Specific convulsions and brain damage in children hospitalized for Omicron BA.5 infection: an observational study using two cohorts.

BACKGROUND: SARS-CoV-2 continues to mutate over time, and reports on children infected with Omicron BA.5 are limited. We aimed to analyze the specific symptoms of Omicron-infected children and to improve patient care. METHODS: We selected 315 consecutively hospitalized children with Omicron BA.5 and 16,744 non-Omicron-infected febrile children visiting the fever clinic at our hospital between December 8 and 30, 2022. Specific convulsions and body temperatures were compared between the two cohorts. We analyzed potential associations between convulsions and vaccination, and additionally evaluated the brain damage among severe Omicron-infected children. RESULTS: Convulsion rates (97.5% vs. 4.3%, P < 0.001) and frequencies (median: 2.0 vs. 1.6, P < 0.001) significantly differed between Omicron-infected and non-Omicron-infected febrile children. The body temperatures of Omicron-infected children were significantly higher during convulsions than when they were not convulsing and those of non-Omicron-infected febrile children during convulsions (median: 39.5 vs. 38.2 and 38.6 °C, both P < 0.001). In the three Omicron-subgroups, the temperature during convulsions was proportional to the percentage of patients and significantly differed ( P < 0.001), while not in the three non-Omicron-subgroups ( P = 0.244). The convulsion frequency was lower in the 55 vaccinated children compared to the 260 non-vaccinated children (average: 1.8 vs. 2.1, P < 0.001). The vaccination dose and convulsion frequency in Omicron-infected children were significantly correlated ( P < 0.001). Fifteen of the 112 severe Omicron cases had brain damage. CONCLUSIONS: Omicron-infected children experience higher body temperatures and frequencies during convulsions than those of non-Omicron-infected febrile children. We additionally found evidence of brain damage caused by infection with omicron BA.5. Vaccination and prompt fever reduction may relieve symptoms.

Characteristics of Carcinoembryonic antigen related cell adhesion molecules and their relationship to cancer.

Carcinoembryonic antigen related cell adhesion molecules (CEACAMs), such as carcinoembryonic antigen (CEA) and the oncofetal glycoprotein family, are tumor markers. The CEACAMs consist of 12 different human CEACAMs and 5 different murine CEACAMs. The CEACAM family of proteins participates in multiple biological processes that include the immune response, angiogenesis, and cancer. CEACAMs play a significant role in cancer initiation and development. Increasing evidence suggests that family members may be new cancer biomarkers and targets in that CEACEAMs tend to be aberrantly expressed and therefore may have potential diagnostic and therapeutic importance. This review systematically summarizes the biogenesis, biological properties, and functions of CEACAMs, with a focus on their relationship with cancer and potential clinical application. As our knowledge of the relationships among CEACAMs and cancer increases, and as our understanding of the involved molecular mechanisms improves, new therapeutic strategies will evolve for cancer prevention and treatment of cancer patients.

Development and validation of a nomogram for predicting hospitalization longer than 14 days in pediatric patients with ventricular septal defect-a study based on the PIC database.

