Anthony Yun et al.

Patent Trials and Appeals Board

Nov 2, 2020

12774616 - (D) (P.T.A.B. Nov. 2, 2020)

UNITED STATES PATENT AND TRADEMARK OFFICE
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
APPLICATION NO. FILING DATE FIRST NAMED INVENTOR ATTORNEY DOCKET NO. CONFIRMATION NO.
12/774,616 05/05/2010 Anthony Joonkyoo Yun PALO-001CIP2CON 8380
93726 7590 11/02/2020
EPA - BOZICEVIC FIELD & FRANCIS LLP
BOZICEVIC, FIELD & FRANCIS
201 REDWOOD SHORES PARKWAY
SUITE 200
REDWOOD CITY, CA 94065
EXAMINER
GETZOW, SCOTT M
ART UNIT PAPER NUMBER
3792
NOTIFICATION DATE DELIVERY MODE
11/02/2020 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):
docket@bozpat.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
________________

BEFORE THE PATENT TRIAL AND APPEAL BOARD
________________

Ex parte ANTHONY JOONKYOO YUN and
PATRICK YUARN-BOR LEE1
________________

Appeal 2020-002273
Application 12/774,616
Technology Center 3700
________________

Before JEFFREY N. FREDMAN, JOHN G. NEW, and DAVID COTTA,
Administrative Patent Judges.

NEW, Administrative Patent Judge.

DECISION ON APPEAL

1 We use the word “Appellant” to refer to “applicant” as defined in 37
C.F.R. § 1.42. Appellant identifies the real party in interest as Palo Alto
Investors. App. Br. 3.
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SUMMARY
Appellant files this appeal under 35 U.S.C. § 134(a) from the
Examiner’s Final Rejection of claims 142, 147–149, 154–156, 159–163, and
167–185. Specifically, claims 149, 154, 155, 160–163, 168, 170, 172, 176–
179, and 184 stand rejected as unpatentable under 35 U.S.C. § 103(a) as
being obvious over the combination of Branham et al. (US 2013/0023688
A1, January 24, 2013) (“Branham”) and either Kuo (US 2003/0097075 A1,
May 22, 2003) (“Kuo”) or Childre et al. (US 7,163,512 B1, January 16,
2007) (“Childre”).
Claims 149, 154, 155, 160–163, 168, 170, 172, 176–179, and 183 also
stand rejected as unpatentable under 35 U.S.C. § 103(a) as being obvious
over Watkins et al. (US 2002/0128171 A1, September 12, 2002)
(“Watkins”) and either Kuo and Childre.
Claims 149, 154, 155, 160–163, 168, 170, 172, 176–179, and 183 also
stand rejected as unpatentable under 35 U.S.C. § 103(a) as being obvious
over Rezai (US 2002/0116030 A1, August 22, 2002) (“Rezai”) and either
Kuo or Childre.
Claims 142, 147–149, 154–156, 159–163, and 167–185 stand rejected
as unpatentable under 35 U.S.C. § 103(a) as being obvious over Ivanova et
al. (US 2004/0048795 A1, March 11, 2004) (“Ivanova”) and either Kuo and
Childre.
Claims 142, 147, 148, 156, 159, 167, 169, 171, 173–175, 180, and 181
stand rejected as unpatentable under 35 U.S.C. § 103(a) as being obvious
over Cohen et al. (US 2008/0147137 A1, June 19, 2008) (“Cohen”) and
either Kuo and Childre.
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Claims 176–178 stand rejected under 35 U.S.C. § 103(a) as being
obvious over the combination of either Branham or Watkins or Rezai, and
either Kuo and Childre, and Shapland (US 5,042,497, August 27, 1991)
(“Shapland”).
Claims 173–178 stand rejected under 35 U.S.C. § 103(a) as being
obvious over the combination of Ivanova and either Kuo and Childre, and
Shapland.
Claims 173–175 stand rejected under 35 U.S.C. § 103(a) as being
obvious over the combination of Cohen, and either Kuo and Childre, and
Shapland.
We have jurisdiction under 35 U.S.C. § 6(b).
We AFFIRM-IN-PART.

NATURE OF THE CLAIMED INVENTION
Appellant’s invention is directed to a method for treating a subject for
a condition by modulating at least a portion of the subject’s autonomic
nervous system. Abstract.

REPRESENTATIVE CLAIM
Independent claims 142 and 149 are representative of the claims on
appeal. Claim 142 recites:
142. A method of treating a subject for a condition associated
with a systemic loss of parasympathetic function, the method
comprising:
measuring the subject’s parasympathetic/sympathetic
activity ratio to detect that the subject has the systemic loss of
parasympathetic function; and
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electrically modulating at least a portion of the
parasympathetic nervous system of the subject, based on the
subject’s detected systemic loss of parasympathetic function,
with an electrical energy application device to modulate the
parasympathetic activity/sympathetic activity ratio in a manner
effective to treat said subject for the condition, wherein the
condition is selected from the group consisting of: multi-system
atrophy, systemic inflammation, constipation, erectile
dysfunction, fluid retention, and Alzheimer’s

App. Br. 57. Claim 149 recites:
149. A method of treating a subject for a condition associated
with a systemic loss of parasympathetic function, the method
comprising:
measuring the subject’s parasympathetic/sympathetic
activity ratio to detect that the subject has the systemic loss of
parasympathetic function; and
administering a pharmacological agent to the subject,
based on the subject’s detected systemic loss of parasympathetic
function, sufficient to provide systemic pharmacological
modulation of said subject’s autonomic nervous system to
modulate the parasympathetic activity/sympathetic activity ratio
in a manner effective to treat said subject for the condition,
wherein the condition is selected from the group consisting of:
multi-system atrophy, systemic inflammation, constipation,
erectile dysfunction, fluid retention, and Alzheimer’s.
Id. at 157–158.

