting the diminished TFH development, we detected lower frequency of phospho-STAT-3+ TFH in immunized neonatal T cells after IL-6 stimulation than adult cells. Moreover, IL-6 induced more phospho-STAT-3+ TFR in neonatal cells than adult cells. We also measured lower expression of IL-6R on TFH cells and higher expression on TFR cells in neonatal cells than adult cells, a possible explanation for the difference in IL-6 induced signaling in different age groups. Supporting the flow cytometry findings, microscopic examination revealed the localization of Treg cells in the splenic interfollicular niches of immunized adult mice compared to splenic follicles in neonatal mice. In addition to the limitations in the formation of IL-21 producing TFH cells, neonatal mice GC B cells also expressed lower levels of IL-21R in comparison to the adult mice cells. These findings point to diminished IL-6 activity on neonatal TFH cells as an underlying mechanism of the increased TFR: TFH ratio in immunized neonatal mice

A case of strangulated ileus caused by internal hernia through a defect in the broad ligament of the uterus

A 41-year-old woman was admitted to our hospital because of lower abdominal pain. She had no history of laparotomy. An abdominal CT scan at the time of admission indicated closed-loop intestinal obstruction of the small intestine within the pelvis and deviation of the uterus to the right. We diagnosed this as a strangulated internal hernia and decided to conduct an emergency operation. The ileum had herniated through a defect in the broad ligament of the uterus. The strangulated intestinal loop, which was about 25cm long, was released, and the defect of the broad ligament was closed. The postoperative course was uneventful. The differential diagnosis of intestinal obstruction should include internal hernia, especially in the absence of a previous laparotomy. An abdominal CT scan is quite useful for the preoperative and prompt diagnosis of internal hernia through a defect in the broad ligament of the uterus