LINC00968 accelerates the progression of epithelial ovarian cancer via mediating the cell cycle progression.

OBJECTIVE: The aim of this study was to clarify the potential role of LINC00968 in the progression of epithelial ovarian cancer (EOC) and the underlying mechanism. PATIENTS AND METHODS: The relative expression level of LINC00968 in EOC tissues (n=40) and normal ovarian tissues (n=40) was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). LINC00968 expression in human-derived ovarian cancer cell lines was examined by qRT-PCR as well. After transfection of LINC00968 small-interfering RNA (siRNA) in ovarian cancer cells, cell cycle progression and cell proliferation were evaluated through flow cytometry, Cell Counting Kit-8 (CCK-8) and colony formation assay, respectively. Tumor xenograft was conducted in nude mice to elucidate the function of LINC00968 in EOC tumorigenesis in vivo. Furthermore, the relative expression levels of cell cycle factors and protein kinase B/extracellular-signal-regulated kinase (AKT/ERK) in ovarian cancer cells influenced by LINC00968 were detected by Western blot. RESULTS: LINC00968 was significantly up-regulated in EOC tissues when compared with normal control tissues. Meanwhile, LINC00968 expression was positively correlated with the prognosis of EOC. Transfection of LINC00968 siRNA in HEY and HO8910 cells markedly attenuated proliferative ability and arrested cell cycle in the G1 phase. Knockdown of LINC00968 remarkably suppressed tumor growth of EOC in nude mice. The silence of LINC00968 significantly downregulated Cyclin D, Cyclin E and CDK4, whereas upregulated p16 and p21. In addition, AKT and ERK pathways were inhibited by knockdown of LINC00968 in ovarian cancer cells. CONCLUSIONS: LINC00968 expression is markedly upregulated in EOC. Meanwhile, it arrests the cell cycle in the G1 phase by inhibiting the ERK and AKT pathways, thus accelerating EOC progression.

Quantum self-contained refrigerator in terms of the cavity quantum electrodynamics in the weak internal-coupling regime.

We present two schemes to implement the self-contained refrigerator in the framework of the cavity quantum electrodynamics. The considered refrigerators are composed of three interacting microcavities (or two microcavities simultaneously interacting with one three-level atom) separately coupling to a thermal bath with a certain temperature. Despite the local master equation employed, the proposed analytic procedure shows the perfect thermodynamical consistency. It is also demonstrated that the heat is stably extracted from the lowest temperature bath with a fixed efficiency only determined by the intrinsic properties of the refrigerators, i.e., the frequency ratio of the two cavities in contact with the two higher temperature baths. These two schemes indicate that the system with the weak internal coupling in the infinite dimensional Hilbert space can be used to realize the quantum self-contained refrigerator on the principle completely the same as the original self-contained refrigerator.

LncRNA GIHCG promotes development of ovarian cancer by regulating microRNA-429.

OBJECTIVE: To explore whether lncRNA GIHCG participates in the pathogenic progression of ovarian cancer (OC) and its underlying mechanism. PATIENTS AND METHODS: Expression levels of GIHCG and microRNA-429 in 30 OC tissues and normal ovarian tissues were detected by quantitative Real time-polymerase chain reaction (qRT-PCR). Subsequently, 15 pairs of OC tissues and paracancerous tissues were selected for correlation analyses of GIHCG, microRNA-429 and the overall survival (OS) of OC patients using Kaplan-Meier method. Pearson correlation analyses were conducted for investigating the correlation between GIHCG and microRNA-429. GIHCG expression in OC cell lines (HEY, A2780 and HO8910) and normal epithelial OC cell line (IOSE-386) was detected by qRT-PCR. After transfection of GIHCG overexpression plasmid in HEY cells, cell cycle, proliferation and colony formation ability were detected by flow cytometry, cell counting kit-8 (CCK-8) and colony formation assay. MicroRNA-429 expression in HEY cells overexpressing GIHCG was detected by qRT-PCR. Rescue experiments were conducted by co-transfection of GIHCG overexpression plasmid and microRNA-429 mimics, followed by cell cycle and colony formation detection. RESULTS: GIHCG was highly expressed, whereas microRNA-429 was lowly expressed in OC tissues than that of paracancerous tissues. OC patients with higher expression of GIHCG showed shorter OS than those with lower expression. However, OC patients with higher expression of microRNA-429 had longer OS than those with lower expression. GIHCG expression was positively correlated to microRNA-429. In vitro experiments showed that GIHCG was highly expressed in HEY, A2780 and HO8910 cells than that of IOSE-386 cells. GIHCG overexpression in HEY cells promoted cell cycle and colony formation abilities, which were reversed by microRNA-429 overexpression. CONCLUSIONS: GIHCG is highly expressed in OC, which promotes OC development by stimulating cell cycle progression and cell proliferation by regulating microRNA-429.

