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週間人気論文ランキング - 閲覧数 (2012/01/28/ 06時更新)

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Neuropathological alterations in Alzheimer disease.

Serrano-Pozo Alberto , Frosch Matthew P , Masliah Eliezer , Hyman Bradley T
Cold Spring Harb Perspect Med.2011 Sep ; 1(1):a006189.
PMID: 22229116[]

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The neuropathological hallmarks of Alzheimer disease (AD) include "positive" lesions such as amyloid plaques and cerebral amyloid angiopathy, neurofibrillary tangles, and glial responses, and "negative" lesions such as neuronal and synaptic loss. Despite their inherently cross-sectional nature, postmortem studies have enabled the staging of the progression of both amyloid and tangle pathologies, and, consequently, the development of diagnostic criteria that are now used worldwide. In addition, clinicopathological correlation studies have been crucial to generate hypotheses about the pathophysiology of the disease, by establishing that there is a continuum between "normal" aging and AD dementia, and that the amyloid plaque build-up occurs primarily before the onset of cognitive deficits, while neurofibrillary tangles, neuron loss, and particularly synaptic loss, parallel the progression of cognitive decline. Importantly, these cross-sectional neuropathological data have been largely validated by longitudinal in vivo studies using modern imaging biomarkers such as amyloid PET and volumetric MRI.

Common Variants in 6 Lipid-Related Genes Discovered by High-Resolution DNA Melting Analysis and Their Association with Plasma Lipids.

Carlquist John F , McKinney Jason T , Horne Benjamin D , Camp Nicola J , Cannon-Albright Lisa , Muhlestein Joseph B , Hopkins Paul , Clarke Jessica L , Mower Chrissa P , Park James J , Nicholas Zachary P , Huntinghouse John A , Anderson Jeffrey L
J Clin Exp Cardiolog.2011 Jul 10 ; 2(138):.
PMID: 22229114[]

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BACKGROUND: Total cholesterol was among the earliest identified risk factors for coronary heart disease (CHD). We sought to identify genetic variants in six genes associated with lipid metabolism and estimate their respective contribution to risk for CHD. METHODS: For 6 lipid-associated genes (LCAT, CETP, LIPC, LPL, SCARB1, and ApoF) we scanned exons, 5' and 3' untranslated regions, and donor and acceptor splice sites for variants using Hi-Res Melting® curve analysis (HRMCA) with confirmation by cycle sequencing. Healthy subjects were used for SNP discovery (n=64), haplotype determination/tagging SNP discovery (n=339), and lipid association testing (n=786). RESULTS: In 17,840 bases of interrogated sequence, 90 variant SNPs were identified; 19 (21.1%) previously unreported. Thirty-four variants (37.8%) were exonic(16 non-synonymous), 28 (31.1%) in intron-exon boundaries, and 28 (31.1%) in the 5' and 3' untranslated regions. Compared to cycle sequencing, HRMCA had sensitivity of 99.4% and specificity of 97.7%. Tagging SNPs (n=38) explained >90% of the variation in the 6 genes and identified linkage disequilibrium (LD) groups. Significant beneficial lipid profiles were observed for CETP LD group 2, LIPC LD groups 1 and 7, and SCARB1 LD groups 1, 3 and 4. Risk profiles worsened for CETP LD group 3, LPL LD group 4. CONCLUSIONS: These findings demonstrate the feasibility, sensitivity, and specificity of HRMCA for SNP discovery. Variants identified in these genes may be used to predict lipid-associated risk and reclassification of clinical CHD risk.

Small protein-mediated quorum sensing in a gram-negative bacterium.

Han Sang-Wook , Sriariyanun Malinee , Lee Sang-Won , Sharma Manoj , Bahar Ofir , Bower Zachary , Ronald Pamela C
PLoS One.2011 ; 6(12):e29192.
PMID: 22174954[]

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The rice XA21 pattern recognition receptor binds a type I secreted sulfated peptide, called axY(S)22, derived from the Ax21 (activator of XA21-mediated immunity) protein. The conservation of Ax21 in all sequenced Xanthomonas spp. and closely related genera suggests that Ax21 serves a key biological function. Here we show that the predicted N-terminal sequence of Ax21 is cleaved prior to secretion outside the cell and that mature Ax21 serves as a quorum sensing (QS) factor in Xanthomonas oryzae pv. oryzae. Ax21-mediated QS controls motility, biofilm formation and virulence. We provide genetic evidence that the Xoo RaxH histidine kinase serves as the bacterial receptor for Ax21. This work establishes a critical role for small protein-mediated QS in a Gram-negative bacterium.

Quality, patient safety, and the board.

Curran Connie R , Totten Mary K
Nurs Econ.2010 Jul-Aug ; 28(4):273-5.
PMID: 21761613[]

213view,270users 保存 要約 閉じる

It is now broadly recognized that good outcomes for patients depend on more than a clinician's knowledge and skills and use of proven, effective practices or evidence-based medicine. Good outcomes also depend on the organization's culture, which affects how well providers and patients work together. Boards play a key role in helping their hospitals improve the quality and safety of the care they deliver--a governance imperative to ensure hospitals meet the needs of key stakeholders and perform effectively in an environment of reform. Nurse leaders who understand this key board responsibility will be better prepared to serve on boards and contribute to effective governance.

Effect of valsartan or olmesartan addition to amlodipine on ankle edema in hypertensive patients.

Fogari Roberto , Malamani Gian , Corradi Luca , Mugellini Amedeo , Preti Paola , Zoppi Annalisa , Derosa Giuseppe
Adv Ther.2010 Feb 19 ; ():.
PMID: 20174905[]

211view,37users 保存 要約 閉じる

INTRODUCTION: The objective of this study was to compare the effect on ankle edema of adding valsartan (V) or olmesartan (O) to amlodipine (A) in the treatment of hypertension. METHODS: After a 4-week placebo period, 74 adult outpatients with essential hypertension (diastolic blood pressure [DBP] >90 and <110 mmHg, and systolic blood pressure [SBP] >140 mmHg) were treated with A 10 mg once daily for 4 weeks. Thereafter, nonresponder patients (DBP >90 mmHg and/or SBP >140 mmHg; n=51) were randomized to receive additional V 160 mg once daily or O 20 mg once daily for 8 weeks in two crossover periods, each separated by a 4-week placebo period. Clinic blood pressure (BP), heart rate, and ankle/foot volume (AFV) were evaluated and blood samples were drawn to evaluate plasma norepinephrine (NE) levels. RESULTS: Both V/A and O/A induced a greater SBP/DBP reduction than A monotherapy (-26.4/-20.8 mmHg and -24.4/-19.1 mmHg, respectively; all P<0.001 vs. baseline and P<0.01 vs. A). A monotherapy increased AFV by 24%, P<0.001 vs. baseline, while the addition of either V or A reduced such increases. However, with V/A the AFV increase (+9.7%, P<0.05 vs. baseline, P<0.01 vs. A) was lower than with O/A (+16.7%, P<0.01 vs. baseline, P<0.05 vs. A); the difference between the two combinations was significant. Plasma NE levels were significantly increased by A (+44.6%) and values did not change with the addition of V (+35.2%) or O (+33.7%). Plasma active renin (PAR) was unchanged by A but increased by V/A (+214.4%, P<0.05 vs. baseline) and further by O/A (+325.6%, P<0.01 vs. baseline; difference between the 2 combinations: P<0.05). An inverse correlation was found between the AFV decrease and PAR increase (r=-0.31, P<0.05). CONCLUSION: Adding V or O to A reduced ankle edema, but this effect was more pronounced with V. The greater degree of renin-angiotensin system activation observed with Ocould be related to such a difference.

Blood pressure goal achievement with olmesartan medoxomil-based treatment: additional analysis of the OLMEBEST study.

Barrios Vivencio , Escobar Carlos , Calderon Alberto , Böhm Michael
Vasc Health Risk Manag.2009 ; 5():723-9.
PMID: 19756164[]

177view,705users 保存 要約 閉じる

AIMS: Guidelines recommend blood pressure (BP) in hypertensive patients should be <140 systolic BP (SBP) and <90 diastolic BP (DBP) mmHg. This analysis assessed goal rate achievement in hypertensive patients receiving olmesartan-based treatment in the OLMEBEST study. METHODS: Patients with essential hypertension (DBP > or = 90 mmHg and <110 mmHg) received open-label olmesartan medoxomil 20 mg/day (n = 2306). After 8 weeks, patients with DBP > or = 90 mmHg (n = 627) were randomized to 4 weeks' double-blind treatment with olmesartan 40 mg/day monotherapy or olmesartan 20 mg/day plus hydrochlorothiazide (HCTZ) 12.5 mg/day. For this analysis, the numbers and proportions of patients who achieved SBP < 140 mmHg and/or DBP < 90 mmHg at the end of the 4 weeks were calculated. RESULTS: In patients who achieved DBP normalization (<90 mmHg) at week 8 (n = 1546) and continued open-label olmesartan 20 mg/day, 66.7% achieved SBP/DBP < 140/90 mmHg at Week 12. In patients who did not achieve DBP normalization at Week 8, 26.8% of those randomized to olmesartan 40 mg/day and 42.5% of those randomized to olmesartan 20 mg/day plus HCTZ 12.5 mg/day achieved a SBP/DBP < 140/90 mmHg at Week 12. CONCLUSION: Olmesartan 40 mg/day and olmesartan 20 mg/day plus HCTZ 12.5 mg/day allow substantial proportions of patients to achieve BP goals.

