Buccal acupuncture combined with ultrasound-guided dry needle-evoked inactivation of trigger points to treat cervical and shoulder girdle myofascial pain syndrome.

BACKGROUND: Myofascial pain syndrome (MPS) is a common disease with easy persistence and recurrence. In clinical practice, although many methods have been adopted to prevent and treat MPS, the control of MPS is still not satisfactory. OBJECTIVE: To compare the safety and effectiveness of buccal acupuncture, inactivation of trigger points (MTrPs), and their combination in the treatment of MPS. METHODS: Two hundred MPS patients in the pain clinic were randomly divided into four groups (n= 50) to receive oral drugs (Group A), oral drugs + buccal needle (Group B), oral drugs + MTrP inactivation (Group C), or oral drugs + buccal needle + MTrP inactivation (Group D). RESULTS: The visual analogue scale (VAS) and cervical range of motion (ROM) of Group D were significantly lower than those of the other three groups, and the pressure pain threshold (PPT) value of labelled MTrPs was significantly higher than those of the other three groups (P< 0.05). The excellent rate and total effective rate of Group D were significantly higher than those of the other three groups. Group C had the highest pain score and the lowest acceptance score. The results showed that buccal acupuncture combined with ultrasound-guided dry needle-evoked inactivation of MTrPs can significantly reduce the VAS score of MPS patients, improve the range of motion of the cervical spine, and improve patient satisfaction. CONCLUSIONS: This study provides a highly accepted and satisfactory treatment for MPS, which is worthy of clinical promotion.

MiR-19a/miR-96-mediated low expression of KIF26A suppresses metastasis by regulating FAK pathway in gastric cancer.

Gastric cancer (GC) is one of the most common malignant neoplasms. Invasion and metastasis are the main causes of GC-related deaths. Recently, kinesins were discovered to be involved in tumor development. The aim of this study was to elucidate the roles of kinesin superfamily protein 26A (KIF26A) in GC and its underlying molecular mechanism in regulating tumor invasion and metastasis. Using real-time quantitative polymerase chain reaction (qPCR) and immunohistochemistry (IHC), we showed that KIF26A expression was lower in GC tissues without lymph node metastasis (LNM) than in nontumorous gastric mucosa, and even lower in GC tissues with LNM than in GC tissues without LNM. Functional experiments showed that KIF26A inhibited migration and invasion of GC cells. We further identified focal-adhesion kinase (FAK), phosphatidylinositol 3-kinase regulatory subunit alpha (PI3KR1), VAV3, Rac1 and p21-activated kinase 2, and ß-PAK (PAK3) as downstream effectors of KIF26A in the focal-adhesion pathway, and we found that KIF26A could regulate FAK mRNA expression through inhibiting c-MYC by MAPK pathway. c-MYC could bind to the promoter of FAK and activate FAK transcription. Moreover, we found that KIF26A-mediated inactivation of the focal-adhesion pathway could reduce the occurrence of the epithelial-to-mesenchymal transition (EMT) by increasing expression of E-cadherin and reducing that of Snail. Luciferase assays and Western blotting revealed that miR-19a and miR-96 negatively regulate KIF26A. Finally, we found that decreased expression of KIF26A has been positively correlated with histological differentiation, Lauren classification, LNM, distal metastasis, and clinical stage, as well as poor survival in patients with GC. These data indicate that KIF26A could inhibit GC migration and invasion by regulating the focal-adhesion pathway and repressing the occurrence of EMT.

Effects of Stellate Ganglion Block Through Different Approaches Under Guidance of Ultrasound.

