Author Correction: Long non-coding RNA HEIH modulates CDK8 expression by inhibiting miR-193a-5p to accelerate nasopharyngeal carcinoma progression.

Correction to: European Review for Medical and Pharmacological Sciences 2021; 25 (2): 770-778-DOI: 10.26355/eurrev_202101_24638-PMID: 33577031, published online 31 January 2021. After publication, the authors found some mistakes in the article. There are amendments to this paper. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/24638.

Long non-coding RNA HEIH modulates CDK8 expression by inhibiting miR-193a-5p to accelerate nasopharyngeal carcinoma progression.

OBJECTIVE: Nasopharyngeal carcinoma (NPC) is the commonest malignant tumor. In this article, we aimed to examine the molecular role of lncRNA HEIH in the progression of NPC. PATIENTS AND METHODS: We assessed the expression of HEIH, miR-193a-5p and CDK8 in NPC tissues and cells by real-time PCR. The cell proliferation, invasion and migration of SUNE-1 cells were examined by CCK-8 and transwell assay. Western blot assay was adopted to measure the protein expression level of CDK8. Dual-Luciferase reporter assay was adopted to evaluate the correlation between HEIH, miR-193a-5p and CDK8. RESULTS: We discovered that HEIH was high expressed and miR-193a-5p was reduced in both NPC tissues and cells. The upregulation of HEIH facilitated cell proliferation, migration and invasion of SUNE-1 cells. In addition, overexpression of miR-193a-5p restrained cell progression of SUNE-1 cells. Moreover, HEIH was proved to be a molecular sponge of miR-193a-5p in NPC. Besides that, CDK8 was found to be a direct target gene of miR-193a-5p in NPC. Furthermore, CDK8 knockdown suppressed cell progression of SUNE-1 cells. CONCLUSIONS: Our data demonstrated that HEIH overexpression promoted cell progression by sponging miR-193a-5p and upregulating CDK8.

LncRNA BC200 regulates the cell proliferation and cisplatin resistance in non-small cell lung cancer via PI3K/AKT pathway.

OBJECTIVE: Long non-coding RNA (lncRNA) exerts tissue specificity and regulates the occurrence and progression of tumors. Previous bioinformatics showed that lncRNA BC200 is served as an oncogene. However, the specific role of BC200 in lung cancer (LC) is rarely reported. The aim of this study is to elucidate the regulatory effects of BC200 on tumor development and cisplatin resistance in non-small cell lung cancer (NSCLC). PATIENTS AND METHODS: The expression level of BC200 in 76 pairs of NSCLC tissues and adjacent normal tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Correlation analyses were conducted to investigate the relation between BC200 expression and prognosis of NSCLC patients. Subsequently, BC200 expression in LC cell lines was detected. After construction of si-BC200 and si-NC, the cellular functions of LC cells were detected through colony formation, flow cytometry and transwell assay, respectively. Western blot was performed to detect the protein expressions of key genes in the PI3K/AKT pathway in LC cells. Finally, cell counting kit-8 (CCK-8) assay was carried out to explore the effect of BC200 on cisplatin resistance of LC cells via calculating IC50. RESULTS: Higher expression of BC200 was found in NSCLC tissues than that of adjacent normal tissues. BC200 expression was positively correlated with tumor stage, lymph node metastasis and distant metastasis of NSCLC patients, whereas not correlated to age and sex. Knockdown of BC200 inhibited proliferation, invasion and migration of LC cells. Western blot results showed that protein expressions of PI3K, AKT and STAT3 were downregulated after BC200 knockdown in LC cells. Additionally, the IC50 in H1299/DDP cells transfected with si-BC200 was lower than in those transfected with si-NC. The apoptotic rate in H1299 cells transfected with si-BC200 was remarkably lower than those transfected with si-NC. CONCLUSIONS: BC200 is highly expressed in NSCLC, which is positively correlated with tumor stage and metastasis of NSCLC patients. BC200 promotes the malignant progression of NSCLC via regulating cisplatin-induced apoptosis of H1299/DDP cells.

Complement deposition on renal histopathology of patients with diabetic nephropathy.

