Abstract: An apparatus is designed for holding the tail of an animal to one side while the animal is on a milking platform. The apparatus consists of a structure mounted to the rail along or around the milking platform which holds the tail such that the pathway to the udder between the animal's rear legs is unobstructed by the tail.

Abstract: A robotic milking system suitable for use with conventional milking clusters. Clusters are withdrawn to a generally known position upon release from a cow with the cups hanging down below the bowl. The cups are then located in a confined region from where they are picked up by a robotic arm and attached to teats of a cow. The arrangement allows a single robotic arm to service multiple bales of a rotary milking parlor.

Abstract: An apparatus is designed for holding the tail of an animal to one side while the animal is on a milking platform. The apparatus consists of a structure mounted to the rail along or around the milking platform which holds the tail such that the pathway to the udder between the animal's rear legs is unobstructed by the tail.

Abstract: Although it can be farnesylated, the mutant lamin A protein expressed in Hutchinson Gilford Progeria Syndrome (HGPS) cannot be defarnesylated because the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (called “progerin”) that alters normal lamin A function as a dominant negative, as well as assuming its own aberrant function through its association with the nuclear membrane. The retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) (both direct effectors and indirect inhibitors) will inhibit the formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression.

Abstract: Although it can be farnesylated, the mutant lamin A protein expressed in Hutchinson Gilford Progeria Syndrome (HGPS) cannot be defarnesylated because the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (called “progerin”) that alters normal lamin A function as a dominant negative, as well as assuming its own aberrant function through its association with the nuclear membrane. The retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) (both direct effectors and indirect inhibitors) will inhibit the formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression.

Abstract: A robotic milking system suitable for use with conventional milking clusters. Clusters are withdrawn to a generally known position upon release from a cow with the cups hanging down below the bowl. The cups are then located in a confined region from where they are picked up by a robotic arm and attached to teats of a cow. The arrangement allows a single robotic arm to service multiple bales of a rotary milking parlour.

Abstract: Although it can be farnesylated, mutant lamin A expressed in Hutchinson Gilford Progeria Syndrome cannot be defarnesylated; the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (“progerin”) that alters normal lamin A function as a dominant negative, and assumes its own aberrant function through its association with the nuclear membrane. Retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) will inhibit formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression. Similarly, treatment with FTIs should improve disease status in progeria and other laminopathies.

Abstract: A robotic milking system suitable for use with conventional milking clusters. Clusters are withdrawn to a generally known position upon release from a cow with the cups hanging down below the bowl. The cups are then located in a confined region from where they are picked up by a robotic arm and attached to teats of a cow. The cups may be located into recesses or slots or be drawn through a guide. The arrangement allows a single robotic arm to service multiple bales of a rotary milking parlor. The application of a vacuum to milking cups may be controlled by applying sufficient pressure to the pulsation line of a cup to collapse the cup liner when that cup is not attached to a teat or by bending a feed line to a cup to close the flow path.

Abstract: Although it can be farnesylated, mutant lamin A expressed in Hutchinson Gilford Progeria Syndrome cannot be defarnesylated; the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (“progerin”) that alters normal lamin A function as a dominant negative, and assumes its own aberrant function through its association with the nuclear membrane. Retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) will inhibit formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression. Similarly, treatment with FTIs should improve disease status in progeria and other laminopathies.

Abstract: Although it can be farnesylated, the mutant lamin A protein expressed in Hutchinson Gilford Progeria Syndrome (HGPS) cannot be defarnesylated because the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (called “progerin”) that alters normal lamin A function as a dominant negative, as well as assuming its own aberrant function through its association with the nuclear membrane. The retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) (both direct effectors and indirect inhibitors) will inhibit the formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression.

Abstract: A robotic milking system suitable for use with conventional milking clusters. Clusters are withdrawn to a generally known position upon release from a cow with the cups hanging down below the bowl. The cups are then located in a confined region from where they are picked up by a robotic arm and attached to teats of a cow. The cups may be located into recesses or slots or be drawn through a guide. The arrangement allows a single robotic arm to service multiple bales of a rotary milking parlour. The application of a vacuum to milking cups may be controlled by applying sufficient pressure to the pulsation line of a cup to collapse the cup liner when that cup is not attached to a teat or by bending a feed line to a cup to close the flow path.

Abstract: Although it can be farnesylated, the mutant lamin A protein expressed in Hutchinson Gilford Progeria Syndrome (HGPS) cannot be defarnesylated because the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (called “progerin”) that alters normal lamin A function as a dominant negative, as well as assuming its own aberrant function through its association with the nuclear membrane. The retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) (both direct effectors and indirect inhibitors) will inhibit the formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression.

Abstract: Although it can be farnesylated, the mutant lamin A protein expressed in Hutchison Gilford Progeria Syndrome (HGPS) cannot be defarnesylated because the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (called “progerin”) that alters normal lamin A function as a dominant negative, as well as assuming its own aberrant function through its association with the nuclear membrane. The retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) (both direct effectors and indirect inhibitors) will inhibit the formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression.

Abstract: Although it can be farnesylated, the mutant lamin A protein expressed in Hutchison Gilford Progeria Syndrome (HGPS) cannot be defarnesylated because the characteristic mutation causes deletion of a cleavage site necessary for binding the protease ZMPSTE24 and effecting defarnesylation. The result is an aberrant farnesylated protein (called “progerin”) that alters normal lamin A function as a dominant negative, as well as assuming its own aberrant function through its association with the nuclear membrane. The retention of farnesylation, and potentially other abnormal properties of progerin and other abnormal lamin gene protein products, produces disease. Farnesyltransferase inhibitors (FTIs) (both direct effectors and indirect inhibitors) will inhibit the formation of progerin, cause a decrease in lamin A protein, and/or an increase prelamin A protein. Decreasing the amount of aberrant protein improves cellular effects caused by and progerin expression.

Abstract: A hand mounted holiday tester includes a control unit with electrical sensing apparatus for detecting a completed circuit between a positive pole and a negative pole of the control unit. The tester further includes a hand receiving mitten, constructed of non-electrically conductive, flexible material with a front surface generally adjacent and parallel to the palm of a hand in the mitten. A flat sponge is fixedly attached to the front surface of the mitten with the front surface of the sponge substantially parallel to the front surface of the mitten. An electrical contact to the sponge includes a loop of wire embedded in the sponge and electrically coupled to one of the positive pole and the negative pole of the control unit.