Exploring biomarkers for prognosis and neoadjuvant chemosensitivity in rectal cancer: Multi-omics and ctDNA sequencing collaboration.

Introduction: This study aimed to identified the key genes and sequencing metrics for predicting prognosis and efficacy of neoadjuvant chemotherapy (nCT) in rectal cancer (RC) based on genomic DNA sequencing in samples with different origin and multi-omics association database. Methods: We collected 16 RC patients and obtained DNA sequencing data from cancer tissues and plasma cell-free DNA before and after nCT. Various gene variations were analyzed, including single nucleotide variants (SNV), copy number variation (CNV), tumor mutation burden (TMB), copy number instability (CNI) and mutant-allele tumor heterogeneity (MATH). We also identified genes by which CNV level can differentiate the response to nCT. The Cancer Genome Atlas database and the Clinical Proteomic Tumor Analysis Consortium database were used to further evaluate the specific role of therapeutic relevant genes and screen out the key genes in multi-omics levels. After the intersection of the screened genes from differential expression analysis, survival analysis and principal components analysis dimensionality reduction cluster analysis, the key genes were finally identified. Results: The genes CNV level of principal component genes in baseline blood and cancer tissues could significantly distinguish the two groups of patients. The CNV of HSP90AA1, EGFR, SRC, MTOR, etc. were relatively gained in the better group compared with the poor group in baseline blood. The CNI and TMB was significantly different between the two groups. The increased expression of HSP90AA1, EGFR, and SRC was associated with increased sensitivity to multiple chemotherapeutic drugs. The nCT predictive score obtained by therapeutic relevant genes could be a potential prognostic indicator, and the combination with TMB could further refine prognostic prediction for patients. After a series of analysis in multi-omics association database, EGFR and HSP90AA1 with significant differences in multiple aspects were identified as the key predictive genes related to prognosis and the sensitivity of nCT. Discussion: This work revealed that effective combined application and analysis in multi-omics data are critical to search for predictive biomarkers. The key genes EGFR and HSP90AA1 could serve as an effective biomarker to predict prognose and neoadjuvant chemosensitivity.

The effect of sacrificing the posterior cruciate ligament on total knee arthroplasty with cruciate retaining highly congruent rotating platform prosthesis.

OBJECTIVE: To analyze the effect of sacrificing the posterior cruciate ligament (PCL) on the early postoperative outcome of cruciate retaining (CR) highly congruent rotating platform TKA. METHODS: From May 2018 to September 2019, 105 cases of total knee arthroplasty (TKA) with CR highly congruent rotating platform prosthesis were retrospectively analyzed. According to the tension of posterior cruciate ligament, they were divided into sacrifice group (29 cases, 27.6%) and retention group (76 cases, 72.4%). Preoperative and postoperative The Hospital for Special Surgery (HSS) score, range of motion (ROM) were compared between the two groups. In addition, postoperative infection, prosthesis loosening, bearing dislocation, and other complications were also compared. RESULTS: All patients were followed up for 11~24 months (mean 18.14 ± 3.52) months. There was no significant difference in general data, preoperative HSS score, and ROM between the two groups (P > 0.05). At the last follow-up, HSS score and ROM of the two groups were better than those before operation (P < 0.05). However, there was no significant difference between the two groups (P > 0.05). Moreover, there were no complications such as infection, loosening of prosthesis, and bearing dislocation in all cases. CONCLUSION: In CR, highly congruent rotating platform TKA with or without tension of the PCL can achieve satisfactory outcomes. Tension-free PCL do not cause joint instability.

