Drug addiction is a serious public health problem worldwide,for which there are currently no established therapeutic medications.Since the legalization of cannabis and the approval of cannabidiol(CBD)by the US Food and Drug Administration,its therapeutic potential for the treatment of substance abuse has been widely explored.Numerous studies have shown that CBD can reduce drug reward in animal models of addiction such as self-administration,conditioned positional preference,and intracranial self-stimulation.CBD can also reduce withdrawal symptoms from substances such as amphetamines,opioids,cocaine,marijuana,alcohol,and nicotine.The mechanisms by which CBD modulates drug addiction,however,are complex and understudied.Here we review studies of CBD related to addictive drugs to clarify the regulatory mechanisms of CBD in drug addiction and provide references for related studies on substance abuse.

The accuracy of medical imaging diagnosis will directly impact the clinical forensic evaluation's scientific validity and objectivity.This study systematically analyzed the primary causes of misdiagnosis and missed diagnosis in imaging examinations,focusing on representative cases,including rib fractures,traumatic subarachnoid hemorrhage,joint injuries with ligament damage,nasal fractures,congenital skeletal variations,and epiphyseal injuries.Key contributing factors encompassed limitation of imaging technologies,the insufficient interpretive experience of examiners,the complexity of injury mechanisms,and inadequate post-traumatic dynamic imaging follow-up.To address these issues,improvement strategies are proposed,which were establishing standardized imaging review protocols,implementing multimodal imaging approaches,rigorous evaluation of original imaging data,and enhancing professional knowledge regarding anatomical variations and injury differentiation.These measures aim to elevate the quality of forensic imaging diagnosis,providing more precise and reliable strategies for forensic clinical identifications.

Drug addiction is a serious public health problem worldwide,for which there are currently no established therapeutic medications.Since the legalization of cannabis and the approval of cannabidiol(CBD)by the US Food and Drug Administration,its therapeutic potential for the treatment of substance abuse has been widely explored.Numerous studies have shown that CBD can reduce drug reward in animal models of addiction such as self-administration,conditioned positional preference,and intracranial self-stimulation.CBD can also reduce withdrawal symptoms from substances such as amphetamines,opioids,cocaine,marijuana,alcohol,and nicotine.The mechanisms by which CBD modulates drug addiction,however,are complex and understudied.Here we review studies of CBD related to addictive drugs to clarify the regulatory mechanisms of CBD in drug addiction and provide references for related studies on substance abuse.

The accuracy of medical imaging diagnosis will directly impact the clinical forensic evaluation's scientific validity and objectivity.This study systematically analyzed the primary causes of misdiagnosis and missed diagnosis in imaging examinations,focusing on representative cases,including rib fractures,traumatic subarachnoid hemorrhage,joint injuries with ligament damage,nasal fractures,congenital skeletal variations,and epiphyseal injuries.Key contributing factors encompassed limitation of imaging technologies,the insufficient interpretive experience of examiners,the complexity of injury mechanisms,and inadequate post-traumatic dynamic imaging follow-up.To address these issues,improvement strategies are proposed,which were establishing standardized imaging review protocols,implementing multimodal imaging approaches,rigorous evaluation of original imaging data,and enhancing professional knowledge regarding anatomical variations and injury differentiation.These measures aim to elevate the quality of forensic imaging diagnosis,providing more precise and reliable strategies for forensic clinical identifications.

Background/Aims: Previous studies have shown that diet and physical activity can influence constipation. However, the combined effect of diet and physical activity on constipation remains unclear. Methods: Constipation was defined based on stool consistency and frequency, while overall diet quality was assessed using Healthy Eating Index (HEI)-2015 scores. Participants were categorized into low (metabolic equivalent [MET]-min/wk < 500) and high physical activitygroups (MET-min/wk ≥ 500). The association between diet and constipation across physical activity groups was analyzed using surveylogistic regression and restricted cubic splines. Results: Higher HEI-2015 scores were associated with reduced constipation risk in the high physical activity group when constipation was defined by stool consistency (odds ratio [OR], 0.98; 95% confidence interval [CI], 0.97-0.99). However, in the low physical activity group, increased HEI-2015 scores did not significantly affect constipation risk (OR, 1.01; 95% CI, 0.97-1.05). Similar results were found when constipation was defined based on stool frequency. In the high physical activity group, increased HEI-2015 scores were significantly associated with a reduced constipation risk (OR, 0.96; 95% CI, 0.94-0.98). Conversely, in the low physical activity group, increased HEI-2015 scores did not affect the risk of constipation (OR, 0.96; 95% CI, 0.90-1.03). Conclusions Our findings suggest that a higher HEI-2015 score is negatively associated with constipation among individuals with high physical activity levels but not among those with low physical activity levels. This association was consistent when different definitions of constipation were used. These results highlight the importance of combining healthy diet with regular physical activity to alleviate constipation.

