Staphylococcus cohnii is a potentially biotherapeutic skin commensal alleviating skin inflammation.

Host-microbe interactions orchestrate skin homeostasis, the dysregulation of which has been implicated in chronic inflammatory conditions such as atopic dermatitis and psoriasis. Here, we show that Staphylococcus cohnii is a skin commensal capable of beneficially inhibiting skin inflammation. We find that Tmem79 mice spontaneously develop interleukin-17 (IL-17)-producing T-cell-driven skin inflammation.

Prebiotics protect against acute graft-versus-host disease and preserve the gut microbiota in stem cell transplantation.

Acute graft-versus-host disease (aGVHD) is a major cause of morbidity and mortality after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Therefore, management of aGVHD is important for successful transplantation. Mucosal damage and alteration of the gut microbiota after allo-HSCT are key factors in the development of aGVHD.

TH1 cell-inducing strain identified from the small intestinal mucosa of patients with Crohn's disease.

Dysbiotic microbiota contributes to the pathogenesis of Crohn's disease (CD) by regulating the immune system. Although pro-inflammatory microbes are probably enriched in the small intestinal (SI) mucosa, most studies have focused on fecal microbiota. This study aimed to examine jejunal and ileal mucosal specimens from patients with CD via double-balloon enteroscopy.

A defined commensal consortium elicits CD8 T cells and anti-cancer immunity.

There is a growing appreciation for the importance of the gut microbiota as a therapeutic target in various diseases. However, there are only a handful of known commensal strains that can potentially be used to manipulate host physiological functions. Here we isolate a consortium of 11 bacterial strains from healthy human donor faeces that is capable of robustly inducing interferon-γ-producing CD8 T cells in the intestine.

Palladacycles: Effective Catalysts for a Multicomponent Reaction with Allylpalladium(II)-Intermediates.

Palladium(II) complexes with an bidentate ligand featuring one C-Pd bond and a Pd-N-donor bond (palladacycles) have been shown to afford improved yields of homoallylic amines from a three-component coupling of boronic acids, allenes and imines in comparison to the yields of homoallylic amines achieved with the originally reported catalyst (Pd(OAc)/P(-Bu)), thus extending the scope of the reaction. P NMR monitoring studies indicate that distinct intermediates featuring Pd-P bonds originate in the reactions catalyzed by either Pd(OAc)/P(-Bu) or the pallada(II)cycle/P(-Bu) systems, suggesting that the role of the pallada(II)cycles is more complex than just precatalysts. The importance of an additional phosphine ligand in the reactions catalyzed the pallada(II)cycles was established, and its role in the catalytic cycle has been proposed.

The counterregulating role of ACE2 and ACE2-mediated angiotensin 1-7 signaling against angiotensin II stimulation in vascular cells.

To clarify the role of endogenous angiotensin (Ang)-converting enzyme 2 (ACE2) and its cleavage product, Ang 1-7, in the atherogenic stimulation of vascular cells, we investigated the effect of pharmacological inhibition of ACE2 and Mas, an Ang 1-7 receptor, on cellular responses against Ang II stimulation. We measured extracellular signal-regulated kinase (ERK) 1/2 phosphorylation by western blot, smooth muscle cell (SMC) proliferation by WST assay and the adhesion of monocytes labeled with PKH67 to endothelial cells (ECs) by fluorescence microplate reader. Cells were pretreated with Ang 1-7, olmesartan (Ang II type 1 receptor (AT1) blocker), DX600 (ACE2 inhibitor), -Ala7-Ang1-7 (D-Ala; Mas antagonist), or combinations of treatments before the application of Ang II.

Macrophage inflammatory protein-1beta induced cell adhesion with increased intracellular reactive oxygen species.

Unlabelled: To investigate the role of macrophage inflammatory protein-1 beta (MIP-1beta) in the development of atherosclerosis, we designed an in vitro study to elucidate the mechanisms of monocyte-endothelium adhesion via intracellular reactive oxygen species (ROS). Angiotensin II (AngII) was used as a positive control. Furthermore, we examined the efficacy of MIP-1beta as a predictor of stroke and cardiovascular events in hypertensive patients.

