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Background α-1-syntrophin (SNTA1), a protein encoded by SNTA1, is highly expressed in human cardiomyocytes. Mutations in SNTA1 are associated with arrhythmia and cardiomyopathy. Previous research on SNTA1 has been based on nonhuman cardiomyocytes. Our study was designed to identify phenotype of SNTA1-deficient using human cardiomyocytes. Methods SNTA1 was knocked out in H9 cell line using CRISPR-Cas9 system. H9SNTA1KO cells were then induced to differentiate into cardiomyocytes using small molecule inhibitors. The phenotypic discrepancies associated with SNTA1-deficient cardiomyocytes were investigated. Results SNTA1 was truncated in PH1 domain by a stop codon (TGA) using CRISPR-Cas9 system. SNTA1-deficient did not affect the pluripotency of H9SNTA1KO, and they retain their in vitro ability to differentiate into cardiomyocytes. However, H9SNTA1KO derived cardiomyocytes exhibited increased structural components, weak calcium transient intensity, low levels of calcium in sarcoplasmic reticulum, lower cardiac contractility, and shorter field potential duration. Early treatment of SNTA1-deficient cardiomyocytes with ranolazine improved the calcium transient intensity and cardiac contractility. Conclusions SNTA1-deficient cardiomyocytes can be used to research the etiology, pathogenesis, and potential therapies for myocardial diseases. The SNTA1-deficient cardiomyocyte model suggests that the maintenance of cardiac calcium homeostasis is a key target in the treatment of myocardial-related diseases.

Objective To determine the prevalence of post traumatic stress disorder (PTSD) in the army officers and soldiers (AOSs), and identify its relationship with functional gastrointestinal disorders (FGIDs). Methods PTSD and FGIDs were diagnosed based on the PTSD checklist-civilian (PCL-C) and Rome Ⅲ Modular Questionnaire respectively, the overlaps of PTSD and FGIDs and their correlation were diagnosed. The correlation of PTSD with traumatic and stressful events was investigated using Trauma History and Stressful Event Screening Questionnaire. The coexistence and relationship of PTSD and FGIDs were analyzed. Results Of 927 AOSs, 33 were diagnosed with PTSD. The prevalence of PTSD was 3.56%. FGIDs were identified in 435 subjects and the incidence of FGIDs was 46.93%. Among 33 AOSs with PTSD, 28 were diagnosed as having FGIDs and the prevalence of FGIDs was 84.85%, which was significantly higher than that of non-PTSD group (45.53%, P

During the 1980s, a novel nonvolatile memory product was introduced, referred to as flash electrically erasable program-mable read-only memory (EEPROM). The basic operating prin-ciple of the nonvolatile memory device is to store charges in the gate oxide of a metal-oxide semiconductor field-effect transistor (MOSFET). If charges can be stored in the oxide of a MOSFET, the threshold voltage of the MOSFET can be modified to switch between two distinct values, conventionally defined as the erase state and the program state. The terms erase and program are used to denote operations that charge and discharge through ox-ide. The threshold voltage shift between the two states is caused by the storage of charge in oxide. The program state is usually obtained from a channel hot electron, while the erase state uses Fowler-Nordheim (F-N) tunneling through a thin gate oxide. The storage of charges in the gate oxide of the nonvolatile memory device can be realized by surrounding a conducting layer by an oxide. Since this layer acts as a completely electrically isolated gate, this type of device is commonly referred to as a floating gate device.An EEPROM cell containing an n-well and metal-insulator-metal (MIM) capacitor was fabricated using a 0.18 μm stan-dard complementary MOS (CMOS) process. In recent efforts, a stacked metal-insulator-metal (MIM) and an n-well capacitor have been applied to a single polysilicon EEPROM cell in order to increase memory capacity [1-4]. The application of the single polysilicon EEPROM is becoming more popular due to its low process cost and satisfactory reliability [5-7]. Optimal charac-teristics of EEPROM include fast program/erase speed, high endurance performance, and low leakage current. Although the MIM capacitor cell performs well, it requires a large device-size. The n-well control gate cell inherently possesses high junction capacitance and high sheet resistance. In this paper, we propose an EEPROM cell that does not re-quire additional cell area in order to obtain a high capacitance. Additionally, the proposed EEPROM provided a satisfactory control gate coupling ratio contributing to the junction capaci-tance between the control gate and the n-well. Because the n-well depletion capacitor was isolated by shallow trench iso-lation (STI) and the MIM capacitor was located just above the n-well capacitor, the cell containing two capacitors connected in parallel was expected to be very reliable and to provide noise immunity.

A simulation study of a current‐mode direct current (DC)‐DC buck converter is presented in this paper. The converter, with a fully integrated power module, is implemented by using sense method metal‐oxide‐semiconductor field‐effect transistor (MOSFET) and bipolar complementary metal–oxide–semiconductor (BiCMOS) technology. When the MOSFET is used in a current sensor, the sensed inductor current with an internal ramp signal can be used for feedback control. In addition, the BiCMOS technology is applied in the converter for an accurate current sensing and a low power consumption. The DC‐DC converter is designed using the standard 0.35 μm CMOS process. An off‐chip LC filter is designed with an inductance of 1 mH and a capacitance of 12.5 nF. The simulation results show that the error be‐ tween the sensing signal and the inductor current can be controlled to be within 3%. The characteristics of the error amplification and output ripple are much improved, as compared to converters using conventional CMOS circuits.