Methamphetamine (METH) is a highly addictive synthetic psychoactive drug that is often abused as a psychostimulant.Chronic exposure to METH induces neurotoxic effects through oxidative stress,impairment of mitochondrial function,activation of astrocytes and microglia,and amino acid excitability.METH abuse increases the chance of developing neurodegenerative diseases such as Alzheimer's disease,Parkinson's disease,Huntington's disease.However,the mechanism behind METH-induced neurotoxicity remains incompletely understood.So far,there is no specific treatment for METH-induced neurotoxicity.This paper reviews some of the potential mechanisms of METH-induced neurotoxicity in recent years,such as neuroinflammation,glutamatergic excitotoxicity,oxidative stress,and mitochondrial toxicity,and discusses the current therapeutic strategies related to mitigating the neurotoxic effects of METH in the brain through different pathways.

Objective To investigate the regulatory role of nuclear factor erythroid 2-related factor 2(Nrf2)in the activation and polarization of microglia induced by methamphetamine(METH).Methods BV2 and HMC3 cells were studied in vitro and wild-type mice and Nrf2-knockout mice were studied in vivo.In vivo and in vitro toxicity models induced by METH were established,respectively.The activation and polarization of microglia in each group were examined using immunofluorescence and Western blot,respectively.Results METH treatment significantly increased the fluorescence level of inducible nitric oxide synthase(iNOS)in BV2 and HMC3 cells(P＜0.001),and significantly decreased the fluorescence level of Arginase1(Arg1)(P＜0.05,P＜0.01).METH exposure activated microglia in the cortex,increased expression levels of ionized calcium binding adaptor molecule-1(IBA1)and iNOS(P＜0.001,P＜0.05),and decreased the expression of Arg1(P＜0.01).The number of activated microglia was significantly increased after Nrf2 gene knockout(P＜0.01),compared with the WT METH group,while the expression levels of IBA1 and iNOS were also increased(P＜0.001,P＜0.01)and the expression level of Argl was decreased(P＜0.01).Conclusions Nrf2 plays an important role in regulating the activation and polarization of microglia induced by METH.Nrf2 may thus be a potential target for the treatment of neuroinflammation induced by METH.

Methamphetamine(METH)is a new type of abused drug with a strong central stimulant effect.Its excitatory pathway involves a series of central higher-level functions,including drug-related rewards and motivation,learning and memory,decision-making,and execution.METH not only causes neurotoxicity,but its long-term use may also cause cognitive dysfunction,loss of personality,and may lead to serious social violence in addicts.Exosomes,as a novel cell-to-cell carrier,are involved in the occurrence and development of drug addiction,and exosome microRNAs are important biomarkers for METH addiction and are also involved in various aspects of METH-induced neurotoxicity.Eoxosmes may thus be useful therapeutic carriers providing a new approach for the diagnosis and treatment of METH abuse.

Objective To investigate the regulatory role of nuclear factor erythroid 2-related factor 2(Nrf2)in the activation and polarization of microglia induced by methamphetamine(METH).Methods BV2 and HMC3 cells were studied in vitro and wild-type mice and Nrf2-knockout mice were studied in vivo.In vivo and in vitro toxicity models induced by METH were established,respectively.The activation and polarization of microglia in each group were examined using immunofluorescence and Western blot,respectively.Results METH treatment significantly increased the fluorescence level of inducible nitric oxide synthase(iNOS)in BV2 and HMC3 cells(P＜0.001),and significantly decreased the fluorescence level of Arginase1(Arg1)(P＜0.05,P＜0.01).METH exposure activated microglia in the cortex,increased expression levels of ionized calcium binding adaptor molecule-1(IBA1)and iNOS(P＜0.001,P＜0.05),and decreased the expression of Arg1(P＜0.01).The number of activated microglia was significantly increased after Nrf2 gene knockout(P＜0.01),compared with the WT METH group,while the expression levels of IBA1 and iNOS were also increased(P＜0.001,P＜0.01)and the expression level of Argl was decreased(P＜0.01).Conclusions Nrf2 plays an important role in regulating the activation and polarization of microglia induced by METH.Nrf2 may thus be a potential target for the treatment of neuroinflammation induced by METH.

Methamphetamine(METH)is a new type of abused drug with a strong central stimulant effect.Its excitatory pathway involves a series of central higher-level functions,including drug-related rewards and motivation,learning and memory,decision-making,and execution.METH not only causes neurotoxicity,but its long-term use may also cause cognitive dysfunction,loss of personality,and may lead to serious social violence in addicts.Exosomes,as a novel cell-to-cell carrier,are involved in the occurrence and development of drug addiction,and exosome microRNAs are important biomarkers for METH addiction and are also involved in various aspects of METH-induced neurotoxicity.Eoxosmes may thus be useful therapeutic carriers providing a new approach for the diagnosis and treatment of METH abuse.