ISSUES AND ANALYSES
We agree with and adopt the Examiner’s reasoning, findings of fact,
and conclusions as to those claims on appeal that we find are obvious over
the combined cited prior art. We address the arguments raised by Appellant
below.
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A. Procedural Posture
Appellant’s claims 142, 147–149, 154–156, 159–163, and 167–172 of
this application were the subject of a prior appeal, 2016-007642, before this
panel. The panel affirmed the Examiner’s Final Rejection of all of the
claims on appeal on the grounds of obviousness, and reversed the
Examiner’s conclusion that the claims were directed to nonstatutory subject
matter. See Decision, filed September 13, 2007 at 28 (the “Prior Decision”).
The application was returned to prosecution and Appellant amended
independent claims 42 and 49 as follows:
142. A method of treating a subject for a condition associated
with a systemic loss of parasympathetic function, the method
comprising:
measuring the subject’s parasympathetic/sympathetic
activity ratio to detect that the subject has the systemic loss of
parasympathetic function; and
electrically modulating at least a portion of said subject’s
the parasympathetic nervous system of the subject, based on the
subject’s detected systemic loss of parasympathetic function,
with an electrical energy application device to modulate the
parasympathetic activity/sympathetic activity ratio in a manner
effective to treat said subject for the condition, wherein the
condition is selected from the group consisting of: multi-system
atrophy, systemic inflammation, constipation, erectile
dysfunction, fluid retention, and Alzheimer’s.
App. Br. 57 (italics represent added text, deleted text is struck through); see
also Prior Decision 5. Similarly, claim 49 was amended as follows:
149. A method of treating a subject for a condition associated
with a systemic loss of parasympathetic function, the method
comprising:
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measuring the subject’s parasympathetic/sympathetic
activity ratio to detect that the subject has the systemic loss of
parasympathetic function; and
administering a pharmacological agent to the said subject,
based on the subject’s detected systemic loss of parasympathetic
function, sufficient to provide systemic pharmacological
modulation of said subject’s autonomic nervous system to
modulate the parasympathetic activity/sympathetic activity ratio
in a manner effective to treat said subject for the condition,
wherein the condition is selected from the group consisting of:
multi-system atrophy, systemic inflammation, constipation,
erectile dysfunction, fluid retention, and Alzheimer’s.
App. Br. 57–58; see also Prior Decision 5–6. Appellant also added new
dependent claims 173–185. All of these claims are before us in the present
appeal.
Each of the claims in the prior appeal were rejected by the Examiner
as unpatentable under 35 U.S.C. § 103(a) as follows:
Claims Rejected Reference
149, 154, 155, 160–163, 168,
170, 172
Branham
149, 154, 155, 160–163, 168,
170, 172
Watkins
149, 154, 155, 160–163, 168, 170,
172
Rezai
142, 147-149, 154–156, 159-163,
167–172
Ivanova
142, 147, 148, 156, 159, 167,
169, 171
Cohen

Prior Decision 2, 28. The Examiner has now added Kuo and Childre to each
of these rejections as teaching or suggesting the amendments to the
respective claims, specifically, “measuring the subject’s parasympathetic/
sympathetic activity ratio to detect that the subject has the systemic loss of
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parasympathetic function” and basing the subsequent treatment on the
measurements. See, e.g., Non-Final Act. 2–3 (filed November 9, 2018).2
We incorporate herein by reference the findings and conclusions of
our Prior Decision that the pre-amendment claims are obvious over the
respective cited prior art. See, generally, Prior Decision. We are then left
with the task of determining: (1) whether Kuo or Childre teaches or suggests
the new limitations introduced in amended independent claims 142 and 149,
viz., “measuring the subject’s parasympathetic/sympathetic activity ratio to
detect that the subject has the systemic loss of parasympathetic function”
and using that measurement in the subsequent treatment of the patient; and
(2) whether it would have been obvious to a person of ordinary skill in the
art to combine the references. We consider the newly-added dependent
claims 173–185 separately.

B. Claims 142, 147–149, 154–156, 159–163, and 167–172 (Appellant’s
Groups I and II): Obviousness of the added limitations over Kuo and
Childre

Issue 1
Appellant argues that the Examiner erred in finding that the cited prior
art teaches or suggests the limitation reciting “measuring the
parasympathetic/sympathetic activity ratio in a subject with a recited

2 We cite generally herein to the Examiner’s Non-Final Office Action of
November 9, 2018 with respect to the Examiner’s findings of fact and
conclusions of law, because the subsequent Final Office Action (filed April
8, 2019) generally refers back to, and incorporates, the findings and
conclusions of the Non-Final Action. See, e.g., Final Act. 3–7.
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condition to detect that the subject has the systemic loss of parasympathetic
function and modulating based on the detected loss of parasympathetic
function.” App. Br. 5–6.

