Serum Levels Of CK Research Articles

Compound Yuye Decoction protects diabetic rats against cardiomyopathy by inhibiting myocardial apoptosis and inflammation via regulating the PI3K/Akt signaling pathway

To explore the therapeutic mechanism of compound Yuye Decoction against diabetic cardiomyopathy (DCM). Drugbank, Gene Cards, OMIM and PharmGKb databases were used to obtain DCM-related targets, and the core targets were identified and functionally annotated by protein-protein interaction network analysis followed by GO and KEGG enrichment analysis. The "Traditional Chinese Medicine-Key Component-Key Target-Key Pathway" network was constructed using Cytoscape 3.9.1, and molecular docking was carried out for the key components and the core targets. In the animal experiment, Wistar rat models of DCM were treated with normal saline or Yuye Decoction by gavage at low (0.29 g/kg) and high (1.15 g/kg) doses for 8 weeks, and the changes in cardiac electrophysiology and histopathology were evaluated. The changes in serum levels of LDH, CK, and CK-MB were examined, and myocardial expressions of PI3K, P-PI3K, Akt, P-AKT, BAX, IL-6, and TNF-α were detected using Western blotting. We identified 61 active compounds in Yuye Decoction with 1057 targets, 3682 DCM-related disease targets, and 551 common targets between them. Enrichment of the core targets suggested that apoptosis, inflammation and the PI3K/Akt pathways were the key signaling pathways for DCM treatment. Molecular docking studies showed that the active components in Yuye Decoction including gold amidohydroxyethyl ester and kaempferol had strong binding activities with AKT1 and PIK3R1. In DCM rat models, treatment with Yuye Decoction significantly alleviated myocardial pathologies, reduced serum levels of LDH, CK and CK-MB, lowered myocardial expressions of BAX, IL-6 and TNF-α, and increased the expressions of P-PI3K and P-AKT. The therapeutic effect of compound Yuye Decoction against DCM is mediated by its multiple active components that act on multiple targets and pathways to inhibit cardiomyocyte apoptosis and inflammatory response by regulating the PI3K/Akt signaling pathway.

Clinical efficacy of ganciclovir combined with transfer factor oral solution for pediatric infectious mononucleosis

This study investigates the clinical efficacy of ganciclovir combined with transfer factor oral solution in the treatment of patients with infectious mononucleosis (IM) to provide a reference for clinical application. A total of 150 children with IM who received treatment in our hospital from 2020 to 2022 were randomly selected as the research subjects. They were randomly divided into a control group receiving intravenous administration of ganciclovir (n = 75) and an observation group receiving transfer factor oral liquid in combination with intravenous administration of ganciclovir (n=75). The results showed that after treatment, the serum levels of CK-MB, CK, CRP, IL-6, and TNF-α were significantly reduced in both groups. The observation group showed lower levels than the control group. Additionally, peripheral blood CD4+ T cells, CD4+/CD8+ ratio, and Tfr expression were higher in the observation group compared to the control group, while the level of CD8+ T cells was lower than that of the control group. Furthermore, there were no significant changes in the levels of IgA, IgM, and IgG antibodies in the two groups before and after treatment. In conclusion, the combination therapy of transfer factor oral solution and ganciclovir demonstrates favorable clinical efficacy and safety in the treatment of children with IM, as it effectively reduces inflammatory reactions, regulates cellular immune function, promotes Tfr differentiation, and shortens recovery time.

Creatine kinase serum levels in children revisited: New reference intervals from a large cohort of healthy children and adolescents

BackgroundCreatine Kinase (CK) has become increasingly important in pediatrics as a commonly used laboratory screening parameter for neuromuscular diseases. Recent research suggests that hyperCKemia in children is not always associated with pathology and can occur due to several reasons. Little is known of various clinical factors that may influence CK throughout child development. ObjectiveThis study aimed to establish reliable age- and sex-specific reference ranges for serum CK levels in healthy infants, children, and adolescents. In addition, the effect of puberty, oral contraceptive (OC) use as well as steroid hormones on CK was examined. Materials and methodsThe data was collected from subjects of the longitudinal population-based “LIFE Child”-cohort between 2011 and 2016 in Leipzig, Germany. 5238 blood samples of 2707 healthy children, aged between 0.14 months and 18 years, were analyzed. ResultsSerum CK levels raised during the first year of life, peaking shortly after age one (P50girls = 2.7 µkat/L, P50boys = 2.90 µkat/L). There was a pronounced difference in the 97.5th percentile between boys and girls during adolescence with its maximum at age 18 (P97.5girls = 5.74 µkat/L, P97.5boys= 14.48 µkat/L). Also, mean CK serum levels were significantly higher in boys (bboys = 0.29, pboys < 0.001). Intake of oral contraceptives (OC), extreme underweight, underweight and obesity revealed a significant inverse correlation with CK serum levels. ConclusionAge, sex, OC intake and weight status affect serum CK levels, particularly during infancy and puberty. We recommend the use of age- and sex-specific reference values for CK serum levels to assess the clinical relevance of measurements.