New research advances in relationship of endoplasmic reticulum stress and cardiovascular diseases / 生理学报

Endoplasmic reticulum (ER) is an important organelle for protein folding, post-transcriptional modification and transport, which plays an important role in maintaining cell homeostasis. A variety of internal and external environmental stimuli can cause the accumulation of misfolded or unfolded proteins in the endoplasmic reticulum, and then result in ER stress. ER stress activates the unfolded protein response (UPR) and initiates a cluster of downstream signals to maintain ER homeostasis. However, severe and persistent ER stress activates UPR, which eventually leads to apoptosis and diseases. In recent years, a lot of researches suggest that ER stress plays an important role in the pathogenesis of various cardiovascular diseases (CVD), including ischemic heart disease, diabetic cardiomyopathy, heart failure, atherosclerosis and vascular calcification, high blood pressure and aortic aneurysm. ER stress might be one of the important targets for treatment of multiple CVD. Herein, the regulation mechanism of ER stress by activating UPR pathways in various common CVD and the new research advances in relationship of ER stress and CVD are briefly reviewed.

Microscopic Minimally Invasive Keyhole Technique for Surgical Resection of Spinal Dumbbell Tumors.

BACKGROUND: Multiple surgical modalities have been developedl and applied for surgical excision of spinal dumbbell tumors. The microscopic minimally invasive keyhole technique has not yet been well characterized for this purpose. We report our experience with 1-stage surgical resection of both intraforaminal and extraforaminal/paraspinal components of spinal dumbbell tumors using the microsurgical keyhole technique. METHODS: We retrospectively reviewed 12 cases of spinal dumbbell tumors treated via 1-stage surgical resection by the same senior spinal surgeon from January 2013 to April 2017. All patients were treated surgically using the microsurgical keyhole technique through a tubular retractor. Demographic data, perioperative variables, and associated complications were recorded. The clinical outcomes were evaluated at the last follow-up using a visual analog scale and the American Spinal Injury Association scale. RESULTS: Mean duration of surgical resection was 184.58 minutes, and mean estimated total blood loss was 208.33 mL. The mean hospitalization time was 9.17 days. Postoperatively, 11 patients (91.67%) who originally presented with pain had a significantly lower visual analog scale score, indicating a reduction in their pain intensity. All patients demonstrated neurologic stability or improvement by 1-3 grades: 16.67% remained stable, 41.67% improved by 1 grade, 33.33% improved by 2 grades, and 8.33% improved by 3 grades. CONCLUSIONS: The microscopic minimally invasive keyhole technique can be used successfully for resection of spinal dumbbell tumors. Further comparative studies are warranted to demonstrate the benefits of the microsurgical keyhole technique compared with traditional open procedures for surgical resection of spinal dumbbell tumors.

Protection Effect of Exogenous Fibroblast Growth Factor 21 on the Kidney Injury in Vascular Calcification Rats / 中华医学杂志(英文版)

<p><b>Background</b>Chronic kidney disease (CKD) is closely related to the cardiovascular events in vascular calcification (VC). However, little has known about the characteristics of kidney injury caused by VC. Fibroblast growth factor 21 (FGF21) is an endocrine factor, which takes part in various metabolic actions with the potential to alleviate metabolic disorder diseases. Even FGF21 has been regarded as a biomarker in CKD, the role of FGF21 in CKD remains unclear. Therefore, in this study, we evaluate the FGF21 on the kidney injury in VC rats.</p><p><b>Methods</b>The male Sprague-Dawley rats were divided into three groups: (1) control group, (2) Vitamin D3 plus nicotine (VDN)-induced VC group, (3) FGF21-treated VDN group. After 4 weeks, the rats were killed and the blood was collected for serum creatinine, urea nitrogen, calcium, and phosphate measurement. Moreover, the renal tissues were homogenized for alkaline phosphatases (ALPs) activity and calcium content. The levels of FGF21 protein were measured by radioimmunoassay. The levels of β-Klotho and FGF receptor 1 (FGFR1) protein were measured by enzyme-linked immunosorbent assay (ELISA). The structural damage and calcifications in aortas were stained by Alizarin-red S. Moreover, the structure of kidney was observed by hematoxylin and eosin staining.</p><p><b>Results</b>The renal function impairment caused by VDN modeling was ameliorated by FGF21 treatment, inhibited the elevated serum creatinine and urea level by 20.5% (34.750 ± 4.334 μmol/L vs. 27.630 ± 2.387 μmol/L) and 4.0% (7.038 ± 0.590 mmol/L vs. 6.763 ± 0.374 mmol/L; P < 0.01), respectively, together with the structural damages of glomerular atrophy and renal interstitial fibrosis. FGF21 treatment downregulated the ALP activity, calcium content in the kidney of VC rats by 42.1% (P < 0.01) and 11.7% (P < 0.05) as well as ameliorated the aortic injury and calcification as compared with VDN treatment alone group, indicating an ameliorative effect on VC. ELISA assays showed that the expression of β-Klotho, a component of FGF21 receptor system, was increased in VDN-treated VC rats by 37.4% (6.588 ± 0.957 pg/mg vs. 9.054 ± 0.963 pg/mg; P < 0.01), indicating an FGF21-resistant state. Moreover, FGF21 treatment downregulated the level of β-Klotho in renal tissue by 16.7% (9.054 ± 0.963 pg/mg vs. 7.544 ± 1.362 pg/mg; P < 0.05). However, the level of FGFR1, the receptor of FGF21, kept unchanged under VDN and VDN plus FGF21 administration (0.191 ± 0.0376 ng/mg vs. 0.189 ± 0.032 ng/mg vs. 0.181 ± 0.034 ng/mg; P > 0.05).</p><p><b>Conclusions</b>In the present study, FGF21 was observed to ameliorate the kidney injury in VDN-induced VC rats. FGF21 might be a potential therapeutic factor in CKD by cutting off the vicious circle between VC and kidney injury.</p>

