Childhood Mycoplasma pneumoniae: epidemiology and manifestation in Northeast and Inner Mongolia, China.

Mycoplasma pneumoniae (MP) is commonly detected in children. However, the epidemiological trends of MP in Northeast (NE) China are unclear. This retrospective study aimed to investigate the prevalence of MP infections in this understudied region. The clinical manifestations and bronchoscopic findings observed in hospitalized patients with severe Mycoplasma pneumoniae pneumonia (SMPP) were collected from comprehensive data obtained from six tertiary hospitals in NE and Inner Mongolian (IM) China, from 1 January 2017 to 31 December 2023. A total of 5,593,530 children who visited the outpatient and emergency departments, and 412,480 inpatient hospitalized children were included in the study. The positivity rate of MP immunoglobulin M (IgM) in the children who visited the outpatient and emergency departments varied from 7.80% to 10.12%, whereas that of MP infection in hospitalized children ranged from 27.18% to 30.10%. Children hospitalized for MP infection were mainly concentrated in the 1- to 4-year (41.39%) and 4- to 7-year (24.25%) age groups. Before 2020, the season with the highest incidence of MP was winter. After the implementation of non-pharmaceutical interventions (NPIs), the MP epidemic season changed, and the number of children with MP infections decreased; however, the proportion of MP infections in hospitalized children did not change significantly. Starting from August 2023, the MP infection rate in outpatient, emergency, and hospitalized children increased sharply, with SMPP and its complications (e.g., plastic bronchitis and pleural effusion) increasing significantly. MP is prevalent in NE and IM, China. When the NPIs ended, MP infection showed a delayed outbreak trend, and the number of children with severe infection increased significantly. IMPORTANCE: In Northeastern (NE) and Inner Mongolia (IM), the incidence of Mycoplasma pneumoniae (MP) infections, including severe Mycoplasma pneumoniae pneumonia (SMPP), is high, posing health risks and imposing substantial economic burdens on the local population. Therefore, it is imperative to prioritize the study of MP prevalence and address the research gaps in MP epidemiology in these areas of China. We obtained a comprehensive collection of pediatric outpatient, emergency, and inpatient data from six public Grade III hospitals. We believe that our study makes a significant contribution to the literature because understanding regional variations in MP infections can help healthcare professionals tailor prevention and treatment strategies, and studying bronchoscopic manifestations can provide insights into the impact of the disease on the respiratory system, potentially leading to a more effective clinical management.

The structural and functional properties of soybean protein-polyglutamic acid complex effected the stability of W/O/W emulsion encapsulated Nattokinase.

Nattokinase (NK) derived from food is a sustainable thrombolytic agent. In this study, to protect vulnerable biological activity of NK, the targeted modified W/O/W emulsions were fabricated from complexes of soybean isolate protein (SPI) and polyglutamic acid (PGA). The results showed that the SPI-PGA complex formed a tighter internal structure through non-covalent bonds. The secondary structure, α-helix and ß-sheet content of the 1:3 (v/v) ratio complex of SPI to PGA increased by 6.14% and 8.62%, respectively. The emulsification and stability of the complexes were improved by refining structural properties as against SPI. The W/O/W emulsions coated by complexes formed the stronger network structure with higher encapsulation efficiency, better interfacial features, and better storage stability. Moreover, the highest bioavailability was achieved by W/O/W emulsions coated with 1:3 ratio complex at 80.69%. This study provided a new strategy towards tailoring ideal emulsion vehicles and expanded the NK application in food formulations.

Effects of Bacillus subtilis BSNK-5-Fermented Soymilk on the Gut Microbiota by In Vitro Fecal Fermentation.

