Ex Parte Sharma et al

Patent Trial and Appeal Board

Aug 22, 2018

13672781 (P.T.A.B. Aug. 22, 2018)

UNITED STA TES p A TENT AND TRADEMARK OFFICE
APPLICATION NO. FILING DATE
13/672,781 11/09/2012
28524 7590 08/24/2018
SIEMENS CORPORATION
INTELLECTUAL PROPERTY DEPARTMENT
3501 Quadrangle Blvd Ste 230
Orlando, FL 32817
UNITED ST A TES OF AMERICA
FIRST NAMED INVENTOR
Puneet Sharma
UNITED STATES DEPARTMENT OF COMMERCE
United States Patent and Trademark Office
Address: COMMISSIONER FOR PATENTS
P.O. Box 1450
Alexandria, Virginia 22313-1450
www .uspto.gov
ATTORNEY DOCKET NO. CONFIRMATION NO.
2011P25614US01 2691
EXAMINER
COOK, BRIANS
ART UNIT PAPER NUMBER
2123
NOTIFICATION DATE DELIVERY MODE
08/24/2018 ELECTRONIC
Please find below and/or attached an Office communication concerning this application or proceeding.
The time period for reply, if any, is set in the attached communication.
Notice of the Office communication was sent electronically on above-indicated "Notification Date" to the
following e-mail address(es):
ipdadmin.us@siemens.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte PUNEET SHARMA, LUCIAN MIHAI ITU,
BOGDAN GEORGESCU, VIOREL MIHALEF, ALI KAMEN, and
DORIN COMANICIU
Appeal 2018-002114
Application 13/672, 781
Technology Center 2100
Before ERIC B. CHEN, MATTHEW R. CLEMENTS, and
SCOTT E. BAIN, Administrative Patent Judges.
CHEN, Administrative Patent Judge.
DECISION ON APPEAL
This is an appeal under 35 U.S.C. § 134(a) from the final rejection of
claims 1--43, which constitute all the claims pending in the application. We
have jurisdiction under 35 U.S.C. § 6(b). We reverse.
Appeal 2018-002114
Application 13/672,781
INVENTION
Appellants' invention, a "method and system for multi-scale
anatomical and functional modeling of coronary circulation" (Title),
provides a "patient-specific anatomical model of coronary arteries and the
heart ... generated from medical image data of a patient" (Abstract). "The
predictive nature of the multi-scale coupled model of the coronary
circulation is intrinsically linked to its coupling with cellular models[,
which] makes it possible to track the initiation, and subsequent growth of
coronary plaques and their effect on the overall circulation." (Spec. ,r 46.)
Claim 1 is exemplary, with disputed limitations in italics:
1. A method, comprising:
generating a patient-specific anatomical model of
coronary arteries and a heart from medical image data of a
patient;
generating a multi-scale functional model of coronary
circulation based on the patient-specific anatomical model;
coupling, to the multi-scale functional model of coronary
circulation, a cellular model of endothelial cell function that
simulates changes in a mechanical property of a vascular wall
due to a response of endothelial cells to hemodynamic forces,
wherein a wall shear-stress value calculated by the multi-scale
functional model of coronary circulation is used to couple the
multi-scale functional model of coronary circulation to the
cellular model of endothelial function through a
mechanotransduction model; and
simulating blood flow in at least one stenosis region of at
least one coronary artery and changes in a mechanical property
of a vascular wall in the at least one stenosis region of the at least
one coronary artery due to a response of endothelial cells in the
vascular wall to hemodynamic forces from the simulated blood
flow using the multi-scale functional model of coronary
circulation and the cellular model of endothelial cell function
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Application 13/672,781
coupled to the multi-scale functional model of coronary
circulation.
EXAMINER'S REJECTIONS
Claims 1-5, 7-12, 15-19, 21-25, 27-34, and 36-43 stand rejected
under 35 U.S.C. § I03(a) as unpatentable over Taylor (US 2012/0041739
Al; Feb. 16, 2012), Ionasec (US 2010/0070249 Al; Mar. 18, 2010), and
NIH 1 (C.A. Taylor et al., Open Problems in Computational Vascular
Biomechanics: Hemodynamics and Arterial Wall Mechanics, 198 COMPUT.
