Abstract: Provided herein are methods of nucleic acid synthesis. In some embodiments, a method of nucleic acid synthesis comprises selectively activating and deactivating an engineered terminal deoxynucleotidyl transferase (TdT). In some embodiments, a method of nucleic acid synthesis comprises activating a pH sensitive enzyme to digest and remove a TdT.

Abstract: Methods and compositions are provided for oxidizing peptides and forming disulfide bonds. In some aspects, a rapid, green, and facile oxidation of peptides (e.g., cysteine containing peptides) is performed (e.g., to promote the formation of 1-3 or more disulfide bonds). In some aspects, methods are conducted in aqueous solutions, in air, utilizing a biocompatible corrin ring-containing compound (e.g., dicyanocobinamide). In some aspects, reaction times are under 1 hour and a simple one step removal of the catalyst can be performed.

Abstract: The invention involves the coupling of compounds that can be bound by Haptocorrin (R-binder; Transcobalamin I; HC) to a target drug to improve pharmacokinetics, avoid undesirable side effects, and/or modify CNS access and localization. The pharmaceutical effect may be improved by conjugating the drug to haptocorrin binding substrate. This allows the conjugate to become bound to unsaturated haptocorrin in the blood, thereby protecting the drug from metabolism or excretion to increase protein half-life while not interfering with the efficacy of the protein drug. The conjugation may additionally prevent the drug from reaching the central nervous system or modify where the drug localizes and produces undesirable side effects such as nausea or hypophagia. Such a route also would prevent, in all case save for actual vitamin B12, binding by serum transcobalamin II (TCII), and thus not cause B12 deficiency with long term use.

Abstract: The present invention provides compositions and methods for lowering blood glucose. More specifically, the present invention provides compositions comprising a complex comprising IF and B12 conjugated to a peptide comprising a GLP-1 agonist. Advantageously, the composition may be delivered subcutaneously.

Abstract: A method of making a hydroxyl-terminated thioketal diol is provided, the method comprising reacting a thioketal ester with a non-pyrophoric reducing agent to form a hydroxyl-terminated thioketal diol. The hydroxyl-terminated thioketal diol can be 2,2-(propane-2,2-diylbis(sulfanediyl)) diethanol. The non-pyrophoric reducing agent can be a sodium aluminum hydride, for example, sodium bis (2-methoxyethoxy)aluminum hydride. The thioketal ester can be dimethyl 2,2-(propane-2,2-diylbis(sulfanediyl)) diacetate. A biodegradable matrix prepared by reacting a hydroxyl-terminated thioketal diol with an isocyanate is provided. A method of making a biodegradable polyurethane composite is also provided.

Abstract: The present disclosure provides pharmaceutical formulations and methods for delivering a therapeutic, diagnostic, or imaging agent to CD206. In an aspect, the present disclosure encompasses a pharmaceutical formulation for administration. The pharmaceutical formulation comprises a recombinantly produced intrinsic factor (IF), wherein the IF has a glycosylation pattern that enables binding to CD206.

Abstract: The invention involves the coupling of compounds that can be bound by Haptocorrin (R-binder; Transcobalamin I; HC) to a target drug to improve pharmacokinetics, avoid undesirable side effects, and/or modify CNS access and localization. The pharmaceutical effect may be improved by conjugating the drug to haptocorrin binding substrate. This allows the conjugate to become bound to unsaturated haptocorrin in the blood, thereby protecting the drug from metabolism or excretion to increase protein half-life while not interfering with the efficacy of the protein drug. The conjugation may additionally prevent the drug from reaching the central nervous system or modify where the drug localizes and produces undesirable side effects such as nausea or hypophagia. Such a route also would prevent, in all case save for actual vitamin B12, binding by serum transcobalamin II (TCII), and thus not cause B12 deficiency with long term use.

Abstract: The present invention relates to engineered peptides and to methods of making engineered peptides. The present invention also relates to methods of treatment comprising administration of the engineered peptides to a subject in need thereof.

Abstract: The present invention provides compositions and methods for lowering blood glucose. More specifically, the present invention provides compositions comprising a complex comprising IF and B12 conjugated to a peptide comprising a GLP-1 agonist. Advantageously, the composition may be delivered subcutaneously.

Abstract: The invention involves the coupling of compounds that can be bound by Haptocorrin (R-binder; Transcobalamin I; HC) to a target drug to improve pharmacokinetics, avoid undesirable side effects, and/or modify CNS access and localization. The pharmaceutical effect may be improved by conjugating the drug to haptocorrin binding substrate. This allows the conjugate to become bound to unsaturated haptocorrin in the blood, thereby protecting the drug from metabolism or excretion to increase protein half-life while not interfering with the efficacy of the protein drug. The conjugation may additionally prevent the drug from reaching the central nervous system or modify where the drug localizes and produces undesirable side effects such as nausea or hypophagia. Such a route also would prevent, in all case save for actual vitamin B12, binding by serum transcobalamin II (TCII), and thus not cause B12 deficiency with long term use.