Phenotypic and Therapeutic Evaluation of Humanized C3 Transgenic Mice as a Model for C3 glomerulopathy-Like Autoimmune Disease

Abstract C3 glomerulopathy (C3G) encompasses a range of kidney disorders with autoimmune and genetic origins, where dysregulated alternative pathway (AP) complement activation stands as the underlying cause. This study develops a transgenic mouse strain that overexpresses human C3, thereby spontaneously generating a rapidly progressing and severe murine model of C3G. The C3G phenotype observed in humanized C3 transgenic mice may arise from a dysregulated interaction between human C3 protein and various mouse complement proteins, resulting in uncontrolled C3 activation via the AP. Male humanized C3 transgenic mice exhibit increased morbidity early in life. Proteinuria initiates at 4 weeks of age, accompanied by an elevation in the albumin/creatinine ratio. Significantly increased serum levels of ALT, AST, ALP, LDH, and CK in humanized C3 transgenic male mice compared to wild-type mice indicate liver and heart injuries. Moreover, serum T-CHOL and HDL levels are significantly reduced, suggesting anemia and malnutrition. Pathohistological analysis of the kidney reveals various renal lesions. Oral administration of Lnp023, a small-molecule inhibitor of complement factor B, effectively increases body weight and serum hC3 levels, improves anemia, and preserves liver, heart, and renal function. In conclusion, this novel model contributes significantly to unraveling the mechanisms underlying C3G and exploring potential therapeutic interventions.

An enhanced cardio-protective effect of nanoparticles loaded with active components from Polygonum orientale L. against isoproterenol-induced myocardial ischemia in rats

In this study, nanoparticles loaded with active components from Polygonum orientale L. (PO), a traditional Chinese herb known for its anti-myocardial ischemic properties, were investigated for cardio-protective properties. Specifically, OVQ-Nanoparticles (OVQ-NPs) with Orientin (Ori), Vitexin (Vit), and Quercetin (Que) was obtained by double emulsion-solvent evaporation method. The OVQ-NPs exhibited a spherical shape, with a uniform size distribution of 136.77 ± 3.88 nm and a stable ζ-potential of −13.40 ± 2.24 mV. Notably, these nanoparticles exhibited a favorable sustained-release characteristic, resulting in an extended circulation time within the living organism. Consequently, the administration of these nanoparticles resulted in significant improvements in electrocardiograms and heart mass index of myocardial ischemic rats induced by isoproterenol, as well as decreased serum levels of CK, LDH, and AST. Furthermore, the results of histopathological examination, such as H&E staining and TUNEL staining, confirmed a reduced level of cardiac tissue pathology and apoptosis. Moreover, the quantification of biochemical indicators (SOD, MDA, GSH, NO, TNF-α, and IL-6) demonstrated that OVQ-NPs effectively mitigated myocardial ischemia by regulating oxidative stress and inflammatory pathways. In conclusion, OVQ-NPs demonstrate promising therapeutic potential as an intervention for myocardial ischemia, providing a new perspective on traditional Chinese medicine treatment in this area.

