[Cytomegalovirus detoxification and associated factors among preschool children in Yi'nan County].

Objective: To investigate cytomegalovirus detoxification and associated factors among preschool children in Yinan County, Shandong Province. Methods: Two kindergartens were selected from the county and township of Yinan respectively. A total of 250 children were investigated in October 2018. Case information was obtained through the child's guardian. Saliva samples of children and their mothers were collected for cytomegalovirus realtime-PCR detection.The status of CMV detoxification of children was explored and the associated factors were analyzed. Results: A total of 242 preschool children were investigated, and the detoxification rate of cytomegalovirus among them was 22.31% (54/242, 95%CI: 17.0%-27.6%). Logistic regression analysis showed that the rate of detoxification was higher in children whose mothers were cytomegalovirus detoxified (OR=12.39, 95%CI:1.73-88.65)and whose school was located in the county (OR=3.58, 95%CI:1.34-9.55). Conclusions: The detoxification rate of cytomegalovirus in preschool children is high, and there is mutual transmission between children and mothers. Women of childbearing age should pay attention to prevent congenital cytomegalovirus infection when they come into contact with children.

Long noncoding RNA UCA1 promotes proliferation and metastasis of thyroid cancer cells by sponging miR-497-3p.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding RNA UCA1 promotes proliferation and metastasis of thyroid cancer cells by sponging miR-497-3p, by H. Gao, J.-Y. Yang, L.-X. Tong, H. Jin, C.-Z. Liu, published in Eur Rev Med Pharmacol Sci 2020; 24 (2): 728-734-DOI: 10.26355/eurrev_202001_20052-PMID: 32016975" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/20052.

Long noncoding RNA UCA1 promotes proliferation and metastasis of thyroid cancer cells by sponging miR-497-3p.

OBJECTIVE: Recently, long noncoding RNAs (lncRNAs) have attracted much attention for their roles in tumor progression. The aim of this study was to investigate the exact role of lncRNA UCA1 in the development of thyroid cancer (TC) and to explore the possible underlying mechanism. PATIENTS AND METHODS: UCA1 expression in both TC cells and tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Colony formation assay, cell proliferation, and transwell assay were conducted in vitro. Subsequent luciferase reporter gene assay was applied to investigate the underlying mechanism. Furthermore, the function of UCA1 in vivo was monitored as well. RESULTS: UCA1 expression level in TC samples was significantly higher than that of corresponding normal tissues. After UCA1 was knocked down in vitro and in vivo, the proliferation, migration, and invasion of TC cells were significantly inhibited. Moreover, the expression of miR-497-3p was repressed after the knockdown of UCA1. Furthermore, miR-497-3p was directly targeted by UCA1. CONCLUSIONS: Knockdown of UCA1 could inhibit TC cell proliferation and metastasis via sponging miR-497-3p. Our findings might offer a new therapeutic intervention for TC patients.

Gene polymorphism of adiponectin in restenosis after coronary stenting.

OBJECTIVE: The objective of the present study was to investigate the relationship between adiponectin (APN)+45T/G and +276G/T polymorphisms and in-stent restenosis (ISR). PATIENTS AND METHODS: A total of 150 patients treated with percutaneous coronary intervention (PCI) were divided into the ISR group and non-ISR group. The levels of blood biochemical indicators were measured, and APN+45T/G and +276G/T polymorphisms were detected by TaqMan probes. RESULTS: Cholesterol levels in the IRS group were significantly higher than those in the non-ISR group (p<0.05). The frequency of the GG genotype and G allele of the APN+45T/G locus in the ISR group were significantly higher than those in the non-ISR group (p<0.05). The frequency of the GG genotype and G allele of the APN+276G/T locus in the ISR group were significantly higher than those in the non-ISR group (p<0.05). CONCLUSIONS: APN+45T/G and +276G/T polymorphisms were associated with susceptibility to ISR, and carrying the G allele of the APN+45T/G and +276G/T loci can significantly increase the risk of ISR.

Rasagiline, an inhibitor of MAO-B, decreases colonic motility through elevating colonic dopamine content.