Background: Ventricular septal defect is a common congenital heart disease. As the disease progresses, the likelihood of lung infection and heart failure increases, leading to prolonged hospital stays and an increased likelihood of complications such as nosocomial infections. We aimed to develop a nomogram for predicting hospital stays over 14 days in pediatric patients with ventricular septal defect and to evaluate the predictive power of the nomogram. We hope that nomogram can provide clinicians with more information to identify high-risk groups as soon as possible and give early treatment to reduce hospital stay and complications. Methods: The population of this study was pediatric patients with ventricular septal defect, and data were obtained from the Pediatric Intensive Care Database. The resulting event was a hospital stay longer than 14 days. Variables with a variance inflation factor (VIF) greater than 5 were excluded. Variables were selected using the least absolute shrinkage and selection operator (Lasso), and the selected variables were incorporated into logistic regression to construct a nomogram. The performance of the nomogram was assessed by using the area under the receiver operating characteristic curve (AUC), Decision Curve Analysis (DCA) and calibration curve. Finally, the importance of variables in the model is calculated based on the XGboost method. Results: A total of 705 patients with ventricular septal defect were included in the study. After screening with VIF and Lasso, the variables finally included in the statistical analysis include: Brain Natriuretic Peptide, bicarbonate, fibrinogen, urea, alanine aminotransferase, blood oxygen saturation, systolic blood pressure, respiratory rate, heart rate. The AUC values of nomogram in the training cohort and validation cohort were 0.812 and 0.736, respectively. The results of the calibration curve and DCA also indicated that the nomogram had good performance and good clinical application value. Conclusion: The nomogram established by BNP, bicarbonate, fibrinogen, urea, alanine aminotransferase, blood oxygen saturation, systolic blood pressure, respiratory rate, heart rate has good predictive performance and clinical applicability. The nomogram can effectively identify specific populations at risk for adverse outcomes.

Influence of systolic blood pressure trajectory on in-hospital mortality in patients with sepsis.

BACKGROUND: Numerous studies have investigated the mean arterial pressure in patients with sepsis, and many meaningful results have been obtained. However, few studies have measured the systolic blood pressure (SBP) multiple times and established trajectory models for patients with sepsis with different SBP trajectories. METHODS: Data from patients with sepsis were extracted from the Medical Information Mart for Intensive Care-III database for inclusion in a retrospective cohort study. Ten SBP values within 10 h after hospitalization were extracted, and the interval between each SBP value was 1 h. The SBP measured ten times after admission was analyzed using latent growth mixture modeling to construct a trajectory model. The outcome was in-hospital mortality. The survival probability of different trajectory groups was investigated using Kaplan-Meier (K-M) analysis, and the relationship between different SBP trajectories and in-hospital mortality risk was investigated using Cox proportional-hazards regression model. RESULTS: This study included 3034 patients with sepsis. The median survival time was 67 years (interquartile range: 56-77 years). Seven different SBP trajectories were identified based on model-fit criteria. The in-hospital mortality rates of the patients in trajectory classes 1-7 were 25.5%, 40.5%, 11.8%, 18.3%, 23.5%, 13.8%, and 10.5%, respectively. The K-M analysis indicated that patients in class 2 had the lowest probability of survival. Univariate and multivariate Cox regression analysis indicated that, with class 1 as a reference, patients in class 2 had the highest in-hospital mortality risk (P < 0.001). Subgroup analysis indicated that a nominal interaction occurred between age group and blood pressure trajectory in the in-hospital mortality (P < 0.05). CONCLUSION: Maintaining a systolic blood pressure of approximately 140 mmHg in patients with sepsis within 10 h of admission was associated with a lower risk of in-hospital mortality. Analyzing data from multiple measurements and identifying different categories of patient populations with sepsis will help identify the risks among these categories.

Association between glucocorticoid use and all-cause mortality in critically ill patients with heart failure: A cohort study based on the MIMIC-III database.

Background: Heart failure (HF) is the terminal stage of various heart diseases. Conventional treatments have poor efficacy, and diuretic resistance can present. Previous studies have found that the use of glucocorticoids can enhance the diuretic effect of patients with heart failure and reduce heart failure symptoms. However, the relationship between glucocorticoid use and mortality in patients with heart failure in intensive care units is unclear. Objectives: The aim of this study was to determine the association between glucocorticoid use and all-cause mortality in critically ill patients with heart failure. Methods: The information on patients with heart failure in this study was extracted from the MIMIC-III (Medical Information Mart for Intensive Care-III) database. Patients in the glucocorticoid and non-glucocorticoid groups were matched using propensity scores. The Kaplan-Meier method was used to explore the difference in survival probability between the two groups. A Cox proportional-hazards regression model was used to analyze the hazard ratios (HRs) for the two patient groups. Subgroup analyses were performed with prespecified stratification variables to demonstrate the robustness of the results. Results: The study included 9,482 patients: 2,099 in the glucocorticoid group and 7,383 in the non-glucocorticoid group. There were 2,055 patients in each group after propensity-score matching. The results indicated that the non-glucocorticoid group was not significantly associated with reduced mortality in patients with heart failure during the 14-day follow-up period [HRs = .901, 95% confidence interval (CI) = .767-1.059]. During the follow-up periods of 15-30 and 15-90 days, the mortality risk was significantly lower in the non-glucocorticoid group than in the glucocorticoid group (HRs = .497 and 95% CI = .370-.668, and HRs = .400 and 95% CI = .310-.517, respectively). Subgroup analyses indicated no interaction among each stratification variable and glucocorticoid use. Conclusion: Glucocorticoid use was associated with an increased mortality risk in critically ill patients with heart failure.