Analysis
The Examiner refers to our Prior Decision as finding that the various
conditions listed in the independent claims “are known to be mediated by the
activity of the sympathetic or parasympathetic system neurons” and
therefore finds that a skilled artisan would consider evaluating the
autonomic nervous system (“ANS”)3 to best treat the relevant conditions.
Non-Final Act. 2. The Examiner finds that Kuo teaches that many
conditions are influenced by the ANS, and that analyzing heart rate
variability (“HRV”), including the high frequency spectral component
(“HF”) and low frequency spectral component (“LF”), as well as the LF:HF
ratio, gives an indication of parasympathetic/sympathetic balance. Id.
(citing, e.g., Kuo ¶¶ 4–11, 29, 30). The Examiner concludes that it would
have been obvious to a person of ordinary skill in the art that measuring the
systemic loss of parasympathetic function by this method could reveal the
underlying cause of the conditions recited in independent claims 142 and
149, because the ANS is considered to control the end organs and systems
that are known in the art to influence those conditions. Id. at 2–3.

3 The autonomic nervous system is collectively composed of the
preganglionic and postganglionic nerves of the sympathetic and
parasympathetic nervous systems. See L.H. Hyman, COMPARATIVE
VERTEBRATE ANATOMY (19th ed.) 428 (1962).
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The Examiner similarly finds that Childre teaches that by applying
“spectral analysis techniques to the HRV waveform, its different frequency
components, which represent the activity of the sympathetic or
parasympathetic branches of the autonomic nervous system, can be
discerned.” Non-Final Act. 3 (citing Childre col. 3, ll. 3–6; col. 5, ll. 46–55,
col. 9, ll. 1–66; col. 2, ll. 1–65). The Examiner concludes that a person of
ordinary skill in the art would have found it obvious to use the techniques
taught by Childre to measure the parasympathetic/sympathetic ratio to reveal
the underlying cause of the conditions recited in independent claims 142 and
149, because the ANS is known in the art to control the end organs and
systems that influence those conditions. Id.
Appellant points out that the sole references (e.g., Ivanova, Rezai,
etc.), cited in our Prior Decision with respect to the claims prior to their
amendment, do not teach or suggest the disputed limitation, which was
added to the claims subsequent to our Prior Decision. See, e.g., App. Br. 6.
Appellant also argues that Kuo and Childre are silent with respect to the
conditions recited in claim 142 or 149, and therefore fail to remedy the
alleged deficiency of the sole references cited in our Prior Decision. Id.
Appellant contends that, because Ivanova does not teach or suggest the
newly-added limitation, and because Kuo and Childre are silent with respect
to subjects having the listed conditions, the combined references fail to teach
or suggest measuring the parasympathetic/sympathetic activity ratio of a
subject with any of the listed conditions to detect a systemic loss of
parasympathetic function in the subject. Id.
Appellant also argues that, even if, arguendo, Kuo or Childre teach
that certain “manner[s] of checking the parasympathetic nervous system” are
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well-known in the art, that does not teach or suggest measuring the
parasympathetic/sympathetic activity ratio of a subject with any of the
conditions listed in the claim, let alone detecting a systemic loss of
parasympathetic function in such a subject and modulating treatment based
thereon. App. Br. 7.
We are not persuaded by Appellant’s argument. Kuo teaches that:
Investigators have discovered that, based on frequency analysis,
HRV can be characterized into two main components: the high
frequency (HF) component and the low frequency (LF)
component…. Currently, researchers agree that the high
frequency (HF) or total power (TP) represents the
parasymapthetic control of the heart rate, whereas the ratio
LF/HF is considered to mirror the sympathovagal balance or to
reflect the sympathetic modulations. Besides being indicative of
the function of the autonomic nervous system, HRV has been
documented to reflect other pathological conditions.

Kuo ¶ 9 (internal citations omitted). Kuo further teaches that:
The power spectrum [of the HRV waveform] is subsequently
quantified by means of integration into standard frequency-
domain parameters including low-frequency (LF 0.04-0.15 Hz)
and high-frequency (HF 0.15-0.40 Hz), total power (TP) and
ratio of low frequency to high frequency (LF/HF) (step 120).
The analyzed results, which include the various ANS indices, the
frequency spectrums and recommendations, can be sent back to
the Client (step 122) through the Network. The user is thereby
immediately brought to the attention of his/her health condition.
In the case of impairments in the sympathetic and/or
parasympathetic functions, whether they are too high or too low,
the Server can also design to automatically notify a physician or
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other medical professions to provide a prompt assistance to the
user.

Id. ¶¶ 29–30 (emphasis added). Kuo thus teaches determining the relative
balance of sympathetic and parasympathetic nervous activity, i.e.,
“measuring the parasympathetic/sympathetic activity ratio of a subject,” and
then, “based on the subject’s detected systemic loss of parasympathetic
function,” administering the appropriate treatment.
Similarly, Childre teaches that:
The analysis of HRV can provide important information relative
to the function and balance of the autonomic nervous system, as
it can distinguish sympathetic from parasympathetic regulation
of heart rate.
Frequency domain analysis decomposes the heart rate
tachogram or waveform into its individual frequency
components and quantifies them in terms of their relative
intensity, in terms of power spectral density (PSD). By applying
spectral analysis techniques to the HRV waveform, its different
frequency components, which represent the activity of the
sympathetic or parasympathetic branches of the autonomic
nervous system, can be discerned. The HRV power spectrum is
divided into three frequency ranges or bands: very low frequency
(VLF), 0.033 to 0.04 Hz; low frequency (LF), 0.04 to 0.15 Hz;
and high frequency (HF), 0.15 to 0.4 Hz.

