Organic carbon preservation in wetlands: Iron oxide protection vs. thermodynamic limitation.

The sequestration of organic carbon (OC) in wetland sediments is influenced by the presence of oxygen or lack thereof. The mechanisms of OC sequestration under redox fluctuations, particularly by the co-mediation of reactive iron (Fe) protection and thermodynamic limitation by the energetics of the OC itself, remain unclear. Over the past 26 years, a combination of field surveys and remote sensing images had revealed a strong decline in both natural and constructed wetland areas in Tianjin. This decline could be attributed to anthropogenic landfill practices and agricultural reclamation efforts, which may have significant impacts on the oxidation-reduction conditions for sedimentary OC. The Fe-bound OC (CBD extraction) decreased by 2 to 10-fold (from 8.3 to 10% to 0.7-4.5%) with increasing sediment depth at three sites with varying water depths (WD). The high-resolution spectro-microscopy analysis demonstrated that Fe (oxyhydr)oxides were colocalized with sedimentary OC. Corresponding to lower redox potential, the nominal oxidation state of C (NOSC), which corresponds to the energy content in OC, became more negative (energy content increased) with increasing sediment depth. Taken together, the preservation of sedimentary OC is contingent on the prevailing redox conditions: In environments where oxygen availability is high, reactive Fe provides protection for OC, while in anoxic environments, thermodynamic constraints (i.e., energetic constraints) limit the oxidation of OC.

Mechanistic insights into poly(C)-binding protein hnRNP K resolving i-motif DNA secondary structures.

I-motifs are four-strand noncanonical secondary structures formed by cytosine (C)-rich sequences in living cells. The structural dynamics of i-motifs play essential roles in many cellular processes, such as telomerase inhibition, DNA replication, and transcriptional regulation. In cells, the structural dynamics of the i-motif can be modulated by the interaction of poly(C)-binding proteins (PCBPs), and the interaction is closely related to human health, through modulating the transcription of oncogenes and telomere stability. Therefore, the mechanisms of how PCBPs interact with i-motif structures are fundamentally important. However, the underlying mechanisms remain elusive. I-motif structures in the promoter of the c-MYC oncogene can be unfolded by heterogeneous nuclear ribonucleoprotein K (hnRNP K), a PCBP, to activate its transcription. Here, we selected this system as an example to comprehensively study the unfolding mechanisms. We found that the promoter sequence containing 5 C-runs preferred folding into type-1245 to type-1234 i-motif structures based on their folding stability, which was further confirmed by single-molecule FRET. In addition, we first revealed that the c-MYC i-motif structure was discretely resolved by hnRNP K through two intermediate states, which were assigned to the opposite hairpin and neighboring hairpin, as further confirmed by site mutations. Furthermore, we found all three KH (hnRNP K homology) domains of hnRNP K could unfold the c-MYC i-motif structure, and KH2 and KH3 were more active than KH1. In conclusion, this study may deepen our understanding of the interactions between i-motifs and PCBPs and may be helpful for drug development.

[Robot-assisted radical prostatectomy: An update].

The incidence of prostate cancer (PCa) is on a gradual rise. For localized PCa, radical prostatectomy is a main treatment option among many others, and laparoscopic radical prostatectomy is even considered as a gold treatment standard. However, with the development of robots and improvement of clinicians' surgical experience and understanding of prostatic anatomy, robot-assisted radical prostatectomy has been gaining a wide application. This review focuses on the development, advantages and disadvantages of robot-assisted radical prostatectomy with a view to providing some reference for clinicians.

Genome-wide characterization and expression profiling of B3 superfamily during ethylene-induced flowering in pineapple (Ananas comosus L.).

