We claim:
1. A method for forming a prion-physiological structure, comprising:
providing an abnormal prion that has a transforming power over a normal prion; and
covalently bonding a linker molecule to the abnormal prion, wherein a polymer is covalently attached to the linker molecule to form a polymerized abnormal prion that does not have the transforming power over the normal prion.
2. The method of claim 1, wherein the polymer is selected from the group consisting of polyethylene glycol, methoxypolyethylene glycol, ethoxypolyethylene glycol, dextran, ficoll, and arabinogalactan.
3. The method of claim 1, wherein the linker molecule is selected from the group consisting of cyanuric chloride, imidazolyl formate, succinimidyl succinate, succinimidyl glutarate, N-hydroxysuccinimide, 4-Nitrophenol, 2,4,5-trichlorophenol, and a chloroformate.
4. The method of claim 1, wherein the abnormal prion has human significance.
5. The method of claim 1, wherein the abnormal prion has veterinary significance.
6. The method of claim 1, wherein covalently bonding the linker molecule to the abnormal prion includes covalently bonding the linker molecule to an amino acid at the abnormal prion.
7. The method of claim 1, wherein covalently bonding the linker molecule to the abnormal prion includes covalently bonding the linker molecule to a lysine group at the abnormal prion.
8. The method of claim 1, wherein covalently bonding the linker molecule to the abnormal prion includes covalently bonding the linker molecule to a carbohydrate at the abnormal prion.
9. The method of claim 1, wherein covalently bonding the linker molecule to the abnormal prion includes covalently bonding the linker molecule to a sulfhydryl group at the abnormal prion.
10. A method for forming a prion-physiological structure, comprising:
providing an abnormal prion that has a transforming power over a normal prion; and
covalently bonding a linker molecule to the abnormal prion, wherein a polymer is covalently attached to the linker molecule to form a polymerized abnormal prion, and wherein the polymer has a long chain length that inactivates the transforming power.
11. A method for forming a prion-physiological structure, comprising:
providing an abnormal prion that has a transforming power over a normal prion; and
covalently bonding a linker molecule to the abnormal prion, wherein a polymer is covalently attached to the linker molecule to form a polymerized abnormal prion, and wherein a camouflaging by the polymer of a charge site at the abnormal prion inactivates the transforming power.
12. A method for forming a prion-physiological structure, comprising:
providing an abnormal prion that has a transforming power over a normal prion;
covalently bonding a linker molecule to the abnormal prion, wherein a polymer is covalently attached to the linker molecule to form a polymerized abnormal prion that does not have the transforming power over the normal prion;
providing an animal that includes the normal prion; and
introducing the polymerized abnormal prion into the animal.
13. The method of claim 12, wherein the animal is a human animal.
14. The method of claim 12, wherein the animal is a veterinary animal.
15. A method for forming a prion-physiological structure, comprising:
providing a medium that includes proteinaceous matter, said proteinaceous matter including an abnormal prion or not including the abnormal prion, said abnormal prion having a transforming power over a normal prion;
providing a linker molecule to which a polymer is covalently attached; and
introducing the linker molecule into the medium such that if the medium includes the abnormal prion then said introducing results in the linker molecule covalently bonding to the abnormal prion to form a polymerized abnormal prion that does not have the transforming power over the normal prion.
16. The method of claim 15, wherein the proteinaceous matter includes blood albumin.
17. A method for forming a prion-physiological structure, comprising:
providing a medium that includes proteinaceous matter, said proteinaceous matter including an abnormal prion or not including the abnormal prion, said abnormal prion having a transforming power over a normal prion;
providing a linker molecule to which a polymer is covalently attached;
introducing the linker molecule into the medium such that if the medium includes the abnormal prion then said introducing results in the linker molecule covalently bonding to the abnormal prion to form a polymerized abnormal prion that does not have the transforming power over the normal prion;
providing an animal that includes the normal prion; and
after introducing the linker molecule, introducing a portion of the medium into the animal.
18. The method of claim 17, wherein the proteinaceous matter includes blood albumin.
19. The method of claim 17, wherein the animal is a human animal.
20. The method of claim 17, wherein the animal is a veterinary animal.
21. A prion-physiological structure, comprising:
an abnormal prion that has a transforming power over a normal prion; and
a linker molecule covalently bonded to the abnormal prion, wherein a polymer is covalently attached to the linker molecule to form a polymerized abnormal prion that does not have the transforming power over the normal prion.