Development and validation of a simple nomogram for predicting the short-term prognosis of patients with pulmonary embolism.

BACKGROUND: Pulmonary embolism (PE) is a disease caused by blood clots, tumor embolism, and other emboli within the pulmonary arteries. Various scoring scales are used for PE. One such same is the PESI, but it has 12 variables, making it inconvenient for clinical application. OBJECTIVES: The aim of this study was to develop a new simple nomogram model to assess 30-day survival in PE patients. The new nomogram makes it easier and faster for clinicians to assess the prognosis of patients with PE. METHODS: We collected data about the patients with PE from the Medical Information Mart for Intensive Care-III (MIMIC-III) database and used the receiver operating characteristic (ROC) curve, area under the ROC curve (AUROC), calibration plot, integrated discrimination improvement (IDI), and decision curve analysis (DCA) to evaluate the predictive power of the new model, and compared these with the PESI. RESULTS: According to the multivariable Cox regression model results, alongside the actual clinical conditions, we included the following seven variables: race, bicarbonate, age, tumor, systolic blood pressure (SBP), body temperature, and oxygen saturation (Spo2). The AUROC of the new model was greater than 0.70. Its IDI exceeded 0, but with P-value>0.05. CONCLUSION: The predictive performance of the new model was not worse than the PESI, but the new model only has seven variables, and is therefore more convenient for clinicians to use.

Association of lactate to albumin ratio and bicarbonate with short-term mortality risk in patients with acute myocardial infarction.

BACKGROUND: Previous studies have indicated that the ratio of lactate/albumin (L/A) has predictive value for the prognosis of critically ill patients with heart failure. Some studies have also indicated that a low serum bicarbonate concentration is inversely related to the mortality risk of patients with cardiogenic shock. However, the value of bicarbonate and the L/A ratio for predicting the mortality risk of patients with acute myocardial infarction (AMI) is still unclear. We therefore conducted a retrospective study to research this problem. METHODS: The subjects of this study were patients with AMI, and the data source was the Medical Information Mart for Intensive Care III database. The primary endpoint was 30-day all-cause mortality after admission. The Receiver operating characteristic (ROC) curve was used to compare the predictive value of L/A ratio, lactate and albumin for end-point events. The effects of different L/A ratio levels and different bicarbonate concentrations on 7-day and 30-day all-cause mortality were compared using Kaplan-Meier (K-M) curves. Hazard ratios for different L/A ratio and different bicarbonate concentrations were investigated using COX proportional hazards models. RESULTS: The Area Under Curve (AUC) of L/A ratio, lactate, and albumin were 0.736, 0.718, and 0.620, respectively. (1) L/A ratio: The patients were divided into three groups according to their L/A ratio: tertile T1 (L/A ratio ≤ 0.47), tertile T2 (L/A ratio ≤ 0.97), and tertile T3 (L/A ratio > 0.97). The T2 and T3 groups had higher 30-day all-cause mortality risks than the T1 group. The restricted cubic spline (RCS) model indicated that there was a nonlinear relationship between L/A ratio and 30-day mortality (P < 0.05). (2) Bicarbonate concentration: The patients were also divided into three groups based on their bicarbonate concentration: G1 (22-27 mmol/L), G2 (< 22 mmol/L), and G3 (> 27 mmol/L). The G2 and G3 groups had higher 30-day all-cause mortality risks than the G1 group. The RCS model indicated that there was a nonlinear relationship between bicarbonate concentration and 30-day mortality (P < 0.05). The RCS model indicated that there was a nonlinear relationship between hemoglobin level and 30-day all-cause mortality (P < 0.05). CONCLUSION: L/A ratio and bicarbonate concentration and hemoglobin level have predictive value for predicting 30-day mortality in patients with acute myocardial infarction.

