[Regularity of meridian-acupoint reactions of foot three yin meridians in primary dysmenorrhea and secondary dysmenorrhea patients].

OBJECTIVE: To observe the meridian-acupoint reactions of foot three yin meridians in primary dysmenorrhea(PD) and secondary dysmenorrhea(SD) patients, so as to summarize the rules of meridian-acupoint reaction and acupoints selection. METHODS: Thirty-five patients with PD (PD group), 34 patients with SD (SD group) and 35 healthy subjects (healthy group) were recruited. The compression method was used to examine the lower leg segment of the foot three yin meridians. Positive reactions(palpable skin changes, including cords, nodules, depressions) and tenderness of meridians and acupoints were recorded. The visual analogue scale (VAS) was used to evaluate the tenderness severity of acupoints. RESULTS: Compared with the healthy group, the probability of positive reactions and tenderness in foot three yin meridians were higher in PD and SD groups (P<0.01,P<0.05). Compared with the PD group, the probability of positive reactions in Spleen and Liver Meridians were higher in the SD group, with higher probability of tenderness in Liver Meridian(P<0.05). The probability of positive reactions and tenderness in the Spleen Meridian of PD and SD groups was significantly higher than that in the Kidney Meridian (P<0.01), while the probability of tenderness in the Spleen Meridian of the PD group was significantly higher than that in the Liver Meridian (P<0.05). Positive reactions and tenderness were concentrated at Yinlingquan (SP9), Diji (SP8) and Sanyinjiao (SP6) of Spleen Meridian and Xiguan (LR7) and Ligou (LR5) in Liver Meridian of PD and SD groups. In comparison with the PD group, the probability of positive reactions, tenderness and VAS score of SP8 and LR5 of the SD group were higher (P<0.05, P<0.01). CONCLUSION: The positive reaction occurs most frequently in the Spleen Meridian, followed by the Liver Meridian, and least frequently in the Kidney Meridian. The acupoints with positive reaction are different between PD and SD, which suggests that the Spleen Meridian acupoints should be the main acupoints when treating the two kinds of dysmenorrhea, and acupoints should also be selected according to the meridian and acupoint examination results.

Influence of sport dance courses on female college students / Influência de cursos de dança esportiva em estudantes universitárias / Influencia de los cursos de danza deportiva en las estudiantes universitarias

ABSTRACT Introduction Dance sport is a project that integrates art and sport. In it, female students can exercise and improve their self-conscious sports skills with music. Objective Study the effects of special sport dance courses on the physical health of female college students. Methods 108 female college students were selected as volunteers for the experiment, the experimental statistics and observations were performed from the aspects related to shape, flexibility and body composition. Results The female college students who were trained in the special sports dance course significantly improved their shape, flexibility and body composition. Conclusion Considering the current scenario of continuous decline of college students' physical health, this paper discusses the positive role of optional sport dance courses in improving college students' physical fitness from the aspects of form, flexibility, and body composition, and other related factors. Level of evidence II; Therapeutic studies - investigation of treatment outcomes.

RESUMO Introdução A dança esportiva é um projeto que integra arte e esporte. Nela, as estudantes podem exercitar e melhorar suas habilidades esportivas autoconscientes com a música. Objetivo Estudar os efeitos dos cursos especiais de dança esportiva sobre a saúde física das estudantes universitárias. Métodos Foram selecionadas 108 estudantes universitárias como voluntárias para o experimento, as estatísticas e observações experimentais foram realizadas a partir dos aspectos relacionados à forma, flexibilidade e composição corporal. Resultados As alunas universitárias que foram treinadas no curso especial de dança esportiva melhoraram significativamente sua forma, flexibilidade e composição corporal. Conclusão Considerando o cenário atual de declínio contínuo da saúde física das estudantes universitárias, este trabalho discute o papel positivo dos cursos optativos de dança esportiva na melhoria da aptidão física das estudantes universitárias a partir dos aspectos da forma, flexibilidade, e composição corporal, além de outros fatores relacionados. Nível de evidência II; Estudos terapêuticos - investigação dos resultados do tratamento.

