• Title, Summary, Keyword: Hypertrophy

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Neurogenic muscle hypertrophy: a case report

  • Shin, Hyun Ho;Jeon, Young Hoon;Jang, Seung Won;Kim, Sae Young
    • The Korean Journal of Pain
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    • v.29 no.4
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    • pp.270-273
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    • 2016
  • Muscular hypertrophy is caused mainly due to myopathic disorder. But, it is also rarely produced by neurogenic disorder. A 74-year-old woman complained of right calf pain with hypertrophy for several years. Recent lumbar spine magnetic resonance imaging (MRI) showed central and lateral canal narrowing at the L4-L5 intervertebral space. Lower extremity MRI revealed fatty change of right medial head of the gastrocnemius and soleus, causing right calf hypertrophy. Electrodiagnostic examinations including electromyography and nerve conduction velocity testing demonstrated $5^{th}$ lumbar and $1^{st}$ sacral polyradiculopathy. Integrating all the results, the diagnosis was neurogenic muscle hypertrophy. Neurogenic muscle hypertrophy is very rare, but we recommend that clinicians consider this problem when a patient complains of lower limb hypertrophy and pain.

Relationship of Urinary Symptom, Urinary Discomfort and Quality of Life in Bladder Cancer and Benign Prostatic Hypertrophy of Male Patients (남성 방광암환자와 전립성비대증 환자에서 배뇨증상, 배뇨 불편감 및 삶의 만족도와의 관계에 관한 연구)

  • Kim, Keum-Soon;Choi, Eun-Sook
    • The Korean Journal of Rehabilitation Nursing
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    • v.7 no.1
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    • pp.78-87
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    • 2004
  • Purpose: The purpose of this study was to identify relationship of urinary symptom, urinary discomfort and quality of life among the bladder cancer patients and benign prostate hypertrophy patients, and to contribute health promotion of such patients and nursing intervention development based on this results. Method: Study sample recruited bladder cancer patents(n=49) and benign prostate hypertrophy patients who admitted Seoul National University Hospital from June, 2002 to June, 2003. Both group patients were operated, and prostate hypertrophy patients group (mean 67.8 years old) were older than bladder cancer patients group(60.82 years old). Instruments was composed of general characteristics, urinary symptom scale(19 items), urinary discomfort scale(19 items) and quality of life scale(21 items). Data was analysed SPSS PC + 10. using mean, standard deviation, pearson correlation coefficient. Result as follows: 1. There was a statistically significant difference in occupation between two groups (p=.027). Hypertrophy patients group's age was more older than bladder cancer patients group. 2. The prostate hypertrophy patients group had the significantly higher score in urinary symptom (p=000) and nighttime urination frequency. However, there was no significant difference in incontinence symptoms and the symptoms associated bladder cancer between two groups. 3. The prostate hypertrophy patients group had significantly higher score in urinary discomfort (p=000) than the bladder cancer patients group. However, there was no significant difference incontinence discomfort and the discomfort associated bladder cancer between two groups. 4. The prostate hypertrophy patients group suffered more urinary discomfort than the bladder cancer patients group did. The quality of life the prostate hypertrophy patients group was lower than the quality of life the bladder cancer patients group. Quality of life was no statistically significant difference between two groups (p=000). 5. There was a positive correlation between urinary symptoms and urinary discomfort. However, there was a negative correlation between the quality of life and urination symptoms and discomfort. Conclusions: The prostate hypertrophy patients group had significantly higher score in urinary symptom and urinary discomfort (p=000) than the bladder cancer patients group. The quality of life the prostate hypertrophy patients group was lower than the quality of life the bladder cancer patients group. This means that urinary symptom and urinary discomfort in prostate hypertrophy patient group is more important problem. So, prostate hypertrophy patient group need to control the symptom. Therefore, nurses will be provide the intervention program to improve the bladder function after prostate hypertrophy surgery.

