We, our agents and our service providers, including our manufacturers, may be subject to various environmental, health and safety laws and regulations, including those governing air emissions, water and wastewater discharges, noise emissions, the use, management and disposal of hazardous, radioactive and biological materials and wastes and the cleanup of contaminated sites. We believe that our business, operations and facilities, including, to our knowledge, those of our agents and service providers, are being operated in compliance in all material respects with applicable environmental and health and safety laws and regulations. All information with respect to any chemical substance is filed and stored as a Material Safety Data Sheet, as required by applicable environmental regulations. Based on information currently available to us, we do not expect environmental costs and contingencies to have a material adverse effect on us. However, significant expenditures could be required in the future if we, our agents or our service providers are required to comply with new or more stringent environmental or health and safety laws, regulations or requirements.

        If we are found to infringe a third party’s intellectual property rights, we could be forced, including by court order, to cease developing, manufacturing or commercializing the infringing product candidate or product. Alternatively, we may be required to obtain a license from such third party in order to use the infringing technology and continue developing, manufacturing or marketing the infringing product candidate or product. However, we may not be able to obtain any required license on commercially reasonable terms or at all. Even if we were able to obtain a license, it could be non-exclusive, thereby giving our competitors access to the same technologies licensed to us; alternatively, or additionally it

Lu, Y., Hu, Y., Kong, X. & Wang, D. Selection of component drug in activating blood flow and removing blood stasis of Chinese herbal medicinal formula for dairy cow mastitis by hemorheological method. J Ethnopharmacol. 116, 313–317 (2008).

Activation of hypoxia-inducible factor 1α (HIF-1α) is the primary hypoxia-driven signaling pathway in the pulmonary vasculature10,11. HIF-1α is a heterodimeric transcription factor that is composed of a regulatory α subunit and a constitutive β subunit (HIF-1β/ARNT). HIF-1α is selectively stabilized under hypoxia, so it can translocate into the nucleus to combine with the β subunit and bind to the hypoxia responsive elements (HREs) and activate transcription of genes that promote vascular cell growth and development, glycolytic metabolism and cell cycle events12. In heterozygous HIF-1α knockout mice, hypoxia-induced pulmonary hypertension and vascular remodeling are notably reduced13. Also, HIF-2α heterozygous deficient mice do not develop pulmonary hypertension even after exposure to prolonged hypoxia14. However, the key molecular and cellular pathways that are influenced by HIF are still being described.

        We have never declared or paid cash dividends on our common stock, and we do not expect to pay any cash dividends on our common stock in the foreseeable future. Payment of future dividends, if any, on our common stock will be at the discretion of our board of directors after taking into account various factors, including our financial condition, operating results, anticipated cash needs, and plans for expansion.

一系列的证据证明激素在肿瘤转移当中扮演辅助角色。一种理论认为过量的激素刺激目标器官会使其细胞分裂增多；分裂过程中偶发的基因传递差错日积月累就导致肿瘤形成。激素依赖组织相关的肿瘤占美国新诊断的肿瘤中的20%以上。治疗前列腺癌的目标就是移除雄激素的刺激，而治疗乳腺癌要降低雌激素刺激。只有肿瘤细胞含有相应的甾体激素受体时这种治疗方法才能发挥作用。

Lange, I. et al. TRPM2 functions as a lysosomal Ca2+-release channel in beta cells. Sci. Signal. 2, ra23 (2009).

Herrmann, S., Stieber, J., Stockl, G., Hofmann, F. & Ludwig, A. HCN4 provides a ‘depolarization reserve’ and is not required for heart rate acceleration in mice. EMBO J 26, 4423–32 (2007).

I notice that many people use Sangre de Drago on wounds. I’ve used C60 in olive oil for this purpose and it works very well.

OGD was achieved using methods published49. Briefly, 24 h after HUVECs were seeded in different culture plates and the culture medium was changed to the glucose-free DMEM containing either β-BA at different final concentrations in 0.2% (w/v) DMSO in the β-BA -treated groups or 0.2% DMSO in the model-treated groups for 24 h. Then cells were placed into an anaerobic chamber that was flushed with 5% CO2 and 95% N2 (v/v). The cell cultures within the anaerobic chamber were kept in a humidified incubator at 37 °C for various time intervals in different experiments. To terminate the OGD, the culture medium was changed to normal medium containing the same concentration of β-BA in DMSO or DMSO alone before returning to the normoxic incubating conditions. In the control groups, the cell cultures were subjected to the same experimental procedures with vehicle only and without exposure to the glucose-free DMEM or anoxia.

(2) Audit related services consist of services that were reasonably related to the performance of the audit or reviews of our financial statements and not included under “Audit Fees” above, including, principally, providing consents for registration statement filings.

In the presence of L-NAME, the relaxation observed in response to the β-BA was significantly smaller than under control and β-BA (200 mg/kg) groups (Fig. 5a). Pretreatment of NO synthase inhibitor L-NAME reduced basal NO formation in the rats of the model group, treatment showed better contractile response in aorta compared with the model group, suggesting a higher NO formation in the vessel. eNOS phosphorylation and cell viability were increased by β-BA under OGD treatment in HUVECs (Fig. 5b), and the protective effect of β-BA was attenuated by knockdown of eNOS (Fig. 5b) (P < 0.01). All the aforementioned results indicate that eNOS is essential for β-BA mediated protection of endothelium function.