RESUMEN Introducción La danza deportiva es un proyecto que integra arte y deporte. En él, los alumnos pueden ejercitarse y mejorar sus habilidades deportivas con música. Objetivo Estudiar los efectos de los cursos especiales de danza deportiva en la salud física de las estudiantes universitarias. Métodos Se seleccionaron 108 estudiantes universitarias como voluntarias para el experimento, se realizaron estadísticas experimentales y observaciones de los aspectos relacionados con la forma, la flexibilidad y la composición corporal. Resultados Las universitarias que recibieron formación en el curso especial de danza deportiva mejoraron notablemente su forma, flexibilidad y composición corporal. Conclusión Teniendo en cuenta el escenario actual de continuo deterioro de la salud física de las estudiantes universitarias, este artículo analiza el papel positivo de los cursos optativos de danza deportiva en la mejora de la forma física de las estudiantes universitarias desde los aspectos de la forma, la flexibilidad y la composición corporal, y otros factores relacionados. Nivel de evidencia II; Estudios terapéuticos - investigación de los resultados del tratamiento.

MD2 deficiency prevents high-fat diet-induced AMPK suppression and lipid accumulation through regulating TBK1 in non-alcoholic fatty liver disease.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is the most predominant form of liver diseases worldwide. Recent evidence shows that myeloid differentiation factor 2 (MD2), a protein in innate immunity and inflammation, regulates liver injury in models of NAFLD. Here, we investigated a new mechanism by which MD2 participates in the pathogenesis of experimental NAFLD. METHODS: Wild-type, Md2-/- and bone marrow reconstitution mice fed with high-fat diet (HFD) were used to identify the role of hepatocyte MD2 in NAFLD. Transcriptomic RNA-seq and pathway enrich analysis were performed to explore the potential mechanisms of MD2. In vitro, primary hepatocytes and macrophages were cultured for mechanistic studies. RESULTS: Transcriptome analysis and bone marrow reconstitution studies showed that hepatocyte MD2 may participate in regulating lipid metabolism in models with NAFLD. We then discovered that Md2 deficiency in mice prevents HFD-mediated suppression of AMP-activated protein kinase (AMPK). This preservation of AMPK in Md2-deficient mice was associated with normalized sterol regulatory element binding protein 1 (SREBP1) transcriptional program and a lack of lipid accumulation in both hepatocytes and liver. We then showed that hepatocyte MD2 links HFD to AMPK/SREBP1 through TANK binding kinase 1 (TBK1). In addition, MD2-increased inflammatory factor from macrophages induces hepatic TBK1 activation and AMPK suppression. CONCLUSION: Hepatocyte MD2 plays a pathogenic role in NAFLD through TBK1-AMPK/SREBP1 and lipid metabolism pathway. These studies provide new insight into a non-inflammatory function of MD2 and evidence for the important role of MD2 in NALFD.

Astaxanthin inhibits homocysteine­induced endothelial cell dysfunction via the regulation of the reactive oxygen species­dependent VEGF­VEGFR2­FAK signaling pathway.

Increased plasma levels of homocysteine (Hcy) can cause severe damage to vascular endothelial cells. Hcy­induced endothelial cell dysfunction contributes to the occurrence and development of human cerebrovascular diseases (CVDs). Our previous studies have revealed that astaxanthin (ATX) exhibits novel cardioprotective activity against Hcy­induced cardiotoxicity in vitro and in vivo. However, the protective effect and mechanism of ATX against Hcy­induced endothelial cell dysfunction requires further investigation. In the present study, treatment of human umbilical vascular endothelial cells (HUVECs) with Hcy inhibited the migration, invasive and tube formation potentials of these cells in a dose­dependent manner. Hcy treatment further induced a time­dependent increase in the production of reactive oxygen species (ROS), and downregulated the expression of vascular endothelial growth factor (VEGF), phosphorylated (p)­Tyr­VEGF receptor 2 (VEGFR2) and p­Tyr397­focal adhesion kinase (FAK). On the contrary, ATX pre­treatment significantly inhibited Hcy­induced cytotoxicity and increased HUVEC migration, invasion and tube formation following Hcy treatment. The mechanism of action may involve the effective inhibition of Hcy­induced ROS generation and the recovery of FAK phosphorylation. Collectively, our findings suggested that ATX could inhibit Hcy­induced endothelial dysfunction by suppressing Hcy­induced activation of the VEGF­VEGFR2­FAK signaling axis, which indicates the novel therapeutic potential of ATX in treating Hcy­mediated CVD.