Incidence, prognosis, and risk factors of sepsis-induced cardiomyopathy.

BACKGROUND: At present, large-scale studies on the clinical characteristics of sepsis-induced cardiomyopathy (SIC) are lacking. AIM: To investigate the clinical characteristics of SIC. METHODS: Based on the analysis of the MIMIC-III public database, we performed a large-scale retrospective study involving sepsis patients who were admitted to the intensive care unit (ICU) and had no concomitant cardiac disease. We used propensity score matching analysis and multivariate logistic regression to ensure the robustness of the results. The primary outcome was hospital mortality, and the secondary outcomes included the number of patients who received mechanical ventilation or renal replacement therapy during their hospital stay, the number of patients administered with vasopressors, the length of ICU stay, and the length of hospital stay. RESULTS: In the present study, after screening 38605 patients, 3530 patients with sepsis were included. A total of 997 patients met the SIC diagnostic criteria, and the incidence of SIC was 28.20% (95% confidence interval [CI]: 26.80%-29.70%). Compared to patients in the non-SIC group, patients in the SIC group were of older age and had a higher Simplified Acute Physiology Score (SAPS)-I score, SAPS-II score, and Elixhauser comorbidity index (ECI). A total of 367 (36.8%) of 997 patients in the SIC group and 818 (32.3%) of 2533 patients in the non-SIC group died in the hospital, which resulted in a significant between-group difference (odds ratios = 1.22, 95%CI: 1.05-1.42; P = 0.011). For the secondary outcomes, more patients in the SIC group received mechanical ventilation and vasopressors. Multivariate logistic regression analysis showed that age, male sex, ECI, hemoglobin level, diabetes, and mechanical ventilation use on the first day of ICU admission were risk factors for SIC. CONCLUSION: Compared with non-SIC patients, hospital mortality is higher in SIC patients.

Management of an Adult with Goodpasture's Syndrome Following Brain Trauma with Extracorporeal Membrane Oxygenation: A Case Report.

A 22-year-old man suffered from acute pulmonary hemorrhage and deteriorated renal function occurred within 3 days after traumatic brain injury. Mechanical ventilation cannot correct his severe hypoxemia, therefore, venoarterial extracorporeal membrane oxygenation (VA-ECMO) support was initiated and finally resolved his hypoxemia. Concomitantly, continuous renal replacement therapy was performed to improve his kidney function. Although no anti-glomerular basement membrane (anti-GBM) antibody was detected in serum, Goodpasture's syndrome was considered. After treated with methylprednisolone pulse therapy and plasmapheresis, his renal function was significantly improved. ECMO was eventually discontinued after 60 hours of treatment and extubated on day 10. He was discharged home with normal pulmonary and renal functions.

Improvement of Left Ventricular Remodelling by Inhibition of NF-κB in a Rat Model of Myocardial Infarction.

