Advances in drug and alcohol research最新文献

{"title":"Vascular Contributions to the Neurobiological Effects of Prenatal Alcohol Exposure.","authors":"Sarah Z Momin, Jacqueline T Le, Rajesh C Miranda","doi":"10.3389/adar.2023.10924","DOIUrl":"https://doi.org/10.3389/adar.2023.10924","url":null,"abstract":"Background: Fetal alcohol spectrum disorders (FASD) are often characterized as a cluster of brain-based disabilities. Though cardiovascular effects of prenatal alcohol exposure (PAE) have been documented, the vascular deficits due to PAE are less understood, but may contribute substantially to the severity of neurobehavioral presentation and health outcomes in persons with FASD. Methods: We conducted a systematic review of research articles curated in PubMed to assess the strength of the research on vascular effects of PAE. 40 pertinent papers were selected, covering studies in both human populations and animal models. Results: Studies in human populations identified cardiac defects, and defects in vasculature, including increased tortuosity, defects in basement membranes, capillary basal hyperplasia, endarteritis, and disorganized and diminished cerebral vasculature due to PAE. Preclinical studies showed that PAE rapidly and persistently results in vasodilation of large afferent cerebral arteries, but to vasoconstriction of smaller cerebral arteries and microvasculature. Moreover, PAE continues to affect cerebral blood flow into middle-age. Human and animal studies also indicate that ocular vascular parameters may have diagnostic and predictive value. A number of intervening mechanisms were identified, including increased autophagy, inflammation and deficits in mitochondria. Studies in animals identified persistent changes in blood flow and vascular density associated with endocannabinoid, prostacyclin and nitric oxide signaling, as well as calcium mobilization. Conclusion: Although the brain has been a particular focus of studies on PAE, the cardiovascular system is equally affected. Studies in human populations, though constrained by small sample sizes, did link pathology in major blood vessels and tissue vasculature, including brain vasculature, to PAE. Animal studies highlighted molecular mechanisms that may be useful therapeutic targets. Collectively, these studies suggest that vascular pathology is a possible contributing factor to neurobehavioral and health problems across a lifespan in persons with a diagnosis of FASD. Furthermore, ocular vasculature may serve as a biomarker for neurovascular health in FASD.","PeriodicalId":72092,"journal":{"name":"Advances in drug and alcohol research","volume":"3 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10191416/pdf/nihms-1891941.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9499270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex differences in cocaine self-administration by Wistar rats after predator odor exposure.","authors":"Taylor J Templeton, Siga Diarra, Nicholas W Gilpin","doi":"10.3389/adar.2023.11245","DOIUrl":"10.3389/adar.2023.11245","url":null,"abstract":"<p><p>Traumatic stress disorders are defined in part by persistent avoidance of trauma-related contexts. Our lab uses a preclinical model of traumatic stress using predator odor (i.e., bobcat urine) in which some but not all rats exhibit persistent avoidance of odor-paired stimuli, similar to what is seen in humans. Bobcat urine exposure increases alcohol consumption in male Avoider rats, but it has not been tested for its effects on intake of other drugs. Here, we tested the effect of bobcat urine exposure on cocaine self-administration in adult male and female Wistar rats. We did not observe any effect of bobcat urine exposure on cocaine self-administration in male or female rats. We observed that (1) female rats with long access (6 hours) to cocaine self-administer more cocaine than long-access males, (2) long-access males and females exhibit escalation of cocaine intake over time, (3) stressed rats gain less weight than unstressed rats following acute predator odor exposure, (4) baseline cocaine self-administration is predictive of subsequent cocaine self-administration. The results of this study may inform future work on predator odor effects on cocaine self-administration.