Elucidation for the pharmacological effects and mechanism of Shen Bai formula in treating myocardial injury based on energy metabolism and serum metabolomic approaches

Ethnopharmacological relevanceShen Bai formula (SBF) is a proven effective traditional Chinese medicine for treating viral myocarditis (VMC) sequelae in clinic, and myocardial injury is the pathological basis of VMC sequelae. However, the pharmacological action and mechanism of SBF have not been systematically elucidated. Aim of the studyIn present research, the doxorubicin-induced myocardial injury rat model was used to evaluate the efficacy of SBF, and energy metabolism and metabolomics approaches were applied to elucidate the effects of SBF on myocardial injury. Materials and methodsThrough energy metabolism measurement system and UPLC-Q-TOF-MS/MS oriented blood metabolomics, directly reflected the therapeutic effect of SBF at a macro level, and identified biomarkers of myocardial injury in microcosmic, revealing its metabolomic mechanism. ResultsResults showed that SBF significantly improved the electrocardiogram (ECG), heart rate (HR), extent of myocardial tissue lesion, and ratio of heart and spleen. In addition, the serum levels of AST, CK, LDH, α-HBDH, cTnI, BNP, and MDA decreased, whereas SOD and ATP activity and content increased. Moreover, SBF increased locomotor activity and basic daily metabolism in rats with myocardial injury, restoring their usual level of energy metabolism. A total of 45 potential metabolomic biomarkers were identified. Among them, 44 biomarkers were significantly recalled by SBF, including representative biomarkers arachidonic acid (AA), 12-HETE, prostaglandin J2 (PGJ2), 15-deoxy-Δ-12,14-PGJ2, 15-keto-PGE2, 15(S)-HPETE, 15(S)-HETE, 8,11,14-eicosatrienoic acid and 9(S)-HODE, which involved AA metabolism, biosynthesis of unsaturated fatty acids and linoleic acid metabolism. ConclusionWe successfully replicated a myocardial injury rat model with the intraperitoneal injection of doxorubicin, and elucidated the mechanism of SBF in treating myocardial injury. This key mechanism may be achieved by targeting action on COX, Alox, CYP, and 15-PGDH to increase or decrease the level of myocardial injury biomarker, and then emphatically interven in AA metabolism, biosynthesis of unsaturated fatty acids and linoleic acid metabolism, and participate in regulating purine metabolism, sphingolipid metabolism, primary bile acid biosynthesis, and steroid hormone synthesis.

Effects of N-acetyl-L-cysteine against apical periodontitis in rats with adriamycin-induced cardiomyopathy and nephropathy.

This study aimed to investigate the potential protective effects of N-acetyl-L-cysteine (NAC) against apical periodontitis (AP) in rats with adriamycin (ADR)-induced kidney and heart diseases. Fourty-eight Wistar albino rats were divided into six groups: (1) Control group, (2) ADR group (1 mg/kg/day ip for 10 days), (3) AP Group (1st mandibular molar tooth), (4) AP + ADR Group, (5) AP + NAC group (150 mg/kg/day ip), and (6) AP + ADR + NAC group. After 3 weeks, the rats were decapitated and blood and tissue samples (heart, kidney, and jaw) were collected. Tissue samples were evaluated by biochemical (inflammatory cytokines and hemodynamic parameters) and radiological analyses. One-way anova with Tukey post hoc tests was used to compare data, considering p < .05 as statistically significant. The serum levels of TNF-α, IL-1β, BUN, Creatinine, CK, and LDH were elevated in the test groups compared with the control group, and treatment with NAC reduced these levels (p < .05). Heart and kidney tissue analysis showed a higher heart-to-body weight ratio (HW/BW) and kidney-to-body weight ratio (KW/BW) in the test groups compared with the control group (p < .05). No significant differences in HW/BW and KW/BW were found between the control and AP + NAC groups. Volumetric apical bone resorption analysis showed an increase in periapical radiolucencies in AP-induced groups indicating apical periodontitis. NAC treatment reduced the total area and volume of resorption cavities (p < .05). The results suggest that NAC's antioxidant and anti-inflammatory effects can reduce adriamycin-mediated heart and kidney damage and may have a positive effect on apical periodontitis in individuals with nephropathy and cardiomyopathy.

PLGA nanoparticles enhanced cardio-protection of scutellarin and paeoniflorin against isoproterenol-induced myocardial ischemia in rats

