Acute kidney injury (AKI) is a common kidney disorder that affects public health and the incidence of AKI. Sepsis, acute ischemia or hypoxia is the main reason for the occurrence of AKI. Recently, noncoding RNA that include microRNA and long noncoding RNA (lncRNAs) were reported to play important roles in AKI as well as have the potential to serve as a biomarker or therapeutic target for the development of the diagnostic and prognostic strategies of AKI. In the current study, we aimed to investigate the expression and biological function of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in ischemia‐induced AKI in patients' sample and in vitro. The expressions of NEAT1 and miR‐27a‐3p in ischemia/reperfusion‐induced AKI patients were examined by quantitative reverse transcription polymerase chain reaction. Cell injury was induced by treatment of human kidney tubular cells (HK‐2) with CoCl2. After treatment, the influences of NEAT1 and miR‐27a‐3p on the cell apoptosis in the CoCl2‐stimulated HK‐2 were tested by flow cytometry. The flow analysis results showed that the expression of NEAT1 was markedly higher in the ischemia‐induced AKI patients compared with normal control. Moreover, repression the expression of NEAT1 decreased CoCl2‐induced injury in HK‐2. The expression of miR‐27a‐3p was negatively regulated by NEAT1. Inhibition the expression of NEAT1 attenuated overexpression of miR‐27a‐3p enhanced CoCl2‐induced injury. In summary, an ischemia‐induced injury may be enhanced by a high level of NEAT1 through targeting miR‐27a‐3p. Thus, NEAT1 has the potential to be explored as a biomarker for diagnosis and target for therapeutic strategies in ischemia‐induced AKI.

BackgroundGrowing evidence has supported that long non-coding RNAs (lncRNAs) could play vital roles in the development, progression, and prognosis of colorectal cancer (CRC). However, little is known about the clinical significance of BRAF-activated non-coding RNA (BANCR) in CRC. The aim of this study is to explore the clinical value of lncRNA BANCR in CRC patients.MethodsThe expression of lncRNA BANCR was measured in 106 CRC tissues and 65 adjacent normal tissues using the quantitative real-time PCR.ResultsThe study showed that lncRNA BANCR was highly expressed in CRC tissues compared with adjacent normal tissues (P < 0.001). In addition, high expression of lncRNA BANCR was positively correlated with the lymph node metastasis (P < 0.001). Kaplan–Meier analysis showed that patients with high lncRNA BANCR expression had a shorter overall survival (OS) compared with the low lncRNA BANCR expression group (P = 0.001). Interestingly, for the group of patients with the lymph node metastasis, we found the similar result that high lncRNA BANCR expression was related to poor OS (P = 0.004). Furthermore, the multivariate Cox regression model analysis indicated that high expression of lncRNA BANCR was an independent poor prognostic factor in CRC patients (HR 2.24, 95% CI 1.22–4.16, P = 0.009).ConclusionsUpregulation of lncRNA BANCR may be associated with the lymph node metastasis and poor survival of CRC. LncRNA BANCR could be served as a novel and useful biomarker for CRC lymph node metastasis and prognosis.

To evaluate safety and efficacy of one-vs. two-session radiofrequency ablation (RFA) of parathyroid hyperplasia for patients with secondary hyperparathyroidism (SHPT) and to compare the outcome of both methods on hypocalcemia. Patients with secondary hyperparathyroidism underwent ultrasound guided RFA of parathyroid hyperplasia. Patients were alternately assigned to either group 1 (n = 28) with RFA of all 4 glands in one session or group 2 (n = 28) with RFA of 2 glands in a first session and other 2 glands in a second session. Serum parathyroid hormone (PTH), calcium, phosphorus and alkaline phosphatase (ALP) values were measured at a series of time points after RFA. RFA parameters, including operation duration and ablation time and hospitalization length and cost, were compared between the two groups. Mean PTH decreased in group 1 from 1865.18 ± 828.93 pg/ ml to 145.72 ± 119.27 pg/ml at 1 day after RFA and in group 2 from 2256.64 ± 1021.72 pg/ml to 1388.13 ± 890.15 pg/ml at 1 day after first RFA and to 137.26 ± 107.12 pg/ml at 1 day after second RFA. Group 1's calcium level decreased to 1.79 ± 0.31 mmol/L at day 1 after RFA and group 2 decreased to 1.89 ± 0.26 mmol/L at day 1 after second session RFA (P < 0.05). Multivariate analysis showed that hypocalcemia was related to serum ALP. Patients with ALP ≥ 566 U/L had lower calcium compared to patients with ALP < 566 U/L up to a month after RFA (P < 0.05). Group 1's RFA time and hospitalization were shorter and had lower cost compared with Group 2. US-guided RFA of parathyroid hyperplasia is a safe and effective method for treating secondary hyperparathyroidism. Single-session RFA was more cost-effective and resulted in a shorter hospital stay compared to two sessions. However, patients with two-session RFA had less hypocalcemia, especially those with high ALP.Secondary hyperparathyroidism (SHPT) commonly occurs in patients with end stage renal disease (ESRD) when low calcium levels and high phosphorus levels over time stimulate increased PTH secretion 1-3 . SHPT increases the risk for osteoporosis and kidney stones, as well as for parathyroid hyperplasia, a condition that can cause mental abnormalities, renal osteodystrophy, calcific uremic arteriolopathy, vascular calcification, muscle spasms and even lead to respiratory or cardiac arrest 4 .Treatment for SHPT includes vitamin D sterols, intravenous vitamin D analogs and cinacalcet 5-10 to improve biochemical profiles and other surrogate markers 11 . Patients with severe SHPT may be candidates for parathyroidectomy (PTX), which increases long-term survival and reduces the risk of fracture in ESRD patients 12 . However, hyperparathyroidism recurs in up to 30% of patients treated with PTX due to incomplete excision of all hyperplasic parathyroid glands 13,14 . Meanwhile, PTX can potentially result in permanent hypoparathyroidism if the parathyroid glands are over-excised 15 .