The gut microbiota of soymilk intervention is beneficial to maintaining human health. Bacillus subtilis fermented soymilk has brought much interest, due to its richness of thrombolytic nattokinase and the strain of potential probiotic properties. In this study, soymilk was fermented by B. subtilis BSNK-5, and the BSNK-5-fermented soymilk (SMF) on the production of short chain fatty acids (SCFAs) and the regulation of fecal microbiota was initially evaluated by in vitro fecal fermentation. SMF supplementation obviously increased the levels of SCFAs from 32.23 mM to 49.10 mM, especially acetic acid, propionic acid, and isobutyric acid. Additionally, SMF changed the composition and microbial diversity of gut microbiota. After 24 h of anaerobic incubation in vitro, SMF decreased the Firmicutes/Bacteroidota ratio favoring weight loss, increased Lachnospiraceae_UCG-004 and the other beneficial bacteria producing SCFAs, as well as suppressing pathogenic Streptococcus genus. These results revealed the potential use of BSNK-5-fermented soymilk as a potential candidate to promote gut health.

Identification of molecular patterns and diagnostic biomarkers in juvenile idiopathic arthritis based on the gene expression of m6A regulators.

The role of N 6-methyladenosine modification in immunity is increasingly being appreciated. However, the landscape of m6A regulators in juvenile idiopathic arthritis (JIA) is poorly understood. Thus, this study explored the impact of m6A modification and related lncRNAs in JIA immune microenvironment. Fourteen m6A regulators and eight lncRNAs were identified as potential diagnostic biomarkers for JIA. Two diagnostic models for JIA were also constructed. The putative molecular regulatory mechanism of FTO-mediated m6A modification in JIA was hypothesized. Three distinct m6A patterns mediated by 26 m6A regulators and three diverse lncRNA clusters mediated by 405 lncRNAs were thoroughly investigated. They exhibited dramatically diverse immune microenvironments and expression of HLA genes. The identification of two separate subtypes of enthesitis-related arthritis implies that our work may aid in the establishment of a more precise categorization system for JIA. m6A modification-related genes were obtained, and their underlying biological functions were explored. The m6Ascore system developed for individual JIA patients may be utilized to evaluate the immunological state or molecular pattern, thereby offering therapy recommendations. In short, through the investigation of the m6A regulators in JIA, the current work may contribute to our knowledge of the pathophysiology of JIA.

Recent Advances in Nattokinase-Enriched Fermented Soybean Foods: A Review.

With the dramatic increase in mortality of cardiovascular diseases (CVDs) caused by thrombus, this has sparked an interest in seeking more effective thrombolytic drugs or dietary nutriments. The dietary consumption of natto, a traditional Bacillus-fermented food (BFF), can reduce the risk of CVDs. Nattokinase (NK), a natural, safe, efficient and cost-effective thrombolytic enzyme, is the most bioactive ingredient in natto. NK has progressively been considered to have potentially beneficial cardiovascular effects. Microbial synthesis is a cost-effective method of producing NK. Bacillus spp. are the main production strains. While microbial synthesis of NK has been thoroughly explored, NK yield, activity and stability are the critical restrictions. Multiple optimization strategies are an attempt to tackle the current problems to meet commercial demands. We focus on the recent advances in NK, including fermented soybean foods, production strains, optimization strategies, extraction and purification, activity maintenance, biological functions, and safety assessment of NK. In addition, this review systematically discussed the challenges and prospects of NK in actual application. Due to the continuous exploration and rapid progress of NK, NK is expected to be a natural future alternative to CVDs.

Recent Advances in Microbial Synthesis of Poly-γ-Glutamic Acid: A Review.

Poly-γ-glutamic acid (γ-PGA) is a natural, safe, non-immunogenic, biodegradable, and environmentally friendly glutamic biopolymer. γ-PGA has been regarded as a promising bio-based materials in the food field, medical field, even in environmental engineering field, and other industrial fields. Microbial synthesis is an economical and effective way to synthesize γ-PGA. Bacillus species are the most widely studied producing strains. γ-PGA biosynthesis involves metabolic pathway of racemization, polymerization, transfer, and catabolism. Although microbial synthesis of γ-PGA has already been used extensively, productivity and yield remain the major constraints for its industrial application. Metabolic regulation is an attempt to solve the above bottleneck problems and meet the demands of commercialization. Therefore, it is important to understand critical factors that influence γ-PGA microbial synthesis in depth. This review focuses on production strains, biosynthetic pathway, and metabolic regulation. Moreover, it systematically summarizes the functional properties, purification procedure, and industrial application of γ-PGA.

