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Key Clinical Message: Maxillary canines are often impacted, which can result in tooth disorders and adversely affect occlusal and facial development. The case report describes complete bilateral impaction of maxillary canines and significant root resorption of a central incisor. The multidisciplinary approach is the optimal strategy for addressing impacted maxillary canines. [ABSTRACT FROM AUTHOR]

Deep learning is applied to many complex tasks in the field of wireless communication, such as modulation recognition of spectrum waveforms, because of its convenience and efficiency. This leads to the problem of a malicious third party using a deep learning model to easily recognize the modulation format of the transmitted waveform. Some existing works address this problem directly using the concept of adversarial examples in the computer vision field without fully considering the characteristics of the waveform transmission in the physical world. Therefore, we propose two low‐interception waveforms (LIWs) generation methods, the LIW and ULIW algorithms, which can reduce the probability of the modulation being recognized by a third party without affecting the reliable communication of the friendly party. Among them, ULIW improves LIW algorithm by simulating channel noise during training cycle, and substantially reduces the perturbation magnitude while maintaining low interception accuracy. Our LIW and ULIW exhibit significant low‐interception performance in both numerical simulations and hardware experiments. Key Points: Define the low‐interception question, and give the mathematical model, application scenarios, and evaluation criteriaPropose the ULIW algorithm based on our LIW algorithm, which substantially reduces perturbation while maintaining low interception accuracyVerify the low‐interception performance of LIW and ULIW in both the digital and physical worlds [ABSTRACT FROM AUTHOR]

Objective: Seizures are a common clinical presentation in patients with glioma and substantially impact patients' quality of life. Hyperhomocysteinemia is defined as abnormally high serum levels of homocysteine (Hcy) and is reportedly linked to susceptibility to various nervous system diseases. However, it remains unclear whether and how hyperhomocysteinemia and its associated genetic polymorphisms promote seizures in glioma patients. Methods: We retrospectively reviewed all medical data from 127 patients with malignant gliomas, who underwent initial tumor resection by our team between July 2019 and June 2021 and had preoperative measurements of serum Hcy levels. According to whether they had at least one seizure before surgery, they were divided into the seizure and nonseizure groups. We also detected polymorphisms in the methylenetetrahydrofolate reductase (MTHFR) gene and measured intratumoral Hcy levels in these patients. Results: Hyperhomocysteinemia was a susceptibility factor for preoperative seizures in glioma patients according to both univariate analyses (P < 0.001) and multivariate logistic regression analyses (OR 1.239, 95% CI 1.062–1.445, P = 0.007). Patients with the MTHFR C677T variant exhibited elevated serum Hcy levels (P = 0.027) and an increased prevalence of preoperative seizures (P = 0.019). Intratumoral Hcy levels were positively correlated with serum Hcy levels (R = 0.231, P = 0.046) and were elevated in patients with hyperhomocysteinemia (P = 0.031), the MTHFR C677T variant (P = 0.002) and preoperative seizures (P = 0.003). High intratumoral Hcy levels, rather than hyperhomocysteinemia or the MTHFR C677T variant, emerged as an independent risk factor for preoperative seizures (OR 1.303, 95% CI 1.015–1.673, P = 0.038). Furthermore, the effects of hyperhomocysteinemia on epileptic susceptibility were reduced to nonsignificance when intratumoral Hcy was controlled to the same level between groups. Significance: Glioma patients with hyperhomocysteinemia and the MTHFR C677T variant were susceptible to preoperative seizures, suggesting their potential as biomarkers for the management of seizures in glioma patients. The elevation of intratumoral Hcy is a possible mechanism underlying this susceptibility. [ABSTRACT FROM AUTHOR]

The chemical interactions between thorium(IV) and O2- in the LiF-BeF2 (2 : 1 mol%) (FLiBe) and LiF-NaF-KF (46.5 : 11.5 : 42 mol%) (FLiNaK) molten salt systems were studied at 873 K. The precipitation-dissolution behavior of Th(IV) oxide/oxyfluoride species, as well as the speciation law of these species and their relationship with oxide concentration in fluoride melts, were clarified. The results showed that the interactions between Th(IV) and O2- in the FLiBe melt would only produce ThO2. The saturated solubility of ThO2 in the FLiBe melt was 0.057 mol/kg, and its corresponding apparent solubility product ( K s p ′ ) was 8.8 ± 0.1 × 10 − 4 mol3/kg3 and 8.6 ± 0.7 × 10 − 4 mol3/kg3 by dissolution and oxide titration methods, respectively. However, in the FLiNaK melt, the interactions between Th(IV) and O2- were more complex than that in FLiBe, and Th(IV) oxyfluoride species (i.e., Th2OF104- and ThOF2) were produced. Th2OF104- was initially formed with the ratio of r ≤ 0.5 (r = O 2 − added / Th IV initial ), and the Th2OF104- was converted to ThOF2 precipitate when r > 0.5. Therefore, the soluble Th2OF104- is the important intermediate between Th(IV), O2-, and ThOF2 precipitation. The difference in results of the FLiBe and FLiNaK melts was attributed to the difference of free F- content in the two systems. The present work provided important reference and fundamental data for understanding the nature of thorium fuel precipitation and how to control it in the molten fluoride media, which is of significant importance for the safe operation of molten salt reactor (MSR). [ABSTRACT FROM AUTHOR]

A novel self‐healing poly(vinyl alcohol) (PVA)‐based hydrogel is developed by cross‐linking PVA chains through multi dynamic covalent bonds by use of a small cross‐linker composed by 4‐formylphenylboric acid (FPBA) and lysine (Lys). The dynamic borate‐imine‐imine‐borate bond structure between PVA chains endows the hydrogel excellent stretchability and ultra‐fast self‐healing ability without external stimulation. The self‐healing efficiency can attain 94% and the elongation at break can reach up to near 1000% after only 3 min healing. Moreover, the self‐healing of the hydrogel through the contact of two faces from both the same cut position and different cut positions has similar excellent efficiency. The hydrogel with the unusual self‐healing performance and stretchability is used as an ideal material in strain sensors monitoring human movement and tiny vibrations caused by human voice. Interestingly, the sensor can continue to function normally after self‐healing for only ≈3 s. It is expected that this simple strategy of fabricating self‐healing hydrogels with multi dynamic bonds will provide new opportunities in the design and preparation of PVA‐based hydrogels to expand their potential applications in sensors and other various fields. [ABSTRACT FROM AUTHOR]

