Fisetin Inhibits UVA-Induced Expression of MMP-1 and MMP-3 through the NOX/ROS/MAPK Pathway in Human Dermal Fibroblasts and Human Epidermal Keratinocytes.

Fisetin is a flavonoid found in plants and has been reported to be effective in various human diseases. However, the effective mechanisms of ultraviolet-A (UVA)-mediated skin damage are not yet clear. In this study, we investigated the protective mechanisms of fisetin regarding UVA-induced human dermal fibroblasts (HDFs) and human epidermal keratinocytes (HEKs) damages. Fisetin showed a cytoprotective effect against UVA irradiation and suppressed matrix metalloproteinases (MMPs), MMP-1, and MMP-3 expression. In addition, fisetin was rescued, which decreased mRNA levels of pro-inflammatory cytokines, reactive oxygen species production, and the downregulation of MAPK/AP-1 related protein and NADPH oxidase (NOX) mRNA levels. Furthermore, UVA-induced MMP-1 and MMP-3 were effectively inhibited by siRNAs to NOX 1 to 5 in HDFs and HEKs. These results indicate that fisetin suppresses UVA-induced damage through the NOX/ROS/MAPK pathway in HDFs and HEKs.

Sleep Reactivity and Sleep Efforts in Shift Workers.

OBJECTIVE: The current study aimed to investigate the differences in sleep reactivity and sleep effort differs among late night shift workers (LSWs) and non-late night shift workers (non-LSWs), and non-shift workers (non-SWs). METHODS: In total, 6,023 participants (1,613 non-SWs, 3,339 LSWs, and 1,071 non-LSWs) were recruited. Non-SWs was defined as those who works at fixed schedules during standard daylight. LSWs was defined as who work late night hours (10 PM-6 AM), while non-LSWs was SWs who did not work during late night. All completed the Ford Insomnia Response to Stress Test (FIRST), the Glasgow Sleep Effort Scale (GSES), the Pittsburgh Sleep Quality Index (PSQI), the Epworth Sleepiness Scale (ESS), the Insomnia Severity Index (ISI), and the short-term Center for Epidemiologic Studies-Depression scale (CES-D) through online survey. RESULTS: LSWs and non-LSWs reported higher FIRST, GSES scores than non-SWs. In addition, LSWs reported higher FIRST, GSES scores than non-LSWs. FIRST scores were correlated with CES-D, PSQI, ISI, and ESS for LSWs, non-LSWs, and non-SWs alike. GSES scores were also correlated with CES-D, PSQI, ISI, and ESS for LSWs, non-LSWs, and non-SWs alike. CONCLUSION: SWs showed higher sleep reactivity and sleep effort than non-SWs. LSWs had higher sleep reactivity and sleep effort than non-LSWs, and these variables are associated with insomnia, daytime sleepiness, and depressive symptoms. Our findings suggests that late night schedule, may increase sleep reactivity and sleep effort, which are associated with sleep and mood disturbances.

Protaetia brevitarsis Extract Attenuates RANKL-Induced Osteoclastogenesis by Inhibiting the JNK/NF-κB/PLCγ2 Signaling Pathway.

Protaetia brevitarsis (PB)-derived bioactive substances have been used as food and medicine in many Asian countries because of their antioxidant, antidiabetic, anti-cancer, and hepatoprotective properties. However, the effect of PB extracts (PBE) on osteoclast differentiation is unclear. In this study, we investigated the effect of PBE on RANKL-induced osteoclastogenesis in mouse bone marrow-derived macrophages (BMMs). To investigate the cytotoxicity of PBE, the viability of BMMs was confirmed via MTT assay. Tartrate-resistant acid phosphatase (TRAP) staining and pit assays were performed to confirm the inhibitory effect of PBE on osteoclast differentiation and bone resorption. The expression levels of osteoclast differentiation-related genes and proteins were evaluated using quantitative real-time PCR and Western blotting. PBE attenuated osteoclastogenesis in BMMs in TRAP and pit assays without cytotoxicity. The expression levels of osteoclast marker genes and proteins induced by RANKL were decreased after PBE treatment. PBE suppressed osteoclastogenesis by inhibiting the RANKL-induced activated JNK/NF-κB/PLCγ2 signaling pathway and the expression of NFATc1 and c-Fos. Collectively, these results suggest that PBE could be a potential therapeutic strategy or functional product for osteoclast-related bone disease.

