Morphometrics of the Metatarsal Bone and Regression Equation of the Metatarsal Length in Korean / 체질인류학회지

As the interest in health is increasing and the population enjoyed the leisure sports is steadily increasing, the stress fracture, fracture or variant of metatarsal bone of foot has been shown frequently. The mistaken estimation about the length and rank of metatarsal bones during the osteotomy of the metatarsal bones of foot can be complicated. It is essential to have detailed knowledges about the anatomical structure of surgical region. This study aimed to investigate the metatarsal bones of foot and to develop a regression equation that can predict the length of metatarsal bones during the osteotomy. The subject of this study is fifty four feet (30M/224F). We measured the whole length and the article length of metatarsal bone. Also, we measured the whole width and the article width in the head, body, base of the metatarsal bone. The data was analyzed using SPSS win 13.0. The regression equation models of length of the metatarsal bones were developed by multiple regression analysis. The regression equation predicted first metatarsal length was second metatarsal articular length x0.770+7.780, second metatarsal length was third metatarsal length x0.976+6.050, third metatarsal length was fourth metatarsal length x1.000+0.922, fourth metatarsal length was third metatarsal length x0.917+4.167, fifth metatarsal length was fourth metatarsal length x0.901+7.972. The results of this study would be useful to clarify the characteristics of the metatarsal bone of the foot, to develop a regression equation for prediction of the length of the metatarsal bone.

Effects of Remote Ischemic Preconditioning on the Expressions of NOS and Akt in the Rat Myocardium / 체질인류학회지

Remote ischemic preconditioning (IP), brief tolerating cycles of ischemia and reperfusion in remote non-vital organs, can reduce ischemic injury of the heart. IP induces cardiac protection by down-regulating iNOS or up-regulating eNOS. In addition, Akt has been known to protect myocardium against ischemia-reperfusion injury. This study was undertaken to observe the expression of iNOS, eNOS, Akt and phospho-Akt (p-Akt) in the rat myocardium after IP. Thirty-five weeks-old male Sprague-Dawley rats were divided into control and IP groups. The IP group was further subdivided into 3 groups based on the number of cycles of IP. For IP, left commom iliac artery was occluded 3, 6 and 10 cycles for 5 min of ischemia alternating with 5 min of reperfusion. The rat were sacrificed at 0, 3, 6, 24 and 72 hours of IP and the heart was removed. The expression of iNOS, eNOS, Akt and p-Akt in the rat myocardium was examined by immunohistochemical staining and Western blot analysis. The expression of iNOS was increased by IP and was higher in 10IP groups than 3IP and 6IP group. The expression of eNOS was increased or decreased by IP and was showed no difference with increasing episode of IP. The expression of Akt was decreased by IP at 24 and 72 hours after reperfusion, and showed no differences with increasing episode of IP. The expression of p-Akt was increased by IP and showed no difference with increasing episode of IP. These results suggest that hind limb ischemic preconditioning provides cardiac protection through up-regulation of eNOS and phosphorylation of Akt, however excessive episodes of remote preconditioning may induce the myocardial ischemic injury through overexpression of iNOS.

The Effects of Ischemic Preconditioning and K(ATP) channel Activation on the Expression of the PKC-epsilon, NF-kappaB and AP-1 in Ischemia-reperfused Rat Heart / 체질인류학회지

This study was aimed to elucidate the effects of K(ATP) activation during IPC on the PKC-epsilon, NF-kappaB and AP-1 in ischemia-reperfused rat hearts. SD male rats weighting from 300 to 350 g were split into 9 groups, such as sham control (S), IPC, 3 cycles of 5 min ischemia and 5 min reperfusion, continuous preconditioning (CP), 8 cycles of 5 min ischemia and 5 min reperfusion, K(ATP) opening (KO) with pinacidil (1.0 mg/kg), K(ATP) blocking with glibenclamide (1.0 mg/kg) injection, ischemia (IS), 30 min ischemia, IPC followed by IS, 8) K(ATP) blocking and IPC followed by IS (KB+IPC+IS), IS and K(ATP) opening (KO+IS). Heart were subjected to ligation of left descending coronary artery and reperfusion in groups of IPC, CP, IS with or without IPC. Immunohistochemistry and Western blotting for PKC-epsilon, NF-kappaB and AP-1 were performed at 3, 6, 24 hours after reperfusion or treatment. Immunoreactivities against PKC-epsilon antibody were observed stronger in the groups of IPC, KO, IPC+IS and KO+IS than groups of KB, IS and KB+IPC+IS. NF-kappaB activation and translocation were only observed in the groups of including 30 min ischemia and reperfusion. AP-1 activation and translocation were opposite to the results of PKC-epsilon activation. In the group of CP, KB, IS and KB+IPC+IS, reactivities of AP-1 antibody were stronger than IPC+IS, KO+IS, and weaker in the groups of S, IPC and KO. These results suggest that K(ATP) opening with IPC or pharmacological methods may direct effect on the PKC-epsilon activation and that K(ATP) blocking has effect on the AP-1 activation and translocation in the heart of ischemiareperfused of rats.

