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Abstract The effects of ultraviolet (UV) radiation on brain function have previously been investigated; however, the specific neurotransmitter-mediated mechanisms responsible for UV radiation-induced neurobehavioral changes remain elusive. In this study, we aimed to explore the mechanisms underlying UV radiation-induced neurobehavioral changes. In a mouse model, we observed that UV irradiation of the skin induces deficits in hippocampal memory, synaptic plasticity, and adult neurogenesis, as well as increased dopamine levels in the skin, adrenal glands, and brain. Chronic UV exposure altered the expression of genes involved in dopaminergic neuron differentiation. Furthermore, chronic peripheral dopamine treatments resulted in memory deficits. Systemic administration of a dopamine D1/D5 receptor antagonist reversed changes in memory, synaptic plasticity, adult neurogenesis, and gene expression in UV-irradiated mice. Our findings provide converging evidence that chronic UV exposure alters dopamine levels in the central nervous system and peripheral organs, including the skin, which may underlie the observed neurobehavioral shifts, such as hippocampal memory deficits and impaired neurogenesis. This study underscores the importance of protection from UV exposure and introduces the potential of pharmacological approaches targeting dopamine receptors to counteract the adverse neurological impacts of UV exposure.

We present a method to efficiently apply turbo coding to OFDM in-phase/quadrature index modulation (OFDM-IQ-IM) for both cases of presence and absence of puncturing. We show that using the posterior probabilities of turbo-coded bits in the Bahl-Cocke-Jelinek-Raviv (BCJR) decoding algorithm yields the same decoding performance as using the likelihood probabilities of turbo-coded bits. We investigate the difference in error rate between systematic bits and parity check bits of systematic turbo coding and the difference in error rate between index selecting bits (ISBs) and symbol selecting bits (SSBs) of OFDM-IQ-IM. Based on the results, we devise a new bit mapping scheme that can efficiently split turbo-coded bits into ISBs and SSBs in OFDM-IQ-IM. Simulations show that the proposed bit mapping scheme improves the bit error rate (BER) of the turbo-coded 4QAM-based OFDM-IQ-IM approach and that the turbo-coded 4QAM-based OFDM-IQ-IM approach applying the proposed bit mapping scheme outperforms the turbo-coded 4QAM-based OFDM approach in the high signal-to-noise ratio (SNR) region.

Background and Purpose The outcomes of acute internal carotid artery (ICA) terminus occlusions are poor. We classified ICA terminus occlusions into 2 groups according to the occlusion pattern of the circle of Willis and hypothesized that clinical outcomes would significantly differ between them. Methods Consecutive patients with acute ICA terminus occlusions evaluated by baseline computed tomographic angiography were enrolled. We investigated the occlusion patterns in the circle of Willis, retrospectively classified patients into simple ICA terminus occlusion (STO; with good Willisian collaterals from neighboring cerebral circulation) and complex ICA terminus occlusion (CTO; with one or more of A2 anterior cerebral artery, fetal posterior cerebral artery occlusion, or hypoplastic/absent contralateral A1; or with poor collaterals from anterior communicating artery) groups, and compared their baseline characteristics and outcomes. Results The STO group (n=58) showed smaller infarct volumes at 72 hours than the CTO group (n=34) (median, 81 mL [interquartile range, 38-192] vs. 414 mL [193-540], P

Based on grouping the pulses that compose the sub-carrier of the time-multiplexed binary offset carrier (TMBOC), we present an unambiguous correlation function that has no side-peaks causing the ambiguity in the TMBOC signal tracking, and also, that has a higher degree of the sharpness of the main-peak (DSM) over those of the conventional unambiguous correlation functions. Splitting the pulses composing the TMBOC sub-carrier into 12 groups, and, subsequently, forming the 12 group correlations corresponding to the 12 groups, we investigate the contribution of each of the 12 group correlations to the side peaks and main peak of the TMBOC autocorrelation function. Then, we propose a combining method of the 12 group correlations based on the investigation to remove the side peaks while improving the DSM. Numerical results demonstrate that the proposed unambiguous correlation function not only has no side-peaks, but also has a higher DSM, and, consequently, has a better tracking error performance than those of the conventional unambiguous correlation functions.

Background and Purpose The goal of stent retriever–based thrombectomy is removal of embolic clots in patients with intracranial large artery occlusion. However, outcomes of stent retrieval may differ between acute arterial occlusions due to intracranial atherosclerotic disease (IAD) and those due to embolism. This case series describes the outcomes of stent retriever–based thrombectomy and rescue treatments in 9 patients with IAD-related occlusion. Methods Among patients who underwent endovascular treatment for acute intracranial large artery occlusion, those in whom stent retrieval was attempted as first-line treatment were included in this review. IAD was defined as significant fixed focal stenosis at the occlusion site, which was evident on final angiographic assessment or observed during endovascular treatment. Results Median number of stent retriever passes was 2 (range, 1-3), and temporary bypass was seen in all patients. Immediate partial recanalization (arterial occlusive lesion grade 2-3) was observed in 7 patients. Immediate modified thrombolysis in cerebral infarction grade 2b-3 was seen in 6 patients, but the lesions often required rescue treatment due to reocclusion or flow insufficiency. In terms of rescue treatments, angioplasty and intra-arterial tirofiban infusion seemed to be effective. Conclusions Our findings suggest that stent retrieval can effectively remove thrombi from stenotic lesions and achieve partial recanalization despite the tendency toward reocclusion in most patients with IAD-related occlusion. Further research into the use of rescue treatments, such as tirofiban infusion and angioplasty, is warranted.