</p>","PeriodicalId":72092,"journal":{"name":"Advances in drug and alcohol research","volume":"3 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10571484/pdf/nihms-1885410.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41241538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-9 utilizes precursor pathways in adaptation to alcohol in mouse striatal neurons.","authors":"Edward Andrew Mead, Yongping Wang, Sunali Patel, Austin P Thekkumthala, Rebecca Kepich, Elizabeth Benn-Hirsch, Victoria Lee, Azra Basaly, Susan Bergeson, Hava T Siegelmann, Andrzej Zbigniew Pietrzykowski","doi":"10.3389/adar.2023.11323","DOIUrl":"10.3389/adar.2023.11323","url":null,"abstract":"<p><p>microRNA-9 (miR-9) is one of the most abundant microRNAs in the mammalian brain, essential for its development and normal function. In neurons, it regulates the expression of several key molecules, ranging from ion channels to enzymes, to transcription factors broadly affecting the expression of many genes. The neuronal effects of alcohol, one of the most abused drugs in the world, seem to be at least partially dependent on regulating the expression of miR-9. We previously observed that molecular mechanisms of the development of alcohol tolerance are miR-9 dependent. Since a critical feature of alcohol action is temporal exposure to the drug, we decided to better understand the time dependence of alcohol regulation of miR-9 biogenesis and expression. We measured the effect of intoxicating concentration of alcohol (20 mM ethanol) on the expression of all major elements of miR-9 biogenesis: three pri-precursors (pri-mir-9-1, pri-mir-9-2, pri-mir-9-3), three pre-precursors (pre-mir-9-1, pre-mir-9-2, pre-mir-9-3), and two mature microRNAs: miR-9-5p and miR-9-3p, using digital PCR and RT-qPCR, and murine primary medium spiny neurons (MSN) cultures. We subjected the neurons to alcohol based on an exposure/withdrawal matrix of different exposure times (from 15 min to 24 h) followed by different withdrawal times (from 0 h to 24 h). We observed that a short exposure increased mature miR-9-5p expression, which was followed by a gradual decrease and subsequent increase of the expression, returning to pre-exposure levels within 24 h. Temporal changes of miR-9-3p expression were complementing miR-9-5p changes. Interestingly, an extended, continuous presence of the drug caused a similar pattern. These results suggest the presence of the adaptive mechanisms of miR-9 expression in the presence and absence of alcohol. Measurement of miR-9 pre- and pri-precursors showed further that the primary effect of alcohol on miR-9 is through the mir-9-2 precursor pathway with a smaller contribution of mir-9-1 and mir-9-3 precursors. Our results provide new insight into the adaptive mechanisms of neurons to alcohol exposure. It would be of interest to determine next which microRNA-based mechanisms are involved in a transition from the acute, intoxicating effects of alcohol to the chronic, addictive effects of the drug.</p>","PeriodicalId":72092,"journal":{"name":"Advances in drug and alcohol research","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10730111/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48777351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute cannabidiol treatment enhances social interaction in adult male mice.","authors":"Livia F Ferreira, Nikhita Pathapati, Stephen T Schultz, Mary C Nunn, Bethany L Pierce, Yatzil R Sanchez, Meredith D Murrell, Brett C Ginsburg, Emmanuel S Onaivi, Georgianna G Gould","doi":"10.3389/adar.2023.11163","DOIUrl":"10.3389/adar.2023.11163","url":null,"abstract":"<p><p>Cannabidiol (CBD) is a non-intoxicating phytochemical from <i>Cannabis sativa</i> that is increasingly used to manage pain. The potential for CBD to ameliorate dimensional behavior symptoms occurring in multiple psychiatric disorders was suggested, including social interaction impairments. To test this hypothesis, adult male BTBRT+Itpr3tf/J (BTBR) mice, a model of idiopathic autism exhibiting social preference deficits and restrictive repetitive behaviors, were acutely treated with vehicle or 0.1, 1, or 10 mg/kg CBD. Social interaction preference was assessed 50 min after treatment, followed by social novelty preference at 60 min, marble burying at 75 min and social dominance at 120 min. CBD (10 mg/kg) enhanced