Abstract: This application relates to a circuit board assembly. The circuit board assembly includes: a first circuit board. The first circuit board is connected to a connector; and a second circuit board. A first connecting portion is disposed on the second circuit board. The first connecting portion is electrically connected to the connector. The second circuit board includes a top surface and a side surface. The top surface intersects and is perpendicular to the side surface. The first connecting portion is disposed on the top surface, and extends towards the side surface. In this disclosure, the top surface intersects and is perpendicular to the side surface, to improve stability of connection between the connector and the first connecting portion, and improve working stability of the second circuit board, so as to improve working performance of the circuit board assembly and improve user experience.

Abstract: Disclosed are probes based on papilloma virus and modified SV40 that can be used for detecting circulating tumor cells (CTCs) in the blood stream, methods for manufacturing such probes, and methods for using such probes.

Abstract: The present invention is directed to the composition and use of a modified Herpes Simplex Virus Type 2 (HSV-2) as a medicament in the treatment of cancer. The modified HSV-2 has fusogenic activity, and comprises a modified/mutated ICP10 polynucleotide encoding a polypeptide having ribonucleotide reductase activity and lacking protein kinase activity.

Abstract: The present invention is directed to the composition and use of a modified Herpes Simplex Virus Type 2 (HSV-2) as a medicament in the treatment of cancer. The modified HSV-2 comprises a modified/mutated ICP10 polynucleotide encoding a polypeptide having ribonucleotide reductase activity and lacking protein kinase activity.

Abstract: The present invention is directed to the composition and use of a modified Herpes Simplex Virus Type 2 (HSV-2) as a medicament in the treatment of cancer. The modified HSV-2 has fusogenic activity, and comprises a modified/mutated ICP10 polynucleotide encoding a polypeptide having ribonucleotide reductase activity and lacking protein kinase activity.

Abstract: The present invention is directed to the composition and use of a modified Herpes Simplex Virus Type 2 (HSV-2) as a medicament in the treatment of cancer. The modified HSV-2 has fusogenic activity, and comprises a modified/mutated ICP 10 polynucleotide encoding a polypeptide having ribonucleotide reductase activity and lacking protein kinase activity.

Abstract: A T cell transduced with a chimeric antigen receptor can be administered to a host to kill cancer cells. The chimeric antigen receptor can include a targeting moiety with a strong binding affinity to ?v?3 integrin, including but not limited to an echistatin polypeptide. The targeting moiety can also be modified to have a reduced binding affinity to ?5?1 integrin.

Abstract: The present invention is directed to the administration of FusOn-H2, an HSV derived oncolytic virus, to treat tumor cells that are resistant to the lytic effect of the virus. Administration of FusOn-H2 induces the patient's innate immune responses to tumor cells via neutrophils, which are able to destroy tumors efficiently when they migrate to the tumor mass. With the induced innate antitumor immunity, FusOn-H2 is effective at eradicating tumors even when it is used at very low doses.

Abstract: The present invention relates to a novel composition and method to potentiate the antitumor effect of an oncolytic virus by providing for resistance against a host's innate interferon response. Particularly, a B18R gene is incorporated into an oncolytic virus. During treatment of a host with the modified oncolytic virus, the oncolytic virus retains its phenotype, and the host's innate immune response has a minimal affect on viral replication.

Abstract: The present invention is directed to the administration of an HSV derived oncolytic virus and a PI3K/AKT/mTOR pathway inhibitor to treat various types of resistant tumors. Therapy-resistant tumor formation is one of the main causes for treatment failure in the clinic. The treatment methods and compositions disclosed herein sensitize resistant tumors to the treatment of herpes simplex virus (HSV)-based oncolytic virotherapy. Pre or co-treatment of resistant tumor cells with the mTOR inhibitor, rapamycin, or certain PI3K inhibitors, such as LY294002, can efficiently sensitize the tumors to HSV derived oncolytic viruses, whereby the replication and spread of the viruses are dramatically enhanced.

Abstract: The present invention is directed to the composition and use of a modified Herpes Simplex Virus Type 2 (HSV-2) as a medicament in the treatment of cancer. The modified HSV-2 has fusogenic activity, and comprises a modified/mutated ICP10 polynucleotide encoding a polypeptide having ribonucleotide reductase activity and lacking protein kinase activity.

Abstract: The present invention is directed to an oncolytic Herpes Simplex Virus having multiple cell membrane fusion mechanisms and preferably comprising a strict late viral promoter for effective conditional replication, such as in a malignant cell. In specific embodiments, the cell membrane fusion mechanisms are either from a mutant virus generated through random mutagenesis or through insertion of a fusogenic membrane glycoprotein, and in further specific embodiments the strict late viral promoter UL38p regulates expression of the glycoprotein.

Abstract: Gene Delivery Vectors and Their Uses

Abstract: Herpesvirus amplicon preparations comprise an origin of replication, a packaging sequence, and at least one inserted gene under control of a promoter, suitable for use as an immunogen or vaccine, in association with helper herpesvirus or DNA, wherein the associated helper virus is of restricted replication competence in a normal host cell; for example where the associated helper virus has an inactivating defect in respect of a gene essential for production of infectious new virus particles, and where the amplicon carries an inserted gene necessary for the propagation of the helper virus.