Introduction: Glioblastoma (GBM) is the most malignant form of glioma and has a poor median survival time. Fibroblast activation protein alpha (FAP) is a dual‐specificity serine protease that is strongly associated with the development and progression of human carcinomas. However, relatively little is known about the function of FAP and its potential as a therapeutic target in GBMs. Aims: In this study, we aimed to explore the role of FAP in GBM through a series of experiments and to evaluate the therapeutic effect of PT100, a small molecule inhibitor of FAP, on GBM. Results: Increased FAP expression was associated with poor survival in glioma. In vitro, FAP knockdown inhibited the process of EMT and caused a decrease in the number of M2 macrophages. In vivo, PT100 was confirmed to suppress the progression of GBMs significantly. Conclusions: FAP could serve as a biomarker and novel therapeutic target for the treatment of GBM and that PT100 is a promising drug for the treatment of GBM. [ABSTRACT FROM AUTHOR]

Inflammasomes are a group of multiprotein signaling complexes located in the cytoplasm. Several inflammasomes have been identified, including NLRP1, NLRP2, NLRP3, AIM2, and NLRC4. Among them, NLRP3 was investigated in most detail, and it was reported that it can be activated by many different stimuli. Increased NLRP3 protein expression and inflammasome assembly lead to caspase‐1 mediated maturation and release of IL‐1β, which triggers inflammation and pyroptosis. The activation of the NLRP3 inflammasome has been widely reported in studies of tumors and neurological diseases, but relatively few studies on the cardiovascular system. Ventricular remodeling (VR) is an important factor contributing to heart failure (HF) after myocardial infarction (MI). Consequently, delaying VR is of great significance for improving heart function. Studies have shown that the NLRP3 inflammasome plays an essential role in the process of VR. Here, we reviewed the latest studies on the activation pathway of the NLRP3 inflammasome, focusing on the effects of the NLRP3 inflammasome in primary cells during VR, and finally discuss future research directions in this field. [ABSTRACT FROM AUTHOR]

Laser current and temperature control circuits have been developed for a distributed feedback laser diode, which is applied as the light source of a tuneable diode laser absorption spectroscopy system. The laser's temperature fluctuation can be limited within the range of −0.02 to 0.02°C, and good operation stability was observed through 15 hours of monitoring on the emitting wavelength of the laser. Response time of temperature modulation was tested which is suitable for the tuning requirements of gas detection systems. Laser current can be injected within the range from 40 to 80 mA. In addition, a linear power supply circuit has been developed to provide stable and low-noise power supply for the system. The physical principles of laser modulation theory are discussed before experiments. Experiments show that the output wavelength of the laser can be tuned accurately through changing the working current and temperature. The wavelength can be linearly controlled by temperature at 0.115 nm/°C (I = 70 mA) and be controlled by current at 0.0140 nm/mA (T = 25°C). This is essential for the tuneable diode laser absorption spectroscopy systems. The proposed cost-effective circuits can replace commercial instruments to drive the laser to meet the requirements of methane detection experiments. It can also be applied to detect other gases by changing the light source lasers and parameters of the circuits. [ABSTRACT FROM AUTHOR]

Supra‐maximum surgical tumor resection without neurological damage is highly valuable for treatment and prognosis of patients with glioblastoma multiforme (GBM). We developed a GBM‐specific fluorescence probe using IRDye800CW (peak absorption/emission, 778/795 nm) and bombesin (BBN), which (IRDye800‐BBN) targets the gastrin‐releasing peptide receptor, and evaluated the image‐guided resection efficiency, sensitivity, specificity, and survivability. Twenty‐nine patients with newly diagnosed GBM were enrolled. Sixteen hours preoperatively, IRDye800‐BBN (1 mg in 20 ml sterile water) was intravenously administered. A customized fluorescence surgical navigation system was used intraoperatively. Postoperatively, enhanced magnetic resonance images were used to assess the residual tumor volume, calculate the resection extent, and confirm whether complete resection was achieved. Tumor tissues and nonfluorescent brain tissue in adjacent noneloquent boundary areas were harvested and assessed for diagnostic accuracy. Complete resection was achieved in 82.76% of patients. The median extent of resection was 100% (range, 90.6–100%). Eighty‐nine samples were harvested, including 70 fluorescence‐positive and 19 fluorescence‐negative samples. The sensitivity and specificity of IRDye800‐BBN were 94.44% (95% CI, 85.65–98.21%) and 88.24% (95% CI, 62.25–97.94%), respectively. Twenty‐five patients were followed up (median, 13.5 [3.1–36.0] months), and 14 had died. The mean preoperative and immediate and 6‐month postoperative Karnofsky performance scores were 77.9 ± 11.8, 71.3 ± 19.2, and 82.6 ± 14.7, respectively. The median overall and progression‐free survival were 23.1 and 14.1 months, respectively. In conclusion, GBM‐specific fluorescent IRDye800‐BBN can help neurosurgeons identify the tumor boundary with sensitivity and specificity, and may improve survival outcomes. [ABSTRACT FROM AUTHOR]

Osteoclasts are responsible for bone destruction in rheumatoid arthritis (RA), and adipose‐derived mesenchymal stromal cells (ADSCs) can inhibit experimental collagen‐induced arthritis model. This study aims to determine whether ADSCs also suppresses osteoclastogenesis and bone erosion in collagen‐induced arthritis (CIA). Osteoclasts were induced from bone marrow‐derived CD11b+ cells with receptor activator of nuclear factor‐κ B ligand (RANKL) and macrophage colony‐stimulating factor (M‐CSF) stimulation and assessed with tartrate‐resistant acid phosphatase (TRAP) staining. For human cells, osteoclasts were produced from human CD14+ cells. ADSCs were generated and added to cultures with different ratios with CD11b+ cells. Transwell and antibody blockade experiments were performed to define the mechanism of action. NF‐κB and RANKL expression were determined by Western blotting and RT‐qPCR. About 2 × 106 ADSCs or fibroblast cells were adoptively transferred to DBA1/J mice on day 14 after immunization with type II collagen/complete Freund's adjuvant (CII/CFA) while the onset and severity of the CIA were monitored. Adipose‐derived mesenchymal stromal cells but not fibroblast cells completely suppressed osteoclastogenesis in vitro for human and mice. ADSCs injected after immunization and before of onset of CIA significantly suppressed disease development. Treatment with ADSCs dramatically decreased the levels of NF‐κB p65/p50 in osteoclasts in vitro and P65/50 and RANKL expression by synovial tissues in vivo. We have demonstrated that ADSCs can inhibit RANKL‐induced osteoclasts genesis via CD39 signals. Our findings also suggest that ADSCs can inhibit osteoclasts genesis without the involvement of regulatory T cells. ADSCs might represent a promising strategy for stem cell‐based therapies for RA. Thus, manipulation of ADSCs may have therapeutic effects on RA and other bone erosion–related diseases. [ABSTRACT FROM AUTHOR]

