MiR-377-3p inhibits cell metastasis and epithelial-mesenchymal transition in cervical carcinoma through targeting SGK3.

OBJECTIVE: In cervical carcinoma (CC), microRNAs (miRNAs) were reported to be involved in its development. In this study, we explored how miR-377-3p regulates cell metastasis and epithelial-mesenchymal transition (EMT) in CC. PATIENTS AND METHODS: Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR), Dual-Luciferase Assay, transwell assays, and Western blot analysis were performed to explore the dysregulation of miR-377-3p. RESULTS: MiR-377-3p expression was decreased in CC, and the downregulation of miR-377-3p could predict poor prognosis in CC patients. Moreover, miR-377-3p overexpression repressed cell invasion and migration in CC. Similarly, miR-377-3p overexpression also inhibited EMT in CC cells. Furthermore, miR-377-3p directly targeted SGK3 in CC cells. SGK3 silence had the same function as miR-377-3p overexpression in CC. Especially, the upregulation of SGK3 abolished the inhibitory action of miR-377-3p in CC. CONCLUSIONS: Taken together, miR-377-3p inhibited cell metastasis and EMT by suppressing SGK3 expression. Moreover, the high miR-377-3p expression could predict good prognosis of CC patients.

[Analysis of the influencing factors of serum bilirubin in workers exposed to occupational hazards factors in a urban area].

Objective: To investigate the effect of exposure to occupational hazard factors on serum bilirubin in workers. Methods: In April 2019, using cluster sampling method 5 433 workers exposed to occupational hazard factors from July 2017 to March 2019 were screened out by questionnaire and laboratory test, the date of serum bilirubin were used by the logistic regression analysis of single factor card test and wilcoxon band symbol rank and test. Results: The bilirubin decreases with age, is higher in male than in female, the han is higher than the uygur, and the unmarried workers is higher than the married one, there was significant difference in the levels of bilirubin between different genders, ages, ethnic groups and marriages (P<0.01) . There were statistically significant differences in bilirubin among the occupational hazard factors (P<0.01) , the bilirubin level is highest in the exposure to physical factors, followed by chemical factors and dust. The multivariate logistic regression analysis showed that the dust was the main factor affecting bilirubin (OR(dusr/TBIL)=2.080, 95%CI: 1.542~2.807, P<0.01) . Abnormal alanine aminotransferase (ALT) and alanine aminotransferase (AST) are consistent with elevated bilirubin. Conclusion: Exposure to occupational hazard factors may lead to elevated serum bilirubin and abnormal liver function transaminase, the prevention and control of occupational hazards and cccupational health monitoring should be strengthened.

Inhibitive effects of microRNA-34a on protecting against ischemia-reperfusion injury of vital organs in hemorrhagic shock pregnant mice.

OBJECTIVE: Hemorrhagic shock is a common vital condition in obstetrics, and major treatment consists of bleeding control and liquid resuscitation. MicroRNA (miR) has been found to regulate multiple diseases. However, its expression profile in hemorrhagic shock or effects on the ischemia-reperfusion injury in pregnant mice has not been reported yet. PATIENTS AND METHODS: This study generated rat hemorrhagic shock pregnant model, on which real-time quantitative PCR was used to measure miR-34a expressions. MiR-34a inhibitor was applied to specifically suppress miR-34a expression. Serum malondialdehyde (MDA) and superoxide dismutase (SOD) levels were measured by using the commercial kit. Ischemia-reperfusion injury on rat kidney, lung, liver and intestine tissues was evaluated by using hematoxylin-eosin (HE) staining. RESULTS: In a hemorrhagic shock pregnant rat model, miR-34a expression level was significantly elevated compared to the Normal group (p < 0.05). Application of miR-34a inhibitor effectively suppressed the miR-34a expression in rat kidney, lung, liver and intestine tissues (p < 0.05 compared to normal group). Model rats also had significantly elevated serum MDA and significantly lower SOD levels compared to Normal group (p < 0.05). miR-34a inhibitor reversed this abnorma lity to certain extents (p < 0.05 compared to model group). HE results showed ischemia-reperfusion damage in rat kidney, lung, liver and intestine tissues. miR-34a inhibitor improved such injury. CONCLUSIONS: Suppression of miR-34a could alleviate multi-organ damage after re-perfusion of hemorrhagic shock pregnant rats, probably due to the suppression of oxidative stress. Suppression of miR-34a might work as the treatment target treating multi-organ damage caused by hemorrhagic shock.

Predictive value of plasma ß2-microglobulin on human body function and senescence.

