Provided are compositions related to HSD17B13 variants, including isolated nucleic acids and proteins related to variants of HSD17B13, and cells comprising those nucleic acids and proteins. Also provided are methods related to HSD17B13 variants. Such methods include methods for modifying a cell through use of any combination of nuclease agents, exogenous donor sequences, transcriptional activators, transcriptional repressors, and expression vectors for expressing a recombinant HSD17B13 gene or a nucleic acid encoding an HSD17B13 protein. Also provided are therapeutic and prophylactic methods for treating a subject having or at risk of developing chronic liver disease.

Neonatal seizure is different from adult seizure, and many anti epileptic drugs that are effective in adults often fail to treat neonatal seizure. Gluconic acid, a natural organic acid enriched in fruits and honey, and the glucose oxidase enzyme, is shown herein to potently inhibit neonatal epilepsy both in vitro and in vivo. Sodium gluconate is shown to inhibit epileptiform burst activity in cell cultures and protect neurons from kainic acid-induced cell death. Sodium gluconate also inhibited epileptiform burst activity in brain slices in a manner that was much more potent in neonatal animals than in older animals. Consistently, in vivo EEC recordings also revealed that sodium gluconate inhibited the epileptic seizure activity in a manner that was much more potent in neonates than in adult animals. Mechanistically, sodium gluconate inhibits voltage-dependent CLC-3 C1.sup.− channels both in neuronal cultures and in hippocampal slices. Together, these data suggest a novel antiepileptic drug gluconate that potently inhibits neonatal seizures through blocking CLC-3 C1.sup.− channels.

Eosinophil peroxidase compositions and methods of their use for killing and/or inhibiting the growth of susceptible microorganisms are provided. The compositions include an eosinophil peroxidase, a peroxide or peroxide source, and amino acids glycine, L-alanine, and L-proline.

The present invention provides a pharmaceutical composition containing 10 mg to about 100 g KRED and/or a long-acting alcohol dehydrogenase as an active ingredient and a pharmaceutically acceptable carrier. Moreover, provided herein methods for lowering blood alcohol level, methods for preventing a symptom or a risk arising from alcohol consumption and methods for treating a subject afflicted with alcoholism by the administration of the pharmaceutical composition of the invention.

Herein are described pharmabiotic compositions and methods of treatment using genetically modified bacteria that include a portion or a variant of human cDNA sequence. Generally, the modified bacterium has a genetic modification that includes the introduction or inclusion of non-native DNA which contain a human cDNA sequence that can be propagated in the genetically altered bacterium. As an example, the non-native DNA can include one or more portions of human cDNA that encode the enzyme phenylalanine hydroxylase. In an embodiment, the modified bacterium can be provided to a patient as a treatment for a metabolic disorder. In a non-limiting example, a modified bacterium including human cDNA encoding the enzyme phenylalanine hydroxylase can be provided to a patient suffering from a deficiency in phenylalanine hydroxylase or suffering from a mutation to the native gene that results in an inactive form of the enzyme. As such, certain embodiments may provide methods for treating phenylketonuria using the modified bacterium.

The present disclosure provides recombinant bacterial cells that have been engineered with genetic circuitry which allow the recombinant bacterial cells to sense a patient's internal environment and respond by turning an engineered metabolic pathway on or off. When turned on, the recombinant bacterial cells complete all of the steps in a metabolic pathway to achieve a therapeutic effect in a host subject. These recombinant bacterial cells are designed to drive therapeutic effects throughout the body of a host from a point of origin of the microbiome. Specifically, the present disclosure provides recombinant bacterial cells comprising a heterologous gene encoding a branched chain amino acid catabolism enzyme. The disclosure further provides pharmaceutical compositions comprising the recombinant bacteria, and methods for treating disorders involving the catabolism of branched chain amino acids using the pharmaceutical compositions disclosed herein.

The present invention provides for a composition, as disclosed herein, for delivery of an active agent. The composition includes a peptide coacervate, wherein the peptide coacervate includes one or more peptides derived from histidine-rich proteins, and an active agent encapsulated in the peptide coacervate. Further provided are a method for encapsulation of an active agent in a peptide coacervate, a method for delivery of an active agent, and a method for treating or diagnosing a condition or disease in a subject in need thereof.

Provided are compositions related to HSD17B13 variants, including nucleic acid molecules and polypeptides related to variants of HSD17B13, and cells comprising those nucleic acid molecules and polypeptides. Also provided are methods related to HSD17B13 variants. Such methods include methods for detecting the presence of the HSD17B13 rs72613567 variant in a biological sample comprising genomic DNA, for detecting the presence or levels of any one of variant HSD17B13 Transcripts C, D, E, F, G, and H, and particularly D, in a biological sample comprising mRNA or cDNA, or for detecting the presence or levels of any one of variant HSD17B13 protein Isoforms C, D, E, F, G, or H, and particularly D, in a biological sample comprising protein. Also provided are methods for determining a subject's susceptibility to developing a liver disease or of diagnosing a subject with liver disease.

An object is to provide a preparation for forming emboli highly safe in a living body and capable of retaining and controlled-releasing an anticancer agent, occluding a blood vessel when injected into the blood vessel, unlikely to be washed out and having a controlled decomposition time (i.e., occludes a blood vessel for a while and quickly decomposes to prevent the necrosis of the entire tissues when the function is completed). The preparation for forming emboli according to the present invention comprises a solution comprising a phenolic hydroxyl group-modified polymer represented by the following formula (1): wherein P is a biocompatible polymer, A is a single bond or an —OCO—C.sub.2-C.sub.4-alkenylene group, a —CONH—C.sub.1-C.sub.4-alkylene group or an —HNCO—C.sub.1-C.sub.4-alkylene group, and X is hydrogen or a C.sub.1-C.sub.3-alkoxy group, a solution comprising at least one selected from a peroxidase, a laccase, a tyrosinase, a catalase and an iron porphyrin complex and a solution comprising hydrogen peroxide.

##STR00001##

Chimeric polypeptides comprising a dihydrotestosterone (DHT) reductase moiety, such as 3 alpha-hydroxysteroid dehydrogenase (3α-HSD), fused to a signal peptide moiety, polynucleotides encoding same, and compositions comprising at least one microorganism cell capable of secreting the chimeric polypeptide, are provided. Further provided are methods and kits for treating, preventing or ameliorating androgen-dependent disorders, including but not limited to androgenic alopecia.