• 제목/요약/키워드: Hypertrophy

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배뇨력 측정을 통한 하부요로계의 보상성기능항진 평가 (Estimation of compensatory hypertrophy in lower urinary system using void force measurement)

  • 정도운;전계록
    • 센서학회지
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    • 제15권6호
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    • pp.449-456
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    • 2006
  • The purpose of urodynamic investigation is to obtain the information on the function of the urinary system. The aim of this study is to acquire the useful information of lower urinary tract symptom (LUTS) diagnosis through void force signal as noninvasive method. The system which could evaluate the function of compensatory hypertrophy with noninvasive and comfortable method was implemented to measure uroflow and void force during urination. The implemented system composes of the sensor parts, signal conditioning parts and PC monitoring program. For the evaluation of the implemented system, the simulation of control part of the system was performed and the model system for the lower urinary system was designed. The superiority of a measuring characteristic of the implemented system was verified using the model system. From the evaluation of the model system, we have found out that the void force was dependent on the occlusion degree and compensatory hypertrophy significantly.

Bow Hunter's Stroke Caused by a Severe Facet Hypertrophy of C1-2

  • Chough, Chung-Kee;Cheng, Boyle C.;Welch, William C.;Park, Chun-Kun
    • Journal of Korean Neurosurgical Society
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    • 제47권2호
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    • pp.134-136
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    • 2010
  • Bow hunter's stroke is a rare symptomatic vertebrobasilar insufficiency in which vertebral artery (VA) is mechanically occluded during head rotation. Various pathologic conditions have been reported as causes of bow hunter's stroke. However, bow hunter's stroke caused by facet hypertrophy of C1-2 has not been reported. A 71-year-old woman presented with symptoms of vertebrobasilar insufficiency. Spine computed tomography showed massive facet hypertrophy on the left side of C1-2 level. A VA angiogram with her head rotated to the right revealed significant stenosis of left VA. C1-2 posterior fixation and fusion was performed to prevent serious neurologic deficit from vertebrobasilar stroke.

Intramuscular Hemangioma Misdiagnosed as Unilateral Masseter Hypertrophy: A Case Report

  • Lee, So-Youn;Byun, Jin-Seok;Jung, Jae-Kwang;Choi, Jae-Kap
    • Journal of Oral Medicine and Pain
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    • 제41권1호
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    • pp.26-29
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    • 2016
  • Intramuscular hemangioma is a rare type of hemangiomas and sometimes overlooked by orofacial pain specialist who encountered various types of masticatory muscle problems. A 42-year-old male, presented with feeling of unilateral hypertrophy on left mandibular area, is finally diagnosed as hemangioma with thrombus by excisional biopsy. However, he was initially treated by injection of botulinum toxin A due to misdiagnosis as unilateral masseter hypertrophy. In the present report, we remind the importance of careful examination and diagnostic images to orofacial pain clinicians in early detection of intramuscular hemangioma of masticatory muscles.

A Case Report of Juvenile Hypertrophy of the Breast in a 15-Year-Old Girl: Presented with Asymmetric Breast Enlargement and a Focal Mass-like Lesion

  • Park, Jae Yeon;Kim, Sung Hun;Jung, Na Young;Kang, Bong Joo;Lee, Ah Won;Jin, Min-Sun
    • Investigative Magnetic Resonance Imaging
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    • 제23권2호
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    • pp.175-178
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    • 2019
  • Juvenile hypertrophy of the breast is a rare condition, leading to hyperplastic breast anomalies in adolescents. Here, we report a case involving a 15-year-old girl, presented with asymmetric enlargement of the left breast. Pronounced parenchymal thickening was found on initial ultrasonography (US). MRI and second-look US revealed a focal mass-like lesion on the left mid-lateral breast, confirmed as juvenile hypertrophy of the breast on pathology.

KR-39038, a Novel GRK5 Inhibitor, Attenuates Cardiac Hypertrophy and Improves Cardiac Function in Heart Failure

