Notes

Thromboembolic Occasions Throughout Therapy using Cisplatin-based Chemotherapy within Metastatic Testicular Germ-cell Cancers 2000-2014: A Population-based Cohort Review.
NLRP3 inflammasome-associated proteins were greatly decreased in MTDs-induced mouse model. MTDs-induced inflammation and lung injury were alleviated by autophagy enhancement. Autophagy can function as an effective way to alleviate inflammation in MTDs-induced ALI by inhibiting NLRP3 inflammasome and may represent a therapeutic target in modulating MTDs-induced inflammatory response.
Ischemic renal disease (IRD) can cause kidney damage and eventually lead to end-stage renal disease. Adiponectin (APN), a recently discovered collagen-like protein secreted by adipose tissues, plays an important role in regulating energy metabolism and inflammation. This study aimed to explore the specific mechanism by which APN affects IRD.

We cultured human renal tubular epithelial cells (HK-2) and created a mouse model of IRD to detect apoptosis-related indicators in vitro and in vivo.

Compared with those in the control group, the apoptosis rate and expression levels of Bax and Fas increased in the CoCl
-induced hypoxia model group. However, the expression of Bcl-2 decreased, and after the combined treatment with APN, the phenomenon mentioned above was reversed. Moreover, studies have found that stanniocalcin-1 (STC-1) and uncoupling protein3 (UCP3) are also involved in the protective effect of APN. Additionally, we found that the glomeruli of the mice were significantly enlarged after the APN gene was knocked out; furthermore, the number of collagen fibers in the renal tubules, as well as the expression of the corresponding fibrogenic factors, increased significantly. More importantly, after the knockout of the APN gene, the expression of the hypoxia-inducible factors HIF-1α and HIF-1β and the apoptotic rate of renal tissue cells also increased.

These results indicate that APN can alleviate the symptoms of IRD by inhibiting renal cell apoptosis. Thus, in the future, APN may be a new target for the treatment of IRD.

Cobalt chloride (PubChem CID 24643).
Cobalt chloride (PubChem CID 24643).Liver regeneration after partial hepatectomy (PH) is a complex and well-orchestrated process involving multiple factors such as cytokines, growth factors, and signaling pathways. MicroRNAs (miRNAs) participate in various biological processes including liver regeneration after PH. In the current study, we investigated the expression and function of human umbilical cord blood mesenchymal stem cell (hUCB-MSC) derived exosomal miRNAs on liver regeneration using a rat PH model. We found that hUCB-MSC derived exosomes promoted rat liver regeneration and ameliorated liver injury after PH. MicroRNA microarray was performed to identify the differentially expressed miRNAs in hUCB-MSC derived exosomes involving in liver regeneration after PH. We demonstrated that hUCB-MSC derived exosomal miR-124 could promote liver regeneration and prevent against liver injury after PH in rats. Inhibition of miR-124 abrogated the protective role of hUCB-MSC derived exosome in rat liver regeneration after PH. BAY 2416964 ic50 In addition, we identified that transcription factor Foxg1 was a direct target of miR-124 and miR-124 promoted rat liver cell proliferation via suppressing Foxg1 expression. Furthermore, we demonstrated that hUCB-MSC derived exosomal miR-124 enhanced liver regeneration via inhibiting Foxg1 in rats after PH. In summary, our findings suggest that hUCB-MSC-derived exosomal miR-124 could promote rat liver regeneration after PH via downregulating Foxg1.
Cyclophosphamide (CYP) is a potent anticancer agent with well-known cardiotoxicity that limits its clinical applications. Cilostazol is a vosodilating drug, showing a cardioprotective effect in some cardiac disorders; however its effect in CYP-induced cardiotoxicity is still uncertain. We investigated the effect of cilostazol against CYP-induced cardiotoxicity and the contribution of SIRT1 signaling.

7week-old male Wistar albino rats were treated with cilostazol (30mg/kg/day, orally) in the absence or presence of SIRT1 inhibitor, EX-527 (5mg/kg/day, IP) for 10days and injected with CYP (200mg/kg, IP) on the 7th day of the study. Age-matched rats were used as control group. On the 11th day, hearts were harvested for biochemical, immunoblotting and histological analyses. Markers of cardiac injury were assessed in plasma samples.

CYP injection contributed to cardiac injury manifested as significant increases in plasma activities of heart enzymes and cardiac troponin I levels. Cilostazol attenuated cardiac injury and minimized the histological lesions in hearts of CYP-treated rats. Cilostazol induced 3 fold up-regulation of SIRT1 and promoted the antioxidant defense response through FoxO1-related mechanism in hearts of CYP-treated rats. Cilostazol suppressed the CYP-induced up-regulation of PARP1 and p53, and blocked the NF-kB p65-mediated inflammatory response in hearts of CYP-treated rats. All the beneficial effects of cilostazol were almost abolished by EX-527.

These data provided insights into the mechanism underlying the cardioprotective effect of cilostazol in CYP-treated rats through upregulation of SIRT1 signaling, suggesting that cilostazol might be a candidate modality for CYP-induced cardiotoxicity.
These data provided insights into the mechanism underlying the cardioprotective effect of cilostazol in CYP-treated rats through upregulation of SIRT1 signaling, suggesting that cilostazol might be a candidate modality for CYP-induced cardiotoxicity.
This study aimed to elucidate the role of microRNAs (miRNAs) during myocardial infarction (MI) development in vivo and in vitro.