Effects of Repetitive Ischemic Preconditioning on the Phosphorylation of Akt and Expression of HSP72 and HSP90 in the Rat Tibialis Anterior and Soleus Muscles / 체질인류학회지

Akt, heat shock protein (HSP72)72, and HSP90 induced by ischemic preconditioning protect cells from the ischemic injury. The purpose of this study was to examine the alterations of the level of phospho-Akt, HSP72, and HSP90 in the rat tibialis anterior and soleus muscles after cyclic episodes of ischemic preconditioning. Sprague-Dawley rats aged 35 weeks were divided into control and ischemic preconditioning (IP) groups. The IP group was divided into 3 subgroups based on cycles of IP. Left common iliac artery was occluded 3, 6, and 10 times for 5 minutes, followed by 5 minutes reperfusion. The experimental animals were sacrificed at 0, 3, 6, 24, and 72 hours after reperfusion, and left tibialis anterior and soleus muscles were removed. The expression of phospho-Akt, HSP72, and HSP90 were examined with immunohistochemical methods and Western blot analysis. The results were as follows; 1. In the 3 and 6 times of IP groups, the expression of phospho-Akt (p-Akt) was increased at 0 and 3 hours after reperfusion, compared with control group. The expression of p-Akt in the 10 times of IP group was lower than that in 3 and 6 times of IP groups. At 72 hours after reperfusion, the expression of p-Akt showed no difference among the IP groups. The expression of p-Akt was higher in Soleus than that in Tibialis anterior. 2. The expression of HSP72 in 3 times of IP group increased at 0 and 3 hours after reperfusion, compared with 6 and 10 times of IP groups. The expression of HSP72 in the 10 times of IP group was lower than that in 3 and 6 times of IP groups. At 72 hours after reperfusion, the expression of HSP72 showed no difference among the IP groups. The expression of HSP72 was higher in Soleus than that in Tibialis anterior. 3. In the 3 and 6 times of IP groups, the expression of HSP90 increased at 0 and 3 hours after reperfusion, compared with control group. The expression of HSP90 in the 10 times of IP group was lower than that in 3 and 6 times of IP groups. At 24 hours after reperfusion, the expression of HSP90 showed no difference with increasing episode of IP. The expression level of HSP90 was higher in Soleus than that in Tibialis anterior. These findings suggest that ischemic preconditioning increases the expression of p-Akt, HSP72 and HSP90 at early phase after reperfusion in the rat tibialis anterior and soleus muscles. However, increased cycles of ischemic preconditioning may not induce the expression of them.

Expression Pattern of Nitric Oxide Synthases in Rat Skeletal Muscle after Cyclic Episodes of Short Ischemia and Reperfusion / 체질인류학회지

The ischemic preconditioning was initially identified as a protective maneuver induced by brief periods of ischemia followed by reperfusion. Although ischemic preconditioning can reduce ischemic injury of heart, skeletal muscle and neuronal tissue, it's protective mechanism remains elusive. Recently, several investigations suggest the associations of nitric oxide with protection from ischemic injury. Nitric oxide synthesized by a member of nitric oxide synthase (NOS) family has been known to increase or decrease the ischemic injury. The purpose of this study was to observe the expression patterns of NOS 1, NOS 2 and NOS 3 in the rat skeletal muscle after cyclic episodes of short ischemia and reperfusion. Nine and thirty-five weeks-old male Sprague-Dawley rats were divided into control and cyclic short ischemia and reperfusion groups. The experimental group was further divided into 3 groups based on cycles of short ischemia and reperfusion. For cyclic short ischemia and reperfusion, left commom iliac artery was occluded 3, 6 and 10 times for 5 minutes ischemia followed by 5 minutes reperfusion using rodent vascular clamps. The animals were sacrificed at hours 0, 3, 6, 24 and 72 after reperfusion and the left rectus femoris muscles were removed. The expression profiles and distribution of NOS 1, NOS 2 and NOS 3 were examined with immunohistochemical staining. The results were as follows; In the cyclic of short ischemia and reperfusion groups, the mortality was increased with increasing of cyclic episodes at 72 hours after reperfusion, and aging. In the control group, NOS 1, NOS 2 and NOS 3 immunoreactivities showed no differenes with aging. In the 9 weeks-old rats, NOS 1 immunoreactivities were observed moderate at 24 hours after 6 times of short ischemia and reperfusion, and moderate and strong at 24 hours after 10 times of short ischemia and reperfusion. In the 35 weeks-old rats, NOS 1 immunoreactivities were observed trace or mild at 24 hours after 6 and 10 times of short ischemia and reperfusion. At 3 hours after 3 times of short ischemia and reperfusion, NOS 2 immunoreactivities were observed moderate or strong, and trace in the 9 and 35 weeks-old rats, respectively. At 3 hours after 10 times of short ischemia and reperfusion, NOS 3 immunoreactivities were observed mild or moderate, and trace or negative in the 9 and 35 weeks-old rats, respectively. In summary, the expression profile of NOS 1, NOS 2 and NOS 3 were observed differently with increasing episodes of short ischemia and reperfusion. The alteration was the most prominent in NOS 3 than in NOS 1 and NOS 2. These results suggest that the alteration of NOS 3 known to protect tissue against ischemic injury may be associated with increasing mortality after multiple episodes of short ischemia and reperfusion.