Steroid‐insensitive asthma‐related airway inflammation is associated with the expression of epidermal growth factor receptor (EGFR) tyrosine kinase in asthmatic bronchial epithelium. Proinflammatory cytokines IL‐6 and IL‐8 are related to steroid‐insensitive asthma. It is currently unknown how EGFR‐tyrosine kinase inhibitors (EGFR‐TKIs) affects house dust mite (HDM)‐induced asthma in terms of inflammatory cytokines related to steroid‐resistant asthma and further signaling pathway. Cytokine expressions and EGFR signaling pathway were performed by ELISA, reverse transcriptase PCR, real‐time PCR, and Western blot in cell‐line models. AMP‐activated protein kinase (AMPK) pathway‐related inhibitors were applied to confirm the association between EGFR‐TKI and AMPK pathway. HDM induced IL‐6 and IL‐8 in a dose‐dependent manner. Both Erlotinib (Tarceva) and Osimertinib (AZD‐9291) reduced the levels of HDM‐stimulated IL‐6 and IL‐8 levels in BEAS‐2B cells. AZD‐9291 was more effective than Erlotinib in inhibiting phospho‐EGFR, and downstream phosphatidylinositol‐3‐kinase/protein kinase B (PI3K/AKT) and phopho‐signal transducer and activator of transcription 3 (p‐STAT3) pathway signaling. In addition, AMPK pathway‐related inhibitor, Calcium‐/calmodulin‐dependent protein kinase kinase β (CaMKKβ) inhibitor, down‐regulated IL‐8, but EGFR‐TKI had no effect on AMPK pathway. Our findings highlight EGFR‐TKIs, Tarceva, and AZD‐9291, attenuate HDM‐induced inflammatory IL‐6 and IL‐8 cytokines via EGFR signaling axis pathway, but not AMPK signaling pathway. [ABSTRACT FROM AUTHOR]

Abstract: Background and Aims: No ideal therapeutic method currently exists for refractory idiopathic supraorbital neuralgia patients who do not respond to conservative therapy, including medications and nerve blocks. Pulsed radiofrequency is a neuromodulation technique that does not produce sequelae of nerve damage after treatment. However, the efficacy of percutaneous pulsed radiofrequency for the treatment of refractory idiopathic supraorbital neuralgia is still not clear. The purpose of our study was to evaluate the efficacy and safety of pulsed radiofrequency treatment of the supraorbital nerve for refractory supraorbital neuralgia patients. Methods: We prospectively investigated the long‐term effects of ultrasound‐guided percutaneous pulsed radiofrequency in the treatment of 22 refractory idiopathic supraorbital neuralgia patients. A reduction in the verbal pain numeric rating scale score of more than 50% was used as the standard of effectiveness. The effectiveness rates at different time points within 2 years were calculated. Results: After a single pulsed radiofrequency treatment, the effectiveness rate at 1 and 3 months was 77%, and the rates at 6 months, 1 year, and 2 years were 73%, 64%, and 50%, respectively. Except for a small portion of patients (23%) who experienced mild upper eyelid ecchymosis that gradually disappeared after approximately 2 weeks, no obvious complications were observed. Conclusions: In conclusion, the results of our study demonstrate that for patients with refractory idiopathic supraorbital neuralgia, percutaneous pulsed radiofrequency may be an effective and safe treatment choice. [ABSTRACT FROM AUTHOR]

We find that exchange rate networks are significantly similar from the perspective of topological structure, though with relatively great differences in fluctuation characteristics from perspective of exchange rate time series. First, we transform central parity rate time series of US dollar, Euro, Yen, and Sterling against CNY into exchange rate networks with visibility graph algorithm and find consistent topological characteristics in four exchange rate networks, with their average path lengths 5 and average clustering coefficients 0.7. Further, we reveal that all four transformed exchange rate networks show hierarchical structure and small-world and scale-free properties, with their hierarchy indexes 0.5 and power exponents 1.5. Both of the US dollar network and Sterling network exhibit assortative mixing features, while the Euro network and Yen network exhibit disassortative mixing features. Finally, we research community structure of exchange rate networks and uncover the fact that the communities are actually composed by large amounts of continuous time point fractions and small amounts of discrete time point fractions. In this way, we can observe that the spread of time series values corresponding to nodes inside communities is significantly lower than the spread of those values corresponding to nodes of the whole networks. [ABSTRACT FROM AUTHOR]

Background: TGFβ1 and Smad3 play an important role in the process of EMT. TGFβ1 regulates the expression of Jagged1 by modulating Notch signaling. Jagged1 is related to tumor invasion, metastasis, chemotherapy resistance, and tumor immune escape. The aims of this study are to examine deregulation of TGFβ1-Smad3-Jagged1-Notch1-Slug signaling in TSCC and to investigate its roles in TSCC progression.Materials and Methods: Notch1, Smad3, Jagged1 and Slug proteins and mRNA expression were detected in specimens from 89 cases of patients. We analyzed the correlation between their expressions and histological grade, clinical stage and lymph node metastasis.Results: Notch1, Smad3, Jagged1 and Slug mRNA expressions in TSCC were higher than normal tissue (P <0.05). The protein expression of Notch1 and Smad3 in TSCC were higher (χ(2) =7.30, P <0.01 and χ(2) = 5.84, P <0.05). Notch1 and Smad3 expressions were correlated with clinical stage (χ(2) =18.81, P<0.01; χ(2) =22.29, P<0.01), but not Jagged1 (χ(2) =0.53, P>0.05). The Slug protein expression was correlated with clinical stage. The positive rate of Notch1 was higher in lymph node metastases positive cases (χ(2) =7.30, P<0.01). Moreover, higher expression of Jagged1 was found in lymph node positive cases (χ(2) =10.82, P<0.01).Conclusions: The key protein expression in TGFβ1-Smad3-Jagged1-Notch1-Slug signaling pathway significantly correlated with the clinicopathological features of TSCC patients. It's potential as a biomarker and a novel therapeutic target for TSCC patients at risk of metastasis. It may play an irreplaceable role in TSCC progression which may attribute to promoting EMT which enhances cell migration, invasion and metastasis. [ABSTRACT FROM AUTHOR]