This study aims to examine the impact of the microfluidic preparation process on the quality of poly (lactic-co-glycolic acid) (PLGA) nanoparticles (NPs) co-delivered with scutellarin (SCU) and paeoniflorin (PAE) in comparison to a conventional emulsification method and to evaluatethe potential cardio-protective effect of SCU-PAE PLGA NPs produced through emulsification method. As compared with microfluidics, the nanoparticles prepared by emulsification method exhibited a smaller size, higher encapsulation efficiency, higher drug loading and lower viscosity for injection. Subsequently, a rat myocardial ischemia (MI) was established using male Sprague-Dawley (SD) rats (250 ± 20 g) subcutaneously injected with 85 mg/kg isoproterenol (ISO) for two consecutive days. The pharmacokinetic findings demonstrated that our SCU-PAE PLGA NPs exhibited prolonged blood circulation time in MI rats, leading to increased levels of SCU and PAE in the heart. This resulted in significant improvements in electrocardiogram and cardiac index, as well as reduced serum levels of CK, LDH, AST. Histopathological analysis using H&E and TUNEL staining provided further evidence of improved cardiac function and decreased apoptosis. Additionally, experiments measuring SOD, MDA, GSH, NO, TNF-α and IL-6 levels indicated that SCU-PAE PLGA NPs may effectively treat MI through oxidative stress and inflammatory pathways, thereby establishing it as a promising therapeutic intervention.

Bradykinin receptor participates in doxorubicin-induced cardiotoxicity by modulating iNOS signal pathway.

Doxorubicin (DOX), an effective and broad-spectrum anthracycline antibiotic, is widely used in the treatment of numerous malignancies. However, dose-dependent cardiotoxicity limits the clinical application of DOX, and the molecular mechanisms are still unknown. In this study, we used the BK receptor B1/B2 double-knockout (B1B2 -/- ) mice to observe the role of BK receptor in cardiotoxicity induced by DOX and the underlying mechanisms. DOX induced myocardial injury with increased serum levels of AST, CK, and LDH, upregulated tissue expression of bradykinin B1/B2 receptor, FABP4 and iNOS, and downregulated expression of eNOS. However, these altered releases of myocardial enzyme and the expression level of iNOS were significantly prevented in the B1B2-/- mice. We concluded that the activation of both B1 and B2 receptors of BK were involved in the DOX-induced acute myocardial injury, possibly mediated through iNOS signaling pathways.

Potential combined effect of Spirulina platensis and Momordica charantia fruits on attenuation of isoproterenol-induced myocardial infarction in rats: identification and prediction its mechanism

We established in vivo models of isoproterenol-induced myocardial infarction (MI) to determine the cardioprotective effect of Spirulina platensis (Spi), Momordica charantia fruit (MC) and their combination. MI was induced in six groups of Male Wistar albino with isoproterenol, and cardioprotection was evaluated by measuring SGOT, SGPT, LDH, CK, CK-MB with commercially available test kits and analyzing histopathology. Online PASS was used to predict the mechanism of action of a marker compound in Spi and MC. Rat serum levels of LDH, SGOT, CK-MB, and CK were significantly reduced by the Spi and MC combination extract (P &amp;lt; 0.05). The combination extract at a dose of 50:50 mg/kg body weight preserve the integrity of the myocardial cell membrane. Identified compounds by LC-MS/MS in the ethanol extract of Momordica charantia are (3β,16α-Dihydroxy-lanosta-8,24-dien-21-oic acid), Eclalbasaponin II, Epianhydrobelachinal, Epianhydrobelachinal, Paeonenolide F, Ziyu glycoside II. Identified compounds by LC-MS/MS in Spirulina platensis extract are d-Lirioferine, Lycopodine, Yuanhunine, Candidate Mass C18H26N2O5 and Candidate Mass C36H38N4O5. In PASS analysis, Phycocyanobilin’s cardioprotective mechanism of action is predicted to be kinase inhibitor, cytoprotectant, and platelet aggregation inhibitor, with Probable activities (Pa) of 0.06, 0.53, and 0.443, respectively. The Pa values for cholesterol antagonist, proliferative disease treatment, nitric oxide scavenger, and anti-inflammatory agents in Momordicoside A are respectively 0.841, 0.666, 0.59, and 0.55. These findings suggest that the cardioprotective activity of the combination of Spi and MC extracts at a dose of 50 mg/kg was synergistic.

Vitamin D3 supplementation could ameliorate the inflammatory and redox status in the muscular phase of trichinellosis.