BACKGROUND: Dopamine (DA) is a negative modulator of gut motility. Monoamine oxidase-B (MAO-B) is an important metabolic enzyme degrading DA. Rasagiline, an irreversible MAO-B inhibitor, is used to treat Parkinson's disease because of its neuroprotective effect and increasing central DA. However, it is unclear whether MAO-B exists in the colon and rasagiline increases colonic DA, thereby affecting colonic motility. METHODS: Immunohistochemistry, western blotting, enzyme activity assay, colonic motility recording, gut transit test, and high-performance liquid chromatography-electrochemical detection were employed in this study. KEY RESULTS: Monoamine oxidase-B was distributed in the colonic muscular layers including neurons and glias of rat and human. When oral treatment of rats with rasagiline for 4 weeks, in vitro colonic motility was significantly reduced, but it was greatly reversed by SCH-23390, an antagonist of DA D1 receptor. The rasagiline-treated rats also manifested decreased MAO-B activity and increased DA content in the colonic muscular layer, but no alterations were detected in the protein expressions of D1 and D2 receptors, and MAO-A and MAO-B, as well as in the content of 5-hydroxytryptamine and noradrenaline. Moreover, acute administration of rasagiline did not affect the colonic motility in vitro and the colonic DA level in rats, although MAO-B activity was significantly inhibited. CONCLUSIONS & INFERENCES: Monoamine oxidase-B is abundant in the colonic muscular layer including myenteric plexus of rat and human. Long-term administration of rasagiline can increase colonic DA thereby inhibiting colonic motility, suggesting that colonic MAO-B could be a potential drug target for colonic dysmotility.

[Expression of nucleolar protein 14 and CD31 in pancreatic cancer mouse model and its correlation with tumor progression].

Objective: To investigate expression of nucleolar protein 14(NOP14) and CD31 in pancreatic cancer mouse model and its correlation with tumor progression. Methods: Clinicopathological data of 5 patients with pathologically confirmed pancreatic ductal adenocarcinoma(PDAC) and hepatic metastasis between January 2013 and December 2015 was collected in Department of General Surgery, Peking Union Medical College Hospital. Immunohistochemistry staining was employed to detect the expression of NOP14 in matched primary PDAC and relevant metastasis.Pancreatic cancer cells with NOP14 stably knocked down were established by transfecting lentivirus with NOP14 targeted silencing RNA.The inhibition efficacy was detected by quantitative real time PCR and western blot.Microvascular density(MVD) in pancreatic cancer transplantation mouse model was determined by CD31 immunohistochemistry staining analysis and correlated with NOP14 expression and tumor progression. Results: NOP14 had a significant higher expression in liver metastasis than primary pancreatic adenocarcinoma (2.09±0.45 vs. 1.31±0.27, P=0.028). NOP14 was knocked down 86 percent on mRNA level determined by qPCR and 78 percents on protein level detected by western blot. MVD was significantly decreased in NOP14-inhibited tumor from both pancreatic cancer cells subcutaneously and orthotopically grafted tumor mouse model with the value of 61.40±13.85 vs. 85.53±14.59 (P=0.041) and 38.33±10.91 vs. 59.33±15.37(P =0.037), respectively. Besides, MVD was positively associated with tumor volume(r=0.842, P<0.01) and metastasis (r=0.726, P=0.008). Conclusion: NOP14 presents higher expression in hepatic metastasis of pancreatic adenocarcinoma and might promote tumor progression by increasing microvascular density.

Effect of tobacco smoke on hydrogen sulfide-induced rat thoracic aorta relaxation.

