No abstract available.
Doxorubicin* ; Membrane Potentials* ; Membranes* ; Purkinje Fibers* ; Sodium*

One of the primary functions for which bones have evolved is to act as a structural support. To achieve this, bones remodel throughout life so that their structure remains optimal for the prevailing mechanical environment. Bone remodeling consists of an initial phase of osteoclastic bone resorption followed by a bone formation period. Prostaglandins are potent regulators of bone formation and bone resorption that can have both stimulatory and inhibitory effects. Elevation of intracellular cAMP is an important intracellular signaling mechanism involved in the regulation of the expression of many proteins. In this study we examine whether PGE or DBcAMP affects osteoblastic activation or osteoclastic differentiation in mouse bone marrow cells and osteosarcoma ROS 17/2.8 cells. The effect of PGE and DBcAMP on the cell proliferation was measured by the incorporation of [3H]- thymidine into DNA. As a result, PGE2 (0.5-1 ug/ml) and DBcAMP (0.1-0.5 mM) inhibited the [3H]-thymidine incorporation into DNA in a dose dependent manner. The effect of PGE2 and DBcAMP on the induction of alkaline phosphatase (ALP) was investigated in ROS 17/2.8 cells cultured in medium containing 0.4% fetal bovine serum. PGE and DBcAMP stimulated ALP activity in the cells in a dose- dependent manner. PGE2 also increased the intracellular cAMP content in a dose- dependent fashion with a maximal effect at 0.5 ug/ml. ROS 17/2.8 cells release nitric oxide upon stimulation of PGE2 or DBcAMP with interferon-r. PGE2 and DBcAMP increase the phosphorylation level of CREB (cAMP response element binding protein) without any change on the amount of CREB protein. Also, PGE (10-6 M) and DBcAMP (10-4 M) significantly increase the generation of osteoclasts in mouse bone marrow cell culture system. In conclusion, the results of this study suggested that cAMP appears to be an important regulatory molecule in the processes of bone formation and resorption.
Alkaline Phosphatase ; Animals ; Bone Marrow Cells ; Bone Remodeling ; Bone Resorption ; Bucladesine* ; Cell Proliferation ; Cyclic AMP Response Element-Binding Protein ; Dinoprostone* ; DNA ; Metabolism* ; Mice ; Nitric Oxide ; Osteoblasts ; Osteoclasts ; Osteogenesis ; Osteosarcoma ; Phosphorylation ; Prostaglandins ; Prostaglandins E ; Response Elements ; Thymidine

BACKGROUND: This study was aimed at defining the varying responses of porcine coronary artery(PCA) to various wavelengths of ultraviolet irradiation, and at relating them to the changes in cyclic GMP contents. METHODS: The ring preparations of PCA with intact or removed endothelium were irradiated with the ultraviolet or visible light of wavelengths(240-520mm) from xenon lamp of a spectrofluorometer, and the changes in vascular tension were recorder on polygraph. For cyclic GMP assay, rat thoracic aorta was frozen after irradiation and homogenated. The supernatant was extracted with water-saturated ether and the cyclic GMP contents were measured with radioimmunoassay. RESULTS: Ultraviolet irradiation relaxed the preparations(UVR-relaxation) in resting state and those precontracted by prostaglandin F2alpha, the maximal relaxation occurring at 410nm, and the magnitude depending on the duration of irradiation. The UVR-relaxation was not affected by removing the endothelium, while it was markedly potentiated by pretreatment with Bay K 8644. The Bay K 8644-induced potentiation of UVR-relaxation was abolished by hemoglobin and slightly reduced by wrapping the rings with aluminum foil. Cyclic GMP contents in the increase was markedly potentiated by pretreatment with Bay K 8644. CONCLUSION: The observations suggest that UVR-relaxation in procine coronary artery is caused by activating the nitric oxide-cyclic GMP system, which is most sensitively activated by UVR of 410nm and that its potentiation induced by Bay K 8644 may be related nitrous substance released from the agent upon UVR.
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester* ; Aluminum ; Animals ; Aorta, Thoracic ; Bays* ; Coronary Vessels* ; Cyclic GMP ; Dinoprost ; Endothelium ; Ether ; Light* ; Passive Cutaneous Anaphylaxis ; Radioimmunoassay ; Rats ; Relaxation* ; Ultraviolet Rays ; Vasodilation ; Xenon