Correction to: Reversal of homocysteine-induced neurotoxicity in rat hippocampal neurons by astaxanthin: evidences for mitochondrial dysfunction and signaling crosstalk.

[This corrects the article DOI: 10.1038/s41420-018-0114-x.].

Superior parathyroid blood supply safety in thyroid cancer surgery: A randomized controlled trial.

BACKGROUND: To evaluate the clinical value of a technique protecting blood supply to the superior parathyroid during surgery for thyroid cancer. MATERIALS AND METHODS: The observation group comprised 113 patients admitted to our hospital during the period from January 1, 2016 to December 31, 2016, who were diagnosed with thyroid cancer and treated by surgery using a technique protecting blood supply to the superior parathyroid. The control group comprised 113 patients diagnosed with thyroid cancer who were treated by surgery using the conventional technique. Postoperative parathyroid function damage and blood calcium levels were assessed in both groups. RESULTS: The incidences of hypocalcemia and low parathyroid hormone in the observation and control groups were 10.6% and 31.9%, and 14.2% and 35.4%, respectively. The relative risk (RR) of the control group was increased (RR = 3.009 for control; RR = 2.493 for observation). Univariate logistic regression analysis showed that postoperative temporary hypoparathyroidism was associated with lymph node metastasis, use of the above protective technique, and tumor size [(odds ratio, OR = 1.936, 95%CI 1.029-3.643; P = 0.041), (OR = 0.301, 95%CI 0.156-0.579; P = 0.001) and (OR = 2.022, 95%CI 1.089-3.756; P = 0.026), respectively]. Postoperative temporary hypoparathyroidism was also associated with lymph node dissection (Bilateral vs. No, P = 0.003) and T classification (T3 vs. T1, P = 0.034). Multivariate logistic regression analysis showed that, after including significant independent variables of univariate logistic regression analysis (e.g., lymph node metastasis, lymph node resection, protective technique, tumor size, and T classification), the protective technique was a factor supporting reduced incidence of postoperative temporary hypoparathyroidism (OR = 0.325, 95% CI 0.163-0.648; P = 0.001). CONCLUSION: Application of a technique protecting blood supply to the superior parathyroid during thyroid cancer surgery effectively reduced the incidence of postoperative temporary hypoparathyroidism. However, because of the imbalance in lymph node dissection between the two groups, confounding factors could not be completely eliminated, and matched pair analysis is needed to eliminate these factors.

Reversal of homocysteine-induced neurotoxicity in rat hippocampal neurons by astaxanthin: evidences for mitochondrial dysfunction and signaling crosstalk.

Elevated plasma level of homocysteine (Hcy) represents an independent risk for neurological diseases, and induction of oxidative damage is considered as one of the most important pathomechanisms. Astaxanthin (ATX) exhibits strong antioxidant activity in kinds of experimental models. However, the potential of ATX against Hcy-induced neurotoxicity has not been well explored yet. Herein, the neuroprotective effect of ATX against Hcy-induced neurotoxicity in rat hippocampal neurons was examined, and the underlying mechanism was evaluated. The results showed that ATX pre-treatment completely reversed Hcy-induced neurotoxicity through inhibiting cell apoptosis in rat primary hippocampal neurons. The mechanical investigation revealed that ATX effectively blocked Hcy-induced mitochondrial dysfunction by regulating Bcl-2 family and opening of mitochondrial permeability transition pore (MPTP). ATX pre-treatment also attenuated Hcy-induced oxidative damage via inhibiting the release of intracellular reactive oxide species (ROS) and superoxide anion through regulating MPTP opening. Moreover, normalization of MAPKs and PI3K/AKT pathways also contributed to ATX-mediated protective effects. Taken together, these results above suggested that ATX has the potential to reverse Hcy-induced neurotoxicity and apoptosis by inhibiting mitochondrial dysfunction, ROS-mediated oxidative damage and regulation of MAKPs and AKT pathways, which validated the strategy of using ATX could be a highly effective way in combating Hcy-mediated neurological disorders.

Selenocysteine antagonizes oxygen glucose deprivation-induced damage to hippocampal neurons.