CDDO, a PPAR-γ ligand, inhibits TPA-induced cell migration and invasion through a PPAR-γ-independent mechanism.

Peroxisome proliferator-activated receptor-γ (PPAR-γ) acts as a key factor in breast cancer metastasis. Notably, PPAR-γ can inhibit metalloproteinase (MMP), which is involved in cancer metastasis. Our previous study revealed that PPAR-γ was related to breast cancer metastasis. The present study aimed to investigate whether the PPAR-γ ligand 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid (CDDO) mediated suppression of cell invasion and reduced the expression of MMP-9 in breast cancer cells. The results indicated that CDDO reduced MMP-9 expression, cell migration and invasion of breast cancer cells by inhibiting TPA-induced phosphorylation of mitogen-activated protein kinases, and downregulating the activities of activator protein-1 and nuclear factor κB. Notably, knock-out of PPAR-γ by small interfering RNA in MCF-7 cells revealed that TPA-induced MMP-9 expression occurred through a PPAR-γ-independent pathway. These data indicated that the downregulatory effect of CDDO on MMP-9 expression was affected by a mechanism independent of PPAR-γ. In conclusion, the findings of the present study suggested that CDDO may act as a key agent in the regulation of breast cancer metastasis, suggesting CDDO as a new targeted therapy for breast cancer.

Inhibition of cell invasion and migration by targeting matrix metalloproteinase-9 expression via sirtuin 6 silencing in human breast cancer cells.

Sirtuin 6 (SIRT6) regulation is involved in carcinogenesis. However, its role in breast cancer (BC) metastasis remains unclear. We investigated the effects of SIRT6 on protein kinase C activator- and cytokine-mediated cancer cell invasion and migration in MCF-7 and MDA-MB-231 cells and the association between SIRT6 and matrix metalloproteinase-9 (MMP-9) expression. To assess MMP-9 and SIRT6 expression in patients, protein levels in BC tissues were analyzed. MCF-7 and MDA-MB-231 cell viability was analyzed using MTT assays. SIRT6 was silenced in both cell lines and protein secretion, expression, and mRNA levels were analyzed. Transcription factor DNA activity was investigated using luciferase assays. Matrigel invasion assays were used to assess the effects of SIRT6 in both cell lines. SIRT6 and MMP-9 expression in cancer tissues was significantly higher than in paired normal breast tissues. 12-O-tetradecanoylphorbol-13-acetate (TPA) or tumor necrosis factor-α (TNF-α) increased MMP-9 expression and cell invasion and migration, but SIRT6 knockdown abolished these effects. SIRT6 overexpression additively increased TPA- and TNF-α-induced MMP-9 expression. SIRT6 knockdown suppressed the mitogen-activated protein kinase (MAPK) signaling pathway and thus TPA- and TNF-α-induced MMP-9 expression. SIRT6 silencing suppressed TPA- and TNF-α-induced nuclear factor-κB (NF-κB) and activator protein-1 (AP-1) expressions in both cell lines, and treatment with MAPK, NF-κB, and AP-1 inhibitors reduced MMP-9 expression. The anti-invasive effects of SIRT6 in BC cells might be mediated by suppression of MAPK phosphorylation and reduction in NF-κB and AP-1 DNA activities, leading to MMP-9 downregulation, suggesting that SIRT6 modulation has the potential to target BC metastasis.

Aurora kinase A induces migration and invasion by inducing epithelial-to-mesenchymal transition in colon cancer cells.