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The Characteristics of Electrocardiography Findings in Left Ventricular Remodeling Patterns of Hypertensive Patients

  • Choi, Sun Young
    • Biomedical Science Letters
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    • v.21 no.4
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    • pp.208-217
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    • 2015
  • The exact diagnosis of left ventricular hypertrophy (LVH) is very important in the treatment of hypertension. The purpose of our study is to determine the relationship between left ventricular remodeling patterns and electrocardiography (ECG) findings in hypertensive patients. We divided 137 patients into four groups according to left ventricular mass index (LVMI) and the relative wall thickness: normal, concentric remodeling, concentric hypertrophy, eccentric hypertrophy. LVH on the ECG was defined by three ECG criteria: Sokolow-Lyon voltage criteria, Cornell voltage criteria and Romhilt-Estes point score. LVH on the echocardiography was defined by LVMI. The prevalence of ECG LVH was increased in concentric hypertrophy and eccentric hypertrophy group. The QRS voltages by Sokolow-Lyon voltage criteria (r = 0.494, P = 0.002) and Cornell voltage criteria (r = 0.628, P < 0.001), and Romhilt-Estes point score (r = 0.689, P < 0.001) were positively correlated with LVMI. Also, the QRS voltages and point scores were significantly increased in the concentric hypertrophy and eccentric hypertrophy group with increased LVMI. The QRS voltage and Romhilt-Estes point scores were positively correlated with LVMI. The QRS voltages and Romhilt-Estes point scores were also increased in the left ventricular remodeling groups with increased LVMI.

Proteasome inhibitors attenuated cholesterol-induced cardiac hypertrophy in H9c2 cells

  • Lee, Hyunjung;Park, Jinyoung;Kim, Eunice EunKyeong;Yoo, Young Sook;Song, Eun Joo
    • BMB Reports
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    • v.49 no.5
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    • pp.270-275
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    • 2016
  • The Ubiquitin proteasome system (UPS) plays roles in protein degradation, cell cycle control, and growth and inflammatory cell signaling. Dysfunction of UPS in cardiac diseases has been seen in many studies. Cholesterol acts as an inducer of cardiac hypertrophy. In this study, the effect of proteasome inhibitors on the cholesterol-induced hypertrophic growth in H9c2 cells is examined in order to observe whether UPS is involved in cardiac hypertrophy. The treatment of proteasome inhibitors MG132 and Bortezomib markedly reduced cellular surface area and mRNA expression of β-MHC in cholesterol-induced cardiac hypertrophy. In addition, activated AKT and ERK were significantly attenuated by MG132 and Bortezomib in cholesterol-induced cardiac hypertrophy. We demonstrated that cholesterol-induced cardiac hypertrophy was suppressed by proteasome inhibitors. Thus, regulatory mechanism of cholesterol-induced cardiac hypertrophy by proteasome inhibitors may provide a new therapeutic strategy to prevent the progression of heart failure.

Effects of Phenoxybenzamine and Propranolol on Monocrotaline Induced Pulmonary Vascular Lesion and Right Ventricular Hypertrophy (Phenoxybenzamine 과 Propranolol 이 Monocrotaline 에 의한 백서 폐동맥 및 우심실벽의 비후성 변화에 미치는 효과)

  • 이성광
    • The Korean Journal of Thoracic and Cardiovascular Surgery
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    • v.19 no.1
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    • pp.1-11
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    • 1986
  • Using an experimental model of pulmonary hypertension, the effects of anticonstrictive drugs on the development of pulmonary vascular remodeling and right ventricular hypertrophy were studied. Male Sprague-Dawley rats weighing 200~250 gm were used. For the experimental model of pulmonary hypertension, a group of animal was given by a subcutaneous injection of monocrotaline on a dose of 20mg, 40mg, or 60mg per kg of body weight. After 4 weeks of injection, all animals were sacrificed. Another group of animal was given by a subcutaneous injection of monocrotaline in a dose of 40 mg per kg of body weight. The animals were sacrificed, in which they were kept alive for 1, 2, 3 and 4 weeks, respectively. For the effects of anticonstrictive drugs on the development of pulmonary vascular remodeling and right ventricular hypertrophy, the animals treated with monocrotaline were given daily by an intraperitoneal injection of phenoxybenzamine in a dose of 1.3mg/kg of body weight, and were given propranolol via their drinking water at a concentration of 400mg/liter. The animals were sacrificed after 4 weeks of administration. The hearts and lungs were examined histopathologically and morphometrically. The results obtained were summarized as follows: 1. The rats treated with monocrotaline showed an interstitial pneumonitis, medial thickening of the pulmonary small arteries and hypertrophy of the right ventricular wall. 2. The medial thickening of the pulmonary arteries in rats treated with monocrotaline was due to muscular hypertrophy and hyperplasia, and the right ventricular hypertrophy was due to hypertrophy of cardiac muscles. Both medial thickening of the pulmonary arteries and hypertrophy of right ventricular wall were more marked with time and with dose. 3. The daily intraperitoneal injection of phenoxybenzamine suppressed significantly the percentage medial thickness of pulmonary small arteries and the index of right ventricular hypertrophy in rats given a single subcutaneous injection of monocrotaline, but propranolol has shown no protective effect on the development of medial thickening of pulmonary arteries and right ventricular hypertrophy in treated with monocrotaline. The results described above suggested that monocrotaline is an alkaloid selectively inducing pulmonary hypertension and that a-adrenergic receptor is responsible for the pathogenesis of monocrotaline induced pulmonary hypertension in rat.

