Background Acupuncture points are commonly used by Traditional Chinese Medicine to treat throat discomfort. Transcutaneous electroacupuncture (TEA) is a new therapy combining transcutaneous electrical nerve stimulation with meridian theory. https://www.selleckchem.com/products/z-vad(oh)-fmk.html The efficacy and mechanism of Transcutaneous electroacupuncture for globus pharyngeus has not been reported. The aim of our study was to explore the effect and possible mechanisms of TEA at CV22/LI3/LU11/ST36 for patients with globus. Methods A total of 80 patients with globus pharyngeus were randomly allocated into eight groups. The intervention order in Groups A1/B1/C1/D1 was firstly TEA at CV22/LI3/LU11/ST36 during the first period and sham-TEA in the second period. For participants in Groups A2/B2/C2/D2, the intervention order was the reverse. Before the test, the participants were asked to complete the Glasgow Edinburgh Throat Scale (GETS), visual analog scale (VAS), and the Hamilton Rating Scale Anxiety/Depression and were then asked to test and measure the heart rate variability and serum hormone levels of SP and NPY. At the end of the second period, these tests were manipulated again. Results D-values of GETS and VAS following stimulation at CV22/LU11 were significantly higher than those of sham-stimulating (CV22 13.5 ± 13.09 vs. 1 ± 9.68, P less then 0.002; LU11 17 ± 10.31 vs. 9 ± 9.68, P = 0.011). Heart rate variability, SP, and NPY were showed a significant difference in LU11 stimulation compared to other acupuncture points (P all less then 0.05). Conclusion Stimulation at CV22/LU11 significantly improved symptoms of globus. The results indicated that symptoms may be improved by stimulating the parasympathetic nervous system and secreting SP and NPY when stimulating at LU11. For CV22, it may improve symptoms by direct action on the throat. Stimulating at CV22/LU11 may be a potential therapy for treating globus.Thyroid hormone (TH) and its receptor (TR) are involved in differentiation, metabolic process, and growth regulation in hepatocellular carcinoma (HCC). The TH/TR complexes are ligand-dependent transcriptional factors, functioning through binding to thyroid hormone response elements (TREs) upstream of the target genes. To date, deciphering the biological effects of TH in cancer progression remains challenging. Several lines of evidence suggest a growth inhibitory effect of TH in liver cancer. Mutation and aberrant expression of TRs are highly correlated with several types of cancers including HCC. Several reports show that TH inhibits cell growth in liver cancer through regulation of cell-cycle-related genes and non-coding RNAs. A case-control study indicates that hypothyroidism is associated with an increased risk of HCC. Moreover, TH/TR suppresses hepatocarcinogenesis via selective autophagy. Conversely, other groups have indicated that TH promotes cancer cell proliferation. In vitro and in vivo experiments show that TH/TR enhances cancer cell migration and invasion, anticancer drug resistance, angiogenesis, and cancer stem cell self-renewal. Adding to the complexity of this issue, non-genomic effects of TH mediated by integrin receptor on cell surface can also modulate several biological functions. Accumulating evidence indicate that regulations by genomic and non-genomic effects of TH overlap. Taken together, these observations suggest that the functions of TH depend largely on cell context, and TH/TR plays a duel role in cancer progression. Therefore, understanding the maze of biological effects of TH has become a necessity when attempting to develop effective therapeutic and preventive strategies in liver cancer.Beta hemoglobinopathies are widely spread monogenic lethal diseases. Delta-globin gene activation has been proposed as a possible approach for curing these pathologies. The therapeutic potential of delta-globin, the non-alpha component of Hemoglobin A2 (α2δ2; HbA2), has been demonstrated in a mouse model of beta thalassemia, while its anti-sickling effect, comparable to that of gamma globin, was established some time ago. Here we show that the delta-globin mRNA level is considerably increased in a Deoxyribonuclease II-alpha knockout mouse model in which type 1 interferon (interferon beta, IFNb) is activated. IFNb activation in the fetal liver improves the delta-globin mRNA level, while the beta-globin mRNA level is significantly reduced. In addition, we show that HbA2 is significantly increased in patients with multiple sclerosis under type 1 interferon treatment. Our results represent a proof of principle that delta-globin expression can be enhanced through the use of molecules. This observation is potentially interesting in view of a pharmacological approach able to increase the HbA2 level.Background Machine perfusion (MP) and static cold storage (CS) are two prevalent methods for liver allograft preservation. However, the preferred method remains controversial. Aim To conduct a meta-analysis on the impact of MP preservation on liver transplant outcome. Methods PubMed, EMBASE, and Cochrane Library databases were systematically searched to identify relevant trials comparing the efficacy of MP vs. CS. Odds ratios (OR) and fixed-effects models were calculated to compare the pooled data. Results Ten prospective cohort studies and two randomized controlled trials (RCTs) were included (MP livers vs. CS livers = 315489). Machine perfusion demonstrated superior outcomes in posttransplantation aspartate aminotransferase levels compared to CS (P 0.05). Conclusions Machine perfusion is superior to CS on improving short-term outcomes for human liver transplantation, with a less clear effect in the longer term. Hypothermic machine perfusion but not NMP conducted significantly protective effects on EAD and biliary complications. Further RCTs are warranted to confirm MP's superiority and applications.FAM46A belongs to the FAM46 subfamily of the nucleotidyltransferase-fold superfamily and is predicted to be a non-canonical poly(A) polymerase. FAM46A has been linked to several human disorders including retinitis pigmentosa, bone abnormality, cancer, and obesity. However, its molecular and functional characteristics are largely unknown. We herein report that FAM46A is expressed in cells of the hematopoietic system and plays a role in hemin-induced hemoglobinization. FAM46A is a nucleocytoplasmic shuttle protein modified by Tyr-phosphorylation only in the cytosol, where it is closely associated with ER. On the other hand, it is located proximal to the chromatin regions of active transcription in the nucleus. FAM46A is a cell cycle-dependent poly-ubiquitinated short-lived protein degraded mostly by proteasome and its overexpression inhibits cell growth and promotes hemin-induced hemoglobinization in K562 cell. Site-directed mutagenesis experiments confirm the non-canonical poly(A) polymerase activity of FAM46A is essential for enhanced hemin-induced hemoglobinization.