Psychoactive Plant Database - Neuroactive Phytochemical Collection

1. Luminescence. 2024 Nov;39(11):e70011. doi: 10.1002/bio.70011.

Dual "Turn-On" Fluorescent and Colorimetric Sensing of Permanganate Based on 
Yellow Carbon Dots.

Zeng HH(1), Huang RX(1), Qiu Y(1), Duan JL(1), Jiang SC(1).

Author information:
(1)College of Materials and Chemical Engineering, Pingxiang University, 
Pingxiang, China.

Existing permanganates (MnO4 -) sensing methods suffered from the poor 
selectivity, restricted solubility, and/or less desirable signaling mechanisms 
(e.g., "turn-off" processes), resulting in the false positive result. In this 
work, an effective "turn-on" fluorescence method for MnO4 - detection in aqueous 
media was proposed via yellow fluorescence carbon dots (Y-CDs) with the maximum 
emission peak of 553 nm. Upon the introduction of MnO4 -, the fluorescence of 
Y-CDs increased significantly due to the enhanced surface passivation degree and 
intramolecular charge transfer. In the range of 0.1-10 μM, the fluorescence 
ratio (F/F0) is proportional to the MnO4 - ions concentration, realizing the 
"turn-on" fluorescence sensing of MnO4 -. On the other hand, utilizing the 
significant color change of Y-CDs by MnO4 - ions, the colorimetric analysis can 
also be established for MnO4 - assay. Compared with other probes, the analysis 
results obtained by bimodal sensing tactics of fluorescent and colorimetric can 
be mutually verified to improve the reliability and meet the sensing needs of 
targets in complex environments.

© 2024 John Wiley & Sons Ltd.

DOI: 10.1002/bio.70011
PMID: 39508148 [Indexed for MEDLINE]


2. Arch Insect Biochem Physiol. 2024 Nov;117(3):e70005. doi: 10.1002/arch.70005.

PGE(2) Binding Affinity of Hemocyte Membrane Preparations of Manduca sexta and 
Identification of the Receptor-Associated G Proteins in Two Lepidopteran 
Species.

Khan F(1), Tunaz H(2), Haas E(3), Kim Y(1), Stanley D(4).

Author information:
(1)Department of Plant Medicals, Andong National University, Andong, Korea.
(2)Faculty of Agriculture, Department of Plant Protection, KahramanMaras Situ 
Imam University, KahramanMaras, Turkey.
(3)Department of Chemistry and Biochemistry, Creighton University, Omaha, 
Nebraska, USA.
(4)Biological Control of Insects Research Laboratory, Columbia, Missouri, USA.

Prostaglandin E2 (PGE2) is an eicosanoid that mediates a range of physiological 
actions in vertebrates and invertebrates, including reproduction and immunity. 
The PGE2 receptor was identified and functionally assessed in two lepidopteran 
insects, Manduca sexta and Spodoptera exigua. However, its binding affinity to 
the receptor has not been reported. The PGE2 receptor is a G-protein coupled 
receptor (GPCR) although its corresponding G-protein is not identified. PGE2 
binding assays were performed with membrane preparations from hemocytes of M. 
sexta larvae. We recorded an optimal binding in 4 h reactions conducted at pH 
7.5 with 12 nM tritium-labeled PGE2. We found that hemocytes express a single 
population of PGE2 binding sites with a high affinity (Kd = 35 pmol/mg protein), 
which are specific and saturable. The outcomes of experiments on the influence 
of purine nucleotides suggested these are functional GPCRs. A bioinformatics 
analysis led to a proposed trimeric G-protein in the S. exigua transcriptome, in 
which the Gα subunit is classified into five different types: Gα(o), Gα(q), 
Gα(s), Gα(12), and Gα(f). After confirming expressions of these five types in S. 
exigua, individual RNA interference (RNAi) treatments were applied to the larvae 
using gene-specific double-stranded RNAs. RNAi treatments specific to Gα(s) or 
Gα(12) gene expression significantly suppressed the cellular immune responses 
although the RNAi treatments specific to other three Gα components did not. 
While PGE2 treatments led to elevated hemocyte cAMP or Ca2+ levels, the RNAi 
treatments specific to Gα(s) or Gα(12) genes led to significantly reduced second 
messenger levels under PGE2, although the RNAi treatments specific to the other 
three Gα components did not. These results showed that the PGE2 receptor has 
high PGE2 affinity in the nanomolar range and binds G-proteins containing a 
Gα(s) or Gα(12) trimeric component in S. exigua and M. sexta, and likely, all 
lepidopteran insects.