  • Lee, Jeong Hyun;Seo, Ho Won;Ryu, Jae Yong;Lim, Chae Jo;Yi, Kyu Yang;Oh, Kwang-Seok;Lee, Byung Ho
    • Biomolecules & Therapeutics
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    • 제28권5호
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    • pp.482-489
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    • 2020
  • G protein-coupled receptor kinase 5 (GRK5) has been considered as a potential target for the treatment of heart failure as it has been reported to be an important regulator of pathological cardiac hypertrophy. To discover novel scaffolds that selectively inhibit GRK5, we have identified a novel small molecule inhibitor of GRK5, KR-39038 [7-((3-((4-((3-aminopropyl)amino)butyl)amino)propyl)amino)-2-(2-chlorophenyl)-6-fluoroquinazolin-4(3H)-one]. KR-39038 exhibited potent inhibitory activity (IC50 value=0.02 µM) against GRK5 and significantly inhibited angiotensin II-induced cellular hypertrophy and HDAC5 phosphorylation in neonatal cardiomyocytes. In the pressure overload-induced cardiac hypertrophy mouse model, the daily oral administration of KR-39038 (30 mg/kg) for 14 days showed a 43% reduction in the left ventricular weight. Besides, KR-39038 treatment (10 and 30 mg/kg/day, p.o.) showed significant preservation of cardiac function and attenuation of myocardial remodeling in a rat model of chronic heart failure following coronary artery ligation. These results suggest that potent GRK5 inhibitor could effectively attenuate both cardiac hypertrophy and dysfunction in experimental heart failure, and KR-39038 may be useful as an effective GRK5 inhibitor for pharmaceutical applications.

Right Ventricular Mass Quantification Using Cardiac CT and a Semiautomatic Three-Dimensional Hybrid Segmentation Approach: A Pilot Study

  • Hyun Woo Goo
    • Korean Journal of Radiology
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    • 제22권6호
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    • pp.901-911
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    • 2021
  • Objective: To evaluate the technical applicability of a semiautomatic three-dimensional (3D) hybrid CT segmentation method for the quantification of right ventricular mass in patients with cardiovascular disease. Materials and Methods: Cardiac CT (270 cardiac phases) was used to quantify right ventricular mass using a semiautomatic 3D hybrid segmentation method in 195 patients with cardiovascular disease. Data from 270 cardiac phases were divided into subgroups based on the extent of the segmentation error (no error; ≤ 10% error; > 10% error [technical failure]), defined as discontinuous areas in the right ventricular myocardium. The reproducibility of the right ventricular mass quantification was assessed. In patients with no error or < 10% error, the right ventricular mass was compared and correlated between paired end-systolic and end-diastolic data. The error rate and right ventricular mass were compared based on right ventricular hypertrophy groups. Results: The quantification of right ventricular mass was technically applicable in 96.3% (260/270) of CT data, with no error in 54.4% (147/270) and ≤ 10% error in 41.9% (113/270) of cases. Technical failure was observed in 3.7% (10/270) of cases. The reproducibility of the quantification was high (intraclass correlation coefficient = 0.999, p < 0.001). The indexed mass was significantly greater at end-systole than at end-diastole (45.9 ± 22.1 g/m2 vs. 39.7 ± 20.2 g/m2, p < 0.001), and paired values were highly correlated (r = 0.96, p < 0.001). Fewer errors were observed in severe right ventricular hypertrophy and at the end-systolic phase. The indexed right ventricular mass was significantly higher in severe right ventricular hypertrophy (p < 0.02), except in the comparison of the end-diastolic data between no hypertrophy and mild hypertrophy groups (p > 0.1). Conclusion: CT quantification of right ventricular mass using a semiautomatic 3D hybrid segmentation is technically applicable with high reproducibility in most patients with cardiovascular disease.

Effects of ${\alpha}-,\;{\beta}-Adrenergic$, and Calcium Channel Blockers on Renin- Angiotensin System in Perfused Rat Heart

  • Park, Chang-Gyo
    • The Korean Journal of Physiology and Pharmacology
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    • 제2권1호
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    • pp.55-62
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    • 1998
  • ${\alpha},\;{\beta}-Adrenergics$, and calcium channels were known to be related to inducing cardiac hypertrophy. Recently, it was reported that the cardiac renin-angiotensin system (RAS) was an important factor in ventricular hypertrophy. The present study was aimed to investigate the effects of ${\alpha},\;{\beta}-adrenergic$, and calcium channel blockers that might be involved in the regulation of cardiac RAS. The reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression of renin gene in the perfused rat heart. Changes in angiotensin converting enzyme (ACE) activity and cyclic AMP (cAMP) content which were thought to play a role in inducing cardiac hypertrophy were measured in the perfused rat heart. The expression of renin gene was not only increased by isoproterenol with metoprolol-pretreatment but also increased by vasopressin treatment in the presence of calcium channel blocker, nifedipine or verapamil. Either prazosin alone or norepinephrine with prazosin-pretreatment significantly increased the ACE activity. However, isoproterenol with metoprolol-pretreatment significantly decreased the ACE activity. On the other hand, the ACE activity was not changed by vasopressin, nifedipine, or verapamil treatments. The content of cAMP was significantly increased by either isoproterenol or vasopressin treatment. According to these results, renin gene expression was associated with ${\beta}2$ - adrenoceptor and calcium channel. ACE activity was associated with ${\alpha}-\;and{\beta}2$ - adrenoceptor. In conclusion, ${\beta}2$ - adrenoceptor was important in cardiac renin gene expression and ACE activity and ${\alpha},\;{\beta}$ -adrenergic, and calcium channel blockers might be involved in the regulation of cardiac RAS in a complicated way.