Designing and/or searching for novel antioxidants against oxygen glucose deprivation (OGD)-induced oxidative damage represents an effective strategy for the treatment of human ischemic stroke. Selenium is an essential trace element, which is beneficial in the chemoprevention and chemotherapy of cerebral ischemic stroke. The underlying mechanisms for its therapeutic effects, however, are not well documented. Selenocysteine (SeC) is a selenium-containing amino acid with neuroprotective potential. Studies have shown that SeC can reduce irradiation-induced DNA apoptosis by reducing DNA damage. In this study, the in vitro protective potential and mechanism of action of SeC against OGD-induced apoptosis and neurotoxicity were evaluated in HT22 mouse hippocampal neurons. We cultured HT22 cells in a glucose-free medium containing 2 mM Na2S4O2, which formed an OGD environment, for 90 minutes. Findings from MTT, flow cytometry and TUNEL staining showed obvious cytotoxicity and apoptosis in HT22 cells in the OGD condition. The activation of Caspase-7 and Caspase-9 further revealed that OGD-induced apoptosis of HT22 cells was mainly achieved by triggering a mitochondrial-mediated pathway. Moreover, the OGD condition also induced serious DNA damage through the accumulation of reactive oxygen species and superoxide anions. However, SeC pre-treatment for 6 hours effectively inhibited OGD-induced cytotoxicity and apoptosis in HT22 cells by inhibiting reactive oxygen species-mediated oxidative damage. Our findings provide evidence that SeC has the potential to suppress OGD-induced oxidative damage and apoptosis in hippocampal neurons.

T-cadherin is associated with prognosis in triple-negative breast cancer.

The purpose of the present study was to assess the prognostic impact of T-cadherin expression in patients with triple-negative breast cancer (TNBC). On the basis of the results of immunohistochemical analysis, 106 patients with operable TNBC were divided into two groups, the T-cadherin-positive group and T-cadherin-negative group. Fisher's exact and χ2 tests were employed to analyze clinical data, which included the association between T-cadherin expression and clinicopathological features and prognosis. The log-rank test was used to examine the impact of T-cadherin expression on the 5-year disease-free survival (DFS) and the 5-year overall survival (OS) of these patients. Kaplan-Meier and Cox regression analyses were introduced to analyze DFS and OS. Compared with the T-cadherin-positive group (58.3, 52.8 and 47.2, respectively; P=0.018, P=0.017, and P=0.047), tumor size >2 cm, grade II and III (Elston-Ellis modification of Bloom-Richardson grading system), and positive lymph node status were significantly more common in the T-cadherin-negative group compared with the T-cadherin-positive group (80.0 vs. 58.3%, 75.7 vs. 52.8% and 67.1 vs. 47.2%, respectively) (P=0.018, P=0.017, and P=0.047). Compared with the T-cadherin-positive group, 5-year DFS and OS levels were significantly lower in the T-cadherin-negative group (Z=6.233, P=0.013; Z=5.366, P=0.021). Multivariate analysis revealed that negative T-cadherin expression was an independent prognostic factor for DFS (P=0.009) and OS (P=0.048). The results of the present study indicated that negative T-cadherin expression indicated a worse prognosis for patients with TNBC.

Association of T-cadherin levels with the response to neoadjuvant chemotherapy in locally advanced breast cancer.

PURPOSE: To examine the association of T-cadherin with pathologic complete response (pCR) after neoadjuvant chemotherapy for locally advanced breast cancer. RESULTS: T-cadherin expression before and after neoadjuvant chemotherapy was similar (P = 0.162). The multivariable analysis indicated that negative T-cadherin expression was independently associated with pCR after neoadjuvant TAC chemotherapy (P = 0.001). MATERIALS AND METHODS: A total of 136 patients with locally advanced breast cancer received four cycles of neoadjuvant TAC chemotherapy (docetaxel + epirubicin + cyclophosphamide), followed by surgery. T-cadherin, estrogen receptor (ER), progesterone receptor (PR), HER-2, and Ki-67 were analyzed by immunohistochemistry. The association between T-cadherin expression and pCR after neoadjuvant chemotherapy was analyzed using multivariable logistic analysis. CONCLUSIONS: Negative T-cadherin expression before and after neoadjuvant chemotherapy for locally advanced breast cancer was similar. T-cadherin could be considered an independent factor associated with the efficacy of such therapy.