22. The prion-physiological structure of claim 21, wherein the polymer is selected from the group consisting of polyethylene glycol, methoxypolyethylene glycol, ethoxypolyethylene glycol, dextran, ficoll, and arabinogalactan.
23. The prion-physiological structure of claim 21, wherein the linker molecule is selected from the group consisting of cyanuric chloride, imidazolyl formate, succinimidyl succinate, succinimidyl glutarate, N-hydroxysuccinimide, 4-Nitrophenol, 2,4,5-trichlorophenol, and a chloroformate.
24. The prion-physiological structure of claim 21, wherein the abnormal prion has human significance.
25. The prion-physiological structure of claim 21, wherein the abnormal prion has veterinary significance.
26. The prion-physiological structure of claim 21, wherein covalently bonding the linker molecule to the abnormal prion includes covalently bonding the linker molecule to an amino acid at the abnormal prion.
27. The prion-physiological structure of claim 21, wherein covalently bonding the linker molecule to the abnormal prion includes covalently bonding the linker molecule to a lysine group at the abnormal prion.
28. The prion-physiological structure of claim 21, wherein covalently bonding the linker molecule to the abnormal prion includes covalently bonding the linker molecule to a carbohydrate at the abnormal prion.
29. The prion-physiological structure of claim 21, wherein covalently bonding the linker molecule to the abnormal prion includes covalently bonding the linker molecule to a sulfhydryl group at the abnormal prion.
30. A prion-physiological structure, comprising:
an abnormal prion that has a transforming power over a normal prion; and
a linker molecule covalently bonded to the abnormal prion, wherein a polymer is covalently attached to the linker molecule to form a polymerized abnormal prion, and wherein the polymer has a long chain length that inactivates the transforming power.
31. A prion-physiological structure, comprising:
an abnormal prion that has a transforming power over a normal prion; and
a linker molecule covalently bonded to the abnormal prion, wherein a polymer is covalently attached to the linker molecule to form a polymerized abnormal prion, and wherein a camouflaging by the polymer of a charge site at the abnormal prion inactivates the transforming power.
32. A prion-physiological structure, comprising:
an abnormal prion that has a transforming power over a normal prion;
a linker molecule covalently bonded to the abnormal prion, wherein a polymer is covalently attached to the linker molecule to form a polymerized abnormal prion that does not have the transforming power over the normal prion; and
an animal that includes the normal prion and the polymerized abnormal prion.
33. The prion-physiological structure of claim 32, wherein the animal is a human animal.
34. The prion-physiological structure of claim 32, wherein the animal is a veterinary animal.
35. A prion-physiological structure, comprising a medium having:
proteinaceous matter that includes an abnormal prion or does not include the abnormal prion, wherein the abnormal prion has a transforming power over a normal prion; and
a linker molecule to which a polymer is covalently attached, wherein if the medium includes the abnormal prion then the linker molecule is covalently bonded to the abnormal prion to form a polymerized abnormal prion that does not have the transforming power over the normal prion.
36. The prion-physiological structure of claim 35, wherein the proteinaceous matter includes blood albumin.
37. A prion-physiological structure, comprising an animal that includes a normal prion and a portion of a medium, wherein the medium comprises:
proteinaceous matter that includes an abnormal prion or does not include the abnormal prion, wherein the abnormal prion has a transforming power over the normal prion; and
a linker molecule to which a polymer is covalently attached, wherein if the medium includes the abnormal prion then the linker molecule is covalently bonded to the abnormal prion to form a polymerized abnormal prion that does not have the transforming power over the normal prion.
38. The prion-physiological structure of claim 37, wherein the proteinaceous matter includes blood albumin.
39. The prion-physiological structure of claim 37, wherein the animal is a human animal.
40. The prion-physiological structure of claim 37, wherein the animal is a veterinary animal.
41. A prion-physiological structure, comprising:
an abnormal prion that has a transforming power over a normal prion; and
means for covalently bonding a linker molecule to the abnormal prion, wherein a polymer is covalently attached to the linker molecule to form a polymerized abnormal prion that does not have the transforming power over the normal prion.