Objective. To explore the antiprostate cancer effects of Celastrol on prostate cancer cells’ proliferation, apoptosis, and cell cycle distribution, as well as the correlation to the regulation of hERG. Methods. DU145 cells were treated with various concentrations of Celastrol (0.25–16.0 μmol/L) for 0–72 hours. MTT assay was used to evaluate the inhibition effect of Celastrol on the growth of DU145 cells. Cell apoptosis was detected through both Annexin-V FITC/PI double-labeled cytometry and Hoechst 33258. Cell cycle regulation was examined by a propidium iodide method. Western blot and RT-PCR technologies were applied to assess the expression level of hERG in DU145 cells. Results. Celastrol presented striking growth inhibition and apoptosis induction potency on DU145 cells in vitro in a time- and dose-dependent manner. The IC50 value of Celastrol for 24 hours was 2.349 ± 0.213 μmol/L. Moreover, Celastrol induced DU145 cell apoptosis in a cell cycle-dependent manner, which means Celastrol could arrest DU145 cells in G0/G1 phase; accordingly, cells in S phase decreased gradually and no obvious changes were found in G2/M phase cells. Through transmission electron microscope, apoptotic bodies containing nuclear fragments were found in Celastrol-treated DU145 cells. Overexpression of hERG channel was found in DU145 cells, while Celastrol could downregulate it at both protein and mRNA level in a dose-dependent manner (P<0.01). Conclusions. Celastrol exhibits its antiprostate cancer effects partially through the downregulation of the expression level of hERG channel in DU145 cells, suggesting that Celastrol may be a potential agent against prostate cancer with a mechanism of blocking the hERG channel. [ABSTRACT FROM AUTHOR]

A new bifunctional titanium/Schiff base catalyst was developed for the enantioselective cyanoformylation of aldehydes with ethyl cyanoformate. The reaction proceeded smoothly with a mild reaction condition to afford the cyanohydrin ethyl carbonates in high yields (up to 96%) and good enantioselectivities (up to 85% enantiomeric excess). Copyright © 2013 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Background The changes in Notch signaling are closely related to the occurrence and development of many cancers. We have investigated Notch signaling receptor and its ligand expressions in TSCC cell lines, tissues and its significance. We clarified Notch signaling pathway in TSCC and its mechanism. We regulated Notch signaling pathway of tumor cells, thereby inhibiting tumor cell proliferation and differentiation. Methods We detected Jagged1 protein and mRNA expression levels in specimens (tongue cancer and adjacent tissues) from 74 patients with tongue cancer and in TSCC cell line. The Jagged1-targeted lentiviral vector RNAi system was constructed, and its suppressive effects on the proliferation and invasion of tongue carcinoma cells in in vivo and ex vivo were determined. Results Jagged1 was expressed in tongue squamous cell cancer tissues and cell line, but there were differences in its expression. Jagged1 was knocked down and the tumor growth was inhibited accompanying cell cycle changes. Animal studies also showed that the tumor growth was inhibited. Conclusions Jagged1 may be involved in the differentiation and proliferation of tongue cancer. Targeting Jagged1 RNA interference lentiviral vector can effectively lower Jagged1 mRNA and protein expression levels of Tca8113 cells, thereby preventing the proliferation of TSCC cells. Jagged1 is expected to be a promising new target for curing tongue cancer. In-depth study of the interaction between Jagged1 and other molecules of Notch signaling pathway in the process of carcinogenesis has important theoretical guidance and clinical significance in revealing the mechanism of Jagged1 and its application in the therapy for tongue cancer. [ABSTRACT FROM AUTHOR]

In this article, a surface-enhanced Raman scattering (SERS)-active substrate with great stability and usability is reported. It is composited with a two-dimensional ordered array of Ag spherical caps and an aluminum coating. The ordered aluminum template formed during the synthesis of anodic aluminum oxide film was used as the patterned matrix. After sputtering a Ag layer and then peeling off the aluminum template, the patterned structure was replicated on Ag layer. The aluminum template could serve as a coating that protected Ag from being oxidized. Ultraviolet-visible reflection measurement was performed to monitor the adsorption process of probing molecules. Taking 4-mercaptopyridine as probing molecules, SERS spectra were investigated. Comparing with the ordinary Ag film, the patterned Ag layer exhibited better SERS activity. The convenience for preparing, storing, and using makes it a promising candidate for SERS application in the fast field analysis. Copyright © 2012 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Background: The association between neonatal jaundice and childhood asthma is a new finding of two reports. The purpose of the study was to verify their results. Methods: Data from 11,321 children were collected from the National Health Insurance Research Database. Their claims data were evaluated from birth to 10 yr old. Children were analyzed as case (those with neonatal jaundice) and controls (those without neonatal jaundice). The diagnostic criteria for asthma were as follows: at least four asthma diagnoses at outpatient services and emergency department (ED), or one asthma diagnosis during an admission. In children fitting the asthma criteria, those with no asthma diagnosis after 1 yr of age were excluded. Mantel-Haenszel's odds ratios were calculated after adjustment for the following confounders: preterm/low birth weight, neonatal infection, other respiratory conditions, other birth conditions, and gender. Asthma rate, onset time, the use of drugs, upper respiratory infection and lower respiratory infection (LRI) rates, hospital admission/ED visit rates, and the effect of phototherapy were evaluated. Results: After adjustment for the confounding factors, the rate of asthma was higher in icteric children (OR: 1.64, 95% CI 1.36-1.98, p < 0.001), and the influence in females was stronger. There still was an association between neonatal jaundice and late onset asthma (asthma onset after 3 yr of age). In asthmatic children, those with neonatal jaundice have increased asthma onset rate before age 6, increased use of inhalant steroids, LRI rates, and ED visits for respiratory disease. Conclusions: Neonatal jaundice increased the rate and severity of childhood asthma in subjects aged up to 10 yr and may be a risk factor for childhood asthma. [ABSTRACT FROM AUTHOR]