Methods for quantitative measurement in the computed tomography images of Tusanqi related hepatic sinusoidal obstruction syndrome / 中华消化杂志

Objective To explore the feasibility of applying threshold and region-growing based algorithm in computed tomography (CT) images for the estimation of hepatic lesion volumes in patients with Tusanqi related hepatic sinusoidal obstruction syndrome (SOS).Methods From July 2012 to January 2015,at the First Affiliated Hospital of Anhui Medical University,20 patients who were diagnosed with SOS and had complete CT images were enrolled.Stereology and threshold and regiongrowing based algorithm were performed to estimate volumes of the low-density region in the liver,respectively,and then the measured volumes of hepatic lesion and operation time were compared.Paired samples t test and the Bland-Altman statistical test were performed for statistical analysis.Results The hepatic lesion volumes measured by stereology and threshold and region-growing based algorithm were (1.001±0.327) dm3 and (1.045±0.363) dm3,respectively,and the difference was not statistically significant (P＞0.05).The consistency between the two methods was good.The operation time of threshold and region-growing based algorithm was (597.55±52.86) s (minimum 500 s),which was less than that of stereology (1 251.60 ± 105.88) s (minimum 1 075 s),and the difference was statistically significant (t =32.808,P＜ 0.01).Conclusion There is no statistically significant difference in the measured hepatic lesion volume of patients with SOS between stereology and the threshold and regiongrowing based algorithm,but the operation time of threshold and region-growing based algorithm is shorter.

Cardiovascular effects of intermedin1-53 and its mechanism / 中国应用生理学杂志

<p><b>AIM</b>The present study was designed to determined the cardiovascular effects of IMD1-53 in rats and its possible mechanism.</p><p><b>METHODS</b>Isolated rat hearts were perfused by Iangendorff mode, and ventricular function was measured after IMD1-53 perfusion. Meanwhere, we investigated the effects of IMDI) on arterial pressure after intravenous administration of IMD. And cAMP content was detected in rat ventricular and aortic tissues.</p><p><b>RESULTS</b>The results showed that perfusion with IMD significantly enhanced cardiac function and resulted in higher LVSP, +dp/dt(max) and -dp/dt(max) by 45%, 51% and 37%, respectively, compared with control and increased coronary infusion flow. The effects of IMD1-53 on cardiac function were antagonized by H-89, an inhibitor of PKA. The content of cAMP in the ventricular tissues after IMD perfusion was 131% higher than control. In addition, intravenous administration of IMD induced a potent decrease in arterial pressureand heart rate, and in aortic tissues, IMD incubation resulted in a 236% increase in cAMP content compared with control group.</p><p><b>CONCLUSION</b>The study reveals that IMD can increase cardiac function and decrease arterial pressure in rat and the effects may be related to cAMP pathway.</p>