BTBR social interaction but not social novelty preference, marble burying or dominance, with serum levels = 29 ± 11 ng/mg at 3 h post-injection. Next, acute 10 mg/kg CBD was compared to vehicle treatment in male serotonin transporter (SERT) knock-out mice, since SERT deficiency is an autism risk factor, and in their wildtype background strain controls C57BL/6J mice. CBD treatment generally enhanced social interaction preference and attenuated social novelty preference, yet neither marble burying nor dominance was affected. These findings show acute treatment with as little as 10 mg/kg purified CBD can enhance social interaction preference in male mice that are otherwise socially deficient.</p>","PeriodicalId":72092,"journal":{"name":"Advances in drug and alcohol research","volume":"3 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10237625/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9756822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-resolution imaging in studies of alcohol effect on prenatal development.","authors":"Augustine Meombe Mbolle,&nbsp;Shiwani Thapa,&nbsp;Anna N Bukiya,&nbsp;Huabei Jiang","doi":"10.3389/adar.2023.10790","DOIUrl":"https://doi.org/10.3389/adar.2023.10790","url":null,"abstract":"<p><p>Fetal alcohol syndrome represents the leading known preventable cause of mental retardation. FAS is on the most severe side of fetal alcohol spectrum disorders that stem from the deleterious effects of prenatal alcohol exposure. Affecting as many as 1 to 5 out of 100 children, FASD most often results in brain abnormalities that extend to structure, function, and cerebral hemodynamics. The present review provides an analysis of high-resolution imaging techniques that are used in animals and human subjects to characterize PAE-driven changes in the developing brain. Variants of magnetic resonance imaging such as magnetic resonance microscopy, magnetic resonance spectroscopy, diffusion tensor imaging, along with positron emission tomography, single-photon emission computed tomography, and photoacoustic imaging, are modalities that are used to study the influence of PAE on brain structure and function. This review briefly describes the aforementioned imaging modalities, the main findings that were obtained using each modality, and touches upon the advantages/disadvantages of each imaging approach.</p>","PeriodicalId":72092,"journal":{"name":"Advances in drug and alcohol research","volume":"3 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10433240/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10422620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<ArticleTitle xmlns:ns0=\"http://www.w3.org/1998/Math/MathML\">Alcohol and pregnenolone interaction on cerebral arteries through targeting of vascular smooth muscle <ns0:math><ns0:msup><ns0:mrow><ns0:mi>C</ns0:mi><ns0:mi>a</ns0:mi></ns0:mrow><ns0:mrow><ns0:mn>2</ns0:mn><ns0:mo>+</ns0:mo></ns0:mrow></ns0:msup></ns0:math>- and voltage-gated K⁺ channels of big conductance.","authors":"Kelsey C North, Andrew A Shaw, Luiz Moreira, Anna N Bukiya, Alex M Dopico","doi":"10.3389/adar.2023.11735","DOIUrl":"10.3389/adar.2023.11735","url":null,"abstract":"<p><p>Despite the significant number of people who may be taking pregnenolone supplements while drinking alcohol (ethanol), the widely documented cerebrovascular actions of pregnenolone and ethanol, and the critical dependence of cerebrovascular function on cerebral artery diameter, there are no studies addressing the effect of pregnenolone + ethanol in combination on cerebral artery diameter. We investigated this by evaluating the effect of this combination on middle cerebral artery diameter in male and female C57BL/6J mice, both <i>in vivo</i> and <i>in vitro</i>. The use of de-endothelialized, <i>in vitro</i> pressurized middle cerebral artery segments allowed us to conduct a concentration-response study of constriction induced by pregnenolone ± ethanol, in which drug action could be evaluated independently of circulating and endothelial factors. In both male and female animals, pregnenolone at lower concentrations (≤1 μM) was found to synergize with 50 mM ethanol to cause vasoconstriction. In both sexes, this synergism was lost as one or both vasoconstrictors approached their maximally effective concentrations (75 mM and 