[Clinical efficacy evaluation of minimally invasive cardiac surgery coronary artery bypass grafting in patients with multivessel coronary artery disease].

Objective: To investigate the clinical efficacy of minimally invasive cardiac surgery coronary artery bypass grafting (MICS CABG) in the treatment of patients with multivessel coronary artery disease. Methods: A total of 147 patients with multi-vessel coronary artery disease and coronary heart disease who underwent surgical treatment in Henan Provincial People's Hospital from March 2016 to March 2019 were retrospectively selected. Of which, 69 patients were treated by MICS CABG (minimally invasive group) and 78 patients were treated using the traditional thoracotomy (traditional group). The perioperative indexes, serum myocardial enzyme indexes and renal function indexes of patients before and after operation were compared between the two groups; Two groups of patients were followed up for 2 years; the incidence of adverse cardiovascular events (MACE) was recorded, and survival analysis was performed. Results: The age of the patients in the minimally invasive group and the traditional group were (66.9±5.8) and (68.2±7.0) years old, respectively, and the proportions of males were 60.9% (42 cases) and 51.3% (40 cases) (all P>0.05). All patients in the two groups successfully completed the operation, and no patients in the minimally invasive group were converted to thoracotomy. Before surgery, there was no significant difference in serum cTnI, CK-MB, BUN, Scr, and creatinine clearance between the minimally invasive group and the traditional group (all P>0.05). After re-examination 48 hours after operation, the serum cTnI in the minimally invasive group was (3.109±0.664) µg/L, and the CK-MB was (18.03±3.27) U/L, which were lower than those in the traditional group (3.438±0.715) µg/L, (20.63±4.28) U/L; the difference was statistically significant (all P<0.05). During the 2-year follow-up, there was no statiscally significant difference in the incidence of recurrent myocardial infarction, postoperative atrial fibrillation, postoperative stroke, arrhythmia, heart failure, thrombosis, cardiac death, and MACE events between the minimally invasive group and the traditional group. Statistical significance (all P>0.05). The survival curve analysis showed that the cumulative rates of MACE events in the minimally invasive and traditional groups were 17.39% and 26.92%, respectively (P=0.171). Conclusions: The effect of MICS CABG in the treatment of patients with multivessel coronary artery disease and coronary heart disease is not much different from that of traditional open thoracotomy, but the former is less traumatic, quicker after surgery, and has clinical significance for the recovery of patients' myocardial function.

Differential MicroRNA Expressions in Human Peripheral Blood Mononuclear Cells Are Predictive of Renal Allograft Function.

BACKGROUND: The present diagnostic methods for detecting graft damage after kidney transplantation are either invasive or not available early enough. The microRNAs (miRNAs) in peripheral blood mononuclear cells (PBMCs) have been suggested as promising biomarkers. METHODS: Using quantitative real-time polymerase chain reaction, we identified 9 miRNAs (miR-142-5p, miR-142-3p, miR-223, miR-211, miR-486, miR-155, miR-10b, miR-30a, and let-7c) related to the human renal allograft status in PBMCs from 104 kidney transplant recipients. RESULTS: The miR-142-5p, miR-142-3p, and miR-223 were significantly upregulated and miR-10b was significantly downregulated in recipients with abnormal levels of serum creatinine 3 to 4 weeks after initial sample collection. Moreover, the miR-142-5p and miR-142-3p were also found to be significantly upregulated in recipients with abnormal levels of cystatin C. Through a combination of the validated miRNAs, receiver operating characteristic analyses yielded the highest area under the curve value of 0.7913 and 0.7063 in predicting the levels of serum creatinine and cystatin C, respectively. In the testing stage, the developed models correctly predicted allograft function in 16 to 17 of 22 recipients (false rate, 22.7%-27.2%). CONCLUSIONS: miRNAs in PBMCs of recipients hold great promise to be used as predictive and noninvasive biomarkers after transplantation.

miR-198 regulated the tumorigenesis of gastric cancer by targeting Toll-like receptor 4 (TLR4).

OBJECTIVE: To investigate the role of miR-198 and its target gene Toll-like receptor 4 (TLR4) of tumorigenesis of gastric cancer (GC). MATERIALS AND METHODS: The expression of miR-198 in GC cells was detected by quantitative polymerase chain reaction (qPCR). The proliferation, apoptosis, migration, and invasion of GC cells were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), flow cytometry, transwell chamber, and wound scratch assay. Bioinformatics analysis for the results of protein chip was performed to identify the target genes of miR-198. TLR4 was further confirmed to be the target gene of miR-198 by TLR4 luciferase reporter assay. RESULTS: miR-198 expression level in GC SGC-7901 cells significantly decreased compared with the normal cells. When the miR-198 was overexpressed, the proliferation, migration, and invasion of GC cells were significantly decreased, while the apoptosis was increased. The expression of TLR4 in SGC-7901 cells was significantly higher, while the expression of TLR4 in SGC-7901 cells transfected with miR-198 significantly lowered, which was consistent with the Western blot for TLR4. The luciferase reporter assay confirmed that TLR4 was the target genes of miR-198 in GC SGC7901 cells. CONCLUSIONS: miR-198 could induce apoptosis and inhibit the proliferation, migration, and invasion of GC cells through downregulating TLR4 expression.