OBJECTIVE: To explore the correlation between plasma ß2-microglobulin (ß2-MG) as senescence factor with age, heart, liver and kidney function as well as the predictive value of ß2-MG in human metabolism function and senescence. PATIENTS AND METHODS: 387 cases of healthy people of different ages were selected and the automatic biochemical analyzer was used to test ß2-MG in plasma based on immunoturbidimetry and also all biochemical indexes. The correlation between ß2-MG and age, gender and all biochemical indexes was analyzed. RESULTS: ß2-MG was positively correlated to age, r = 0.373; and the difference was of statistical significance (p < 0.010). It was significantly negative correlated to HDL-C but positively correlated to LP (a), BUN, CREA, UA, CYS-C, LDH, CK-MB, HBDH, AST, GLB and HCY. CONCLUSIONS: ß2-MG was closely correlated to age, heart, kidney and liver biochemical indexes, which can be taken as an important biomarker for human body function and anti-senescence and have significant basic research and clinical guidance values.

A role of pre-mir-10a coding region variant in host susceptibility to coxsackie virus-induced myocarditis.

OBJECTIVE: Acute viral myocarditis (VM) is an important cause of sudden cardiac death and heart failure in healthy young person. Direct virus-mediated injury and secondary immune reactions, including inflammatory and autoimmune responses, have been reported both in animal models and in humans. Recently, genetic variation has been confirmed related to myocarditis process and susceptibility to VM. In this study, we scanned 339bp of pri-miR-10a coding region in CVB3 VM patients, want to found genetic relations between miR-10a and VM susceptibility. PATIENTS AND METHODS: The secondary structure of two genotype 220 bp pri-miR-10a sequences was predicted using RNAfold web server. In vitro biological functional study concluded dual luciferase assay and Western blotting. RESULTS: We found the rare allele T of rs3809783 was accumulated in VM patients and related to VM significantly. Subsequently, we confirmed that ITCH, a NK-κB signaling suppressor, is a direct target of miR-10a. In vitro biological functional study indicated that this site variation reduced mature miR-10a expression and induced a down-regulated cytokine secretion in the cell culture supernatant. CONCLUSIONS: The results suggest that the rare allele T in pri-miR-10a coding region should be involved in the CVB3 caused VM pathogenesis through weakening host anti-virus immune response. This site may be used for clinical genetic evaluation for VM susceptibility.

LNK (SH2B3): paradoxical effects in ovarian cancer.

LNK (SH2B3) is an adaptor protein studied extensively in normal and malignant hematopoietic cells. In these cells, it downregulates activated tyrosine kinases at the cell surface resulting in an antiproliferative effect. To date, no studies have examined activities of LNK in solid tumors. In this study, we found by in silico analysis and staining tissue arrays that the levels of LNK expression were elevated in high-grade ovarian cancer. To test the functional importance of this observation, LNK was either overexpressed or silenced in several ovarian cancer cell lines. Remarkably, overexpression of LNK rendered the cells resistant to death induced by either serum starvation or nutrient deprivation, and generated larger tumors using a murine xenograft model. In contrast, silencing of LNK decreased ovarian cancer cell growth in vitro and in vivo. Western blot studies indicated that overexpression of LNK upregulated and extended the transduction of the mitogenic signal, whereas silencing of LNK produced the opposite effects. Furthermore, forced expression of LNK reduced cell size, inhibited cell migration and markedly enhanced cell adhesion. Liquid chromatography-mass spectroscopy identified 14-3-3 as one of the LNK-binding partners. Our results suggest that in contrast to the findings in hematologic malignancies, the adaptor protein LNK acts as a positive signal transduction modulator in ovarian cancers.

Testing accelerometer rectification error caused by multidimensional composite inputs with double turntable centrifuge.

Rectification error is a critical characteristic of inertial accelerometers. Accelerometers working in operational situations are stimulated by composite inputs, including constant acceleration and vibration, from multiple directions. However, traditional methods for evaluating rectification error only use one-dimensional vibration. In this paper, a double turntable centrifuge (DTC) was utilized to produce the constant acceleration and vibration simultaneously and we tested the rectification error due to the composite accelerations. At first, we deduced the expression of the rectification error with the output of the DTC and a static model of the single-axis pendulous accelerometer under test. Theoretical investigation and analysis were carried out in accordance with the rectification error model. Then a detailed experimental procedure and testing results were described. We measured the rectification error with various constant accelerations at different frequencies and amplitudes of the vibration. The experimental results showed the distinguished characteristics of the rectification error caused by the composite accelerations. The linear relation between the constant acceleration and the rectification error was proved. The experimental procedure and results presented in this context can be referenced for the investigation of the characteristics of accelerometer with multiple inputs.

Suppression of PPN/MG61 attenuates Wnt/beta-catenin signaling pathway and induces apoptosis in human lung cancer.