The effect of angiotensin-converting enzyme inhibitors and aldosterone receptor blockers on cardiac function in calcium-overload rats / 中国应用生理学杂志

<p><b>AIM</b>To observe the effect of angiotensin-converting enzyme inhibitors (ACEI) and aldosterone receptor blockers on cardiac function to explore the mechanism of cardiac function descending and myocardial injury in calcium-overload rats.</p><p><b>METHODS</b>Calcium-overload in rat was induced by administration of Vitamin D3 plus nicotine. To Estimate the extent of calcium-overload by calcium content. Angiotension II and aldosterone levels in the myocardia were measured by radioimmunoassay. Cardiac function (+/- LVdp/dt, LVESP and LVEDP) were measured by Powerlab. The malondialdehyde (MDA) content, activities of lactate dehydrogenase (LDH) and creatine kinase (CPK) were measured by biochemistry.</p><p><b>RESULTS</b>Calcium content increased by 3.2-, 5.8 -fold in myocardial and artery, compared with controls. VDN-treated survivors showed lower + LVdp/dt(max) and -LVdp/dt(max) values, by 27% and 34%, respectively (both P < 0.01). Higher LVESP, and LVEDP by 42 % and 32% (P < 0.01); heart rate and mean arterial pressure were not significantly altered (P > 0.05). The lipid peroxidation products MDA and conjugated diene in myocardia were increased 22% (P < 0.01), 68% (P < 0.05) (P < 0.05), respectively. The plasma activity of CPK and LDH was greatly increased by 4.5-and 3.1-fold (P < 0.01), respectively. ACEI and spironolactone obviously relieved degree of calcium-overload and improved cardiac function and myocardial injury(P < 0.01). Calcium content in myocardia and artery was lower 44%, 39% and 57%, 34%. Lower MDA by 20%, 30%, lower conjugated diene by 44%, 35% than calcium-overload group. The plasma activity of CPK and LDH were obviously decreased 28%, 34% and 20%, 27%, compared with calcium-overload group.</p><p><b>CONCLUSION</b>Calcium-overload could lead to cardiac function descending and myocardial injury in calcium-overload rats by VDN. ACEI and spironolactone could reduce calcium-overload in myocardial and ameliorate cardiac function and decrease myocardial injury.</p>

Changes of intermedin/adrenomedullin 2 and its receptors in the right ventricle of rats with chronic hypoxic pulmonary hypertension / 生理学报

The purpose of the present study was to explore the expression changes of intermedin/adrenomedullin 2 (IMD/ADM2), a novel small molecular bioactive peptide, and its receptors, calcitonin receptor-like receptor (CRLR) and receptor activity modifying proteins (RAMP1, RAMP2, RAMP3) in the right ventricle of rats with chronic hypoxia-induced pulmonary hypertension. Twenty male Sprague-Dawley rats were randomly divided into 4-week hypoxia group and normal control group (each n=10). The rats in hypoxia group were placed in an isobaric hypoxic chamber, in which O(2) content was maintained at 9%-11% by delivering N(2), and CO(2) content was maintained at <3% for 4 weeks (8 h/d, 6 d/week). The rats in the control group were housed in room air. The protein levels of IMD/ADM2 and adrenomedullin (ADM) in blood plasma and right ventricular tissue were measured by radioimmunoassay. The mRNA expressions of IMD/ADM2, ADM and their receptors CRLR, RAMP1, RAMP2, RAMP3 in right ventricular tissue were determined by reverse transcription-polymerase chain reaction (RT-PCR). The results showed that the ratio of right ventricle weight to left ventricle plus septum weight [RV/(LV+S)] and mean pulmonary arterial pressure (mPAP) were higher in hypoxia group than those in the control group (all P<0.01), suggesting that the rat model of pulmonary hypertension was successfully established. However, the mean carotid arterial pressure (mCAP) between the two groups had no significant difference. Compared with that in the control group, ADM contents in plasma and right ventricular tissue in hypoxia group increased by 1.26 and 1.68 folds (all P<0.01), respectively. Likewise, IMD/ADM2 contents in blood plasma and right ventricular tissue in hypoxia group increased by 0.90 and 1.19 folds (P<0.01), respectively, compared with that in the control group. The data of RT-PCR showed that mRNA levels of ADM, IMD/ADM2 and RAMP2 in hypoxia group increased by 155.1% (P<0.01), 80.9% (P<0.01) and 52.9% (P<0.05), respectively, compared with those in the control group. There were no significant differences in mRNA expressions of CRLR, RAMP1 and RAMP3 between the two groups (all P>0.05). Taken together, the results show that the level of IMD/ADM2 increases in the rats with chronic hypoxia-induced pulmonary hypertension.