An alternative method for evaluating lipoprotein(a) excess in plasma.

OBJECTIVE: To estimate the stability and reliability of lipoprotein(a) cholesterol measurement, and explore the possibility to evaluate lipoprotein(a) excess in plasma by using lipoprotein(a)-cholesterol assay alternatively to assay lipoprotein(a). SETTING: Number 255 Hospital of PLA, Tangshan, Hebei, China. PRACTICE DESCRIPTION: A total of 396 plasma samples from 100 healthy people (control), 107 chronic renal failure patients, 114 coronary heart disease patients, and 75 cerebral infarction patients, respectively, were measured for lipoprotein(a) cholesterol and lipoprotein(a) mass; lipoprotein(a) cholesterol and lipoprotein(a) mass levels among control and diseased groups were compared; and lipoprotein(a) cholesterol levels and lipoprotein(a) mass values from the control group were subjected to linear regression analysis. MAIN OUTCOME MEASUREMENTS: The affinity between oligosaccharide contained in lipoprotein(a) and lectin wheat germ agglutinin to isolate lipoprotein(a) from other lipoproteins; lipoprotein(a) cholesterol and lipoprotein(a) mass detected by total cholesterol kits and enzyme linked immunosorbent assay kits, respectively. RESULTS: Both lipoprotein(a) cholesterol and lipoprotein(a) mass levels of the chronic renal failure, coronary heart disease, and cerebral infarction groups were significantly higher than those of the control (P < 0.05 or P < 0.01) whereas no difference was seen among the diseased groups at the 0.05 level. Regression analysis within the control group showed a very high correlation between lipoprotein(a) cholesterol and lipoprotein(a) (r = 0.9932). CONCLUSION: The results suggest that lipoprotein(a) cholesterol assay may be used in the place of lipoprotein(a) measurement for evaluating lipoprotein(a) excess for chronic renal failure, coronary heart disease, and cerebral infarction patients. Further studies about the mechanism of this association between lipoprotein(a) cholesterol and lipoprotein(a) levels are needed.

Keshan disease--an endemic mitochondrial cardiomyopathy in China.

Keshan disease (KD) is a cardiomyopathy endemic in certain areas of China, characterized by severe deterioration and multiple focal necrosis. In the present paper we describe abnormalities of the structure and function of myocardial mitochondria from patients with subacute Keshan disease. Activities of succinate dehydrogenase, succinic oxidase, cytochrome c oxidase, H(+)-ATPase and its sensitivity to oligomycin and the response of membrane potential to energization by ATP were significantly decreased. However, the spectrum of reduced-minus-oxidized cytochromes in patients' mitochondria showed no obvious difference in the content of cytochrome c oxidase (aa3). There was also a marked decrease in lipid fluidity of affected mitochondria, and an abnormal amount of moderately electron dense amorphous inclusions. Electron-microscopic x-ray microanalysis and exposure to protein digestion reagent demonstrated that these inclusions are not Ca3(PO4)2, but are, probably, proteinaceous in nature. Affected mitochondria had markedly decreased selenium content. The defects in myocardial mitochondria from patients with chronic Keshan disease were less extensive than those in patients with subacute Keshan disease. We propose that Keshan disease be classified as a form of "mitochondrial cardiomyopathy".