BACKGROUND: The B3 superfamily (B3s) represents a class of large plant-specific transcription factors, which play diverse roles in plant growth and development process including flowering induction. However, identification and functional surveys of B3 superfamily have not been reported in ethylene-induced pineapple flowering (Ananas comosus). RESULTS: 57 B3 genes containing B3 domain were identified and phylogenetically classified into five subfamilies. Chromosomal localization analysis revealed that 54 of 57 AcB3s were located on 21 Linkage Groups (LG). Collinearity analysis demonstrated that the segmental duplication was the main event in the evolution of B3 gene superfamily, and most of them were under purifying selection. The analysis of cis-element composition suggested that most of these genes may have function in response to abscisic acid, ethylene, MeJA, light, and abiotic stress. qRT-PCR analysis of 40 AcB3s containing ethylene responsive elements exhibited that the expression levels of 35 genes were up-regulated within 1 d after ethephon treatment and some were highly expressed in flower bud differentiation period in stem apex, such as Aco012003, Aco019552 and Aco014401. CONCLUSION: This study provides a basic information of AcB3s and clues for involvement of some AcB3s in ethylene-induced flowering in pineapple.

Analysis of risk factors for early stent thrombosis in the Chinese population: A multicenter restrospective study.

BACKGROUND: The predictive scoring systems for early stent thrombosis (EST) remains blank in China. The study aims to evaluate the risk factors and conduct a prediction model of EST in the Chinese population. METHODS: EST was defined as thrombosis that occurs within the first 30 days after primary percutaneous coronary intervention (PCI). Patients from ten Chinese hospitals diagnosed as stent thrombosis (ST) from January 2010 to December 2016 were retrospectively included as the study group. A control group (1 case:2 controls) was created by including patients without ST, major adverse cardiovascular events, or cerebrovascular events during follow-up. The present study evaluated 426 patients with single-vessel lesions and ultimately included 40 patients with EST and 80 control patients, who were included to identify factors that predicted EST and to develop a prediction scoring system. The other 171 patients without integrated 1:2 pair were used for external validation. RESULTS: EST was independently associated with a low hemoglobin concentration (adjusted odds ratio [OR] 0.946, 95% confidence interval [95% CI] 0.901-0.993, P=0.026), a high pre-PCI Synergy between Percutaneous Coronary Intervention with Taxus and Cardiac Surgery (SYNTAX) score (OR 1.166, 95% CI 1.049-1.297, P=0.004), and a DAPT (DAPT) duration of <30 days (OR 28.033, 95% CI 5.302-272.834, P<0.001). The simple EST prediction score provided an area under the curve (AUC) of 0.854 (95% CI 0.777-0.932, P<0.001) with 70.0% sensitivity and 90.0% specificity, and 0.742 (95% CI 0.649-0.835, P<0.001) with 54.5% sensitivity and 81.0% specificity for external validation dataset. CONCLUSIONS: EST may be independently associated with DAPT discontinuation within 30 days, a low hemoglobin concentration, and a high SYNTAX score. The scoring system also has a good ability to predict the risk of EST and may be useful in the clinical setting.

Protein phosphatase 2ACα gene knock-out results in cortical atrophy through activating hippo cascade in neuronal progenitor cells.

Protein phosphatase 2ACα (PP2ACα), a vital member of the protein phosphatase family, has been studied primarily as a regulator for the development, growth and protein synthesis of a lot of cell types. Dysfunction of PP2ACα protein results in neurodegenerative disease; however, this finding has not been directly confirmed in the mouse model with PP2ACα gene knock-out. Therefore, in this study presented here, we generated the PP2ACα gene knock-out mouse model by the Cre-loxP targeting gene system, with the purpose to directly observe the regulatory role of PP2ACα gene in the development of mouse's cerebral cortex. We observe that knocking-out PP2ACα gene in the central nervous system (CNS) results in cortical neuronal shrinkage, synaptic plasticity impairments, and learning/memory deficits. Further study reveals that PP2ACα gene knock-out initiates Hippo cascade in cortical neuroprogenitor cells (NPCs), which blocks YAP translocation into the nuclei of NPCs. Notably, p73, directly targeted by Hippo cascade, can bind to the promoter of glutaminase2 (GLS2) that plays a dominant role in the enzymatic regulation of glutamate/glutamine cycle. Finally, we find that PP2ACα gene knock-out inhibits the glutamine synthesis through up-regulating the activity of phosphorylated-p73 in cortical NPCs. Taken together, it concludes that PP2ACα critically supports cortical neuronal growth and cognitive function via regulating the signaling transduction of Hippo-p73 cascade. And PP2ACα indirectly modulates the glutamine synthesis of cortical NPCs through targeting p73 that plays a direct transcriptional regulatory role in the gene expression of GLS2.