OBJECTIVE: This study aimed to investigate the effects of stellate ganglion block (SGB) through different approaches under guidance of ultrasound. METHODS: A total of 130 patients undergoing SGB in our hospital between February 2019 and February 2020 were enrolled as the research subjects. According to the random number table method, these subjects were divided into two groups: a modified 6th cervical vertebra (C6) group (n = 65) and a 7th cervical vertebra (C7) group (n = 65). Under the guidance of ultrasound, the subjects in the modified C6 group were punctured at the level of the C6 transverse process, and the subjects in the C7 group were punctured at the level of the C7 transverse process. The operation duration, number of puncture angle adjustments, block effects, and adverse reactions for SGB were compared between the two groups. RESULTS: The modified C6 group showed shorter SGB operation duration and a lower number of puncture angle adjustments than the C7 group, and the differences were statistically significant (P < 0.05). Horner Syndrome occurred in both groups after SGB. The incidence of adverse reactions in the modified C6 group was 4.62%, comprising 1 case of hoarseness and 2 cases of slowed pulse, while that in the C7 group was 6.15%, with 1 case of hoarseness and 3 cases of slowed pulse; the difference between the two groups was not statistically significant (P > 0.05). CONCLUSION: The operation duration for modified SGB guided by ultrasound puncturing at the C6 transverse process is shorter and requires fewer puncture angle adjustments than puncturing at the C7 transverse process; however, there is no significant difference between the incidence of adverse reactions or the blocking effects of the two methods.

The Recombinant Protein EphB4-Fc Changes the Ti Particle-Mediated Imbalance of OPG/RANKL via EphrinB2/EphB4 Signaling Pathway and Inhibits the Release of Proinflammatory Factors In Vivo.

Aseptic loosening caused by wear particles is one of the common complications after total hip arthroplasty. We investigated the effect of the recombinant protein ephB4-Fc (erythropoietin-producing human hepatocellular receptor 4) on wear particle-mediated inflammatory response. In vitro, ephrinB2 expression was analyzed using siRNA-NFATc1 (nuclear factor of activated T-cells 1) and siRNA-c-Fos. Additionally, we used Tartrate-resistant acid phosphatase (TRAP) staining, bone pit resorption, Enzyme-linked immunosorbent assay (ELISA), as well as ephrinB2 overexpression and knockdown experiments to verify the effect of ephB4-Fc on osteoclast differentiation and function. In vivo, a mouse skull model was constructed to test whether the ephB4-Fc inhibits osteolysis and inhibits inflammation by micro-CT, H&E staining, immunohistochemistry, and immunofluorescence. The gene expression of ephrinB2 was regulated by c-Fos/NFATc1. Titanium wear particles activated this signaling pathway to the promoted expression of the ephrinB2 gene. However, ephrinB2 protein can be activated by osteoblast membrane receptor ephB4 to inhibit osteoclast differentiation. In in vivo experiments, we found that ephB4 could regulate Ti particle-mediated imbalance of OPG/RANKL, and the most important finding was that ephB4 relieved the release of proinflammatory factors. The ephB4-Fc inhibits wear particle-mediated osteolysis and inflammatory response through the ephrinB2/EphB4 bidirectional signaling pathway, and ephrinB2 ligand is expected to become a new clinical drug therapeutic target.

Quercetin inhibits macrophage polarization through the p-38α/ß signalling pathway and regulates OPG/RANKL balance in a mouse skull model.

Aseptic loosening caused by wear particles is a common complication after total hip arthroplasty. We investigated the effect of the quercetin on wear particle-mediated macrophage polarization, inflammatory response and osteolysis. In vitro, we verified that Ti particles promoted the differentiation of RAW264.7 cells into M1 macrophages through p-38α/ß signalling pathway by using flow cytometry, immunofluorescence assay and small interfering p-38α/ß RNA. We used enzyme-linked immunosorbent assays to confirm that the protein expression of M1 macrophages increased in the presence of Ti particles and that these pro-inflammatory factors further regulated the imbalance of OPG/RANKL and promoted the differentiation of osteoclasts. However, this could be suppressed, and the protein expression of M2 macrophages was increased by the presence of the quercetin. In vivo, we revealed similar results in the mouse skull by µ-CT, H&E staining, immunohistochemistry and immunofluorescence assay. We obtained samples from patients with osteolytic tissue. Immunofluorescence analysis indicated that most of the macrophages surrounding the wear particles were M1 macrophages and that pro-inflammatory factors were released. Titanium particle-mediated M1 macrophage polarization, which caused the release of pro-inflammatory factors through the p-38α/ß signalling pathway, regulated OPG/RANKL balance. Macrophage polarization is expected to become a new clinical drug therapeutic target.

Pelvic incidence measurement using a computed tomography data-based three-dimensional pelvic model.

