Trajectories of Alcohol and Drug Use and Dependence From Adolescence to Adulthood: The Effects of Familial Alcoholism and Personality.

This study describes trajectories of substance use and dependence from adolescence to adulthood. Identified consumption groups include heavy drinking/heavy drug use, moderate drinking/experimental drug use, and light drinking/rare drug use. Dependence groups include alcohol only, drug only, and comorbid groups. The heavy drinking/heavy drug use group was at risk for alcohol and drug dependence and persistent dependence and showed more familial alcoholism, negative emotionality, and low constraint. The moderate drinking/experimental drug use group was at risk for alcohol dependence but not comorbid or persistent dependence and showed less negative emotionality and higher constraint. Familial alcoholism raised risk for alcohol and drug use and dependence in part because children from alcoholic families were more impulsive and lower in agreeableness. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

"Prospective relations between bulimic pathology, depression, and substance abuse: Unpacking comorbidity in adolescent girls": Correction to Stice et al. (2004).

Reports an error in "Prospective Relations Between Bulimic Pathology, Depression, and Substance Abuse: Unpacking Comorbidity in Adolescent Girls" by Eric Stice, Emily M. Burton and Heather Shaw (Journal of Consulting and Clinical Psychology, 2004[Feb], Vol 72[1], 62-71). The findings of Leon, Fulkerson, Perry, Keel, and Klump ("Three to four year prospective evaluation of personality and behavioral risk factors for later disordered eating in adolescent girls and boys," Journal of Youth and Adolescence, 1999, Vol. 28, No. 2, pp. 181-196), cited on page 62, were incorrectly reported. Leon et al. (1999) found that the latent variable of negative affect/attitudes determined at study entrance significantly correlated with final year eating disorder risk score when conducted with the full sample and when removing Time 1 high eating disorder risk subjects. This latent variable consisted of the GBI Depression, MPQ Negative Emotionality, EDI Ineffectiveness, EDI Interoceptive Awareness, and EDI Body Dissatisfaction scales. A subsequent univariate analysis of Time 1 Negative Emotionality scale score on Time 3 eating disorder risk, adjusting for initial eating disorder risk score, showed a nonsignificant effect size (Stice, E. [2002]. Risk and maintenance factors for eating pathology: A meta-analytic review. Psychological Bulletin, 128, 825-848). (The following abstract of the original article appeared in record 2004-10364-006.) To elucidate the processes that contribute to the comorbidity between bulimic pathology, depression, and substance abuse, the authors tested the temporal relations between these disturbances with prospective data from adolescent girls (N = 496). Multivariate analyses indicated that depressive symptoms predicted onset of bulimic pathology but not of substance abuse, bulimic symptoms predicted onset of depression but not of substance abuse, and substance abuse symptoms predicted onset of depression but not of bulimic pathology. Results suggest that the comorbidity arises because certain disorders are risk factors for the other disorders. Findings also provide support for select etiologic theories and further establish the clinical significance of these conditions by showing that they increase risk for onset of other psychiatric disturbances. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

The Effectiveness of Telephone-Based Continuing Care in the Clinical Management of Alcohol and Cocaine Use Disorders: 12-Month Outcomes.

This study of continuing care for substance dependent patients compared a telephone-based monitoring and brief counseling intervention (TEL) with 2 face-to-face interventions, relapse prevention (RP) and standard 12-step group counseling (STND). The participants were graduates of intensive outpatient programs who had current dependence on alcohol and/or cocaine. Self-report, collateral, and biological measures of alcohol and cocaine use were obtained over a 12-month follow-up. The treatment groups did not differ on abstinence-related outcomes in the complete sample (N = 359) or on cocaine use outcomes in participants with cocaine dependence (n = 268). However, in participants with alcohol dependence only (n = 91), TEL produced better alcohol use outcomes than STND on all measures examined and better outcomes than RP on some of the measures. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Psychometric Evaluation of the Parent Situation Inventory: A Role-Play Measure of Coping in Parents of Substance-Using Adolescents.

This article reports on the generalizability, reliability, and construct validity of the Parent Situation Inventory (PSI), a role-play measure of coping skills in parents experiencing problems from an adolescent's drug and alcohol use. Generalizability was robust (.80) and alternate form and test-retest reliability were satisfactory. PSI skillfulness was negatively related to the parent's own substance use and to the adolescent's alcohol use. The PSI shows promise as a reliable and potentially valid measure of coping in this population and has direct implications for developing and evaluating skill-based parent training programs. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

