Visual and auditory attention defects in children with intermittent exotropia.

Background: Previous studies have shown that children with intermittent exotropia (IXT) have a higher rate of psychiatric abnormalities as they grow up, such as attention deficit. This study explored visual and hearing attention among children with IXT, and evaluated its association with clinical characteristics and cognitive development.

Methods: Forty-nine children with a diagnosis of IXT and 29 children with traditional development were recruited.

STING deletion alleviates podocyte injury through suppressing inflammation by targeting NLRP3 in diabetic kidney disease.

An increasing number of studies have shown that immune inflammatory response plays a vital role in diabetic kidney disease (DKD). Nod-like receptor protein 3 (NLRP3) inflammasome-dependent inflammatory response is a key mechanism in the initiation and development of DKD. The stimulator of interferon genes (STING) is an adaptor protein that can drive noninfectious inflammation and pyroptosis.

Ox-LDL aggravates contrast-induced injury of renal tubular epithelial cells.

Hypercholesterolemia can aggravate contrast-induced acute kidney injury, and the exacerbation of renal tubular epithelial cell (RTEC) injury is a major cause. However, the exact mechanisms remain obscure. Mitophagy, a type of autophagy, selectively eliminates damaged mitochondria and reduces mitochondrial oxidative stress, which is strongly implicated in cell homeostasis and acute kidney injury.

B‑cell lymphoblastic lymphoma‑associated renal damage: A case report and literature review.

Lymphoblastic lymphoma (LBL) is a highly malignant form of lymphoma with rapid progression and high mortality. According to the World Health Organization immunophenotype, it is classified into T-lymphoblastic lymphoma (T-LBL) and B-lymphoblastic lymphoma (B-LBL). B-LBL often involves lymph nodes and extranodal locations, such as the skin, bones, and soft tissues.

Sirt3 mitigates LPS-induced mitochondrial damage in renal tubular epithelial cells by deacetylating YME1L1.

Acute kidney injury (AKI) is often secondary to sepsis. Increasing evidence suggests that mitochondrial dysfunction contributes to the pathological process of AKI. In this study, we aimed to examine the regulatory roles of Sirt3 in Lipopolysaccharide (LPS)-induced mitochondrial damage in renal tubular epithelial cells (TECs).

SIRT3 deficiency exacerbates early-stage fibrosis after ischaemia-reperfusion-induced AKI.

Background: Sirtuin 3 (SIRT3) is a crucial regulator of mitochondrial function and is associated with injury and repair in acute kidney injury (AKI). To investigate whether mitochondrial damage and early renal fibrosis are associated with decreased renal SIRT3 levels, we established an in vivo model.

Methods: In vivo, we established ischaemia-reperfusion-induced AKI (IR-AKI) models in wild-type (WT) and SIRT3-knockout (SIRT3-KO) mice.

Different Surgical Approaches for treatment of isolated dissociated vertical deviation without inferior oblique overaction.

Purpose: To report the surgical results on superior rectus recession (SRR) and inferior oblique anterior transposition (IOAT) for cases with isolated bilateral dissociated vertical deviation（DVD）without inferior oblique overaction (IOOA).

Methods: A retrospective review was conducted for cases with isolated bilateral DVD without IOOA who were surgically treated using either bilateral SRR (SRR group) or IOAT (IOAT group). Pre- and post-operative ocular motility, ocular alignment, amount of DVD and complications were compared between the two groups.

Roles of SIRT6 in kidney disease: a novel therapeutic target.

SIRT6 is an NAD dependent deacetylase that belongs to the mammalian sirtuin family. SIRT6 is mainly located in the nucleus and regulates chromatin remodeling, genome stability, and gene transcription. SIRT6 extensively participates in various physiological activities such as DNA repair, energy metabolism, oxidative stress, inflammation, and fibrosis.

MicroRNA-214-5p aggravates sepsis-related acute kidney injury in mice.

Acute kidney injury (AKI) is a devastating comorbidity in sepsis and correlates with a very poor prognosis and increased mortality. Currently, we use lipopolysaccharide (LPS) to establish sepsis-related AKI and try to demonstrate the pathophysiological role of microRNA-214-5p (miR-214-5p) in this process. Mice were intravenously injected with the miR-214-5p agomir, antagomir or negative controls for three consecutive days and then received a single intraperitoneal injection of LPS (10 mg/kg) for 24 h to induce AKI.