OBJECTIVES: To introduce a new method of pelvic incidence (PI) measurement based on three-dimensional (3D) pelvic models reconstructed from CT images and to report the normal distribution of PI in normal pelvic anatomy. METHODS: CT images of 320 subjects with normal pelvic anatomy who visited the Radiology Department between 2006 and 2017 were retrospectively selected and saved in Digital Imaging and Communications in Medicine (DICOM) format. A computerized method was employed to determine the bony landmarks required for the measurement of PI. To quantify the method's accuracy and reliability, the intraclass correlation coefficient (ICC) was calculated. A subgroup of 30 DICOM files was randomly selected to perform a validation study. Three independent testers performed all procedures. All measurements were performed twice independently by the three testers on all 10 subjects with an interval of 2 weeks. Independent samples t tests were used to identify statistically significant differences in the PI value between sexes. Pearson correlation coefficient was employed to determine the relationship between PI and age. RESULTS: PI measurement using the new method resulted in an excellent intraobserver reliability (0.9612, range 0.8917-0.9893; p < 0.001) and interobserver reliability (0.9867, range 0.9611-0.9964; p < 0.001). PI was significantly different between sexes, with larger PI in women (p = 0.019). PI was significantly larger in the 40-80-year age group (45.94 ± 9.08°) than the < 40-year age group (43.50 ± 7.39°). We did not find any linear correlation between PI and age in the male (r = 0.140, p = 0.105) or female subgroup (r = 0.119, p = 0.107). A weak correlation between PI and age overall was observed (r = 0.142, p = 0.011). CONCLUSION: Accurate PI measurement could be achieved by a CT data-based 3D pelvic model.

Pelvic incidence variation among individuals: functional influence versus genetic determinism.

Pelvic incidence has become one of the most important sagittal parameters in spinal surgery. Despite its great importance, pelvic incidence can vary from 33° to 85° in the normal population. The reasons for this great variability in pelvic incidence remain unexplored. The objective of this article is to present some possible interpretations for the great variability in pelvic incidence under both normal and pathological conditions and to further understand the determinants of pelvic incidence from the perspective of the functional requirements for bipedalism and genetic backgrounds via a literature review. We postulate that both pelvic incidence and pelvic morphology may be genetically predetermined, and a great variability in pelvic incidence may already exist even before birth. This great variability may also serve as a further reminder that the sagittal profile, bipedal locomotion mode, and genetic background of every individual are unique and specific, and clinicians should avoid making universally applying broad generalizations of pelvic incidence. Although PI is an important parameter and there are many theories behind its variability, we still do not have clear mechanistic answers.

Protocadherin 7 inhibits cell migration and invasion through E-cadherin in gastric cancer.

The protocadherin 7 is a member of the protocadherin family that expressed aberrantly in many types of human cancers. However, its expression, function, and underlying mechanisms are little known in gastric cancer. In this study, we detected protocadherin 7 expression in gastric cancer tissues and non-tumorous gastric mucosa tissues by real-time quantitative polymerase chain reaction and immunohistochemistry. The association of protocadherin 7 expression with the clinicopathological characteristics and the prognosis was subsequently analyzed. MTS ((3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium)) and transwell assays were performed to assess the effect of protocadherin 7 on proliferation, migration, and invasion in gastric cancer cell lines. Moreover, real-time quantitative polymerase chain reaction and western blot were used to detect the expression of epithelial-mesenchymal transition markers. Protocadherin 7 expression was decreased gradiently from normal tissue to gastric cancer, especially in gastric cancer tissue with lymph node metastasis. Low expression of protocadherin 7 was significantly associated with Lauren's classification ( p = 0.0005), lymph node metastases ( p = 0.0002), and tumor node metastasis stage ( p = 0.0221), as well as poor prognosis ( p < 0.05). Furthermore, down-regulation of protocadherin 7 in gastric cancer cell lines significantly increased their migration and invasion abilities (both p < 0.05), while it had no influence on the gastric cancer cell proliferation ( p > 0.05). Additionally, our results demonstrated that E-cadherin expression was down-regulated in gastric cancer cells with protocadherin 7 depletion. Our data indicated that protocadherin 7 may play important roles in the invasion and metastasis of gastric cancer, and protocadherin 7 could suppress cell migration and invasion through E-cadherin inhibition. Protocadherin 7 can serve as a novel biomarker for diagnostic and prognosis in patients with gastric cancer.