加工工艺对香榧籽油中挥发性物质组成的影响

旨在为风味香榧籽油的开发提供理论支持,考察了不同加工工艺（烘烤温度和压榨工艺）对香榧籽油理化指标的影响,并采用电子鼻、顶空固相微萃取-气质联用（HS-SPME-GC-MS/MS）等技术研究不同烘烤温度（140、150、160、170、180 ℃）和压榨工艺（螺杆压榨和液压压榨）对香榧籽油中挥发性物质组成的影响。结果表明：烘烤温度和压榨工艺对香榧籽油酸值影响较小,随烘烤温度的升高,螺杆压榨和液压压榨对香榧籽油过氧化值的影响不同,但不同烘烤温度和压榨工艺条件下制取的香榧籽油酸值和过氧化值均符合GB 2716—2018中的要求;电子鼻分析表明氮氧化合物、硫化物、芳香成分、甲基类物质对香榧籽油风味的影响较大;液压压榨和螺杆压榨香榧籽油风味最浓郁的烘烤温度分别为140 ℃和170 ℃;香榧籽油中共检出挥发性物质7类42种,其中萜烯类物质占主导;不同温度烘烤后液压压榨制取的香榧籽油中共有5种挥发性物质的相对含量发生显著变化,而螺杆压榨制取的香榧籽油中有18种挥发性物质的相对含量发生显著变化,柏木脑和香芹酮为两种压榨工艺共有的相对含量发生显著变化的物质。综上,压榨工艺会影响香榧籽油达到浓郁风味所需要的热风烘烤条件,且螺杆压榨相较于液压压榨,其风味物质种类变化更加丰富。     

Upregulation of miR145 and miR126 in EVs from Renal Cells Undergoing EMT and Urine of Diabetic Nephropathy Patients

Simple SummaryDiabetic nephropathy is one of the most frequent complications of diabetes, resulting from diffuse damage to different kidney cells. The identification of subjects at risk is mandatory to prevent its development and provide appropriate therapies reducing the unmanageable evolution towards end-stage kidney disease. The aim of this work was to identify urinary-derived extracellular vesicles (EVs) miRNA cargo to be used as biomarker of kidney damage in diabetic patients. The miRNA profile was then correlated with the molecular mechanism associated with the glomerular and tubular damage using a diabetic-like model. In patients, miR145 and miR126 in urinary EVs increased together with albuminuria. MiR145 and miR126 increased in parallel in EVs from renal epithelial cells undergoing transition to a fibrotic mesenchymal phenotype. These data unveiled a role for miR126 and miR145 as the biomarkers of damage progression and proteinuria development in diabetic nephropathy. AbstractDiabetic nephropathy (DN) is a severe kidney-related complication of type 1 and type 2 diabetes and the most frequent cause of end-stage kidney disease. Extracellular vesicles (EVs) present in the urine mainly derive from the cells of the nephron, thus representing an interesting tool mirroring the kidney’s physiological state. In search of the biomarkers of disease progression, we here assessed a panel of urinary EV miRNAs previously related to DN in type 2 diabetic patients stratified based on proteinuria levels. We found that during DN progression, miR145 and miR126 specifically increased in urinary EVs from diabetic patients together with albuminuria. In vitro, miRNA modulation was assessed in a model of TGF-β1-induced glomerular damage within a three-dimensional perfusion system, as well as in a model of tubular damage induced by albumin and glucose overload. Both renal tubular cells and podocytes undergoing epithelial to mesenchymal transition released EVs containing increased miR145 and miR126 levels. At the same time, miR126 levels were reduced in EVs released by glomerular endothelial cells. This work highlights a modulation of miR126 and miR145 during the progression of kidney damage in diabetes as biomarkers of epithelial to mesenchymal transition.     

Circ_0011129 Encapsulated by the Small Extracellular Vesicles Derived from Human Stem Cells Ameliorate Skin Photoaging

Photoaging is not only the main cause of skin aging caused by exogenous factors, it is also related to a variety of skin diseases and even malignant tumors. Excessive and repeated exposure to ultraviolet radiation, especially UVA induces oxidative stress, DNA damage, inflammation, and collagen and elastin degeneration, ultimately leads to skin photoaging, manifested by skin redness, coarse wrinkles, and pigmentation even skin cancer. There has been a large demand of effective prevention and medications but approaches in the current management of photoaging are very limited. In the previous study, we found that a non-coding circular RNA circ_0011129 acts as a miR-6732-5p adsorption sponge to inhibit the reduction of type I collagen and the denaturation and accumulation of elastin in UVA-induced HDF cells photoaging model. However, in vivo instability and efficient delivery to the target cell of circRNA is a major challenge for its clinical application. Therefore, improving its stability and delivery efficiency are desired. In this study, we proposed a strategy of delivering circ_0011129 with small extracellular vesicles (sEVs) from human adipose-derived stem cells (hADSCs) to intervene in the photoaging process. The results showed that sEVs from hADSCs in 3D bioreactor culture (3D-sEVs) can prevent photoaging. Consequently, by overexpressing circ_0011129 in hADSCs, we successfully loaded it into 3D-sEVs (3D-circ-sEVs) and its protective effect was better. Our studies provide a novel approach to preventing skin photoaging, which has important clinical significance and application value for the development of non-coding RNA drugs to treat skin photoaging. We first screened out hADSCs-derived sEVs with excellent anti-oxidant effects. We then compared the sEVs collected from traditional 2D culture with 3D bioreactor culture. By miRNA-seq and GEO data analysis, we found that miRNAs in 3D-sEVs were enriched in cell activities related to apoptosis, cellular senescence, and inflammation. Subsequently, we prepared circ_0011129-loaded 3D-sEVs (3D-circ-sEVs) by overexpressing it in hADSCs for the treatment of photoaging in vitro. We proved that 3D-circ-sEVs can interfere with the process of cell photoaging and protect cells from UVA radiation damage, as well as in a H2O2-induced oxidative stress model.     

