ContextRoutine repeat testing of critical values is a long-standing practice in many clinical laboratories; however, its usefulness and necessity remain to be empirically established and no regulatory requirements yet exist for verification of the critical value results obtained by repeat analysis.ObjectiveTo determine whether repeat testing of critical values is useful and necessary in a clinical chemistry laboratory.MethodsA total of 601 chemistry critical values (potassium, n = 255; sodium, n = 132; calcium, n = 108; glucose, n = 106) obtained from 72,259 routine clinical chemistry specimens were repeat tested. The absolute value and the percentage of difference between the two testing runs were calculated for each of the four critical values and then compared with the allowable error limit put forth in the College of American Pathologists (CAP).ResultsAmong the repeat data for the 601 critical values, a total of 24 showed large differences between the initial result and the repeated result which exceeded the CAP limits for allowable error. The number and rates (%) of large differences for within and outside the analytical measurement range (AMR) were 12 (2.1%) and 12 (41.4%), respectively. For the 572 critical values within the AMR for each test category, the mean absolute difference (mmol/L) and difference(%) between the two testing runs were: potassium, 0.1 mmol/L (2.7%); sodium, 2.1 mmol/L (1.7%); calcium, 0.05 mmol/L (3.0%); glucose, 0.18 mmol/L (2.6%).ConclusionsWhen the initial chemistry critical values are within the AMR, repeated testing does not improve accuracy and is therefore unnecessary. When the initial chemistry critical values are outside the AMR, however, the benefit of repeated testing justifies its performance and makes it necessary. Performing repeat clinical testing on a case-by-case, rather than routine, basis can improve patient care by delivering critical values more rapidly while providing savings on reagent costs associated with unnecessary repeat testing.

Hypoxia is identified as one of the microenvironmental features of most solid tumors and is involved in tumor progression. In the present research, we demonstrate that lncRNA extracellular leucine rich repeat and fibronectin type III domain-containing 1-antisense RNA 1 (ELFN1-AS1) is upregulated by hypoxia in colon cancer cells. Knockdown of ELFN1-AS1 in hypoxic colon cancer cells can reduce cell proliferation and restore the invasion to non-hypoxic levels. Fluorescence in situ hybridization results show that ELFN1-AS1 is distributed in the cytoplasm of colon cancer cells, so we further analyze the potential targets for ELFN1-AS1 as a competing endogenous RNA (ceRNA). MiR-191-5p contains a binding sequence with ELFN1-AS1 and is downregulated by ELFN1-AS1 in colon cancer cells. Then, there is a binding site between miR-191-5p and the 3′ untranslated region of tripartite motif TRIM 14 (TRIM14). The expression of TRIM14 is inhibited by ELFN1-AS1 siRNA or miR-191-5p mimics in LoVo and HT29 cells. The treatment of the miR-191-5p inhibitor in ELFN1-AS1 knockdown cells can significantly increase cell proliferation and invasion ability. Overexpression of TRIM14 in miR-191-5p-mimic-treated cells can rescue the inhibition of proliferation and invasion caused by miR-191-5p mimics. In conclusion, ELFN1-AS1 operates as a downstream target of hypoxia, promotes proliferation and invasion, and inhibits apoptosis through upregulating TRIM14 by sponging miR-191-5p in the colon cancer cells. Our results enrich our understanding of colon cancer progression and provide potential targets for clinical treatment of colon cancer.

Aim of the studyWe measured the impact of changing KLK6 expression levels on the pathological grade of gliomas and on proliferation rate, cell cycle progression, and apoptosis in the U251 glioblastoma cell line.Material and methodsThe expression of KLK6 in 35 brain glioma tissues and adjacent noncancerous tissues was measured using real-time quantitative polymerase chain reaction (PCR) and the relationship between KLK6 expression and pathological grades was analysed.ResultsThe KLK6 expression in U251 cells was silenced by a specific siRNA, and the effects on proliferation, the cell cycle, and apoptosis were compared to wild type cells. Expression of KLK6 was downregulated in gliomas relative to matched noncancerous tissue. There was no obvious relationship between patient sex, pathological grade, or tumour classification and the expression of KLK6. In the U251 cell line, cell proliferation was enhanced and the fractions of cells in the G2 and S phases were increased by siRNA-mediated KLK6 silencing.ConclusionsExpression of KLK6 inhibits tumour growth. Decreased KLK6 expression may be a possible risk factor for glioma.

Persistent symptoms of depression indicate the adaptive involvement of stable molecules in the brain that may be manifested at the level of chromatin remodeling, such as histone acetylation. Former studies have identified alterations in histone acetylation and deacetylation in several animal models about depression. However, the specific histone deacetylases related with depression are needed to be explored. Here, social avoidance behaviors, anxiety-, and depression-like behaviors were all found in mice suffered from chronic social defeat stress. Moreover, we also discovered that the amount of the class II histone deacetylase, HDAC7 rather than HDAC2, was significantly decreased in the nucleus accumbens of defeated mice, which suggested that HDAC7 might be a crucial histone deacetylase in a chronic social defeat stress model. Our data showed that the depressive-like behaviors induced by chronic social defeat stress were associated with HDAC7 reduction in nucleus accumbens. HDAC7 might be a promising therapeutic target for depression.

Peroxiredoxin 2 (PRDX2), a member of the peroxiredoxin family of antioxidant enzymes, has been revealed to be an important player in cancer progression. However, the biological role of PRDX2 in the progression of non-small cell lung cancer (NSCLC) is poor reported. In the present study, the loss-of-function experiments were performed to investigate the specific role of PRDX2 in the growth and invasion of NSCLC. The results revealed that knockdown of PRDX2 by siRNA interference significantly suppressed the proliferation, migration, and invasion of A549 and H1299 cells, as well as diminished the activity of MMP9. Additionally, the decrease in PRDX2 expression significantly promoted apoptosis in NSCLC cells by downregulating expression of Bcl-2 and upregulating the expression of Bax, cleaved caspase 3 and cleaved caspase 9, but had no significant effect on the apoptosis of normal lung epithelial cells BEAS-2B. Moreover, PRDX2 inhibitor also inhibited the proliferation, migration, and invasion of A549 cells and promoted apoptosis. Further, our data demonstrated that silencing of PRDX2 markedly reduced the phosphorylation of Akt and mTOR and expression of downstream proteins Cyclin D1 and p70S6k. In conclusion, our findings indicate that PRDX2 exerts a prooncogenic role in the progression of NSCLC and might be a potential therapeutic target for NSCLC treatment.