To investigate the dynamic expression of p-signal transducer and activator of transcription 3 (STAT3) and vascular endothelial growth factor (VEGF) in the formation of gastric tumors induced by drinking water containing N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in Wistar rats.One hundred and twenty Wistar rats were randomly divided into two groups (60 in each group): Control group and Model group. The rats in each group were then randomly divided into three groups (20 in each group): C/M15, C/M25 and C/M40 (15, 25 and 40 represent the number of feeding weeks from termination). Rats in the control group received normal drinking water and rats in the model group received drinking water containing 100 μg/mL MNNG. Stomach tissues were collected at the end of the 15(th), 25(th) and 40(th) week, respectively, for microscopic measurement using hematoxylin and eosin staining. The expression of p-STAT3 and VEGF in different pathological types of gastric tissue, including normal, inflammation, atrophy, hyperplasia and gastric stromal tumor, was observed by immunohistochemistry and Western blot, and the corelation between p-STAT3 and VEGF was analyzed.(1) The expression of p-STAT3 in tissue with gastritis, atrophy, dysplasia and gastric stromal tumor were significantly increased in the model group compared with the control group (2.5 ± 1.0, 2.75 ± 0.36, 6.2 ± 0.45, 5.67 ± 0.55 vs 0.75 ± 0.36, P = 0.026, 0.035, 0.001, 0.002, respectively); the expression of p-STAT3 in tissue with dysplasia was higher than that in samples with gastritis or atrophy (6.2 ± 0.45 vs 2.5 ± 1.0, P = 0.006; 6.2 ± 0.45 vs 2.75 ± 0.36, P = 0.005, respectively); however, the expression of p-STAT3 in gastritis and atrophy was not significantly different (P0.05); (2) the expression of VEGF in tissue with gastritis, atrophy, dysplasia and gastric stromal tumor was significantly increased in the model group compared with normal gastric mucosa; and the expression of VEGF in tissue with dysplasia was higher than that in tissue with inflammation and atrophy (10.8 ± 1.96 vs 7.62 ± 0.25, P = 0.029; 10.8 ± 1.96 vs 6.26 ± 0.76, P = 0.033, respectively); similarly, the expression of VEGF in tissue with gastritis and atrophy was not significantly different (P0.05); and (3) the expression of VEGF was positively correlated with p-STAT3.p-STAT3 plays an important role in gastric cancer formation by regulating the expression of VEGF to promote the progression of gastric tumor from gastritis.

OBJECTIVE: To investigate the cytotoxicity of silk fibroin/gelatin (SF/G) composite scaffolds in vitro as well as their biocompatibility and degradation in vivo. METHODS: The proliferation and relative growth rate of human hepatic QZG cells grown on different blends of two-dimensional (2-D) SF/G scaffolds were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Flow cytometry was used to evaluate apoptotic rate of QZG cells on different blends of 2-D SF/G scaffolds. The effect of silk protein materials on cell growth was observed by scanning electron microscopy. Three-dimensional (3-D) SF/G scaffolds of three different ratios (diameter 10 mm, thickness 1 mm) were implanted into subcutaneous pockets on male Sprague–Dawley (SD) rats. On the 7th, 14th and 30th day post-implantation, the rats were sacrificed. The scaffold area including the surrounding tissues was retrieved. Hematoxylin and eosin staining was performed for observation under a light microscope. RESULTS: Significant cell attachment and proliferation on the SF/G scaffolds were observed. As the increased gelatin concentration, SF/G scaffolds became more amenable to cell adhesion. After the subcutaneous implantation of the SF/G scaffolds in SD rats, immunological rejection tests showed only slight inflammation, measured by the presence of inflamed cells on day 7 and 14. By day 30, each scaffold had been completely infiltrated and organized by fibroblasts and inflamed cells. The greater the gelatin concentration in the scaffold, the faster the degradation rate. CONCLUSION: Composite SF/G scaffolds are a promising candidate matrix for implantable bio-artificial livers.

To evaluate the preventive potential of intraoperative or early postoperative local administration of peptide PIII into the abdominal cavity against peritoneal carcinomatosis.Human gastric cancer cells of the line GC9811 were inoculated subcutaneously into nude mice to cause subcutaneous carcinoma. The 8th generation cancer was taken out to isolate the cancer cells to be inoculated into the serous membrane at the greater curvature of the stomach. Forty-eight nude BALB/C-nu/nu mice underwent implantation of the 8th generation cancer cells into the serous membrane at the greater curvature of the stomach via minilaparotomy so as to establish models of peritoneal carcinoma The 48 mice were randomly divided into 3 equal groups: Group 1 (control group); Group 2, undergoing intraperitoneal perfusion of 100 microg of peptide PIII, and post-operative intraperitoneal perfusion of 2 mg/kg peptide PIII twice; and Group 3, undergoing post-operative intraperitoneal perfusion of 100 microg/kg peptide PIII twice. Six mice in every group were sacrificed on the day 23 to undergo pathological examination. The other mice in every group were used to evaluate the survival rate. The tumor-bearing mice showing manifestations of failure were killed to undergo pathology.The weight of individual tumor was not significantly different among the 3 groups. The number of peritoneal metastatic nodules of Group 2 was (9.2 +/- 1.3), significantly less than those of Group 1 and 3 [(126.3 +/- 9.6) and (64.2 +/- 8.3) respectively, both P0.01]. The number of metastatic nodules2 mm of Group 2 was 1.6 +/- 0.2, significantly less then those of Groups 1 and 3 [(51.2 +/- 3.6) and (21.7 +/- 4.9) respectively, both P0.01]. The survival rate of Group 2 was significantly longer than those of Groups 1 and 3 (both P0.01).Peptide PIII does not significantly inhibit the growth of GC, but significantly reduce the peritoneal metastasis of GC. An ideal targeting chemotherapy, intra-operative application of peptide PIII into the abdominal cavity plus intraperitoneal perfusion is an attractive and promising strategy to prevent peritoneal metastasis of GC.