Management of hepatitis B in developing countries.

Abbas Zaigham , Siddiqui Adeel R
World J Hepatol.2011 Dec 27 ; 3(12):292-9.
PMID: 22216369[]

177view,0users 保存 要約 閉じる

Hepatitis B is one of the leading causes of chronic hepatitis in developing countries, with 5% to 15% of the population carrying virus. The high prevalence is due to failure to adopt appropriate measure to confine the spread of infection. Most hepatitis B patients present with advanced diseases. Although perinatal transmission is believed to be an important mode, most infections in the developing world occur in childhood and early adulthood. Factors in developing countries associated with the progression of chronic hepatitis B (CHB) include co-infections with human immunodeficiency virus, delta hepatitis virus, hepatitis C virus, alcohol intake and aflatoxin. Treatment protocols extrapolated from developed countries may need modifications according to the resources available. There is some controversy as to when to start treatment, with what medication and for how long? There is now enough evidence to support that hepatitis B patients should be considered for treatment if they show persistently elevated abnormal aminotransferase levels in the last 6 mo, checked on at least three separate occasions, and a serum hepatitis B virus DNA level of > 2000 IU/mL. Therapeutic agents that were approved by Pure Food and Drug Administration are now available in many developing countries. These include standard interferon (INF)-α, pegylated INF-α, lamivudine, adefovir, entecavir and telbivudine. Drug resistance has emerged as a major challenge in the management of patients with CHB. The role of the universal vaccination program for effective control of hepatitis B cannot be emphasized enough.

Nanog and β-catenin: A new convergence point in EpSC proliferation and differentiation.

Yin Delong , Tian Linqiang , Ye Yaping , Li Kunpeng , Wang Jiang , Cheng Peng , Chen Anmin , Guo Fengjing , Huang Hui
Int J Mol Med.2011 Dec 29 ; ():.
PMID: 22211239[]

171view,0users 保存 要約 閉じる

Skin tissue homeostasis is maintained by the balanced proliferation and differentiation of certain types of proliferating cells such as epidermal stem cells (EpSCs). The proliferation and differentiation of EpSCs are complex processes which are not well understood. This study aimed to find the internal relationship between the Nanog pathway and the Wnt/β-catenin pathway in the proliferation and differentiation process of EpSCs. In brief, EpSCs were isolated from rat epidermis and cultured. The MTT assay, western blotting, polymerase chain reaction (PCR) and immunocytochemistry were performed during the proliferation and differentiation process of EpSCs. Our results showed that 10-7 M neuropeptide substance P could effectively stimulate proliferation of EpSCs and that a possible link exists between the Nanog pathway and the Wnt/β-catenin pathway.

A new phylogenetic method for identifying exceptional phenotypic diversification.

Revell Liam J , Mahler D Luke , Peres-Neto Pedro R , Redelings Benjamin D
Evolution.2012 Jan ; 66(1):135-46.
PMID: 22220870[]

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Currently available phylogenetic methods for studying the rate of evolution in a continuously valued character assume that the rate is constant throughout the tree or that it changes along specific branches according to an a priori hypothesis of rate variation provided by the user. Herein, we describe a new method for studying evolutionary rate variation in continuously valued characters given an estimate of the phylogenetic history of the species in our study. According to this method, we propose no specific prior hypothesis for how the variation in evolutionary rate is structured throughout the history of the species in our study. Instead, we use a Bayesian Markov Chain Monte Carlo approach to estimate evolutionary rates and the shift point between rates on the tree. We do this by simultaneously sampling rates and shift points in proportion to their posterior probability, and then collapsing the posterior sample into an estimate of the parameters of interest. We use simulation to show that the method is quite successful at identifying the phylogenetic position of a shift in the rate of evolution, and that estimated rates are asymptotically unbiased. We also provide an empirical example of the method using data for Anolis lizards. [This article was published online on September 20, 2011. An error in a co-author's name was subsequently identified. This notice is included in the online and print versions to indicate that both have been corrected September 21, 2011.].

New mixed metal selenites and tellurites containing Pd(2+) ions in a square planar geometry.

Zhang Su-Yun , Hu Chun-Li , Mao Jiang-Gao
Dalton Trans.2011 Dec 16 ; ():.
PMID: 22175062[]

168view,0users 保存 要約 閉じる

Four novel mixed metal selenites or tellurites containing PdO(4) squares, namely, BaPd(SeO(3))(2), Bi(2)Pd(SeO(3))(4), and Pb(2)Pd(QO(3))(2)Cl(2) (Q = Se, Te), have been prepared and structurally characterized by single crystal X-ray diffraction analyses. These compounds exhibit three different types of anionic structures. BaPd(SeO(3))(2) contains one-dimensional (1D) [Pd(SeO(3))(2)](2-) anionic chains composed of PdO(4) units linked by SeO(3)(2-) groups in a bidentate bridging fashion. Bi(2)Pd(SeO(3))(4) exhibits a complicated 3D architecture constructed by [Bi(SeO(3))](+) and [Pd(SeO(3))(2)](2-) layers that are alternating along the a-axis. The [Pd(SeO(3))(2)](2-) layers are composed of Pd(2+) ions bridged by SeO(3)(2-) anions in a bidentate fashion. Pb(2)Pd(QO(3))(2)Cl(2) (Q = Se, Te) features zero-dimensional (0D) [Pd(QO(3))Cl(2)](4-) (Q = Se, Te) anionic clusters, which are further bridged by Pb(2+) cations into a 3D network. The results of optical diffuse-reflectance spectrum measurements and band structure calculations based on DFT methods indicate that all the compounds are wide-band-gap semiconductors.

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週間人気論文ランキング - 保存数 (2012/01/28/ 06時更新)

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Blood pressure goal achievement with olmesartan medoxomil-based treatment: additional analysis of the OLMEBEST study.

Barrios Vivencio , Escobar Carlos , Calderon Alberto , Böhm Michael
Vasc Health Risk Manag.2009 ; 5():723-9.
PMID: 19756164[]

177view,705users 保存 要約 閉じる

AIMS: Guidelines recommend blood pressure (BP) in hypertensive patients should be <140 systolic BP (SBP) and <90 diastolic BP (DBP) mmHg. This analysis assessed goal rate achievement in hypertensive patients receiving olmesartan-based treatment in the OLMEBEST study. METHODS: Patients with essential hypertension (DBP > or = 90 mmHg and <110 mmHg) received open-label olmesartan medoxomil 20 mg/day (n = 2306). After 8 weeks, patients with DBP > or = 90 mmHg (n = 627) were randomized to 4 weeks' double-blind treatment with olmesartan 40 mg/day monotherapy or olmesartan 20 mg/day plus hydrochlorothiazide (HCTZ) 12.5 mg/day. For this analysis, the numbers and proportions of patients who achieved SBP < 140 mmHg and/or DBP < 90 mmHg at the end of the 4 weeks were calculated. RESULTS: In patients who achieved DBP normalization (<90 mmHg) at week 8 (n = 1546) and continued open-label olmesartan 20 mg/day, 66.7% achieved SBP/DBP < 140/90 mmHg at Week 12. In patients who did not achieve DBP normalization at Week 8, 26.8% of those randomized to olmesartan 40 mg/day and 42.5% of those randomized to olmesartan 20 mg/day plus HCTZ 12.5 mg/day achieved a SBP/DBP < 140/90 mmHg at Week 12. CONCLUSION: Olmesartan 40 mg/day and olmesartan 20 mg/day plus HCTZ 12.5 mg/day allow substantial proportions of patients to achieve BP goals.

Sodium-translocating NADH:Quinone oxidoreductase as a redox-driven ion pump.

Verkhovsky Michael I , Bogachev Alexander V
Biochim Biophys Acta.2010 Jan 4 ; ():.
PMID: 20056102[]

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The Na(+)-translocating NADH:ubiquinone oxidoreductase (Na(+)-NQR) is a component of the respiratory chain of various bacteria. This enzyme is an analogous but not homologous counterpart of mitochondrial Complex I. Na(+)-NQR drives the same chemistry and also uses released energy to translocate ions across the membrane, but it pumps Na(+) instead of H(+). Most likely the mechanism of sodium pumping is quite different from that of proton pumping (for example, it could not accommodate the Grotthuss mechanism of ion movement); this is why the enzyme structure, subunits and prosthetic groups are completely special. This review summarizes modern knowledge on the structural and catalytic properties of bacterial Na(+)-translocating NADH:quinone oxidoreductases. The sequence of electron transfer through the enzyme cofactors and thermodynamic properties of those cofactors are discussed. The resolution of the intermediates of the catalytic cycle and localization of sodium-dependent steps are combined in a possible molecular mechanism of sodium transfer by the enzyme.

Anthocyanins in cardiovascular disease.

Wallace Taylor C
Adv Nutr (Bethesda).2011 Jan ; 2(1):1-7.
PMID: 22211184[]

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Anthocyanins are a group of abundant and widely consumed flavonoid constituents that occur ubiquitously in the plant kingdom, providing the bright red-orange to blue-violet colors present in many fruit- and vegetable-based food products. Their intake has been estimated to be up to 9-fold higher than that of other dietary flavonoids. Anthocyanins have become increasingly important to the food industry as their use as natural alternatives to artificial colors has become widespread and knowledge of their health-promoting properties has become more evident. Epidemiological studies suggest that increased consumption of anthocyanins lowers the risk of cardiovascular disease (CVD), the most common cause of mortality among men and women. Anthocyanins frequently interact with other phytochemicals, exhibiting synergistic biological effects but making contributions from individual components difficult to decipher. Over the past 2 decades, many peer-reviewed publications have demonstrated that in addition to their noted in vitro antioxidant activity, anthocyanins may regulate different signaling pathways involved in the development of CVD. This review summarizes the latest developments on the bioavailability/bioactivity and CVD preventative activities of anthocyanins, including results from in vitro cell culture and in vivo animal model systems as related to their multiple proposed mechanisms of action. Limited yet promising data from epidemiological studies and human clinical trials are also presented. Future studies aimed at enhancing the absorption of anthocyanins and characterizing their metabolic and/or breakdown products are necessary to ultimately evaluate their use for protection/prevention against the development of CVD.

