OBJECTIVETo investigate the expression of the estrogen receptors(ER) in breast hypertrophy and micromastia.

METHODSThe quantity of ER within breast tissue in 13 patients with mammary hypertrophy strictly elected was determined using DCC single dot test. The results were compared with that measured in 13 patients with micromastia.

RESULTSThe average of the quantity of the ER was respectively (5.33 +/- 5.70) fmol/mg and (1.17 +/- 0.86) fmol/mg in mammary hypertrophy ground and in the micromastia group. There was obvious significant between the two groups in a statistics basis (P < 0.05) .

CONCLUSIONSThe breast hypertrophy is related to the excessive expression of ER within breast tissue,while the micromastia and breast hypotrophy are related to the lower level or the expression inhibition of ER.

Adolescent ; Adult ; Breast ; abnormalities ; metabolism ; pathology ; Female ; Humans ; Hypertrophy ; metabolism ; pathology ; Middle Aged ; Receptors, Estrogen ; metabolism ; Young Adult

AIMTo investigate the relations between left ventricular hypertrophy and systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), neuropeptide Y (NPY) during cardiac hypertrophy and regression.

METHODSBlood pressure and heart rate were recorded with polygraph channel biologic message system. NPY in plasma and myocardium were measured with Radioimmunoassay. Correlation coefficient were calculated with SPSS software.

RESULTSThere were positive correlations between SBP, DBP, MAP, NPY in the cardiac tissue and cardiac coefficient (LVW/BW). There was no correlations between cardiac coefficient and heart rate (HR), NPY in plasma.

CONCLUSIONHypertension is one of cardiac hypertrophy factors, SBP correlate better with LVW/ BW than DBP. SBP, DBP, MAP, NPY in cardiac tissue has correlative tendency with LVW/BW.

Animals ; Blood Pressure ; Heart Rate ; Hypertension ; metabolism ; physiopathology ; Hypertrophy, Left Ventricular ; metabolism ; physiopathology ; Male ; Neuropeptide Y ; metabolism ; Rats ; Rats, Wistar

OBJECTIVETo investigate the expression status of the P450arom mRNA in breast tissue of pubertal mammary hypertrophy and then explore the possible etiology of pubertal mammary hypertrophy.

METHODS15 patients were selected for pubertal mammary hypertrophy group. Breast hypertrophy tissue specimens were collected from the gland excised during reduction mammaplasty. 15 patients with pathologically simple fibroadenoma were used as another control group. Patient approval of participation in this study was obtained preoperatively. The expression of P450arom mRNA was detected by RT-PCR in all the cases above.

RESULTSThere was no significant difference between the pubertal mammary hypertrophy groups and normal groups on the expression rates of P450arom mRNA. But among the positive cases, the expression of P450arom mRNA within breast tissue were 0.202 +/- 0.048 in pubertal mammary hypertrophy group; and 0.159 +/- 0.068 in normal group. There was significant difference between the pubertal mammary hypertrophy and normal groups (P < 0.05).

CONCLUSIONThe expression of P450arom mRNA in pubertal mammary hypertrophy are significantly higher than in normal mammary glandular tissue. The pubertal mammary hypertrophy may be related to the expression status of P450arom mRNA within breast tissue.

Adolescent ; Adult ; Aromatase ; genetics ; metabolism ; Breast ; metabolism ; pathology ; Female ; Humans ; Hypertrophy ; metabolism ; pathology ; Puberty ; RNA, Messenger ; genetics ; Young Adult

We investigated the effect of phenylephrine (PE)- and isoproterenol (ISO)-induced cardiac hypertrophy on subcellular localization and expression of caveolin-3 and STAT3 in H9c2 cardiomyoblast cells. Caveolin-3 localization to plasma membrane was attenuated and localization of caveolin-3 to caveolae in the plasma membrane was 24.3% reduced by the catecholamine-induced hypertrophy. STAT3 and phospho-STAT3 were up-regulated but verapamil and cyclosporin A synergistically decreased the STAT3 and phospho-STAT3 levels in PE- and ISO-induced hypertrophic cells. Both expression and activation of STAT3 were increased in the nucleus by the hypertrophy. Immunofluorescence analysis revealed that the catecholamine-induced hypertrophy promoted nuclear localization of pY705-STAT3. Of interest, phosphorylation of pS727-STAT3 in mitochondria was significantly reduced by catecholamine-induced hypertrophy. In addition, mitochondrial complexes II and III were greatly down-regulated in the hypertrophic cells. Our data suggest that the alterations in nuclear and mitochondrial activation of STAT3 and caveolae localization of caveolin-3 are related to the development of the catecholamine-induced cardiac hypertrophy.
Animals ; Catecholamines/*pharmacology ; Caveolae/*metabolism ; Caveolin 3/*metabolism ; Cell Line ; Hypertrophy/metabolism ; Mitochondria/*metabolism ; Myocardium/cytology/*pathology ; Myocytes, Cardiac/cytology/*drug effects/metabolism ; Rats ; STAT3 Transcription Factor/*metabolism