A series of new modular bifunctional chiral thiourea organocatalysts were synthesized from natural Cinchona alkaloids and amino acids, and their performance in the aza-Henry reaction of nitroalkanes to imines, the Michael addition of acetylacetone to nitroolefins and the Michael addition of acetone to nitroolefins was investigated. Under the mild conditions, the important building blocks β-nitro amines and γ-nitro carbonyl compounds could be obtained in good yields (up to 95%) with excellent enantioselectivities (up to 99% ee) and diastereoselectivity (up to 17:1). [ABSTRACT FROM AUTHOR]

We have investigated CaMgO(CMO) film by E-beam(EB) and plasma gun(PG). By varying different deposition conditions, film show difference in contamination level, structure and discharge voltage characteristic. The film analysis is critical to develop manufacture process for high efficiency PDP with CMO. [ABSTRACT FROM AUTHOR]

Acute bacterial meningitis caused by Klebsiella pneumoniae ( K. pneumoniae) is a major health threat with a high mortality rate and severe neuro-cognitive sequelae. The intense pro-inflammatory cytokine released from calcium-mediated microglial activation plays an important role in eliciting neuronal damage in the hippocampal region. Considering melatonin possesses anti-inflammatory and immuno-modulatory properties, the present study determined whether melatonin can effectively decrease inflammatory responses and prevent hippocampal damage in animals subjected to K. pneumoniae. Adult rats inoculated with K. pneumoniae received a melatonin injection immediately thereafter at doses of 5, 25, 50, or 100 mg/kg. Following 24 h of survival, all experimental animals were processed for time-of-flight secondary ion mass spectrometry (for detecting glial calcium intensity), isolectin-B4 histochemistry (reliable marker for microglial activation), pro-inflammatory cytokine measurement as well as cytochrome oxidase and in situ dUTP end-labeling (representing neuronal bio-energetic status and apoptotic changes, respectively). Results indicate that in K. pneumoniae-infected rats, numerous calcium-enriched microglia, enhanced pro-inflammatory cytokine, and various apoptotic neurons with low bio-energetic activity were detected in hippocampus. Following melatonin administration, however, all parameters including glial calcium intensity, microglial activation, pro-inflammatory cytokine levels, and number of apoptotic neurons were successfully decreased with maximal change observed at a melatonin dose of 100 mg/kg. Enzymatic data corresponded well with above findings in which all surviving neurons displayed high bio-energetic activity. As effectively reducing glia-mediated inflammatory response is neuro-protective to hippocampal neurons, the present study supports the clinical use of melatonin as a potential therapeutic agent to counteract K. pneumoniae meningitis-induced neuro-cognitive damage. [ABSTRACT FROM AUTHOR]

Although the effects of coumestrol on osteoblasts and osteoclasts can be summarized as increasing the bone density and preventing bone resorption, direct and detailed effects of coumestrol on bone marrow stromal cells remain obscure. In the present study, the effects of coumestrol on proliferation and osteoblastic differentiation of rat bone marrow stromal cells (BMSCs) have been investigated; the regulative effect of coumestrol on BMSCs and skeletal system has also been discussed. The results showed that treatment with coumestrol increased cellular activities (analyzed by MTT assay), alkaline phosphatase (ALP), type I collagen and osteocalcin (OCN) activity as well as the protein and gene expression of OPG, gene expression ratio of OPG/RANKL and gene expression of estrogen receptor α(ERα). These results demonstrate that phytoestrogen coumestrol has a direct enhancing effect on the proliferation and osteogenic differentiation of bone marrow stromal cells, which would lead to stimulation of bone formation, and it can also protect the whole skeletal system by regulating OPG/RANKL expression, and these effects may be mediated by ERα. © 2009 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2009 [ABSTRACT FROM AUTHOR]

Aim: Acute pyelonephritis is a common infectious disease in children and can result in permanent renal damage. Interleukin (IL)-1β is an important inflammatory mediator that appears early during bacterial infection. This prospective study examined urine IL-1β levels in children with acute pyelonephritis documented by 99mTc-dimercaptosuccinic acid (DMSA) scan, and also evaluated whether this cytokine correlated with renal scarring. Methods: A total of 75 children aged 1–121 months with a diagnosis of first-time febrile urinary tract infection (UTI) were studied. The following inflammatory markers were assessed: fever, white blood cell (WBC), neutrophil, C-reactive protein (CRP) and urine IL-1β. Urine samples were collected for IL-1β measurement by enzyme-linked immunosorbent assay before and after antibiotic treatment of the infection. Follow-up DMSA scan was performed at 6–12 months after the acute pyelonephritis to detect renal scarring. Twenty children with other febrile illnesses served as non-renal febrile controls. Results: The 75 children were divided into acute pyelonephritis ( n = 41) and lower UTI ( n = 34) groups according to the findings of DMSA scans. Fever, WBC count, neutrophil count and CRP were significantly higher in the children with acute pyelonephritis than in those with lower UTI (all P < 0.001). The initial urine IL-1β levels of children with acute pyelonephritis were significantly higher when compared with lower UTI and non-renal febrile controls ( P < 0.001). Urine IL-1β in children with acute pyelonephritis was positively correlated with fever, CRP, WBC, neutrophil and leucocyturia. Renal scarring was found in 12 (29.3%) of the 41 children with acute pyelonephritis. The mean age was significantly lower in the children with renal scarring compared with those without ( P < 0.05). Conclusion: These results have shown that urine IL-1β level may serve as a useful marker for the early detection of acute pyelonephritis in febrile children. Young children are at a risk of the development of renal scarring following acute pyelonephritis. [ABSTRACT FROM AUTHOR]