© 2024 Wiley Periodicals LLC.

DOI: 10.1002/arch.70005
PMID: 39508136 [Indexed for MEDLINE]


3. Arterioscler Thromb Vasc Biol. 2024 Nov 7. doi: 10.1161/ATVBAHA.123.319460. 
Online ahead of print.

Cure of Congenital Purpura Fulminans via Expression of Engineered Protein C 
Through Neonatal Genome Editing in Mice.

Togashi T(1)(2), Baatartsogt N(2), Nagao Y(3), Kashiwakura Y(2)(4), Hayakawa 
M(2)(4), Hiramoto T(2), Fujiwara T(5)(6), Morishita E(1), Nureki O(7), Ohmori 
T(2)(4).

Author information:
(1)Department of Clinical Laboratory Science, Division of Health Sciences, 
Graduate School of Medical Science, Kanazawa University, Ishikawa, Japan (T.T., 
E.M.).
(2)Department of Biochemistry, Jichi Medical University School of Medicine, 
Tochigi, Japan (T.T., N.B., Y.K., M.H., T.H., T.O.).
(3)Center for Experimental Medicine, Center for Molecular Medicine, Jichi 
Medical University, Tochigi, Japan. (Y.N.).
(4)Center for Gene Therapy Research, Center for Molecular Medicine, Jichi 
Medical University, Tochigi, Japan. (Y.K., M.H., T.O.).
(5)Division of Cell and Molecular Medicine, Center for Molecular Medicine, Jichi 
Medical University, Tochigi, Japan (T.F.).
(6)Department of Cardiovascular Medicine, The University of Tokyo Hospital, 
Japan (T.F.).
(7)Department of Biological Sciences, Graduate School of Science, The University 
of Tokyo, Japan (O.N.).

BACKGROUND: PC (protein C) is a plasma anticoagulant encoded by PROC; mutation 
in both PROC alleles results in neonatal purpura fulminans-a fatal systemic 
thrombotic disorder. In the present study, we aimed to develop a genome editing 
treatment to cure congenital PC deficiency.
METHODS: We generated an engineered APC (activated PC) to insert a 
furin-cleaving peptide sequence between light and heavy chains. The engineered 
PC was expressed in the liver of mice using an adeno-associated virus vector or 
CRISPR/Cas9 (clustered regularly interspaced short palindromic repeats/clustered 
regularly interspaced short palindromic repeat-associated 9)-mediated genome 
editing using an adeno-associated virus vector in vivo.
RESULTS: The engineered PC could be released in its activated form and 
significantly prolonged the plasma coagulation time independent of the cofactor 
activity of PS (protein S) in vitro. The adeno-associated virus vector-mediated 
expression of the engineered PC, but not wild-type PC, prolonged coagulation 
time owing to the inhibition of activated coagulation FV (factor V) in a 
dose-dependent manner and abolished pathological thrombus formation in vivo in 
C57BL/6J mice. The insertion of EGFP sequence conjugated with self-cleaving 
peptide sequence at Alb locus via neonatal in vivo genome editing using 
adeno-associated virus vector resulted in the expression of EGFP in 7% of liver 
cells, mainly via homology-directed repair, in mice. Finally, we succeeded in 
improving the survival of PC-deficient mice by expressing the engineered PC via 
neonatal genome editing in vivo.
CONCLUSIONS: These results suggest that the expression of engineered PC via 
neonatal genome editing is a potential cure for severe congenital PC deficiency.