Childre cols, 2–3, ll. 60–10 (emphasis added). Childre thus teaches that it is
possible to “measure[e] the parasympathetic/sympathetic activity ratio of a
subject, as recited in the claim.”
We agree with Appellant that neither Kuo nor Childre teach the
various conditions recited in claims 142 and 149, i.e., multi-system atrophy,
systemic inflammation, constipation, erectile dysfunction, fluid retention,
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and Alzheimer’s. However, as we explained in our Prior Decision, a person
of ordinary skill in the art would understand that the various references cited
therein teach the claimed methods of treatment of those conditions. See
Prior Decision 14–17, 23–25.
Furthermore,
The test for obviousness is not whether the features of a
secondary reference may be bodily incorporated into the
structure of the primary reference; nor is it that the claimed
invention must be expressly suggested in any one or all of the
references. Rather, the test is what the combined teachings of the
references would have suggested to those of ordinary skill in the
art.
In re Keller, 642 F.2d 413, 425 (C.C.P.A. 1981). In the appeal before us, we
find that Kuo and/or Childre teach the newly added limitations of the
amended claims, and we incorporate by reference the reasoning of our Prior
Decision that the cited references teach the remaining limitations of those
claims. We consequently conclude that the combined cited references teach
all of the limitations of the amended claims on appeal.

Issue 2
Appellant next argues that the Examiner erred because there is no
reason or guidance in the cited art as to why one ordinarily skilled in the art
would modify any method of the references cited with respect to the pre-
amendment claims. App. Br. 9.

Analysis
Appellant contends that the combined cited prior art references do not
demonstrate a sufficient reason why one of ordinary skill in the art would
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start with the teachings of the prior art cited with respect to the pre-
amendment claims and modify those teachings according to Childre or Kuo
to arrive at the methods recited in the claims on appeal. App. Br. 9.
According to Appellant, because the references neither teach nor suggest the
new limitation, the cited prior art fails to demonstrate that an ordinarily
skilled artisan would have had a reason or been guided to measure the
parasympathetic/sympathetic activity ratio in subjects with the listed
conditions to attempt to detect a systemic loss of parasympathetic function,
let alone proceed to modulate at least a portion of such a subject’s
parasympathetic nervous system based on the detected systemic loss of
parasympathetic function. Id. at 9–10. Appellant asserts that there is no
nexus between the treatment methods of prior art and the evaluation methods
of Childre and Kuo, such that an ordinarily skilled artisan would have had a
reason or guidance to perform the modification. Id. at 10.
Appellant points to the Prior Decision’s reasoning that it was well
known in the art that:
[T]he use of pharmaceutical compounds to treat conditions,
including constipation, inflammation, and erectile dysfunction,
known to be mediated by the activity of the sympathetic or
parasympathetic systems of the ANS and by increasing and or
decreasing the activity of sympathetic or parasympathetic
neurons and thus, inherently, altering the sympathetic/
parasympathetic activity ratio.

App. Br. 10 (quoting Prior Decision 16–17). Appellant argues that, even if
that statement by the Board is adopted, it does not show that any of the
conditions listed were known to be caused at least in some cases by an
underlying systemic loss of parasympathetic activity or that a subject having
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such a condition could be treated using a method that includes measuring the
parasympathetic/sympathetic activity ratio to detect a systemic loss of
parasympathetic activity and modulating a subject’s ANS based on the
detected loss. Id.
We are not persuaded by Appellant’s arguments. As an initial matter,
it is not required that a reference directly teach or suggest the combination of
references proposed by the Examiner. Rather, “the test is what the
combined teachings of the references would have suggested to those of
ordinary skill in the art.” Keller, 642 F.2d at 425. In this instance, our Prior
Decision determined that the claimed methods of “modulat[ing] the
parasympathetic activity/sympathetic activity ratio in a manner effective to
treat said subject for the condition, wherein the condition is selected from
the group consisting of: multi-system atrophy, age related inflammation,
systemic inflammation, constipation, insomnia, erectile dysfunction, fluid
retention, type-2 diabetes and Alzheimer’s” were obvious over the cited
prior art. See Prior Decision 11–19, 22–25.
Because we found that the prior art teaches that the recited conditions
are “known to be mediated by the activity of the sympathetic or
parasympathetic systems of the ANS,” we agree with the Examiner’s
conclusion that a person of ordinary skill in the art would have found it
obvious to combine methods of measuring the relative balance sympathetic
and parasympathetic neural activity, as taught by Kuo and Childre, as a
preliminary diagnostic step, with the subsequent methods of treatment of the
recited conditions, as taught by the references cited in our Prior Decision.
See Ans. 7. Furthermore, we conclude that a person of ordinary skill would
have been motivated to combine the references because an accurate
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diagnosis of sympathetic/parasympathetic imbalance would be beneficial in
prescribing an appropriate treatment for the recited conditions caused by
such an imbalance. “A person of ordinary skill is also a person of ordinary
creativity, not an automaton.” KSR, 550 US at 421. We consequently affirm
the Examiner’s rejection of claims 142, 147–149, 154–156, 159–163, and
167–172.