10 μM for ethanol and pregnenolone, respectively), whether this was evaluated <i>in vitro</i> or <i>in vivo</i> using a cranial window. Vasoconstriction by pregnenolone + ethanol was abolished by 1 μM paxilline, indicating BK channel involvement. Moreover, cell-free recordings of BK channel activity in cerebral artery myocyte membranes showed that 10 μM pregnenolone and pregnenolone +50 mM ethanol reduced channel activity to an identical extent, suggesting that these drugs inhibit cerebrovascular BK channels <i>via</i> a common mechanism or mechanisms. Indeed, pregnenolone was found to disrupt allosteric coupling to <math><msup><mrow><mi>C</mi><mi>a</mi></mrow><mrow><mn>2</mn><mo>+</mo></mrow></msup></math>-driven gating, as previously reported for ethanol.</p>","PeriodicalId":72092,"journal":{"name":"Advances in drug and alcohol research","volume":"3 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10578043/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41241537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Substance abuse and early development.","authors":"Anna N Bukiya,&nbsp;Declan W Ali","doi":"10.3389/adar.2023.11836","DOIUrl":"https://doi.org/10.3389/adar.2023.11836","url":null,"abstract":"While misuse of psychoactive substances can be traced back to pre-historic times, their effects on invisible target—such as the developing fetus—only gained recognition within the last century [1–4]. Initial seminal findings in humans and laboratory rodents quickly grew from isolated observations to well-planned, multidisciplinary studies. Despite the involvement of numerous methodologies, large teams of researchers, and widely different experimental organisms, there has been an unusual consensus on the meaning of findings: principally that prenatal exposure to drugs of misuse has deleterious consequences for the developing fetus.","PeriodicalId":72092,"journal":{"name":"Advances in drug and alcohol research","volume":"3 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10424723/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10358891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microglial knockdown does not affect acute withdrawal but delays analgesic tolerance from oxycodone in male and female C57BL/6J mice.","authors":"Omar El Jordi, Kathryn D Fischer, Timothy B Meyer, Brady K Atwood, Adrian L Oblak, Raymond W Pan, David L McKinzie","doi":"10.3389/adar.2022.10848","DOIUrl":"10.3389/adar.2022.10848","url":null,"abstract":"<p><p>Opioid Use Disorder (OUD) affects approximately 8%-12% of the population. In dependent individuals, abrupt cessation of opioid taking results in adverse withdrawal symptoms that reinforce drug taking behavior. Considerable unmet clinical need exists for new pharmacotherapies to treat opioid withdrawal as well as improve long-term abstinence. The neuroimmune system has received much scientific attention in recent years as a potential therapeutic target to combat various neurodegenerative and psychiatric disorders including addiction. However, the specific contribution of microglia has not been investigated in oxycodone dependence. Chronic daily treatment with the CSF1R inhibitor Pexidartinib (PLX3397) was administered to knockdown microglia expression and evaluate consequences on analgesia and on naloxone induced withdrawal from oxycodone. In vivo results indicated that an approximately 40% reduction in brain IBA1 staining was achieved in the PLX treatment group, which was associated with a delay in the development of analgesic tolerance to oxycodone and maintained antinociceptive efficacy. Acute withdrawal behavioral symptoms, brain astrocyte expression, and levels of many neuroinflammatory markers were not affected by PLX treatment. KC/GRO (also known as CXCL1) was significantly enhanced in the somatosensory cortex in oxycodone-treated mice receiving PLX. Microglial knock-down did not affect the expression of naloxoneinduced opioid withdrawal but affected antinociceptive responsivity. The consequences of increased KC/GRO expression within the somatosensory cortex due to microglial reduction during opioid dependence are unclear but may be important for neural pathways mediating opioid-induced analgesia.