Sirt6-mediated Nrf2/HO-1 activation alleviates angiotensin II-induced DNA DSBs and apoptosis in podocytes.

Recent studies suggested that DNA double-strand breaks (DSBs) were associated with the pathogenesis of chronic kidney disease (CKD). The purpose of this investigation was to determine the role of Sirtuin6 (Sirt6), a histone deacetylase related to DNA damage repair, in angiotensin (Ang) II-induced DNA DSBs and the cell injury of podocytes and explore the possible mechanism. Here we showed that an increase of DNA DSBs was accompanied by a reduction in Sirt6 expression in the glomeruli of patients with hypertensive nephropathy (HN).

Efficacy and Safety of Long-Term Corticosteroid Monotherapy in 26 Cases of Nephrotic Syndrome with Biopsy-Proven Membranous Nephropathy Induced by Seronegative Hepatitis B Virus-Associated Glomerulonephritis.

Background: Hepatitis B virus-associated glomerulonephritis (HBV-GN) can occur in patients with negative HBV serological antigens. Little is known about the treatment of seronegative HBV-GN (sn HBV-GN). The aim of this prospective study was to evaluate the efficacy and safety of corticosteroids in the treatment of sn HBV-GN.

Sirt6 deficiency aggravates angiotensin II-induced cholesterol accumulation and injury in podocytes.

Disturbed renal lipid metabolism, especially cholesterol dysregulation plays a crucial role in the pathogenesis of chronic kidney disease (CKD). We recently reported that angiotensin (Ang) II could induce cholesterol accumulation and injury in podocytes. However, the underlying mechanisms for these alterations remain unknown.

Rapamycin attenuates mitochondrial injury and renal tubular cell apoptosis in experimental contrast-induced acute kidney injury in rats.

Reactive oxygen species (ROS) overproduction and renal tubular epithelial cell (TEC) apoptosis are key mechanisms of contrast-induced acute kidney injury (CI-AKI). Mitochondria are the main source of intracellular ROS. In the present study, the characteristics of mitophagy and the effects of rapamycin on contrast-induced abnormalities in oxidative stress, mitochondrial injury and mitophagy, TEC apoptosis and renal function were investigated in a CI-AKI rat model.

TOFA induces cell cycle arrest and apoptosis in ACHN and 786-O cells through inhibiting PI3K/Akt/mTOR pathway.

Cancer cells usually have a high requirement for fatty acids in order to meet the rapid proliferation and metabolism. Acetyl-CoA carboxylase-α(ACCA) catalyzes the carboxylation of acetyl-CoA to malonyl-CoA and has been a rate-limiting enzyme in the synthesis of long chain fatty acid and cellular energy storage. 5-tetradecyloxy-2-furoic acid (TOFA) is well known as an allosteric inhibitor of ACCA.

Role of reactive oxygen species-mediated endoplasmic reticulum stress in contrast-induced renal tubular cell apoptosis.

Background: Renal tubular cell apoptosis is a key mechanism of contrast-induced acute kidney injury. It has been reported that endoplasmic reticulum (ER) stress is the underlying mechanism of high osmolar contrast-induced renal tubular cell apoptosis. Whether ER stress is involved in low osmolar contrast-induced renal tubular cell injury remains unclear.

IgA Nephropathy with Pathologic Features of Membranoproliferative Glomerulonephritis following Burn Injury.

IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide, accounting for approximately 30-40% of patients undergoing renal biopsy in Asia. The characteristic and diagnostic lesion of IgAN is the deposition of glomerular IgA. The morphological lesions observed by light microscopy are extremely variable.

Role of intracellular Ca2+ and Na+/Ca2+ exchanger in the pathogenesis of contrast-induced acute kidney injury.

The precise mechanisms underlying contrast-induced acute kidney injury (CI-AKI) are not well understood. Intracellular Ca(2+) overload is considered to be a key factor in CI-AKI. Voltage-dependent Ca(2+) channel (VDC) and Na(+)/Ca(2+) exchanger (NCX) system are the main pathways of intracellular Ca(2+) overload in pathological conditions.