C. Claims 174 and 177 (Appellant’s Group III)
Issue
Dependent claim 174 is representative and recites: “The method
according to claim 173, wherein the one or more indicators comprises heart
rate variability and the measuring comprises measuring low HRV frequency
peak (LF), high HRV frequency peak (HF), the HRV LF/HF ratio or a
combination thereof. App. Br. 60. Appellant argues that neither Ivanova,
Kuo, nor Childre teach or suggest measuring the parasympathetic/
sympathetic activity ratio of a subject with any of the listed conditions to
detect a systemic loss of parasympathetic function in the subject. App. Br.
13. Therefore, argues Appellant, the references also fail to teach the
additional limitations of claims 174 and 177. Id.

Analysis
Appellant contends that, because Kuo, Childre, and the prior
references cited in our Prior Decision do not teach or suggest measuring the
parasympathetic/sympathetic activity ratio of a subject with any of the
recited conditions, the references also do not suggest measuring that
employs heart rate variability, including measuring low HRV LF, high HRV
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HF, the HRV LF/HF ratio or a combination thereof, to determine the
parasympathetic/sympathetic activity ratio and detect a systemic loss of
parasympathetic function in the subject having any of the listed conditions.
App. Br. 13. Appellant contends that even if, arguendo, a skilled artisan
would be expected to “determine if the nerves which control the action of
the colon are malfunctioning” in a subject with intractable constipation, none
of the cited art teach or suggest that this action would necessarily involve the
measuring set forth in the claims of Group Ill. Id. at 14.
Appellant points to the Examiner’s finding that “[T]o measure the
systemic loss of parasympathetic function is considered to be obvious in that
it would reveal an underlying cause tor the ailment since the ANS is
considered to control the end organs and systems that are implicated in the
various ailments listed in the independent claims.” App. Br. 15 (quoting
Adv. Act. 5, filed June 28, 2019). Appellant contends that this reasoning is
clearly an application of impermissible hindsight, because it cannot be said
that an unknown result of performing an action renders performing the
action obvious. Id. Appellant argues that, although the Examiner bases the
obviousness of performing the measurement on the premise that it “reveal an
underlying cause tor the ailment,” the Examiner has not established, or
provided any evidence to support, that the underlying cause for the
conditions listed of systemic loss of parasympathetic function was known
before the relevant priority date. Id. Therefore, argues Appellant, it cannot
be said that it would have been obvious to a skilled artisan to perform the
recited measuring in the recited subjects to detect a systemic loss of
parasympathetic function and modulate based on the detected loss. Id.
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We are not persuaded. As we explained in our Prior Decision, it was
well known in the prior art that art that an underlying cause of the recited
conditions was an imbalance in sympathetic/parasympathetic function. See,
e.g., Prior Decision 23–25. Kuo and Childre explicitly teach a method of
determining sympathetic/parasympathetic balance by measuring “low HRV
frequency peak (LF), high HRV frequency peak (HF), the HRV LF/HF ratio
or a combination thereof,” as recited in claim 174. See Kuo ¶ 29; Childre
col. 8, ll. 24–36. In other words, both Kuo and Childre expressly teach
employing the methods claimed in claims 174 and 177 for “rapid diagnosis”
(Kuo ¶ 30). We consequently affirm the Examiner’s rejection of these
claims.

D. Claim 180 (Appellant’s Group IV): Obviousness over Ivanova or
Cohen, and Kuo or Childre

Issue
Claim 180 recites: “The method according to Claim 142, wherein the
condition is multi-system atrophy.” App. Br. 61. Appellant contends that
the combined cited prior art neither teaches nor suggests that the condition to
be treated is multi-system atrophy (MSA). Id. at 15, 51.