We synthesized lead-free piezoelectric (Bi0.5Na0.5-xKx)TiO3 (BNKT) ceramics using a conventional solid-state reaction method. We have investigated the structural and electrical properties of the materials with x = 0.05 to 0.40. The X-ray diffraction (XRD) analysis suggests that the BNKT ceramics show the transition from rhombohedral to tetragonal structure. The ratio of the tetragonal structure increased continuously in accordance with the increasing composition of x. The sample of x = 0.10 showed a similar ratio between the tetragonal and rhombohedral structures. Frequency-dependent dielectric measurements showed a sort of relaxor properties emerged with increasing x composition, this effect may be interpreted in terms of the formation of polar nano-regions (PNRs) in samples. The value of remnant polarization (Pr) decreases rapidly as x increases beyond the point of x = 0.10 from 25.3 μC/cm2 to 5.9 μC/cm2. On the contrary, as for inverse piezoelectric coefficient (d33*), a higher value of d33* (336 pm/V) at x = 0.10, was observed when compared with x = 0.05 (d33* = 51 pm/V). These results can be explained by the formation of PNRs and their variations with the external applied field. We here propose a possible mechanism showing the effects of dipolar defects, which can be resulted from the K ion substitution on (Bi,Na)TiO3 (BNT) ceramics.

SHP2 is an unusual protein phosphatase that functions as an activator for several signaling pathways, including the RAS pathway, while most other phosphatases suppress their downstream signaling cascades. The physiological and pathophysiological roles of SHP2 have been extensively studied in the field of cancer research. Mutations in the PTPN11 gene which encodes SHP2 are also highly associated with developmental disorders, such as Noonan syndrome (NS), and cognitive deficits including learning disabilities are common among NS patients. However, the molecular and cellular mechanism by which SHP2 is involved in cognitive functions is not well understood. Recent studies using SHP2 mutant mice or pharmacological inhibitors have shown that SHP2 plays critical role in learning and memory and synaptic plasticity. Here, we review the recent studies demonstrating that SHP2 is involved in synaptic plasticity, and learning and memory, by the regulation of the expression and/or function of glutamate receptors. We suggest that each cell type may have distinct paths connecting the dots between SHP2 and glutamate receptors, and these paths may also change with aging. [ABSTRACT FROM AUTHOR]

The article introduces a new media storage and transportation system that utilizes Movable and Deployable information and communication technology (ICT) Resource Unit (MDRU) in disaster areas. Topics include the concept of layered coding in a cache server, disaster resilient layered data transmission, and the Joint Photographic Experts Group (JPEG) 2000 standard for layered image/video coding. It also discusses network distributed storage and forward error correction (FEC).

Background and objective Although several studies have shown an association between ferritin level and hypertension, only a few studies have investigated the longitudinal relationship between them. Thus, we evaluated the incidental risk for hypertension according to baseline ferritin level. Patients and methods A total of 7104 healthy Korean men matched by a propensity score, who had participated in a medical health check-up program in 2005, were followed up from 2005 to 2010. They were divided into four groups according to baseline serum ferritin level (first quartile-fourth quartile). The incidence of hypertension was compared among the four groups, and the Cox-proportional hazard model was used to assess whether the development of hypertension was associated with higher baseline serum ferritin level. Results A total of 1252 (17.6%) cases had newly developed hypertension during the 26,339.5 person-years of follow-up between 2006 and 2010. The adjusted hazard ratios (HRs) (95% confidence intervals, CIs) for incident hypertension were 1.00 (reference), 1.09 (0.91-1.30), 1.21 (1.01-1.45) and 1.28 (1.07-1.52), respectively (Pfor trend = 0.003) through the quartiles of serum ferritin levels, respectively, after adjusting for multiple confounders. For the log-transformed serum ferritin levels as a continuous variable, adjusted HRs and 95% CIs for HTN were 1.15 (1.02-1.29). Conclusions Elevated serum ferritin level was independently associated with the incidental risk for hypertension in Korean men. This finding suggests the value of elevated ferritin level as an early predictor of hypertension. [ABSTRACT FROM AUTHOR]