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A Case Report of Treating Adenoidal Hypertrophy by Gwakyangjeonggisan-gamibang (곽향정기산가미방(藿香正氣散加味方) 투여로 호전된 아데노이드 비대 치험 1례)

  • Lee, Sun Jung;Park, Eun Jeong
    • The Journal of Pediatrics of Korean Medicine
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    • v.30 no.4
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    • pp.8-18
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    • 2016
  • Objectives The purpose of this case study is to report the effect of Gwakyangjeonggisangamibang on adenoidal hypertrophy. Methods The subject was a child with adenoidal hypertrophy. This patient was treated with oriental herbal medicine. The improvement was observed by subjective symptoms and A/N ratio, and OSA-18 survey was performed to compare quality of life before and after the treatment. Results After the treatment, the symptoms of adenoidal hypertrophy were relieved. A/N ratio of this child went down from 0.9 to 0.65. Also, the significant OSA-18 score change demonstrated that the patient's quality of life was improved. Conclusions This study showed that a conservative treatment using herbal medicine can be an effective choice for adenoidal hypertrophy before deciding to performing an adenoidectomy.

False Vocal Fold Hypertrophy Caused by Thyroid Cartilage Inward Bowing (갑상연골 내굴곡에 인한 가성대의 비대)

  • Kwon, Jin Ho;Choi, Byeong Il;Hong, Hyun Jun;Choi, Hong-Shik
    • Journal of the Korean Society of Laryngology, Phoniatrics and Logopedics
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    • v.24 no.1
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    • pp.51-54
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    • 2013
  • False vocal fold hypertrophy caused by diverse pathologic lesion, such as laryngeal amyloidosis, laryngeal lipidosis, laryngocele, saccular cyst and sulcus vocalis. False vocal fold hypertrophy, however, is also caused laryngeal structure deformity, irrespective of pathologic lesions. In this article, we report some cases of false vocal fold hypertrophy caused by inward bowing of thyroid cartilage. At the clinic of the department of otorhinolaryngology in Gangnam Severance Hospital, with 3 male complained of hoarseness as subjects, and comfirmed of false vocal fold hypertrophy using the stroboscopy and larynx CT we checked vocal fold and laryngeal structure. Three patients with apparent hypertrophy of false vocal fold were investigated with computerized tomography (CT). In all patients, marked concavity of thyroid cartilage was revealed in CT scan at the level of the false vocal fold, and this deformity of the thyroid cartilage seemed to cause a protrusion of false vocal fold which taken as hypertrophy in stroboscopy. Careful palpation of the larynx and a CT scan taken at the level of the false vocal fold should be useful in determining whether hypertrophy of the false vocal fold is pathologic. For the next articles, It is necessary to discuss for the cause, diagnosis, treatment and prevention of inward bowing of thyroid cartilage.