Aurora kinase is a family of serine/threonine kinases intimately associated with mitotic progression and the development of human cancers. Studies have shown that aurora kinases are important for the protein kinase C (PKC)-induced invasion of colon cancer cells. Recent studies have shown that aurora kinase A promotes distant metastasis by inducing epithelial-to-mesenchymal transition (EMT) in colon cancer cells. However, the role of aurora kinase A in colon cancer metastasis remains unclear. In this study, we investigated the effects of aurora kinase A on PKC-induced cell invasion, migration, and EMT in human SW480 colon cancer cells. Treatment with 12-O-tetradecanoylphorbol- 13-acetate (TPA) changed the expression levels of EMT markers, increasing α-SMA, vimentin, and MMP-9 expression and decreasing E-cadherin expression, with changes in cell morphology. TPA treatment induced EMT in a PKC-dependent manner. Moreover, the inhibition of aurora kinase A by siRNAs and inhibitors (reversine and VX-680) suppressed TPA-induced cell invasion, migration, and EMT in SW480 human colon cells. Inhibition of aurora kinase A blocked TPA-induced vimentin and MMP-9 expression, and decreased E-cadherin expression. Furthermore, the knockdown of aurora kinase A decreased the transcriptional activity of NF-κB and AP-1 in PKC-stimulated SW480 cells. These findings indicate that aurora kinase A induces migration and invasion by inducing EMT in SW480 colon cancer cells. To the best of our knowledge, this is the first study that showed aurora kinase A is a key molecule in PKC-induced metastasis in colon cancer cells. [BMB Reports 2022;55(2): 87-91].

Triptolide inhibits matrix metalloproteinase-9 expression and invasion of breast cancer cells through the inhibition of NF-κB and AP-1 signaling pathways.

Triptolide is a diterpenoid epoxide that is endogenously produced by the thunder god vine, Tripterygium wilfordii Hook F. Triptolide has demonstrated a variety of biological activities, including anticancer activities, in previous studies. Invasion and metastasis are the leading causes of mortality for patients with breast cancer, and the increased expression of matrix metalloproteinase-9 (MMP-9) has been shown to be associated with breast cancer invasion. Therefore, the aim of the present study was to investigate the effect of triptolide on 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced cell invasion and MMP-9 expression in breast cancer cells. The expression of signal molecules was examined by western blotting, zymography and quantitative polymerase chain reaction; an electrophoretic mobility gel shift assay was also used, and cell invasiveness was measured by an in vitro Matrigel invasion assay. The MCF-7 human breast cancer cell line was treated with triptolide at the highest concentrations at which no marked cytotoxicity was evident. The results demonstrated that triptolide decreased the expression of MMP-9 through inhibition of the TPA-induced phosphorylation of extracellular signal-regulated kinase (ERK) and the downregulation of nuclear factor-κB (NF-κB) and activator protein-1 (AP-1) activity. In addition, a Transwell assay revealed that triptolide reduced the ability of MCF-7 cells to invade Matrigel. These data demonstrate that the anti-invasive effect of triptolide is associated with the inhibition of ERK signaling and NF-κB and AP-1 activation, and suggest that triptolide may be a promising drug for breast cancer.

Aqueous extract of Chrysanthemum morifolium Ramat. inhibits RANKL-induced osteoclast differentiation by suppressing the c-fos/NFATc1 pathway.

OBJECTIVE: The flower of chrysanthemum, used worldwide as a medicinal and edible product, has shown various bioactivities, such as anti-inflammatory, antioxidant, anti-tumorigenic, and hepatoprotective activities, as well as cardiovascular protection. However, the effect of Chrysanthemum morifolium Ramat. on the regulation of osteoclast differentiation has not yet been reported. In this study, we aimed to investigate the inhibitory effect of Chrysanthemum morifolium Ramat. water extract (CME) on RANKL-induced osteoclast differentiation in mouse bone marrow-derived macrophages (BMMs). STUDY DESIGN: Bone marrow-derived macrophages (BMMs) isolated from the C57BL/6 J mice. The viability of BMMs was detected with MTT assays. Inhibitory effects of CME on osteoclast differentiation and bone resorption was measured by TRAP staining and Pit assay. Osteoclast differentiation-associated gene expression were assessed by Real-time quantitative polymerase chain reaction. Intracellular signaling molecules was assessed by western blot. RESULTS: CME significantly inhibited osteoclast differentiation in BMMs without cytotoxicity, besides inhibiting MAPK/c-fos and PLCγ2/CREB activation. The inhibitory effects of CME on differentiation-related signaling molecules resulted in significant repression of NFATc1 expression, which is a key transcription factor in osteoclast differentiation, fusion, and activation. CONCLUSION: Our results confirmed the inhibition of RANKL-induced PLCγ2/CREB/c-fos/NFATc1 activation by CME during osteoclast differentiation. The findings collectively suggested CME as a traditional therapeutic agent for osteoporosis, RA, and periodontitis.