METHODS APPLIED MECH. & ENG'G. 3514--3523 (2009)). (Final Act. 11-
38.)
Claims 6, 26, and 35 stand rejected under 35 U.S.C. § I03(a) as
unpatentable over Taylor, Ionasec, NIH, and Passerini (T. Passerini et al., A
3D/1D Geometrical Multiscale Model of Cerebral Vasculature, 64 J. ENG'G
MATH 319-330 (2009)). (Final Act. 38--40.)
Claim 13 stands rejected under 35 U.S.C. § I03(a) as unpatentable
over Taylor, Ionasec, NIH, and Naghavi (US 2011/0270051 Al; Nov. 3,
2011). (Final Act. 40--43.)
Claim 14 stands rejected under 35 U.S.C. § I03(a) as unpatentable
over Taylor, Ionasec, NIH, and Algranati (D. Algranati et al., Mechanisms of
Myocardium-Coronary Vessel Interaction, 298 AM. J. PHYSIOLOGY-HEART
& CIRCULATORY PHYSIOLOGY, H86I-H873 (2010). (Final Act. 44--45.)
Claim 20 stands rejected under 35 U.S.C. § I03(a) as unpatentable
over Taylor, Ionasec, NIH, and Holzapfel (G. Holzapfel et al., A
Layer-Specific Three-Dimensional Model for the Simulation of Balloon
1 Accessed as an author manuscript from the National Institutes of Health.
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Angioplasty Using Magnetic Resonance Imaging and Mechanical Testing,
30 ANNALS OF BIOMEDICAL ENG'G. 753-767 (2002)). (Final Act. 45--48.)
ANALYSIS
§ 103 Rejection-Taylor, Ionasec, and NIH
We are persuaded by Appellants' arguments (App. Br. 7-8; see also
Reply Br. 5-7) that the combination of Taylor, Ionasec, and NIH would not
have rendered obvious independent claim 1, which includes the limitation "a
cellular model of endothelial cell function that simulates changes in a
mechanical property of a vascular wall due to a response of endothelial cells
to hemodynamic forces."
The Examiner found that the description of hypertension in NIH, the
description of arterial hemodynamic conditions in NIH, and the development
of multiscale models ( e.g., endothelial dysfunction) in NIH, collectively
correspond to the limitation "a cellular model of endothelial cell function
that simulates changes in a mechanical property of a vascular wall due to a
response of endothelial cells to hemodynamic forces." (Final Act. 19; see
also Ans. 8-10.) We do not agree with the Examiner's findings.
NIH relates to "highlighting[] some past successes of vascular
biomechanics, but emphasizes the need for research that synthesizes
complementary advances in molecular biology, biomechanics, medical
imaging, computational methods, and computing power for purposes of
increasing our understanding of vascular physiology and pathophysiology."
(Abstract.) With respect to pulmonary hypertension, NIH explains that
"[t]his form of the disease occurs primarily due to an increased
vasoconstriction followed by significant remodeling of the walls of medium-
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and small-diameter arteries." (§ 3.2, para. 3.) With respect to arterial
hemodynamic conditions, NIH explains that "[a]rteries retain a remarkable
ability to adapt to changing hemodynamic conditions throughout life" and
"[t]he best known examples are that arteries increase (or decrease) in caliber
in response to sustained increases ( or decreases) in blood flow induced wall
shear stresses and they increase ( or decrease) in thickness in response to
sustained increases (or decreases) in blood pressure." (§ 4.5, para. 1
(footnotes omitted).) Moreover, in the "Open Problems" section, NIH
explains that "there is a need to begin to develop multiscale models that
combine knowledge of molecular mechanisms with clinical manifestation,"
and "subclasses of such models [fluid-solid-growth models] are possible and
should be pursued for specific clinical problems based on dominate
underlying processes (e.g., endothelial dysfunction)." (§ 5.4.)