Metabolomics Approaches for the Comprehensive Evaluation of Fermented Foods: A Review.

Fermentation is an important process that can provide new flavors and nutritional and functional foods, to deal with changing consumer preferences. Fermented foods have complex chemical components that can modulate unique qualitative properties. Consequently, monitoring the small molecular metabolites in fermented food is critical to clarify its qualitative properties and help deliver personalized nutrition. In recent years, the application of metabolomics to nutrition research of fermented foods has expanded. In this review, we examine the application of metabolomics technologies in food, with a primary focus on the different analytical approaches suitable for food metabolomics and discuss the advantages and disadvantages of these approaches. In addition, we summarize emerging studies applying metabolomics in the comprehensive analysis of the flavor, nutrition, function, and safety of fermented foods, as well as emphasize the applicability of metabolomics in characterizing the qualitative properties of fermented foods.

SGK1 enhances Th9 cell differentiation and airway inflammation through NF-κB signaling pathway in asthma.

This study aimed to explore the effect of Sgk1 on Th9 differentiation and the underlying mechanism in asthma. The asthmatic mouse model induced by ovalbumin (OVA) and CD4+T cells which were cultured with TGF-ß, IL-2, IL-4, and anti-IFN-γ were applied in vivo and in vitro, respectively. Flow cytometry, quantitative real-time PCR (qRT-PCR), and ELISA were performed to detect T-helper 9 (Th9) cells, IL-9 expression, and IL-9 release. Western blot was performed to examine phosphorylated(p)-IKKα, p-IκBα, p-p65, and IRF4 levels. Hematoxylin/eosin (H&E) staining was adopted to assess pathological changes of lung tissues. Inhibition of Sgk1 dramatically reversed elevated Th9 cells and IL-9 expression in the lung tissues of asthmatic mice. In vitro, Sgk1 promoted Th9 differentiation and elevated p-IKKα, p-IκBα, p-p65, and IRF4 levels, but inhibition of IKKα/IκBα/p65 pathway and IRF4 both reversed enhanced Th9 differentiation by Sgk1. Sgk1→IKKα/IκBα/NF-κBp65→IRF4→Th9 axis may be implicated in asthma development.

Exogenous H2S switches cardiac energy substrate metabolism by regulating SIRT3 expression in db/db mice.

Hydrogen sulfide (H2S) is involved in diverse physiological functions, such as anti-hypertension, anti-proliferation, regulating ATP synthesis, and reactive oxygen species production. Sirtuin 3 (SIRT3) is a NAD + -dependent deacetylase that regulates mitochondrial energy metabolism. The role of H2S in energy metabolism in diabetic cardiomyopathy (DCM) may be related to regulate SIRT3 expression; however, this role remains to be elucidated. We hypothesized that exogenous H2S could switch cardiac energy metabolic substrate preference by lysine acetylation through promoting the expression of SIRT3 in cardiac tissue of db/db mice. Db/db mice, neonatal rat cardiomyocytes, and H9c2 cell line with the treatment of high glucose, oleate, and palmitate were used as animal and cellular models of type 2 diabetes. Using LC-MS/MS, we identified 76 proteins that increased acetylation, including 8 enzymes related to fatty acid ß-oxidation and 7 enzymes of the tricarboxylic acid (TCA) cycle in the db/db mice hearts compared to those with the treatment of NaHS. Exogenous H2S restored the expression of NAMPT and the ratio of NAD+/NADH enhanced the expression and activity of SIRT3. As a result of activation of SIRT3, the acetylation level and activity of fatty acid ß-oxidation enzyme LCAD and the acetylation of glucose oxidation enzymes PDH, IDH2, and CS were reduced which resulted in activation of PDH, IDH2, and CS. Our finding suggested that H2S induced a switch in cardiac energy substrate utilization from fatty acid ß-oxidation to glucose oxidation in DCM through regulating SIRT3 pathway. KEY MESSAGES: H2S regulated the acetylation level and activities of enzymes in fatty acid oxidation and glucose oxidation in cardiac tissues of db/db mice. Exogenous H2S decreased mitochondrial acetylation level through upregulating the expression and activity of SIRT3 in vivo and in vitro. H2S induced a switch in cardiac energy substrate utilization from fatty acid oxidation to glucose.

