Meat adulteration is a global problem which undermines market fairness and harms people with allergies or certain religious beliefs. In this study, a novel framework in which a one-dimensional ...convolutional neural network (1DCNN) serves as a backbone and a random forest regressor (RFR) serves as a regressor, named 1DCNN-RFR, is proposed for the quantitative detection of beef adulterated with pork using electronic nose (E-nose) data. The 1DCNN backbone extracted a sufficient number of features from a multichannel input matrix converted from the raw E-nose data. The RFR improved the regression performance due to its strong prediction ability. The effectiveness of the 1DCNN-RFR framework was verified by comparing it with four other models (support vector regression model (SVR), RFR, backpropagation neural network (BPNN), and 1DCNN). The proposed 1DCNN-RFR framework performed best in the quantitative detection of beef adulterated with pork. This study indicated that the proposed 1DCNN-RFR framework could be used as an effective tool for the quantitative detection of meat adulteration.
This study examined whether depression was a risk factor for onset of dementia including Alzheimer's disease (AD), vascular dementia (VD) and any dementia, and mild cognitive impairment (MCI) by ...using a quantitative meta-analysis of longitudinal studies.
EMBASE and MEDLINE were searched for articles published up to February 2011. All studies that examined the relationship between depression and the onset of dementia or MCI were included. Pooled relative risk was calculated using fixed-effects models.
Twelve studies met our inclusion criteria for this meta-analysis. All subjects were without dementia or MCI at baseline. Four, two, five, and four studies compared the incidence of AD, VD, any dementia, and MCI between subjects with or without depression, respectively. After pooling all the studies, subjects with depression had higher incidence of AD (relative risk (RR):1.66, 95% confidence interval (CI): 1.29-2.14), VD (RR: 1.89, 95% CI: 1.19-3.01), any dementia (RR: 1.55, 95% CI: 1.31-2.83), and MCI (RR: 1.97, 95% CI: 1.53-2.54) than those without depression.
The quantitative meta-analysis showed that depression was a major risk factor for incidence of dementia (including AD, VD, and any dementia) and MCI.
Objective We examined the association between nonalcoholic fatty liver disease and lumbar spine bone mineral density in individuals with and without type 2 diabetes. Methods The lumbar BMD of 1088 ...subjects was measured using dual-energy X-ray absorptiometry (DXA). Liver fat content was quantified via B-mode ultrasound. Multivariable linear regression was used to study the association between NAFLD and lumbar BMD in participants with and without T2DM. Results The lumbar BMD in the T2DM group and the non-diabetes group was higher in the NAFLD group than in the non-NAFLD group (P < 0.001). Multivariate regression analysis in the T2DM group showed that after adjusting for confounders, the positive association between lumbar spine BMD and NAFLD remained (P = 0.027). In the non-diabetes group, after adjusting for confounders, the association between NAFLD and lumbar spine BMD disappeared. Conclusions The relationship between nonalcoholic fatty liver disease and lumbar bone mineral density may differ in individuals with and without diabetes. The effect of nonalcoholic fatty liver disease on bone mineral density needs to be evaluated in different clinical contexts. Keywords: Nonalcoholic fatty liver, Diabetes, Lumbar, Bone mineral density
Glaucoma is the leading cause of irreversible blindness worldwide, and pathologically elevated intraocular pressure (IOP) is the major risk factor. Neuroprotection is one of the potential therapies ...for glaucomatous retinal damage. Intravitreal mesenchymal stem cell (MSC) transplantation provides a viable therapeutic option, and human umbilical cord- (hUC-) MSCs are attractive candidates for cell-based neuroprotection. Here, we investigated the ability of transplanted hUC-MSCs to survive and migrate within the vitreous cavity and their neuroprotective effects on chronic glaucomatous retina. For this, we developed a chronic ocular hypertension (COH) rat model through the intracameral injection of allogeneic Tenon’s fibroblasts. Green fluorescent protein-transduced hUC-MSCs were then injected into the vitreous cavity one week after COH induction. Results showed that a moderate IOP elevation lasted for two months. Transplanted hUC-MSCs migrated toward the area of damaged retina, but did not penetrate into the retina. The hUC-MSCs survived for at least eight weeks in the vitreous cavity. Moreover, the hUC-MSCs were efficient at decreasing the loss of retinal ganglion cells; retinal damage was attenuated through the inhibition of apoptosis. In this study, we have developed a novel COH rat model and demonstrated the prolonged neuroprotective potential of intravitreal hUC-MSCs in chronic glaucoma.