Uterine adenomatoid tumor: a clinicopathologic study of 102 cases.

OBJECTIVE: Uterine adenomatoid tumors (UATs) are tubercle without significant clinical features. The study aims to summarize the clinicopathological characteristics of UATs to improve diagnostic accuracy. METHODS: Between January 2014 and December 2015, 4326 uterine specimens were collected from patients who received hysterectomy or myomectomy, of which 102 cases were pathologically confirmed as UATs. The clinical features, pathological parameters and immunohistochemical staining were analyzed. RESULTS: One hundred and two UATs were identified by gross and microscopic examination, which accounts for 2.4% of all the uterine tumors. UATs were usually located in the uterus myometrium, near the serosa or cornua. Most of them were solitary, without an enveloping membrane or clear demarcation. Microscopically, typical features were glandular structures and cavities with various sizes and shapes found within the hyperplastic smooth muscle tissues. Immunohistochemical staining showed that all tumors were positive for HBME-1 and CK (pan). Most of them were positive for CR (89.6%) and D2-40 (92.4%), negative for CD31 and CEA, while cast-off cells in glandular cavities and lymphocytes were positive for LCA. CONCLUSION: Adenomatoid tumors are not very rare in the uterus. The diagnosis of UATs can be improved by carefully gross and microscopic examination. Immnohistachemical staining is helpful for diagnosis and differential diagnosis of UATs.

MicroRNA-27b, microRNA-101 and microRNA-128 inhibit angiogenesis by down-regulating vascular endothelial growth factor C expression in gastric cancers.

Vascular Endothelial Growth Factor C (VEGF-C) has critical roles in angiogenesis in human cancers; however, the underlying mechanisms regulating VEGF-C expression remain largely unknown. In the present study, VEGF-C protein expression and the density of blood vessels or lymphatic vessels were determined by immunohistochemistry in 103 cases of gastric cancer tissues. Suppression of VEGF-C by miR-27b, miR-101 and miR-128 was investigated by luciferase assays, Western blot and ELISA. The miRNAs expression levels were detected in human gastric cancers by real-time quantitative PCR. Cell proliferation, migration and invasion assays were performed to assess the effect of miRNAs on gastric cancer cells and human umbilical vascular endothelial cells (HUVECs). Our data showed that high VEGF-C expression was significantly associated with increased tumor size, advanced TNM classification and clinical stage, higher microvessel density (MVD) and lymphatic density (LVD), as well as poor survival in patients with gastric cancer. Furthermore, VEGF-C was found to be a direct target gene of miR-27b, miR-101, and miR-128. The expression levels of the three miRNAs were inversely correlated with MVD. Overexpression of miR-27b, miR-101, or miR-128 suppressed migration, proliferation activity, and tube formation in HUVECs by repressing VEGF-C secretion in gastric cancer cells. We conclude that miR-27b, miR-101 and miR-128 inhibit angiogenesis by down-regulating VEGF-C expression in gastric cancers.

[Effect of Janus kinase inhibitor AG490 on invasion and metastasis of human breast cancer cells].

OBJECTIVE: To investigate the effect of Janus kinase (JAK) inhibitor AG490 on invasion and metastasis of the human breast cancer cell MDA-MB-231, and to explore the regulating role of JAK-STAT3 signaling pathway when the breast cancer occurs to the invasiveness and metastasis. METHODS: The human breast cancer cell MDA-MB-231 was used as the research object, and AG490 was as Janus kinase inhibitor. The adhesion of MDA-MB-231 cell attaching to matrigel was measured with MTT assay. The invasion and metastasis potential were evaluated with transwell chamber. The P-STAT3 protein in cell was detected by Western-blot. RESULTS: Janus kinase inhibitor AG490 could make that the expression of P-STAT3 in human breast cancer cell MDA-MB-231 became weak, and that the abilities of adhesion, invasion and metastasis were also dropping down as compared with the control group (P < 0.01). CONCLUSION: JAK-STAT3 signaling pathway participates in regulating the invasion and metastasis of human breast cancer. Inhibiting the activation of JAK-STAT3 signaling pathway can suppress the invasion and metastasis of human breast cancer.