Dysfunction of myocardial sarcoplasmic reticulum in rats with myocardial calcification.

We investigated the relationship between cardiac dysfunction and Ca2+ transport in the myocardial sarcoplasmic reticulum (SR) during the pathogenesis of cardiovascular calcification in rats. The possible mechanism of SR dysfunction was explored by detecting the alteration of the nitric oxide/nitric oxide synthase (NO/NOS) pathway in the SR. Using the vitamin D plus nicotine (VDN treatment for 2 week and 6 week) experimental model of cardiac calcification, cardiac function and sarcoplasmic reticulum function were measured. Inhibition of cardiac functions in vivo (peak rate of contraction and peak rate of relaxation, P < 0.05 or P < 0.01) were observed in all calcification groups, simultaneously, Ca2+ release and uptake in the SR as well as the Ca2+ release channel and Ca2+ pump activity were inhibited. Myocardial Ca2+ concentration and cardiac and SR dysfunction were inversely related (P < 0.05). The specific NO/NOS pathway (NO production, NOS activity and nNOS expression in the SR) was upregulated in the SR and associated with calcification (both 2- and 6 week VDN groups). These results indicate that cardiac dysfunction associated with myocardial calcification might be mediated by SR dysfunction, which may result from an impaired SR-specific NO/NOS pathway.

Clinical research of heart rate turbulence on predictive value in patients with acute myocardial infarction / 中华心血管病杂志

<p><b>OBJECTIVE</b>To assess the predictive value of heart rate turbulence (HRT) in patients with acute myocardial infarction.</p><p><b>METHODS</b>One hundred and twenty-five patients with acute myocardial infarction were enrolled in this study. During the period from 6 to 21 days after onset of acute myocardial infarction, they were undergone 24-hour Holter recordings to collect the mean RR interval and heart rate variability (HRV) SDNN. The Holter files were processed with software of "HRT! View V0.60-1" to obtain the value of Turbulence Onset (TO) and Turbulence Slope (TS) and the value of "heart rate variability (HRV) SDNN". LVEF and EDD were measured by Ultrasonic Cardiography. Endpoint of follow-up was cardiac death. According to the results, patients were divided into two groups (the "survivors" and the "nonsurvivors"). The predictive value for high-risk patients with acute myocardial infarction was assessed by variables between the two groups.</p><p><b>RESULTS</b>In the period of follow-up (mean 225.4 +/- 99.8 days), 14 patients died and 111 patients survived. In the univariate Cox regression analysis, "TS" was a strong univariate predictor of mortality (hazard ratio 11.46, P < 0.01); "TO" was a relatively weak predictor and the hazard ratio was 2.76 (P > 0.05). Combination of abnormal TO and abnormal TS was the strongest mortality predictor (hazard ratio 26.70, P < 0.01); in the multivariate Cox regression analysis, TS < or = 2.5 ms/RR and EDD > or = 5.6 cm were the independent predictors of mortality with hazard ratios 9.49 (P < 0.01) and 3.64 (P < 0.05), respectively.</p><p><b>CONCLUSIONS</b>The absence of the heart rate turbulence after ventricular premature beats is a very potent post-infarction risk predictor which is independent of and stronger than other known risk predictors.</p>

