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Several intracellular pathological processes have been reported to be regulated by the FAM19A5/S1PR1 signaling pathway. However, the role of FAM19A5/S1PR1 signaling pathway in the viability and proliferation of mantle cell lymphoma is not been completely understood. The task of this study is to explore the influence of FAM19A5/S1PR1 signaling pathway in affecting the survival and growth of mantle cell lymphoma. shRNAs against FAM19A5 or S1PR1 were transfected into mantle cell lymphom. Cell viability and proliferation were measured through MTT assay and CCK8 assay, respectively. Our results demonstrated that loss of FAM19A5 significantly reduced the viability of mantle cell lymphom, an effect that was followed by a drop in cell proliferation capacity. Besides, inhibition of S1PR1 also impairs cell survival and interrupt mantle cell lymphom proliferation in vitro. Taken together, our results illustrate that FAM19A5/S1PR1 signaling pathway is associated with the regulation of mantle cell lymphom viability and proliferation. This finding will provide a potential target for the treatment of malignant lymphoma in the clinical practice.PINK1 and PRKN, which cause Parkinson disease when mutated, form a quality control mitophagy pathway that is well-characterized in cultured cells. The extent to which the PINK1-PRKN pathway contributes to mitophagy in vivo, however, is controversial. This is due in large part to conflicting results from studies using one of two mitophagy reporters mt-Keima or mito-QC. Studies using mt-Keima have generally detected PINK1-PRKN mitophagy in vivo, whereas those using mito-QC generally have not. Here, we directly compared the performance of mito-QC and mt-Keima in cell culture and in mice subjected to a PINK1-PRKN activating stress. We found that mito-QC was less sensitive than mt-Keima for mitophagy, and that this difference was more pronounced for PINK1-PRKN mitophagy. These findings suggest that mito-QC's poor sensitivity may account for conflicting reports of PINK1-PRKN mitophagy in vivo and caution against using mito-QC as a reporter for PINK1-PRKN mitophagy.Alzheimer's disease (AD) is associated with an impairment of autobiographical memories, leading to the production of nonspecific memories. Recent research has demonstrated that odor can serve as a powerful cue for the retrieval of autobiographical memories in AD. Moreover, studies conducted in young adults have showed that odor-evoked autobiographical memories are evoked with more details compared with memories triggered by other sensory modalities. Building on the latter research, we compared specificity, subjective experience, emotional characteristics and retrieval time of autobiographical memories evoked by odor cue, visual cue and verbal cue. To this end, we invited participants with mild AD and control participants to retrieve autobiographical memories after the presentation of an odor, a visual representation of the odorant, or a verbal label of the odorant. Results showed more specificity, higher arousal and more positive memories after odor exposure compared to the visual cue and verbal cue in AD and control participants. In AD participants, autobiographical were retrieved faster after odor-exposure compared to memories evoked by a visual cue and a verbal cue, suggesting the automatic nature of odor-evoked autobiographical memories. Overall, these findings demonstrate that odor is more effective than visual or verbal cues for autobiographical retrieval in AD.
A comprehensive understanding of vascular calcification pathology is significant for the development of cardiovascular disease therapy in high-risk populations. This cross-sectional study aimed to evaluate the prevalence and characteristics of radial artery calcification (RAC) and to identify the factors that are associated with RAC in end-stage kidney disease (ESKD).
Detailed medical histories of 180 patients with ESKD were recorded. Fragments of the radial artery obtained during the creation of arteriovenous fistula for hemodialysis access were stained with alizarin red S.
Calcification was localized in the arterial media layer. The prevalence of positive calcification staining in the radial arteries was 21.1% (
= 38). Patients with RAC had a higher glycated hemoglobin level (
< 0.01), higher prevalence of dialysis duration >5 years (
= 0.022), and diabetes mellitus (
< 0.01) than those without RAC. Multiple logistic regression models showed dialysis duration >5 years (odds ratio [RAC. Thus, the combination of prolonged dialysis and hyperglycemic conditions exerts a synergistic effect on RAC.
Chronic kidney disease (CKD) and diabetes mellitus increase atherosclerotic cardiovascular diseases (ASCVD) risk. However, the association between renal outcome of diabetic kidney disease (DKD) and ASCVD risk is unclear.
This retrospective study enrolled 218 type 2 diabetic patients with biopsy-proven DKD, and without known cardiovascular diseases. Baseline characteristics were obtained and the 10-year ASCVD risk score was calculated using the Pooled Cohort Equation (PCE). Eprenetapopt molecular weight Renal outcome was defined as progression to end-stage renal disease (ESRD). The association between ASCVD risk and renal function and outcome was analyzed with logistic regression and Cox analysis.
Among all patients, the median 10-year ASCVD risk score was 14.1%. The median of ASCVD risk score in CKD stage 1, 2, 3, and 4 was 10.9%, 12.3%, 16.5%, and 14.8%, respectively (
= 0.268). Compared with patients with lower ASCVD risk (<14.1%), those with higher ASCVD risk had lower eGFR, higher systolic blood pressure, and more severe renal interstitial inflammation. High ASCVD risk (>14.1%) was an independent indicator of renal dysfunction in multivariable-adjusted logistic analysis (OR, 3.997; 95%CI, 1.385-11.530;
= 0.010), though failed to be an independent risk factor for ESRD in patients with DKD in univariate and multivariate Cox analysis.
DKD patients even in CKD stage 1 had comparable ASCVD risk score to patients in CKD stage 2, 3, and 4. Higher ASCVD risk indicated severe renal insufficiency, while no prognostic value of ASVCD risk for renal outcome was observed, which implied macroangiopathy and microangiopathy in patients with DKD were related, but relatively independent.
DKD patients even in CKD stage 1 had comparable ASCVD risk score to patients in CKD stage 2, 3, and 4. Higher ASCVD risk indicated severe renal insufficiency, while no prognostic value of ASVCD risk for renal outcome was observed, which implied macroangiopathy and microangiopathy in patients with DKD were related, but relatively independent.
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