Search

Taraxasterol is one of the bioactive triterpenoids found in dandelion, a member of the family Asteraceae. In the animal or cellular models of several ailments, including liver damage, gastritis, colitis, arthritis, pneumonia, tumors, and immune system diseases, taraxasterol has been shown to have significant preventive and therapeutic effects. This review aims to evaluate the current state of research and provide an overview of the possible applications of taraxasterol in various diseases. The reported phytochemical properties and pharmacological actions of taraxasterol, including anti-inflammatory, anti-oxidative, and anti-carcinogenic properties, and its potential molecular mechanisms in developing these diseases are highlighted. Finally, we further explored whether taraxasterol has protective effects on neuronal death in neurodegenerative diseases. In addition, more animal and clinical studies are also required on the metabolism, bioavailability, and safety of taraxasterol to support its applications in pharmaceuticals and medicine.

Multiple risk factors of stroke are associated with telomere length shortening. Although leukocyte telomere length (LTL) is shorter in patients with stroke, the heterogeneity is high. Risk factors may be differentially associated with LTL in male and female patients contributing to the heterogeneity. However, the gender difference in associations between LTL and risk factors in stroke patients has not been investigated. In this study, we investigated the gender difference in associations between LTL and risk factors in 312 stroke patients. Real-time quantitative PCR was used to determine relative LTL, and multiple linear regression analysis was applied for association analyses. We found that LTL was negatively associated with triglyceride (TG) in all patients [β(95% CI) = −0.69 (−1.26, −0.11), P < 0.05] after adjusting confounders. Importantly, LTL was negatively associated with lack of exercise [β(95% CI) = −1.80 (−3.12, −0.49), P < 0.05] and LDL levels [β(95% CI) = −3.22 (−6.05, −0.390), P < 0.05] in male patients, while LTL was negatively associated with dyssomnia [β(95%CI) = −2.00 (−3.96, −0.07), P < 0.05] and diabetes [β(95%CI) = −2.13 (−4.10, −0.27), P < 0.01] in female patients. Our study showed that LTL is differently associated with risk factors in male and female patients with stroke, indicating that gender difference should be considered when LTL is potentially applied as an index of risk and prognosis for stroke. Our study also provides an insight into that gender differences should be considered when developing intervention strategies for stroke prevention and treatment.

Diabetic foot ulcer (DFU) is considered as one of the most serious and prevailing complications of diabetes mellitus, while it is the major cause of amputations in diabetic patients. Herein, we reported an acquired severe traumatic DFU with an intermediate cuneiform hairline fracture and displacement in a 55-year old male (Grade IV of Wagner classification; Grade III of IWGDF classification). The Pseudomonas aeruginosa was identified in pus culture. Data of antibiotic susceptibility testing indicated that the isolates of Pseudomonas aeruginosa were multi-drug resistant. Routine debridement, clearing displaced intermediate cuneiform and drainage were performed to facilitate the outflow of pus and pressure mitigation. Dressing with Prontosan solution and gel was applied to the wound, and meropenem was systemically administrated in addition to effective glycemic control. The DFU has been fully healed after ~40-day treatment. For this case, clearing the displaced and fractured intermediate cuneiform is essential for the heal of the DFU in addition to the common strategy for DFU treatment, i.e., the combination of debridement, pressure mitigation, wound dressing with Prontosan, antibiotic selection and effective glycemic control. This case report might have value for the treatment of complex DFU with bone fracture and displacement, reducing the risk of amputation.

Isolated congenital coronary artery fistula (ICCAF) is an exceedingly rare anomaly in which there is a direct abnormal connection between a coronary artery and other cardiac chambers or any of great vessels. The left circumflex artery (LCX) is the least common source of ICCAF. Here we reported a rare case of large ICCAF originated from the LCX in a 9-year-old boy. He presented fatigability, murmurs and NYHA class II. Echocardiography and cardiac CT revealed that an aneurysmal dilatation of the LCX along with the dilated coronary sinus entered into the right atrium (RA) through the great cardiac vein. However, it showed that the dilated LCX directly drained into the RA by coronary angiography, which was confirmed by the surgery. During the surgical procedure, the LCX fistula was identified in a 3*3 cm bulbous structure, the aneurysmal dilation of RA tissue. The end of fistula was located in the lower-middle interatrial septum, which was near the coronary sinus and above the opening of inferior vena cava (IVC). Transcardiac chamber closure with cardiopulmonary bypass (CPB) was successfully performed for the correction of the fistula. It indicated that preoperative angiography is essential to define the details of large ICCAF with aneurysmal dilation. Moreover, transcardiac chamber closure with CPB is the optimal procedure for the treatment of large ICCAF, while interventional catheterization is not feasible due to the presence of aneurysmal dilation of the LCX. The description of this rare case might have great value for the diagnosis and treatment of large ICCAF originated from the LCX.

Ubiquitin-proteasome pathway (UPS) and autophagy-lysosome pathway (ALP) are the two major protein degradation pathways, which are critical for proteostasis. Growing evidence indicates that proteasome inhibition-induced ALP activation is an adaptive response. Transcription Factor EB (TFEB) is a master regulator of ALP. However, the characteristics of TFEB and its role in proteasome inhibition-induced ALP activation are not fully investigated. Here we reported that the half-life of TFEB is around 13.5 h in neuronal-like cells, and TFEB is degraded through proteasome pathway in both neuronal-like and non-neuronal cells. Moreover, proteasome impairment not only promotes TFEB accumulation but also facilitates its dephosphorylation and nuclear translocation. In addition, proteasome inhibition-induced TFEB accumulation, dephosphorylation and nuclear translocation significantly increases the expression of a number of TFEB downstream genes involved in ALP activation, including microtubule-associated protein 1B light chain-3 (LC3), particularly LC3-II, cathepsin D and lysosomal-associated membrane protein 1 (LAMP1). Furthermore, we demonstrated that proteasome inhibition increases autophagosome biogenesis but not impairs autophagic flux. Our study advances the understanding of features of TFEB and indicates that TFEB might be a key mediator of proteasome impairment-induced ALP activation.

Stroke is one of the leading causes of death and disability worldwide. Age is associated with increased risk of stroke, while telomere length shortening plays a pivotal role in the process of aging. Moreover, telomere length shortening is associated with many risk factors of stroke in addition to age. Accumulated evidence shows that short leukocyte telomere length is not only associated with stroke occurrence but also associated with post-stroke recovery in the elderly population. In this review, we aimed to summarize the association between leukocyte telomere length and stroke, and discuss that telomere length might serve as a potential biomarker to predict the risk and prognosis of stroke.