Factors influencing the functional significance in intermediate coronary stenosis.

OBJECTIVE: To analyze the influencing factors of the functional significance determined by fractional flow reserve (FFR) in intermediate coronary artery stenosis. METHODS: The study enrolled 143 patients with 203 intermediate coronary lesions. Pressure-derived FFR of these lesions was gained at maximal hyperemia induced by intravenous adenosine infusion. An FFR < 0.80 was considered as abnormal functional significance. Anatomic parameters at the lesion sites were obtained by off-line quantitative coronary angiography analysis (QCA). The predictive value of the demographic characteristics and anatomic parameters for FFR in these intermediate lesions was assessed using multiple linear and binary logistic regression analysis. RESULTS: Overall, FFR < 0.8 was found in 70 (34%) of the total 203 intermediate coronary lesions. FFR values were positively correlated with QCA-measured minimum lumen diameters (MLD, r = 0.372, P = 0.000) and the reference vessel diameters (RVD, r = 0.217, P = 0.002) were negatively correlated with percent area stenosis (AS, r = -0.251, P = 0.000) and percent diameter stenosis (DS, r = -0.210, P = 0.000). Age, MLD and the lesion location in different coronary arteries were the independent determinants of FFR < 0.8. CONCLUSIONS: MLD can predict the functional significance of intermediate coronary stenosis, while age and the lesion location in different coronary arteries should be taken into account as important influencing factors of FFR values.

Usefulness of lumen area parameters determined by intravascular ultrasound to predict functional significance of intermediate coronary artery stenosis.

BACKGROUND: Coronary artery disease is the leading cause of death in China. Percutaneous coronary intervention is a recent milestone technology for treatment coronary artery disease. However, clinical decision making for patients with intermediate coronary stenosis is still controversial. We designed this study to assess the optimal intravascular ultrasound (IVUS) criteria for predicting functional significance of intermediate coronary lesions. METHODS: We enrolled 141 patients with 165 intermediate coronary lesions located in vessels with a diameter ≥ 2.50 mm. IVUS of intermediate coronary lesions were performed before intervention. Pressure-derived fractional flow reserve (FFR) was measured at maximal hyperemia induced by adenosine infusion. An FFR < 0.80 was considered as abnormal functional significance. RESULTS: For the overall 165 lesions, the mean FFR value was 0.84 ± 0.09. The diameter of the stenosis by visual estimation on angiogram was (59.63 ± 11.29)%. Minimum lumen diameter (MLD), minimum lumen area (MLA) and plaque burden (PB) were (2.00 ± 0.36) mm, (3.88 ± 1.34) mm(2), (67.28 ± 9.89)% respectively by IVUS measurements. An FFR < 0.80 was seen in 43 lesions (30.5%). There was a moderate correlation between IVUS parameters and FFR, including MLD (r = 0.372, P < 0.001), MLA (r = 0.442, P < 0.001) and PB (r = -0.172, P < 0.05). MLA was a predictor for FFR as a continuous variable independent of possible confounding variables (P < 0.05), and MLA and PB, were predictors for FFR < 0.80 as binary variables (P < 0.05). The best cutoff value of MLA to predict FFR < 0.80 was < 3.15 mm(2), with a 73.6% diagnostic accuracy; sensitivity 71.4%, specificity 67.0%, AUC = 0.709, and P < 0.001. The cutoff value of the PB to predict FFR < 0.80 was 65.45%; sensitivity 82.6%, specificity 41.2%, AUC = 0.644, and P < 0.01. If both MLA and PB were taken into account, the negative predictive value and the positive predictive value were 88.7% and 64.8% respectively. CONCLUSIONS: Anatomic measurements of intermediate coronary lesions obtained by IVUS showed a moderate correlation to FFR values. IVUS-derived MLA ≥ 3.15 mm(2) may be useful to exclude FFR < 0.80, but poor specificity limits its applicability for physiological assessment of lesions < 3.15 mm(2). MLA was one of many factors affecting coronary flow hemodynamics. Both MLA and PB should be taken into account when determining functional ischemia.