Nutritional supplements, particularly vitamin D, have been widely used worldwide in the treatment of various infections, including parasites. This study aimed to evaluate the potential effects of vitamin D3 supplementation on the muscular phase of trichinellosis in experimental animals. Mice were divided as follows: (group I): infected untreated, (group IIa) infected and treated with vitamin D3 for 12 doses beginning 2weeks before infection and continuing after infection, (group IIb) infected and treated with vitamin D3 for 8 doses beginning on the same day of infection, (group III) normal control, (group IVa) which received vitamin D3 for 12 doses and (group IVb) which received vitamin D3 for 8 doses. Mice were sacrificed 35days after infection and total muscle larval count, and histopathological examination of muscle samples with immunohistochemical staining of cyclooxygenase 2 (COX2) and inducible nitric oxide synthase (iNOS) were performed. Muscle relative cathelicidin mRNA expression was assessed, as well as serum levels of muscle enzymes CK and LDH, interleukin-4 (IL-4), IL-10, IL-17 and interferon-gamma (INF-γ). Vitamin D3 supplementation significantly reduced muscle larval count, inflammatory cellular infiltration, COX2 and iNOS expression. Furthermore, it increased cathelicidin gene expression, decreased serum levels of CK and LDH and affected serum cytokine levels, increasing serum IL-4 and IL10 levels while decreasing serum INF γ and IL-17. In conclusion, vitamin D3 supplementation has favorable outcomes on the muscle phase of trichinellosis, including anti-inflammatory, antioxidant, and immunomodulatory effects.

Exploring the potential molecular mechanism of trastuzumab-induced cardiotoxicity based on RNA sequencing and bioinformatics analysis

The cardiotoxicity of trastuzumab (TRZ) seriously affects the prognosis of breast cancer patients, but the underlying mechanisms remains to be elucidated. This study aimed to investigate the potential molecular mechanisms of TRZ-induced cardiotoxicity based on RNA sequencing (RNA-Seq) and bioinformatics analysis. Kunming mice were exposed to 10 mg/kg TRZ for 6 and 10 days, followed by echocardiography, histopathology and serum biochemical analysis to evaluate the cardiotoxicity model. The results showed no significant changes after 6 days administration of TRZ. After 10 days administration of TRZ, the mice showed cardiac dysfunction, myocardial injury and fibrosis, and the serum levels of LDH, CK, CK-MB and cTnI were increased compared to the control [CON (Day 10)] group, indicating the cardiotoxicity model was successfully established. We compared gene expression levels in mice cardiac tissues by RNA-Seq and screened out 593 differentially expressed genes (DEGs). Results based on Gene Ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, protein–protein interaction (PPI) network analysis and RT-PCR revealed that the CD74/STAT1 signaling pathway might play an important role in TRZ-induced cardiotoxicity. In the TRZ group, the protein expressions of CD74, p-STAT1 (Tyr) and p-STAT1 (Ser) were increased. The TUNEL staining showed increased apoptosis of cardiomyocytes. In addition, an increased expressions of Bax, Caspase-3, IFN-γ and TNF-α and a decreased expression of Bcl-2 were observed in Western blot results, indicating the apoptosis and inflammation levels were increased. These findings suggested that TRZ may induce cardiotoxicity in mice by activating the CD74/STAT1 signaling pathway, which might be related to the induction of apoptosis and inflammation.

The effect of atorvastatin therapy on skeletal muscle function in hyperlipidemia patients in khartoum

Background: Atorvastatin is a lipid-lowering medication that causes skeletal muscle side effects by altering serum levels of skeletal muscle biomarkers. The aim of this study is to assess the effect of atorvastatin on muscle function and biomarker serum levels of CK, LDH, AST, Myoglobin, and Troponin I in Sudanese patients. Method: The total study group of hindered participants, including 60 case group (under Atorvastatin treatment) and 40 healthy as a control group, was matched with age and sex for the case group. The serum CK, LDH, myoglobin, and lipid profiles in the study groups were estimated by automated chemistry analyzers in this study. Result: Muscle pain was reported in case studies (55 = 91%). There was a significant increase in CK, LDH, and myoglobin among case studies when compared to the control group. The dose of drug showed no significant difference among the studied parameters. No correlation was found between CK and LDH with the duration of drug administration. Conclusion: Atorvastatin medication causes skeletal muscle pain among case study and increase muscle biomarkers such as CK, LDH, and myoglobin levels.

Ponciri Fructus Immaturus ethanol extract attenuates septic shock through inhibition of the STAT1 signaling pathway.