Effects of bacterial toxins on endothelial tight junction in vitro: a mechanism-based investigation.

Singh Ashok K , Jiang Yin , Gupta Shveta
Toxicol Mech Methods.2007 ; 17(6):331-47.
PMID: 20020957[]

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ABSTRACT Lipopolysaccharide (LPS) and lipoteichoic acid (LTA), principal cell wall components of Gram-negative and Gram-positive bacteria, respectively, play a central role in altering the blood-brain barrier and facilitate bacterial infection of the host brain. Despite the significance of bacterial toxins in disease pathogenesis, mechanisms by which toxins impair the barrier are not yet known. This study, using an in vitro cell culture model, showed that LPS and LTA interacted with the endothelial cells and disrupted the tight junction between the cells that increased the barrier's permeability. Both toxins increased inducible nitric oxide synthase (iNOS) mRNA that is indicative of an increase in intracellular NO release, disrupted architecture of the tight junction proteins, suppressed zonula occludens-1 (ZO-1) and occludin (OCL) and junctional adhesive molecules (JAM) mRNA levels, and increased tumor necrosis factor alpha (TNFalpha) and interleukin-1 beta (IL-1beta) mRNA levels. Anti-CD14 antibodies blocked the increase in TNFalpha and IL-1beta mRNA levels but did not affect either changes in the tight junction or iNOS, ZO-1, OCL, and JAM mRNA levels in endothelial cells and astrocytes. Although both toxins did not cross the endothelial barrier, the abluminal neurons exhibited high inflammatory activity characterized by a sequential increase in TNFalpha, IL-1beta, external receptor kinase (ERK), and RelA-p50 that induced inflammation, followed by an increase in anti-inflammatory/apoptotic factors including IL-10 and cysteine-aspartic acid protease-8 (CASPASE-8), which resolve inflammation and induce apoptosis. Anti-CD14 antibodies in luminal buffer blocked the pro- and anti-inflammatory effects of the toxins in neurons. Thus, the CD14-TLR cascade that participates in the inflammatory effects of toxins may not participate in the toxin-induced barrier disruption in vitro. Since the toxins did not cross the endothelial barrier, induction of inflammation in neurons was due to a release of proinflammatory cytokines in the abluminal fluid.

The RNase III enzyme Dicer is essential for germinal center B-cell formation.

Xu Shengli , Guo Ke , Zeng Qi , Huo Jianxin , Lam Kong-Peng
Blood.2011 Nov 23 ; ():.
PMID: 22117047[]

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MicroRNAs (miRNAs) are short non-coding RNAs that regulate gene expression and are important for pre-B and follicular B lymphopoiesis as demonstrated respectively, by mb-1-Cre- and cd19-Cre-mediated deletion of Dicer, the RNase III enzyme critical for generating mature miRNAs. To explore the role of miRNAs in B cell terminal differentiation, we use Aicda-Cre to specifically delete Dicer in activated B cells where activation-induced cytidine deaminase (AID) is highly expressed. We demonstrate that mutant mice fail to produce high-affinity class-switched antibodies and generate memory B and long-lived plasma cells (PCs) upon immunization with a T cell-dependent antigen. More importantly, germinal center (GC) B cell formation is drastically compromised in the absence of Dicer, as a result of defects in cell proliferation and survival. Dicer-deficient GC B cells express higher levels of cell cycle inhibitor genes and proapoptotic protein Bim. Ablation of Bim could partially rescue the defect in GC B cell formation in Dicer-deficient mice. Taken together, our data suggest that Dicer and likely, miRNAs are critical for GC B cell formation during B cell terminal differentiation.

Germinal center B and follicular helper T cells: siblings, cousins or just good friends?

Nutt Stephen L , Tarlinton David M
Nat Immunol.2011 Jun ; 12(6):472-7.
PMID: 21739669[]

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Humoral immunity requires interaction between specialized populations of B cells and CD4(+) T cells, called follicular helper T cells (T(FH) cells), in the germinal center (GC) to produce memory B cells and long-lived plasma cells. Molecular crosstalk between GC B cells and T(FH) cells influences the survival, proliferation and differentiation of each cell type. This pairing of GC B cells and T(FH) cells also occurs at the transcriptional level as the Bcl-6–IRF4–Blimp-1 axis, which is crucial for B cell differentiation, is also essential for the T(FH) cell identity. Less is known about the memory B cells that arise from the GC pool, as they seem to be distinctly 'programmed' on the basis of their antigen receptor affinity to enter the long-lived memory pool.

Contribution of chymase-dependent angiotensin II formation to the progression of tubulointerstitial fibrosis in obstructed kidneys in hamsters.

Fan Yu-Yan , Nishiyama Akira , Fujisawa Yoshihide , Kobori Hiroyuki , Nakano Daisuke , Matsuura Junji , Hase Naoki , Hitomi Hirofumi , Kiyomoto Hideyasu , Urata Hidenori , Kohno Masakazu
J Pharmacol Sci.2009 Sep ; 111(1):82-90.
PMID: 19721329[]

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Recent studies indicate a role of chymase in the regulation of angiotensin II (AngII) formation in cardiovascular and renal tissues. We investigated a possible contribution of chymase to AngII formation and to renal fibrosis in unilateral ureteral obstruction (UUO). Eight-week-old Syrian hamsters were subjected to UUO and treated with vehicle, the specific chymase inhibitor (CI) 4-[1-(4-methyl-benzo[b]thiophen-3-ylmethyl)-1H-benzimidazol-2-ylsulfanyl]-butyric acid (50 mg/kg, twice a day, p.o.), or the selective AT(1)-receptor blocker olmesartan (10 mg/kg per day, p.o.) for 14 days. UUO-induced renal interstitial fibrosis was associated with increases in renal mRNA levels of alpha-smooth muscle actin (SMA), type I collagen, and transforming growth factor (TGF)-beta. The UUO hamsters showed markedly higher AngII contents and increased AT(1)-receptor mRNA level in the obstructed kidney than sham-operated ones. In contrast, angiotensin-converting enzyme (ACE) protein expression was significantly lower in UUO hamsters. In UUO hamsters, treatment with CI or olmesartan significantly decreased AngII levels in renal tissue and mRNA levels of alpha-SMA, type I collagen, and TGF-beta and ameliorated tubulointerstitial injury. On the other hand, neither CI nor olmesartan changed systolic blood pressure, renal ACE, and AT(1)-receptor protein levels. These data suggest that chymase-dependent intrarenal AngII formation contributes to the pathogenesis of interstitial fibrosis in obstructed kidneys of hamsters.

Comparison of the long-term effects of candesartan and olmesartan on plasma angiotensin II and left ventricular mass index in patients with hypertension.

Hypertens Res.2009 Nov 20 ; ():.
PMID: 19927151[]

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In general, treatment with most angiotensin receptor blockers (ARBs) increases plasma angiotensin II (Ang II) level because of a lack of negative feedback on renin activity. Olmesartan is a potential ARB inducing activation of angiotensin-converting enzyme 2 (ACE2) that hydrolyzes Ang II to Ang 1-7, and has shown a beneficial effect on ventricular remodeling. Indeed, a previous study reported that olmesartan treatment resulted in decreased plasma levels of Ang II and aldosterone. However, there has not yet been a study showing the relationship of chronic effects of olmesartan on Ang II and the left ventricular mass index (LVMI) in comparison with those of other ARB.A total of 50 stable outpatients with essential hypertension who had received candesartan for more than 1 year were randomized into two groups: control group (n=25): continuous candesartan treatment at a stable dose; and olmesartan group (n=25): candesartan (8 mg day(-1)) was changed to olmesartan given at a dose of 20 mg day(-1). There was no difference in the baseline characteristics between the two groups. In the control group, there were no significant changes in blood pressure, LVMI or biomarkers during 12 months of study. In the olmesartan group, blood pressure did not change and plasma levels of Ang II decreased during 12 months of study, whereas LVMI was significantly decreased after 12 months (135+/-36 vs. 123+/-29 g m(-2); P<0.01).These findings indicate that replacing candesartan with olmesartan decreased LVMI in association with a sustained decrease of plasma Ang II over a 12-month period without changing blood pressure or plasma aldosterone in patients with essential hypertension.Hypertension Research advance online publication, 20 November 2009; doi:10.1038/hr.2009.192.

Hospitals, providers collaborate on transitions.

Hosp Case Manag.2012 Jan ; 20(1):11-2.
PMID: 22263244[]

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Baystate Health, a three-hospital system with headquarters in Springfield, MA, is partnering with post-acute providers to improve transitions as patients move through the continuum of care. A multidisciplinary post-acute performance team partnered with post-acute providers to determine why patients are readmitted to the hospital and to work on ways to avoid readmissions. Facilities share information with the hospitals how they operate and what they need to ensure patients receive the care they need. The health system's director of post-acute services holds regular meetings with providers to brainstorm on improving patient care.

