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Objective To present a technical note on how to perform upper extremity peripheral nerve stimulators for three major nerves: median, ulnar, and radial. Design Literature review and expert opinion. Setting Single academic center. Results Peripheral nerve stimulation has recently become popular with the development and availability of peripheral nerve stimulators with an external pulse generator. Here, we describe ultrasound anatomy and technical details for peripheral nerve stimulation in the upper extremity for three major nerves: median, ulnar, and radial. Conclusions Upper extremity peripheral nerve stimulation can be considered as an option for refractory neuropathic upper extremity pain.

The aryl hydrocarbon receptor (AHR) signaling pathway participates in immune regulation of multiple autoimmune diseases, including rheumatoid arthritis (RA). We conducted this study to investigate the association of AHR signaling pathway genes (AHR, ARNT, AHRR) single nucleotide polymorphisms (SNPs), as well as their methylation levels, with RA susceptibility. Nine SNPs (AHR gene rs2066853, rs2158041, rs2282885, ARNT gene rs10847, rs1889740, rs11204735, AHRR gene rs2292596, rs2672725, rs349583) were genotyped via improved multiple ligase detection reaction (iMLDR) in 479 RA patients and 496 healthy controls. We used the Illumina Hiseq platform to detect methylation levels of these genes in 122 RA patients and 123 healthy controls. A significant increase in rs11204735 C allele frequency was observed in RA patients when compared to controls. Further, rs11204735 polymorphism was associated with a decreased risk of RA under the dominant model. ARNT CCC haplotype frequency was significantly increased in RA patients in comparison to controls. In the AHRR gene, rs2672725 GG genotype, G allele frequencies were significantly related to an increased risk of RA and rs2292596, rs2672725 polymorphism were significantly associated with an increased risk of RA under the dominant model, recessive model, respectively. However, no significant association was identified between AHR gene polymorphism and RA susceptibility. The AHR methylation level in RA patients was significantly higher than the controls, while AHRR methylation level was abnormally reduced in RA patients. In addition, AHRR rs2672725 genotype distribution was significantly associated with the AHRR methylation level among RA patients. In summary, ARNT rs11204735, AHRR rs2292596, and rs2672725 polymorphisms were associated with RA susceptibility and altered AHR, AHRR methylation levels were related to the risk of RA.

Objective Although extensive research has been carried out on CD4 + T cells infiltrating the labial glands in patients with primary Sjögren’s Syndrome (pSS), it is still unclear how CD4 + T cells remain in the labial gland tissue and develop into tissue resident cells. The aim of this study was to investigate the molecular mechanism by which CD4 + T reside in labial glandular tissue of pSS patients. Methods Lymphocyte infiltration in labial salivary glands (LSG) of pSS patients was detected by H&E staining. Expression of sphingosine-1-phosphate receptor 1 (S1PR1) in LSG was examined by Immunohistochemistry. Immunofluorescence analyses were utilized to detect the co-expression of CD4, CD69 and S1PR1 in T cells of LSG of pSS patients. Expression of gene S1pr1 in peripheral blood CD4 + T cells of healthy controls and pSS patients was detected by quantitative real-time PCR (QPCR). QPCR was used to examine the expression of gene S1pr1, Klf2, and Cd69 in the CD4 + T cells that were co-cultured in vitro with cytokines TNF-α, TGF-β, and IL-33. Results S1PR1 was expressed in the infiltrating monocytes in LSG of pSS patients, and S1PR1 was weakly or even not expressed in cytoplasm of CD4 + CD69 + T RM cells of LSG in patients with pSS. Expression of gene S1pr1 in peripheral blood CD4 + T cells of pSS patients was about three-fifths of that of healthy controls (P < 0.05). Expression of genes S1pr1 (P < 0.001) and Klf-2 (P < 0.001) was significantly decreased, and the expression of gene Cd69 (P < 0.05) was significantly increased in peripheral blood CD4 + T cells of pSS patients co-cultured in vitro with cytokines TNF-α, TGF-β, and IL-33. Conclusion Our study suggests that the decrease of S1pr1 gene expression may provide a molecular basis for promoting the tissue retention and development of CD4 + CD69 + T RM cells.

The rapid growth of wireless electronic devices has raised concerns about the harmful effects of leaked electromagnetic radiation (EMR) on human health. Even though numerous studies have been carried out to explore the biological effects of EMR, no clear conclusions have been drawn about the effect of radio frequency (RF) EMR on oligodendrocytes. To this end, we exposed oligodendroglia and three other types of brain cells to 2.4 GHz EMR for 6 or 48 h at an average input power of 1 W in either a continuous wave (CW-RF) or a pulse-modulated wave (PW-RF, 50 Hz pulse frequency, 1/3 duty cycle) pattern. RNA sequencing, RT-qPCR, and Western blot were used to examine the expression of C/EBPβ and its related genes. Multiple reaction monitoring (MRM) was used to examine the levels of expression of C/EBPβ-interacting proteins. Our results showed that PW-RF EMR significantly increased the mRNA level of C/EBPβ in oligodendroglia but not in other types of cells. In addition, the expression of three isoforms and several interacting proteins and targeted genes of C/EBPβ were markedly changed after 6-h PW-RF but not CW-RF. Our results indicated that RF EMR regulated the expression and functions of C/EBPβ in a waveform- and cell-type-dependent manner.