AIMS: As the potential role of the complement system in diabetic nephropathy (DN) is increasingly reported, this study aimed to investigate C1q and C3c deposition as seen on renal histopathology, as well as its association with clinical and pathological parameters, in DN patients. METHODS: Renal biopsy specimens from 161 DN patients were investigated using direct immunofluorescence, light, and electron microscopy. For direct immunofluorescence, staining for C1q and C3c on fresh-frozen renal tissue was performed immediately after biopsy. Complement deposition was defined as the presence of C1q or C3c of at least 1 + on a 0-4 + Scale. The association between complement deposition and clinicopathological data was also analyzed. RESULTS: On direct immunofluorescence microscopy, C1q and C3c were detected in specimens from 44/161 (27.3%) and 89/161 (55.3%) patients, respectively. Regarding clinical data, patients with C1q deposition had a significantly higher level of urinary protein (7.25 ± 4.20 g/24 h vs. 4.97 ± 3.76 g/24 h; P < 0.01) and significantly lower estimated glomerular filtration rate (eGFR; 34.16 ± 25.21 mL/min/1.73 m2 vs. 51.17 ± 31.56 mL/min/1.73 m2, respectively; P < 0.01), whereas patients with vs. without C3c deposition had a significantly lower eGFR (40.09 ± 27.97 mL/min/1.73 m2 vs. 54.48 ± 32.49 mL/min/1.73 m2, respectively; P < 0.01). On renal histopathology, patients with C1q deposition had significantly higher Scores for interstitial fibrosis and tubular atrophy (IFTA), interstitial inflammation and vascular lesions (P < 0.01, P < 0.05 and P < 0.05, respectively), whereas patients with C3c deposition had significantly higher IFTA Scores and proportions of global sclerosis (P < 0.01 and P < 0.01, respectively). CONCLUSION: Complement deposition of C1q and C3c on renal histopathology is associated with more severe kidney damage in patients with DN.

The novel KIR3DS1*084 allele identified in a southern Chinese Han individual.

KIR3DS1*084 allele differs from the closest allele KIR3DS1*01301 at nucleotide 308 C>T in exon 3.

The novel KIR3DS1*083 allele identified in a southern Chinese Han individual.

KIR3DS1*083 allele differs from the closest allele KIR3DS1*01301 by 3 mutations in exon 4.

A novel HLA-E allele, HLA-E*01:01:01:07, identified in a Chinese leukemia patient.

A novel HLA-E allele, HLA-E*01:01:01:07, was identified in a Chinese leukemia patient.

The novel KIR3DS1*085 allele identified in a southern Chinese Han individual.

KIR3DS1*085 allele differs from the closest allele KIR3DS1*01301 at nucleotide 934 C>T in exon 5.

The novel KIR3DS1*082 allele identified in a southern Chinese Han individual.

KIR3DS1*082 allele differs from the closest allele KIR3DS1*01301 at nucleotide 1114T>C in exon 8.

The novel KIR3DS1*078 allele identified in a southern Chinese Han individual.

KIR3DS1*078 allele differs from the closest allele KIR3DS1*01301 at nucleotide 775 G>C in exon 5.

A novel HLA-E allele, HLA-E*01:01:01:06, identified in a Chinese Leukemia patient.

A novel HLA-E allele, HLA-E*01:01:01:06, was identified in a Chinese leukemia patient.

A 3-year follow-up of a patient with acute renal failure caused by thrombotic microangiopathy related to antiphospholipid syndrome: case report.

Background Microvascular manifestations of antiphospholipid antibody syndrome in the kidneys include acute renal failure, thrombotic microangiopathy and hypertension. Therapy has been largely empiric. Case report A 49-year-old Chinese man presented with anuric acute renal failure without abundant proteinuria and heavy haematuria, but markedly low levels of urinary sodium, potassium and chlorine upon admission. On day 1 of hospitalization, his thrombocytopenia, anaemia and renal failure showed rapid progression. The presence of lupus anticoagulant and vascular ischaemia of the small vessels in renal arteriography were also observed. Anticoagulants, continuous renal replacement therapy, glucocorticoids and six sessions of plasma exchange were started. After the fourth plasma exchange (on day 20), his urine output increased and began to normalize. On day 25, haemodialysis was stopped and his general condition gradually improved. A renal biopsy was subsequently performed, and the histopathological diagnosis was thrombotic microangiopathy due to antiphospholipid antibody syndrome. A further 3-year follow-up showed that his haemoglobin level, platelet count and serum creatinine were within the normal range, with stable blood pressure. Conclusion Treatment modalities such as anticoagulation, immunosuppression and plasma exchange are likely to be necessary when severe acute renal failure combined with thrombotic microangiopathy present in nephropathy of antiphospholipid antibody syndrome.

Shear stress regulates endothelial cell autophagy via redox regulation and Sirt1 expression.