DOI: 10.1161/ATVBAHA.123.319460
PMID: 39508105


4. Sichuan Da Xue Xue Bao Yi Xue Ban. 2024 Sep 20;55(5):1063-1070. doi: 
10.12182/20240960201.

[Clinical Value of Dual Tracer PET Imaging With (68)Ga-PSMA and (18)F-FDG in 
Patients With Metastatic Prostate Cancer].

[Article in Chinese]

Dai H(1), Huang S(1), Tian T(1), Hou N(1), Zeng H(1), Wei Q(1), Huang R(1).

Author information:
(1)（ 610041） Department of Nuclear Medicine, West China Hospital, Sichuan 
University, Chengdu 610041, China.

OBJECTIVE: In this study, we retrospectively analyzed the imaging 
characteristics of dual-tracer 68Ga-prostate specific membrane antigen (PSMA) 
and 18F-flurodeoxyglucose (FDG) positron emission tomography (PET)/computed 
tomography (CT) in metastatic prostate cancer (mPCa) patients. We analyzed the 
uptake modes of the dual tracers, explored clinical pathological parameters 
affecting the 18F-FDG uptake in the lesions, and evaluated their prognostic 
implications for prostate specific antigen progression-free survival (PSA-PFS).
METHODS: A total of 41 mPCa patients who underwent dual-tracer PET/CT (68Ga-PSMA 
and 18F-FDG) scans between September 2021 and January 2024 were retrospectively 
enrolled. One patient had negative uptake of both PSMA and FDG. According to the 
uptake patterns of the 2 tracers, the other patients, 40 in total, were 
categorized in 2 groups, including group A consisting of 33 cases who showed 
PSMA and FDG dual and those who showed FDG only avidity, and group B consisting 
of 7 cases who showed PSMA avidity only. Comparative analyses of clinical 
pathological characteristics between group A and group B were conducted. The 
relationship between various parameters and PSA-PFS was analyzed by the 
Kaplan-Meier method.
RESULTS: A total of 26 patients (63.4%) were diagnosed with metastatic 
castration-resistant prostate cancer (mCRPC), and 38 cases (92.7%) had a Gleason 
score of 8-9. Bone metastasis, the predominant type of distant metastasis, 
occurred in 36 cases (87.8%). The skeletal and distant lymph node metastases 
mostly showed a dual positive uptake pattern for both PSMA and FDG (85.7% 
[24/28] and 81.8% [9/11]). 37.5% (3/8) of the metastases to organs showed FDG 
only positive uptake pattern. The serum levels of prostate specific antigen 
(PSA) in group A were significantly higher than those in group B (P=0.013). A 
total of 13 patients of special pathological classification (intraductal 
carcinoma and neuroendocrine differentiation) were all found to be in group A. 
Among the 41 cases, 16 were lost to follow-up. Of the 25 patients who completed 
follow-up, 9 patients, with a median PSA value of 104 ng/mL, experienced PSA 
progression, while the 16 other patients, with a median PSA of 0.34 ng/mL, did 
not incur any PSA progression. There was significant difference in the median 
PSA between patients showing PSA progression and those who did not show PSA 
progression (P<0.001). Kaplan-Meier survival analysis revealed that the median 
PSA-PFS of patients of specific pathological classifications was 7 months, which 
was shorter than the 16 months of the patients with typical prostate cancer, 
with the difference between the two groups being statistically meaningful 
(P=0.043). The median PSA-PFS for group A was 30 months. With more than half of 
the patients in the group not experiencing any PSA progression, group B did not 
reach the median PSA-PFS (P=0.645).
CONCLUSION: Dual-tracer PET/CT imaging with 68Ga-PSMA and 18F-FDG commonly 
exhibits avidity for both tracers in mPCa. Serum PSA level is a reliable 
biomarker for predicting FDG-positive lesions. mPCa presented with intraductal 
carcinoma and neuroendocrine differentiation tends to exhibit FDG avidity and is 
more susceptible to PSA progression.

© 2024《四川大学学报（医学版）》编辑部 版权所有Copyright ©2024 Editorial Office of Journal of 
Sichuan University (Medical Sciences).