Roles of JNK/Nrf2 Pathway on Hemin-Induced Heme Oxygenase-1 Activation in MCF-7 Human Breast Cancer Cells.

Heme oxygenase-1 (HO-1) is highly induced in various human disease states, including cancer, indicating that HO-1 is an emerging target of cancer therapy. In this study, we investigated that the mechanisms of hemin-induced HO-1 expression and its signaling pathways in human breast cancer cell. We used MCF-7 cells, a human breast cancer cell line. Hemin increased HO-1 expression in MCF-7 cells in a dose- and time-dependent manner. Hemin enhanced HO-1 expression through the activation of c-Jun N-terminal kinases (JNK) signaling pathway. Hemin also induced activation of Nrf2, a major transcription factor of HO-1 expression. These responses in MCF-7 cells were completely blocked by pretreatment with brazilin, a HO-1 regulator. These results indicated that brazilin inhibits hemin-induced HO-1 expressions through inactivation of JNK/Nrf2 in MCF-7 cells. Thus, our findings suggest that HO-1 is an important anticancer-target of brazilin in human breast cancer.

15d-PGJ2 inhibits NF-κB and AP-1-mediated MMP-9 expression and invasion of breast cancer cell by means of a heme oxygenase-1-dependent mechanism.

Activation of peroxisome proliferator-activated receptor γ (PPARγ) serves as a key factor in the proliferation and invasion of breast cancer cells and is a potential therapeutic target for breast cancer. However, the mechanisms underlying this effect remain largely unknown. Heme oxygenase-1 (HO-1) is induced and overexpressed in various cancers and is associated with features of tumor aggressiveness. Recent studies have shown that HO-1 is a major downstream target of PPARγ. In this study, we investigated the effects of induction of HO-1 by PPARγ on TPAinduced MMP-9 expression and cell invasion using MCF-7 breast cancer cells. TPA treatment increased NF-κB /AP-1 DNA binding as well as MMP-9 expression. These effects were significantly blocked by 15d-PGJ2, a natural PPARγ ligand. 15d-PGJ2 induced HO-1 expression in a dose-dependent manner. Interestingly, HO-1 siRNA significantly attenuated the inhibition of TPA-induced MMP-9 protein expression and cell invasion by 15d-PGJ2. These results suggest that 15d-PGJ2 inhibits TPA-induced MMP- 9 expression and invasion of MCF-7 cells by means of a heme oxygenase-1-dependent mechanism. Therefore, PPARγ/HO-1 signaling- pathway inhibition may be beneficial for prevention and treatment of breast cancer. [BMB Reports 2020; 53(4): 212-217].

Oral administration of Ulmus davidiana extract suppresses interleukin-1ß expression in LPS-induced immune responses and lung injury.

BACKGROUND: Ulmus davidiana (UD) is a traditional Korean herb medicine that is used to treat inflammatory disorders. UD has been shown to modulate a number of inflammatory processes in vitro or in vivo studies. However, the molecular mechanisms of UD on lipopolysaccharide (LPS)-induced acute lung injury remain to be understood. OBJECTIVE: The primary objective of this study is to determine the effect of UD bark water extract on LPS-induced immune responses and lung injury using both in vitro and in vivo models. METHODS: RAW 264.7 cells and a rat model of acute lung injury (ALI) were used to study the effects of UD on several parameters. Nitrite level, lactate dehydrogenase (LDH) level, and superoxide dismutase (SOD) activities were measured. Tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and plasma transaminase activities in blood were also determined. Pathological investigations were also performed. RESULTS: LPS infusion resulted in elevated IL-1ß mRNA expression, nitrite levels, TNF-α expression, and IL-1ß expression in RAW 264.7 cells. LPS infusion also increased levels of nitrite/nitrate, total protein, LDH, and TNF-α in bronchoalveolar lavage fluid, but reduced SOD levels in ex vivo and in vivo models. UD administration ameliorated all these inflammatory markers. In particular, treatment with UD reduced LPS-induced nitrite production in RAW 264.7 cells in a dose-dependent manner. UD treatment also counteracted the LPS-induced increase in alanine aminotransferase (ALT) and aspartate transaminase (AST) activity in rat plasma, leading to a significant reduction in ALT and AST activity. CONCLUSIONS: The results revealed that UD treatment reduces LPS-induced nitrite production, IL-1ß mRNA expression, and TNF-α expression. In addition, LPS-induced decrease in SOD level is significantly elevated by UD administration. These results indicate that UD extract merits consideration as a potential drug for treating and/or preventing ALI.