Role of adiponectin and its receptors in anti-atherosclerotic effects of pioglitazone on ApoE knocked out mice / 北京大学学报(医学版)

Objective:To study the effects of pioglitazone on atherosclerosis on ApoE-/-mice,and to investigate the roles of adiponectin and its receptors.Methods:ApoE-/-mice were fed with high-fat chow for the induction of atherosclerosis and were divided into three subgroups:placebo(n=10),low-dose[10 mg/(kg?d),n=10] pioglitazone therapy,and high-dose[20 mg/(kg?d),n=10] pioglitazone therapy.C57BL/6J wild type mice(n=9) were used as control.Aortic atherosclerosis and intima-media thickness(intima-media thickness,IMT) of abdominal aorta were monitored,and plasma adiponectin was also measured.Expression levels of the adiponectin receptor 1(AdipoR1)and adiponectin receptor 2(AdipoR2) in vessels were analyzed(RT-PCR).Results:(1) Aortic atherosclerotic lesions were observed in ApoE-/-mice but not in wild type mice.Interestingly,these lesions were significantly prevented by high-dose pioglitazone therapy.Compared with wild type mice,ApoE-/-mice had increased IMT of abdominal aorta [(0.290?0.063 vs 0.178?0.012) cm,P

Levels of adrenomedullin and proadrenomedullin N-terminal 20 peptide in myocardium and aorta of spontaneously hypertensive rats and Wistar-Kyoto rats / 生理学报

In this study, we observed the levels of adrenomedullin (ADM) and proadrenomedullin N-terminal 20 peptide (PAMP) in myocardium and aorta of spontaneously hypertensive rats (SHRs) in comparison with Wistar-kyoto (WKY) rats. Contents of ADM and PAMP were measured by radioimmunoassay (RIA) in plasma, myocardium and aorta. The amount of Pro-ADM mRNA of myocardium and aorta was determined by competitive quantitative reverse transcription polymerase chain reaction (RT-PCR). In SHRs the amounts of Pro-ADM mRNA of myocardium and aorta were 66.7% (P<0.01) and 73% (P<0.01) higher than those in WKY rat, respectively. In SHRs, the levels of ADM in plasma, myocardium and aorta were 29%, 76.7% and 79% (all P<0.01) higher than those in WKY rats, respectively. The level of PAMP in SHRs was increased by 42.5% in plasma (P<0.01), 47.2% in myocardium (P<0.0.1) and 27.3% in aorta (P<0.05) compared to WKY rats, respectively. In addition, the ratio of ADM content to PAMP content in SHRs group was increased compared with that in WKY group (2.0+/-0.25 vs 1.64+/-0.3 and 2.2+/-0.18 vs 1.56+/-0.28, in myocardium and aorta, respectively, P<0.01). These results suggest that ProADM gene expression is up-regulated and the increase in ADM and PAMP is different in SHRs. The significance of inconsistency of increase in ADM and PAMP in SHRs needs to be further investigated.

Changes in adrenomedullin and receptor activity-modifying protein 2 mRNA in myocardium and vessels during L-NNA-induced hypertension in rats / 生理学报

To explore the changes in adrenomedullin (ADM) and receptor activity-modifying protein 2 (RAMP2) mRNA in myocardium and vessels in hypertension, a hypertensive rat model was prepared by administering L-NNA. Contents of ADM in plasma, myocardium and vessels were measured by radioimmunoassay (RIA). The levels of pro-ADM mRNA of myocardium and vessels were determined by competitive quantitative RT-PCR. The results showed that L-NNA induced hypertension and cardiomegaly. The ratio of heart to body weight increased by 35.5% (P<0.01). In hypertensive rats the ir-ADM in plasma, myocardium and vessels was increased by 80%, 72% and 57% (P<0.01), respectively compared with the control. The amounts of ADM mRNA in myocardium and vessels were increased by 50% and 109.2% (P<0.05), respectively, and the amounts of RAMP2 mRNA was increased by 132% and 87% (P<0.01), respectively, compared with control. The levels of ADM in myocardium and vessels were positively correlated with RAMP2 mRNA, the correlation coefficients were 0.741 and 0.885 (P<0.01), respectively. The results obtained indicate that in hypertensive rats, ADM is elevated in plasma, myocardium and ves-myocardium and vessel, and ADM and RAMP2 mRNA are up-regulated in myocardium and vessel. The ADM/RAMP2 system may play an important role in the pathogenesis of hypertension.