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유전적 고혈압 발병에 대한 Calcineurin 및 PKB/Akt의 연관성 (Involvement of calcineurin and PKB/Akt in development of hereditary hypertension)

  • 홍용근;조재현;김주헌
    • 대한수의학회지
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    • 제44권1호
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    • pp.7-13
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    • 2004
  • Severe hypertension (>180 mmHg) develops in spontaneously hypertensive rats (SHR) after 12 wk-old; however, it is not clear whether what kinds of molecular mechanism leads to altered cardiac performance following developmental stages in SHR. Also, although the effect of calcineurin (Cn) to promote cardiomyocyte hypertrophy in vivo and in vitro is established, its overall necessity as a hypertrophic mediator is currently an area of ongoing debate. Thus, we have examined i) body weight and blood pressure, ii) differences of expression and distribution of signaling molecules such as Cn, protein kinase B/Akt (PKB/Akt), and extracellular signal-regulated kinase (ERK) between SHR and their age-matched control Wistar-Kyoto (WKY) rats following developmental stages. In 16 wk-old SHR compared with WKY, 2-dimentional echocardiography showed cardiac enlargement and hypertrophy of left ventricle, significantly. Taken together, we suggest that Cn is associated with hereditary cardiac hypertrophy, the process being related to the molecular signaling mechanisms involving PKB/Akt and ERK.

C2C12 골격근 세포에서 백출의 분화 조절 효능 (Effect of Root of Atractylodes macrocephala Koidzumi on Myogenesis in C2C12 Cells)

  • 송미영
    • 한방비만학회지
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    • 제15권1호
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    • pp.38-44
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    • 2015
  • Objective: Skeletal muscle is a crucial tissue from the perspectives of mitochondrial dysfunction and insulin resistance, it is formed by myogenesis which is dynamic multistep process to be myotubes. The authors could found that root of Atractylodes macrocephala Koidzumi (Atractylodis Rhizoma Alba, ARA) enhanced glucose and lipid metabolism in C2C12 myotubes via mitochondrial regulation. However its action in myogenesis process is not known. The aim of this work was the study of ARA on proliferation, differentiation and hypertrophy in C2C12 cells. Methods: To study proliferation phase, cells were incubated in growth medium with or without ARA (0.2 or 1.0 mg/ml) for 24 hours. To examine differentiation, at 70% confluence, cells were transferred in differentiation medium both with/without ARA (0.2 or 1.0 mg/ml) for 96 hours. And after 72 hours of differentiation, cells were treated with or without ARA (0.2 or 1.0 mg/ml) for 24 hours, the genesis of hypertrophy in myotubes were analyzed. Results: In proliferation phase, ARA could make difference in morphologic examination. In differentiation phase, it also made morphologic difference furthermore ARA (1.0 mg/ml) increased mRNA expressions of Myogenic regulatory factors and muscle-specific proteins synthesis. In late differentiation, ARA induced hypertrophic morphological changes in neo-formed myotubes. Conclusions: ARA might control cell cycle promoting myogenesis and hypertrophy in C2C12 cells.

Salubrinal Alleviates Pressure Overload-Induced Cardiac Hypertrophy by Inhibiting Endoplasmic Reticulum Stress Pathway

  • Rani, Shilpa;Sreenivasaiah, Pradeep Kumar;Cho, Chunghee;Kim, Do Han
    • Molecules and Cells
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    • 제40권1호
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    • pp.66-72
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    • 2017
  • Pathological hypertrophy of the heart is closely associated with endoplasmic reticulum stress (ERS), leading to maladaptations such as myocardial fibrosis, induction of apoptosis, and cardiac dysfunctions. Salubrinal is a known selective inhibitor of protein phosphatase 1 (PP1) complex involving dephosphorylation of phospho-eukaryotic translation initiation factor 2 subunit $(p-eIF2)-{\alpha}$, the key signaling process in the ERS pathway. In this study, the effects of salubrinal were examined on cardiac hypertrophy using the mouse model of transverse aortic constriction (TAC) and cell model of neonatal rat ventricular myocytes (NRVMs). Treatment of TAC-induced mice with salubrinal ($0.5mg{\cdot}kg^{-1}{\cdot}day^{-1}$) alleviated cardiac hypertrophy and tissue fibrosis. Salubrinal also alleviated hypertrophic growth in endothelin 1 (ET1)-treated NRVMs. Therefore, the present results suggest that salubrinal may be a potentially efficacious drug for treating pathological cardiac remodeling.