DOI: 10.12182/20240960201
PMCID: PMC11536228
PMID: 39507973 [Indexed for MEDLINE]

Conflict of interest statement: 
利益冲突　本文作者魏强是本刊编委会编委。该文在编辑评审过程中所有流程严格按照期刊政策进行，且未经其本人经手处理。除此之外，所有作者声明不存在利益冲突。


5. J Allergy Clin Immunol Glob. 2024 Sep 21;4(1):100345. doi: 
10.1016/j.jacig.2024.100345. eCollection 2025 Feb.

Atopic dermatitis and tobacco smoke exposure during childhood and adolescence.

Al-Alusi NA(1), Ramirez FD(2), Chan LN(1), Ye M(3), Langan SM(4), McCulloch 
C(5), Abuabara K(3).

Author information:
(1)School of Medicine, University of California, San Francisco, Calif.
(2)Department of Pediatrics, University of California, San Francisco, Calif.
(3)Department of Dermatology, University of California, San Francisco, Calif.
(4)Department of Non-communicable Disease Epidemiology, London School of Hygiene 
and Tropical Medicine, London, United Kingdom.
(5)Division of Epidemiology and Biostatistics, University of California, San 
Francisco, Calif.

BACKGROUND: Tobacco smoke may affect atopic dermatitis (AD) because of its known 
effects on humoral and cellular immunity, but prior studies lack data on disease 
severity and biomarkers over time.
OBJECTIVE: We investigated the association between passive and active tobacco 
smoke exposure (TSE) during childhood and adolescence and the activity and 
severity of AD.
METHODS: A birth cohort of 10,521 individuals was followed through adolescence 
as part of the Avon Longitudinal Study of Parents and Children. We used 
mixed-effect models to determine the risk of AD (based on repeated assessments) 
with passive smoke exposure during childhood, active TSE during adolescence, and 
using a serum biomarker of tobacco exposure (cotinine) at 3 time points.
RESULTS: After adjusting for confounding factors, there was no evidence of a 
relationship between passive TSE and concurrent AD activity in childhood 
(adjusted odds ratio, 0.95; 95% confidence interval, 0.83, 1.07) or of an 
increased risk between active smoking and AD activity in adolescence (adjusted 
odds ratio, 0.57; 95% confidence interval, 0.44, 0.75). Secondary analyses 
demonstrated no dose-response relationship and no increased severity of AD with 
passive or active TSE. Furthermore, we found no increased risk of AD with a 
cumulative measure of passive TSE across childhood (adjusted relative risk 
ratio, 0.98; 95% confidence interval, 0.96, 1.00).
CONCLUSION: Neither active nor passive TSE was associated with AD during 
childhood and adolescence.

© 2024 The Authors.

DOI: 10.1016/j.jacig.2024.100345
PMCID: PMC11536054
PMID: 39507926

Conflict of interest statement: Funded by National Institutes of Health grants 
via Arthritis and Musculoskeletal and Skin Diseases Career Development Award 
K23AR073915 (to K.A.), National Center for Advancing Translational Sciences 
award UCSF-CTSI grant UL1 TR001872 (to C.E.M.), and UCSF-CTSI grant TL1TR001871 
(to F.R.). Funding was also received from a Wellcome Trust Senior Research 
Fellowship in Clinical Science (award 205039/Z/16/Z to S.M.L.); and from the 
UCSF Summer Explore Fellowship (to N.A.A. and L.N.C.). The funders had no role 
in study design, data collection and analysis, decision to publish, or 
preparation of the report. The findings and conclusions in this report are those 
of the authors and do not necessarily represent the views of the funders. The UK 
Medical Research Council and Wellcome (grant 217065/Z/19/Z) and the University 
of Bristol provide core support for ALSPAC. This publication is the work of the 
authors and will serve as guarantors for its contents. A comprehensive list of 
grant funding is available on the ALSPAC website 
(www.bristol.ac.uk/alspac/external/documents/grant-acknowledgements.pdf). 
Disclosure of potential conflict of interest: K. Abuabara reports receipt of 
consulting fees from TARGET RWE and grants to her institution from Pfizer and 
Cosmetique International SNC. The rest of the authors declare that they have no 
relevant conflicts of interest.