Analysis
Appellant points to the Examiner’s finding, that paragraph [0055] of
Ivanova teaches “use for tissue and organ necrosis, multiple sclerosis,
paralysis, each of which is considered to result in multisystem atrophy.”
App. Br. 16 (quoting Final Act. 3). Appellant contends that none of these
conditions cited by the Examiner constitutes multi-system atrophy, and that
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the Examiner’s interpretation is inconsistent with how the term would be
understood by a skilled artisan. Id. In support of this contention, Appellant
points to National Institutes of Health, What is multiple system atrophy?
available at: www.ninds.nih.gov/Disorders/Patient-Caregiver-
Education/Fact-Sheets/MultipleSystem-Atrophy (of record) (“NIH”).
Appellant contends that NIH teaches that multi-system atrophy (MSA) is a
distinct disorder, specifically: “a progressive neurodegenerative disorder
characterized by a combination of symptoms that affect both the autonomic
nervous system ... and movement.” Id.
Appellant therefore contends that regardless of whether Ivanova
describes “tissue and organ necrosis, multiple sclerosis, [and] paralysis” as
alleged, this does not represent a teaching or suggestion of multi-symptom
atrophy, let alone practicing the instantly claimed method in a subject with
multi-system atrophy. App. Br. 16–17. Therefore, argues Appellant, in
view of how the term would be commonly understood, Ivanova does not
teach or suggest performing the instantly claimed method with a subject
having multi-system atrophy. Id. at 17.
The Examiner responds that he considers the term “multi-system
atrophy” to be broader than is reflected in the definition supplied by
Appellant. Adv. Act. 6. Nevertheless, the Examiner finds that, as
Appellant’s definition suggests, a physician of ordinary skill would, in order
to rule out a diagnosis of multi-system atrophy, determine whether the ANS
was properly balanced and functioning normally, so as to rule out multi-
system atrophy. Id. at 6–7.
We are not persuaded by the Examiner’s reasoning. The Examiner
adduces no evidence to support his reasoning that a skilled artisan would
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understand the definition of multi-system atrophy to exceed the definition
provided by NIH. See also Multiple System Atrophy Fact Sheet, available
at: https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Fact-
Sheets/Multiple-System-Atrophy (last visited October 16, 2020) for the
current version of NIH.
We agree with Appellant that Ivanova is silent with respect to multi-
system atrophy. Absent citation by the Examiner of a prior art reference
showing that multi-system atrophy was known at the time of invention to be
a result of sympathetic/parasympathetic system dysfunction, we cannot
sustain the Examiner’s rejection of claim 180 over Ivanova, Kuo and
Childre.
With respect to Cohen, Appellant disputes the Examiner’s reasoning
that “[i]f the disease of anorexia is treated, then the symptom of atrophy is
treated as well.” App. Br. 51 (quoting Adv. Act. 9). Appellant argues that
the interpretation of multi-system atrophy as being merely a symptom of
anorexia is in consistent with the commonly understood definition of multi-
system atrophy, as taught by NIH. Id.
Again, we agree with Appellant. The Examiner adduces no prior art
evidence that a person of ordinary skill in the art would understand that
anorexia, as taught by Cohen, is a form of multi-system atrophy. More
importantly, and as we explained with respect to the rejection over Ivanova,
the Examiner has provided no evidence of record that a skilled artisan would
understand that multi-system atrophy was known at the time of invention to
be a result of sympathetic/parasympathetic system dysfunction. Absent any
such evidence, we do not sustain the Examiner’s rejection of claim 180 over
Ivanova, Kuo, and Childre.
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E. Claim 181 (Appellant’s Group V): Obviousness over Ivanova or
Cohen, and Kuo or Childre

Issue
Claim 181 recites: “The method according to Claim 142, wherein the
condition is fluid retention.” App. Br. 61. Appellant contends that the
Examiner erred because the combined cited prior art neither teaches nor
suggests the condition of fluid retention. Id. at 18, 52.

Analysis
With respect to the rejection over Ivanova, and Kuo or Childre,
Appellant notes the Examiner’s finding that “¶ 6 of Ivanova teaches
congestive heart failure, which causes fluid retention and ¶ 8 teaches
pulmonary edema.” App. Br. 18 (quoting Final Act. 3). However, argues
Appellant, paragraph [0006] of Ivanova is specifically related to “[d]isorders
where inflammatory cytokine cascades are involved at least in part” and the
mention of “pulmonary edema” in paragraph [0008] of Ivanova is
specifically related to “various cardiac disorders” in which “TNF has been
implicated.” Id.
Appellant therefore contends that these passages of Ivanova do not
represent a teaching or suggestion of measuring the parasympathetic/
sympathetic activity ratio of a subject with fluid retention to detect that the
subject has a systemic loss of parasympathetic function. App. Br. 18. Nor,
according to Appellant, do the above cited paragraphs demonstrate that it
would have been obvious to a skilled artisan to perform such measuring in a
subject with fluid retention to detect a systemic loss of parasympathetic
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function and electrically modulate at least a portion of the parasympathetic
nervous system to treat said subject for fluid retention. Id. at 18–19.
We are not persuaded. Appellant’s Specification provides no
definition of the claim term “fluid retention.” We consequently adopt the
broadest reasonable definition of the claim term consistent with the
disclosures of the Specification. See Phillips v. AWH Corp., 415 F.3d 1303,
1316 (Fed. Cir. 2005). “Pulmonary edema,” which may be defined as a
condition caused by excess fluid in the lungs4, may reasonably be construed
as a form of “fluid retention”; a point that is not contested by Appellant.
Ivanova teaches:
Tumor necrosis factor [TNF] is known to be a major pro-
inflammatory cytokine mediator of various acute and chronic
inflammatory diseases, e.g., gram negative bacterial sepsis,
multi-system organ failure (MSOF), circulatory collapse and
death. The primary source of circulating TNF following a septic
challenge is the liver.….
….

TNF has been implicated in various cardiac disorders including
cardiac failure secondary to septic cardiomyopathy, bi-
ventricular dysfunction, and pulmonary edema.