Levels of hydrogen sulfide (H2S), a gaseous signaling molecule, are reduced in the serum of individuals who smoke. We hypothesized that tobacco smoke influenced smooth muscle relaxation by decreasing H2S levels and this effect could also influence expression of cystathionine γ-lyase (CSE) and sulfonylurea receptor-2 (SUR-2). The aim of this study was to explore the effect of tobacco smoke on H2S-mediated rat thoracic aorta relaxation and its possible mechanism. Thirty-two Sprague-Dawley rats were divided into four groups: control (C) group, short-term smoker (SS) group, mid-term smoker (MS) group, and long-term smoker (LS) group. H2S concentrations in serum, action of H2S on rat aortic vascular relaxation, and expression of CSE and SUR-2 in thoracic aortic smooth muscle were measured. Although there was no significant difference in H2S between the C and the SS groups, concentration of H2S was significantly reduced in both the LS and MS groups compared to control (P<0.01). Furthermore, H2S was significantly lower in the LS than in the MS group (P<0.05). Rat aortic vascular relaxation was lower in all three treatment groups compared to the control, with the most significant decrease observed in the LS group (P<0.05 compared to the MS group). Expression of CSE and SUR-2 was reduced in the LS and MS groups compared to control (P<0.05), with the lowest levels observed in the LS group (P<0.05). Therefore, tobacco smoke reduced expression of CSE and SUR-2 in rat thoracic aorta, which may inhibit H2S production and vascular dilation.

[The effect and factors associated with outcome of extracorporeal membrane oxygenation in refractory cardiogenic shock patients].

Objective: To observe the clinical efficacy and factors associated with outcome of extracorporeal membrane oxygenation (ECMO) in refractory cardiogenic shock patients. Methods: Patients with refractory cardiogenic shock received ECMO treatment in our hospital from May 2013 to November 2015 were retrospectively analyzed. The clinical status before ECMO support, ECMO timing, complications and outcome were observed and analyzed.The hemodynamic data and the amount of vasoactive drugs at 2 hours before ECMO support and at 2, 6, 24 and 48 hours after ECMO support were collected and compared. Results: Ten refractory cardiogenic shock patients were included in this study (5 acute fulminant myocarditis patients, 4 acute myocardial infarction patients, 1 myocardial rupture patient (6 males, 4 females, age ranged 12 to 56 years). Before ECMO, the mean left ventricular ejection fraction (LVEF) was (31.4±10.2)%, the mean score of APACHE Ⅱ was 26.6±10.8. Eight patients developed cardiac arrests and the duration of CPR ranged from 10 to 300 minutes and three patients received IABP. CVP decreased, BP increased, HR decreased, ScVO2 increased, dose of dobutamine decreased at 2 hours after ECMO support. After ECMO support for 6 hours, lactate decreased, dose of norepinephrine decreased. After ECMO support for 24 and 48 hours, hemodynamics became stable and shock was significantly improved. Complication including infection of limb and catheterization site occurred in 3 patients, femoral arterial thrombosis occurred in 2 patients, critical limb ischemia occurred in 2 patients, hemorrhage at the catheterization site occurred in 2 patients. The duration of ECMO ranged from 2 to 220 hours. Nine patients could be weaned off ECMO support and 6 patients survived to hospital discharge. Two patients died due to too late ECMO support, the other two patients died due to severe complication of limb. Conclusions: ECMO can rapidly improve hemodynamic stability of patients with cardiogenic shock. Accurate assessing the timing of ECMO support and decreasing complication of limb play a critical role on improving outcome in refractory cardiogenic shock patients.

Association between HLA-A and -B polymorphisms and susceptibility to Henoch-Schönlein purpura in Han and Mongolian children from Inner Mongolia.

We examined a possible association between HLA-A and -B polymorphisms and susceptibility to Henoch-Schönlein purpura (HSP) in Han and Mongolian children in Inner Mongolia, through a case-control study. Two hundred and sixty-eight unrelated children were enrolled, including 56 Mongolian and 50 Han children with HSP, 66 healthy Mongolian and 96 healthy Han children as a control group. HLA-A and -B alleles were indentified by PCR-sequence-specific oligonucleotide analysis and were further analyzed by PCR-sequencing-based typing (SBT). Frequencies of HLA-A*11, HLA-B*15 in Mongolian patients and HLA-A*26, HLA-B*35, HLA-B*52 in Han patients were higher than those in the corresponding control group (P < 0.05), while frequencies of HLA-B*07 and -B*40 in Mongolian HSP patients were lower than those in the control group (P < 0.05). Further analysis using PCR-SBT showed that all HLA-A*11 were HLA-A*1101, and most HLA-B*15 were HLA-B*1501 in Mongolian HSP patients. All HLA-A*26 were HLA-A*2601 and HLA-B*35 were mostly HLA-B*3503 in Han patients. There were more Han patients with severe manifestations than Mongolian patients (P < 0.05). Frequencies of HLA-A*26, HLA-B*35 and HLA-B*52 in Han patients were higher than in Mongolian patients (P < 0.05). We conclude that HLA-A*11(*1101) and -B*15(*1501) are associated with susceptibility to HSP in Mongolian children and HLA-A*26(*2601), HLA-B*35(*3503) and HLA-B*52 are associated with susceptibility to HSP in Han children. HLA-B*07 and -B*40 may be protective genes in Mongolian children. The different frequencies of HLA-A and -B in Mongolian and Han children may be responsible for the different manifestations in these two ethnic groups.