Quality, patient safety, and the board.

Curran Connie R , Totten Mary K
Nurs Econ.2010 Jul-Aug ; 28(4):273-5.
PMID: 21761613[]

213view,270users 保存 要約 閉じる

It is now broadly recognized that good outcomes for patients depend on more than a clinician's knowledge and skills and use of proven, effective practices or evidence-based medicine. Good outcomes also depend on the organization's culture, which affects how well providers and patients work together. Boards play a key role in helping their hospitals improve the quality and safety of the care they deliver--a governance imperative to ensure hospitals meet the needs of key stakeholders and perform effectively in an environment of reform. Nurse leaders who understand this key board responsibility will be better prepared to serve on boards and contribute to effective governance.

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週間人気ジャーナルランキング - 閲覧数 (2012/01/28/ 07時更新)

保存数ランキング

The Journal of biological chemistry

9,347view , 462users

Proceedings of the National Academy of Sciences of the United States of America

6,195view , 272users

PloS one

5,425view , 301users

Physical review letters

3,905view , 0users

Science (New York, N.Y.)

3,773view , 107users

Journal of immunology (Baltimore, Md. : 1950)

3,551view , 257users

Journal of the American Chemical Society

3,334view , 0users

Biochemical and biophysical research communications

3,232view , 154users

Blood

3,074view , 503users

Biochimica et biophysica acta

3,048view , 747users

※view数：合計 user数：合計

週間人気ジャーナルランキング - 保存数 (2012/01/28/ 06時更新)

閲覧数ランキング

Biochimica et biophysica acta

3,048view , 747users

Vascular health and risk management

0view , 711users

Advances in nutrition (Bethesda, Md.)

0view , 570users

Toxicology mechanisms and methods

0view , 528users

Blood

3,074view , 503users

The Journal of biological chemistry

9,347view , 462users

Nature immunology

0view , 399users

Hypertension research : official journal of the Japanese Society of Hypertension

0view , 353users

PloS one

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Hospital case management : the monthly update on hospital-based care planning and critical paths

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BDNF induces polarized signaling of small GTPase (Rac1) at the onset of Schwann cell myelination through partitioning-defective 3 (Par3).

Tep Chhavy , Kim Mi Lyang , Opincariu Laura I , Limpert Allison S , Chan Jonah R , Appel Bruce , Carter Bruce D , Yoon Sung Ok
J Biol Chem.2011 Nov 29 ; ():.
PMID: 22128191[]

2011/11/30 保存 要約 閉じる

BDNF was shown to play a role in Schwann cell myelination by recruiting Par3 to exon-glial interface, but the underlying mechanism has remained unclear. Here we report that Par3 regulates Rac1 activation by BDNF, but not by NRG1-Type III in Schwann cells, although both ligands activate Rac1 in vivo. During development, active Rac1 signaling is localized in a polarized manner to axon-glial interface in Schwann cells. Knockdown of p75 and Par3 individually inhibits Rac1 activation, while constitutive activation of Rac1 disturbs the polarized activation of Rac1 in vivo. Polarized Rac1 activation is necessary for myelination as Par3 knockdown attenuates myelination in mouse sciatic nerves as well as in zebrafish. Specifically, Par3 knockdown in zebrafish disrupts proper alignment between the axon and Schwann cells without perturbing Schwann cell migration, suggesting that localized Rac1 activation at the axon-glial interface helps identifying the initial wrapping sites. We therefore conclude that polarized activation of Rac1 activation is critical for myelination.

Mutational analysis supports a core role for Drosophila α-Catenin in adherens junction function.

Sarpal Ritu , Pellikka Milena , Patel Ridhdhi R , Hui Felix Yan Wai , Godt Dorothea , Tepass Ulrich
J Cell Sci.2012 Jan 20 ; ():.
PMID: 22266901[]

2012/01/23 保存 要約 閉じる

α-catenin associates the cadherin-catenin complex with the actin cytoskeleton. α-catenin binds to β-catenin, which links it to the cadherin cytoplasmic tail, and F-actin, but also to a multitude of actin-associated proteins. These interactions suggest a highly complex cadherin-actin interface. Moreover, mammalian αΕ-catenin has been implicated in a cadherin-independent cytoplasmic function in Arp2/3-dependent actin regulation, and in cell signaling. The function and regulation of individual molecular interactions of α-catenin, in particular during development, are not well understood. We have generated mutations in Drosophila α-Catenin (α-Cat) to investigate α-Catenin function in this model, and to establish a setup for testing α-Catenin-related constructs in α-Cat-null mutant cells in vivo. Our analysis of α-Cat mutants in embryogenesis, imaginal discs and oogenesis reveals defects consistent with a loss of cadherin function. Compromising components of the Arp2/3 complex or its regulator SCAR ameliorate the α-Cat loss-of-function phenotype in embryos but not in ovaries, suggesting negative regulatory interactions between α-Catenin and the Arp2/3 complex in some tissues. We also show that the α-Cat mutant phenotype can be rescued by the expression of a DE-cadherin::α-Catenin fusion protein, which argues against an essential cytosolic, cadherin-independent role of Drosophila α-Catenin.

A crucial role for Nox 1 in redox-dependent regulation of Wnt-β-catenin signaling.

Kajla Seheli , Mondol Abdus S , Nagasawa Atsushi , Zhang Yugen , Kato Masayoshi , Matsuno Kuniharu , Yabe-Nishimura Chihiro , Kamata Tohru
FASEB J.2012 Jan 25 ; ():.
PMID: 22278940[]

2012/01/26 保存 要約 閉じる

Canonical Wnt signaling critically regulates cell fate and proliferation in developmental stages and adult tissues. Redox regulation through nucleoredoxin (NRX) has recently been identified in canonical Wnt signaling. However, the source of reactive oxygen species (ROS) affecting the redox state of NRX remains elusive. Our principal aim in this study was to investigate whether superoxide-generating NADPH oxidase1 (Nox1) is involved in NRX-regulated Wnt signaling in intestinal and colon epithelial cells. Here, we demonstrate that Wnt treatment of mouse intestinal cells induces production of ROS through Nox1. This Nox1 action is regulated by Rac1 GTPase through Wnt-induced activation of the Rac1 guanine nucleotide exchange factor Vav2 by Src-mediated tyrosine phosphorylation. Nox1-generated ROS oxidize and inactivate NRX, thereby releasing the NRX-dependent suppression of Wnt-β-catenin signaling through dissociation of NRX from Dvl. Nox1 small-interference RNA inhibits cell response to Wnt, including stabilization of β-catenin, expression of cyclin D1 and c-Myc via the TCF transcription factor, and accelerated cell proliferation. Nox1 mediates Wnt-induced cell growth in colon cancer cells with the normal Wnt pathway, but not in APC-deficient colon cancer cells, which are constitutively active in Wnt signaling. Together, these results suggest the mediating role of Nox1 in redox-dependent regulation of canonical Wnt-β-catenin signaling and provide further insight into the regulatory mechanism of the Wnt pathway.-Kajla, S., Mondol, A. S., Nagasawa, A., Zhang, Y., Kato, M., Matsuno, K., Yabe-Nishimura, C., Kamata, T. A crucial role for Nox 1 in redox-dependent regulation of Wnt-β-catenin signaling.

Diabetes, fracture, and bone fragility.

Schwartz Ann V , Sellmeyer Deborah E
Curr Osteoporos Rep.2007 Sep ; 5(3):105-11.
PMID: 17925191[]

2007/10/10 保存 要約 閉じる

Recent studies have added to the evidence that type 1 and type 2 diabetes are associated with increased risk of hip fracture and other fractures. More frequent falls probably account for some of this increased risk, but reduced bone strength may also play a role. Although type 1 diabetes is associated with lower bone density, those with type 2 diabetes usually have elevated bone density. Yet for both types of diabetes, bone appears to be more fragile for a given density. Diabetes can affect bone through multiple pathways-some with contradictory effects-including obesity, insulin levels, hyperglycemia, and advanced glycation end products in collagen. Treatment with thiazolidinediones may increase fracture risk, at least in older women. Clinicians need to be aware of the increased fracture risk associated with diabetes. Additional research is needed to clarify the mechanisms underlying this increased risk and the best approaches to fracture prevention.

Type 2 diabetes and bone fractures.

Moseley Kendall F
Curr Opin Endocrinol Diabetes Obes.2012 Jan 18 ; ():.
PMID: 22262002[]

2012/01/20 保存 要約 閉じる

PURPOSE OF REVIEW: To discuss current literature and hypotheses pertaining to the pathophysiology of increased bone fragility and fracture in men and women with type 2 diabetes mellitus. RECENT FINDINGS: Despite high bone mineral density, studies have shown that men and women with type 2 diabetes mellitus (T2DM) are at increased risk for fracture. Complications of T2DM including retinopathy and autonomic dysfunction may contribute to bone fracture by increasing fall risk. Nephropathy may lead to renal osteodystrophy. Lean mass and potentially fat mass, may additionally contribute to skeletal health in diabetes. There is increasing acknowledgement that the marrow microenvironment is critical to efficient bone remodeling. Medications including thiazolidinediones and selective serotonin reuptake inhibitors may also impair bone remodeling by acting on mesenchymal stem cell differentiation and osteoblastogenesis. T2DM is associated with significant alterations in systemic inflammation, advanced glycation end-product accumulation and reactive oxygen species generation. These systemic changes may also directly and adversely impact the remodeling cycle and lead to bone fragility in T2DM, though more research is needed. SUMMARY: Fracture is a devastating event with dismal health consequences. Identifying the extrinsic and intrinsic biochemical causes of bone fracture in T2DM will speed the discovery of effective strategies for fracture prevention and treatment in this at-risk population.

