The present invention relates to a method of treating lymphedema comprising administering an effective amount of a composition to a patient in need thereof. The composition consisting essentially of cyclodextrin or a pharmaceutically acceptable salt, solvate or prodrug thereof. The present invention also relates to a composition consisting essentially of cyclodextrin.

A topical composition comprising a nanonised L-glutathione and cyclodextrin complex, together with ascorbic acid in a weight ratio of glutathione to ascorbic acid from 7:1 to 15:1 and from 1:1 to 1:15 and a further compound comprising dexpanthenol, thiamine, benzalkonium chloride, sodium hyaluronate or acetyl-L-cysteine, which composition is topically administered for treating the symptoms of viral infection including COVID-19 and influenza, and for treating herpes simplex, herpes zoster, post herpetic neuralgia, genital herpes, alcohol detoxification, high triglycerides, age or liver spots and lupus.

A topical composition comprising a nanonised L-glutathione and cyclodextrin complex, together with ascorbic acid in a weight ratio of glutathione to ascorbic acid from 7:1 to 15:1 and from 1:1 to 1:15 and a further compound comprising dexpanthenol, thiamine, benzalkonium chloride, sodium hyaluronate or acetyl-L-cysteine, which composition is topically administered for treating the symptoms of viral infection including COVID-19 and influenza, and for treating herpes simplex, herpes zoster, post herpetic neuralgia, genital herpes, alcohol detoxification, high triglycerides, age or liver spots and lupus.

Disclosed are a fibrinogen solution and a thrombin solution. The fibrinogen solution comprises fibrinogen at a concentration of at least 40 mg/ml, factor XIII, pharmaceutically acceptable additives and water. The dynamic viscosity of the fibrinogen solution measured at 20° C. increases at most by 35% after storing the solution at 20° C. for 30 days. The thrombin solution comprises thrombin, pharmaceutically acceptable additives and water. The thrombin activity decreases at most by 15% after storing the solution at 25° C. for 14 days. Also disclosed is a fibrin sealant kit with a first container comprising the fibrinogen solution and a second container comprising the thrombin solution. Further, methods for preparing a fibrin sealant and methods for treating a wound are disclosed.

Disclosed are a fibrinogen solution and a thrombin solution. The fibrinogen solution comprises fibrinogen at a concentration of at least 40 mg/ml, factor XIII, pharmaceutically acceptable additives and water. The dynamic viscosity of the fibrinogen solution measured at 20° C. increases at most by 35% after storing the solution at 20° C. for 30 days. The thrombin solution comprises thrombin, pharmaceutically acceptable additives and water. The thrombin activity decreases at most by 15% after storing the solution at 25° C. for 14 days. Also disclosed is a fibrin sealant kit with a first container comprising the fibrinogen solution and a second container comprising the thrombin solution. Further, methods for preparing a fibrin sealant and methods for treating a wound are disclosed.

In the present invention, inventors have used high throughput sequencing to identify novel mutations in ABCA1 in CM ML patient samples. Further studies in a mouse model of myelomonocytic leukemia driven by hematopoietic Tet2 deficiency have shown that these somatic mutations abrogate the tumor suppressor function of WT ABCA1, resulting in the failure to suppress canonical IL3-receptor beta signaling-driven myelopoiesis. The loss of the myelo-suppressive function of ABCA1 mutants can be overcome by raising HDL levels through overexpression of the human apolipoprotein A-1 (apoA-1) transgene. Inventors have also shown that both IL-3Rbeta blocking antibody and cyclodextrin prevented the proliferation of ABCA1 mutant-transduced Tet2 deficient BM cells similar to the effect of ABCA1-WT overexpression. Accordingly, the invention relates to a method for predicting the survival time of a subject NI suffering from CM ML comprising the step identifying at least one ABCA1 and to a method for treating said subject with HDL/ABCA recombinant (ApoA-1); cylodextrin and/or anti-IL-3Rbeta antibody.

In the present invention, inventors have used high throughput sequencing to identify novel mutations in ABCA1 in CM ML patient samples. Further studies in a mouse model of myelomonocytic leukemia driven by hematopoietic Tet2 deficiency have shown that these somatic mutations abrogate the tumor suppressor function of WT ABCA1, resulting in the failure to suppress canonical IL3-receptor beta signaling-driven myelopoiesis. The loss of the myelo-suppressive function of ABCA1 mutants can be overcome by raising HDL levels through overexpression of the human apolipoprotein A-1 (apoA-1) transgene. Inventors have also shown that both IL-3Rbeta blocking antibody and cyclodextrin prevented the proliferation of ABCA1 mutant-transduced Tet2 deficient BM cells similar to the effect of ABCA1-WT overexpression. Accordingly, the invention relates to a method for predicting the survival time of a subject NI suffering from CM ML comprising the step identifying at least one ABCA1 and to a method for treating said subject with HDL/ABCA recombinant (ApoA-1); cylodextrin and/or anti-IL-3Rbeta antibody.

In the present invention, inventors have used high throughput sequencing to identify novel mutations in ABCA1 in CM ML patient samples. Further studies in a mouse model of myelomonocytic leukemia driven by hematopoietic Tet2 deficiency have shown that these somatic mutations abrogate the tumor suppressor function of WT ABCA1, resulting in the failure to suppress canonical IL3-receptor beta signaling-driven myelopoiesis. The loss of the myelo-suppressive function of ABCA1 mutants can be overcome by raising HDL levels through overexpression of the human apolipoprotein A-1 (apoA-1) transgene. Inventors have also shown that both IL-3Rbeta blocking antibody and cyclodextrin prevented the proliferation of ABCA1 mutant-transduced Tet2 deficient BM cells similar to the effect of ABCA1-WT overexpression. Accordingly, the invention relates to a method for predicting the survival time of a subject NI suffering from CM ML comprising the step identifying at least one ABCA1 and to a method for treating said subject with HDL/ABCA recombinant (ApoA-1); cylodextrin and/or anti-IL-3Rbeta antibody.

The invention provides the use of a formulation containing cyclodextrin, quercetin and zinc at appropriate concentrations to mitigate infections by enveloped viruses. While the different forms of cyclodextrin prevent the entry of coated viruses into host cells by extracting and sequestering cholesterol molecules at the virus envelope and at the host cell plasma membrane, the ionophore quercetin enables cellular entry of zinc, thereby inhibiting viral replication by altering polymerase activity in the host cell.

The invention provides the use of a formulation containing cyclodextrin, quercetin and zinc at appropriate concentrations to mitigate infections by enveloped viruses. While the different forms of cyclodextrin prevent the entry of coated viruses into host cells by extracting and sequestering cholesterol molecules at the virus envelope and at the host cell plasma membrane, the ionophore quercetin enables cellular entry of zinc, thereby inhibiting viral replication by altering polymerase activity in the host cell.