Magnesium mediated change in physical state of phospholipid modulates membrane ATPase activity.

During reconstitution of pig heart mitochondrial H(+)-ATPase in soybean phospholipid liposomes by the cholate dialysis method, Mg2+ greatly enhanced 32Pi-ATP exchange activity, ATPase activity and the sensitivity to oligomycin or DCCD of the reconstituted enzyme complex. The effect of Mg2+ on the lipid packing or fluidity of the reconstituted proteoliposomes was measured by means of spin labels, fluorescent probes and pyrene excimer formation efficiency. A difference in fluidity seemed to be localized near the polar faces of lipid bilayers of the reconstituted enzyme complex. Fluidity was less in the presence of Mg2(+)-containing and the Mg2(+)-'free' samples. Based on the results obtained a hypothetical scheme was proposed for Mg2(+)-mediated change in the physical state of phospholipid modulates incorporating H(+)-ATPase in liposomes. It postulated that Mg2+ may play a role in altering the lipid fluidity of the bilayers, which would induce a change of conformation of F0 portion (buried in the lipid core) of H(+)-ATPase complex. Such change could be transmitted to the soluble F1 portion, the conformation of which is in turn altered, resulting in higher enzymatic activity. Such an assumption was further supported by the results of a series of biochemical and biophysical experiments. Similar to its effect in the reconstitution of porcine heart mitochondrial H(+)-ATPase in liposomes, Mg2+ may also enhance the enzyme activity of reconstituted cytochrome C oxidase, porcine kidney medulla Na,K-ATPase, Ca-ATPase from rabbit sarcoplasmic reticulum and chloroplast H(+)-ATPase, in liposomes. It may be inferred that the structure and function of many membrane proteins are similarly modulated by Mg2+.(ABSTRACT TRUNCATED AT 250 WORDS)

Mg2+-mediated change in lipid fluidity enhances the reconstituted H+-ATPase activity.

The results by using ANS fluorescent probe and spin labels 5-NS show that the fluidity of L. (H+-ATPase) +Mg2+ (H+-ATPase from pig heart mitochondria reconstituted in the presence of Mg2+) is less than that of L. (H+-ATPase) -Mg2+ (proteoliposome reconstituted in the absence of Mg2+). But no significant difference in fluidity has been observed when both reconstituted systems were monitored by using spin labels 12-NS and 16-NS. This indicates that Mg2+ may cause changes in fluidity of the lipid molecules near the surfaces of the bilayers, but does not affect significantly the fluidity of the deeper layer of the reconstituted system. It is tentatively supposed that in the presence of Mg2+, enhancement of activities of reconstituted H+-ATPase may be due to the Mg2+-mediated change in physical state of the lipids in the more superficial region of lipid bilayers so as to ensure a suitable conformation of ATPase complex, thereby possessing higher activity.

Studies on incorporation of membrane protein into liposomes--effect of divalent cations on reconstitution of pig heart mitochondrial H+-ATPase into liposomes.

During the process of reconstitution of pig heart mitochondrial H+-ATPase on liposomes by cholate dialysis method, 1 mM Mg2+ in the dialysis medium can obviously increase activities of the reconstituted H+-ATPase (32Pi-ATP exchange, enzyme activity and its sensitivity to oligomycin or DCCD and ATP-dependent ANS 1) fluorescence). Besides Mg2+, effects of other divalent cations and spermidine on the H+-ATPase reconstitution have been compared. The effectiveness of the divalent cation activation of 32Pi-ATP exchange of the reconstituted H+-ATPase, decreased in the order: Mg2+ greater than Ca2+ greater than Mn2+ greater than Sr2+, while that of increasing the sensitivity to the inhibitors: Ca2+ greater than Mg2+ greater than Mn2+ greater than Sr2+. No significant effect on the H+-ATPase reconstitution has been found with Cd2+, Zn2+ and spermidine3+. Mechanism of action of the divalent cations on reconstitution has been discussed.