</p>","PeriodicalId":72092,"journal":{"name":"Advances in drug and alcohol research","volume":" ","pages":"10848"},"PeriodicalIF":0.0,"publicationDate":"2022-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10880796/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49657983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal exposure to alcohol: mechanisms of cerebral vascular damage and lifelong consequences.","authors":"Partha S Saha, William G Mayhan","doi":"10.3389/adar.2022.10818","DOIUrl":"10.3389/adar.2022.10818","url":null,"abstract":"<p><p>Alcohol is a well-known teratogen, and prenatal alcohol exposure (PAE) leads to a greater incidence of many cardiovascular-related pathologies. Alcohol negatively impacts vasculogenesis and angiogenesis in the developing fetal brain, resulting in fetal alcohol spectrum disorders (FASD). Ample preclinical evidence indicates that the normal reactivity of cerebral resistance arterioles, which regulate blood flow distribution in response to metabolic demand (neurovascular coupling), is impaired by PAE. This impairment of dilation of cerebral arteries may carry implications for the susceptibility of the brain to cerebral ischemic damage well into adulthood. The focus of this review is to consolidate findings from studies examining the influence of PAE on vascular development, give insights into relevant pathological mechanisms at the vascular level, evaluate the risks of ethanol-driven alterations of cerebrovascular reactivity, and revisit different preventive interventions that may have promise in reversing vascular changes in preclinical FASD models.</p>","PeriodicalId":72092,"journal":{"name":"Advances in drug and alcohol research","volume":" ","pages":"10818"},"PeriodicalIF":0.0,"publicationDate":"2022-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10880760/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44921352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CB1 Cannabinoid Receptor is a Target for Neuroprotection in Light Induced Retinal Degeneration.","authors":"Manuel Soliño, Ignacio M Larrayoz, Ester María López, Manuel Rey-Funes, Mariana Bareiro, Cesar Fabián Loidl, Elena Girardi, Laura Caltana, Alicia Brusco, Alfredo Martínez, Juan José López-Costa","doi":"10.3389/adar.2022.10734","DOIUrl":"10.3389/adar.2022.10734","url":null,"abstract":"<p><p>In the last few years, an increasing interest in the neuroprotective effect of cannabinoids has taken place. The aim of the present work was to study the effects of modulating cannabinoid receptor 1 (CB1) in the context of light induced retinal degeneration (LIRD), using an animal model that resembles many characteristics of human age-related macular degeneration (AMD) and other degenerative diseases of the outer retina. Sprague Dawley rats (<i>n</i> = 28) were intravitreally injected in the right eye with either a CB1 agonist (ACEA), or an antagonist (AM251). Contralateral eyes were injected with respective vehicles as controls. Then, rats were subjected to continuous illumination (12,000 lux) for 24 h. Retinas from 28 animals were processed by GFAP-immunohistochemistry (IHC), TUNEL technique, Western blotting (WB), or qRT-PCR. ACEA-treated retinas showed a significantly lower number of apoptotic nuclei in the outer nuclear layer (ONL), lower levels of activated Caspase-3 by WB, and lower levels of glial reactivity by both GFAP-IHC and WB. qRT-PCR revealed that ACEA significantly decreased the expression of Bcl-2 and CYP1A1. Conversely, AM251-treated retinas showed a higher number of apoptotic nuclei in the ONL, higher levels of activated Caspase-3 by WB, and higher levels of glial reactivity as determined by GFAP-IHC and WB. AM251 increased the expression of Bcl-2, Bad, Bax, Aryl hydrocarbon Receptor (AhR), GFAP, and TNFα. In summary, the stimulation of the CB1 receptor, previous to the start of the pathogenic process, improved the survival of photoreceptors exposed to LIRD. The modulation of CB1 activity may be used as a neuroprotective strategy in retinal degeneration and deserves further studies.</p>","PeriodicalId":72092,"journal":{"name":"Advances in drug and alcohol research","volume":" ","pages":"10734"},"PeriodicalIF":0.0,"publicationDate":"2022-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10880786/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49332573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}