A large-scale, randomized clinical study on functional dyspepsia treatment with mosapride or teprenone: Japan Mosapride Mega-Study (JMMS).

Hongo Michio , Harasawa Shigeru , Mine Tetsuya , Sasaki Iwao , Matsueda Kei , Kusano Motoyasu , Hanyu Nobuyasu , Nakada Koji , Shibata Chikashi
J Gastroenterol Hepatol.2011 Oct 17 ; ():.
PMID: 22004457[]

2011/10/18 保存 要約 閉じる

Background and Aims: Functional dyspepsia (FD) is a common condition seen in primary gastroenterology practice. The present study was conducted to compare the clinical effectiveness of mosapride and teprenone in patients with FD. Methods: Prospective clinical comparative study with random allocation of open labeled medications was performed as a multicenter trial in Japan. 1,042 patients presenting symptoms of FD, either with gastric stasis (GSS) and/or epigastric pain (EPS), were enrolled. After initial endoscopic evaluation, medication either with mosapride 5 mg tid or teprenone 50 mg tid was started. Severity and frequency of GSS and EPS, health-related quality-of-life (HR-QOL) by the SF-36 Japanese version, and patients' compliance to medication was evaluated. Results: Organic lesions were found in 90 patients (9%) in the 1,027 patients examined by endoscopy. Among those without any specific lesions detected by endoscopy, gastrointestinal symptoms were resolved within one week after the endoscopy in 264 (28%) patients before initiating medication. 618 patients who remained symptomatic were randomized to medication either with mosapride (n = 311) or teprenone (n = 307). Two-week treatment with mosapride significantly improved GSS and EPS, while teprenone tended to improve only GSS. Mosapride also improved HR-QOL. 91% patients treated with mosapride, while 52% patients with teprenone favored their medication. Conclusions: Endoscopic evaluation at patients' presentation was effective to find active lesions and to improve FD symptoms. Mosapride was more favorably accepted than teprenone by the patients with sufficient safety and efficacy.

The take-it-or-leave-it option allows small penalties to overcome social dilemmas.

Sasaki Tatsuya , Brännström Ake , Dieckmann Ulf , Sigmund Karl
Proc Natl Acad Sci U S A.2012 Jan 9 ; ():.
PMID: 22232694[]

2012/01/10 保存 要約 閉じる

Self-interest frequently causes individuals engaged in joint enterprises to choose actions that are counterproductive. Free-riders can invade a society of cooperators, causing a tragedy of the commons. Such social dilemmas can be overcome by positive or negative incentives. Even though an incentive-providing institution may protect a cooperative society from invasion by free-riders, it cannot always convert a society of free-riders to cooperation. In the latter case, both norms, cooperation and defection, are stable: To avoid a collapse to full defection, cooperators must be sufficiently numerous initially. A society of free-riders is then caught in a social trap, and the institution is unable to provide an escape, except at a high, possibly prohibitive cost. Here, we analyze the interplay of (a) incentives provided by institutions and (b) the effects of voluntary participation. We show that this combination fundamentally improves the efficiency of incentives. In particular, optional participation allows institutions punishing free-riders to overcome the social dilemma at a much lower cost, and to promote a globally stable regime of cooperation. This removes the social trap and implies that whenever a society of cooperators cannot be invaded by free-riders, it will necessarily become established in the long run, through social learning, irrespective of the initial number of cooperators. We also demonstrate that punishing provides a "lighter touch" than rewarding, guaranteeing full cooperation at considerably lower cost.

The take-it-or-leave-it option allows small penalties to overcome social dilemmas.

Sasaki Tatsuya , Brännström Ake , Dieckmann Ulf , Sigmund Karl
Proc Natl Acad Sci U S A.2012 Jan 9 ; ():.
PMID: 22232694[]

2012/01/10 保存 要約 閉じる

Self-interest frequently causes individuals engaged in joint enterprises to choose actions that are counterproductive. Free-riders can invade a society of cooperators, causing a tragedy of the commons. Such social dilemmas can be overcome by positive or negative incentives. Even though an incentive-providing institution may protect a cooperative society from invasion by free-riders, it cannot always convert a society of free-riders to cooperation. In the latter case, both norms, cooperation and defection, are stable: To avoid a collapse to full defection, cooperators must be sufficiently numerous initially. A society of free-riders is then caught in a social trap, and the institution is unable to provide an escape, except at a high, possibly prohibitive cost. Here, we analyze the interplay of (a) incentives provided by institutions and (b) the effects of voluntary participation. We show that this combination fundamentally improves the efficiency of incentives. In particular, optional participation allows institutions punishing free-riders to overcome the social dilemma at a much lower cost, and to promote a globally stable regime of cooperation. This removes the social trap and implies that whenever a society of cooperators cannot be invaded by free-riders, it will necessarily become established in the long run, through social learning, irrespective of the initial number of cooperators. We also demonstrate that punishing provides a "lighter touch" than rewarding, guaranteeing full cooperation at considerably lower cost.

Activation-Induced B Cell Fates Are Selected by Intracellular Stochastic Competition.

Duffy Ken R , Wellard Cameron J , Markham John F , Zhou Jie H S , Holmberg Ross , Hawkins Edwin D , Hasbold Jhagvaral , Dowling Mark R , Hodgkin Philip D
Science.2012 Jan 5 ; ():.
PMID: 22223740[]

2012/01/06 保存 要約 閉じる

In response to stimulation, B lymphocytes pursue a large number of distinct fates important for immune regulation. Whether each cell's fate is determined by external direction, internal stochastic processes, or directed asymmetric division is unknown. Measurement of times to isotype switch, to develop into a plasmablast, and to divide or to die for thousands of cells indicated that each fate is pursued autonomously and stochastically. As a consequence of competition between these processes, censorship of alternative outcomes predicts intricate correlations that are observed in the data. Stochastic competition can explain how the allocation of a proportion of B cells to each cell fate is achieved. The B cell may exemplify how other complex cell differentiation systems are controlled.

B Cell-Derived IL-10 Does Not Regulate Spontaneous Systemic Autoimmunity in MRL.Faslpr Mice.

Teichmann Lino L , Kashgarian Michael , Weaver Casey T , Roers Axel , Müller Werner , Shlomchik Mark J
J Immunol.2011 Dec 9 ; ():.
PMID: 22156495[]

2011/12/13 保存 要約 閉じる

B cells contribute to the pathogenesis of chronic autoimmune disorders, like systemic lupus erythematosus (SLE), via multiple effector functions. However, B cells are also implicated in regulating SLE and other autoimmune syndromes via release of IL-10. B cells secreting IL-10 were termed "Bregs" and were proposed as a separate subset of cells, a concept that remains controversial. The balance between pro- and anti-inflammatory effects could determine the success of B cell-targeted therapies for autoimmune disorders; therefore, it is pivotal to understand the significance of B cell-secreted IL-10 in spontaneous autoimmunity. By lineage-specific deletion of Il10 from B cells, we demonstrated that B cell-derived IL-10 is ineffective in suppressing the spontaneous activation of self-reactive B and T cells during lupus. Correspondingly, severity of organ disease and survival rates in mice harboring Il10-deficient B cells are unaltered. Genetic marking of cells that transcribe Il10 illustrated that the pool of IL-10-competent cells is dominated by CD4 T cells and macrophages. IL-10-competent cells of the B lineage are rare in vivo and, among them, short-lived plasmablasts have the highest frequency, suggesting an activation-driven, rather than lineage-driven, phenotype. Putative Breg phenotypic subsets, such as CD1d(hi)CD5(+) and CD21(hi)CD23(hi) B cells, are not enriched in Il10 transcription. These genetic studies demonstrated that, in a spontaneous model of murine lupus, IL-10-dependent B cell regulation does not restrain disease and, thus, the pathogenic effects of B cells are not detectably counterbalanced by their IL-10-dependent regulatory functions.

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Effects of bacterial toxins on endothelial tight junction in vitro: a mechanism-based investigation.

Singh Ashok K , Jiang Yin , Gupta Shveta
Toxicol Mech Methods.2007 ; 17(6):331-47.
PMID: 20020957[]

先週： 50位 12,177view,1users 保存 要約 閉じる

ABSTRACT Lipopolysaccharide (LPS) and lipoteichoic acid (LTA), principal cell wall components of Gram-negative and Gram-positive bacteria, respectively, play a central role in altering the blood-brain barrier and facilitate bacterial infection of the host brain. Despite the significance of bacterial toxins in disease pathogenesis, mechanisms by which toxins impair the barrier are not yet known. This study, using an in vitro cell culture model, showed that LPS and LTA interacted with the endothelial cells and disrupted the tight junction between the cells that increased the barrier's permeability. Both toxins increased inducible nitric oxide synthase (iNOS) mRNA that is indicative of an increase in intracellular NO release, disrupted architecture of the tight junction proteins, suppressed zonula occludens-1 (ZO-1) and occludin (OCL) and junctional adhesive molecules (JAM) mRNA levels, and increased tumor necrosis factor alpha (TNFalpha) and interleukin-1 beta (IL-1beta) mRNA levels. Anti-CD14 antibodies blocked the increase in TNFalpha and IL-1beta mRNA levels but did not affect either changes in the tight junction or iNOS, ZO-1, OCL, and JAM mRNA levels in endothelial cells and astrocytes. Although both toxins did not cross the endothelial barrier, the abluminal neurons exhibited high inflammatory activity characterized by a sequential increase in TNFalpha, IL-1beta, external receptor kinase (ERK), and RelA-p50 that induced inflammation, followed by an increase in anti-inflammatory/apoptotic factors including IL-10 and cysteine-aspartic acid protease-8 (CASPASE-8), which resolve inflammation and induce apoptosis. Anti-CD14 antibodies in luminal buffer blocked the pro- and anti-inflammatory effects of the toxins in neurons. Thus, the CD14-TLR cascade that participates in the inflammatory effects of toxins may not participate in the toxin-induced barrier disruption in vitro. Since the toxins did not cross the endothelial barrier, induction of inflammation in neurons was due to a release of proinflammatory cytokines in the abluminal fluid.