Exogenous H2S facilitating ubiquitin aggregates clearance via autophagy attenuates type 2 diabetes-induced cardiomyopathy.

Diabetic cardiomyopathy (DCM) is a serious complication of diabetes. Hydrogen sulphide (H2S), a newly found gaseous signalling molecule, has an important role in many regulatory functions. The purpose of this study is to investigate the effects of exogenous H2S on autophagy and its possible mechanism in DCM induced by type II diabetes (T2DCM). In this study, we found that sodium hydrosulphide (NaHS) attenuated the augment in left ventricular (LV) mass and increased LV volume, decreased reactive oxygen species (ROS) production and ameliorated H2S production in the hearts of db/db mice. NaHS facilitated autophagosome content degradation, reduced the expression of P62 (a known substrate of autophagy) and increased the expression of microtubule-associated protein 1 light chain 3 II. It also increased the expression of autophagy-related protein 7 (ATG7) and Beclin1 in db/db mouse hearts. NaHS increased the expression of Kelch-like ECH-associated protein 1 (Keap-1) and reduced the ubiquitylation level in the hearts of db/db mice. 1,4-Dithiothreitol, an inhibitor of disulphide bonds, increased the ubiquitylation level of Keap-1, suppressed the expression of Keap-1 and abolished the effects of NaHS on ubiquitin aggregate clearance and ROS production in H9C2 cells treated with high glucose and palmitate. Overall, we concluded that exogenous H2S promoted ubiquitin aggregate clearance via autophagy, which might exert its antioxidative effect in db/db mouse myocardia. Moreover, exogenous H2S increased Keap-1 expression by suppressing its ubiquitylation, which might have an important role in ubiquitin aggregate clearance via autophagy. Our findings provide new insight into the mechanisms responsible for the antioxidative effects of H2S in the context of T2DCM.

Post-traumatic stress disorder after typhoon disaster and its correlation with platelet 5-HT concentrations.

OBJECTIVE: To investigate residents' psychological stress factors and research the correlation between post-traumatic stress disorder (PTSD) and platelet 5-HT concentrations so as to provide scientific bases for diagnosis and treatment of PTSD and psychological intervention for people in the disaster area. METHODS: A questionnaire survey of 5500 residents who have accepted psychological help was conducted by the emphatic investigation method. While high performance liquid chromatography was used to detect the platelet serotonin concentration of 100 PTSD patients and 100 healthy people. RESULTS: (1) Of the 5114 cases, 3167 (61.93%) showed positive results in screening for psychological stress symptoms, and 399 (7.8%) were tested having apparent PTSD symptoms. Male and female prevalence showed no significant difference (χ(2) = -0.380, P = 0.704). The differences of prevalence between different age groups were statistically significant (χ(2) = 381.89, P = 0.000). (2) The differences in the level of platelet 5-HT between PTSD patients and normal control group were statistically significant. CONCLUSIONS: The typhoon of Hainan Province caused relatively large psychological problems to the disaster victims. Compared with normal control group, the platelet 5-HT levels of PTSD patients in the disaster areas are lower. It may be related to incidents exposure levels, cultural background, religious ideas, social concerns and psychological rescue of the residents who live in the disaster areas of Hainan.

