ABSTRACT
Information on anatomy of the Cun position at wrist is lacking; whether the blood vessel taking pulse in Cun is the radial artery or the superficial palmar branch is also clinically controversial. The objective was to investigate the boundaries and contents, and the vascular distribution and their pulse points in Cun. Thirty-two upper extremities of 16 human cadavers were investigated for dissection and observation. The boundaries, contents, and blood vessel distribution in Cun were observed; the location of pulse points in Cun was identified; the length of the superficial palmar branch in wrist pulse (L1), the pulp width of the index finger (L2), and the angle between the radial artery and the superficial palmar branch were measured. The results showed that the Cun was located in the region formed by the bulge of the prominent bone proximal to the palm, the radial flexor tendon, the tubercle of scaphoid, and the abductor longus muscle tendon. In this area, the radial artery could be pulsed part in the medial side of the abductor longus muscle tendon, while the superficial palmar branch lied near the surface and was easy to pulse in the lateral side of the radial flexor tendon and the medial side of the tubercle of scaphoid. The ratio of L1 to L2 was 1.2±0.8, and the angle was 23.3±9.9°. The results suggested that it could not be generalized that the blood vessel taking pulse in Cun was the radial artery or the superficial palmar branch; it might depend on the vascular distribution in Cun, the region of finger positioning, and the patient's pulse condition.
ABSTRACT
Neuregulin-1 (NRG-1) is a member of the epidermal growth factor family. Our previous study showed that NRG-1 protected neurons from apoptosis following focal cerebral ischemia by the inhibition of caspase-3 and TNF-alpha expression. However, the molecular signaling mechanisms for this action of NRG-1 following cerebral ischemia are not fully understood. Presently, activation of the PI3K/Akt pathway has been implicated as a major contributor to neuronal survival after an ischemic insult. In the present study, we investigated whether NRG-1 modulates the activation of Akt and its downstream targets Bad and Bcl-2 expression after transient focal cerebral ischemia by intraluminal blockade of the middle cerebral artery. Western blot was employed to analyze the change of phosphorylated Akt (p-Akt) expression; reverse transcription and polymerization chain reaction (RT-PCR) were used to measure changes of Bcl-2 mRNA. The level of phosphorylation of Bad (p-Bad) was determined using an enzyme-linked immunosorbent assay (ELISA). Our results showed that recombinant human NRG-1(3.0 ng.kg-1) significantly increased the expression of p-Akt protein, Bcl-2 mRNA, and the level of p-Bad, respectively, whereas administration of LY294002, a specific inhibitor of PI3K, significantly decreased the expression of p-Akt, p-Bad, and Bcl-2 induced by NRG-1 after a 60 min ischemic insult, followed by 24 h of reperfusion. These results indicate that NRG-1 may be involved in regulating the expression of Bcl-2 and p-Bad through the PI3K/Akt pathway after transient focal cerebral ischemia.