Association between serum resistin level and cardiovascular events in postmenopausal women with acute coronary syndrome undergoing percutaneous coronary intervention.

BACKGROUND: As an adipocytokine, resistin has been proposed as a link between inflammation, metabolic disorder and atherosclerosis. The aim of the study is to evaluate whether serum resistin is associated with acute coronary syndrome (ACS) and major adverse cardiovascular events (MACEs) among postmenopausal women with ACS undergoing percutaneous coronary intervention (PCI). METHODS: A total of 106 consecutive postmenopausal women who underwent coronary angiography for evaluation of suspected myocardial ischemia were enrolled. Pre-procedure serum resistin, inflammatory and metabolic biomarkers were measured. All participants were followed for seven years for MACEs, including cardiovascular death, recurrent nonfatal myocardial infarction, and re-PCI. RESULTS: Patients with ACS (n = 69) had significantly higher resistin levels than those without coronary artery disease (CAD) (n = 37) (4.61 (1.79 - 10.80) ng/ml vs. 2.36 (0.85 - 4.15) ng/ml, P = 0.002). Correlation analysis revealed positive correlations between resistin levels and inflammatory and metabolic factors (P < 0.05). A follow-up of a mean of 83.4 months showed that patients with ACS suffered more MACEs than those without (13.0% vs. 2.7%, P = 0.05). Adjusted for cardiovascular risks, inflammatory and metabolic factors, multiple Logistic regression analysis indicated that an elevated resistin level was an independent predictor of ACS onset (OR = 1.139, 95%CI 1.024 - 1.268, P = 0.017) and of MACEs after PCI (OR = 1.099, 95%CI 1.015 - 1.189, P = 0.019). To clarify the association between resistin levels and MACEs, ACS patients were divided into two subgroups on the basis of resistin levels. Compared with the low resistin subgroup (≤ 4.35 ng/ml, n = 32), patients in the high resistin subgroup (> 4.35 ng/ml, n = 37) were more prone to suffer MACEs (21.6% vs. 3.1%, P = 0.015). Kaplan-Meier analysis showed a significantly lower event-free survival rate in ACS patients with high resistin levels than in the low resistin subgroup (78.4% vs. 96.9%, Log rank 5.594, P = 0.018). CONCLUSION: An elevated serum resistin level is associated with ACS and cardiovascular events and acts as a predictor in progression of ACS in postmenopausal women.

The relationship between kidney function and angiographically-derived SYNTAX score.

BACKGROUND: Chronic kidney disease (CKD) is highly prevalent in patients with coronary artery disease (CAD) and is an independent risk factor for adverse cardiovascular disease (CVD) and all-cause mortality in patients with acute coronary syndromes. SYNTAX score (SXscore) can predict the outcomes of patients undergoing percutaneous coronary intervention. However, the association between kidney function and SXscore has not been previously reported. METHODS: The estimated glomerular filtration rate (eGFR) and SXscore were retrospectively collected in 2262 patients with established CAD undergoing coronary angiography at Peking University Third Hospital from March 2005 to September 2010. Ordinal logistic regression and Pearson and partial correlation were used to analyze the association between eGFR and SXscore. RESULTS: Patients with renal dysfunction were older, more likely to be female, and have a history of hypertension and diabetes. The unadjusted correlation coefficient of eGFR and SXscore was -0.125 (P<0.001).This remained significant after adjustment for age, sex, hypertension, diabetes, hyperlipidemia, or current smoking (r=-0.075, P=0.019). Ordinal logistic regression showed that age, gender, diabetes, and eGFR exerted independent influences on SXscore. CONCLUSIONS: Kidney function was an independent predictor of SXscore in patients with established CAD. This helps explain the increased risk of cardiovascular disease events and mortality in patients with renal dysfunction. Further prospective multicentre studies are needed to confirm this finding.

Impact of primary hypertension on hematuria of the patients with benign prostatic hyperplasia.