Disruption of NF-κB signaling by fluoxetine attenuates MGMT expression in glioma cells.

BACKGROUND: Resistance to temozolomide (TMZ) in glioma is modulated by the DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT). This study aimed to examine the effects of fluoxetine (FLT) on MGMT expression in glioma cells and to investigate its underlying mechanisms. MATERIALS AND METHODS: Expression of MGMT, GluR1, or IκB kinase ß (IKKß) was attenuated using short hairpin RNA-mediated gene knockdown. The 3-(4,5-dimethylthiazol -2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to evaluate the growth inhibition induced by FLT or TMZ. Terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling (TUNEL) was conducted to detect apoptotic cells. Western blotting was conducted to analyze the protein expression of MGMT, IKKß, and NF-κB/p65 following FLT treatment. The murine subcutaneous xenograft model was used to evaluate the combinational effect of TMZ and FLT. RESULTS: FLT markedly reduced MGMT expression in glioma cells, which was independent of GluR1 receptor function. Further, FLT disrupted NF-κB/p65 signaling in glioma cells and consequently attenuated NF-κB/p65 activity in regulating MGMT expression. Importantly, FLT sensitized MGMT-expressing glioma cells to TMZ, as FLT enhanced TMZ's ability to impair the in vitro tumorigenic potential and to induce apoptosis in glioma cells. Knockdown of MGMT or IKKß expression abolished the synergistic effect of FLT with TMZ in glioma cells, which suggested that FLT might sensitize glioma cells to TMZ through down-regulation of MGMT expression. Consistently, TMZ combined with FLT markedly attenuated NF-κB/p65 activity, reduced MGMT expression, and suppressed in vivo tumor growth in the murine subcutaneous xenograft model. CONCLUSION: Our findings demonstrated that FLT attenuated MGMT expression by disrupting NF-κB signaling and sensitized glioma cells to TMZ, which may warrant further investigation toward possible clinical application in MGMT-expressing glioma.

Nicorandil protects against ischaemia-reperfusion injury in newborn rat kidney.

Ischaemia-reperfusion injury (IRI) is the predominant cause of acute kidney injury. Nevertheless, the underlying molecular mechanisms are still unclear. The current study investigated the effects of nicorandil on ATP-sensitive potassium (KATP) channels and the potential signal transduction pathway(s) in a rat kidney IRI model and in cultured tubular HK-2 cells subjected to oxygen and glucose deprivation/reoxygenation (OGD/R) injury. The standard procedure for IRI was performed in newborn rat kidneys. Pretreatment with nicorandil (10 mg/kg) 2 h prior to induction of IRI improved renal function, attenuated tubule damage, and prevented apoptosis of tubule cells, infiltration of neutrophils and macrophages, and production of inflammatory cytokines interleukin (IL)-6, IL-17 and tumour necrosis factor-α. Ischaemia-reperfusion-induced reduction of KIR6.2 was restored to normal levels by nicorandil. The activation of the phosphoinositide-3-kinase (PI3K)-Akt-nuclear factor (NF)-κB axis was detected in this rat kidney IRI model, which was blocked by nicorandil. The renoprotection of nicorandil against IRI was abolished by its inhibitor glibenclamide (1 mg/kg). Similar results were obtained in OGD/R-damaged HK-2 cells. Taken together, our findings demonstrated the specific renoprotective role of nicorandil in the newborn rat IRI kidney by decreasing the production of inflammatory cytokines, and restoring the expression of KIR6.2 potentially through the PI3K-Akt-NF-κB axis.

Activation of integrin ß1-focal adhesion kinase-RasGTP pathway plays a critical role in TGF beta1-induced podocyte injury.