Differentially expressed miRNAs between heart tissue from the MI mouse model and the control mouse were identified via microarray. Quantitative PCR (qPCR) and western blotting (WB) were performed to examine the expression levels of miRNAs and proteins, respectively. EdU-staining and colony formation assay were performed to assess cell viability and growth. Annexin V- and PI-staining-based flow cytometry was used to assess cell apoptosis. An MI mouse model was also established to study the function of miR-1278 in vivo.

The levels of miR-1278 were reduced in the infarct regions of heart tissues of the MI mouse model and in H
O
-treated newborn murine ventricular cardiomyocytes (NMVCs) compared to those in the heart tissues of healthy mice and non-treated NMVCs. H
O
treatment suppressed the proliferation of NMVCs, while miR-1278 upregulation improved it. Moreover, we found that miR-1278 inhibited the upregulation of IL-22 and CXCL14 expression in H
O
-treated NMVCs by directly binding with the 3'-UTRs of both IL-22 and CXCL14. Furthermore, restoration of IL-22 and CXCL14 in H
O
-treated NMVCs promoted miR-1278-induced inflammation and apoptosis. Administration of agomiR-1278 to the MI mouse model significantly improved cardiac activity.

Collectively, our findings illustrate that the expression of miR-1278 is low in H
O
-treated NMVCs and post-MI cardiac tissues, and the overexpression of miR-1278 in these protects against cell death by modulating IL-22 and CXCL14 expression.
Collectively, our findings illustrate that the expression of miR-1278 is low in H2O2-treated NMVCs and post-MI cardiac tissues, and the overexpression of miR-1278 in these protects against cell death by modulating IL-22 and CXCL14 expression.
Proton pump inhibitors (PPIs) are widely used drugs recently linked to chronic kidney disease. However, the invloved mechanisms remained elusive. Since defective autophagy is identified as a new culprit in the pathogenesis of diabetic nephropathy (DN), we aimed to trace the link of autophagy blockade by PPIs to the progression of DN with and without the standard therapy of metformin and enalapril.

Male CD1 albino mice (20-25g) were randomly assigned to normal control or diabetic mice. Diabetes was induced by intraperitoneal streptozotocin (35mg/kg) injection combined with high fat diet. DN mice were randomized to receive vehicle, lansoprazole (5mg/kg), metformin (200mg/kg), lansoprazole+metformin, metformin+enalapril (0.5mg/kg) or the three drugs together, orally daily for four weeks. At the study end, albuminuria, fasting plasma glucose, HbA1c, renal functions and malondialdehyde were assessed. Renal tissues were examined microscopically, and autophagic changes were evaluated by immunohistochemical detection of LC3-II and p62.

Consistent with autophagic blockade, lansoprazole increased both LC3II and p62 in the glomerular and tubular cells. This was associated with impaired creatinine clearance and renal functions, enhanced albuminuria, oxidative stress and augmented DN histopathological changes. Opposite effects on autophagy markers were observed by single or combined treatment of metformin with enalapril; which also ameliorated glycemic control and signs of DN. This improvement was mitigated by combination with lansoprazole.

Autophagy blockade by lansoprazole augmented diabetic nephropathy and opposed the reno-protective effects of metformin and enalapril. The use of PPIs in diabetes should be considered with great caution.
Autophagy blockade by lansoprazole augmented diabetic nephropathy and opposed the reno-protective effects of metformin and enalapril. The use of PPIs in diabetes should be considered with great caution.
Although chemotherapeutic agents have highly beneficial effects against cancer, they disturb the body's normal homeostasis. One of the critical side effects of chemotherapeutic agents is their deleterious effect on the cardiac system, which causes limitations of their clinical usage. Taurine constitutes more than 50% of the amino acids in the heart. The use of taurine might prevent chemotherapy-induced cardiotoxicity. This systematic study aims to evaluate the protective role of taurine against cardiotoxicity induced by chemotherapy.

A systematic search was performed in databases up to November 2020, and the review is designed on PRISMA guidelines. The search keywords were selected based on our study target and were searched in the title and abstract. After the consecutive screening, out of a whole of 94 articles, 8 articles were included according to our inclusion and exclusion criteria.

According to the study results, chemotherapy decreases body and heart weight and increases mortality. Also, it inducination simultaneously.
To describe the academic concerns and risk strata of children with sickle cell disease (SCD) as identified through a parent-directed screening tool and to compare the rates of these concerns with actual school service utilization in the clinic population.

We completed a retrospective review of patients with SCD referred to the school intervention program during the 2017-2018 and 2018-2019 school years because of a school-related concern raised by parents or noted by the clinical team. All parents completed the Brief School Needs Inventory (BSNI), a validated parent-response tool used to stratify academic risk. Rates of special education services, grade retention, and results from neuropsychologic testing were captured. Clinical history, the use of disease-modifying therapy, and results from laboratory and neuroimaging studies were also obtained. Descriptive statistics were performed to examine demographic information, clinical history, and BSNI results.

In total, 137 unique patients (age range, 14months to 19years) completed the BSNI during the study period, for 181 events.
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