PURPOSE: Venous malformation(VM) which often causes pain and discomfort is the most common type of vascular malformations. Although it is presented with disfigured appearance and associated soft tissue or skeletal hypertrophy, the molecular bases of VMs are poorly understood. Differentially expressed genes(DEGs) of VMs were investigated to illuminate the molecular mechanism of the disease entity. METHODS: Gene expressions of VM patients' subcutaneous tissue were studied in comparison with normal persons' by GeneFishing(TM) technique using the annealing control primers (ACPs) to identify DEGs. Candidate genes were sequenced and screened by basic local alignment search tool (BLAST) afterwards. RESULTS: Among seventy DEGs identified, forty DEGs which had shown significantly different expression pattern were sequenced. Twenty eight out of 40 were up- regulated while 12 were down-regulated. BLAST searches revealed that 37 were known genes and 3 were unknown genes. Many genes were involved in the differentiation and remodeling of smooth muscle cells, opposed to the previous hypothesis that a lot of angiogenetic genes would be involved. Furthermore, several transcription factors and related genes, as well as cell signaling and metabolism regulators, were up regulated. CONCLUSION: It suggests that analysis of DEGs in VMs provide basic knowledge about its pathophysiology. and new therapeutic approaches.
Gene Expression* ; Genes, vif ; Hypertrophy ; Metabolism ; Myocytes, Smooth Muscle ; Subcutaneous Tissue ; Transcription Factors ; Vascular Malformations

Adenoid hypertrophy is a disease that mostly occurs among children of 3-5 years old. It is caused by repeated inflammation and infection of nasopharynx and its adjoin parts, or the adenoid itself, which will finally leads to pathological hyperplasia of adenoid. With so much information we have acquired about this disease, its specific mechanism remains unknown. In recent years, some researches have indicated that adenoid hypertrophy may have something to do with extra-gastroesophageal reflux, in which pepsin plays a very important role, and pepsin will do a series of pathological damages to the upper airway as it reaches the upper respiratory tract. Based on relative domestic and foreign literature, this paper attempts to make a review about the relationship between gastroesophageal reflux and adenoid hypertrophy.
Adenoids ; pathology ; Child ; Gastroesophageal Reflux ; complications ; Humans ; Hypertrophy ; complications ; Nasopharynx ; pathology ; Pepsin A ; metabolism

Heart failure with preserved ejection fraction (HFpEF) is a type of heart failure characterized by left ventricular diastolic dysfunction with preserved ejection fraction. With the aging of the population and the increasing prevalence of metabolic diseases, such as hypertension, obesity and diabetes, the prevalence of HFpEF is increasing. Compared with heart failure with reduced ejection fraction (HFrEF), conventional anti-heart failure drugs failed to reduce the mortality in HFpEF due to the complex pathophysiological mechanism and multiple comorbidities of HFpEF. It is known that the main changes of cardiac structure of in HFpEF are cardiac hypertrophy, myocardial fibrosis and left ventricular hypertrophy, and HFpEF is commonly associated with obesity, diabetes, hypertension, renal dysfunction and other diseases, but how these comorbidities cause structural and functional damage to the heart is not completely clear. Recent studies have shown that immune inflammatory response plays a vital role in the progression of HFpEF. This review focuses on the latest research progress in the role of inflammation in the process of HFpEF and the potential application of anti-inflammatory therapy in HFpEF, hoping to provide new research ideas and theoretical basis for the clinical prevention and treatment in HFpEF.
Humans ; Heart Failure ; Stroke Volume/physiology* ; Hypertrophy, Left Ventricular/metabolism* ; Ventricular Dysfunction, Left/metabolism* ; Inflammation/complications* ; Obesity ; Hypertension

OBJECTIVETo investigate the pathophysiological role of the cardiac adrenomedullin (AM) system, including the ligand and amidating activity in the hypertrophied heart in severe hypertension.

METHODSThe following four groups were studied: control Wistar Kyoto rats (WKY), spontaneously hypertensive stroke-prone rats (SHR-SP), 8 weeks captopril-treated SHR-SP, and 8 weeks trichlormethiazide-treated SHR-SP. AM precursor was converted to inactive glycine-extended AM (AM-Gly) and subsequently AM-Gly was converted to active mature AM (AM-m) by enzymatic amidation. AM-m, AM-total (AM-T; AM-T = AM-m + AM-Gly), atrial natriuretic peptide (ANP) in the plasma and left ventricle (LV) by immunoradiometric assay, and gene expression of AM and ANP were measured.

RESULTSSHR-SP had increased blood pressure, LV weight, plasma and LV ANP levels and mRNA levels of ANP compared with WKY. AM-m and AM-T levels in the plasma (AM-m: +31%; AM-T: +56%) and in the LV (AM-m: +84%; AM-T: +31%) were significantly higher in SHR-SP than those in WKY. The LV tissue AM-m/AM-T ratio was significantly higher in SHR-SP (93.2%) than that in WKY. The mRNA levels of AM in the LV were significantly higher in SHR-SP than those in WKY. Captopril and trichlormethiazide similarly decreased blood pressure and LV hypertrophy with the reduction of the LV AM-m and AM-T levels and mRNA abundance of AM.