Surface Modification and Planar Defects of Calcium Carbonates by Magnetic Water Treatment.

Powdery calcium carbonates, predominantly calcite and aragonite, with planar defects and cation-anion mixed surfaces as deposited on low-carbon steel by magnetic water treatment (MWT) were characterized by X-ray diffraction, electron microscopy, and vibration spectroscopy. Calcite were found to form faceted nanoparticles having 3x (01̄14) commensurate superstructure and with well-developed {112̄0} and {101̄4} surfaces to exhibit preferred orientations. Aragonite occurred as laths having 3x (01̄1) commensurate superstructure and with well-developed (01̄1) surface extending along [100] direction up to micrometers in length. The (hkil)-specific coalescence of calcite and rapid lath growth of aragonite under the combined effects of Lorentz force and a precondensation event account for a beneficial larger particulate/colony size for the removal of the carbonate scale from the steel substrate. The coexisting magnetite particles have well-developed {011} surfaces regardless of MWT.

Alleviating the ischemia-reperfusion injury of donor liver by transfection of exogenous hTERT genes.

BACKGROUND: Ischemia-reperfusion (I/R) injury had been linked to primary graft dysfunction in transplantation. To find effective methods to alleviate donor liver injury from I/R, we transferred exogenous human telomerase reverse transcriptase (hTERT) genes into donor rats before liver transplantation. METHODS: SD rats (age, 16 months) were divided into 3 groups: group A were donors pretreated with exogenous hTERT gene; group B were donors pretreated with adenovirus vector only; and group C were donors pretreated with physiologic saline. Alanine aminotransferase (ALT), apoptotic index, telomerase activity, and histological evaluation were calculated after liver transplantation. RESULTS: The levels of ALT and apoptotic index of group A were significantly lower than those of group B or group C (P < .05), at the same time, a mild histological injury and increased telomerase activity were also observed in group A. CONCLUSIONS: Exogenous hTERT gene provides protection against I/R injury, which depends on exogenous hTERT gene-mediated inhibition of apoptosis.

On the process capability of the solid free-form fabrication: a case study of scaffold moulds for tissue engineering.

This study applies the methodology and procedure of process capability to investigate a solid free-form fabrication technique as a manufacturing method to produce scaffold moulds for tissue engineering. The process capability Cpk and process performance Ppk of scaffold mould manufacture using a solid free-form fabrication technique has been analysed with respect to the dimension deviations. A solid free-form fabrication machine T66 was used to fabricate scaffold moulds in this study and is able to create features that ranged from 200 microm to 1000 microm. The analysis showed that the printing process under the normal cooling conditions of the printing chamber was in statistical control but gave low process capability indices, indicating that the process was 'inadequate' for production of 'dimension-consistent' scaffold moulds. The study demonstrates that, by lowering the temperature of the cooling conditions, the capability Cpk of the printing process can be improved (about threefold) sufficiently to ensure the consistent production of scaffold moulds with dimension characteristics within their specification limits.

Novel 3D collagen scaffolds fabricated by indirect printing technique for tissue engineering.