A G-protein gamma subunit mimic is a general antagonist of prion propagation in Saccharomyces cerevisiae.

Ishiwata Masao , Kurahashi Hiroshi , Nakamura Yoshikazu
Proc Natl Acad Sci U S A.2009 Jan 20 ; 106(3):791-6.
PMID: 19129493[]

先週： 63位 1,219view,1users 保存 要約 閉じる

The Gpg1 protein is a Ggamma subunit mimic implicated in the G-protein glucose-signaling pathway in Saccharomyces cerevisiae, and its function is largely unknown. Here we report that Gpg1 blocks the maintenance of [PSI(+)], an aggregated prion form of the translation termination factor Sup35. Although the GPG1 gene is normally not expressed, over-expression of GPG1 inhibits propagation of not only [PSI(+)] but also [PIN(+)], [URE3] prions, and the toxic polyglutamine aggregate in S. cerevisiae. Over-expression of Gpg1 does not affect expression and activity of Hsp104, a protein-remodeling factor required for prion propagation, showing that Gpg1 does not target Hsp104 directly. Nevertheless, prion elimination by Gpg1 is weakened by over-expression of Hsp104. Importantly, Gpg1 protein is prone to self-aggregate and transiently colocalized with Sup35NM-prion aggregates when expressed in [PSI(+)] cells. Genetic selection and characterization of loss-of-activity gpg1 mutations revealed that multiple mutations on the hydrophobic one-side surface of predicted alpha-helices of the Gpg1 protein hampered the activity. Prion elimination by Gpg1 is unaffected in the gpa2Delta and gpb1Delta strains lacking the supposed physiological G-protein partners of Gpg1. These findings suggest a general inhibitory interaction of the Gpg1 protein with other transmissible and nontransmissible amyloids, resulting in prion elimination. Assuming the ability of Gpg1 to form G-protein heterotrimeric complexes, Gpg1 is likely to play a versatile function of reversing the prion state and modulating the G-protein signaling pathway.

Germinal center B and follicular helper T cells: siblings, cousins or just good friends?

Nutt Stephen L , Tarlinton David M
Nat Immunol.2011 Jun ; 12(6):472-7.
PMID: 21739669[]

先週： 64位 515view,1users 保存 要約 閉じる

Humoral immunity requires interaction between specialized populations of B cells and CD4(+) T cells, called follicular helper T cells (T(FH) cells), in the germinal center (GC) to produce memory B cells and long-lived plasma cells. Molecular crosstalk between GC B cells and T(FH) cells influences the survival, proliferation and differentiation of each cell type. This pairing of GC B cells and T(FH) cells also occurs at the transcriptional level as the Bcl-6–IRF4–Blimp-1 axis, which is crucial for B cell differentiation, is also essential for the T(FH) cell identity. Less is known about the memory B cells that arise from the GC pool, as they seem to be distinctly 'programmed' on the basis of their antigen receptor affinity to enter the long-lived memory pool.

Germinal center B and follicular helper T cells: siblings, cousins or just good friends?

Nutt Stephen L , Tarlinton David M
Nat Immunol.2011 Jun ; 12(6):472-7.
PMID: 21739669[]

先週： 64位 1view,1users 保存 要約 閉じる

Humoral immunity requires interaction between specialized populations of B cells and CD4(+) T cells, called follicular helper T cells (T(FH) cells), in the germinal center (GC) to produce memory B cells and long-lived plasma cells. Molecular crosstalk between GC B cells and T(FH) cells influences the survival, proliferation and differentiation of each cell type. This pairing of GC B cells and T(FH) cells also occurs at the transcriptional level as the Bcl-6–IRF4–Blimp-1 axis, which is crucial for B cell differentiation, is also essential for the T(FH) cell identity. Less is known about the memory B cells that arise from the GC pool, as they seem to be distinctly 'programmed' on the basis of their antigen receptor affinity to enter the long-lived memory pool.

A fine romance: T follicular helper cells and B cells.

King Cecile
Immunity.2011 Jun 24 ; 34(6):827-9.
PMID: 21703537[]

先週： 65位 343view,1users 保存 要約 閉じる

T follicular helper (Tfh) cells help B cells to generate affinity-matured antibodies. Three papers in this issue of Immunity (Choi et al., 2011; Kerfoot et al., 2011; Kitano et al., 2011) provide information about the reciprocal relationship between B cells and Tfh cells.

Programmed Cell Death 1 Suppresses B-1b Cell Expansion and Long-Lived IgG Production in Response to T Cell-Independent Type 2 Antigens.

Haas Karen M
J Immunol.2011 Oct 14 ; ():.
PMID: 22003198[]

先週： 66位 289view,1users 保存 要約 閉じる

B-1b cells play a key role in producing Abs against T cell-independent type 2 Ags. However, the factors regulating Ab production by this unique B cell subset are not well understood. In this study, a detailed analysis of the B cell response to 2,4,6-trinitrophenol (TNP)-Ficoll was performed using normal mice. TNP-Ficoll delivered i.p. or i.v. induced rapid Ag-specific B-1b cell activation, expansion, isotype switching, and plasmablast/plasma cell differentiation. Ag-specific B-1b cell numbers peaked at day 5 and then gradually declined in the spleen but remained elevated in the peritoneal cavity beyond 40 d postimmunization. In addition to expressing CD43, CD44, and CD86, Ag-activated B-1b cells transiently expressed programmed cell death 1 (PD-1), which functionally suppressed BCR-induced B-1b cell in vitro proliferation when additional costimulatory signals were lacking. Inhibiting PD-1:PD-1 ligand interactions during TNP-Ficoll immunization significantly enhanced Ag-specific B-1b cell expansion and the frequency of IgG isotype switching and plasmablast/plasma cell differentiation. Remarkably, PD-1 mAb blockade during the first week following immunization resulted in significantly increased numbers of both splenic and bone marrow Ag-specific IgG3-secreting cells, but not IgM-secreting cells, at both early (day 5) and late (week 6) time points. Moreover, Ag-specific serum IgG3 levels, as well as IgG2c, IgG2b, and IgA levels, remained significantly elevated in PD-1 mAb-treated mice relative to control Ab-treated mice for ≥6 wk postimmunization. Thus, PD-1:PD-1 ligand interactions occurring shortly after initial T cell-independent type 2 Ag encounter play a critical role in suppressing Ag-specific B-1b cell expansion and the development of long-term IgG-producing bone marrow and spleen cells.

Immunization induces activation of bone marrow eosinophils required for plasma cell survival.

Chu Van Trung , Berek Claudia
Eur J Immunol.2011 Nov 7 ; ():.
PMID: 22057654[]

先週： 67位 197view,1users 保存 要約 閉じる

Eosinophils have multiple functions as effector cells of the innate immune system but also as modulators of immune responses. As producers of cytokines required for plasma cell survival, they are essential for the long-term maintenance of plasma cells in the bone marrow (BM). Here we show that activation of eosinophils both in vitro and in vivo enhances expression of the plasma cell survival factors APRIL, IL-6, IL-4, IL-10 and TNF-α. The in vivo activation of eosinophils is independent of the type of adjuvant used for primary immunization. Although eosinophils are activated by adjuvant itself, a stable activation and a constant increase in BM eosinophils is observed only in the presence of antigen. Thus, the numbers and the quality of eosinophils are dependent on priming the adaptive immune system. With secondary immunization and re-activation of antigen dependent memory cells, the ability of eosinophils to promote plasma cell survival is further increased. These findings suggest that in T cell-dependent immune responses eosinophils are conditioned so as to support the long-term survival of plasma cells in the BM. It implies that through accelerated numbers of eosinophils stable plasma cell survival niches are established and the long term survival of plasma cells is ensured.

Low density lipoprotein receptor-related protein 5 (LRP5) mutations and osteoporosis, impaired glucose metabolism and hypercholesterolaemia.