No abstract available.
Doxorubicin* ; Membrane Potentials* ; Membranes* ; Papillary Muscles*

Here, a case of a 59-year-old man with rotator cuff tear and impingement syndrome caused by an ossified coracoacromial ligament is presented. Ossification of the coracoacromial ligaments can occur because of degenerative changes due to trauma or repeated stress, which can lead to impingement syndrome. Therefore, when coracoacromial ligament ossification is present, rotator cuff damage due to impingement syndrome should be considered. Here, we conducted arthroscopic subacromial decompression, removal of the ossified coracoacromial ligament, and supraspinatus and subscapularis tendon repairs. We achieved satisfactory surgical outcomes without relapse; therefore, we report this case with a literature review.
Decompression ; Humans ; Ligaments* ; Middle Aged ; Recurrence ; Rotator Cuff ; Shoulder ; Shoulder Impingement Syndrome* ; Tears ; Tendons

BACKGROUND: Hypertonic solutions are using in emergency patients including refractory shock. The effects of the hyperosmotic solutions for the cardiac contractile effect has remained unclear. To study the mechanism of increase in twitch force by hypertonic solution, memberane potential, intracellular sodium activities(aNia), and twitch force were measured simultaneously in 1 Hz-driven canine Purkinje fibers and guinea pig papillary muscles. METHODS: To increase osmolarity, 20, 40, and 80 mOsm glucose, NaCl or mannitol was added to normal Tyrode solution. We used the conventional and Na(+)-selective microelectrodes, to study the membrane potential and intracellular sodium activity. Changes in twitch force were evaluated also by tension tranducer. RESULTS: 1) Hyperosmolar glucose or NaCl added to normal Tyrode solution produced membrane pontential hyperpolarization, increase in aNia, and increase in twitch force in dog Purkinje fibers. Increase in twitch force was related to decrease in the ratio of aNia to extracellular sodium activity(aNoa). NaCl-inducedd aNia increase was not blocked by 10(-5)M tetrodotoxin, a fast sodium channel blocker. 2) Hyperosmolar glucose or mannitol added to normal Tyrode solution produced membrane potential hyperpolarization, increase in aNia, and increase in twitch force in guinea pig papillary muscles. However, the addition of hyperosmolar NaCl did not affect on membrane potential, but produced increase in aNia, and decrease in twitch force. 3) Prolonging effect of hyperosmolar glucose on duration of action potential was smaller than that of NaCl or mannitol in Purkinje fibers and papillary muscles. 4) Increase in twich force produced by ECF Na+reduction or by hyperosmotic solution was reated to decrase in the aNia ratio. 5) Relationship curve between increase in twitch force and aNoa/aNia ratio in hyperosmolr solution was less steeper than that in ECF Na(+)-reduced solution. CONCLUSION: The above results suggested that hyperosmolar solution-induced twitch force change was related to aNoa/aNia ratio change which influenced intracellular calcium activity via Na(+)-Ca(2+)exchange.
Action Potentials ; Animals ; Calcium ; Dogs ; Emergencies ; Glucose ; Guinea Pigs ; Humans ; Hypertonic Solutions ; Mannitol ; Membrane Potentials* ; Membranes* ; Microelectrodes ; Muscles* ; Osmolar Concentration ; Papillary Muscles ; Purkinje Fibers* ; Shock ; Sodium Channels ; Sodium* ; Tetrodotoxin

BACKGROUND: The effects of a newly synthesized potassium channel opener, KR-30816((-)(nitro-2-hydroxymethyl-2-methy-2H-1-benzopyran-4-y1)pyridine oxide) on the action potential of papillary muscles of guinea pigs and the ATP-sensitive potassium channel current(IKATP) of single ventricular muscle cells of rats were examined to make clear its action mechanism of the KATPchannel. METHODS: We used the conventional microelectrode and the excised inside-out patch configuration. RESULTS: KR-30816 caused a shortening of the action potential duration in dose-dependent manner, which was inhibited by glibenclamide(3microM). Before run-down of the K+channel, KR-30816 activated the cardiac ATP-sensitive K+ channel only in the presence of ATP and shifted the dose-response relation curve between [ATP]i and the channel activity to the right in parallel. After run-down of the KATP channel, KR-30816 did not after the channel opening either in the absence or in the presence of UDP. CONCLUSION: These results suggest that KR-30816 antagonizes the inhibitory effect of ATP on the KATPchannel in a competitive manner, thereby enhancing the channel openings.
Action Potentials ; Adenosine Triphosphate ; Animals ; Guinea Pigs ; Heart ; Microelectrodes ; Muscle Cells ; Papillary Muscles ; Potassium Channels* ; Potassium* ; Rats ; Uridine Diphosphate