CONCLUSIONSThese results suggested that cardiac AM system was upregulated in the hypertrophied heart in this hypertension model. Considering that AM being as an antiremodeling autocrine and(or) paracrine factor, upregulation of the AM system may modulate the pathophysiological course in LV hypertrophy.

Adrenal Glands ; metabolism ; Adrenomedullin ; metabolism ; Animals ; Hypertension ; metabolism ; pathology ; Hypertrophy, Left Ventricular ; metabolism ; Male ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Up-Regulation

Chronic treatment with Salvia Miltiorrhiza preventing left ventricular hypertrophy (LVH) and its possible mechanism--inhibiting the action of cardiac aldosterone in spontaneously hypertensive rats (SHR) were investigated. Normotensive Wistar-kyoto (WKY) rats and SHRs were used. Part of SHRs was treated with Salvia Miltiorrhiza for 12 weeks. Systolic blood pressure (SBP) and left ventricular mass index were measured. Sections of heart tissue were stained with HE method and VanGieson method. Collagen volume fraction was determined in the left ventricle by automatically quantitative morphometry. Cardiac aldosterone concentration was measured by radioimmunoassay. The results indicated that compared with WKY rats, SHRs exhibited higher SBP, left ventricular collagen volume fraction, and aldosterone concentration (all P < 0.05). After the treatment with Salvia Miltiorrhiza, SBP, left ventricular collagen volume fraction, and aldosterone concentration in SHR were decreased as compared with control group (P < 0.05) except SBP. It was concluded that chronic treatment with Salvia Miltiorrhiza could prevent left ventricular hypertrophy in SHR, significantly inhibit collagen compositions in left ventricle. The mechanism was probably related with the inhibition of the cardiac aldosterone action.
Aldosterone ; metabolism ; Animals ; Drugs, Chinese Herbal ; pharmacology ; Hypertension ; metabolism ; physiopathology ; Hypertrophy, Left Ventricular ; metabolism ; prevention & control ; Male ; Myocardium ; metabolism ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Salvia miltiorrhiza

The aim of this study is to investigate the effects of chronic intermittent hypobaric hypoxia (IHH) and chronic continuous hypobaric hypoxia (CHH) on hemodynamics under basic normoxia and acute hypoxia conditions and to find the difference of two types of chronic hypoxia. Forty adult male Sprague-Dawley (SD) rats were randomly divided into 5 groups: Control group (CON), 28 days IHH group (IHH28), 42 days IHH group (IHH42), 28 days CHH group (CHH28) and 42 days CHH group (CHH42). The rats in IHH groups were treated with intermittent hypoxia (11.1% O2) mimicking 5 000 m altitude in a hypobaric chamber for 28 or 42 d, 6 h a day, respectively. The rats in CHH groups lived in the hypobaric chamber with the same degree of hypoxia like IHH rats except half an hour in normoxia each day for feeding and cleaning. The body weight of rats was measured once a week. The parameters in hemodynamics, such as mean artery blood pressure (MAP), heart rate (HR), left ventricular systolic pressure (LVSP), maximum change rate of left ventricular pressure (+/-LVdP/dt(max)) were recorded under basic normoxia and acute hypoxia conditions through catheterization technique. The superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in myocardium of rats were measured by biochemical method. The weights of whole heart, left and right ventricles were measured separately. The results showed: (1) The basic HR and MAP in CHH42 rats were lower than those in CON, IHH and CHH28 rats (P<0.05). (2) IHH showed a cardioprotection against acute hypoxia and reoxygenation injury, manifested as the result that the changes of HR, MAP, LVSP, and +/- LVdP/dt(max) were smaller than those in CON rats during acute hypoxia and reoxygenation. CHH showed a rather strong cardioprotection during acute hypoxia, manifested as the result that the decreases of HR, MAP, LVSP, and +/- LVdP/dt(max)were much smaller, but it did damage during reoxygenation, manifested as the result that the recovery of hemodynamics was the worst among three groups (P<0.05). (3) The antioxygenation of heart was increased in both IHH and CHH rats compared with that in CON rats manifested by the increased SOD activity and decreased MDA content (P<0.05, P<0.01). (4) IHH had no effect on heart weight, but CHH rats showed an obvious right ventricular hypertrophy compared with CON and IHH animals (P<0.01). The result indicates that IHH can induce a more effective cardioprotection with no much side effect, which might have a potential value for practical use.
Altitude ; Animals ; Heart ; physiopathology ; Hemodynamics ; Hypertrophy, Right Ventricular ; pathology ; Hypoxia ; metabolism ; Male ; Malondialdehyde ; metabolism ; Myocardium ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; metabolism