Subscribe: Nature Medicine - Issue - science feeds
Added By: Feedage Forager Feedage Grade B rated
Language: English
anti  bowel disease  cells  cystic fibrosis  cystic  disease  fibrosis  hiv  inflammatory bowel  inflammatory  macrophages  therapy  tumor 
Rate this Feed
Rate this feedRate this feedRate this feedRate this feedRate this feed
Rate this feed 1 starRate this feed 2 starRate this feed 3 starRate this feed 4 starRate this feed 5 star

Comments (0)

Feed Details and Statistics Feed Statistics
Preview: Nature Medicine - Issue - science feeds

Nature Medicine

A biomedical research journal devoted to publishing the latest and most exciting advances in biomedical research for scientists and physicians.


The curse of uncertainty


Proposed US budget cuts and the impending exit of the UK from the European Union have the potential to destabilize the global biomedical-research enterprise. In the meantime, the uncertainty of not knowing just how bad the effects will be will inflict its own damage.



A role for oncostatin M in inflammatory bowel disease


A new study identifies oncostatin M (OSM) as a potential biomarker and therapeutic target for anti-tumor necrosis factor (TNF)-refractory inflammatory bowel disease (IBD), and pinpoints mucosal stromal cells as key players in OSM-mediated inflammation.

Thymosin α1: a single drug with multiple targets in cystic fibrosis


A new study in mice suggests that a single drug, thymosin α1, may simultaneously rectify the impaired trafficking of the cystic fibrosis transmembrane conductance regulator (CFTR) in cystic fibrosis (CF) and reduce inflammation, offering new hope for CF treatment.

HIV persistence in macrophages


A recent study using a humanized mouse model shows that HIV-1 can persist in macrophages during antiretroviral therapy (ART), and suggests that macrophages may represent an obstacle to efforts to cure HIV-1 infection.

Is autoimmunity the Achilles' heel of cancer immunotherapy?


In this Perspective, June, Bluestone and Warshauer discuss potential cellular and molecular explanations for the autoimmunity often associated with immunotherapy, and propose additional research and changes to reporting practices to aid efforts to understand and minimize these toxic side effects.

Diagnosis of Zika virus infection on a nanotechnology platform


Antibody-based diagnosis of Zika virus (ZIKV) infection is complicated by cross-reactivity with antibodies against dengue virus. Hongjie Dai and colleagues report their development of a new IgA- and IgG-based diagnostic test that detects ZIKV with high specificity.

VISTA is an inhibitory immune checkpoint that is increased after ipilimumab therapy in patients with prostate cancer


Prostate cancer is refractory to anti-CTLA-4 therapy, but the reason why is unclear. Padmanee Sharma and colleagues report that the inhibitory molecule VISTA, which negatively regulates T cells, is upregulated on macrophages in prostate tumors that have been treated with anti-CTLA-4 and may play a role in resistance to this immunotherapy.

Dectin 1 activation on macrophages by galectin 9 promotes pancreatic carcinoma and peritumoral immune tolerance


Activation of dectin-1-dependent signaling in macrophages through ligation by galectin 9 promotes an immunosuppressive, protumorigenic microenvironment in pancreatic adenocarcinoma (PDA). Blocking dectin 1 ligation restores anti-tumor immunity and delays tumor growth, thus offering a novel strategy for improving the effectiveness of immunotherapy in patients with PDA.

A stemness-related ZEB1–MSRB3 axis governs cellular pliancy and breast cancer genome stability


During malignant transformation, the ability of mammary epithelial cells to cope with oncogene-induced DNA damage and avoid chromosomal instability is determined by stemness-related expression of the canonical epithelial-to-mesenchymal transition transcription factor ZEB1 and its target MSRB3, a methionine sulfoxide reductase involved in antioxidant defense.

Oncostatin M drives intestinal inflammation and predicts response to tumor necrosis factor–neutralizing therapy in patients with inflammatory bowel disease


The cytokine oncostatin M drives intestinal inflammation in mice, and its abundance in the intestine of patients with inflammatory bowel disease predicts response to tumor necrosis factor–neutralizing therapy.

Thymosin α1 represents a potential potent single-molecule-based therapy for cystic fibrosis


Thymosin α1 is used in the clinic as a treatment in viral disease and acts as an anti-inflammatory. Here it was found to also correct the misfolding of mutant CTFR and potentiate its activity, thus improving outcome in a mouse model of cystic fibrosis.

Marginal zone B cells control the response of follicular helper T cells to a high-cholesterol diet


Splenic marginal zone B cells suppress atherosclerosis in mice by dampening the proatherogenic T follicular helper response via a PDL1-dependent interaction with T follicular helper cells.

A heart–brain–kidney network controls adaptation to cardiac stress through tissue macrophage activation


The ability of the heart to withstand pressure overload, as occurs in heart failure, depends on a multi-organ circuit, in which sympathetic activation of the kidney leads to release of the cytokine CSF2 into the circulation, stimulating cardiac-resident macrophages that protect the heart.

Alternatively activated macrophages do not synthesize catecholamines or contribute to adipose tissue adaptive thermogenesis


In contrast to previously reported findings, M2-like polarized macrophages are not a source of catecholamines and do not contribute to browning of the fat.

The cold-induced lipokine 12,13-diHOME promotes fatty acid transport into brown adipose tissue


Cold stimulation induces the synthesis and release of the lipid species 12,13-diHOME from brown adipose tissue. This ‘lipokine’ then acts on brown adipocytes to promote the uptake of fatty acids to fuel this cell type's heat production.

HIV persistence in tissue macrophages of humanized myeloid-only mice during antiretroviral therapy


Persistence of HIV is attributed primarily to latent infection of CD4+ T cells. Honeycutt et al. report that in humanized mice lacking T cells HIV can rebound from myeloid cells after antiretroviral treatment interruption, suggesting that persistence of HIV could involve other cell types.