Chronic metabolic disorders such as obesity and diabetes are associated with accelerated rates of macrovascular and microvascular complications, which are leading causes of morbidity and mortality worldwide. Further understanding of the underlying molecular mechanisms can aid in the development of novel drug targets and therapies to manage these disorders more effectively. Long non-coding RNAs (lncRNAs) that do not have protein-coding potential are expressed in a tissue- and species-specific manner and regulate diverse biological processes. LncRNAs regulate gene expression in cis or in trans through various mechanisms, including interaction with chromatin-modifying proteins and other regulatory proteins and via posttranscriptional mechanisms, including acting as microRNA sponges or as host genes of microRNAs. Emerging evidence suggests that major pathological factors associated with diabetes such as high glucose, free fatty acids, proinflammatory cytokines, and growth factors can dysregulate lncRNAs in inflammatory, cardiac, vascular, and renal cells leading to altered expression of key inflammatory genes and fibrotic genes associated with diabetic vascular complications. Here we review recent reports on lncRNA characterization, functions, and mechanisms of action in diabetic vascular complications and translational approaches to target them. These advances can provide new insights into the lncRNA-dependent actions and mechanisms underlying diabetic vascular complications and uncover novel lncRNA-based biomarkers and therapies to reduce disease burden and mortality.

To compare the cumulative live birth rate (CLBR) of a gonadotropin-releasing hormone (GnRH) antagonist regimen and a progestin-primed ovarian stimulation (PPOS) regimen in low-prognosis patients according to POSEIDON criteria.

Single-center, retrospective, observational study.

Henan Provincial People’s Hospital, Zhengzhou, China.

Women aged ≤40 years, with a body mass index <25 kg/m

, who underwent

fertilization (IVF) or intracytoplasmic sperm microinjection (ICSI) and met POSEIDON low-prognosis criteria.

GnRH or PPOS regimen with IVF or ICSI.

CLBR per oocyte retrieval cycle.

Per oocyte retrieval cycle, CLBR was significantly higher with GnRH antagonist versus PPOS (35.3% vs 25.2%; P<0.001). In multivariable logistic regression analysis, CLBR per oocyte retrieval cycle was significantly lower with PPOS versus GnRH antagonist before (OR 0.62 [95% confidence intervals (CI) 0.46, 0.82; P=0.009]) and after (OR 0.66 [95% CI 0.47, 0.93; P=0.0172]) adjustment for age, body mass index, infertility type, infertility duration, baseline follicle stimulating hormone, anti-Müllerian hormone (AMH), antral follicle count (AFC), and insemination method. CLBR was numerically higher with the GnRH antagonist regimen than with PPOS, across all of the POSEIDON groups, and was significantly higher in patients aged ≥35 years with poor ovarian reserve [AFC <5, AMH <1.2 ng/mL] (unadjusted, P=0.0108; adjusted, P=0.0243).

In this single-center, retrospective, cohort study, patients had a higher CLBR with a GnRH antagonist versus PPOS regimen, regardless of other attributes.

In this single-center, retrospective, cohort study, patients had a higher CLBR with a GnRH antagonist versus PPOS regimen, regardless of other attributes.

We investigated if the concentration and “rangeability” of cystatin C (CysC) influenced the prognosis of coronavirus disease 2019 (COVID-19) in patients suffering from, or not suffering from, type 2 diabetes mellitus (T2DM).

A total of 675 T2DM patients and 572 non-T2DM patients were divided into “low” and “high” CysC groups and low and high CysC-rangeability groups according to serum CysC level and range of change of CysC level, respectively. Demographic characteristics, clinical data, and laboratory results of the four groups were analyzed.

COVID-19 patients with a high level and rangeability of CysC had more organ damage and a higher risk of death compared with those with a low level or low rangeability of CysC. Patients with a higher level and rangeability of CysC had more blood lymphocytes and higher levels of C-reactive protein, alanine aminotransferase, and aspartate aminotransferase. After adjustment for possible confounders, multivariate analysis revealed that CysC >0.93 mg/dL was significantly associated with the risk of heart failure (OR = 2.231, 95% CI 1.125-5.312) and all-cause death (2.694, 1.161-6.252). CysC rangeability >0 was significantly associated with all-cause death (OR = 4.217, 95% CI 1.953-9.106). These associations were stronger in patients suffering from T2DM than in those not suffering from T2DM.

The level and rangeability of CysC may influence the prognosis of COVID-19. Special care and appropriate intervention should be undertaken in COVID-19 patients with an increased CysC level during hospitalization and follow-up, especially for those withT2DM.

The level and rangeability of CysC may influence the prognosis of COVID-19. Special care and appropriate intervention should be undertaken in COVID-19 patients with an increased CysC level during hospitalization and follow-up, especially for those with T2DM.Pheochromocytoma (PCC) is a rare neuroendocrine tumor of the adrenal gland with a high rate of mortality if diagnosed at a late stage. Common symptoms of pheochromocytoma include headache, anxiety, palpitation, and diaphoresis. Different treatments are under observation for PCC but there is still no effective treatment option. Recently, the gene expression profiling of various tumors has provided new subtype-specific options for targeted therapies. In this study, using data sets from TCGA and the GSE19422 cohorts, we identified two distinct PCC subtypes with distinct gene expression patterns. see more Genes enriched in Subtype I PCCs were involved in the dopaminergic synapse, nicotine addiction, and long-term depression pathways, while genes enriched in subtype II PCCs were involved in protein digestion and absorption, vascular smooth muscle contraction, and ECM receptor interaction pathways. We further identified subtype specific genes such as ALK, IGF1R, RET, and RSPO2 for subtype I and EGFR, ESR1, and SMO for subtype II, the overexpression of which led to cell invasion and tumorigenesis.