Effects of phased education on attitudes toward organ donation and willingness to donate after brain death in an Asian country.

BACKGROUND/OBJECTIVE: This study aims to investigate the effects of phased education on attitudes toward organ donation and willingness to donate after brain death. METHODS: A survey was conducted using a questionnaire to examine attitudes toward organ donation of the families of patients admitted to a surgical intensive care unit (SICU) between March 1, 2014 and September 30, 2016. RESULTS: Ninety-two people voluntarily participated in this survey. Before reviewing the educational material, 75.0% had a positive attitude toward organ donation, 60.9% were willing to donate their own organs, and 38.0% were willing to donate a family member's organs. After reviewing the educational material, these figures increased to 92.4%, 80.4%, and 56.5%, respectively. Before receiving an education, there was a significant difference in consistency between people's attitudes and willingness to donate their own organs, versus donating a family member's organs (79.3% vs 54.3%, p < 0.001). With phased education, these percentages increased from 79.3% to 85.9% with regard to donating one's own organs, and from 54.3% to 64.1% with regard to donating a family member's organs. CONCLUSION: Phased education was effective overall, but it had a limited effect on changing the willingness to donate a family member's organs. It increased the consistency between people's attitudes toward organ donation and willingness to donate their own, or a family member's organs.

Troglitazone Inhibits Matrix Metalloproteinase-9 Expression and Invasion of Breast Cancer Cell through a Peroxisome Proliferator-Activated Receptor γ-Dependent Mechanism.

PURPOSE: Peroxisome proliferator-activated receptor γ (PPARγ) is involved in the pathology of numerous diseases including atherosclerosis, diabetes, obesity, and cancer. Matrix metalloproteinases (MMPs) play a significant role in tissue remodeling related to various processes such as morphogenesis, angiogenesis, tissue repair, invasion, and metastasis. We investigated the effects of PPARγ on MMP expression and invasion in breast cancer cells. METHODS: MCF-7 cells were cultured and then cell viability was monitored in an MTT assay. Western blotting, gelatin zymography, real-time polymerase chain reaction, and luciferase assays were performed to investigate the effect of the synthetic PPARγ ligand troglitazone on MMP expression. Transcription factor DNA binding was analyzed by electrophoretic mobility shift assay. A Matrigel invasion assay was used to assess the effects of troglitazone on MCF-7 cells. RESULTS: Troglitazone did not affect MCF-7 cell viability. 12-O-tetradecanoylphorbol-13-acetate (TPA) induced MMP-9 expression and invasion in MCF-7 cell. However, these effects were decreased by troglitazone. TPA increased nuclear factor κB and activator protein-1 DNA binding, while troglitazone inhibited these effects. The selective PPARγ antagonist GW9662 reversed MMP-9 inhibition by troglitazone in TPA-treated MCF-7 cells. CONCLUSION: Troglitazone inhibited nuclear factor κB and activator protein-1-mediated MMP-9 expression and invasion of MCF-7 cells through a PPARγ-dependent mechanism.

Survey Regarding Attitude of Family About Organ Donation After Brain Death in Korea.

BACKGROUND This study examined the attitude of patients' relatives in South Korea toward organ donation after brain death. MATERIAL AND METHODS A structured questionnaire was used to obtain the information on the attitude toward organ donation for relatives of patients who were admitted to the surgical intensive care unit (SICU) between March 1, 2014 and September 30, 2016. In total, 92 persons participated voluntarily. The investigation included general opinion about organ donation; and additional categorical analysis was performed. RESULTS In this study, 75% of participants agreed that they had positive thoughts on organ donation; however, fewer participants (60.9%) showed a positive attitude towards donating their own body, while only a third of participants (38.1%) agreed that they would donate relatives' body. We could confirm specifically concerns about excessive physical damage during organ recovery (34.7%) and ignorance or disrespect by hospital staff (15.2%), as well as consideration of being sacrificed for the benefit of others (26.0%). The participants who agreed to donate relatives' body showed significantly different responses in each categories of the questionnaire compared to the participants who disagreed or were undecided. CONCLUSIONS Despite positive perceptions concerning organ donation after brain death, there were nonetheless several prejudices and misunderstandings to overcome. The findings of this study can be used to establish evidence-based strategies.