Disturbed cell autophagy is found in various cardiovascular disease conditions. Biomechanical stimuli induced by laminar blood flow have important protective actions against the development of various vascular diseases. However, the impacts and underlying mechanisms of shear stress on the autophagic process in vascular endothelial cells (ECs) are not entirely understood. Here we investigated the impacts of shear stress on autophagy in human vascular ECs. We found that shear stress induced by laminar flow, but not that by oscillatory or low-magnitude flow, promoted autophagy. Time-course analysis and flow cessation experiments confirmed that this effect was not a transient adaptive stress response but appeared to be a sustained physiological action. Flow had no effect on the mammalian target of rapamycin-ULK pathway, whereas it significantly upregulated Sirt1 expression. Inhibition of Sirt1 blunted shear stress-induced autophagy. Overexpression of wild-type Sirt1, but not the deacetylase-dead mutant, was sufficient to induce autophagy in ECs. Using both of gain- and loss-of-function experiments, we showed that Sirt1-dependent activation of FoxO1 was critical in mediating shear stress-induced autophagy. Shear stress also induced deacetylation of Atg5 and Atg7. Moreover, shear stress-induced Sirt1 expression and autophagy were redox dependent, whereas Sirt1 might act as a redox-sensitive transducer mediating reactive oxygen species-elicited autophagy. Functionally, we demonstrated that flow-conditioned cells are more resistant to oxidant-induced cell injury, and this cytoprotective effect was abolished after inhibition of autophagy. In summary, these results suggest that Sirt1-mediated autophagy in ECs may be a novel mechanism by which laminar flow produces its vascular-protective actions.

Isolation and identification of epithelial and stromal stem cells from eutopic endometrium of women with endometriosis.

OBJECTIVE: The recent characterization of possible stem/progenitor cells in the endometrium has shed new light on the origins of ectopic endometrial tissue and the mechanism for the pathogenesis of endometriosis, but has raised new questions. Is it possible that abnormal endometrial stem/progenitor cells increase their capacity to implant and establish themselves as ectopic tissue, or that normal stem cells implant in abnormal peritoneum? This study investigated key stem cell properties in cologenic epithelial and stromal cells obtained from eutopic endometrium of women with endometriosis. STUDY DESIGN: Single cell suspensions of endometrial epithelial and stromal cells were cultured at densities of 20, 50, 100 and 200cells/cm(2). Cloning efficiency (CE) was determined, and stem cell phenotypic surface markers were detected using Western blotting and quantitative real-time polymerase chain reaction. RESULTS: CE was significantly higher in cells cultured at a density of 50cells/cm(2) compared with the other groups. After 15 days of culture, small and large colonies were observed. Large-colony-derived epithelial and stromal cells had high proliferative potentials, producing millions of cells in vitro, with strong expression of epithelial and stromal stem cell phenotypic surface markers EMA, CK, CD49f, THY-1(CD90), collagen type I, 5B5 and vimentin. CONCLUSION: Adult stem cells were found in eutopic endometrium of women with endometriosis, and this may play an important role in disease development.

Gankyrin promotes breast cancer cell metastasis by regulating Rac1 activity.

Tumor metastasis is responsible for most cancer patients' deaths. Understanding the mechanism of metastasis is crucial for improving the cure rate for cancer. Here, we report that Gankyrin, a chaperone of ubiquitin-proteasome, has an essential role in breast cancer metastasis. We find that Gankyrin is highly overexpressed in human breast cancers and the expression correlates strongly with lymph node metastasis. Knocking down Gankyrin expression in highly metastatic human breast cancer cells significantly decreases cancer cell migration and invasion. Furthermore, we demonstrate that depletion of Gankyrin inhibits intrinsic Rac1 activity and induces large focal adhesions. Overexpression of Gankyrin accelerates focal adhesion turnover and increases cell migration. Notably, reduction of Gankyrin expression in mouse mammary tumor cell significantly decreases tumor metastasis to lung in animal models. Therefore, our findings suggest that Gankyrin is crucial for breast cancer metastasis and highlight the potential of Gankyrin as a therapeutic target for tumor metastasis.

Do polymorphic variants of chromosomes affect the outcome of in vitro fertilization and embryo transfer treatment?

BACKGROUND The aim of this study was to investigate the effect of chromosomal polymorphic variations on the outcome of IVF and embryo transfer (IVF-embryo transfer) treatment for infertile couples. METHODS During the period from October 2006 to December 2009, 1978 infertile couples who had received their first IVF-embryo transfer treatment cycle in our hospital were selected for this retrospective study, and the frequency of chromosomal polymorphic variations was calculated. From these, 1671 couples were selected and divided into three groups: 1402 couples with normal chromosomes (Group 1/control group), 82 couples with chromosomal polymorphic variations in only females (Group 2) and 187 couples with chromosomal polymorphic variations in only males (Group 3). The clinical pregnancy rates (CPR), early miscarriage rates and ongoing pregnancy rates after IVF-embryo transfer treatment were compared. RESULTS There were no statistically significant differences among the three groups in implantation rates (29.37% in the control group, 29.70% in Group 2 and 31.41% in Group 3, P > 0.05) and CPR (45.86, 46.34 and 51.87%, respectively, P > 0.05). Although there was a trend toward higher first trimester pregnancy loss rates in Group 3 (male chromosomal polymorphic variations), but not in Group 2, compared with normal karyotype couples (10.31 versus 6.84%), the difference did not reach significance (P > 0.05). CONCLUSIONS Chromosomal polymorphic variations appear to have no adverse effects on the outcome of IVF-embryo transfer treatment.

