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Objective: To explore the clinical application of supraclavicular fasciocutaneous island flap (SIF) in the repair of tracheal defect. Methods: From May 2016 to March 2021, the clinical data of 10 patients (8 males,2 females,aged 27-73 years old) were retrospectively analyzed who underwent repair surgery with SIF for trachea defects after resection of cervical or thoracic tumors, including 2 cases of laryngotracheal adenoid cystic carcinoma, 2 cases of laryngeal carcinoma, 3 cases of esophageal carcinoma, 2 cases of thyroid carcinoma and one case of parathyroid carcinoma. All of the primary tumors were at T4. The outcomes of 10 cases with tracheal defect repaired by SIF were evaluated. Results: The areas of the SIF were (3-7) cm × (6-10) cm, the thicknesses of the flaps were 8-11 mm, and the lengths of the pedicles were 10-15 cm. The blood supply of the SIF came from the transverse carotid artery. The skin defects of the donor areas of the shoulders were directly closed. After 1-60 months of follow-up, all the flaps survived. The flaps, tracheas as well as shoulder wounds healed well. Conclusion: The SIF is suitable for the repair of tracheal defects. It has perfect thickness compatible with the trachea. The technique is simple and microsurgical technique is not needed, with a good application prospect.

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Hypohydration exceeding 2% body mass can impair endurance capacity. It is postulated that the brain could be perturbed by hypohydration, leading to impaired motor performance. We investigated the neural effects of hypohydration with magnetic resonance imaging (MRI). Ten men were dehydrated to approximately -3% body mass by running on a treadmill at 65% maximal oxygen consumption (V̇o2max) before drinking to replace either 100% [euhydration (EU)] or 0% [hypohydration (HH)] of fluid losses. MRI was performed before start of trial (baseline) and after rehydration phase (post) to evaluate brain structure, cerebral perfusion, and functional activity. Endurance capacity assessed with a time-to-exhaustion run at 75% V̇o2max was reduced with hypohydration (EU: 45.2 ± 9.3 min, HH: 38.4 ± 10.7 min; P = 0.033). Mean heart rates were comparable between trials (EU: 162 ± 5 beats/min, HH: 162 ± 4 beats/min; P = 0.605), but the rate of rise in rectal temperature was higher in HH trials (EU: 0.06 ± 0.01°C/min, HH: 0.07 ± 0.02°C/min; P < 0.01). In HH trials, a reduction in total brain volume (EU: +0.7 ± 0.6%, HH: -0.7 ± 0.9%) with expansion of ventricles (EU: -2.7 ± 1.6%, HH: +3.7 ± 3.3%) was observed, and vice versa in EU trials. Global and regional cerebral perfusion remained unchanged between conditions. Functional activation in the primary motor cortex in left hemisphere during a plantar-flexion task was similar between conditions (EU: +0.10 ± 1.30%, HH: -0.11 ± 0.31%; P = 0.637). Our findings demonstrate that with exertional hypohydration, brain volumes were altered but the motor-related functional activity was unperturbed. NEW & NOTEWORTHY Dehydration occurs rapidly during prolonged or intensive physical activity, leading to hypohydration if fluid replenishment is insufficient to replace sweat losses. Altered hydration status poses an osmotic challenge for the brain, leading to transient fluctuations in brain tissue and ventricle volumes. Therefore, the amount of fluid ingestion during exercise plays a critical role in preserving the integrity of brain architecture. These structural changes, however, did not translate directly to motor functional deficits in a simple motor task.

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The central nervous system, specifically the brain, is implicated in the development of exertional fatigue under a hot environment. Diverse neuroimaging techniques have been used to visualize the brain activity during or after exercise. Notably, the use of magnetic resonance imaging (MRI) has become prevalent due to its excellent spatial resolution and versatility. This review evaluates the significance and limitations of various brain MRI techniques in exercise studies-brain volumetric analysis, functional MRI, functional connectivity MRI, and arterial spin labeling. The review aims to provide a summary on the neural basis of exertional fatigue and proposes future directions for brain MRI studies. A systematic literature search was performed where a total of thirty-seven brain MRI studies associated with exercise, fatigue, or related physiological factors were reviewed. The findings suggest that with moderate dehydration, there is a decrease in total brain volume accompanied with expansion of ventricular volume. With exercise fatigue, there is increased activation of sensorimotor and cognitive brain areas, increased thalamo-insular activation and decreased interhemispheric connectivity in motor cortex. Under passive hyperthermia, there are regional changes in cerebral perfusion, a reduction in local connectivity in functional brain networks and an impairment to executive function. Current literature suggests that the brain structure and function are influenced by exercise, fatigue, and related physiological perturbations. However, there is still a dearth of knowledge and it is hoped that through understanding of MRI advantages and limitations, future studies will shed light on the central origin of exertional fatigue in the heat.

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Medullary thyroid carcinoma（MTC） is a special type of neuroendocrine tumor originated from C-cells of the thyroid gland, MTC can be divided into sporadic(70%-80%)and hereditary(20%-30%), about 98% of the hereditary MTC patients have RET proto-oncogene germline mutation in exon 10, 11, 13, 14, 15, 16. The mutation of RET proto oncogene is closely related to the pathogenesis of MTC, and different mutation of RET proto oncogene exon may lead to different MTC phenotypes.More than 100 kinds of mutations in the RET gene were reported. This paper reviews the research progress of RET proto-oncogene mutation in MTC.

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Previous case-control studies having investigated the relationship between the X-ray repair cross-complementing group 1 (XRCC1) Arg194Trp polymorphism and thyroid cancer (TC) have drawn inconsistent conclusions. The current study aimed to clarify the role of this polymorphism in susceptibility to TC. An up-to-date search of PubMed and Web of Science databases was conducted, including articles published up to August 2015. Crude odds ratios (ORs) with 95%CIs were calculated to establish the association between the XRCC1 Arg194Trp polymorphism and TC risk. Five studies were used, comprising 911 patients and 1476 controls. Our meta-analysis indicated that this polymorphism is associated with TC risk in Caucasians (TrpTrp vs ArgArg: OR = 5.72, 95%CI = 1.39-23.54; ArgTrp vs ArgArg: OR = 1.20, 95%CI = 0.87-1.66; dominant model: OR = 1.31, 95%CI = 0.96-1.79; recessive model: OR = 0.18, 95%CI = 0.04-0.73). This investigation demonstrates that the XRCC1 Arg194Trp polymorphism constitutes a risk factor for TC in Caucasian individuals.

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Percutaneous coronary intervention is a revolutionary treatment for ischemic heart disease, but in-stent restenosis (ISR) remains a clinical challenge. Inflammation, smooth muscle proliferation, endothelial function impairment, and local thrombosis have been identified as the main mechanisms for ISR. Considering the multifactorial mechanisms of ISR, a novel therapeutic agent with multiple bioactivities is required. Ghrelin is a novel gut-brain peptide predominantly produced by the stomach, and has been shown to play a role in various cardiovascular activities, such as increasing myocardial contractility, improving cardiac output, and inhibiting ventricular remodeling, as well as attenuating cardiac ischemia-reperfusion injury. Recent studies have demonstrated that ghrelin effectively inhibits vascular inflammation and vascular smooth muscle cell proliferation, repairs endothelial cells, promotes vascular endothelial function, inhibits platelet aggregation, and exerts antithrombotic effects. These findings suggest that ghrelin may be an innovative therapeutic candidate for the prevention and treatment of ISR.

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