Cosmetic smears are a form of trace evidence that can link the crime scene, suspects, and victims. Foundation and lipstick are the most common sources of cosmetics that can easily smear, with most current research focused on the evidential analysis of lipsticks. This research aims to create a database of cosmetic foundations on different materials and to access the robustness of using Near-infrared with chemometrics as a non-destructive technique to identify unknown samples collected from a crime scene. Small amounts of six shades of three brands of foundations were smeared on clothing materials, which were then analysed with a combination of Near-infrared with chemometric analysis. Principle component analysis (PCA) was used to reduce data dimensionality and explore potential patterns in sample separation and Linear Discriminant Analysis (LDA) was utilised to assign unknown samples to one of the established classes. The selected techniques proved to be promising for database construction and as a preliminary method of analysis, with 93% of the spectra being correctly classified. Notably, darker foundation shades were less likely to be correctly classified (90% classified correctly) compared to lighter ones (96.7% classified correctly). This could not be improved with Standard Normal Variate (SNV) data pre-treatment or selecting specific NIR regions. This finding is of particular importance; according to the Crime Survey for England and Wales (year ending March 2020) police recorded sexual offences demonstrated that those in Mixed and Black or Black British ethnic groups were significantly more likely to be a victim of sexual assault compared to White, Asian or Other ethnic groups. It is, therefore, crucial to add a wide range of foundation shades, particularly of darker tones, to the future database.

Ethanol is the most commonly encountered drug in forensic toxicology, with widespread use throughout society. For this reason, it is important that there are a variety of reliable and robust methods to detect and quantify the content of alcohol in blood samples of suspected drink drivers. A common method of detection is gas chromatography with flame ionisation detector, with a number of sample preparation techniques employed. Typically, venous blood is sampled and used in the analysis. However, there is currently no legal specification in the UK of the blood sample source. This study investigates the use of capillary blood as an alternative to venous blood alongside two different sample volumes: 100 and 10 µL. Venous and capillary blood were collected from volunteers who had consumed alcohol. All blood sampling was carried out one hour after cessation of drinking. The results show a statistically significant difference between venous and capillary samples, with an average difference of 3.38 ± 1.99 mg/100 mL at 100 μL and approximately 4.13 ± 2.42 mg/100 mL at 10 μL, respectively. Predominantly, venous blood was detected at higher concentrations than the corresponding capillary samples. The deviations in alcohol samples between venous and capillary blood are consistent with previous studies. However, our research indicates that capillary blood is a viable matrix to test for alcohol, albeit one that underestimates blood-alcohol content in relation to venous sampling. There was no statistically significant difference between the 100 and 10 µL sample preparation methods on an individual basis, which infers that micro-volumes of alcohol are suitable for forensic blood-alcohol analysis.

Cannabis is one of the most commonly used recreational drugs worldwide. Rrecent epidemiology studies have linked increased cardiac complications to cannabis use. However, this literature is predominantly based on case incidents and post-mortem investigations. This study elucidates the molecular mechanism of Δ9-tetrahydrocannabinol (THC), and its primary metabolites 11-Hydroxy-Δ9-THC (THC-OH) and 11-nor-9-carboxy-Δ⁹-tetrahydrocannabinol (THC-COOH). Treatment of cardiac myocytes with THC-OH and THC-COOH increased cell migration and proliferation (p < 0.05), with no effect on cell adhesion, with higher doses (250–100 ng/mL) resulting in increased cell death and significant deterioration in cellular architecture. Conversely, no changes in cell morphology or viability were observed in response to THC. Expression of key ECM proteins α-SMA and collagen were up-regulated in response to THC-OH and THC-COOH treatments with concomitant modulation of PI3K and MAPK signalling. Investigations in the planarian animal model Polycelis nigra demonstrated that treatments with cannabinoid metabolites resulted in increased protein deposition at transection sites while higher doses resulted in significant lethality and decline in regeneration. These results highlight that the key metabolites of cannabis elicit toxic effects independent of the parent and psychoactive compound, with implications for cardiotoxicity relating to hypertrophy and fibrogenesis.