BACKGROUND: Both benign prostatic hyperplasia (BPH) and primary hypertension are common in the elderly men. The purpose of this study was to investigate the possible effect of primary hypertension on the hematuria in patients with BPH. METHODS: All patients who underwent transurethral resection of prostate or opening operation had confirmed diagnoses of BPH histologically. comparative analysis of packet was used to analyze the incidence of hematuria in 423 BPH patients with or without hypertension. Immunostaining of CD34 and vascular endothelial growth factor (VEGF) was carried out in tissues of 50 cases of simple BPH and 50 cases of BPH accompanied with hypertension. RESULTS: The incidence of hematuria in the BPH with hypertension was significantly higher than that in the simple BPH (P < 0.01). Furthermore, the incidence of hematuria in patients who had hypertension for more than 10 years was clearly higher than that in the patients who had hypertension for less than 10 years (P < 0.01). Both microvessel density (MVD) based on CD34 immunostaining and VEGF expression were significantly higher in the BPH tissues of patients with hypertension than that in the simple BPH (P < 0.01, P < 0.05). CONCLUSIONS: Long-term hypertension may significantly increase the incidence of hematuria in patients with both BPH and hypertension. Increased MVD level and VEGF expression may account for the higher incidence of hematuria in these patients.

[Intracoronary transfer autologous bone marrow stem cells can improve cardiac function in patients with left ventricular dysfunction after myocardial infarction].

OBJECTIVE: To evaluate the efficacy of intracoronary transfer of autologous bone marrow mononuclear stem cells in patients with heart dysfunction after myocardial infarction. METHODS: Forty-two patients with anterior myocardial infarction [BMSC(bone marrow mononuclear stem cells) group: 13 cases; control group: 29 cases] were treated by standard percutaneous coronary intervention (PCI) and medical therapy. Patients in BMSC group were also transplanted bone marrow mononuclear stem cells through coronary injection. Baseline and 12 months' follow-up evaluations included New York Heart Association Class ( NYHA class) and the level of plasma NT-proBNP, six minutes walk test, single photon emission computed tomography(SPECT). RESULTS: In BMSC group, the NYHA class improved significantly at the end of the 12 months' follow-up (1.54+/-0.27 vs. 2.62+/-0.33, P=0.002) and was better than that of control group (2.45+/-0.21, P=0.02). The level of plasma NTjproBNP reduced significantly [(701.05+/-154.60) ng/L vs. (1,921.70+/-373.70) ng/L, P=0.000 8]. The distances of six minutes walk test of the two groups increased significantly [BMSC group: (432.85+/-27.81) m vs. (363.77+/-20.14) m, P=0.000 6;control group: (381.48+/-17.72) m vs. (339.00+/-9.87) m, P=0.000 5], but the difference was not obvious between the two groups. The score of myocardial blood perfusion improved significantly in BMSC group at the end of the 12 months' follow-up (31.15+/-3.65 vs. 46.31+/-2.87, P=0.002) and was better than that of control group (42.59+/-2.08,P=0.015 7). The area of the perfusion defects in SPECT reduced significantly in BMSC group [(32.23+/-4.40)% vs. (39.54+/-3.76)%, P=0.000 1], but no obvious difference was found between the two groups. Global LVEF of BMSC group increased [(38.54+/-2.94)% vs. (35.38+/-2.16)%, P>0.05). CONCLUSION: Intracoronary transplantation of bone marrow mononuclear cells could improve myocardial blood perfusion and increase the systolic function in patients with heart failure after myocardial infarction.

[Impact of hypertension on angiogenesis in the tissues of benign prostatic hyperplasia].