Evaluation of admission characteristics, hospital length of stay and costs for cerebral infarction in a medium-sized city in China.

BACKGROUND AND PURPOSE: Stroke is a heavy economic and health burden for the patients and society. This study aimed to evaluate hospital length of stay (LOS) by admission characteristics and costs correlated with medical insurance status for cerebral infarction in a medium-sized city in China. METHODS: A total of 557 consecutive patients with principal diagnosis of cerebral infarction were enrolled. Admission characteristics, LOS, and costs were retrospectively analyzed. RESULTS: The mean LOS was 18.5 days (median, 16 days). Our analysis demonstrated that medical insurance status, stroke severity (National Institutes of Health Stroke Scale score, Functional Independence Measure cognitive and motor score, Glasgow coma scale), Oxfordshire Community Stroke Project (OCSP) classification, some comorbidities (coronary heart disease, chronic obstructive pulmonary disease, and hyperlipemia), and raised leukocytes were the main explanatory factors for LOS by stepwise multiple regression model. The mean per patient costs were US $983.0, and mean daily costs US $67.0. Drugs were the most expensive cost subtype, all subtypes costs except non-medical care were significantly higher in patients with state medicine than in those with new cooperative medical scheme (NCMS) (P < 0.001). CONCLUSION: Stroke severity, OCSP classification, raised leukocytes on admission, some comorbidities, and medical insurance status may help to predict LOS for patients with cerebral infarction. Healthcare expenditures were heavy burdens to inhabitants. State medicine patients could shorten unnecessary LOS to improve the resources allocation and cost-efficiency.

Levels of urinary complement factor H in patients with IgA nephropathy are closely associated with disease activity.

Factor H plays a key inhibitory role in control of the activation of alternative pathway of complement system. The aim of the study was to investigate the predictive value of factor H as a biomarker of renal injury in IgA nephropathy (IgAN). Urine factor H concentration from 202 patients was measured and compared with that of 60 healthy volunteers. Forty-eight patients fulfilled Haas-I or II (group 1), 60 fulfilled Haas-III (group 2) and 94 fulfilled Haas-IV or V (group 3). Co-deposition of factor H and C3b in kidneys were investigated using confocal microscope. The levels of urinary factor H, when expressed as a ratio of urinary creatinine, were significantly higher in groups 3 than group 1 and 2, also significantly higher in group 2 than group 1. In addition, the levels of urinary factor H were significantly higher in those with factor H deposition in the kidney than those without deposition. The levels of urinary factor H may be a useful biomarker to evaluate kidney injury in IgAN.

Cardiac autonomic regulation during gastroscopy.

BACKGROUND: Gastroscopy is sometimes associated with adverse cardiovascular events. AIMS: We evaluated the effects of sedation and pharyngeal anaesthesia on cardiac autonomic regulation during gastroscopy. PATIENTS: Two hundred thirteen outpatients undergoing gastroscopy. METHODS: The patients were assigned to 4 groups: (1) sedation with intravenous midazolam and placebo throat spray (midazolam group), (2) placebo sedation and pharyngeal anaesthesia with lidocaine (lidocaine group), (3) placebo sedation and placebo throat spray (placebo group), and (4) no intravenous cannula nor throat spray (control group). Continuous electrocardiogram was recorded. Heart rate variability was assessed; the powers of low frequency (0.04-0.15 Hz) and high frequency (0.15-0.40 Hz) components as well as total power (0.0-0.4 Hz) were calculated. RESULTS: Gastroscopy was associated with a decrease in high frequency normalized units, increases in low frequency normalized units and low frequency/high frequency ratio indicating activation of sympathetic and withdrawal of vagal modulation. Sympathetic activation resulted in a decrease in total power and all components of heart rate variability. The decrease was most prominent in the midazolam treated patients (p<0.001 vs the lidocaine group and p<0.01 vs placebo and control groups during the postendoscopy phase). CONCLUSION: Gastroscopy induces a shift towards dominance of the sympathetic modulation of the heart. Premedication with midazolam potentiates this shift.