Correlation of serum PCSK9 in CHD patients with the severity of coronary arterial lesions.

OBJECTIVE: The present study aims to investigate the correlation between serum level of proprotein convertase subtilisin/kexin type 9 (PCSK9) and the severity of coronary arterial lesion in patients with coronary heart disease (CHD). PATIENTS AND METHODS: Between August 2010 and January 2015, 126 CHD patients and 70 patients with coronary arterial stenosis < 50% (controls) were included in the present study. Serum PCSK9 level was determined using ELISA. Demographic characteristics, relevant clinical data and biochemical data were collected from all patients, and their relationship with PCSK9 was analyzed to evaluate the correlation of PCSK9 expression with the severity of coronary artery disease (CAD). RESULTS: Concentrations of total cholesterol (TC) and fasting blood sugar (FBS) were significantly higher in CHD patients than in controls (p < 0.05). No significant differences were observed in gender, age, body mass index (BMI), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), family history, smoking history and history of hypertension between groups (p > 0.05). Serum PCSK9 levels in the CHD group were significantly higher than those in the control group [(96.4 ± 33.2) ng/mL vs. (81.8 ± 27.6) ng/mL, p < 0.05]. Compared with those of patients with single-vessel or double-vessel disease, PCSK9 levels were significantly elevated in patients with multi-vessel disease (p < 0.05). The Gensini score of the CHD group was significantly lower than that of the control group (11.4 ± 10.5 vs. 37.3 ± 10.3, p < 0.05). The Gensini score of patients with multi-vessel disease was significantly higher compared with patients of single-vessel  or double-vessel disease (p < 0.05). Correlation analysis revealed that PCSK9 was positively correlated with many clinical parameters, including age, BMI, TC, TG, systolic blood pressure, FBS, Gensini score and LDL-C (p < 0.05). However, PCSK9 was not correlated with either gender ratio or diastolic blood pressure (p > 0.05). CONCLUSIONS: Serum PCSK9 level is significantly elevated in CHD patients and its variation is correlated with the severity of CAD.

Palmitate induces ER calcium depletion and apoptosis in mouse podocytes subsequent to mitochondrial oxidative stress.

Pathologic alterations in podocytes lead to failure of an essential component of the glomerular filtration barrier and proteinuria in chronic kidney diseases. Elevated levels of saturated free fatty acid (FFA) are harmful to various tissues, implemented in the progression of diabetes and its complications such as proteinuria in diabetic nephropathy. Here, we investigated the molecular mechanism of palmitate cytotoxicity in cultured mouse podocytes. Incubation with palmitate dose-dependently increased cytosolic and mitochondrial reactive oxygen species, depolarized the mitochondrial membrane potential, impaired ATP synthesis and elicited apoptotic cell death. Palmitate not only evoked mitochondrial fragmentation but also caused marked dilation of the endoplasmic reticulum (ER). Consistently, palmitate upregulated ER stress proteins, oligomerized stromal interaction molecule 1 (STIM1) in the subplasmalemmal ER membrane, abolished the cyclopiazonic acid-induced cytosolic Ca(2+) increase due to depletion of luminal ER Ca(2+). Palmitate-induced ER Ca(2+) depletion and cytotoxicity were blocked by a selective inhibitor of the fatty-acid transporter FAT/CD36. Loss of the ER Ca(2+) pool induced by palmitate was reverted by the phospholipase C (PLC) inhibitor edelfosine. Palmitate-dependent activation of PLC was further demonstrated by following cytosolic translocation of the pleckstrin homology domain of PLC in palmitate-treated podocytes. An inhibitor of diacylglycerol (DAG) kinase, which elevates cytosolic DAG, strongly promoted ER Ca(2+) depletion by low-dose palmitate. GF109203X, a PKC inhibitor, partially prevented palmitate-induced ER Ca(2+) loss. Remarkably, the mitochondrial antioxidant mitoTEMPO inhibited palmitate-induced PLC activation, ER Ca(2+) depletion and cytotoxicity. Palmitate elicited cytoskeletal changes in podocytes and increased albumin permeability, which was also blocked by mitoTEMPO. These data suggest that oxidative stress caused by saturated FFA leads to mitochondrial dysfunction and ER Ca(2+) depletion through FAT/CD36 and PLC signaling, possibly contributing to podocyte injury.

Linear free energy relationships on rate constants for dechlorination by zero-valent iron.

By correlation analysis, molecular structural factors governing surface area-normalized rate constants (k) for dechlorination by zero-valent iron, were identified. Twenty-nine quantum chemical descriptors computed by MNDO, AM1 and PM3 Hamiltonians for gas-phase and the conductor-like screening model (COSMO) for incorporating solvent (H2O) effects were studied. Besides the energy of the lowest unoccupied molecular orbital (E(LUMO)), the character of carbon-chlorine bonds (C-Cl bonds) and especially the strength of C-Cl bonds was found significant in governing the magnitude of log k. By PLS analysis, six two-parameter linear free energy relationships (LFER) were obtained. The best two-parameter LFER model was the one using E(LUMO) and C (the Coulombic interaction energy of the two-center term for the C-Cl bonds) computed by PM3/H2O method as molecular structural descriptors. Chlorinated compounds with high E(LUMO) and C values tend to have low dechlorination rate constants.