Pretreatment with baicalin attenuates hypoxia and glucose deprivation-induced injury in SH-SY5Y cells.

OBJECTIVE: To explore the neuroprotective effects of baicalin against hypoxia and glucose deprivation-reperfusion (OGD/RO)-induced injury in SH-SY5Y cells. METHODS: SH-SY5Y cells were divided into a control group, a OGD/RO group, which was subject to OGD/RO induction; and 3 baicalin groups subject to baicalin (1, 5, 25 µmol/L) for 2 h before induction of OGD/RO (low-, medium-, and high-dose baicalin groups). Cell viability was detected by thiazolyl blue tetrazolium bromide (MTT) assay and flow cytometric analysis was used to detect cell apoptosis. Real-time polymerase chain reaction was performed to determine the mRNA expression of caspase-3 gene. Western blot analysis was conducted to determine the expression of nuclear factor (NF)-κB and N-methyl-daspartic acid receptor-1 (NMDAR1). RESULTS: Baicalin could significantly attenuate OGD/RO mediated apoptotic cell death in SH-SY5Y cells; the apoptosis rates in the low-, medium- and high-dose groups were 12.1%, 7.9%, and 5.4%, respectively. Western blot and real-time PCR analysis revealed that significant decrease in caspase-3 expression in the baicalin group compared with the OGD/RO group (P<0.01). Additionally, down-regulation of NF-κB and NMDAR1 was observed in the baicalin group compared with those obtained from the OGD/RO group. Compared with the low-dose baicalin group, remarkable decrease was noted in the medium- and high-dose groups (P<0.01). CONCLUSION: Baicalin pre-treatment attenuates brain ischemia reperfusion injury by suppressing cellular apoptosis.

Baicalin protects against thrombin induced cell injury in SH-SY5Y cells.

Baicalin, an extract from the dried root of Scutellaria baicalensis Georgi, was shown to be neuroprotective. However, the precise mechanisms are incompletely known. In this study, we determined the effect of baicalin on thrombin induced cell injury in SH-SY5Y cells, and explored the possible mechanisms. SH-SY5Y cells was treated with thrombin alone or pre-treated with baicalin (5, 10, 20 µM) for 2 h followed by thrombin treatment. Cells without thrombin and baicalin treatment were used as controls. Cell viability was detected by MTT assay. Cell apoptosis was analyzed by flow cytometry. Real-time PCR was performed to determine the mRNA expression of protease-activated receptor-1 (PAR-1). Western blotting was conducted to determine the protein expression of PAR-1, Caspase-3 and NF-κB. Baicalin reduced cell death following thrombin treatment in a dose-dependent manner, with concomitant inhibition of NF-κB activation and suppression of PAR-1 expression. In addition, baicalin reduced Caspase-3 expression. The above findings indicated that baicalin prevents against cell injury after thrombin stimulation possibly through inhibition of PAR-1 expression and NF-κB activation.

A whole-mechanical method to establish human embryonic stem cell line HN4 from discarded embryos.

Since the first human embryonic stem cell (hESC) line was generated by Thomson et al. (in Science 282:1145-1147, 1998), hundreds of hESC lines have been reported by different labs, providing resources for basic research and regenerative medicine as well. However it has been widely recognized that hESC lines varied on their properties, in terms of gene expression profile, epigenetic modify profile, and differentiation tendency. Generation of more hESC lines will largely enhance our knowledge of hESCs innate character. In this current work, we reported the generation of HN4, a hESC line derived from grade III IVF human embryo by using a mixture of human foreskin fibroblast (HFF) and mouse embryonic fibroblast (MEF) as feeder layers, and a whole-mechanical method in inner cell mass (ICM) isolation. HN4 satisfied the criteria of hESCs pluripotency, with high expression of hESC surface markers (SSEA-3, SSEA-4, TRA-1-60, TRA-1-81), transcription factors (OCT-4, NANOG, REX-1), and alkaline phosphatase. It is able to differentiate to three germ layer derivatives when cultured in vitro, or in teratoma formation. Moreover, it displayed promising potential in neural differentiation under a proper culture condition, suggesting the advantage of HN4 in further investigation. Additionally, the whole-mechanical protocol for ICM isolation facilitates hESC line generation for its ease to handle.