Status of Superficial Esophageal Cancers Treated by Endoscopy "OESOFARE"

Condition:   Superficial Esophageal Cancers
Intervention:  
Sponsor:   Nantes University Hospital
Not yet recruiting

https://ift.tt/2PKx1yw

Assessing Timing of Enteral Feeding Support in Esophageal Cancer Patients on Muscle functTion and Survival

Conditions:   Esophageal Cancer;   Nutrition Aspect of Cancer;   Postoperative Complications;   Muscle Weakness;   Sarcopenia;   Jejunostomy; Complications
Intervention:   Other: delayed start enteral support @ POD5
Sponsor:   University Hospital, Gasthuisberg
Not yet recruiting

https://ift.tt/2xju7Kr

HRQOL in Thyroid Cancer and Thyroid Tumours

Conditions:   Thyroid Nodule;   Thyroid Cancer;   Quality of Life
Intervention:  
Sponsor:   Oslo University Hospital
Recruiting

https://ift.tt/2PLTZ8j

Status of Superficial Esophageal Cancers Treated by Endoscopy "OESOFARE"

Condition:   Superficial Esophageal Cancers
Intervention:  
Sponsor:   Nantes University Hospital
Not yet recruiting

https://ift.tt/2PKx1yw

Assessing Timing of Enteral Feeding Support in Esophageal Cancer Patients on Muscle functTion and Survival

Conditions:   Esophageal Cancer;   Nutrition Aspect of Cancer;   Postoperative Complications;   Muscle Weakness;   Sarcopenia;   Jejunostomy; Complications
Intervention:   Other: delayed start enteral support @ POD5
Sponsor:   University Hospital, Gasthuisberg
Not yet recruiting

https://ift.tt/2xju7Kr

HRQOL in Thyroid Cancer and Thyroid Tumours

Conditions:   Thyroid Nodule;   Thyroid Cancer;   Quality of Life
Intervention:  
Sponsor:   Oslo University Hospital
Recruiting

https://ift.tt/2PLTZ8j

β-Adrenergic signaling blocks murine CD8 + T-cell metabolic reprogramming during activation: a mechanism for immunosuppression by adrenergic stress

Abstract

Primary and secondary lymphoid organs are heavily innervated by the autonomic nervous system. Norepinephrine, the primary neurotransmitter secreted by post-ganglionic sympathetic neurons, binds to and activates β-adrenergic receptors expressed on the surface of immune cells and regulates the functions of these cells. While it is known that both activated and memory CD8⁺ T-cells primarily express the β2-adrenergic receptor (β2-AR) and that signaling through this receptor can inhibit CD8⁺ T-cell effector function, the mechanism(s) underlying this suppression is not understood. Under normal activation conditions, T-cells increase glucose uptake and undergo metabolic reprogramming. In this study, we show that treatment of murine CD8⁺ T-cells with the pan β-AR agonist isoproterenol (ISO) was associated with a reduced expression of glucose transporter 1 following activation, as well as decreased glucose uptake and glycolysis compared to CD8⁺ T-cells activated in the absence of ISO. The effect of ISO was specifically dependent upon β2-AR, since it was not seen in adrb2^−/− CD8⁺ T-cells and was blocked by the β-AR antagonist propranolol. In addition, we found that mitochondrial function in CD8⁺ T-cells was also impaired by β2-AR signaling. This study demonstrates that one mechanism by which β2-AR signaling can inhibit CD8⁺ T-cell activation is by suppressing the required metabolic reprogramming events which accompany activation of these immune cells and thus reveals a new mechanism by which adrenergic stress can suppress the effector activity of immune cells.

https://ift.tt/2QIhNeT