Background: Inflammation is a common pathophysiological trait found in both hypertension and cardiac vascular disease. Recent evidence indicates that fractalkine (FKN) and its receptor CX3CR1 have been linked to inflammatory response in the brain of hypertensive animal models. Here, we investigated the role of CX3CR1-microglia in nitric oxide (NO) generation during chronic inflammation and systemic blood pressure recovery in the nucleus tractus solitarii (NTS). Methods: The hypertensive rat model was used to study the role of CX3CR1-microglia in NTS inflammation following hypertension induction by oral administration of 10% fructose water. The systolic blood pressure was measured by tail-cuff method of non-invasive blood pressure. The CX3CR1 inhibitor AZD8797 was administered intracerebroventricularly (ICV) in the fructose-induced hypertensive rat. Using immunoblotting, we studied the nitric oxide synthase signaling pathway, NO concentration, and the levels of FKN and CX3CR1, and pro-inflammatory cytokines were analyzed by immunohistochemistry staining. Results: The level of pro-inflammatory cytokines IL-1β, IL-6, TNF-α, FKN, and CX3CR1 were elevated two weeks after fructose feeding. AZD8797 inhibited CX3CR1-microglia, which improved the regulation of systemic blood pressure and NO generation in the NTS. We also found that IL-1β, IL-6, and TNF-α levels were recovered by AZD8797 addition. Conclusion: We conclude that CX3CR1-microglia represses the nNOS signaling pathway and promotes chronic inflammation in fructose-induced hypertension. Collectively, our results reveal the role of chemokines such as IL-1β, IL-6, and TNF-α in NTS neuroinflammation with the involvement of FKN and CX3CR1.

Wearable powered robotic exoskeleton can provide high repetitions and high-intensity gait training. It can promote a sense of well-being when the user is in upright posture to walk around different environment. We present a case of a lady with progressive multiple sclerosis who received 15 sessions of robotic exoskeleton training. Post training, she demonstrated improvement in lower limb strength, sense of well-being and self-esteem that led to improved transfer ability, increased social outings and better quality of life (QOL). Previously, she was depressed and reluctant to go out for social activities. This case suggests the potential of robotic exoskeleton to enhance QOL in people with mobility challenges.

Leukemia is a hematopoietic stem cell disorder and leukemia patients suffer their lost in functional blood cell and the ratio of non-function cell increased. K562 cell was isolated from the pleural effusion of the leukemia patient and was used as a model cell line to study the relationship between the blood cell differentiation and signal transduction. In this report, three different inducers, huangqi (Astragalus membranaceus) extract, chemicals Hemin and HMBA were used to induce K562 cell differentiation and several cluster of differentiation (CD) marker were used to identify the cell linage. Two megakaryocyte markers were up-regulated in these treatments. The CD61, a late marker, was highly expressed in HMBA treated cell and CD41, an earlier marker, was identified in huangqi and HMBA treated cell. In former report, the Gi2α and Gsα was induced by the HMBA administration. Since both G proteins affect their downstream effector, adenylate cyclases (ADCYs), the ADCYs that could be participated in the pathway were examined by RT-PCR. The ADCY1 and ADCY6 were up-regulated in the HMBA-induced K562 cell. The ADCY6 was further studied because it coupled to calcium ion channel. The recombinant ADCY6 transfected cells were treated with three inducers, the results showed that all inducers induceed CD61 expression especially in HMBA treated sample. Also, the CD61 gene was 25 times higher expression as the parental cell. The results imply that the signals activated from HMBA and ADCY6 together may participate in the megakaryocyte differentiation. The study suggested that K562 cells can change the cell destination through the ADCY isoforms expression and other signal genes. These results may be used as the reference of the drug discover for leukemia treatment. Citation Format: Shin Hua Jiang, Chiu Yi Ho, Tai Lin Lee, Yun Shiang Chang, Wei Tung Huang, Meng Feng Tsai, Ang Yuan. Analysis of adenylate cyclase 6 in HMBA induced K562 cell megakaryocyte differentiation. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2132. doi:10.1158/1538-7445.AM2013-2132