Epigallocatechin gallate inhibits the growth of MDA-MB-231 breast cancer cells via inactivation of the ß-catenin signaling pathway.

Epigallocatechin gallate (EGCG), a major constituent of green tea, has potential as a treatment for a variety of diseases, including cancer. EGCG induces apoptosis and inhibits tumorigenesis through multiple signaling pathways in breast cancer cells. ß-catenin signaling modulators could be useful in the prevention and therapy of breast cancer. However, the precise anticancer effect of EGCG through the ß-catenin signaling pathway in breast cancer is unclear. The present study investigated the association between ß-catenin expression and clinicopathological factors of breast cancer patients, and the effect of EGCG on ß-catenin expression in breast cancer cells. ß-catenin expression was analyzed according to the clinicopathological factors of 74 patients with breast cancer. All patients were females diagnosed with invasive ductal carcinoma. Western blot analysis revealed that ß-catenin was expressed at higher levels in breast cancer tissue than in normal tissue. ß-catenin expression was associated with lymph node metastasis (P=0.04), tumor-node-metastasis stage (P=0.03) and estrogen receptor status (P<0.01). EGCG decreased MDA-MB-231 cell viability and significantly downregulated the expression of ß-catenin, phosphorylated Akt and cyclin D1. Remarkably, additive effects of LY294002 and wortmannin, two phosphatidylinositol-3 kinase inhibitors, were observed. The present results suggest that EGCG inhibits the growth of MDA-MB-231 cells through the inactivation of the ß-catenin signaling pathway. Based on these promising results, EGCG may be a potential treatment for triple negative breast cancer patients.

Isolated intracranial fibromuscular dysplasia of the posterior cerebral artery.

Fibromuscular dysplasia (FMD) is a nonatherosclerotic, noninflammatory arterial disease that most commonly affects the renal and internal carotid arteries, but intracranial FMD is very rare. We report a patient with FMD involving the posterior cerebral arteries (PCAs). A 24year old female was presented with a 4day history of right homonymous hemianopsia with throbbing headache in the left temporo-occipital area. The brain magnetic resonance imaging (MRI) revealed an acute ischemic stroke in the left PCA territory, while the Time of Flight (TOF) magnetic resonance angiogram (MRA) showed segmental luminal irregularities in the left proximal PCA. The conventional angiogram revealed the "string of beads" appearance, a characteristic that is pathognomonic for FMD. The patient's inhospital clinical course was stable, while there was no recurrence of stroke. This is the second report of FMD of the PCA. Notwithstanding incredibly rare incidences of isolated intracranial FMD and nonspecific findings of MRA, such a pathophysiology should be considered as the cause for a stroke in young patients, especially those with no cardiovascular risk factor.

Formation of a Surficial Bifunctional Nanolayer on Nb2 O5 for Ultrastable Electrodes for Lithium-Ion Battery.

Safe and long cycle life electrode materials for lithium-ion batteries are significantly important to meet the increasing demands of rechargeable batteries. Niobium pentoxide (Nb2 O5 ) is one of the highly promising candidates for stable electrodes due to its safety and minimal volume expansion. Nevertheless, pulverization and low conductivity of Nb2 O5 have remained as inherent challenges for its practical use as viable electrodes. A highly facile method is proposed to improve the overall cycle retention of Nb2 O5 microparticles by ammonia (NH3 ) gas-driven nitridation. After nitridation, an ultrathin surficial layer (2 nm) is formed on the Nb2 O5 , acting as a bifunctional nanolayer that allows facile lithium (Li)-ion transport (10-100 times higher Li diffusivity compared with pristine Nb2 O5 microparticles) and further prevents the pulverization of Nb2 O5 . With the subsequent decoration of silver (Ag) nanoparticles (NPs), the low electric conductivity of nitridated Nb2 O5 is also significantly improved. Cycle retention is greatly improved for nitridated Nb2 O5 (96.7%) compared with Nb2 O5 (64.7%) for 500 cycles. Ag-decorated, nitridated Nb2 O5 microparticles and nitridated Nb2 O5 microparticles exhibit ultrastable cycling for 3000 cycles at high current density (3000 mA g-1 ), which highlights the importance of the surficial nanolayer in improving overall electrochemical performances, in addition to conductive NPs.

