Objective To evaluate exertional overheating and endurance during and after physical exercise on individuals with hypohidrotic ectodermal dysplasia(HED) ,to assess protective effects of skin cooling device ,and to provide theoretical basis for ex-ternal cooling devices .Methods 12 HED patients and 12 age-matched healthy controls were studied during standardized exercise on a treadmill at ambient temperatures of 25 ℃ and 30 ℃ .Body core temperature ,performance ,heart rate ,respiratory rate ,blood pres-sure and serum lactate were investigated during and after exercise .Results HED subjects experienced a significantly greater rise in body temperature after cycling than healthy controls ,and their body temperature remained elevated longer(P<0 .05) .HED subjects had a lower endurance time(F=9 .985 ,P=0 .005) and increasing speed value(F=7 .158 ,P=0 .014) .However ,serum lactate value of the HED subjects found to be higher than the controls (F=5 .204 ,P=0 .033) .Maximum heart rates ,respiratory rate and blood pressure did not differ significantly between HED and the control groups .However ,compared with controls ,body temperature and endurance time of HED patients equipped with skin cooling device had no statistical significance .Conclusion HED subjects showed a significantly greater rise of body temperature during exercise than the control groups ,and their body temperature remained elevat-ed longer than in healthy subjects ,and had a lower performance .External evaporative skin cooling attenuates exertional overheating in HED patients and may facilitate their participation in athletic activities and professional life .

Objective To investigate the effect of ectodysplasin A (EDA‐A1) gene of hypohidrotic ectodermal dysplasia on pro‐liferation and cell cycle of human umbilical vein endothelial cell (ECV304). Methods Recombinant eukaryotic expression vectors pcDNA3. 1(‐)‐EDA‐A1‐M /W (mutant, M and wild, W) containing the coding sequence were transected into ECV304 cells. EDA‐A1 gene was amplified by reverse transcription polymerase chain reaction (RT‐PCR), and the protein was detected by Western blot. Cell viability and cycle distribution were invested by MTT and Flow cytometry (FCM ). Results The EDA‐A1 gene and pro‐tein were detected respectively by RT‐PCR and Western blot in ECV cells transfected with pcDNA3. 1(‐)‐EDA‐A1‐M /W, but not in ECV cells transfected with plasmid pcDNA3. 1(‐) and cells without transection. And also, compared with control groups, EDA‐A1 gene mutant significantly decreased proliferation of ECV cells and its inhibition rate was 45. 70% ( P < 0. 01), whereas wild EDA‐A1 gene did not cause such growth inhibition (P> 0. 05). A significant increase of the G0 /G1 and S fraction was seen in the ECV cells of mutant group, compared with wild group with an accumulation in S phase and a concomitant decrease in G2 /M phase population (P< 0. 05). Conclusion Mutant and wild EDA‐A1 gene may have distinct biological functions on proliferation and cell cycle distribution of cultured human umbilical vein endothelial cell.

As a crucial regulatory molecule in the context of vascular stenosis, transforming growth factor-β (TGF-β), plays a pivotal role in its initiation and progression. TGF-β, a member of the TGF-β superfamily, can bind to the TGF-β receptor and transduce extracellular to intracellular signals through canonical Smad dependent or noncanonical signaling pathways to regulate cell growth, proliferation, differentiation, and apoptosis. Restenosis remains one of the most challenging problems in cardiac, cerebral, and peripheral vascular disease worldwide. The mechanisms for occurrence and development of restenosis are diverse and complex. The TGF-β pathway exhibits diversity across various cell types. Hence, clarifying the specific roles of TGF-β within different cell types and its precise impact on vascular stenosis provides strategies for future research in the field of stenosis.
Humans ; Transforming Growth Factor beta/metabolism* ; Constriction, Pathologic ; Signal Transduction ; Cell Differentiation ; Vascular Diseases ; Transforming Growth Factors ; Transforming Growth Factor beta1

The cardiovascular patch, served as artificial graft materials to replace heart or vascular tissue defect, is still playing a key role in cardiovascular surgeries. The defects of traditional cardiovascular patch materials may determine its unsatisfactory long-term effect or fatal complications after surgery. Recent studies on many new materials (such as tissue engineered materials, three-dimensional printed materials, etc) are being developed. Patch materials have been widely used in clinical procedures of cardiovascular surgeries such as angioplasty, cardiac atrioventricular wall or atrioventricular septum repair, and valve replacement. The clinical demand for better cardiovascular patch materials is still urgent. However, the cardiovascular patch materials need to adapt to normal coagulation mechanism and durability, promote short-term endothelialization after surgery, and inhibit long-term postoperative intimal hyperplasia, its research and development process is relatively complicated. Understanding the characteristics of various cardiovascular patch materials and their application in cardiovascular surgeries is important for the selection of new clinical surgical materials and the development of cardiovascular patch materials.
Cardiac Surgical Procedures/methods* ; Tissue Engineering ; Heart Ventricles ; Heart Atria ; Treatment Outcome