Cryptosporidium parvum is a highly prevalent zoonotic and anthroponotic protozoan parasite that causes a diarrheal syndrome in children and neonatal livestock, culminating in growth retardation and mortalities. Disclosed herein are inhibitors against the enzymatic activity of recombinant CpLDH protein that were identified. The inhibitors were tested for anti-Cryptosporidium effect using in vitro infection assays of HCT-8 cells monolayers. Compounds NSC158011 and NSC10447 were identified to inhibit the proliferation of intracellular C. parvum in vitro, with IC50 values of 14.88 and 72.65 μM, respectively. At doses tolerable in mice, both NSC158011 and NSC10447 significantly reduced the shedding of C. parvum oocysts in infected immunocompromised mice's feces and prevented intestinal villous atrophy as well as mucosal erosion due to C. parvum. These findings have unveiled anti-Cryptosporidium drug candidates that can be explored further for the development of therapeutic agents against C. parvum infections.

Cryptosporidium parvum is a highly prevalent zoonotic and anthroponotic protozoan parasite that causes a diarrheal syndrome in children and neonatal livestock, culminating in growth retardation and mortalities. Disclosed herein are inhibitors against the enzymatic activity of recombinant CpLDH protein that were identified. The inhibitors were tested for anti-Cryptosporidium effect using in vitro infection assays of HCT-8 cells monolayers. Compounds NSC158011 and NSC10447 were identified to inhibit the proliferation of intracellular C. parvum in vitro, with IC50 values of 14.88 and 72.65 μM, respectively. At doses tolerable in mice, both NSC158011 and NSC10447 significantly reduced the shedding of C. parvum oocysts in infected immunocompromised mice's feces and prevented intestinal villous atrophy as well as mucosal erosion due to C. parvum. These findings have unveiled anti-Cryptosporidium drug candidates that can be explored further for the development of therapeutic agents against C. parvum infections.

The present invention relates to the field of neurological diseases, particularly to neurodegenerative diseases caused by dipeptide repeat toxicity. The invention provides genetic and chemical inhibitors of the protein kinase NEK6 to treat amyotrophic lateral sclerosis and frontotemporal dementia.

The present invention relates to the field of neurological diseases, particularly to neurodegenerative diseases caused by dipeptide repeat toxicity. The invention provides genetic and chemical inhibitors of the protein kinase NEK6 to treat amyotrophic lateral sclerosis and frontotemporal dementia.

Disclosed is use of a composition for preventing and/or eliminating platelet aggregation in an in vitro blood sample. The composition comprises at least one compound selected from the group consisting of formula, R1-NH—R2, and a salt thereof. Also disclosed is an agent, which comprises the compound for reducing platelet aggregation interference in an in vitro blood test, and a method for preventing and/or eliminating platelet aggregation in a sample in an in vitro blood test. The compound of the present invention exhibits a disaggregation effect in multiple types of platelet aggregation circumstances, and the platelet disaggregation takes effect within a short time without additional conditions such as temperature control with water bath, prolonged reaction time and the like, thereby eliminating platelet aggregation in a sample conveniently and thus accurate blood cell detection parameters can be obtained.

The present invention provides compounds, compositions thereof, and methods of using the same.

The present invention provides compounds, compositions thereof, and methods of using the same.

A method of treating cervical cancer in a patient in need is described that includes implanting a fast release implant containing an effective amount of Cis-Pt within a cervical cancer lesion. The implant includes a polymer and a therapeutic load homogenously distributed throughout the polymer. The implant assumes a solid phase at room temperature and assumes a liquid phase at a body temperature of the patient.

A method of treating cervical cancer in a patient in need is described that includes implanting a fast release implant containing an effective amount of Cis-Pt within a cervical cancer lesion. The implant includes a polymer and a therapeutic load homogenously distributed throughout the polymer. The implant assumes a solid phase at room temperature and assumes a liquid phase at a body temperature of the patient.

Described herein are methods of enhancing chromosomal homologous recombination to stimulate a loss of heterozygosity at a gene locus of interest in a living cell. These methods are driven by an enhancer component and a target-specific endonuclease component and proceed through a mechanism whereby: exogenous donor DNA that is homologous to the gene locus of interest is not introduced into the living cell; the desired allele of the gene locus of interest remains uncleaved; and the undesired allele is either uncleaved, cleaved at a single location, or cleaved at multiple locations. These methods have numerous applications, including the repair of risk alleles for disease prevention, the correction of heterozygous mutations in dividing cells, the design of cancer therapeutics, and the design of novel gene-drive strategies.