Menin (MEN1) is a critical modulator of tissue development and maintenance. As such, MEN1 mutations are associated with multiple endocrine neoplasia type 1 (MEN1) syndrome. Although menin is ...abundantly expressed in the nervous system, little is known with regard to its function in the adult brain. Here, we demonstrate that neuron-specific deletion of Men1 (CcKO) affects dendritic branching and spine formation, resulting in defects in synaptic function, learning, and memory. Furthermore, we find that menin binds to the p35 promoter region to facilitate p35 transcription. As a primary Cdk5 activator, p35 is expressed mainly in neurons and is critical for brain development and synaptic plasticity. Restoration of p35 expression in the hippocampus and cortex of Men1 CcKO mice rescues synaptic and cognitive deficits associated with Men1 deletion. These results reveal a critical role for menin in synaptic and cognitive function by modulating the p35-Cdk5 pathway.
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•The tumor suppressor menin is expressed in neurons and increases during maturation•Neuronal menin deficiency leads to impaired learning and memory in mice•Menin binds the p35 promoter locus and promotes p35 transcription•Restoring p35 expression rescues cognitive impairment associated with menin deletion
The biological function of menin in neurons remains unclear. Zhuang et al. report that menin regulates neuronal dendritic branching, spine density, and synaptic plasticity. Menin binds to the p35 promoter to enhance p35 transcription and CDK5 activity. The study demonstrates a role for menin in synaptic and cognitive function.
Dysfunction of parvalbumin (PV) neurons is closely involved in depression, however, the detailed mechanism remains unclear. Based on the previous finding that multiple endocrine neoplasia type 1 ...(Protein: Menin; Gene: Men1) mutation (G503D) is associated with a higher risk of depression, a Menin‐G503D mouse model is generated that exhibits heritable depressive‐like phenotypes and increases PV expression in brain. This study generates and screens a serial of neuronal specific Men1 deletion mice, and found that PV interneuron Men1 deletion mice (PcKO) exhibit increased cortical PV levels and depressive‐like behaviors. Restoration of Menin, knockdown PV expression or inhibition of PV neuronal activity in PV neurons all can ameliorate the depressive‐like behaviors of PcKO mice. This study next found that ketamine stabilizes Menin by inhibiting protein kinase A (PKA) activity, which mediates the anti‐depressant function of ketamine. These results demonstrate a critical role for Menin in depression, and prove that Menin is key to the antidepressant function of ketamine.
Parvalbumin (PV) increases in several depression mice models. Men1 deficiency in PV interneurons (PcKO) increases pvalb transcription and PV expression by H3K27me3 modification and leading to depression‐like behaviors in mice. The depressive‐like behaviors in PcKO mice can be rescued by PV knockdown or Menin restoring. Ketamine stabilizes Menin protein to contribute its's anti‐depressant function.
Highlights • Evidence shows that autophagy is involved in the pathological process of glaucoma. • The crosstalk between autophagy and apoptosis in glaucoma is not fully understood. • Evidence shows ...that autophagy can inhibit or enhance apoptosis in glaucomatous RGCs. • The modulation of autophagy may be a therapeutic option for glaucoma in the future.
Astrocyte dysfunction and inflammation are associated with the pathogenesis of major depressive disorder (MDD). However, the mechanisms underlying these effects remain largely unknown. Here, we found ...that multiple endocrine neoplasia type 1 (Men1; protein: menin) expression is attenuated in the brain of mice exposed to CUMS (chronic unpredictable mild stress) or lipopolysaccharide. Astrocyte-specific reduction of Men1 (GcKO) led to depressive-like behaviors in mice. We observed enhanced NF-κB activation and IL-1β production with menin deficiency in astrocytes, where depressive-like behaviors in GcKO mice were restored by NF-κB inhibitor or IL-1β receptor antagonist. Importantly, we identified a SNP, rs375804228, in human MEN1, where G503D substitution is associated with a higher risk of MDD onset. G503D substitution abolished menin-p65 interactions, thereby enhancing NF-κB activation and IL-1β production. Our results reveal a distinct astroglial role for menin in regulating neuroinflammation in depression, indicating that menin may be an attractive therapeutic target in MDD.
•Astroglia menin deficiency leads to depressive-like behaviors in mice•Menin reduction in astrocytes promotes IL-1β generation through NF-κB activation•NF-κB and IL-1β inhibitors attenuate the depressive-like phenotypes•A MEN1 SNP associated with MDD risk leads to aberrant NF-κB activation
Mechanisms underlying astrocyte-mediated neuroinflammation in depression remain unclear. Menin regulates NF-κB activity in astrocytes to promote neuroinflammation. Clinically, a MEN1 SNP is associated with the onset of depression. This study reveals a distinct role for menin in neuroinflammation and depression.
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