Dysregulation of intracellular Ca2+ homeostasis plays an important role in mediating myocardial injury. We tested the hypothesis that treatment with trimetazidine (TMZ) would improve intracellular Ca2+ handling in myocardial injury of rats. The control group received saline only (10 ml kg−1 day−1,i.p.) for 7 days. In a second group, isoprenaline (ISO; 5 mg kg−1 day−1,s.c.) was administered to rats for 2 days to induce an acute injury of the myocardium. In a third group, treatment with TMZ (10 mg kg−1 day−1,i.p.) was initiated 1 day before ISO administration and continued for 7 days ( n= 7 rats in each group). Histopathological evaluation showed that TMZ prevented ISO-induced myocardial damage. TMZ preserved the ATP levels and decreased the maleic dialdehyde (MDA) content in the hearts compared with ISO-treated rats. The diastolic [Ca2+]i measured by loading with fura-2 AM in isolated cardiomyocytes was increased significantly in ISO-treated rats compared to the control animals. TMZ prevented the rise of diastolic [Ca2+]i and the depression of caffeine-induced Ca2+ transients caused by ISO administration. The reduction in sarcoplasmic reticulum (SR) Ca2+ content in the heart cells and in cardiac SR Ca2+-ATPase activity in ISO-treated rats was abolished by TMZ, although there were no differences in SR Ca2+-ATPase protein levels between the control, ISO and ISO + 7 mz-treated rats. In addition, TMZ prevented the reduction in sarcolemmal L-type Ca2+ current density in the heart cells induced by ISO treatment. These results demonstrate that the treatment of rats with TMZ inhibited the increase of diastolic [Ca2+]i and prevented the decrease of SR Ca2+ content, SR Ca2+-ATPase activity and L-type Ca2+ current density in cardiomyocytes in ISO-mediated myocardial injury of rats. These changes in Ca2+ handling could help to explain the favourable action of TMZ in myocardial injury. [ABSTRACT FROM AUTHOR]

The present study was designed to determine whether or not an increase in endothelial intracellular concentration of calcium ([Ca2+]i) evokes endothelium-dependent contractions in the aorta from normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Acetylcholine, adenosine triphosphate (ATP) and the calcium ionophore, A 23187, produced endothelium-dependent relaxations in isolated aortic rings of both WKY and SHR. These relaxations in response to the three agonists were significantly smaller in the SHR when compared with the WKY. Endothelium-dependent contractions to acetylcholine, ATP and A 23187 were observed only in the aorta isolated from the SHR. In the presence of NG-nitro-L-arginine, an NO synthase inhibitor, the endothelium-dependent contractions in response to acetylcholine, ATP and A 23187 were potentiated significantly in the aorta SHR and were unmasked in that of WKY. However, the contractions were still significantly greater in SHR than in WKY. These contractions were abolished by indomethacin and valeryl salicylate (two cyclo-oxygenase inhibitors) as well as by S 18886 (a TP-receptor antagonist), indicating that the endothelium-dependent contraction produced by the three agonists share the same characteristics. The results of the present study indicate that the release/generation of endothelium-derived contracting factor, requires an increase in endothelial [Ca2+]i. [ABSTRACT FROM AUTHOR]

Experiments were designed to investigate whether or not oxygen-derived free radicals mediate endothelium-dependent contractions to acetylcholine in the aorta of spontaneously hypertensive rat (SHR). Isometric tension was measured in aortic rings taken from adult male SHR and Wistar-Kyoto rat (WKY) in the presence of NG-nitro-L-arginine. Endothelium-dependent contractions to acetylcholine were significantly greater in rings from SHR compared to WKY. Oxygen-derived free radicals, generated from xanthine plus xanthine oxidase, induced contractions that were larger in aortas from SHR than from WKY. Contractions to acetylcholine and free radicals were abolished by a selective TP-receptor antagonist, S 18886, and a preferential inhibitor of cyclo-oxygenase-1, valeryl salicylate, but not by a preferential inhibitor of cyclo-oxygenase-2, NS-398. Allopurinol, deferoxamine and the combination of superoxide dismutase plus catalase inhibited the contractions to oxygen-derived free radicals but did not significantly affect those to acetylcholine. In contrast, diethyldithiocarbamic acid, an inhibitor of superoxide dismutase, or Tiron, a scavenger of superoxide anion, reduced endothelium-dependent contractions to acetylcholine in aortas from SHR. The effect of these two drugs was additive. In SHR chronically treated with dimethylthiourea endothelium-dependent contractions to acetylcholine were decreased, and reduced further by acute in vitro exposure to deferoxamine or the combination of superoxide dismutase plus catalase. These results suggest that in the SHR aorta acetylcholine-induced endothelium-dependent contractions involve endothelial superoxide anion production and the subsequent dismutation into hydroxyl radicals and/or hydrogen peroxide. The free radicals activate cyclo-oxygenase-1, most likely to produce endoperoxides. Activation of TP-receptors is required to observe endothelium-dependent contractions to acetylcholine or endothelium-independent contractions in response to free radical generation. [ABSTRACT FROM AUTHOR]

1 Experiments were designed to investigate whether or not oxygen-derived free radicals mediate endothelium-dependent contractions to acetylcholine in the aorta of spontaneously hypertensive rat (SHR). 2 Isometric tension was measured in aortic rings taken from adult male SHR and Wistar-Kyoto rat (WKY) in the presence of N[supG]-nitro-i-arginine. 3 Endothelium-dependent contractions to acetylcholine were significantly greater in rings from SHR compared to WKY. Oxygen-derived free radicals, generated from van thine plus xanthine oxidase, induced contractions that were larger in aortas from SHR than from WKY. Contractions to acetylcholine and tree radicals were abolished by a selective TP-receptor antagonist, S 18886, and a preferential inhibitor of cyclo-oxygenase-l, valeryl salicylate. but not by a preferential inhibitor of cyclo-oxygenase-2, NS-398. 4 Allopurinol, deferoxainine and the combination of superoxide dismutase plus catalase inhibited the contractions to oxygen-derived free radicals but did not significantly affect those to acetylcholine. In contrast, diethyldithiocarbamic acid, an inhibitor of superoxide dismutase. or Tiron, a scavenger of superoxide anion, reduced endothelium-dependent contractions to acetylcholine in aortas from SHR. The died of these two drugs was additive. 5 In SHR chronically treated with dimethylthiourea endothelium-dependent contractions to acetylcholine were decreased, and reduced further by acute in vitro exposure to deferoxamine or the combination of superoxide dismutase plus catalase. 6 These results suggest that in the SHR aorta acetylcholine-induced endothelium-dependent contractions involve endothelial superoxide anion production and the subsequent dismutation into hydroxyl radicals and or hydrogen peroxide. The free radicals activate cyclo-oxygenase-1 most likely to produce endoperoxides. Activation of TP-receptors is required to observe endothelium-dependent contractions to acetylcholine or endothelium-independent contractions in response to free radical generation. [ABSTRACT FROM AUTHOR]