Ivanova ¶¶ 7–8 (emphasis added). Ivanova further teaches that:
“Vertebrates respond to inflammation caused by inflammatory cytokine
cascades in part through humoral mechanisms of the central nervous system
(activation of the hypothalamus-pituitary adrenal [HPA] axis), by means of

4 See Mayo Clinic, Pulmonary edema, available at:
https://www.mayoclinic.org/diseases-conditions/pulmonary-
edema/symptoms-causes/syc-20377009 (last visited October 19, 2020).
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vagal nerve activation, and by means of peripheral anti-inflammatory
cytokine production (e.g., IL-10 production).” Id. at ¶ 9.
Ivanova further teaches that:
In one set of responses, afferent vagus nerve fibers are activated
by endotoxin or cytokines, stimulating the release of humoral
anti-inflammatory responses through glucocorticoid hormone
release. Cytokines or endotoxin can stimulate the afferent vagus
nerve, which in turn signals a number of critical brain nuclei, and
leads to activation of the HPA anti-inflammatory responses and
down-regulation of endotoxemia and cytokinemia. Similarly,
direct efferent vagus nerve stimulation (VNS) in rats prevents
shock secondary to an induced endotoxic challenge, by
decreasing TNF synthesis in the liver.

Ivanova ¶ 11 (internal citations omitted, emphasis added). In other words,
activation of a major portion of the parasympathetic system (i.e., the vagus
nerve), may inhibit TNF synthesis that contributes to pulmonary edema.
Conversely, we conclude, a person of ordinary skill in the art would have
understood that dysfunction (i.e., decreased activity) of the vagus nerve
would reduce the effectiveness of the parasympathetic system in decreasing
TNF synthesis in the liver, effectively increasing the likelihood of
pulmonary edema.
We therefore conclude that Ivanova teaches the limitation of claim
181.
With respect to the teachings of Cohen, Appellant points to the
Examiner’s finding that “Cohen teaches treating ... CHF [congestive heart
failure] which has as a symptom fluid retention … if the disease of CHF is
treated, the symptom of fluid retention is also treated.” App. Br. 52 (quoting
Adv. Act. 9). Appellant contends that Cohen’s teaching of treating CHF
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necessarily teaches treating fluid retention, and asserts that Cohen is silent as
to fluid retention, let alone treating fluid retention. Id.
We are not persuaded by the Examiner’s reasoning. The Examiner
adduces no evidence of record to support the finding that fluid retention is a
symptom of CHF, nor can we discern any such teaching in the cited prior
art. Absent any such teaching, we cannot sustain the Examiner’s rejection of
claim 181 over Cohen, Kuo, and Childre. However, because we sustain the
Examiner’s rejection over Ivanova, Kuo, and Childre for the reasons we
have explained, we affirm the Examiner’s rejection of claim 181 on that
ground.

F. Claim 182 (Appellant’s Group VI): Obviousness over Ivanova and
Kuo or Childre

Issue
Claim 182 recites: “The method according to Claim 142, wherein the
condition is Alzheimer’s [disease].” App. Br. 62. Appellant argues that the
Examiner erred because the cited art does not teach or suggest the limitation
in which the condition is Alzheimer’s disease. Id. at 20.

Analysis
Appellant argues that that paragraph [0055] of Ivanova, upon which
the Examiner relies, is specifically directed to “diseases characterized by the
presence of deleterious physiological conditions at least partially mediated
by pro-inflammatory cytokine release.” Id. at 20–21. Appellant contends
that the teachings of Ivanova do not teach measuring the parasympathetic/
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sympathetic activity ratio of a subject with Alzheimer’s to detect that the
subject has a systemic loss of parasympathetic function. Id. at 21.
Appellant further disputes the Examiner’s finding that: “[s]ince
inflammation is implicated in causing Alzheimer’s […], and that inhibition
of inflammation is ‘vagus nerve dependent,’ it would be prudent to check the
vagus nerve to see if it were functioning properly in the Alzheimer’s
patient.” App. Br. 21 (quoting Adv. Act. 7 (citing Ivanova ¶¶ 51, 52, 55)).
Appellant argues that this teaching is not found in the reference as cited.
According to Appellant, paragraph [0055] of Ivanova teaches diseases that
are “at least partially mediated by pro-inflammatory cytokine release,” and
paragraph [0051] teaches that “inhibition of proinflammatory cytokine
release and the reduction of peripheral inflammation is vagus nerve-
dependent and can also be reduced by direct stimulation of the vagus nerve
in the brain.” Id. Appellant therefore argues that, even if the cited
paragraphs describe that the vagus nerve can be stimulated to reduce
inflammation, such does not represent a teaching of a systemic loss of
parasympathetic activity in Alzheimer’s subjects. Id.
We disagree. Ivanova teaches that it was well known in the art that
Inflammatory cytokine cascades contribute to deleterious
characteristics of numerous disorders. These deleterious
characteristics include inflammation and apoptosis. Disorders
where inflammatory cytokine cascades are involved at least in
part, include, without limitation, … diseases involving the
central or peripheral nervous system and associated tissues (such
as Alzheimer’s disease, meningitis, encephalitis, multiple
sclerosis, cerebral infarction, cerebral embolism, Guillame-Barre
syndrome, neuritis, neuralgia, spinal cord injury, paralysis, and
uveitis)….