There have been no specific health claims for functional foods. So, a lot of namely functional foods have been produced, and consumers confuse these functional foods with conventional foods. Last year, the Chonbuk National University Hospital established a clinical trial center for functional foods to meet the social needs for the validation of functional foods. For a successful clinical trial for functional foods, their characteristics should be understood. The followings should be considered before clinical trial: (1) The clinical trial for functional foods is different from that for pharmaceuticals, since the subjects for the functional foods should be healthy and sub-healthy persons, not patients. (2) Some clinical trials for functional foods should be done in a larger pool of subjects because functional foods show less significant effects compared to medical agents. (3) The diet should be more tightly regulated for clinical trial of functional foods. (4) Appropriate biomarkers are required for clinical trials for functional foods.
Biomarkers ; Diet ; Functional Food* ; Humans ; Jeollabuk-do

BACKGROUND: Bupivacaine is a potent, and commonly used, long acting local anesthetic. If accidentally injected into the systemic circulation, bupivacaine can cause lethal dysrhythmias and circulatory collapse. Attempts to treat bupivacaine induced cardiac toxicity have been varied and controversial, and they have not been very successful. The aim of this study was to investigate the electrophysiologic effects of bupivacaine in Purkinje fibers. METHODS: Effects of bupivacaine on the membrane potential were studied in 12 isolated canine Purkinje fibers. Purkinje fibers from ventricle were dissected and mounted in a tissue chamber perfused with Tyrode's solution. Transmembrane potentials recorded through glass microelectrodes filled with 3M KCI in the beating or quiescent Purkinje fibers during infusions of bupivacaine at concentratons of 3*10/-7M,10/-6M, 3*10/-6M,10/-5M, and 3*10/-5M. RESULTS: Bupivacaine reduced action potential druation in a dose-dependent manner. Bupivacaine produced a decrease in intracelullar sodium ion activity in driven(1Hz) and quiescent canine Purkinje fibers. Bupivacaine-induced hyperpolarizaton of diastolic membrane potential in quiescent Purkinje fibers was dose dependent, and the hyperpolarization by bupivacaine was attenuated by depolarization induced by high potassium extracellular concentration in part. CONCLUSIONS: These results suggest that bupivacaine decreases the fast inward sodium current, and inhibits pacemaker current in canine Purkinje fibers.
Action Potentials ; Bupivacaine* ; Glass ; Membrane Potentials* ; Membranes* ; Microelectrodes ; Potassium ; Purkinje Fibers ; Shock ; Sodium ; Sodium Channels

The induction of interleukin-6 (IL-6) using combined proinflammatory agents (LPS/IFN-gamma or TNF-alpha/IFN-gamma) was studied in relation to p38 mitogen-activated protein kinase (MAPK) and NF-kappaB transcriptional factor in primary neonatal cardiomyocytes. When added to cultures of cardiomyocytes, the combined agents (LPS/IFN-gamma or TNF-alpha/IFN-gamma) had stimulatory effect on the production of IL-6 and the elevation was significantly reduced by SB203580, a specific p38 MAPK inhibitor. SB203580 inhibited protein production and gene expression of IL-6 in a concentration-dependent manner. In this study, IFN-gamma enhancement of TNF-alpha-induced NF-kappaB binding affinity as well as p38 MAP kinase activation was observed. However, a specific inhibitor of p38 MAPK, SB203580, had no effect on TNF-alpha/IFN-gamma or LPS/IFN-gamma-induced NF-kappaB activation. This study strongly suggests that these pathways about TNF-alpha/IFN-gamma or LPS/IFN-gamma-activated IL-6 release can be primarily dissociated in primary neonatal cardiomyocytes.
Gene Expression ; Interleukin-6* ; Myocytes, Cardiac* ; NF-kappa B ; p38 Mitogen-Activated Protein Kinases ; Protein Kinases*