Sepsis is a systemic inflammatory disease to infections and results in tissue damage and multiple organ failure. Ponciri Fructus Immaturus (PFI) is widely used in traditional medicine for allergic inflammation and gastrointestinal disorders. However, the effect of PFI on sepsis is still unknown. This study investigated the anti-inflammatory and antiseptic effects of PFI ethanol extract (PFIE) in LPS-stimulated J774 macrophages and mice with CLP- or LPS-induced sepsis, respectively. PFIE attenuates the LPS-induced production of the proinflammatory mediator NO by inhibiting the expression of iNOS in J774 cells. Real-time RT-PCR data and ELISA showed that the mRNA and protein levels of TNF-α, IL-1β, and IL-6 increased in LPS-stimulated J774 cells. However, this induction was significantly suppressed in PFIE pre-treated J774 cells. We also found that PFIE administration increased the survival rate of mice with LPS- and CLP-induced sepsis. Decreased serum levels of AST, ALT, and CK were observed after administration of PFIE, which was associated with reduced production of proinflammatory factors, such as NO, TNF-α, IL-1β, and IL-6. Moreover, PFIE suppressed the phosphorylation and nuclear translocation of STAT1 in LPS-stimulated J774 cells, suggesting that PFIE can inhibit LPS- and CLP-induced septic shock by suppressing the STAT1 activation. These findings provide the potential therapeutic relevance of PFIE in treating acute inflammatory disease.

Case report: One child with an autism spectrum disorder who had chronically elevated serum levels of CK and CK-MB

Some patients with autism spectrum disorder (ASD) exhibit elevated serum creatine kinase levels, which are believed to be associated with mitochondrial dysfunction. Although a few articles have reported this situation in the past and the increase mostly ranges from 100 to 300 U/L, there is a paucity of previous study focusing on the serum creatine kinase MB isoenzyme. This article discusses a 5-year-old girl with ASD, whose serum creatine kinase and creatine kinase MB isoenzyme have been rising for nearly 2 years, fluctuating at 584–993 and 111–625 U/L respectively. Except for behavioral and language symptoms associated with ASD, the child appears normal in other aspects. The child's laboratory tests showed no abnormality, except that the serum levels of lactic acid was slightly higher than normal (1.89 mmol/L, normal 1.33–1.78 mmol/L). The child was prescribed with a traditional Chinese medicine during the process and the serum creatine kinase MB isoenzyme level decreased dramatically to 111 U/L after the treatment. This study firstly recorded the serum creatine kinase levels and the MB isoenzyme in patients with autism spectrum disorder for nearly 2 years, indicating that patients with ASD may experience long-term increases in serum creatine kinase and creatine kinase MB isoenzyme, and that the traditional Chinese medicine decoction Xinfukang can temporarily reduce the serum creatine kinase MB isoenzyme level in patients. Nevertheless, the effect is not sustained. Therefore, it is of great importance to conduct long-term longitudinal studies so as to elucidate the potential mechanism responsible for long-term elevation of serum creatine kinase level.

Liquiritigenin protects against myocardial ischemic by inhibiting oxidative stress, apoptosis, and L-type Ca2+ channels.

Liquiritigenin (Lq) offers cytoprotective effects against various cardiac injuries, but its beneficial effects on myocardial ischemic (MI) injury and the related mechanisms remain unclear. In the in vivo study, an animal model of MI was induced by intraperitoneal injection of isoproterenol (Iso, 85 mg/kg). ECG, heart rate, serum levels of CK and CK-MB, histopathological changes, and reactive oxygen species (ROS) levels were all measured. In vitro, H9c2 cells were divided into four groups and treated for 24 hr with liquiritigenin (30 μmol/L and 100 μmol/L) followed with CoCl2 (800 μmol/L) for another 24 hr. Cell viability, apoptosis, mitochondrial membrane potential, and intracellular Ca2+ concentration ([Ca2+ ]i ) were then assessed. The L-type Ca2+ current (ICa-L ) was detected using a patch clamp technique on isolated rat ventricular myocytes. The myocyte contraction and Ca2+ transients were measured using an IonOptix detection system. The remarkable cardiac injury and generation of intracellular ROS induced by Iso were alleviated via treatment with Lq. CoCl2 administration induced cell apoptosis, mitochondrial dysfunction, and Ca2+ overload in H9c2; Lqreduces these deleterious effects of CoCl2 . Meanwhile, Lq blocked ICa-L in a dose-dependent manner. The half-maximal inhibitory concentration of Lq was 110.87 μmol/L. Lq reversibly reduced the amplitude of cell contraction as well as the Ca2+ transients. The results show that Lq protects against MI injury by antioxidation, antiapoptosis, counteraction mitochondrial dysfunction, and inhibition of ICa-L , thus damping intracellular Ca2+ .