OBJECTIVE: To investigate the impact of primary hypertension on angiogenesis in the tissues of benign prostatic hyperplasia (BPH). METHODS: Immunohistochemistry was carried out to examine the expression of CD34, so as to calculate the microvassel density (MVD), and the expression of vascular endothelial growth factor (VEGF) in the tissues of prostatic gland, resected during operation, of 50 simple BPH patients, aged 68.3 (56 approximately 83), and 50 patients with BPH with hypertension, aged 69.0 (55 approximately 91) with a course of hypertension of 16.5 +/- 11.9 years (1 - 41 years). RESULTS: The MVD of the simple BPH group was 23.1 +/- 9.2, significantly lower than that of the BPH complicated with hypertension group (28.2 +/- 9.5, P < 0.01), especially the BPH complicated with hypertension group with a course >/= 15 years (31.3 +/- 8.5). The MVD of the BPH complicated with hypertension group with a course >/= 15 years was significantly higher than that of the BPH complicated with hypertension group with a course < 15 years (25.7 +/- 9.7, P < 0.05). The VEGF positive rate of the stroma of the simple BPH group was 46.0%, significantly lower than that of the BPH complicated with hypertension group (66.0%, P < 0.05), especially that of the BPH complicated with hypertension group with a course >/= 15 years (81.8%). The VEGF positive rate of the stroma of the BPH complicated with hypertension group with a course >/= 15 years was significantly higher than that of the BPH complicated with hypertension group with a course < 15 years (53.6%, P < 0.05). In the group of BPH with hypertension, MVD was positively correlated with the expression of VEGF in the stromal tissue (R = 0.11, P < 0.05). CONCLUSION: Hypertension may be closely related to the increased expression of VEGF in prostatic stroma. The increased expression of VEGF may induce angiogenesis and consequently lead to clinical progression of BPH in patients with hypertension.

[Correlation of benign prostatic hyperplasia with hyperlipemia].

OBJECTIVE: To investigate relationship between benign prostatic hyperplasia (BPH) and hyperlipemia, and to clear out possible factors related to BPH etiology. METHODS: A total of 462 cases of BPH diagnosed by pathological examination were studied retrospectively. RESULTS: Of 462 cases, BPH with hyperlipemia was noted in 232 cases (50.22%). In comparison with the data of simple BPH, both prostate volume (P = 0.029) and residual urine (P = 0.03) were significantly increased in the BPH patients with hyperlipemia. Statistical analysis regarding the effects of different components of serum lipid on BPH clinical factors showed that the level of high density lipoprotein was significantly associated with both the enlargement of prostate volume (P < 0.05) and increasing of serum PSA (P < 0.05) Further study indicated that hypertension was demonstrated in 39.2% patients of BPH with hyperlipemia. Hyperlipemia accompanied with hypertension in BPH patients was significantly related to increased IPSS (P = 0.004). CONCLUSION: The situation of BPH with hyperlipemia is frequently noted in clinics, and the decreased level of high-density lipoprotein is significantly associated with the enlargement of prostate volume. Co-existence of hypertension with hyperlipemia in BPH patients greatly worsens the lower urinary tract symptoms (LUTS) of BPH. Hyperlipemia may be one of the risk factors in the processes of BPH growth and progression.

[Effect of hypertension on cell proliferation and apoptosis in benign prostatic hyperplasia].

OBJECTIVE: To evaluate the effect of hypertension on cell proliferation and apoptosis in benign prostatic hyperplasia (BPH). METHODS: The techniques of immunohistochemistry and terminal deoxynucleotidyl transferase-mediated dUTP biotin nick end labeling(TUNEL) were used to detect the proliferative index (PI) and apoptotic index (AI) in both epithelium and stroma of simple BPH (40 cases) and BPH with hypertension (40 cases), respectively. RESULTS: In both the groups of simple BPH and BPH with hypertension, the value of PI was significantly higher than that of AI in epithelium and stroma (P < 0.05), and PI was closely related to the prostate volume (P < 0.05). As compared with the simple BPH group, PI was significantly increased in epithelium and stroma in the group of BPH with hypertension( P < 0.05), in which the disease history of hypertension was positively associated with PI in epithelium and stroma (p < 0.05). CONCLUSION: Hypertension, particularly persistent hypertension state, may enhance cell proliferation in both epithelium and stroma of BPH, and consequently lead to the enlargement of the prostate.

[Association study between benign prostatic hyperplasia and primary hypertension].