Renal protective effect in hypertensive patients: the high doses of angiotensin II receptor blocker (HARB) study.

Angiotensin receptor blockers (ARBs) are the recommended first-line antihypertensive treatment for managing chronic kidney disease, and strict blood pressure (BP) regulation is crucial for the reduction of proteinuria. Valsartan and candesartan are commonly used ARBs in Japan, with maximum permissible doses of 160 mg/day and 12 mg/day, respectively. We evaluated BP and proteinuria after changeover from the maximum dose of candesartan to the maximum dose of valsartan, in 55 poorly controlled hypertensive patients undergoing candesartan treatment who were unable to achieve optimal BP according to the Japanese Society of Hypertension Guidelines for the Management of Hypertension (JSH 2004).

Renal-protective effect of T-and L-type calcium channel blockers in hypertensive patients: an Amlodipine-to-Benidipine Changeover (ABC) study.

Both strict blood pressure control and efferent artery dilatation are critical in reducing proteinuria, which in turn helps to regulate blood pressure. Benidipine, an L- and T-type calcium channel blocker, has the potential for increased effectiveness compared with L-type-dominant calcium channel blockers such as amlodipine. Therefore, we evaluated blood pressure and proteinuria after changeover from amlodipine to benidipine in poorly controlled hypertensive patients.

Renin-angiotensin inhibition reverses advanced cardiac remodeling in aging spontaneously hypertensive rats.

Background: Many experiments using young hypertensive animal models support the evidence that angiotensin-converting enzyme inhibitor or angiotensin receptor type 1 blocker attenuates the progression of cardiac hypertrophy. However, it is still unclear whether inhibiting the renin-angiotensin system can reverse age-related cardiac hypertrophy. To clarify the role of renin-angiotensin system inhibition in naturally advanced myocardial hypertrophy we treated spontaneously hypertensive, aging rats with an angiotensin-converting enzyme inhibitor or an angiotensin receptor type 1 blocker.

Clinical usefulness and limitations of brachial-ankle pulse wave velocity in the evaluation of cardiovascular complications in hypertensive patients.

The goal of this study was to clarify the clinical usefulness and limitations of brachial-ankle pulse wave velocity (PWV) to evaluate hypertensive complications, in comparison with carotid-femoral PWV. Patients with essential hypertension (n=296, male/female=161/135; age=61.1+/-0.

Evaluation of morning blood pressure elevation and autonomic nervous activity in hypertensive patients using wavelet transform of heart rate variability.

To evaluate morning autonomic nervous activity and blood pressure profiles in hypertensive patients by analyzing heart rate variability and ambulatory blood pressure. Data from 82 patients with untreated essential hypertension were analyzed. We evaluated the 24-h profile of blood pressure and that of indices of autonomic nervous activity, i.

Deletion of angiotensin-converting enzyme 2 accelerates pressure overload-induced cardiac dysfunction by increasing local angiotensin II.

Angiotensin-converting enzyme 2 (ACE2) is a carboxypeptidase that cleaves angiotensin II to angiotensin 1-7. Recently, it was reported that mice lacking ACE2 (ACE2(-/y) mice) exhibited reduced cardiac contractility. Because mechanical pressure overload activates the cardiac renin-angiotensin system, we used ACE2(-/y) mice to analyze the role of ACE2 in the response to pressure overload.

Quantitative angiographic and intravascular ultrasound study >5 years after directional coronary atherectomy.

Aggressive and optimal directional coronary atherectomy (DCA) using intravascular ultrasound (IVUS) guidance provides favorable outcomes within 1 year. However, no previous data are available on the changes that occur in target lesions for the long term after stand-alone DCA. This study's aim evaluates, using quantitative angiography and intravascular ultrasonography, the natural history of changes that occur in target lesions between short- (about 6 months) and long-term (>5 years) follow-up angiography after stand-alone DCA.