Anti-cancer Effect of Cyanidin-3-glucoside from Mulberry via Caspase-3 Cleavage and DNA Fragmentation in vitro and in vivo.

BACKGROUND: Fruits of Morus alba L. (mulberry) have various bioactive compounds such as polyphenols and anthocyanins and used as a herbal medicine. However, the anti-cancer effects and molecular basis have not been elucidated. METHODS: We isolated the cyanidin-3-glucoside in various cultivar of mulberry by acidified-methanol extraction methods. This molecule were compared mass spectroscopic properties by LC-MS/MS and analyzed by 1H and 13C NMR. We examined the anti-cancer effect with molecular mechanisms of the cyanidin-3-glucoside on MDA-MB-453 human breast cancer cells and xenograft animal model. RESULTS: The treatment with the mulberry cyanidin-3-glucoside decreased cell viability in a dose-dependent manner with alteration of apoptotic protein contents, and DNA fragmentation, suggesting that cells undergo apoptosis. Supporting the observations, Treatment with the cyanidin-3-glucoside showed active apoptosis by caspase-3 cleavage and DNA fragmentation through Bcl-2 and Bax pathway. Indeed, cyanidin-3-glucoside inhibits tumor growth in MDA-MB-453 cells-inoculated nude mice. Tumor growth of xenograft nude mouse was significantly reduced compared to the control group by the cyanidin-3-glucoside. CONCLUSION: The data demonstrate that cyanidin-3-glucoside isolated from mulberry induced apoptosis in breast cancer (MDA-MB-453) cells, and therefore, has a potential as an anti-cancer agent. These results show that mulberry cyanidin-3-glucoside inhibit the proliferation and growth in vitro and in vivo model and, indicating the inhibition of tumor progression.

Factors Associated with a Family's Delay of Decision for Organ Donation After Brain Death.

BACKGROUND This study aimed to explore the factors associated with a family's delay of decision for organ donation after brain death, and to investigate the effect of such a delay on organ donation. MATERIAL AND METHODS Medical records and data on counseling about organ donation with the families of 107 brain-dead potential donors between September 2012 and March 2016 at a single tertiary medical center were retrospectively reviewed. RESULTS The final consent rate was 58% (62/107), and successful donation was performed in 40% (43/107). Ninety-two families (86%) made a decision within 48 hours, whereas 15 (14%) required more than 48 hours for a final decision. In univariate and multivariate analyses, the independent factors associated with a decision delay were mean arterial pressure ≤60 mm Hg and coma therapy. In the early decision group (<48 hours), the consent and successful donation rates were 55% (51/92) and 39% (36/92), respectively, whereas in the delayed decision group (≥48 hours), these rates were 73% (11/15) and 47% (7/15), respectively. The consent and successful donation rates were not inferior in the delayed decision group. CONCLUSIONS These findings justify continuous efforts to maintain organ viability and to extend counseling to encourage donation even if the family cannot decide immediately.

Paradoxical vestibular syndrome in a dog from western Newfoundland infected with French heartworm (Angiostrongylus vasorum).

A dog from western Newfoundland was presented with paradoxical vestibular syndrome. First-stage larvae of Angiostrongylus vasorum were detected on fecal examination. Treatment with milbemycin oxime resulted in resolution of signs. This is the first report of the spread of this parasite to western Newfoundland and of paradoxical vestibular syndrome in a dog infected with A. vasorum.

Syndrome vestibulaire paradoxal chez un chien de l'ouest de Terre-Neuve infecté par des vers du cœur(Angiostrongylus vasorum). Un chien de l'ouest de Terre-Neuve a été présenté avec un syndrome vestibulaire paradoxal. Des larves de premier stade d'Angiostrongylus vasorum ont été détectées à l'examen fécal. Le traitement à l'aide d'oxime de milbémycine a produit une disparition des symptômes. Il s'agit du premier rapport de la propagation de ce parasite dans l'ouest de Terre-Neuve et du syndrome vestibulaire paradoxal chez un chien infecté par A. vasorum.(Traduit par Isabelle Vallières).