42. The prion-physiological structure of claim 41, wherein the polymer is selected from the group consisting of polyethylene glycol, methoxypolyethylene glycol, ethoxypolyethylene glycol, dextran, ficoll, and arabinogalactan.
43. The prion-physiological structure of claim 41, wherein the linker molecule is selected from the group consisting of cyanuric chloride, imidazolyl formate, succinimidyl succinate, succinimidyl glutarate, N-hydroxysuccinimide, 4-Nitrophenol, 2,4,5-trichlorophenol, and a chloroformate.
44. The prion-physiological structure of claim 41, wherein the abnormal prion has human significance.
45. The prion-physiological structure of claim 41, wherein the abnormal prion has veterinary significance.
46. The prion-physiological structure of claim 41, wherein covalently bonding the linker molecule to the abnormal prion includes covalently bonding the linker molecule to an amino acid at the abnormal prion.
47. The prion-physiological structure of claim 41, wherein covalently bonding the linker molecule to the abnormal prion includes covalently bonding the linker molecule to a lysine group at the abnormal prion.
48. The prion-physiological structure of claim 41, wherein covalently bonding the linker molecule to the abnormal prion includes covalently bonding the linker molecule to a lysine group at the abnormal prion.
49. The prion-physiological structure of claim 41, wherein covalently bonding the linker molecule to the abnormal prion includes covalently bonding the linker molecule to a sulfhydryl group at the abnormal prion.
50. A prion-physiological structure, comprising:
an abnormal prion that has a transforming power over a normal prion; and
means for covalently bonding a linker molecule to the abnormal prion, wherein a polymer is covalently attached to the linker molecule to form a polymerized abnormal prion, and wherein the polymer has a long chain length that inactivates the transforming power.
51. A prion-physiological structure, comprising:
an abnormal prion that has a transforming power over a normal prion; and
means for covalently bonding a linker molecule to the abnormal prion, wherein a polymer is covalently attached to the linker molecule to form a polymerized abnormal prion, and wherein a camouflaging by the polymer of a charge site at the abnormal prion inactivates the transforming power.
52. A prion-physiological structure, comprising:
an abnormal prion that has a transforming power over a normal prion;
means for covalently bonding a linker molecule to the abnormal prion, wherein a polymer is covalently attached to the linker molecule to form a polymerized abnormal prion that does not have the transforming power over the normal prion;
an animal that includes the normal prion; and
means for introducing the polymerized abnormal prion into the animal.
53. The prion-physiological structure of claim 52, wherein the animal is a human animal.
54. The prion-physiological structure of claim 52, wherein the animal is a veterinary animal.
55. A prion-physiological structure, comprising:
a medium that includes proteinaceous matter, said proteinaceous matter including an abnormal prion or not including the abnormal prion, said abnormal prion having a transforming power over a normal prion;
a linker molecule to which a polymer is covalently attached; and
means for introducing the linker molecule into the medium such that if the medium includes the abnormal prion then said introducing results in the linker molecule covalently bonding to the abnormal prion to form a polymerized abnormal prion that does not have the transforming power over the normal prion.
56. The prion-physiological structure of claim 55, wherein the proteinaceous matter includes blood albumin.
57. A prion-physiological structure, comprising:
a medium that includes proteinaceous matter, said proteinaceous matter including an abnormal prion or not including the abnormal prion, said abnormal prion having a transforming power over a normal prion;
a linker molecule to which a polymer is covalently attached;
means for introducing the linker molecule into the medium such that if the medium includes the abnormal prion then said introducing results in the linker molecule covalently bonding to the abnormal prion to form a polymerized abnormal prion that does not have the transforming power over the normal prion;
an animal that includes the normal prion; and
means for introducing a portion of the medium into the animal.
58. The prion-physiological structure of claim 57, wherein the proteinaceous matter includes blood albumin.
59. The prion-physiological structure of claim 57, wherein the animal is a human animal.
60. The prion-physiological structure of claim 57, wherein the animal is a veterinary animal.
The claims below are in addition to those above.
All refrences to claim(s) which appear below refer to the numbering after this setence.