Saarinen Anne , Saukkonen Tero , Kivelä Tero , Lahtinen Ulla , Laine Christine , Somer Mirja , Toiviainen-Salo Sanna , Cole William G , Lehesjoki Anna-Elina , Mäkitie Outi
Clin Endocrinol (Oxf).2010 Apr ; 72(4):481-8.
PMID: 19673927[]

先週： 68位 1,097view,1users 保存 要約 閉じる

OBJECTIVE: Mutations in the low-density lipoprotein receptor-related protein 5 gene (LRP5) underlie osteoporosis-pseudoglioma syndrome. Animal models implicate a role for LRP5 in lipid and glucose homeostasis. The objective was to evaluate metabolic consequences of LRP5 mutations in humans. DESIGN AND PATIENTS: Thirteen Finnish individuals with homozygous or heterozygous LRP5 mutations were assessed for bone health, glucose and lipid metabolism, and for serum serotonin concentration. Results were compared with findings in family members without mutations. MEASUREMENTS: Bone mineral density (BMD), vertebral morphology, oral and intravenous glucose tolerance tests, lipid profile and serum serotonin concentrations. RESULTS: Two individuals were homozygous for R570W, one compound heterozygous for R570W and R1036Q, and 10 were heterozygous (six for R570W, three for R1036Q and one for R925C). Subjects with two LRP5 mutations had multiple spinal fractures and low BMD. Subjects with one mutation had significantly lower median lumbar spine (P = 0.004) and femoral neck (P = 0.005) BMD Z-scores, and more often vertebral fractures than the 18 individuals without mutations. Of the 12 subjects with LRP5 mutation six had diabetes and one had impaired glucose tolerance. Intravenous glucose tolerance tests suggested impaired beta-cell function; no insulin resistance was observed. Prevalence of hypercholesterolaemia was similar in mutation positive and negative subjects. Serum serotonin concentrations showed a trend towards higher concentrations in subjects with LRP5 mutation. CONCLUSIONS: We found high prevalence of osteoporosis and abnormal glucose metabolism in subjects with LRP5 mutation(s). Further studies are needed to establish the role of LRP5 in glucose and lipid metabolism.

In vitro cell quality of buffy coat platelets in additive solution treated with pathogen reduction technology.

Ostrowski Sisse R , Bochsen Louise , Salado-Jimena José A , Ullum Henrik , Reynaerts Inge , Goodrich Raymond P , Johansson Pär I
Transfusion.2010 Oct ; 50(10):2210-9.
PMID: 20456708[]

先週： 69位 2,319view,1users 保存 要約 閉じる

BACKGROUND: Pathogen reduction technologies (PRTs) may induce storage lesion in platelet (PLT) concentrates. To investigate this, buffy coat PLTs (BCPs) in PLT additive solution (AS; SSP+) with or without Mirasol PRT (CaridianBCT Biotechnologies) were assessed by quality control tests and four-color flow cytometry. STUDY DESIGN AND METHODS: In vitro comparison of PRT and control pooled-and-split BCPs after 2, 3, 6, 7, and 8 days of storage was made. PLT concentration, count per unit, swirl, metabolism, activation (CD62P, PAC1, CD42b/GPIb, CD63, CD40L/CD154, CD40, annexin V), and microparticle, sCD40L, and sCD62P release were evaluated. RESULTS: PRT induced a minor initial PLT loss (Day 2 [mean±SD], 302×10(9) ±44×10(9) PLTs/unit vs. 325× 10(9) ±46×10(9) PLTs/unit; p<0.001) but the decline was comparable to control BCP. Swirling was comparable and declined with similar rates in PRT-treated and control BCPs during storage. PRT enhanced PLT metabolism and activation, evidenced by lower pH(22) ; increased glucose consumption and lactate production rates (p<0.01); early increases in CD62P-, PAC1-, CD63-, CD40L-, CD40-, and annexin V-positive PLTs; reduced GPIb expression; and enhanced release of PLT-derived MPs and sCD40L (all p<0.05). CD62P and PAC1 expression changed with different kinetics during storage and varying GPIb expression was displayed within the CD62P/PAC1-positive PLT subsets. CONCLUSION: PRT treatment of BCP in AS induced a minor initial PLT loss and enhanced metabolism and PLT activation. The clinical relevance for PLT function in vivo of these findings will be investigated in a clinical trial.

Origins of CD4(+) effector and central memory T cells.

Pepper Marion , Jenkins Marc K
Nat Immunol.2011 Jun ; 12(6):467-71.
PMID: 21739668[]

先週： 70位 389view,1users 保存 要約 閉じる

Lineage-committed effector CD4(+) T cells are generated at the peak of the primary response and are followed by heterogeneous populations of central and effector memory cells. Here we review the evidence that T helper type 1 (T(H)1) effector cells survive the contraction phase of the primary response and become effector memory cells. We discuss the applicability of this idea to the T(H)2 cell, T(H)17 helper T cell, follicular helper T cell (T(FH) cell) and induced regulatory T cell lineages. We also discuss how central memory cells are formed, with an emphasis on the role of B cells in this process.

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Association between Interpersonal Trust, Reciprocity, and Depression in South Korea: A Prospective Analysis.

Kim Seung-Sup , Chung Yeonseung , Perry Melissa J , Kawachi Ichiro , Subramanian S V
PLoS One.2012 ; 7(1):e30602.
PMID: 22279597[]

2012/01/26 保存 要約 閉じる

A growing body of empirical evidence indicates that low-level social capital is related to poor mental health outcomes. However, the prospective association between social capital and depression remains unclear, and no published studies have investigated the association with longitudinal data in East-Asian countries.

Unsaturated Fatty acids revert diet-induced hypothalamic inflammation in obesity.

Cintra Dennys E , Ropelle Eduardo R , Moraes Juliana C , Pauli José R , Morari Joseane , de Souza Claudio T , Grimaldi Renato , Stahl Marcela , Carvalheira José B , Saad Mario J , Velloso Licio A
PLoS One.2012 ; 7(1):e30571.
PMID: 22279596[]

2012/01/26 保存 要約 閉じる

In experimental models, hypothalamic inflammation is an early and determining factor in the installation and progression of obesity. Pharmacological and gene-based approaches have proven efficient in restraining inflammation and correcting the obese phenotypes. However, the role of nutrients in the modulation of hypothalamic inflammation is unknown.

Rapid Evaluation in Whole Blood Culture of Regimens for XDR-TB Containing PNU-100480 (Sutezolid), TMC207, PA-824, SQ109, and Pyrazinamide.

Wallis Robert S , Jakubiec Wesley , Mitton-Fry Mark , Ladutko Lynn , Campbell Sheldon , Paige Darcy , Silvia Annette , Miller Paul F
PLoS One.2012 ; 7(1):e30479.
PMID: 22279595[]

2012/01/26 保存 要約 閉じる

There presently is no rapid method to assess the bactericidal activity of new regimens for tuberculosis. This study examined PNU-100480, TMC207, PA-824, SQ109, and pyrazinamide, singly and in various combinations, against intracellular M. tuberculosis, using whole blood culture (WBA). The addition of 1,25-dihydroxy vitamin D facilitated detection of the activity of TMC207 in the 3-day cultures. Pyrazinamide failed to show significant activity against a PZA-resistant strain (M. bovis BCG), and was not further considered. Low, mid, and high therapeutic concentrations of each remaining drug were tested individually and in a paired checkerboard fashion. Observed bactericidal activity was compared to that predicted by the sum of the effects of individual drugs. Combinations of PNU-100480, TMC207, and SQ109 were fully additive, whereas those including PA-824 were less than additive or antagonistic. The cumulative activities of 2, 3, and 4 drug combinations were predicted based on the observed concentration-activity relationship, published pharmacokinetic data, and, for PNU-100480, published WBA data after oral dosing. The most active regimens, including PNU-100480, TMC207, and SQ109, were predicted to have cumulative activity comparable to standard TB therapy. Further testing of regimens including these compounds is warranted. Measurement of whole blood bactericidal activity can accelerate the development of novel TB regimens.

Wiring a Periscope - Ocelli, Retinula Axons, Visual Neuropils and the Ancestrality of Sea Spiders.

Lehmann Tobias , Heß Martin , Melzer Roland R
PLoS One.2012 ; 7(1):e30474.
PMID: 22279594[]

2012/01/26 保存 要約 閉じる

The Pycnogonida or sea spiders are cryptic, eight-legged arthropods with four median ocelli in a 'periscope' or eye tubercle. In older attempts at reconstructing phylogeny they were Arthropoda incertae sedis, but recent molecular trees placed them as the sister group either to all other euchelicerates or even to all euarthropods. Thus, pycnogonids are among the oldest extant arthropods and hold a key position for the understanding of arthropod evolution. This has stimulated studies of new sets of characters conductive to cladistic analyses, e.g. of the chelifores and of the hox gene expression pattern. In contrast knowledge of the architecture of the visual system is cursory. A few studies have analysed the ocelli and the uncommon "pseudoinverted" retinula cells. Moreover, analyses of visual neuropils are still at the stage of Hanström's early comprehensive works. We have therefore used various techniques to analyse the visual fibre pathways and the structure of their interrelated neuropils in several species. We found that pycnogonid ocelli are innervated to first and second visual neuropils in close vicinity to an unpaired midline neuropil, i.e. possibly the arcuate body, in a way very similar to ancestral euarthropods like Euperipatoides rowelli (Onychophora) and Limulus polyphemus (Xiphosura). This supports the ancestrality of pycnogonids and sheds light on what eyes in the pycnogonid ground plan might have 'looked' like. Recently it was suggested that arthropod eyes originated from simple ocelli similar to larval eyes. Hence, pycnogonid eyes would be one of the early offshoots among the wealth of more sophisticated arthropod eyes.

Informatics technology mimics ecology: dense, mutualistic collaboration networks are associated with higher publication rates.