Endogenous Modulation of Extracellular Matrix Collagen during Scar Formation after Myocardial Infarction

Myocardial infarction is remains the leading cause of death in developed countries. Recent data show that the composition of the extracellular matrix might differ despite similar heart function and infarction sizes. Because collagen is the main component of the extracellular matrix, we hypothesized that changes in inflammatory cell recruitment influence the synthesis of different collagen subtypes in myofibroblasts, thus changing the composition of the scar. We found that neutrophils sustain the proliferation of fibroblasts, remodeling, differentiation, migration and inflammation, predominantly by IL-1 and PPARγ pathways (n = 3). They also significantly inhibit the mRNA expression of fibrillar collagen, maintaining a reduced stiffness in isolated myofibroblasts (n = 4–5). Reducing the neutrophil infiltration in CCR1^−/− resulted in increased mRNA expression of collagen 11, moderate expression of collagen 19 and low expression of collagen 13 and 26 in the scar 4 weeks post infarction compared with other groups (n = 3). Mononuclear cells increased the synthesis of all collagen subtypes and upregulated the NF-kB, angiotensin II and PPARδ pathways (n = 3). They increased the synthesis of collagen subtypes 1, 3, 5, 16 and 23 but reduced the expression of collagens 5 and 16 (n = 3). CCR2^−/− scar tissue showed higher levels of collagen 13 (n = 3), in association with a significant reduction in stiffness (n = 4–5). Upregulation of the inflammation-related genes in myofibroblasts mostly modulated the fibrillar collagen subtypes, with less effect on the FACIT, network-forming and globular subtypes (n = 3). The upregulation of proliferation and differentiation genes in myofibroblasts seemed to be associated only with the fibrillar collagen subtype, whereas angiogenesis-related genes are associated with fibrillar, network-forming and multiplexin subtypes. In conclusion, although we intend for our findings to deepen the understanding of the mechanism of healing after myocardial infarction and scar formation, the process of collagen synthesis is highly complex, and further intensive investigation is needed to put together all the missing puzzle pieces in this still incipient knowledge process.     

Evaluation of Circulating Platelet Extracellular Vesicles and Hypertension Mediated Organ Damage

Elevated circulating platelet-derived extracellular vesicles (pEVs) have been associated with arterial hypertension. The role of hypertension-mediated organ damage (HMOD) to induce EV release is still unknown. We studied the micro- and macro-vascular changes (retinal vascular density and pulse wave velocity), endothelial function (flow-mediated vasodilation of brachial artery and finger plethysmography), and assessed the psychosocial status (anxiety and depression) in hypertensive patients to determine their relationship with EV release. Pulse wave velocity showed a significant positive correlation with pEVs (r = 0.33; p = 0.01). Systolic blood pressure (SBP) negatively correlated with retinal vascularity. The superficial retinal vascular plexus density in the whole image showed a significant negative correlation with 24 h SBP (r = −0.38, p < 0.01), day-SBP (r = −0.35, p = 0.01), and night-SBP (r = −0.27, p = 0.04). pEVs did not show significant associations with microvascular damage (retinal vascular density), endothelial function (flow-mediated vasodilation of brachial artery and finger plethysmography), or psychosocial status (anxiety and depression). Our results indicate that the pEV levels were associated with macrovascular damage measured by PWV, whereas no significant association between pEVs and microvascular damage, endothelial function, or emotional status could be detected. The potential utility of pEV in clinical practice in the context of HMOD may be limited to macrovascular changes.     

Update on Innate Immunity in Acute Kidney Injury—Lessons Taken from COVID-19

The serious clinical course of SARS-CoV-2 infection is usually accompanied by acute kidney injury (AKI), worsening prognosis and increasing mortality. AKI in COVID-19 is above all a consequence of systemic dysregulations leading to inflammation, thrombosis, vascular endothelial damage and necrosis. All these processes rely on the interactions between innate immunity elements, including circulating blood cells, resident renal cells, their cytokine products, complement systems, coagulation cascades and contact systems. Numerous simultaneous pathways of innate immunity should secure an effective host defense. Since they all form a network of cross-linked auto-amplification loops, uncontrolled activation is possible. When the actions of selected pathways amplify, cascade activation evades control and the propagation of inflammation and necrosis worsens, accompanied by complement overactivity and immunothrombosis. The systemic activation of innate immunity reaches the kidney, where the damage affecting single tubular cells spreads through tissue collateral damage and triggers AKI. This review is an attempt to synthetize the connections between innate immunity components engaged in COVID-19-related AKI and to summarize the knowledge on the pathophysiological background of processes responsible for renal damage.