1. A system comprising an applier with an anastomosis ring device having proximal, center, and distal rings connected respectively b proximal and distal hinged arms, the ring device having a generally cylindrical shape when unactuated and a rivet shape when actuated, the applier comprising:
an elongate implement portion;
a handle connected to the implement portion;
a first actuating member of the elongate implement portion having a first set of prongs internally engaged to the distal ring of the anastomosis device, the first set of prongs being configured to deflectably disengage from the distal ring of the anastomosis ring device when the anastomosis ring device is actuated;
an arresting member of the elongate implement portion engaged to the proximal ring of the anastomosis device;
a second actuating member of the elongate implement portion having a second set of prongs internally engaged to the center ring of the anastomosis device, the second set of prongs being configured to deflectably disengage from the center ring of the anastomosis ring device when the anastomosis ring device is actuated; and
first control coupled to the handle operably configured to cause proximal movement of the first actuating member and the distal ring engaged thereto toward the arresting member and toward the proximal ring;
a second control coupled to the handle operably configured to cause proximal movement of the second actuating member and the center ring engaged thereto toward the arresting member and toward the proximal ring;
wherein the first and second controls are operable to be selectively positioned to contemporaneously perform both of the following:
(i) reduce a first longitudinal separation between the center ring and a selected one of the proximal and distal rings thereby causing actuating of the interposed hinged arms located between the center ring and the selected one of the proximal and distal rings of the ring device, and
(ii) maintain a second longitudinal separation between the center ring and the other ring thereby preventing actuating of the interposed hinged arms located between the center ring and the other ring of the ring device to configure the anastomosis ring device into a partially actuated ring shape having one set of at least partially actuated arms and one set of unactuated arms; and
wherein the first and second controls are further operable to be selectively positioned to reduce the longitudinal separation between the center ring and both the proximal ring and distal ring, causing actuating of all of the hinged arms of the anastomosis ring device.
2. The system of claim 1, wherein the first actuating member that is engaged to the distal ring of the ring device distally terminates in a catch.
3. The system of claim 2, wherein the prongs of the first actuating member that is engaged to the distal ring of the ring device includes a releasing surface responsive to an actuated condition of the ring device to disengage the first actuating member from the distal ring of the ring device.
4. The system of claim 1, further comprising a distal tip illuminator connected to the implement portion
5. The system of claim 1, wherein the implement portion is dimensionally sized for endoscopic surgical use.
6. An applier for an anastomotic ring device having a center circular portion longitudinally connected by a plurality of proximal arms to a proximal ring and by a plurality of distal arms to a distal ring, the ring expanding each plurality of arms by compressing a respective ring toward the center circular portion, the applier comprising:
a first member having prongs operative to internally engage the distal ring;
a second member having prongs operative to internally engage the center circular portion;
a third member operative to engage the proximal ring; and
a handle;
a first control on the handle operatively configured to position at least one of the first, second and third members to separately actuate the plurality of distal arms; and
a second control on the handle operatively configured to position at least one of the first, second and third members to separately actuate the plurality of proximal arms;
wherein when said center circular portion of said anastomotic ring device is engaged directly with said second member of said applier, movement of said center circular portion is constrained to movement of said second member;
wherein when said proximal ring and said distal ring are adjacent to said center circular portion, said first member and said second member are deflectably disengaged from said distal ring and said center circular portion.
7. The applier of claim 6, wherein the center circular portion of the ring device comprises a center ring, the second member engaged to the center ring.
8. The applier of claim 7, wherein the prongs of first and third members comprise a releasable engagement surface responsive to an actuated condition of the anastomotic device.
9. The applier of claim 6, further comprising a cannula distally supporting the first, second, and third members, wherein the cannula is proximally attached to the handle, operatively configured to distally receive the anastomotic device, and dimensioned for endoscopic use.
10. The system of claim 1, further comprising a locking member extending proximally from the distal ring, wherein the locking member is configured to selectively engage the center ring, thereby preventing distal movement of the distal ring relative to the center ring, when the distal ring has been moved toward the center ring to actuate the distal hinged arms.
11. The system of claim 10, wherein the locking member is further configured to selectively engage the proximal ring, thereby preventing distal movement of the distal ring relative to the proximal ring, when the center ring has been moved toward the proximal ring to actuate the proximal hinged arms.