Human body fluids such as blood and saliva represent the most common source of biological material found at a crime scene. Reliable tissue identification in forensic science can reveal significant insights into crime scene reconstruction and can thus contribute toward solving crimes. Limitations of existing presumptive tests for body fluid identification in forensics, which are usually based on chemoluminescence or protein analysis, are expected to be overcome by RNA-based methods, provided that stable RNA markers with tissue-specific expression patterns are available. To generate sets of stable RNA markers for reliable identification of blood and saliva stains we (1) performed whole-genome gene expression analyses on a series of time-wise degraded blood and saliva stain samples using the Affymetrix U133 plus2 GeneChip, (2) consulted expression databases to obtain additional information on tissue specificity, and (3) confirmed expression patterns of the most promising candidate genes by quantitative real-time polymerase chain reaction including additional forensically relevant tissues such as semen and vaginal secretion. Overall, we identified nine stable mRNA markers for blood and five stable mRNA markers for saliva detection showing tissue-specific expression signals in stains aged up to 180 days of age, expectedly older. Although, all of the markers were able to differentiate blood/saliva from semen samples, none of them could differentiate vaginal secretion because of the complex nature of vaginal secretion and the biological similarity of buccal and vaginal mucosa. We propose the use of these 14 stable mRNA markers for identification of blood and saliva stains in future forensic practice.

/pdf/stable-rna-markers-for-identification-of-blood-and-saliva-2s5dsdndd8.pdf

Stable RNA markers for identification of blood and saliva stains revealed from whole genome expression analysis of time-wise degraded samples.

Fractionation and characterization of biologically-active polysaccharides from Artemisia tripartita

The xenoestrogen bisphenol A (BPA) is commonly ingested by humans. We examined the effects of neonatal exposure to low versus high doses of BPA over the control of estrogen receptor alpha (ERalpha) expression in the preoptic area (POA) of prepubertal female rats. Pups received s.c. injections every 48 h of BPA (high dose, 20 mg/kg and low dose, 0.05 mg/kg) or diethylstilbestrol (DES, 0.02 mg/kg) from postnatal day (PND) 1 to PND7 and were killed at PND8 or PND21. Relative expression of ERalpha transcripts containing alternative 5'-untranslated regions OS, ON, O, OT, and E1 in POA were evaluated by RT-PCR. Methylation status of ERalpha promoters was determined by bisulfited DNA restriction analysis and ERalpha protein by immunohistochemistry. In PND8, the high dose of BPA and DES diminished total ERalpha mRNA levels, mediated by the decreased expression of ERalpha-O and ERalpha-OT variants. In contrast, the low dose of BPA augmented total ERalpha mRNA by increasing the expression of the ERalpha-E1 variant. In PND21, both BPA doses increased total ERalpha mRNA by means of the augmented expression of ERalpha-O and ERalpha-OT variants. In PND21, the methylation status of the ERalpha promoters and the circulating levels of estradiol were similar in all experimental groups. At PND8 and PND21, DES and the high dose of BPA decreased, while the low dose of BPA increased ERalpha protein in the POA. These findings show that neonatal BPA exposure alters the abundance of hypothalamic ERalpha transcript variants and protein in a dose-dependent manner.

/pdf/neonatal-exposure-to-bisphenol-a-modifies-the-abundance-of-2wzgnizd2m.pdf

Neonatal exposure to bisphenol A modifies the abundance of estrogen receptor α transcripts with alternative 5′-untranslated regions in the female rat preoptic area

Cannabidiol (CBD) is a major phytocannabinoid present in Cannabis sativa (Linneo, 1753). This naturally occurring secondary metabolite does not induce intoxication or exhibit the characteristic profile of drugs of abuse from cannabis like Δ9-tetrahydrocannabinol (∆9-THC) does. In contrast to ∆9-THC, our knowledge of the neuro-molecular mechanisms of CBD is limited, and its pharmacology, which appears to be complex, has not yet been fully elucidated. The study of the pharmacological effects of CBD has grown exponentially in recent years, making it necessary to generate frequently updated reports on this important metabolite. In this article, a rationalized integration of the mechanisms of action of CBD on molecular targets and pharmacological implications in animal models and human diseases, such as epilepsy, pain, neuropsychiatric disorders, Alzheimer’s disease, and inflammatory diseases, are presented. We identify around 56 different molecular targets for CBD, including enzymes and ion channels/metabotropic receptors involved in neurologic conditions. Herein, we compiled the knowledge found in the scientific literature on the multiple mechanisms of actions of CBD. The in vitro and in vivo findings are essential for fully understanding the polypharmacological nature of this natural product.

/pdf/the-polypharmacological-effects-of-cannabidiol-2efn3trp.pdf

The Polypharmacological Effects of Cannabidiol

Characterization of 5' untranslated regions of the voltage-gated sodium channels SCN1A, SCN2A, and SCN3A and identification of cis-conserved noncoding sequences.

Variants of the 5'-untranslated region of human NCF2: expression and translational efficiency.

Biased G protein‐coupled receptor (GPCR) ligands preferentially activate G protein‐ or β‐arrestin signaling pathways and are leading to the development of drugs with superior efficacy and reduced side‐effects in heart disease, pain management, and neuropsychiatric disorders. Although GPCRs are implicated in the pathophysiology of Alzheimer’s disease (AD), biased GPCR signaling is an unexplored area of investigation in AD. Previous work demonstrated that Gpr3 deficiency ameliorates amyloid‐β (Aβ) pathology. However, Gpr3‐deficient mice display several adverse phenotypes, including elevated anxiety‐like behavior, reduced fertility, and memory impairment, which are potentially associated with impaired G protein‐signaling. We hypothesized that generation of a G protein‐biased GPR3 mouse model, which maintains G protein‐signaling while eliminating β‐arrestin signaling, would attenuate AD‐associated phenotypes while preserving the beneficial effects of GPR3‐mediated G protein‐signaling.

https://onlinelibrary.wiley.com/doi/pdfdirect/10.1002/alz.063989

G protein‐biased GPR3 signaling induces glial activation and ameliorates amyloid pathology in a preclinical Alzheimer’s disease mouse model

Significance Levels of the orphan G protein–coupled receptor GPR3 are elevated in a subset of patients with Alzheimer’s disease (AD). Our group previously showed that genetic deletion of Gpr3 attenuates amyloid-β (Aβ) pathology in multiple AD mouse models, highlighting the therapeutic potential of GPR3 as a drug target for AD. However, Gpr3-deficient mice display several adverse phenotypes, including anxiety-like behavior and cognitive deficits. Here, we genetically modified Gpr3 in naive mice and in a preclinical AD mouse model and demonstrated that biased GPR3 signaling reduces AD pathology and induces glial activation in the absence of an effect on basal anxiety levels or cognitive function. Thus, biased GPR3 therapeutics are potentially neuroprotective and a safer avenue for therapeutic intervention in AD.

G protein–biased GPR3 signaling ameliorates amyloid pathology in a preclinical Alzheimer’s disease mouse model

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Variants of the 5'-untranslated region of human NCF2: expression and translational efficiency.

G protein‐biased GPR3 signaling induces glial activation and ameliorates amyloid pathology in a preclinical Alzheimer’s disease mouse model

G protein–biased GPR3 signaling ameliorates amyloid pathology in a preclinical Alzheimer’s disease mouse model