Sorani Marco D
PLoS One.2012 ; 7(1):e30463.
PMID: 22279593[]

2012/01/26 保存 要約 閉じる

Information technology (IT) adoption enables biomedical research. Publications are an accepted measure of research output, and network models can describe the collaborative nature of publication. In particular, ecological networks can serve as analogies for publication and technology adoption. We constructed network models of adoption of bioinformatics programming languages and health IT (HIT) from the literature.We selected seven programming languages and four types of HIT. We performed PubMed searches to identify publications since 2001. We calculated summary statistics and analyzed spatiotemporal relationships. Then, we assessed ecological models of specialization, cooperativity, competition, evolution, biodiversity, and stability associated with publications.Adoption of HIT has been variable, while scripting languages have experienced rapid adoption. Hospital systems had the largest HIT research corpus, while Perl had the largest language corpus. Scripting languages represented the largest connected network components. The relationship between edges and nodes was linear, though Bioconductor had more edges than expected and Perl had fewer. Spatiotemporal relationships were weak. Most languages shared a bioinformatics specialization and appeared mutualistic or competitive. HIT specializations varied. Specialization was highest for Bioconductor and radiology systems. Specialization and cooperativity were positively correlated among languages but negatively correlated among HIT. Rates of language evolution were similar. Biodiversity among languages grew in the first half of the decade and stabilized, while diversity among HIT was variable but flat. Compared with publications in 2001, correlation with publications one year later was positive while correlation after ten years was weak and negative.Adoption of new technologies can be unpredictable. Spatiotemporal relationships facilitate adoption but are not sufficient. As with ecosystems, dense, mutualistic, specialized co-habitation is associated with faster growth. There are rapidly changing trends in external technological and macroeconomic influences. We propose that a better understanding of how technologies are adopted can facilitate their development.

ErbB2, EphrinB1, Src Kinase and PTPN13 Signaling Complex Regulates MAP Kinase Signaling in Human Cancers.

Vermeer Paola D , Bell Megan , Lee Kimberly , Vermeer Daniel W , Wieking Byrant G , Bilal Erhan , Bhanot Gyan , Drapkin Ronny I , Ganesan Shridar , Klingelhutz Aloysius J , Hendriks Wiljan J , Lee John H
PLoS One.2012 ; 7(1):e30447.
PMID: 22279592[]

2012/01/26 保存 要約 閉じる

In non-cancerous cells, phosphorylated proteins exist transiently, becoming de-phosphorylated by specific phosphatases that terminate propagation of signaling pathways. In cancers, compromised phosphatase activity and/or expression occur and contribute to tumor phenotype. The non-receptor phosphatase, PTPN13, has recently been dubbed a putative tumor suppressor. It decreased expression in breast cancer correlates with decreased overall survival. Here we show that PTPN13 regulates a new signaling complex in breast cancer consisting of ErbB2, Src, and EphrinB1. To our knowledge, this signaling complex has not been previously described. Co-immunoprecipitation and localization studies demonstrate that EphrinB1, a PTPN13 substrate, interacts with ErbB2. In addition, the oncogenic V660E ErbB2 mutation enhances this interaction, while Src kinase mediates EphrinB1 phosphorylation and subsequent MAP Kinase signaling. Decreased PTPN13 function further enhances signaling. The association of oncogene kinases (ErbB2, Src), a signaling transmembrane ligand (EphrinB1) and a phosphatase tumor suppressor (PTPN13) suggest that EphrinB1 may be a relevant therapeutic target in breast cancers harboring ErbB2-activating mutations and decreased PTPN13 expression.

Whole brain radiation-induced impairments in learning and memory are time-sensitive and reversible by systemic hypoxia.

Warrington Junie P , Csiszar Anna , Mitschelen Matthew , Lee Yong Woo , Sonntag William E
PLoS One.2012 ; 7(1):e30444.
PMID: 22279591[]

2012/01/26 保存 要約 閉じる

Whole brain radiation therapy (WBRT) is commonly used for treatment of primary and metastatic brain tumors; however, cognitive impairment occurs in 40-50% of brain tumor survivors. The etiology of the cognitive impairment following WBRT remains elusive. We recently reported that radiation-induced cerebrovascular rarefaction within hippocampal subregions could be completely reversed by systemic hypoxia. However, the effects of this intervention on learning and memory have not been reported. In this study, we assessed the time-course for WBRT-induced impairments in contextual and spatial learning and the capacity of systemic hypoxia to reverse WBRT-induced deficits in spatial memory. A clinical fractionated series of 4.5Gy WBRT was administered to mice twice weekly for 4 weeks, and after various periods of recovery, behavioral analyses were performed. To study the effects of systemic hypoxia, mice were subjected to 11% (hypoxia) or 21% oxygen (normoxia) for 28 days, initiated 1 month after the completion of WBRT. Our results indicate that WBRT induces a transient deficit in contextual learning, disruption of working memory, and progressive impairment of spatial learning. Additionally, systemic hypoxia completely reversed WBRT-induced impairments in learning and these behavioral effects as well as increased vessel density persisted for at least 2 months following hypoxia treatment. Our results provide critical support for the hypothesis that cerebrovascular rarefaction is a key component of cognitive impairment post-WBRT and indicate that processes of learning and memory, once thought to be permanently impaired after WBRT, can be restored.

Capacities of Migrating CD1b Lymph Dendritic Cells to Present Salmonella Antigens to Naive T Cells.

Olivier Michel , Foret Benjamin , Le Vern Yves , Guilloteau Laurence A
PLoS One.2012 ; 7(1):e30430.
PMID: 22279590[]

2012/01/26 保存 要約 閉じる

Dendritic cells (DCs) are well known as professional antigen-presenting cells (APC) able to initiate specific T-cell responses to pathogens in lymph nodes (LN) draining the site of infection. However, the respective contribution of migratory and LN-resident DCs in this process remains unclear. As DC subsets represent important targets for vaccination strategies, more precise knowledge of DC subsets able to present vaccine antigens to T cells efficiently is required. To investigate the capacities of DCs migrating in the lymph (L-DCs) to initiate a specific T-cell response, we used physiologically generated DCs collected from a pseudoafferent lymphatic cannulation model in sheep. The CD1b(+) L-DCs were assessed for presenting antigens from the vaccine attenuated strain of Salmonella enterica serovar Abortusovis. CD1b(+) L-DCs were able to phagocytose, process and to present efficiently Salmonella antigens to effector/memory T cells in vitro. They were shown to be efficient APC for the priming of allogeneic naive T cells associated with inducing both IFN-γ and IL-4 responses. They were also efficient in presenting Salmonella antigens to autologous naive T cells associated with inducing both IFN-γ and IL-10 responses. The capacities of L-DCs to process and present Salmonella antigens to T cells were investigated in vivo after conjunctival inoculation of Salmonella. The CD1b(+) L-DCs collected after inoculation were able to induce the proliferative response of CD4(+) T cells suggesting the in vivo capture of Salmonella antigens by the CD1b(+) L-DCs, and their potential to present them directly to CD4(+) T cells. In this study, CD1b(+) L-DCs present potential characteristics of APC to initiate by themselves T cell priming in the LN. They could be used as target cells for driving immune activation in vaccinal strategies.

Rectangular coordination polymer nanoplates: large-scale, rapid synthesis and their application as a fluorescent sensing platform for DNA detection.

Zhang Yingwei , Luo Yonglan , Tian Jingqi , Asiri Abdullah M , Al-Youbi Abdulrahman O , Sun Xuping
PLoS One.2012 ; 7(1):e30426.
PMID: 22279589[]

2012/01/26 保存 要約 閉じる

In this paper, we report on the large-scale, rapid synthesis of uniform rectangular coordination polymer nanoplates (RCPNs) assembled from Cu(II) and 4,4'-bipyridine for the first time. We further demonstrate that such RCPNs can be used as a very effective fluorescent sensing platform for multiple DNA detection with a detection limit as low as 30 pM and a high selectivity down to single-base mismatch. The DNA detection is accomplished by the following two steps: (1) RCPN binds dye-labeled single-stranded DNA (ssDNA) probe, which brings dye and RCPN into close proximity, leading to fluorescence quenching; (2) Specific hybridization of the probe with its target generates a double-stranded DNA (dsDNA) which detaches from RCPN, leading to fluorescence recovery. It suggests that this sensing system can well discriminate complementary and mismatched DNA sequences. The exact mechanism of fluorescence quenching involved is elucidated experimentally and its use in a human blood serum system is also demonstrated successfully.

Cytokinesis in Bloodstream Stage Trypanosoma brucei Requires a Family of Katanins and Spastin.

Benz Corinna , Clucas Caroline , Mottram Jeremy C , Hammarton Tansy C
PLoS One.2012 ; 7(1):e30367.
PMID: 22279588[]

2012/01/26 保存 要約 閉じる

Microtubule severing enzymes regulate microtubule dynamics in a wide range of organisms and are implicated in important cell cycle processes such as mitotic spindle assembly and disassembly, chromosome movement and cytokinesis. Here we explore the function of several microtubule severing enzyme homologues, the katanins (KAT80, KAT60a, KAT60b and KAT60c), spastin (SPA) and fidgetin (FID) in the bloodstream stage of the African trypanosome parasite, Trypanosoma brucei. The trypanosome cytoskeleton is microtubule based and remains assembled throughout the cell cycle, necessitating its remodelling during cytokinesis. Using RNA interference to deplete individual proteins, we show that the trypanosome katanin and spastin homologues are non-redundant and essential for bloodstream form proliferation. Further, cell cycle analysis revealed that these proteins play essential but discrete roles in cytokinesis. The KAT60 proteins each appear to be important during the early stages of cytokinesis, while downregulation of KAT80 specifically inhibited furrow ingression and SPA depletion prevented completion of abscission. In contrast, RNA interference of FID did not result in any discernible effects. We propose that the stable microtubule cytoskeleton of T. brucei necessitates the coordinated action of a family of katanins and spastin to bring about the cytoskeletal remodelling necessary to complete cell division.

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