The Examiner cited to: (i) the description in NIH of pulmonary
hypertension, including vasoconstriction; (ii) the description in NIH of
arterial hemodynamic conditions; and (iii) multiscale models of NIH, which
combine molecular mechanisms with clinical manifestation, for example,
endothelial dysfunction. The Examiner, however, has provided insufficient
evidence to support a finding that NIH teaches the limitation "a cellular
model of endothelial cell function that simulates changes in a mechanical
property of a vascular wall due to a response of endothelial cells to
hemodynamic forces." In particular, the Examiner has not demonstrated that
the concepts of vasoconstriction, arterial hemodynamic conditions, and
endothelial dysfunction correspond to "a cellular model of endothelial cell
function that simulates changes in a mechanical property of a vascular wall
due to a response of endothelial cells to hemodynamic forces," as recited in
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claim 1. Moreover, NIH explains that "there is a need to begin to develop
multiscale models" relating to endothelial dysfunction, which is an
indication that such models were not yet developed at the time of NIH.
(§ 5.4; see also Abstract.) We are, therefore, persuaded by Appellants'
arguments that:
[S]ection 5 ofNIH_2009 describes open problems that have not
yet been solved, and section 5.4 describes that "advances in
molecular biology and systems biology promise to enable
modeling of underlying mechanobiology (i.e.,
mechanotransduction, ... " Accordingly, this section states that
such a model of underlying mechanobiology is an expected
advance in the future, but does not describe a cellular model of
endothelial function that can be coupled to a multi-scale model
of coronary circulation. . . . As described in section 3 .2 of
NIH_2009, pulmonary hypertension occurs primarily due to an
increased vasoconstriction followed by significant remodeling of
the walls of medium and small diameter arteries. However, there
is no description of any cellular model that simulates such
changes in a vascular wall due to a response of endothelial cells
to hemodynamic changes. Section 4.5 of NIH_2009 describes
vasoactive molecules that regulate vasodilation and
vasoconstriction, but again, there is no description of a cellular
model that simulates changes in a mechanical property of a
vascular wall due to a response of endothelial cells to
hemodynamic changes.
(App. Br. 8.)
Accordingly, we do not sustain the rejection of independent claim 1
under 35 U.S.C. § 103(a). Claims 2-5, 7-12, 15-19, 21, 22, and 41--43
depend from claim 1. We do not sustain the rejection of claims 2-5, 7-12,
15-19, 21, 22, and 41--43 under 35 U.S.C. § 103(a) for the same reasons
discussed with respect to claim 1.
Independent claims 23 and 32 recite limitations similar to those
discussed with respect to claim 1. We do not sustain the rejection of claims
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23 and 32, as well as its dependent claims 24, 25, 27-31, and 33--40, for the
same reasons discussed with respect to claim 1.
§ 103 Rejection-Taylor, Ionasec, NIH, and Passerini
Claims 6, 26, and 3 5 depend from independent claims 1, 23, and 3 2,
respectively. The Examiner cited Passerini for teaching the additional
features of claims 6, 26, and 35. (Final Act. 38--40.) However, the
Examiner's findings regarding Passerini do not cure the above noted
deficiencies of Taylor, Ionasec, and NIH.
§ 103 Rejection-Taylor, Ionasec, NIH, and Naghavi
Claim 13 depends from independent claim 1. The Examiner cited
Naghavi for teaching the additional features of claim 13. (Final Act. 41--43.)
However, the Examiner's findings regarding Naghavi do not cure the above
noted deficiencies of Taylor, Ionasec, and NIH.
§ 103 Rejection-Taylor, Ionasec, NIH, and Algranati
Claim 14 depends from independent claim 1. The Examiner cited
Algranati for teaching the additional features of claim 14. (Final Act. 44--
45.) However, the Examiner's findings regarding Algranati do not cure the
above noted deficiencies of Taylor, Ionasec, and NIH.
§ 103 Rejection-Taylor, Ionasec, NIH, and Holzapfel
Claim 20 depends from independent claim 1. Holzapfel was cited by
the Examiner for teaching the additional features of claim 20. (Final
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Act. 45--48.) However, the Examiner's findings regarding Holzapfel does
not cure the above noted deficiencies of Taylor, Ionasec, and NIH.
DECISION
The Examiner's decision rejecting claims 1--43 is reversed.
REVERSED
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