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Altered Delayed Rectifier $K^+$ Current of Rabbit Coronary Arterial Myocytes in Isoproterenol-Induced Hypertrophy

  • Kim, Na-Ri;Han, Jin;Kim, Eui-Yong
    • The Korean Journal of Physiology and Pharmacology
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    • v.5 no.1
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    • pp.33-40
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    • 2001
  • The aim of present study was to define the cellular mechanisms underlying changes in delayed rectifier $K^+\;(K_{DR})$ channel function in isoproterenol-induced hypertrophy. It has been proposed that $K_{DR}$ channels play a role in regulation of vascular tone by limiting membrane depolarization in arterial smooth muscle cells. The alterations of the properties of coronary $K_{DR}$ channels have not been studied as a possible mechanism for impaired coronary reserve in cardiac hypertrophy. The present study was carried out to compare the properties of coronary $K_{DR}$ channels in normal and hypertrophied hearts. These channels were measured from rabbit coronary smooth muscle cells using a patch clamp technique. The main findings of the study are as follows: (1) the $K_{DR}$ current density was decreased without changes of the channel kinetics in isoproterenol-induced hypertrophy; (2) the sensitivity of coronary $K_{DR}$ channels to 4-AP was increased in isoproterenol-induced hypertrophy. From the above results, we suggest for the first time that the alteration of $K_{DR}$ channels may limit vasodilating responses to several stimuli and may be involved in impaired coronary reserve in isoproterenol-induced hypertrophy.

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Metformin Inhibits Isoproterenol-induced Cardiac Hypertrophy in Mice

  • Cha, Hye-Na;Choi, Jung-Hyun;Kim, Yong-Woon;Kim, Jong-Yeon;Ahn, Myun-Whan;Park, So-Young
    • The Korean Journal of Physiology and Pharmacology
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    • v.14 no.6
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    • pp.377-384
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    • 2010
  • The present study examined whether metformin treatment prevents isoporterenol-induced cardiac hypertrophy in mice. Chronic subcutaneous infusion of isoproterenol (15 mg/kg/24 h) for 1 week using an osmotic minipump induced cardiac hypertrophy measured by the heart-to-body weight ratio and left ventricular posterior wall thickness. Cardiac hypertrophy was accompanied with increased interleukin-6 (IL-6), transforming growth factor (TGF)-${\beta}$, atrial natriuretic peptide (ANP), collagen I and III, and matrix metallopeptidase 2 (MMP-2). Coinfusion of metformin (150 mg/kg/24 h) with isoproterenol partially inhibited cardiac hypertrophy that was followed by reduced IL-6, TGF-${\beta}$, ANP, collagen I and III, and MMP-2. Chronic subcutaneous infusion of metformin did not increase AMP-activated protein kinase (AMPK) activity in heart, although acute intraperitoneal injection of metformin (10 mg/kg) increased AMPK activity. Isoproterenol increased nitrotyrosine levels and mRNA expression of antioxidant enzyme glutathione peroxidase and metformin treatment normalized these changes. These results suggest that metformin inhibits cardiac hypertrophy through attenuating oxidative stress.

EGCG Blocked Phenylephrin-Induced Hypertrophy in H9C2 Cardiomyocytes, by Activating AMPK-Dependent Pathway

  • Cai, Yi;Zhao, Li;Qin, Yuan;Wu, Xiao-Qian
    • The Korean Journal of Physiology and Pharmacology
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    • v.19 no.3
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    • pp.203-210
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    • 2015
  • AMP-activated protein kinase (AMPK) is a key regulator of energy metabolism. Previous studies have shown that activation of AMPK results in suppression of cardiac myocyte hypertrophy via inhibition of the p70S6 kinase (p70S6K) and eukaryotic elongation factor-2 (eEF2) signaling pathways. Epigallocatechin-3-gallate (EGCG), the major polyphenol found in green tea, possesses multiple protective effects on the cardiovascular system including cardiac hypertrophy. However, the molecular mechanisms has not been well investigated. In this study, we found that EGCG could significantly reduce natriuretic peptides type A (Nppa), brain natriuretic polypeptide (BNP) mRNA expression and decrease cell surface area in H9C2 cardiomyocytes stimulated with phenylephrine (PE). Moreover, we showed that AMPK is activated in H9C2 cardiomyocytes by EGCG, and AMPK-dependent pathway participates in the inhibitory effects of EGCG on cardiac hypertrophy. Taken together, our findings provide the first evidence that the effect of EGCG against cardiac hypertrophy may be attributed to its activation on AMPK-dependent signaling pathway, suggesting the therapeutic potential of EGCG on the prevention of cardiac remodeling in patients with pressure overload hypertrophy.