Dysfunction of myocardial and vascular taurine transport in spontaneously hypertensive rats / 生理学报

The alterations of taurine transport and the expression of taurine transporter (TAUT) mRNA in myocardium and aortic wall were investigated in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. It was demonstrated that plasma taurine concentration and taurine release from myocardium and aortic wall in SHR were higher than those in WKY rats, whereas taurine content, taurine uptake and TAUT mRNA in myocardium and aortic wall of SHR were lower than those of WKY rats. In SHR, the maximal velocity (V(max)) of taurine transportation in myocardium and aortic wall was lower by 24% (P<0.05) and 35% (P<0.05) than that in WKY, their michaelis constants (Km) values were higher by 16% (P<0.05) and 39% (P<0.05), respectively. The results suggest that there is dysfunction of taurine transport in myocardium and aortic wall in SHR, which may be partly resulted from the decrease of TAUT activity and affinity, and down-regulation of TAUT gene expression.

An observation of taurine transport alterations in calcification of myocardial cells in vitro / 中国医学科学院学报

<p><b>OBJECTIVE</b>To observe the alterations of taurine transport, taurine transporter (TAUT) and cysteine sulfinate decarboxylase (CSD) mRNA in the calcification of myocardial cells in vitro.</p><p><b>METHODS</b>3H-taurine measured the amount of taurine uptake. TAUT and CSD mRNA consents were measured using competitive quantitative RT-PCR in cultured and calcified myocardial cells.</p><p><b>RESULTS</b>In calcification of myocardial cells, taurine concentration was decreased by 27% (P < 0.05), taurine uptake was markedly reduced, Vmax reduced by 39% (P < 0.01), there were no statistical significance of Km values between the two groups. TAUT mRNA decreased by 45% (P < 0.01), but CSD mRNA increased by 25% (P < 0.05).</p><p><b>CONCLUSIONS</b>The data suggest that there were impediment of taurine transport in calcification of myocardial cells, as TAUT mRNA level was decreased, but CSD mRNA concentration was improved.</p>

Effects of mitochondrial L-arginine/nitric oxide system on mitochondrial Ca2+ transport in rat myocardium / 中国应用生理学杂志

<p><b>AIM AND METHODS</b>To observe the effect of myocardial mitochondrial L-arginine (L-Arg)/nitric oxide (NO) system on mitochondrial Ca2+ transport by using purified rat mitochondria and incubation of them in vitro.</p><p><b>RESULTS</b>Compared with control group, incubation of mitochondria with L-Arg (10(-4) mol/L, NO substrate) or sodium nitroprusside (5 x 10(-7) mol/L, the donor of exogenous NO, SNP) increased significantly mitochondrial NO2- (66% and 89%, P < 0.01), respectively, and decreased the Ca2+ content (40% and 54%, P < 0.01). After L-Arg or SNP treatment, mitochondrial Ca2+ uptake were decreased by 67% and 85%, respectively (P < 0.01), vs control. The rate of mitochondrial Ca2+ release decreased by 11% and 8%, respectively (P < 0.01). When L-NAME (NO synthase inhibitor) was incubated with mitochondria and the L-Arg together, it inhibited the effects of L-Arg, NO2 on the mitochondrial NO2 formation, Ca2+ content descending, and decrease of Ca2+ uptake and release.</p><p><b>CONCLUSION</b>The data suggest that myocardial mitochondrial L-Arg /NO systems take part in the regulation of cardiomyocytes Ca2+ transportation.</p>