Research Objective: The Home Health Value‐Based Purchasing (HHVBP) Model provides financial incentives for quality improvement to home health agencies in nine states with the goal of improving quality and efficiency of care for Medicare beneficiaries. The maximum Medicare payment adjustment increases during each of the five years of the model, ranging from ±3% in 2018 to ±8% in 2022. Our goal is to understand the early impact of the HHVBP Model on quality, utilization, and Medicare spending during its first three years (2016–2018), which includes the first year in which payment adjustments to agencies took effect. Study Design: CMS randomly selected nine states to participate in the HHVBP Model starting January 2016, with mandatory participation from all agencies. Agencies in these states received performance scores for 20 measures of quality of care used to determine their payment adjustment relative to other agencies within their state. To evaluate the effects of HHVBP, we used a difference‐in‐differences design and multivariate linear regression to compare differences in the changes in outcomes of the nine HHVBP states with those in the 41 comparison states for three years pre‐intervention (2013–2015) through the first three years of the model (2016–2018). We evaluated agency performance using Outcome and Assessment Information Set (OASIS)‐based quality measures and measures of claims‐based Medicare fee‐for‐service (FFS) health care utilization and spending. Population Studied: Medicare and Medicaid patients receiving home health care in the nine HHVBP states and forty‐one comparison states. Principal Findings: We found evidence of slightly greater improvements in most measures of improved functional status used to determine payment adjustments in HHVBP states relative to non‐HHVBP states. Compared to non‐HHVBP states, Medicare FFS beneficiaries who received home health care in the nine HHVBP states had a relative decrease in unplanned hospitalization rate (−1.8%) and in skilled nursing facility (SNF) stays (−4.9%) from pre‐HHVBP implementation average levels. Conversely, we observed a 2.4% increase in emergency department (ED) visits relative to the average pre‐implementation rates for HHVBP states. Overall, we found evidence of a 1.2% reduction in Medicare spending due to HHVBP, corresponding to an average $141 million reduction in annual Medicare spending in HHVBP states over the first three years of the model. The reduction in spending among home health Medicare FFS patients was driven primarily by reductions in inpatient hospital spending (−2%) and SNF spending (−4%). We did not find an appreciable difference in savings between the third year—in which payment adjustments were applied—and the first two years of the model prior to HHVBP agencies receiving payment adjustments. Conclusions: Through the HHVBP Model's first three years—which includes the first year of payment adjustments to agencies—we found modest impacts of HHVBP: lower growth in Medicare spending, declines in unplanned hospitalizations and use of SNFs, somewhat greater increases in ED use, and somewhat greater improvements in many OASIS‐based quality measures among home health patients in the HHVBP states. Implications for Policy or Practice: The findings from current and subsequent research will inform policymakers, home health care patients, and other stakeholders about potential benefits of expanding the model to include agencies in other states. Primary Funding Source: Centers for Medicare and Medicaid Services. [ABSTRACT FROM AUTHOR]

ABSTRACT Aim Tuberous sclerosis complex (TSC) presents with multisystem benign neoplasm induced by dysregulation of the mammalian target of rapamycin pathway. This study aimed to examine the effects of oral everolimus at either 2.5 or 5.0 mg daily on the treatment of TSC-associated renal angiomyolipoma (AML). Methods Between July 2012 and August 2015, patients with TSC-associated renal AML were selected for everolimus therapy protocol. An oral everolimus starting dose at 2.5 mg was administered daily, and was gradually increased to 5.0 mg daily. All patients were evaluated using magnetic resonance imaging or computed tomography scanning at baseline, 12, 24, and 36 months after the start of treatment for measuring the changes of renal AML mass volume. Results Eight patients were finally enrolled for analysis in this study. Everolimus treatment had a statistically significant effect on the renal AML volume reduction during follow-up ( P < 0.05). Renal AML mass volume reduction rates were 10.5-45.3% in four patients with everolimus 2.5 mg and 40.7-73.1% in four patients with everolimus 5.0 mg daily; the difference was statistically significant between the two groups ( P < 0.05). Longitudinal follow-up for response to everolimus showed volume reduction rates to be around 10.5-73.1% in the initial 6-24 months after everolimus treatment, which remained stable during follow-up up to 36 months. Conclusion The results suggest that an oral everolimus is effective and provides a non-invasive way to treat TSC-associated renal AML, and patients are likely to require maintenance therapy to continue to derive benefit. [ABSTRACT FROM AUTHOR]

A range of 9-amino-9-deoxyepiquinine-based thiourea catalysts are synthesized and applied to the asymmetric oxaziridination of aldimines for the first time. [ABSTRACT FROM AUTHOR]

An abstract of the article "Construction of Chiral Quaternary Carbon Center via Catalytic Asymmetric Aza-Henry Reaction with α-Substituted Nitroacetates," by M. Li and colleagues is presented.

Angiopoietin-like protein (ANGPTL) 4 is a key factor in the regulation of lipid and glucose metabolism in metabolic diseases. ANGPTL4 is highly expressed in various cancers, but the regulation of energy metabolism in tumours remains to be determined. This study explored the role of ANGPTL4 in aerobic glycolysis, glutamine consumption and fatty acid oxidation in nonsmall cell lung cancer (NSCLC) cells. Two NSCLC cell lines (A549 and H1299) were used to investigate the role of ANGPTL4 in energy metabolism by tracer techniques and with Seahorse XF technology in ANGPTLs4 knockdown cells. RNA microarrays and specific inhibitors were used to identify targets in ANGPTLs4-overexpressing cells. The results showed that knockdown of ANGPTLs4 could inhibit energy metabolism and proliferation in NSCLC. ANGPTLs4 had no significant effect on glycolysis but affected glutamine consumption and fatty acid oxidation. Knockdown of ANGPTLs4 also significantly inhibited tumour metastasis and energy metabolism in mice and had a weak effect on glycolysis. RNA microarray analysis showed that ANGPTLs4 significantly affected glutaminase (GLS) and carnitine palmitoyl transferase 1 (CPT1). ANGPTLs4-overexpressing cells were exposed to a glutamine deprivation environment, and cell proliferation and energy metabolism were significantly decreased but still differed from normal NSCLC cells. Treatment of ANGPTLs4-overexpressing cells with GLS and CPT1 inhibitors simultaneously prevented the regulatory effects on cell proliferation and energy metabolism. ANGPTLs4 could promote glutamine consumption and fatty acid oxidation but not glycolysis or accelerate energy metabolism in NSCLC., (© 2022 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)