Clinical and electrocardiogram presentations of patients with high serum potassium concentrations within emergency settings: a prospective study

BackgroundElevated potassium level is a common and reversible peri-arrest condition. Diagnosis and management of hyperkalemia in a short time is critical, where electrocardiogram (ECG) alterations might be helpful. We aimed to investigate the role of clinical features and ECGs in early diagnosing and treating hyperkalemia.MethodsProspectively, adult patients who presented to the emergency department (ED) from July 2019 to March 2020 with hyperkalemia (serum potassium ≥5.5mmol/L) were included. History was obtained, and laboratory investigations and ECGs were performed at the presentation and before initiating hyperkalemia therapy. Hyperkalemia severity was divided into mild (5.5–5.9mmol/L), moderate (6.0–6.4mmol/L), and severe (≥6.5mmol/L). A cardiologist and emergency physician blinded to laboratory values, study design, and patients’ diagnoses interpreted ECGs and presenting symptoms independently to predict hyperkalemia.ResultsSixty-seven hyperkalemic patients with a mean (±SD) serum potassium level of 6.5±0.7mmol/L were included in this study. The mean age was 63.9±15.1, and 58.2% were females. Hyperkalemia was mild in 10.4%, moderate in 40.3%, and severe in 49.3%. Almost two thirds of patients (71.6%) had hypertension, 67.2% diabetes, and 64.2% chronic kidney disease. About one-quarter of patients (22.4%) were asymptomatic, while fatigue (46.3%), dyspnea (28.4%), and nausea/vomiting (20.9%) were the most common presenting symptoms. Normal ECGs were observed in 25.4% of patients, while alterations in 74.6%. Atrial fibrillation (13.4%), peaked T wave (11.9%), widened QRS (11.9%), prolonged PR interval (10.5%), and flattening P wave (10.5%) were the most common. Peaked T wave was significantly more common in severe hyperkalemia (87.5%) than in mild and moderate hyperkalemia (12.5%, 0.0%, respectively) (p=0.041). The physicians’ sensitivities for predicting hyperkalemia were 35.8% and 28.4%, improved to 51.5% and 42.4%, respectively, when limiting the analyses to severe hyperkalemia. The mean (±SD) time to initial hyperkalemia treatment was 63.8±31.5 min. Potassium levels were positively correlated with PR interval (r=0.283, p=0.038), QRS duration (r=0.361, p=0.003), peaked T wave (r=0.242, p=0.041), and serum levels of creatinine (r=0.347, p=0.004), BUN (r=0.312, p=0.008), and CK (r=0.373, p=0.039).ConclusionsThe physicians’ abilities to predict hyperkalemia based on ECG and symptoms were poor. ECG could not be solely relied on, and serum potassium tests should be conducted for accurate diagnosis.

NEUROMUSCULAR JUNCTION RELATED DISORDERS: EP.295 Brachio-cervical inflammatory myopathy associated with myasthenia gravis

Among idiopathic inflammatory myopathies (IIM), brachio-cervical inflammatory myopathy (BCIM) constitutes a rare entity basically characterized by progressive weakness in the proximal regions of the arms and neck, the frequent association with other autoimmune diseases, and peculiar histopathological features at muscle biopsy. A 57-year-old woman presented with a 1-yr history of weight loss (-10kg), cervicalgia, bulbar signs and weakness in upper limbs. Clinical examination showed drop head with cervical muscle atrophy, severe proximal muscle weakness in upper limbs and nasal voice with swallowing disorders. No sign of scleroderma. Biological assessment disclosed increased CK serum levels and anti-AChR and anti-Scl autoantibodies. EMG showed myogenic changes in upper limbs but no decrement. Deltoid muscle biopsy revealed type-II fiber atrophy, randomly distributed active myonecrosis, and nodular inflammatory infiltrates, mainly perivascular. Immunohistochemical techniques showed ubiquitous myofiber expression of major histocompatibility complex (MHC)-class I and multifocal MHC-II-expressing myofibers. B-cells (CD20) were majority in infiltrates. C5b-9 immunostaining showed deposition in endomysium and capillaries walls. Significant clinical improvement was observed under medical treatment (anticholinesterase, corticosteroid, immunoglobulin and rituximab), ventilatory and nutritional support. Present case enlightened the specificities of BCIM, including (i) the remarkable distribution of muscle deficit, (ii) the frequent association with myasthenia gravis, and (iii) the highly recognizable histopathological pattern with active myopathy, C5b-9 staining of endomysium, focal perivascular and perimysial inflammation often with a prominent B cell component. Treatment is usually modeled on that of IIM, but considering histopathological features and the association with myasthenia, BCIM could constitute a privileged indication for anti-CD20 biotherapy.

