Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add more filters










Database
Publication year range
1.
Zhonghua Shao Shang Za Zhi ; 37(9): 900-904, 2021 Sep 20.
Article in Chinese | MEDLINE | ID: mdl-34645159

ABSTRACT

As the largest organ in mammals, skin is the first protective barrier against external stimuli. Sweat glands are one of the important cutaneous appendages and play an important role in maintaining electrolyte balance and regulating body temperature. Patients with extensive deep burns usually suffer from damage to deep dermis or the entire skin layer. The damaged sweat glands are difficult to repair and even unable to regenerate, which seriously affects patients' sweating and thermo-regulation function, reduces patients' quality of lives. How to achieve the functionalization of sweat glands has become one of the important researches in regenerative medicine of damaged skin. This review summarizes the translational and application technology of sweat gland regeneration and repair using stem cells and tissue engineering, in order to provide a theoretical basis for the research of sweat gland regeneration.


Subject(s)
Sweating , Tissue Engineering , Animals , Humans , Regeneration , Stem Cells , Sweat Glands
2.
Neuroscience ; 307: 151-9, 2015 Oct 29.
Article in English | MEDLINE | ID: mdl-26318331

ABSTRACT

Identifying novel neuroprotectants that can halt or even reverse the effects of stroke is of interest to both clinicians and scientists. Neuregulin 1 (NRG1) is an effective neuroprotectant, but its molecular mechanisms are largely unclear. In this study, NRG1 rescued cortical neurons from oxygen-glucose deprivation (OGD) model, but the effect was blocked by neutralizing NRG1 and ErbB4 inhibition. In addition, γ-Aminobutyric acid (GABA) receptor agonists had no synergistic effect with NRG1, and the neuroprotective effect of NRG1 against OGD was partly blocked by GABA receptor antagonists. Importantly, NRG1 neuroprotection against brain ischemia was abolished in the mice with specific deletion of ErbB4 in parvalbumin (PV)-positive interneurons. In summary, NRG1 protects against ischemic brain injury via ErbB4 receptors by enhancing GABAergic transmission.


Subject(s)
Brain Injuries/metabolism , Brain Injuries/prevention & control , Neuregulin-1/therapeutic use , Neuroprotective Agents/therapeutic use , Receptor, ErbB-4/metabolism , Synaptic Transmission/drug effects , gamma-Aminobutyric Acid/metabolism , Animals , Apoptosis/drug effects , Apoptosis/physiology , Brain Injuries/etiology , Cell Hypoxia/drug effects , Cells, Cultured , Disease Models, Animal , GABA Agonists/pharmacology , Infarction, Middle Cerebral Artery/complications , Infarction, Middle Cerebral Artery/genetics , Male , Mice , Mice, Transgenic , Neuregulin-1/pharmacology , Neurons/drug effects , Neuroprotective Agents/pharmacology , Parvalbumins/metabolism , Rats , Receptor, ErbB-4/genetics , Synaptic Transmission/genetics
SELECTION OF CITATIONS
SEARCH DETAIL
...