The depletion of glomerular podocytes is the key mechanism of glomerulosclerosis and progressive renal failure. Transforming growth factor-ß (TGFß) is a central mediator of signaling networks that control a diverse set of cellular processes, such as cell proliferation, differentiation, and apoptosis. Though many key events in TGFß1 signaling have been documented at cellular and molecular level in podocytes, the complete effects of TGFß1 on podocyte integrity are still elusive. In this study, the function of adhesion protein integrin ß1, focal adhesion kinase (FAK), and a small GTPase Ras was explored in TGFß1-induced podocyte injury. In cultured mouse podocyte, caspase 3-positive cells were counted by flow cytometry to evaluate podocyte damage at different time points after TGFß1 treatment. Immunoblotting assay showed that integrin ß1, FAK, Src kinase, and an adaptor protein Grb2 were activated rapidly after TGFß1 stimulation. Active Ras Pull-Down assay revealed that the active Ras (GTP-bound Ras) level was upregulated in TGFß1-treated cell. Immunoprecipitation results displayed that TGFß1 enhanced the complex formation of integrin ß1, FAK and Src kinase, as well as FAK, Grb2 and Ras. The FAK inhibitor TAE226 and the specific knockdown of Grb2 remarkably alleviated TGFß1-induced podocyte apoptosis. The activation of p38MAPK and Erk1/2, and the nuclear translocation of NFκB(p65) were increased evidently in TGFß1-treated cell, which could be dramatically prohibited by the application of the p38MAPK inhibitor SB202190 and the Ras inhibitor FPT Inhibitor III. The Src kinase inhibitor PP2 obviously prevented the activation of FAK and Ras, as well as the translocation of NFκB(p65) from cytoplasm to nuclei. The PP2, FPT Inhibitor III, and SB202190 significantly decreased TGFß1-induced podocyte apoptosis. Taken together, these data demonstrated that the activation of integrin ß1/Src/FAK and Grb2/RasGTP should be responsible for TGFß1-induced podocyte damage through the p38MAPK and Erk1/2-mediated nuclear translocation of NFκB(p65).

ApoER2 and VLDLR in the developing human telencephalon.

The Reelin-Dab1 signaling pathway plays a crucial role in regulating the migration and position of cortical neurons during the development of the cerebral cortex. Mutation in Reelin may result in severe developmental disorders such as autosomal recessive lissencephaly. Apolipoprotein E receptor type-2 (ApoER2) and very low-density lipoprotein receptor (VLDLR) are canonical receptors of Reelin, through which extracellular Reelin activates the intracellular adapter, Disabled1(Dab1), and subsequently interacts with other molecules. Although it is widely accepted that ApoER2 and VLDLR are indispensable components of the Reelin signaling pathway, little is known of their expression pattern in the laminated developing human brain. Here, we collected 18 cases of human fetal brains of 6-18 gestational weeks (GW) old and examined the expression of ApoER2 and VLDLR in the their telencephalon using immunocytochemical staining. We found that both receptors were absent in the preplate (PP) and the earliest stage of the cortical plate (CP). In later stages of CP development, ApoER2 was expressed earlier than VLDLR in the migrating neurons. Thus, the Reelin-Dab1 signaling pathway may not be involved in the formation of the preplate and deep layers of the CP. Instead, the pathway may act on neurons that are destined to form the more superficial layers of the CP. In addition, the pathway required ApoER2 only rather than both ApoER2 and VLDLR at the initiation of activity.

Calcium-sensing receptors regulate cardiomyocyte Ca2+ signaling via the sarcoplasmic reticulum-mitochondrion interface during hypoxia/reoxygenation.

