• Journal of Chest Surgery
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• v.42 no.6
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• pp.800-802
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• 2009

A 43-year-old male patient visited our hospital because of intermittent chest pain and exertional dyspnea. This patient was diagnosed as suffering with pulmonary stenosis that was caused by muscle hypertrophy of the subpulmonic area, and the diagnosis was made by performing echocardiography and cardiac catheterization. A sternal foramen of the chest wall was found on the operation field. We report here on this case and we also review the relevant literature.

• The Korean Journal of Physiology and Pharmacology
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• v.27 no.3
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• pp.209-220
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• 2023

This study is to determine the regulation of nitric oxide synthase 3 (NOS3) by edaravone in mice with hypoxic pulmonary hypertension (HPH). C57BL/6J mice were reared in a hypoxic chamber. HPH mice were treated with edaravone or edaravone + L-NMMA (a NOS inhibitor). Lung tissue was collected for histological assessment, apoptosis analysis, and detection of malondialdehyde, superoxide dismutase, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and NOS3. The levels of serum TNF-α and IL-6 were also measured. Immunohistochemistry was used to visualize the expression of α-smooth muscle actin (SMA) in pulmonary arterioles. Edaravone treatment improved hemodynamics, inhibited right ventricular hypertrophy, increased NOS3 expression, and reduced pathological changes, pulmonary artery wall thickness, apoptotic pulmonary cells, oxidative stress, and the expression of TNF-α, IL-6, and α-SMA in HPH mice. L-NMMA treatment counteracted the lung protective effects of edaravone. In conclusion, edaravone might reduce lung damage in HPH mice by increasing the expression of NOS3.

• The Korean Journal of Physiology and Pharmacology
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• v.24 no.1
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• pp.111-119
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• 2020

In vascular smooth muscle, K⁺ channels, such as voltage-gated K⁺ channels (Kv), inward-rectifier K⁺ channels (Kir), and big-conductance Ca²⁺-activated K⁺ channels (BK_Ca), establish a hyperpolarized membrane potential and counterbalance the depolarizing vasoactive stimuli. Additionally, Kir mediates endothelium-dependent hyperpolarization and the active hyperemia response in various vessels, including the coronary artery. Pulmonary arterial hypertension (PAH) induces right ventricular hypertrophy (RVH), thereby elevating the risk of ischemia and right heart failure. Here, using the whole-cell patch-clamp technique, we compared Kv and Kir current densities (I_Kv and I_Kir) in the left (LCSMCs), right (RCSMCs), and septal branches of coronary smooth muscle cells (SCSMCs) from control and monocrotaline (MCT)-induced PAH rats exhibiting RVH. In control rats, (1) I_Kv was larger in RCSMCs than that in SCSMCs and LCSMCs, (2) I_Kv inactivation occurred at more negative voltages in SCSMCs than those in RCSMCs and LCSMCs, (3) I_Kir was smaller in SCSMCs than that in RCSMCs and LCSMCs, and (4) I_BKCa did not differ between branches. Moreover, in PAH rats, I_Kir and I_Kv decreased in SCSMCs, but not in RCSMCs or LCSMCs, and I_BKCa did not change in any of the branches. These results demonstrated that SCSMC-specific decreases in I_Kv and I_Kir occur in an MCT-induced PAH model, thereby offering insights into the potential pathophysiological implications of coronary blood flow regulation in right heart disease. Furthermore, the relatively smaller I_Kir in SCSMCs suggested a less effective vasodilatory response in the septal region to the moderate increase in extracellular K⁺ concentration under increased activity of the myocardium.

• Journal of Oral Medicine and Pain
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• v.30 no.2
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• pp.247-255
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• 2005

The purpose of this study is to evaluate the effect of botulinum toxin type A on masseter muscle atrophy and the extent of masseter muscle affected from the injection site in relation to injection dose, with and without occlusal splint therapy through computed tomographic measurement. 32 volunteers were divided into four groups - group 25U (injection dose of 25 unit), group 25Us (injection dose of 25 unit with occlusal splint), group 35U (injection dose of 35 unit), group 35Us (injection dose of 35 unit with occlusal splint). Each group consisted of 8 people. 3 positions (position 1, 2, 3 - 10mm, 20mm and 40mm from the inferior border of the mandible, respectively) were selected for the evaluation of the masseter muscle change. The following results were obtained. 1. The thickness and the cross-sectional area of the masseter muscle had reduced in all groups except for the right side thickness at position 3 of group 25U and group 25Us, and the right side thickness as well as the left side cross-sectional area at position 3 of group 35Us. In group 35Us, the thickness and the cross-sectional area of the masseter muscle had reduced significantly in all positions (P < 0.05). 2. There was no significant difference in the masseter muscle change between the injection dose of 25unit and that of 35unit. 3. The groups with occlusal splint showed greater reduction of the masseter muscle thickness than the other groups (P < 0.05). From the above results, botulinum toxin type A injection together with occlusal splint therapy in the treatment of masseter muscle hypertrophy would be clinically effective.