OBJECTIVE: To assess whether primary hypertension affects the occurrence and progression of benign prostatic hyperplasia (BPH). METHODS: A total of 423 cases of BPH, undergoing transurethral resection of prostate (TURP) or open surgery due to severe low urinary tract symptoms, were reviewed and analyzed. All cases were verified to be BPH postoperatively following histopathological examination. RESULTS: Of 423 patients, 295 cases (69.7%) were simple BPH (group BPH-NT); 128 cases (30.3%) were BPH with hypertension (group BPH-HT). The mean age and the incidence of haematuria were significantly higher in group BPH-HT than those in group BPH-NT (P < 0.05). The time of BPH occurrence and surgical treatment in group BPH-HT with mean diastolic blood pressure >/= 90 mmHg was significantly earlier than those with diastolic blood pressure < 90 mmHg (P < 0.05; P < 0.01). As compared with group BPH-NT, the time of BPH occurrence was significantly earlier in group BPH-HT with more than 10 years hypertension; the rate of urinary retention and haematuria was significantly higher and prostatic volume was significantly greater in group BPH-HT with more than 20 years hypertension; (all P < 0.05). Additionally, prostatic volume was positively correlated with the years of hypertension in group BPH-HT (Rsq = 0.056, P = 0.009). CONCLUSIONS: The present results demonstrate that BPH may be frequently accompanied by the disease of hypertension. A long-term hypertension, particularly the condition of high diastolic blood pressure may improve the occurrence and clinical progression of BPH.

[Clinical manifestation and prognosis of myocardial bridge].

OBJECTIVE: To study the clinical manifestation, angiographic features, and prognosis of myocardial bridge. METHODS: A retrospective analysis was made on the data of the clinical manifestation, coronary angiography, and prognosis of 35 patients with myocardial bridge, 29 males and 6 females, with an average age of 52.0 +/- 9.5 years, out of 2 871 patients undergoing coronary angiography 1 January 1996 - 20 February 2001. RESULTS: The detection rate of myocardial bridge, mostly in the middle or distal parts of left anterior descending branch and 24 being isolated myocardial bridge, was 1.22% in coronary angiography. There was a significant difference in the extent of diameter stenosis during systolic stage between the group with atherosclerosis (68% +/- 15%, n = 15) and the group without atherosclerosis (54% +/- 14%, n = 20) in the vessel proximal to myocardial bridge (P < 0.01). The systolic diameter stenosis was more severe in the abnormal ECG group (63% +/- 13%, n = 12) than in the normal ECG group (54% +/- 14%, n = 12), P < 0.05. However, the systolic stenosis extent of myocardial bridge in the patients with typical angina pectoris (58% +/- 15%, n = 11) was not significantly different from that in the patients with atypical angina pectoris (54% +/- 15%, n = 13). The systolic stenosis extent of myocardial bridge were 69% +/- 9% (n = 7) and 58% +/- 16% (n = 26) in the patients with and without left ventricular wall hypertrophy respectively (P = 0.09). No malignant event occurred during the follow-up period of 3 - 50 months. CONCLUSION: (1) The more severe the extent of systolic diameter stenosis, the more severe the myocardial ischemia and the more the possibility of abnormal ECG. (2) Myocardial bridge tends to promote or accelerate the atherosclerosis of the vessels proximal to it. (3) Left ventricular wall hypertrophy may promote the formation of myocardial bridge clinically. (4) The prognosis of myocardial bridge is good.

Mitochondrial ATPase subunit 6 and cytochrome B gene polymorphisms in young obese adults.

We hypothesized that the mutational strand asymmetry is more strongly exerted upon the mitochondrial cytochrome b (Cytb) gene, which is distant from the origin of the light-strand replication (Ori(L)), than upon the ATPase subunit 6 (ATP6) gene, which is close to the Ori(L). To test this hypothesis, we determined the sequences of these two genes in 96 Japanese young obese adults. The frequency of G-->A transitions was significantly higher than that of C-->T transitions in the Cytb gene, whereas the frequencies of G-->A and C-->T transitions were not significantly different in the ATP6 gene. The marked mutational strand asymmetry in the Cytb gene can be explained by the deamination of C to uracil in the long single-stranded state of the heavy strand during replication. The ratio of the nonsynonymous substitutions at the second codon positions to those at the first codon positions was significantly lower in the Cytb gene than in the ATP6 gene. The physicochemical differences between the standard and the replaced amino acid residues were significantly smaller in the Cytb gene than in ATP6 one. The present study indicates that amino acid sequences are less variable for Cytb than for ATP6 in spite of the strong mutational strand asymmetry for the Cytb gene.