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In the study, an adsorptive removal strategy as a straightforward and fast procedure was developed to remove four aflatoxins, including aflatoxin B1 (AF-B1), aflatoxin B2 (AF-B2), aflatoxin G1 (AF-G1), and aflatoxin G2 (AF-G2). A simple and green sorbent consisting of two components (activated nanobentonite and Fe 3 O 4 nanoparticles) was synthesized based on three steps using acidic treatment, ultrasonic procedure, and chemical precipitation method. The sorbent was characterized by several techniques such as FTIR, FESEM, TEM, XRD, and VSM to determine the sorbent structure and morphology. An experimental design based on a central composite design was utilized to optimize factors in the removal of AFs. The optimum values of the factors (pH, sorbent amount, shaking rate) were 6.8, 0.076 g, and 160 rpm, respectively. Three models, including pseudo-first-order, pseudo-second-order, and intra-particle diffusion models, were used to investigate the kinetics of the removal process. The removal of AFs using magnetic nanobentonite was fitted with the pseudo-second-order model better than other models with an equilibrium time lower than 30 min. The thermodynamic data show that the adsorption of AFs on the sorbent is a spontaneous and feasible process due to negative values of the Gibbs-free energy change (ΔG) at different temperatures. Two models (Langmuir and Freundlich models) were chosen to study the isotherm of the removal procedure, indicating that the Freundlich model describes the results better than the Langmuir model. The maximum adsorption capacity of the sorbent for removing AF-B1, AF-B2, AF-G1, and AF-G2 is 357.14, 400.0, 370.37, and 400.0 mg g -1 , respectively. The sorbent reusability was also evaluated to study the sorbent's ability for the removal of AFs, indicating that the sorbent was used for 5 cycles without a significant reduction in the ability to remove AFs., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

The dose-limiting salivary gland toxicity of 225 Ac-labelled PSMA for treatment of metastatic, castration-resistant prostate cancer remains unresolved. Suppressing the metabolism of the gland by intraparenchymal injections of botulinum toxin appears to be a promising method to reduce off-target uptake. A 68 Ga-PSMA PET/CT scan performed 45 days after injection of 80 units of botulinum toxin A into the right parotid gland in a 63-year-old patient showed a decrease in the SUVmean in the right parotid gland of up to 64% as compared with baseline. This approach could be a significant breakthrough for radioprotection of the salivary glands during PSMA radioligand therapy., Competing Interests: Compliance with Ethical StandardsRichard P. Baum, Thomas Langbein, Aviral Singh, Mostafa Shahinfar, Christiane Schuchardt, Gerd Fabian Volk, Harshad Kulkarni declare that they have no conflict of interest.All procedures performed in this study involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the principles of the1964 Declaration of Helsinki and its later amendments or comparable ethical standards.Informed consent was obtained from the patient who was the subject of the study.

In molecular radiotherapy with 177Lu-labeled prostate specific membrane antigen (PSMA) peptides, kidney and/or salivary glands doses limit the activity which can be administered. The aim of this work was to investigate the effect of the ligand amount and injected activity on the tumor-to-normal tissue biologically effective dose (BED) ratio for 177Lu-labeled PSMA peptides. For this retrospective study, a recently developed physiologically based pharmacokinetic model was adapted for PSMA targeting peptides. General physiological parameters were taken from the literature. Individual parameters were fitted to planar gamma camera measurements (177Lu-PSMA I&T) of five patients with metastasizing prostate cancer. Based on the estimated parameters, the pharmacokinetics of tumor, salivary glands, kidneys, total body and red marrow was simulated and time-integrated activity coefficients were calculated for different peptide amounts. Based on these simulations, the absorbed doses and BEDs for normal tissue and tumor were calculated for all activities leading to a maximal tolerable kidney BED of 10 Gy2.5/cycle, a maximal salivary gland absorbed dose of 7.5 Gy/cycle and a maximal red marrow BED of 0.25 Gy15/cycle. The fits yielded coefficients of determination > 0.85, acceptable relative standard errors and low parameter correlations. All estimated parameters were in a physiologically reasonable range. The amounts (for 25-29 nmol) and pertaining activities leading to a maximal tumor dose, considering the defined maximal tolerable doses to organs of risk, were calculated to be 272±253 nmol (452±420 μg) and 7.3±5.1 GBq. Using the actually injected amount (235±155 μg) and the same maximal tolerable doses, the potential improvement for the tumor BED was 1-3 fold. The results suggest that currently given amounts for therapy are in the appropriate order of magnitude for many lesions. However, for lesions with high binding site density or lower perfusion, optimizing the peptide amount and activity might improve the tumor-to-kidney and tumor-to-salivary glands BED ratio considerably., Competing Interests: The authors have declared that no competing interests exist.

Galactocerebrosidase (GALC) is responsible for the lysosomal catabolism of certain galactolipids, including galactosylceramide and psychosine. Patients with GALC deficiency have an autosomal recessive disorder known as globoid cell leukodystrophy (GLD) or Krabbe disease. Storage of undegraded glycolipids results in defective myelin and the characteristic globoid cells observed on pathological examination of the central and peripheral nervous systems. Most patients have the infantile form of GLD, although older individuals are also diagnosed. Recently the human, mouse, and canine GALC genes were cloned, and mutations causing GLD have been identified. We now describe the construction of a vector containing human GALC cDNA (MFG-GALC), and the transduction of cultured skin fibroblasts from molecularly characterized Krabbe disease patients, as well as rat brain astrocytes and human CD34(+) hematopoietic cells, using retrovirus produced by the psi-CRIP amphotropic packaging cell line. The transduced fibroblasts showed extremely high GALC activity (up to 20,000 times pretreatment levels, about 100 times normal). GALC was secreted into the media and was taken up by untransduced fibroblasts from the same or a different patient. Mannose-6-phosphate receptor-mediated uptake was only partially responsible for the efficient transfer of GALC to neighboring cells. Additional studies confirmed the presence of normal GALC cDNA and mRNA in the transduced cells. The GALC produced by the transduced cells and donated to neighboring untransduced cells was localized to lysosomes as demonstrated by the normal metabolism of [14C]stearic acid-labeled galactosylceramide produced from endocytosed [14C]sulfatide.

Molecular analysis and clinical updates are provided on a previously reported mother and adult son with Gaucher disease; two other children died with acute neuronopathic (type 2) Gaucher disease. The mother and son have the identical genotype (370/444) but very different clinical manifestations. These findings illustrate the need for additional studies before families with newly diagnosed Gaucher disease undergo counseling.