BACKGROUND: To investigate the effects of inhibition of NF-κB activation on left ventricular (LV) remodelling in a rat model of myocardial infarction (MI). METHODS: The acute MI model was established by ligation of left anterior descending coronary artery. Pyrrolidine dithiocarbamate (PDTC) (20mg/kg, Qd) was administered intraperitoneally to inhibit NF-κB activation. Eight weeks later, the cardiac structure and LV ejection fraction were assessed with echocardiography. The rat body, heart, and LV weights were measured to calculate LV mass indices. Activation of NF-κB in non-infarcted myocardium was detected by a TransAM NF-κB p65 Transcription Factor Assay Kit. Cardiac collagen volume fraction was evaluated by Masson staining. RESULTS: Eight weeks after the MI model was established, the LV posterior wall thickness in PDTC and MI group was 1.75±0.07mm and 1.85±0.07mm respectively (p<0.05). The LV mass index in the PDTC group (2.53±0.09) was lower than in the MI group (2.65±0.08, p<0.05). The LVEF in the PDTC group (63.89%±4.21%) was higher than in the MI group (42.73%±8.94%, p<0.05). The interstitial collagen deposition in the non-infarcted myocardium in the PDTC group was less than in the MI group (7.25%±1.88% vs. 10.09%±2.19%, p<0.05). CONCLUSION: Inhibition of activation of NF-κB may result in improvement of myocardial remodelling after myocardial infarction, which is possibly attributable to reduced collagen deposition in non-infarcted areas.

Effect of glutamine on caspase-3 mRNA and protein expression in the myocardium of rats with sepsis.

: Apoptosis and caspase-3 play an important role in the pathogenesis of sepsis. In this study, the authors monitored myocardial apoptosis and investigated caspase-3 protein expression change in rats with sepsis. In addition, we investigated the protective effect of glutamine (Gln) on myocardial injury in septic rats. A rat model of sepsis was established by intraperitoneal injection of lipopolysaccharide (LPS). Rats were divided into control group, endotoxin (LPS) group and LPS + Gln group, which were further divided into 4 subset groups (0, 6, 12 and 24 hour subgroups; n = 6). The rate of myocardial apoptosis, caspase-3 mRNA expression and caspase-3 protein expression were examined. Data were analyzed using the F-test or linear correlation test. The results revealed that the rate of myocardial apoptosis in the LPS group was significantly higher than that in the control group (P < 0.05). Compared with the control group, LPS group has an upregulated caspase-3 mRNA expression level. However, the caspase-3 protein was low expressed (P < 0.05). The LPS + Gln group has significant lower myocardial apoptosis rate compared with the LPS group (P < 0.05). In addition, caspase-3 mRNA expression levels and caspase-3 protein expression levels were lower in the LPS + Gln group (P < 0.05). We found that Gln reduces the extent of myocardial apoptotic cell death by decreasing the gene and protein expression of caspase-3. Therefore, Gln may be used to prevent the onset of sepsis at an early stage.

[Effects of Notch signaling pathway and vascular endothelial growth factor gene on the functions of endothelial cells derived from rat bone marrow mesenchymal stem cells].

OBJECTIVE: To explore the effects of Notch signaling pathway and the vascular endothelial growth factor [VEGF(165)] gene on the functions of endothelial cells derived from rat bone marrow mesenchymal stem cells (MSCs). METHODS: Isolated and cultivated rat bone marrow MSCs in vitro, then the cells were treated by VEGF165 and basic fibroblast growth factor (bFGF) for 2 weeks to induce them to differentiate into endothelial cells. The gene of VEGF165 was transfected into differentiated endothelial cells to promote the functions of the cells. The receptor Notch1 and the ligand Jagged1 of the Notch signaling were detected by reverse transcription-polymerase chain reaction (RT-PCR) before and after the transfection. γ-secretase inhibitor L-685458 was used to block Notch pathway. Migration ability of cells was detected by scarification test. Cells were inoculated on semisolid gel to study their ability of forming capillary-like structure. RESULTS: After transfection, VEGF165 mRNA could be detected on the differentiated endothelial cells. The expression of Jagged1 mRNA was up regulated(1.08 ± 0.01 vs. 1.01 ± 0.02,P < 0.01) and there was no change in Notch1 mRNA(0.60 ± 0.02 vs. 0.59 ± 0.01,P > 0.05). The ability of migration was enhanced (number of cells on the scratched area:46.45 ± 4.46 vs. 41.61 ± 1.42,P < 0.05), and the ability of forming capillary-like structure on semisolid gel showed no change (cells classification: 3.00 ± 0.89 vs. 2.00 ± 0.89,P > 0.05). After the transfection, using the γ-secretase inhibitor L-685458 to block the Notch signaling transduction, the ability of migration of the differentiated endothelial cells (number of cells on the scratched area: 51.72 ± 3.47 vs. 46.45 ± 4.46,P < 0.05), and that of forming capillary--like structure (cells classification: 4.17 ± 0.75 vs. 3.00 ± 0.89, P < 0.05), was also further enhanced. CONCLUSION: Transfection of the gene of VEGF165 into the differentiated endothelial cells can reinforce the function of these cells, and when Notch signaling was blocked, this effect can be further amplified.