This article reports the mechanical properties and in vitro evaluation of a collagen scaffold fabricated using an indirect 3D printing technique. Collagen scaffolds, featuring predefined internal channels and capillary networks, were manufactured using phase change printing. It was observed that the collagen scaffolds featured internal channels and a hierarchical structure that varied over length scales of 10-400 microm. In vitro evaluation using hMSCs demonstrated that the resultant collagen based scaffolds have the ability to support hMSC cell attachment and proliferation; cells can migrate and survive deep within the structure of the scaffold. The cell numbers increased 2.4 times over 28 days in culture for the lysine treated scaffolds. The cells were spread along the collagen fibers to form a 3D structure and extracellular matrix was detected on the surface of the scaffolds after 4 weeks in culture. The crosslinking treatment enhanced the biostability and dynamic properties of the collagen scaffolds significantly.

Micro- and nano-injectable composite biomaterials containing calcium phosphate coated with poly(DL-lactide-co-glycolide).

Calcium phosphate/poly(dl-lactide-co-glycolide) (CP/DLPLG) composite biomaterial, in which each CP particle was coated with DLPLG, was synthesized. Two kinds of composites were prepared: microcomposite, with particles 150-200mum in size, and nanocomposite, with the particles 40+/-5nm in size. Using nanoparticles, a new class of injectible composite biomaterials was produced. Based on scanning electron microscopy, atomic force microscopy, differential thermal analysis, thermogravimetric analysis, differential scanning calorimetry and Fourier transform infrared analyses, the structure and phase organization in both biomaterials was identified and in both studied cases CP particles were coated with DLPLG polymer. An injectable composite biomaterial, the characteristics of which depend on the ratio of the phases, was prepared by mixing physiological solution with the nano-CP/DLPLG composite. Rheological studies indicated a possible agglomeration of particles of the injectable nano-CP/DLPLG composite biomaterial with a CP content of 65%.

Increased expression of type 2 3alpha-hydroxysteroid dehydrogenase/type 5 17beta-hydroxysteroid dehydrogenase (AKR1C3) and its relationship with androgen receptor in prostate carcinoma.

Type 2 3alpha-hydroxysteroid dehydrogenase (3alpha-HSD) is a multi-functional enzyme that possesses 3alpha-, 17beta- and 20alpha-HSD, as well as prostaglandin (PG) F synthase activities and catalyzes androgen, estrogen, progestin and PG metabolism. Type 2 3alpha-HSD was cloned from human prostate, is a member of the aldo-keto reductase (AKR) superfamily and was named AKR1C3. In androgen target tissues such as the prostate, AKR1C3 catalyzes the conversion of Delta(4)-androstene-3,17-dione to testosterone, 5alpha-dihydrotestosterone to 5alpha-androstane-3alpha,17beta-diol (3alpha-diol), and 3alpha-diol to androsterone. Thus AKR1C3 may regulate the balance of androgens and hence trans-activation of the androgen receptor in these tissues. Tissue distribution studies indicate that AKR1C3 transcripts are highly expressed in human prostate. To measure AKR1C3 protein expression and its distribution in the prostate, we raised a monoclonal antibody specifically recognizing AKR1C3. This antibody allowed us to distinguish AKR1C3 from other AKR1C family members in human tissues. Immunoblot analysis showed that this monoclonal antibody binds to one species of protein in primary cultures of prostate epithelial cells and in LNCaP prostate cancer cells. Immunohistochemistry with this antibody on human prostate detected strong nuclear immunoreactivity in normal stromal and smooth muscle cells, perineurial cells, urothelial (transitional) cells, and endothelial cells. Normal prostate epithelial cells were only faintly immunoreactive or negative. Positive immunoreactivity was demonstrated in primary prostatic adenocarcinoma in 9 of 11 cases. Variable increases in immunoreactivity for AKR1C3 was also demonstrated in non-neoplastic changes in the prostate including chronic inflammation, atrophy and urothelial (transitional) cell metaplasia. We conclude that elevated expression of AKR1C3 is highly associated with prostate carcinoma. Although the biological significance of elevated AKR1C3 in prostatic carcinoma is uncertain, AKR1C3 may be responsible for the trophic effects of androgens and/or PGs on prostatic epithelial cells.

Dynamic creep and mechanical characteristics of SmartSet GHV bone cement.