Mechanism of Ursolic Acid Inhibiting Myocardial Injury in Mice

Ursolic acid can clear free radicals and prevent the formation of non-enzymatic glycosylation products. Our study assessed the inhibitory effect of UA on the myocardial tissue of mice. 36 healthy mice were equally and randomly divided into 3 groups by double blind method, sham operation group, model group and ursolic acid group. Myocardial injury model was established and treated with ursolic acid followed by analysis of cell morphological structure and apoptosis; levels of serum CK, AST, LDH activity and IL-6, IL-1β and TNF-α levels, as well as expression of p-AKT, AKT and PI3K in myocardial tissue. The morphological structure and apoptosis of ursolic acid group were improved compared to model group (P &lt; 0.05). CK, AST, LDH, p-AKT and PI3K level in serum of ursolic acid group was significantly decreased (P &lt;0.05) along with significantly downregulate IL-6, IL-1β, TNF-α (P &lt;0.05). Ursolic acid ameliorates myocardial injury in mice possibly through inhibition of AKT/P13K signaling pathway to reduce inflammatory cascade in the body.

Functional Outcome and Inflammatory Response of Patients with Extra-Articular Distal Humeral Fractures following Implantation of Anatomically Precontoured Locking Compression Plates through a Posterior Approach.

Distal humeral fractures are challenging injuries to surgically correct and account for up to 2% of all adult fractures. Surgical management of extra-articular distal humeral fractures is challenging considering surgical approach, implant selection, and position of the implant owing to the availability of different precontoured implants and plate configurations. Anatomically precontoured locking compression plates (APLCPs) allow the placement of angular stable screws right underneath the reduced joint surface fragments. To date, there is a lack of evidence supporting its superiority to conventional locking plate osteosynthesis (LPO) in treating extra-articular distal humeral fractures. The objective of the study is to evaluate the efficacy and safety of APLCPs in the treatment of extra-articular distal humeral fractures. A total of 100 patients diagnosed with humeral fractures and receiving treatments in our hospital between May 2018 and May 2020 fulfilled inclusion and exclusion criteria and were randomly assigned to LPO and APLCP groups according to the odd-even of the order of hospital admission, 50 cases per groups. Clinical endpoints were assessed including operation time; in-bed time; length of hospital stay; volume of intraoperative blood loss; VSA scores before and 24, 48, and 72 h after surgery; MEPS scores before and 3, 6, and 12 months after surgery; range of motion, flexion, and extension of the elbow; serum levels of CK, CRP, and IL-6; and incidence of complications after surgery. It was found that the APLCP group exhibited shortened operation time and in-bed time, decreased length of hospital stay, and reduced volume of intraoperative blood loss compared to the LPO group (all P < 0.001). The two groups had declined VSA scores concomitant with increased MEPS scores after surgery in a time-dependent manner (P < 0.001). Notably, the VSA scores in the APLCP group were all lower than those in the LPO group at indicated time points (24, 48, and 72 h) after surgery (P < 0.001). Besides, the MEPS scores in the APLCP group were all higher than those in the LPO group at indicated time points (3, 6, and 12 months) after surgery (P < 0.001). It was revealed that the patients receiving extra-articular distal humeral APLCP through posterior approaches exhibited greater ranges of motion, flexion, and extension of the elbow than those receiving LPO after surgery (P < 0.001). The patients receiving extra-articular distal humeral APLCP through posterior approaches exhibited lower serum levels of IL-6, CRP, and CK than those receiving LPO after surgery (IL-6: P=0.007, CRP: P=0.001, CK: P=0.001). The APLCP had a lower total incidence rate of complication than the LPO group (48.00% vs. 18.00%, P=0.003). In conclusion, these data support the notion that the implantation of anatomically precontoured APLCP through a posterior approach allows for improved functional outcomes and attenuated inflammatory response and prevents the incidence of postoperative complications compared to conventional LPO for internal fixation of extra-articular distal humeral fractures.