[The role of Notch signaling during the differentiation of rat bone marrow mesenchymal stem cells into endothelial cells].

OBJECTIVE: To research the role of Notch signaling during the differentiation of bone marrow mesenchymal stem cells (MSCs) into endothelial cells and its effect on the functions of the differentiated cells. METHODS: Rat bone marrow MSCs were isolated and cultured in vitro, then the cells were treated with vascular endothelial growth factor (VEGF165) and basic fibroblast growth factor (bFGF) for 2 weeks to induce it to differentiate into endothelial cells. The differentiated cells were identified by fluorescence immunoassay. The receptors and ligands of the Notch signaling were detected by reverse transcription-polymerase chain reaction (RT-PCR) before and after the differentiation. γ-secretase inhibitor was used to block Notch pathway. Migration ability of cells were assessed by scarification test. Cells were inoculated on semisolid gel to study their ability of forming the capillary-like structure. RESULTS: After inducing MSCs to differentiate into endothelial cells by VEGF165 and bFGF, MSCs gained the characteristics of the endothelial cells with expression of CD31 and Flk1. There were Notch1 mRNA and Jagged1 mRNA expressions in rat bone marrow MSCs. The expression changes in the receptor Notch1 were not statistically significant on the differentiated cells (0.59±0.01 vs. 0.59±0.01, P>0.05), but there was a trend towards an increase of Jagged1 mRNA (1.01±0.02 vs. 0.99±0.03, P>0.05). When Notch pathway was blocked, the differentiated cells' migration ability was increased (number of cells on the scratched area: 44.61±4.34 vs. 40.06±2.43, P<0.05), and the ability of forming capillary-like structure was also increased (cells classification: 3.67±0.82 vs. 2.00±0.89, P<0.01). CONCLUSION: Notch signaling may have an important role during the differentiation of MSCs into endothelial cells. The function of differentiated cells were strengthened when Notch pathway was blocked.

[Changes in expressions of the myocardial Toll-like receptor 4, tumor necrosis factor-alpha and interleukin-6 mRNA in rat with sepsis].

OBJECTIVE: To investigate the relationship between apoptosis of myocardial cell in the rats with sepsis and the expressions of Toll-like receptor 4 (TLR4), tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) mRNA, and the protective effect of glutamine (Gln) against apoptosis of myocardial cell. METHODS: Rat model of sepsis was reproduced by peritoneal injection with lipopolysaccharide (LPS), and the animals were divided into control group, LPS group and Gln group. Rats in each group were further divided into four subgroups, 0, 6, 12 and 24 hours ( n =6). Apoptosis of myocardial cells was surveyed, and TLR4, TNF-alpha and IL-6 mRNA expressions were assessed with reverse transcription-polymerase chain reaction (RT-PCR). The pathological changes in myocardial cells were observed. RESULTS: Myocardial apoptosis rate in LPS group was higher. Compared with the control group, expressions of TLR4 mRNA, TNF-alpha mRNA and IL-6 mRNA were significantly higher at all time points after LPS administration in the LPS group and the Gln group (all P<0.05). Compared with the LPS group, the rate of myocardial apoptosis in Gln group was lower, and expression of TLR4 mRNA in the Gln group was significantly lower at 12 hours and 24 hours; the expression of TNF-alpha mRNA was obviously lower at 6 hours and 24 hours; the expression of IL-6 mRNA in the Gln group was significantly lower at 12 hours (all P<0.05). CONCLUSION: TLR4, TNF-alpha and IL-6 gene expressions play extremely important role in apoptosis of myocardial cell in the rat with sepsis. Gln can affect apoptosis-related gene expressions, thus alleviating the apoptosis of myocardial cell.