Bloom syndrome is a rare genetic disorder characterized by genomic instability and cancer predisposition. The disease is caused by mutations of the Bloom syndrome protein (BLM). Here we report the crystal structure of a RecQ C-terminal (RQC) domain from human BLM. The structure reveals three novel features of BLM RQC which distinguish it from the previous structures of the Werner syndrome protein (WRN) and RECQ1. First, BLMRQClacks an aromatic residue at the tip of the β-wing, a key element of the RecQ-family helicases used for DNA-strand separation. Second, a BLM-specific insertion between the N-terminal helices exhibits a looping-out structure that extends at right angles to the β-wing. Deletion mutagenesis of this insertion interfered with binding to Holliday junction. Third, the C-terminal region of BLM RQC adopts an extended structure running along the domain surface, which may facilitate the spatial positioning of an HRDC domain in the full-length protein. [ABSTRACT FROM AUTHOR]

Threats of electronic warfare, especially to global positioning systems (GPSs), have been rapidly increasing. The development of the Chinese navigation satellite system BeiDou has been extended to a global navigation satellite system (GNSS). In December 2011, the Chinese government released a specification document-a test version of a civil BeiDou-II signal called B1(I). A strong possibility exists that BeiDou-II (Chinese GNSS) will be adopted by North Korea in the near future. Therefore, research on BeiDou-II is essential. Since BeiDou-II is a newly-built system, few jamming effect analyses of its positioning signals have been performed. Thus, in this study, we analyze quality factors (Q) and the tolerable jamming signal power among two BeiDou-II civil signals, and two GPS civil signals, in three jamming conditions: band-limited white noise (BLWN), matched spectrum (MS), and continuous wave (CW). In addition, we present each jamming propagation range. [ABSTRACT FROM AUTHOR]

Cigarette smoking causes apoptotic death, senescence, and impairment of repair functions in lung fibroblasts, which maintain the integrity of alveolar structure by producing extracellular matrix (ECM) proteins. Therefore, recovery of lung fibroblasts from cigarette smoke-induced damage may be crucial in regeneration of emphysematous lung resulting from degradation of ECM proteins and subsequent loss of alveolar cells. Recently, we reported that bone marrow-derived mesenchymal stem cell-conditioned media (MSC-CM) led to angiogenesis and regeneration of lung damaged by cigarette smoke. In this study, to further investigate reparative mechanisms for MSC-CM-mediated lung repair, we attempted to determine whether MSC-CM can recover lung fibroblasts from cigarette smoke-induced damage. In lung fibroblasts exposed to cigarette smoke extract (CSE), MSC-CM, not only inhibited apoptotic death, but also induced cell proliferation and reversed CSE-induced changes in the levels of caspase-3, p53, p21, p27, Akt, and p-Akt. MSC-CM also restored expression of ECM proteins and collagen gel contraction while suppressing CSE-induced expression of cyclooxygenase-2 and microsomal PGE2 synthase-2. The CSE-opposing effects of MSC-CM on cell fate, expression of ECM proteins, and collagen gel contraction were partially inhibited by LY294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor. In rats, MSC-CM administration also resulted in elevation of p-Akt and restored proliferation of lung fibroblasts, which was suppressed by exposure to cigarette smoke. Taken together, these data suggest that MSC-CM may recover lung fibroblasts from cigarette smoke-induced damage, possibly through inhibition of apoptosis, induction of proliferation, and restoration of lung fibroblast repair function, which are mediated in part by the PI3K/Akt pathway. [ABSTRACT FROM AUTHOR]

Emphysema is one of the characteristic features of chronic obstructive pulmonary disease, which is caused mainly by cigarette smoking. Recent data have suggested that apoptosis and cell cycle arrest may contribute to the development of emphysema. In this study, we addressed the question of whether and how cigarette smoke affected Akt, which plays a critical role in cell survival and proliferation. In normal human lung fibroblasts, cigarette smoke extract (CSE) caused cell death, accompanying degradation of total and phosphorylated Akt (p-Akt), which was inhibited by MG132. CSE exposure resulted in preferential ubiquitination of the active Akt (myristoylated), rather than the inactive (T308A/S473A double mutant) Akt. Consistent with cytotoxicity, CSE induced a progressive decrease of phosphorylated human homolog of mouse double minute homolog 2 (p-HDM2) and phosphorylated apoptosis signal regulating kinase 1 (p-ASK1) with concomitant elevation of p53, p21, and phosphorylated p38 MAPK. Forced expression of the active Akt reduced both CSE-induced cytotoxicity and alteration in HDM2/p53/p21 and ASK1/p38 MAPK, compared with the inactive Akt. Of note, CSE induced expression of the tetratrico-peptide repeat domain 3 (TTC3), known as a ubiquitin ligase for active Akt. TTC3 siRNAs suppressed not only CSE-induced Akt degradation but also CSE-induced cytotoxicity. Accordingly, rat lungs exposed to cigarette smoke for 3 months showed elevated TTC3 expression and reduced Akt and p-Akt. Taken together, these data suggest that cigarette smoke induces cytotoxicity, partly through Akt degradation via the ubiquitin-proteasome system, in which TTC3 acts as a ubiquitin ligase for active Akt. [ABSTRACT FROM AUTHOR]