The restrained dynamic creep behaviour and mechanical properties of SmartSet GHV bone cement have been investigated at both room temperature and body temperature. It was found that the bone cement behaves significant differently at room temperature from that at body temperature. The test temperature had a strong effect on the creep performance of the bone cements with a higher creep rate observed at body temperature at each loading cycle. For both temperatures, two stages of creep were identified with a higher creep rate during early cycling followed by a steady state creep rate. The relationship between creep deformation and loading cycle can be expressed by a Hyperb 1 model. As a visco-elastic material, the sensitivity of bone cement to the temperature change was evident during mechanical testing. Compared to the mechanical strength at room temperature, a decreased value was demonstrated at body temperature. The bending modulus was very sensitive to the change in testing temperature, where a reduction of 52% was recorded. A significant reduction in compressive and bending strength, 31 and 23% were recorded respectively. The effect of temperature on bending strength was less apparent, where only 13% reduction was exhibited at body temperature compared to room temperature.

Transient atypical monocytosis mimic acute myelomonocytic leukemia in post-chemotherapy patients receiving G-CSF: report of two cases.

Granulocyte colony-stimulating factor (G-CSF) is now widely used in patients with malignant disorders receiving intensive chemotherapy to increase leukocyte count and to upregulate phagocyte function during neutropenia. Monocytosis associated with G-CSF has been reported in anecdotal literature. We report two cases of pseudoleukemia secondary to G-CSF administration. Both patients initially presented with myelodysplastic syndrome with chromosome 7 abnormalities that evolved into acute myeloid leukemia. Case one had deletion 7q while case two initially had monosomy 7 and subsequently developed a balanced translocation between the short (p) arm of chromosome 1 and long (q) arm of chromosome 15. Following the induction chemotherapy and G-CSF administration, both of these patients developed pseudoleukemia. Patient 1 had white blood cell (WBC) count of 26 x 10(9)/l with 72% monocytes, while patient two had WBC of 14.1 x 10(9)/l with 30% monocytes. In both patients the monocytosis resolved after the discontinuation of G-CSF therapy. In summary, patients treated with G-CSF should be followed closely. In those cases with pseudoleukemia discontinuation of the drug with no supplemental chemotherapy is probably enough to control the atypical monocytosis.

Artemisia judaica L.: micropropagation and antioxidant activity.

Artemisia judaica L., an Egyptian medicinal plant used in the treatment of gastrointestinal disorders, was mass-propagated and grown using solid, paper-bridge-support liquid, liquid-flask and bioreactor cultures. The liquid-flask culture using 50 ml MS liquid medium in 250 ml flask yielded significantly greater shoot proliferation than either solid cultures or paper-bridge-support liquid cultures. Increasing flask capacity from 100 to 500 ml improved shoot proliferation and growth. Mass-propagation efficiencies of various bioreactor systems, viz. temporary immersion reactors and bubble column reactors, were also compared. The temporary immersion bioreactor was found to have significant advantages for A. judaica shoot proliferation. The shoot cultures from the temporary immersion reactor formed complete plantlets when subcultured onto a medium containing 1 micromoll(-1) indole-3-butyric acid (IBA), and mature plants were established, acclimatized and thrived in standard greenhouse conditions. Assays of antioxidant activity and total flavonoid content of in vitro and in vivo grown tissues were evaluated as gross parameters of medicinal efficacy. Significantly higher antioxidant activity and flavonoid contents were observed in the tissues of mature greenhouse-grown plants. The efficient in vitro production systems developed in this study provided sterile, consistent tissues for investigation of bioactivity and germplasm conservation of A. judaica.

Regeneration of the Egyptian medicinal plant Artemisia judaica L.

An in vitro propagation system for Artemisia judaica L., a traditional Egyptian medicinal plant, has been developed. De novo shoot organogenesis was induced by culturing etiolated hypocotyls and intact seedlings on medium supplemented with thidiazuron [N-phenyl-N'-(1,2,3-thidiazol-yl) urea] via callusing at the cotyledonary notch region. Up to 16 shoots formed per seedling cultured on a medium containing 1 micro mol l(-1) thidiazuron for an optimal duration of exposure of 20 days. Regenerated shoots formed roots when subcultured onto a medium containing 1 micromol l(-1) indole-3-butyric acid. The regeneration protocol developed in this study provides a basis for germplasm conservation and for further investigation of medicinally active constituents of A. judaica.