• Journal of the Korean Society of Physical Medicine
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• v.3 no.1
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• pp.27-37
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• 2008

Purpose : Today, it enjoys a sports and a leisure where the anterior cruciate ligament(ACL) injury patient increase. The knee joint is important means of human body movement and to do an important duty when it encounters ACL injuries of the knee joint and the many restriction follows in the life which is ordinary. When it is damaged ACL, it comes to determinate that ACL reconstruction and preservation treatment that the according to condition of ligament and knee joint. After ACL reconstruction, that is the fact which already becomes known the exercise treatment advances a recovery and to reduce a sequela. Methods : we researched the method of exercise treatment after anterior cruciate ligament reconstruction operation by journal of science direct and KISS in daecu university. Results : The representative exercise treatment is isometric exercise, isokinetic exercise isotonic exercise and complex exercise but what kind of exercise treatment most is effective, it revealed and support it was not. The method of exercise treatment is very various, so It causes a confusion made to the therapist and patients. So it executes once again it sought the kinetic therapeutic method which is efficient from this research and it tried to observe preceding research after ACL reconstruction. To operation a various the exercise treatments, operation only the treatment which is general compared to it was effective in muscular power and muscle functional improvement. But this like improve despite with the exercise treatment consequence which is continuous from research of most the pain leg compares to the health leg, it appeared the discrepancy which is a muscular power, a muscular endurance and a hypertrophy muscle etc, to the health leg or before operating 100% of muscular power to having gets the many therapy time was the recovery rate. Conclusion : Therefore after ACL reconstruction, it will become the many research continuously which is improve the muscle functional and ROM of the exercise treatment method and From therapeutic site of the patients it does to memorizes knowledge in advance about ACL injuries and the application the isokinetic treatment or exercise program are the set of necessary, frequency and amusement that considers complex what kind of therapeutic exercise becomes accomplished with the patient take care of attention.

• Journal of Life Science
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• v.25 no.2
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• pp.231-236
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• 2015

Angiotensin II (AngII) is an essential hormone that affects vascular physiology. For example, stimulation of vascular smooth muscle cells (VSMCs) rapidly induces vasoconstriction and results in the up-regulation of blood pressure. Chronic stimulation of VSMCs with AngII also results in hypertrophy. In this study, we confirmed an involvement of phosphatidylinositol 3-kinase (PI3K)-dependent calcium mobilization in AngII-induced generation of reactive oxygen species (ROS). Stimulation of rat aortic smooth muscle cells (RASMCs) with AngII significantly induced the generation of ROS in a dose- and time-dependent manner. AngII-induced generation of ROS was completely abolished by pharmacological inhibition of PI3K (with LY294002), but inhibition of the ERK signaling pathway had no effect. AngII-induced calcium mobilization was completely blocked by inhibition of PI3K, whereas inhibition of the ERK signaling pathway by PD98059 was ineffective. Depletion of extracellular calcium or inhibition of the L-type calcium channel by nifedipine completely blocked AngII-induced calcium mobilization. Depletion of extracellular calcium by EGTA and incubation of RASMCs with calcium-free medium both significantly blocked AngII-induced ROS generation. Inhibition of the L-type calcium channel also significantly blocked AngII-induced ROS generation. These results suggest that AngII-induced ROS generation is regulated by calcium mobilization, which, in turn, is modulated by a PI3K/L-type calcium channel signaling pathway.

• Journal of the Korea Society of Computer and Information
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• v.29 no.5
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• pp.111-121
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• 2024

With strength training comes the risk of injury and the benefits of exercise. Lack of knowledge and experience or repetitions at excessive intensity can lead to injury. Adequate feedback on an exercise's progress can increase the exercise's effectiveness and reduce injuries by providing scientific data and psychological motivation. This study aimed to validate EMG equipment and examine the effects of 8 weeks of biofeedback training with wireless electromyography. A correlation analysis between the Noraxon device and Fitsig^®(EMG Prototype), a well-known instrument in the field of research, showed a moderate correlation. Statistically significant differences in humeral circumference, humeral muscle mass, and biceps and triceps strength were found between the left and right sides of the body over time, with no differences in the type of exercise. Feedback training with real-time EMG was found to be favorable for hypertrophic growth and strength improvement. Future studies should be conducted to investigate its application in sports activities further.