Communication between the SR (sarcoplasmic reticulum, SR) and mitochondria is important for cell survival and apoptosis. The SR supplies Ca2+ directly to mitochondria via inositol 1,4,5-trisphosphate receptors (IP3Rs) at close contacts between the two organelles referred to as mitochondrion-associated ER membrane (MAM). Although it has been demonstrated that CaR (calcium sensing receptor) activation is involved in intracellular calcium overload during hypoxia/reoxygenation (H/Re), the role of CaR activation in the cardiomyocyte apoptotic pathway remains unclear. We postulated that CaR activation plays a role in the regulation of SR-mitochondrial inter-organelle Ca2+ signaling, causing apoptosis during H/Re. To investigate the above hypothesis, cultured cardiomyocytes were subjected to H/Re. We examined the distribution of IP3Rs in cardiomyocytes via immunofluorescence and Western blotting and found that type 3 IP3Rs were located in the SR. [Ca2+]i, [Ca2+]m and [Ca2+]SR were determined using Fluo-4, x-rhod-1 and Fluo 5N, respectively, and the mitochondrial membrane potential was detected with JC-1 during reoxygenation using laser confocal microscopy. We found that activation of CaR reduced [Ca2+]SR, increased [Ca2+]i and [Ca2+]m and decreased the mitochondrial membrane potential during reoxygenation. We found that the activation of CaR caused the cleavage of BAP31, thus generating the pro-apoptotic p20 fragment, which induced the release of cytochrome c from mitochondria and the translocation of bak/bax to mitochondria. Taken together, these results reveal that CaR activation causes Ca2+ release from the SR into the mitochondria through IP3Rs and induces cardiomyocyte apoptosis during hypoxia/reoxygenation.

Calcium-sensing receptors induce apoptosis in rat cardiomyocytes via the endo(sarco)plasmic reticulum pathway during hypoxia/reoxygenation.

The calcium-sensing receptor (CaR) is a G protein-coupled receptor. The CaR stimulation elicits phospholipase C-mediated inositol triphosphate formation, leading to an elevation in the level of intracellular calcium released from endoplasmic reticulum (ER). Depletion of ER Ca(2+) leads to ER stress, which is thought to induce apoptosis. Intracellular calcium overload-induced apoptosis in cardiac myocytes during hypoxia-reoxygenation (H/Re) has been demonstrated. However, the links between CaR, ER stress and apoptosis during H/Re are unclear. This study hypothesized that the CaR could induce apoptosis in neonatal rat cardiomyocytes during H/Re via the ER stress pathway. Neonatal rat cardiomyocytes were subjected to 3 hr of hypoxia, followed by 6 hr of reoxygenation. CaR expression was elevated and the number of apoptotic cells was significantly increased, as shown by transferase-mediated dUTP nick end-labelling, with exposure to CaCl(2), a CaR activator, during H/Re. The intracellular calcium concentration was significantly elevated and the Ca(2+) concentration in the ER was dramatically decreased during H/Re with CaCl(2); both intracellular and ER calcium concentrations were detected by laser confocal microscopy. Expression of GRP78 (glucose-regulated protein 78), the cleavage products of ATF6 (activating transcription factor 6), phospho-PERK [pancreatic ER kinase (PKR)-like ER kinase], the activated fragments of caspase-12, and phospho-JNK (c-Jun NH(2)-terminal kinase) were increased following exposure to CaCl(2) during H/Re. Our results confirmed that the activated CaR can induce cardiomyocyte apoptosis via ER stress-associated apoptotic pathways during H/Re.

[Numerical analysis of the anti-fracture intensity of packed and repaired tooth in different cavity capacities].

This study was aimed to assess the stress distribution of different capacity of class I cavity after composite resin filling. A three-dimensional finite element made of the maxillary second molar was constructed by spiral CT scan technology. Based on this model, stress distribution in tooth was analyzed before and after post-core restorations with 5 different capacities of class I cavity. When the circle triangle of class I cavities being under 50N vertical pressures, the cavity capacity increased from 3.3 mm to 3.7 mm, the maximum tensile stress values of the composite resin restorations being 3 times those of normal tooth, which were 14.872 MPa, 16.682 MPa and 17.589 MPa, 17.307 MPa and17.912 MPa. Obviously, the effect of different capacities of class I cavity on the maximum stress value enduring ability of teeth was samll, but in the analysis model, the enduring ability of teeth was reduced when the molars were filled with resin.