[Effects of selective inhibition of reverse mode of Na(+)/Ca(2+) exchanger on rats with contrast-induced acute kidney injury].

Objective: Intracellular Ca(2+) overload is a key factor in contrast-induced renal tubular toxicity. Na(+)/Ca(2+) exchanger (NCX) system is one of main pathways of intracellular Ca(2+) overload. We explore the effects of KB-R7943, an inhibitor of reverse mode of NCX, on contrast-induced acute kidney injury (CI-AKI).

Selective inhibition of the reverse mode of Na(+)/Ca(2+) exchanger attenuates contrast-induced cell injury.

Background: The precise mechanisms underlying radiocontrast nephropathy (RCN) are not well understood. Intracellular Ca(2+) overload is considered to be a key factor in RCN. The Na(+)/Ca(2+) exchanger (NCX) system is one of the main pathways of intracellular Ca(2+) overload.

Na+/Ca2+ exchange inhibitor, KB-R7943, attenuates contrast-induced acute kidney injury.

Background: Intracellular Ca2+ overload is considered to be a key factor in contrast-induced acute kidney injury (CI-AKI). The Na+/Ca2+ exchanger (NCX) system is one of the main pathways of intracellular Ca2+ overload. We investigated the effects of KB-R7943, an inhibitor of the reverse mode of NCX, on CI-AKI in a rat model.

[Effects of hypercholesterolemia on contrast media-induced nephrotoxicity in rats].

Objective: To explore the effects of short- and long-term dietary hypercholesterolemia on contrast media-induced nephrotoxicity in rats.

Methods: The male Wistar rats were fed either a normal rodent diet or a high cholesterol diet. At the end of 2 and 8 weeks, 8 rats from each group received a tail vein injection of either Iohexol injection (groups NC and HC) or vehicle (groups N and H).

Effects of short- and long-term hypercholesterolemia on contrast-induced acute kidney injury.

Background: Whether hypercholesterolemia is a risk factor for contrast-induced acute kidney injury (CI-AKI) remains unclear. In the present study, the effects of short- and long-term dietary hypercholesterolemia on contrast media-induced nephrotoxicity were evaluated.

Methods: Rats were fed either a normal rodent diet (N) or high-cholesterol diet (H).

Candesartan attenuates Angiotensin II-induced mesangial cell apoptosis via TLR4/MyD88 pathway.

Angiotensin II (Ang II) can stimulate Toll-like receptor 4 (TLR4) expression in mesangial cells (MCs), but the role of TLR4 in the Ang II-induced apoptosis and the effect of candesartan on TLR4 expression remain unclear. Here, we report that Ang II-induced MC apoptosis in a time-dependent manner and up-regulated TLR4/MyD88 expression, and that the intracellular ROS was subsequently increased. We also show that candesartan attenuated the Ang II-induced MC apoptosis, and that this protective effect was dependent on decreased TLR4/MyD88 expression as well as reduced intracellular ROS formation.

CD19+CD5+ B cells in primary IgA nephropathy.

The source of IgA and the mechanism for deposition of IgA in the mesangium remain unknown for primary IgA nephropathy. Because CD19(+)CD5(+) B cells are important producers of IgA and contribute to several autoimmune diseases, they may play an important role in IgA nephropathy. In this study, flow cytometry, quantitative PCR, and confocal microscopy were used to assess the frequency, distribution, Ig production, CD phenotypes, cytokine production, and sensitivity to apoptosis of CD19(+)CD5(+) B cells in the peripheral blood, peritoneal fluid, and kidney biopsies of 36 patients with primary IgA nephropathy.

Fluvastatin prevents oxidized low-density lipoprotein-induced injury of renal tubular epithelial cells by inhibiting the phosphatidylinositol 3-kinase/Akt-signaling pathway.

Background: Lipid abnormalities may play a role in the progression of nephrosis. Recent studies have demonstrated that oxidized low-density lipoprotein (oxLDL) appears to be a detrimental factor for the glomerular mesangium and podocytes. The aim of the present study is to identify the potential effects of oxLDL on tubular epithelial cells (TECs) in vitro and to investigate its associated signal transduction pathway, as well as to examine whether fluvastatin reverses the responses of TECs to oxLDL.