• Asian-Australasian Journal of Animal Sciences
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• v.21 no.7
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• pp.928-935
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• 2008

The myostatin gene of seven important meat (Beltex (Australia), Beltex$\times$Huyang (F1), Meat and Multi-Prolific Chinese Merino Fine Wool, Meat Chinese Merino Fine Wool and Dorper (South Africa)) and non-meat (Huyang and Kazak) sheep breeds was analyzed to study the genetic basis of muscular hypertrophy (double muscling) phenotype in sheep. SNPs, four in regulatory regions and several in the introns in the myostatin gene, were identified, and the former four SNPs were used for further studies. Twelve haplotypes were predicted by PHASE program, of which four main haplotypes (1, 3, 7, 9) were present in 90% of the 364 sheep in the study. Haplotypes 1-4 were mainly present in meat breeds while haplotypes 7 and 9 dominated the non-meat breeds. The association between haplotypes and average daily gain (ADG) was analyzed among 116 sheep with production data, Haplo2 (CGAA) and Haplo8 (TGAA) were identified to have significant (p<0.05) effect on ADG by the model (JMP5.1 software) taking into account the effects of breed, family background, haplotype, birth weight and sex. ADG of these haplotype groups also correlated well (r = 0.82) with hypertrophic phenotype scores. In conclusion, the mutations -956 (T$\rightarrow$C), -41 (C$\rightarrow$A) and 6223 (G$\rightarrow$A) involved in Haplo2 and 8 may be associated with the double-muscling trait by influencing myostatin function and be suitable markers in selecting meat sheep.

• Journal of Oral Medicine and Pain
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• v.32 no.3
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• pp.337-346
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• 2007

This study aimed to evaluate a relation of bruxism with clinical effects of botulinum toxin type A(BTX-A) injection. 5 bruxers and 5 nonbruxers with bilateral masseter hypertrophy were participated in this study. After injecting 25 unit of BTX-A(Allergen Inc, $Botox^{(R)}$) into each masseter muscle, the thickness of masseter(Mm) and anterior temporalis(Ta) muscles was measured by ultrasonography and the maximum bite force was evaluated during a 9-month period. Self-estimation on the recovery of occlusal force during mastication was done as well. Regardless of presence of bruxsim, all subjects showed significantly reduced Ms thickness(p<0.001) and maximum bite force at $1^{st}$ molars(p=0.027) with their peak at 3 months after injection, which then started to return. No significant difference was observed in Ta thickness and the bite force at the central incisors. While self-estimated occlusal force was the least at 2 weeks after injection and then rapidly returned to the baseline level with full recovery at the time of 6 to 9 months after injection, the maximum bite force measured by bite force recorder did not recover the original value, particularly in the nonbruxer group. It is assumed that nocturnal bruxism can influence recovery of atrophic masseter and decreased occlusal force due to BTX-A injection. These findings suggest a need of occlusal appliance to control bruxism or clenching habit for longer clinical effect of BTX-A injection.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.6
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• pp.499-506
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• 2015

Angiotensin II (Ang II), a key mediator of hypertensive, causes structural changes in the arteries (vascular remodeling), which involve alterations in cell growth, vascular smooth muscle cell (VSMC) hypertrophy. Ang II promotes fibrotic factor like IGFBP5, which mediates the profibrotic effects of Ang II in the heart and kidneys, lung and so on. The purpose of this study was to identify the signaling pathway of IGFBP5 on cell proliferation and migration of Ang II-stimulated VSMC. We have been interested in Ang II-induced IGFBP5 and were curious to determine whether a Pitavastatin would ameliorate the effects. Herein, we investigated the question of whether Ang II induced the levels of IGFBP5 protein followed by proliferation and migration in VSMC. Pretreatment with the specific Angiotensin receptor type 1 (AT1) inhibitor (Losartan), Angiotensin receptor type 2 (AT2) inhibitor (PD123319), MAPK inhibitor (U0126), ERK1/2 inhibitor (PD98059), P38 inhibitor (SB600125) and PI3K inhibitor (LY294002) resulted in significantly inhibited IGFBP5 production, proliferation, and migration in Ang II-stimulated VSMC. In addition, IGFBP5 knockdown resulted in modulation of Ang II induced proliferation and migration via IGFBP5 induction. In addition, Pitavastatin modulated Ang II induced proliferation and migration in VSMC. Taken together, our results indicated that Ang II induces IGFBP5 through AT1, ERK1/2, P38, and PI3K signaling pathways, which were inhibited by Pitavastatin. These findings may suggest that Pitavastatin has an effect on vascular disease including hypertension.