Improved radiation hybrid map of rat chromosome 2: colocalization of the genes encoding corticotropin-releasing hormone and IL6-receptor with quantitative trait loci regulating the inflammatory response.

We established a radiation hybrid (RH) map of several genes and anonymous markers in the lower half of rat chromosome 2, a chromosome region that contains quantitative trait loci (QTLs) for blood pressure, diabetes and inflammatory response. Two of the newly localized genes (Crh and Il6r) encode proteins involved in the regulation of inflammatory and immune events. Our data show that they reside within regions that were genetically defined as QTLs controlling the inflammatory response. These genes are thus both functional and positional candidates.

Analysis of candidate genes included in the mammary cancer susceptibility 1 (Mcs1) region.

The rat strain COP is resistant to spontaneous and carcinogen-induced mammary cancer, whereas the strain WF is susceptible. Using genetic linkage analysis of (WF x COP) F1 x WF backcrosses, LC Hsu, LA Shepel and co-workers showed that a region at the centromeric end of Chromosome (Chr) 2 (2q1) segregates with the sensitivity to mammary cancer development. The responsible locus was named Mcs1 (for mammary cancer susceptibility 1). We have developed the chromosome map of the 2q1 region by localizing 18 genes, 4 ESTs, and several anonymous markers, using radiation hybrids and fluorescence in situ hybridization. The region containing Mcs1 was delineated to 2q12-q14. Five of the genes (Mef2c, Map1b, Ccnh, Rasa, Rasgrf2) were assigned to this region and were shown to be expressed in the rat mammary glands, while three possible functional candidate genes, Pi3kr1, Rad17, and Naip, were excluded from the critical region. Since cyclin H, encoded by Ccnh, plays an important role in the control of the cell cycle and since the proteins encoded by Rasa and Rasgrf2 control the activity of the RAS oncoprotein, the corresponding genes appeared as both functional and positional Mcs1 candidates. RT-PCR experiments on RNA extracted from mammary glands of the two rat strains (COP, WF) was done. No amino acid sequence difference was found between the two strains. These results argue against the hypothesis that any of these three genes is Mcs1.

Localization of new, microdissection- generated, anonymous markers and of the genes Pcsk1, Dhfr, Ndub13, and Ccnb1 to rat chromosome region 2q1.

The centromeric region of rat chromosome 2 (2q1) harbors unidentified quantitative trait loci of genes that control tumor growth or development. To improve the mapping of this chromosome region, we microdissected it and generated 10 new microsatellite markers, which we included in the linkage map and/or radiation hybrid map of 2q1, together with other known markers, including four genes: Pcsk1 (protein convertase 1), Dhfr (dihydrofolate reductase), Ndub13 (NADH ubiquinone oxidoreductase subunit b13), and Ccnb1 (cyclin B1). To generate anchor points between the different maps, the gene Ndub13 and the microsatellite markers D2Ulb25 and D2Mit1 were also localized cytogenetically. The radiation map generated in region 2q1 extends its centromeric end of about 150 cR.

Sternocleidomastoid pseudotumor of infants and congenital muscular torticollis: fine-structure research.

Fifty cases, 16 with sternocleidomastoid pseudotumor of infants (SCMPOI) and 34 with congenital muscular torticollis (CMT), were investigated by light and electron microscopy. The ultrastructure of the pseudotumor revealed that there were myoblasts, fibroblasts, myofibroblasts, and mesenchyme-like cells, which consisted of fibrous tissue and were regarded as fibroblasts only in the literature. The myoblasts showed the various stages of differentiation and degeneration. For those cases without mass, the collagen fibrils and fibrocytes were often arranged in tight parallel bundles in which some muscles showed normal structure and some with decreased myofibrillae. The mesenchyme-like cells and myoblasts found in the pseudotumor may be the key point to its pathologic characteristics.

[Studies on serum regulatory protein for cell growth in patients with lung cancer exposed to indoor coal-burning].

Seven kinds of serum regulatory gene coding protein for cell growth were determined with enzyme linked immunodotting in 19 indoor coal-burning exposed patients with lung cancer (Group A), 22 exposed cases without lung cancer (Group B), and 19 nonexposed cases without lung cancer (Group C) to study pathogenesis of lung cancer patients exposed to indoor coal-burning. Results showed that serum concentrations of ras, p53 and neu protein in Group A were significantly higher than those in Groups B and C, with a statistically significant difference (P < 0.05) or a very significant difference (P < 0.01). Six cases in Group A were positive for ras protein (with two strong positive), three for p53, neu and jun each, and one for p16. Two in Group B were positive for ras protein and one for p16. It suggests that serum regulatory protein for cell growth can be regarded as biological markers for environment-related lung cancer.