Effect of intracoronary tirofiban in patients undergoing percutaneous coronary intervention for acute coronary syndrome.

BACKGROUND: To investigate the efficacy of intracoronary tirofiban during primary percutaneous coronary intervention (PCI) for patients with acute coronary syndrome (ACS). METHODS AND RESULTS: The 118 patients aged 70 years and above (average age 75+/-2) were divided into study (n = 58, intracoronary bolus tirofiban) and control (n = 57, intravenous tirofiban) groups. The culprit vessels were targeted with primary PCI in all patients. Compared with the control group, the study group showed better Thrombolysis In Myocardial Infarction (TIMI) flow grades and TIMI myocardial perfusion grades (TMPG) immediately after PCI (p = 0.016 and 0.026, respectively). The 14-day composite major adverse cardiac events rate was lower in the study group (3.5% vs 17.5%, p = 0.030), but was similar between the 2 groups at 30 days following PCI (7.0% vs 1.7%, p = 0.350). The left ventricular ejection fraction in the study group was higher than in the control group 30 days following PCI (67.4+/-6.2% vs 60.7+/-4.6%, p = 0.033). The 14-day bleeding complication (p = 0.201) and platelet reduction rates (p = 0.984) were similar between the 2 groups. CONCLUSION: In patients with ACS undergoing primary PCI, intracoronary bolus administration of tirofiban is superior to intravenous bolus injection for improving coronary flow, myocardial perfusion and short-term clinical outcomes.

[Urotensin II induces hypertrophy of in vitro cultured neonatal rat cardiac myocytes].

OBJECTIVE: To examine whether urotensinII (UII) induces hypertrophy of neonatal rat cardiomyocytes cultured in vitro. METHODS: The primary cardiac myocytes cultured for 40 h followed by further culture in serum-free media for another 24 h were subjected to exposure to UII of varied concentrations for 24 h, after which the changes in the size of the cells were analyzed by flow cytometry with (3)H-leucine incorporation also measured. RESULTS: At the concentration of 1x10(-7) mol/L, UIIcould increase the size of the cultured cardiac myocardial cells (P=0.021) and 3H-Leucine incorporation (P=0.015). CONCLUSION: UII may induce hypertrophy of neonatal rat cardiac myocytes cultured in vitro.

[Effects of urotensin II on cultured cardiac fibroblast proliferation and collagen type I mRNA expression].

OBJECTIVE: To observe the effect of urotensin II on cultured cardiac fibroblast collagen type I mRNA expression and proliferation, thereby to explore the role of urotensin II in myocardial remodeling in the event of cardiac failure. METHODS: Cardiac fibroblasts of neonatal Sprague-Dawley rats isolated by trypsin digestion method were stimulated by urotensin II at varied concentrations when the cells reached growth arrest. MTT assay was employed to measure the proliferation and determine the number of the cells, and reverse transcriptional (RT)-PCR used to detect the collagen mRNA expression. RESULTS: With the increase of urotensin II concentration, the optical density at 570 nm of the fibroblasts as shown by MTT assay first increased but then decreased, and remained at a significantly higher level in the cells treated with 1x10(-8) or 1x10(-9) mol/L urotensin II as compared with the control (P<0.05). The collagen type I mRNA levels of the cells treated with 1x10(-7), 1x10(-8) or 1x10(-9) mol/L urotensin II were significantly higher than that of the control cells (P<0.01). CONCLUSION: Urotensin II can directly induce cardiac fibroblast proliferation and significantly increase collagen type I mRNA expression, suggesting the crucial role of urotensin II in myocardial remodeling.