Abstract: The present disclosure relates to metal di-amino acid chelates and metal tri-amino acid chelates.

Abstract: The present disclosure relates to metal di-amino acid chelates and metal tri-amino acid chelates.

Abstract: A head-mounted display device is provided, including an at least partially see-through display, an electrical device, and a flexible printed circuit board (FPC) arranged on a surface of a see-through portion of the display. The FPC may include a plurality of electrical traces electrically coupled to the electrical device. Each electrical trace may be separated from at least one other electrical trace by one or more respective see-through gaps. The FPC may further include a transparent material arranged between the electrical traces in each see-through gap.

Abstract: A method of making a hydroxyl-terminated thioketal diol is provided, the method comprising reacting a thioketal ester with a non-pyrophoric reducing agent to form a hydroxyl-terminated thioketal diol. The hydroxyl-terminated thioketal diol can be 2,2-(propane-2,2-diylbis(sulfanediyl)) diethanol. The non-pyrophoric reducing agent can be a sodium aluminum hydride, for example, sodium bis (2-methoxyethoxy)aluminum hydride. The thioketal ester can be dimethyl 2,2-(propane-2,2-diylbis(sulfanediyl)) diacetate. A biodegradable matrix prepared by reacting a hydroxyl-terminated thioketal diol with an isocyanate is provided. A method of making a biodegradable polyurethane composite is also provided.

Abstract: A method of making a hydroxyl-terminated thioketal diol is provided, the method comprising reacting a thioketal ester with a non-pyrophoric reducing agent to form a hydroxyl-terminated thioketal diol. The hydroxyl-terminated thioketal diol can be 2,2-(propane-2,2-diylbis(sulfanediyl)) diethanol. The non-pyrophoric reducing agent can be a sodium aluminum hydride, for example, sodium bis(2-methoxyethoxy)aluminum hydride. The thioketal ester can be dimethyl 2,2-(propane-2,2-diylbis(sulfanediyl)) diacetate. A biodegradable matrix prepared by reacting a hydroxyl-terminated thioketal diol with an isocyanate is provided. A method of making a biodegradable polyurethane composite is also provided.

Abstract: A computer-assisted method to provide timely multi-channel notification of treatments to healthcare providers and patients, the method including receiving de-identified longitudinal medical records, treatment prescription records of healthcare providers, and notification data. Relationships between the healthcare providers, the anonymized patients, and the notifications are identified using the de-identified longitudinal medical records, the treatment prescription records of the healthcare providers, and the notification data. An impact of notifications being received by both the healthcare provider for the anonymized patient and the anonymized patient on whether the anonymized patient received the treatment is determined.

Abstract: A method of making a hydroxyl-terminated thioketal diol is provided, the method comprising reacting a thioketal ester with a non-pyrophoric reducing agent to form a hydroxyl-terminated thioketal diol. The hydroxyl-terminated thioketal diol can be 2,2-(propane-2,2-diylbis(sulfanediyl)) diethanol. The non-pyrophoric reducing agent can be a sodium aluminum hydride, for example, sodium bis(2-methoxyethoxy)aluminum hydride. The thioketal ester can be dimethyl 2,2-(propane-2,2-diylbis(sulfanediyl)) diacetate. A biodegradable matrix prepared by reacting a hydroxyl-terminated thioketal diol with an isocyanate is provided. A method of making a biodegradable polyurethane composite is also provided.

Abstract: The present invention relates to the digestion of peptides by pancreatic proteases and, more specifically, to compositions and methods for protecting against protease digestion.

Abstract: The invention involves the coupling of compounds that can be bound by Haptocorrin (R-binder; Transcobalamin I; HC) to a target drug to improve pharmacokinetics, avoid undesirable side effects, and/or modify CNS access and localization. The pharmaceutical effect may be improved by conjugating the drug to haptocorrin binding substrate. This allows the conjugate to become bound to unsaturated haptocorrin in the blood, thereby protecting the drug from metabolism or excretion to increase protein half-life while not interfering with the efficacy of the protein drug. The conjugation may additionally prevent the drug from reaching the central nervous system or modify where the drug localizes and produces undesirable side effects such as nausea or hypophagia. Such a route also would prevent, in all case save for actual vitamin B12, binding by serum transcobalamin II (TCII), and thus not cause B12 deficiency with long term use.

Abstract: Peptide sequences that can serve as agonists of both the glucagon-like peptide 1 receptor (GLP-IR) and the neuropeptide Y2 receptor (NPYR2). The peptide sequences include regions that correspond to certain aspect of natural substrates and known agonists of the glucagon-like peptide 1 receptor (GLP-IR) and the neuropeptide Y2 receptor (NPYR2) in a single sequence.