Wingless and int homologue (Wnt) family proteins have been shown to have important roles in the decision of cell fate and behavior at multiple stages during the development and tumorigenesis. One of the Drosophila segment polarity genes, porcupine (porc) gene, encodes an evolutionarily conserved endoplasmic reticulum membrane protein involving in the post-translational processing of the Wnt family proteins. Here, we report that human homologue of Drosophila porc gene, PPN/MG61, was abundantly expressed in human cancer cell lines, but not in normal cells. We also found that PPN/MG61 was overexpressed in primary lung cancer tissue samples, compared to their matched normal tissue samples. Furthermore, when we used small interfering RNA to knock down PPN/MG61 mRNA in lung cancer cells expressing the gene, we observed apoptosis induction, along with decreased activity of Wnt pathway in those lung cancer cells. These data suggest that PPN/MG61 may be a novel marker for human lung cancer and that post-translational modification of the Wnt signal molecules by PPN/MG61 may be important for the function of Wnt pathway in lung cancer.

[One-pot synthesis of dl-naproxen by rearrangement].

AIM: To synthesize dl-naproxen by rearrangement method. METHODS: dl-Naproxen was synthesized by halogenation, ketalization, rearrangement and hydrolysis, using cupric halide as halogenation agent. RESULTS: Total yields were 74.0%-92.6% based on 6-methoxy-2-propionyl naphthalene. CONCLUSION: Total yield was higher by one-pot rearrangement approach.

Development of olfactory marker protein and tyrosine hydroxylase immunoreactivity in the transplanted rat olfactory bulb.

Evidence suggests that tyrosine hydroxylase (TH) expression by juxtaglomerular (JG) neurons of the olfactory bulb (OB) is dependent upon input from primary olfactory neurons (ONs), which are identifiable using immunocytochemical localization (ICC-L) methods for olfactory marker protein (OMP). When the input from the continuously regenerating ONs is temporarily removed (either surgically or chemically), JG cells cease TH production until ON contact is reestablished. We are studying this transneuronal regulation using the rat OB in a transplantation (TX) model. Fetal OBs, labeled in utero with tritiated thymidine, were transplanted (TX) into a site vacated by removal of a neonatal host OB. Host animals were sacrificed at varying periods after TX. Alternate sets of frozen sections were then processed for autoradiography or using ICC-L for TH and OMP. As early as 1 week post-TX, OMP-positive fibers and glomerulus-like structures were seen throughout the TX OB. Despite this extensive and rapid OMP reinnervation, TH expression returned very slowly and the number of TH expressing cells never approached control levels. The reduced TH activity in TXs may be due to failure of JG cells to survive or to develop the correct phenotype under TX conditions. Alternatively, input from ON fibers may only be necessary, but not sufficient, for the expression of TH.

Age-related development of olfactory bulb transplants in rats.

We are using the rat olfactory system to study developmental aspects of neurotransplantation (TX). Age-related TX maturation and subsequent establishment of connections are of special concern. Previous studies of deafferentation by olfactory bulb (OB) removal suggested "critical" periods of plasticity in the system. We present here preliminary attempts at relating age of host receiving TX to maturation of the TX and its connections. This investigation used hosts of postnatal age (PN) 13-14 days with fetal donors at Embryonic Day 15; the former having one OB ablated and receiving a fetal donor OB TX immediately placed in the vacated space. The fetal tissue was labeled previously in utero with tritiated thymidine. After 2 months a small coagulation lesion was placed in the OB TX and 2 days later the tissue was taken, serially sectioned, and processed for [3H] autoradiography, degeneration, and olfactory marker protein (OMP). Extensively 3H-labeled OB TXs with localized small lesions were studied. The cellular architecture of the TX is less well organized than in normals but substantial OMP reactivity occurs throughout. Degeneration occurs mainly near the lesion and little if any degeneration is seen beyond the 3H-labeled TX tissue. The results show that OB TX survive and develop in the PN 13-14 age group as they do in the younger animals and that primary olfactory neurons likewise reinnervate the TX but that PN 13-14 TX efferent projections are far more limited than those of younger hosts.

Neurological and electroneuromyographic assessment of the adverse effects of acrylamide on occupationally exposed workers.

Seventy-one acrylamide workers and fifty-one unexposed referents were studied. Weak legs and numb hands and feet, preceded by skin peeling from the hands, were the early symptoms of the acrylamide workers; their early signs were impairment of vibration sensation in their toes and loss of ankle reflexes. Three cases had cerebellar involvement followed by polyneuropathy due to heavy exposure. Electroneuromyographic changes, including a decrease in the sensory action potential amplitude, neurogenic abnormalities in electromyography, and prolongation of the ankle tendon reflex latency, are of greater importance in the early detection of acrylamide neurotoxicity since they can precede the neuropathic symptoms and signs. The diagnostic criteria for occupational acrylamide intoxication of this study revealed three severe poisonings, six moderate poisonings, and 43 mild poisonings. The total prevalence of acrylamide poisoning was 73.2%. The prevention of dermal exposure to acrylamide should be emphasized.