Multislice spiral computed tomography imaging in congenital inner ear malformations.

OBJECTIVE: The purpose of this study is to evaluate the usefulness of multislice spiral computed tomography (CT) in the diagnosis of congenital inner ear malformations. METHODS: Forty-four patients with sensorineural hearing loss were examined on a Somatom Sensation 16 (Siemens) CT scanner. The 3-dimensional reconstructions and multiplanar reformation (MPR) were performed using the volume-rendering technique (VRT) on the workstation. RESULTS: Of the 44 patients examined for this study, 25 patients were found to be normal and 19 patients (36 ears) were diagnosed with congenital inner ear malformations. Of the malformations, the axial, MPR, and VRT images can all display the site and degree in 33 of the ears. Volume-rendering technique images were superior to the axial images in displaying the malformations in 3 ears with small lateral semicircular canal malformations. The common malformations were Michel deformity (1 ear), common cavity deformity (3 ears), incomplete partition I (3 ears), incomplete partition II (Mondini deformity) (5 ears), vestibular and semicircular canal malformations (14 ears), enlarged vestibular aqueduct (16 ears, 6 of which had other malformations), and internal auditory canal malformation (8 ears, all accompanied by other malformations). CONCLUSIONS: Multislice spiral CT allows a comprehensively assessment of various congenital inner ear malformations through high-quality MPR and VRT reconstructions. Volume-rendering technique images can display the site and degree of the malformation 3-dimensionally and intuitionisticly. This is very useful to the cochlear implantation.

Comparative study on 16-slice CT coronary angiography vs conventional coronary angiography--a report of 38 cases.

The clinical application of 16-slice CT coronary angiography (CTCA) and the impact of plaques differently characterized on assessing coronary artery stenosis were evaluated. Thirty-eight patients with coronary artery disease diagnosed by conventional coronary angiography (CAG) underwent 16-slice CTCA (collimation: 16x0.75 mm; rotation time: 420 msec; kernel: 35f; effective current: 500 mAs; tube voltage: 120 kV). The interval between CTCA and CAG was within one month. CTCA was evaluated by consensus of two independent experienced radiologists unknowing CAG findings. Original images, maximum intensity projections and multiplanar reconstructions were used to assess coronary artery stenosis. For a determined plaque an attenuation value > or = 130 HU was considered as calcified, and <130 HU noncalcified. The plaques were then classified into significant calcification (extensive calcification), medium calcification (small isolated calcification) and noncalcification. The diagnostic accuracy of 16-slice CTCA findings as well as to detect > or = 50% stenoses caused by plaques was evaluated respectively regarding CAG as the standard of reference. In comparison with CAG findings, the sensitivity, specificity, positive and negative predictive value derived from CTCA for mild stenosis (<50%) were 72.7%, 38.5%, 50%, 62.5%, respectively; for moderate stenosis (50%-75%) 82.4%, 72.7%, 70%, 84.2%, respectively; and for severe coronary stenosis (>75%) 85%, 90.5%, 81%, 92.7% respectively. With the increase of stenoses degree, the value of CTCA was greater. For the classification of the plaque calcification with > or = 50% stenosis CTCA attained the sensitivity, specificity, positive and negative predictive value for severe calcification 73.3%, 22.2%, 61.1% and 33.3%, respectively; for moderate calcification 70%, 55.6%, 63.6% and 62.5%, respectively; for noncalcification 93.8%, 85.7%, 93.8% and 85.7% respectively. CTCA was restricted in assessing coronary artery stenosis in the presence of calcification, but CTCA value was much improved in assessing non-calcified stenosis. It was concluded that 16-slice CTCA could provide useful information about coronary artery stenosis, especially for severe stenosis > or = 50%) and non-calcified plaque. Since CTCA is a noninvasive technique, it may be useful in screening coronary artery disease.