Emerging evidence indicates that the dysregulation of protein ubiquitination plays a crucial role in aging-associated diseases. Smad-dependent canonical BMP signaling pathway is indispensable for osteoblastic bone formation, which could be disrupted by the ubiquitination and subsequent proteasomal degradation of Smad1/5, the key molecules for BMP signaling transduction. However, whether the dysregulation of Smad1/5 ubiquitination and disrupted BMP signaling pathway is responsible for the age-related bone formation reduction is still underexplored. Pleckstrin homology domain-containing family O member 1 (PLEKHO1) is a previously identified ubiquitination-related molecule that could specifically target the linker region between the WW domains of Smurf1 to promote the ubiquitination of Smad1/5. Here, we found an age-related increase in the expression of PLEKHO1 in bone specimens from either fractured patients or aging rodents, which was associated with the age-related reduction in Smad-dependent BMP signaling and bone formation. By genetic approach, we demonstrated that loss of Plekho1 in osteoblasts could promote the Smad-dependent BMP signaling and alleviated the age-related bone formation reduction. In addition, osteoblast-specific Smad1 overexpression had beneficial effect on bone formation during aging, which could be counteracted after overexpressing Plekho1 within osteoblasts. By pharmacological approach, we showed that osteoblast-targeted Plekho1 siRNA treatment could enhance Smad-dependent BMP signaling and promote bone formation in aging rodents. Taken together, it suggests that the increased PLEKHO1 could suppress Smad-dependent BMP signaling to inhibit bone formation during aging, indicating the translational potential of targeting PLEKHO1 in osteoblast as a novel bone anabolic strategy for reversing established osteoporosis during aging., (© 2016 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.)

Membrane sialic acid (SA) plays an important role in the survival of red blood cells (RBCs), the age-related reduction in SA content negatively impacts both the structure and function of these cells. We have therefore suggested that remodelling the SA in the membrane of aged cells would help recover cellular functions characteristic of young RBCs. We developed an effective method for the re-sialylation of aged RBCs by which the cells were incubated with SA in the presence of cytidine triphosphate (CTP) and α-2,3-sialytransferase. We found that RBCs could be re-sialylated if they had available SA-binding groups and after the re-sialylation, aged RBCs could restore their membrane SA to the level in young RBCs. Once the membrane SA was restored, the aged RBCs showed recovery of their biophysical and biochemical properties to similar levels as in young RBCs. Their life span in circulation was also extended to twofold. Our findings indicate that remodelling membrane SA not only helps restore the youth of aged RBCs, but also helps recover injured RBCs., (© 2015 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.)

The aim of the present study was to investigate the effects of salvianolic acid B on lipopolysaccharide (LPS)-induced disseminated intravascular coagulation (DIC) in rabbits. Continuous infusion of LPS was used to induce a DIC model in rabbits. Treatment with salvianolic acid B (1, 3 or 6 mg/kg) was started simultaneously with LPS infusion (0.5 mg/kg LPS in 60 mL saline; 10 mL/h over a period of 6 h) through the contralateral marginal ear vein. Activated partial thromboplastin time (APTT), prothrombin time (PT), platelet count and fibrinogen concentration were determined, as were plasma levels of fibrin-fibrinogen degradation products (FDP), alanine aminotransferase (ALT), blood urea nitrogen (BUN), protein C activity, antithrombin III (ATIII) and tumour necrosis factor (TNF)-α concentration. The gradual impairment of haemostatic parameters was induced by continuous infusion of LPS. There were marked increases in APTT, PT, BUN, ALT and plasma TNF-α and marked decreases in the platelet count, fibrinogen, FDP, protein C and ATIII. The intravenous administration of 1, 3 or 6 mg/kg salvianolic acid B attenuated the increases in APTT, PT, BUN, ALT and plasma TNF-α and the decreases in fibrinogen, platelet, FDP, protein C and ATIII induced by LPS infusion. These observations indicate that salvianolic acid B has an effect against LPS-induced DIC in rabbits., (© 2014 Wiley Publishing Asia Pty Ltd.)

The midterm effects of cardiac telocytes (CTs) transplantation on myocardial infarction (MI) and the cellular mechanisms involved in the beneficial effects of CTs transplantation are not understood. In the present study, we have revealed that transplantation of CTs was able to significantly decrease the infarct size and improved cardiac function 14 weeks after MI. It has established that CT transplantation exerted a protective effect on the myocardium and this was maintained for at least 14 weeks. The cellular mechanism behind this beneficial effect on MI was partially attributed to increased cardiac angiogenesis, improved reconstruction of the CT network and decreased myocardial fibrosis. These combined effects decreased the infarct size, improved the reconstruction of the LV and enhanced myocardial function in MI. Our findings suggest that CTs could be considered as a potential cell source for therapeutic use to improve cardiac repair and function following MI, used either alone or in tandem with stem cells., (© 2014 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.)

Recently, cardiac telocytes were found in the myocardium. However, the functional role of cardiac telocytes and possible changes in the cardiac telocyte population during myocardial infarction in the myocardium are not known. In this study, the role of the recently identified cardiac telocytes in myocardial infarction (MI) was investigated. Cardiac telocytes were distributed longitudinally and within the cross network of the myocardium, which was impaired during MI. Cardiac telocytes in the infarction zone were undetectable from approximately 4 days to 4 weeks after an experimental coronary occlusion was used to induce MI. Although cardiac telocytes in the non-ischaemic area of the ischaemic heart experienced cell death, the cell density increased approximately 2 weeks after experimental coronary occlusion. The cell density was then maintained at a level similar to that observed 1-4 days after left anterior descending coronary artery (LAD)-ligation, but was still lower than normal after 2 weeks. We also found that simultaneous transplantation of cardiac telocytes in the infarcted and border zones of the heart decreased the infarction size and improved myocardial function. These data indicate that cardiac telocytes, their secreted factors and microvesicles, and the microenvironment may be structurally and functionally important for maintenance of the physiological integrity of the myocardium. Rebuilding the cardiac telocyte network in the infarcted zone following MI may be beneficial for functional regeneration of the infarcted myocardium., (© 2012 The Authors. Published by Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.)