The UK, as the “cocaine capital of Europe,” currently accounts for ∼75% of all cocaine-related hospital admissions in Europe. This study aims to analyze the trends in cocaine-related deaths in England, Wales and Northern Ireland over 20 years (2000–2019). Cases reported to the National Programme on Substance Abuse Deaths (NPSAD) occurring between 2000 and 2019 where cocaine was detected at post-mortem (PM) were extracted for analysis. A total of 5,339 cases were retrieved, with an increase in the rate of reporting over time. Cocaine was deemed a cause of death and quantified in PM blood samples along with its major metabolite benzoylecgonine in 685 cases. Of these 685 cases, 25% (n = 170/685) occurred following acute use, 22% (n = 154/685) following chronic/binge use, 40% (n = 271/685) in combination with morphine, 4% (n = 29/685) in drug packer/swallower circumstances and 9% (n = 61/685) in a suicide context. Cardiac complications were evident in 22% of cases (n = 154/685). The average concentration of cocaine detected in cardiac cases (900 ng/mL) was considerably lower than that detected in cases where acute (19,100 ng/mL) or chronic/binge (6,200 ng/mL) dosing was evident. This is the first cocaine-related mortality study in these geographical areas. Deaths following cocaine use continue to rise despite its Class A drug listing in the UK. While underlying and external risk factors including polydrug use, cardiac complications and mental health can all contribute to the incidence of fatal drug toxicity following cocaine use, this study demonstrates that the risk of a cocaine overdose cannot be attributed to a specific blood concentration range.

Cocaine is one of the most widely abused illicit drugs due to its euphoric and addictive properties. Cocaine‐mediated cognitive impairments are the result of dynamic cytoskeletal rearrangements involved in mediating structural and behavioural plasticity. Cytoskeletal changes initiated following cocaine abuse are regulated by the Rho family of GTPases with significant downstream activity in key actin binding proteins. Moreover, signalling via the endoplasmic reticulum chaperone protein, sigma‐1 receptor has highlighted the possibility of cocaine regulated pathology in other organ systems. However, the question of whether upstream stimulation of such a high affinity binding receptor is directly involved in cocaine‐mediated cytoskeletal changes at present remains unknown. In this review, we describe the functional role of key cytoskeletal regulators in response to cocaine‐induced signalling cues. In addition, we ascertain the extent of whether global cytoskeletal modulators involved in cocaine‐induced neurological stimulation can be used as a platform for future studies into elucidating its fibrotic potential within the hepatic microenvironment. A focus on aspects still poorly understood relating to the nonneuronal pathological impact of cocaine is discussed in the sphere of hepatic dysregulation. Lastly, we suggest that cocaine may mediate its pathological capacity via the sigma1 receptor in regulating hepatoxicity, hepatic stellate cells activity, cytoskeletal dynamics, and the transcriptional regulation of key hepato‐fibrogenic modulators.

Ethanol is the most commonly used recreational drug worldwide. This study describes the development and validation of a headspace gas chromatography flame ionisation detection (HS-GC-FID) method using dual columns and detectors for simultaneous separation and quantitation. The use of a dual-column, dual-detector HS-GC-FID to quantitate ethanol is a common analytical technique in forensic toxicology; however, most analytical systems utilise pressure-balance injection rather than a simplified gas-tight syringe, as per this technique. This study is the first to develop and validate a technique that meets the specifications of the United Kingdom’s requirements for road traffic toxicology testing using a Shimadzu GC-2014 gas-tight syringe. The calibration ranged from 10 to 400 mg/100 mL, with a target minimum linearity of r2 > 0.999, using tertiary butanol as the internal standard marker. The method has an expanded uncertainty at 99.73% confidence of 3.64% at 80 mg/100 mL, which is the blood alcohol limit for drink driving in England and Wales. In addition, at 200 mg%—the limit at which a custodial sentence may be imposed on the defendant—the expanded uncertainty was 1.95%. For both the 80 mg% and 200 mg% concentrations, no bias was present in the analytical method. This method displays sufficient separation for other alcohols, such as methanol, isopropanol, acetaldehyde, and acetone. The validation of this technique complies with the recommended laboratory guidelines set out by United Kingdom and Ireland Association of Forensic Toxicologists (UKIAFT), the recently issued Laboratory 51 guidelines by the United Kingdom Accreditation Service (UKAS), and the criteria set out by the California Code of Regulations (CCR), 17 CCR § 1220.1.