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Ivanova ¶ 6 (emphasis added); see also id. ¶ 55. Furthermore, Ivanova also
teaches that:
These methods [e.g., directly stimulating a vagus nerve pathway
in the brain of the vertebrate5] are useful for preventing the
release of pro-inflammatory cytokines in any vertebrate. In
preferred embodiments, the vertebrate is a mammal. In
particularly preferred embodiments, the vertebrate is a human.
The vertebrate is preferably a patient suffering from, or at risk
for, a condition mediated by an inflammatory cytokine cascade.
As used herein, a patient can be any vertebrate individual from a
species that has a vagus nerve. Preferably, the condition is …
Alzheimer’s disease….
Ivanova ¶ 60. Ivanova thus teaches that vagal stimulation is useful in
preventing release of pro-inflammatory cytokines that may be a cause of,
inter alia, Alzheimer’s disease. As we have explained supra, a person of
ordinary skill in the art would therefore have understood that
parasympathetic system (e.g., vagus nerve) dysfunction, would exert a
disinhibiting effect on the release of pro-inflammatory cytokines, and a
concurrent promotion of inflammation related to Alzheimer’s. We therefore
conclude that Ivanova teaches the disputed limitation of claim 182, and we
affirm the Examiner’s rejection of that claim.

G. Claim 183 (Appellant’s Group VII): Obviousness over Ivanova,
Watkins, or Rezai, and Kuo or Childre

Issue
Claim 183 recites: “The method according to Claim 149, wherein the
condition is multi-system atrophy.” App. Br. 62. Appellant argues that the

5 See Ivanova Abstr.
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Examiner erred because the cited art does not teach or suggest the limitation
in which the condition is multi-system atrophy. Id. at 20.
Analysis
We have explained supra why we conclude that Ivanova neither
teaches nor suggests the claim term “multi-system atrophy,” and we
incorporate by reference that reasoning with respect to claim 183.
With respect to the teachings of Watkins, Appellant disputes the
Examiner’s determination that, in its broadest reasonable interpretation “the
term ‘multisystem atrophy’ is considered to be consistent with anorexia-
nervosa since anorexia nervosa results in multi-system atrophy.” App. Br.
40 (quoting Adv. Act. 8).
We do not find such tautological reasoning by the Examiner
persuasive, particularly in view of the fact that the Examiner adduces no
evidence in support of the conclusion that anorexia causes multi-system
atrophy. Nor is the Examiner’s interpretation consistent with our adopted
interpretation of the claim term “multi-system atrophy” supra. Absent any
persuasive evidence that there is a link between anorexia nervosa and multi-
system atrophy, we do not sustain the Examiner’s rejection.
With respect to the teachings of Rezai, Appellant points to the
Examiner’s finding that Rezai teaches “atrophy can be treated at least
indirectly by stimulating the ANS.” App. Br. 45 (quoting Adv. Act. 9
(citing Rezai ¶ 50)). Appellant contends that Rezai refers to “atrophy” in
paragraph [0050] only in the context of the symptoms of “[a] syndrome of
total body pain due to CRPS [complex regional pain syndrome].” Id.
(quoting Rezai ¶ 50). Specifically, Appellant argues, Rezai refers to “skin
changes such as atrophy, dryness, and scaling.” Id. Appellant asserts that
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the atrophy referred to in Rezai could not be reasonably understood by a
skilled artisan to refer to multi-system atrophy as recited in the claims. Id.
We agree with Appellant’s reasoning. The paragraph of Rezai relied
upon by the Examiner teaches, in relevant part:
Complex regional pain syndrome (CRPS) type I, commonly
known as reflex sympathetic dystrophy syndrome, or RSDS, was
described 25 years ago.…

Spontaneous pain develops in the territory of the affected nerve
that may then spread beyond that region. Vasomotor
abnormalities and focal edema may occur alone or in
combination in both CRPS types I and II. These are a severely
disabling group of illness with simultaneous involvement of
nerve, skin, muscle, blood vessels, and bones. While there are
many symptoms associated with CRPS, the only common
denominator is pain. The pain usually appears in one or more
extremities, and is described as chronic, burning and constant in
nature. A syndrome of total body pain due to CRPS has been
described as well. The remainder of symptoms may or may not
occur. These symptoms include swelling, limited motor function
which may lead to atrophy or dystrophy, tremor focal dystonia
or spasm, skin changes such as atrophy, dryness, and scaling, as
well as bony changes with joint tenderness and swelling.

Rezai ¶ 50 (emphasis added). We are not persuaded by the Examiner’s
reasoning that Rezai’s teaching of atrophy of motor function, as a possible
symptom of CRPS, corresponds to multi-system atrophy, which we have
defined supra as “a progressive neurodegenerative disorder characterized by
a combination of symptoms that affect both the autonomic nervous system ...
and movement.” NIH. Simply put, the Examiner has not provided us with
any evidence of record of a nexus between CRPS and multi-system atrophy,
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as thus defined. Absent any such evidence, we do not sustain the
Examiner’s rejection of claim 183.

H. Claim 184 (Appellant’s Group VIII): Obviousness over Ivanova or
Branham, and Kuo or Childre

Issue
Claim 184 recites: “The method according to Claim 149, wherein the
condition is fluid retention.” App. Br. 62. Appellant argues that the
Examiner erred because the cited art does not teach or suggest the limitation
in which the condition is fluid retention. Id. at 23, 33–34.

Analysis
With respect to the teachings of Ivanova, we have explained supra
why we find that the reference teaches the disputed limitation. We therefore
sustain the Examiner’s rejection upon this ground.
With respect to the teachings of Branham, Appellant points to the
Examiner’s finding that “¶ 198 of Branham … teaches use as a diuretic.”
App. Br. 34 (quoting Final Act. 4). Appellants argues that paragraph [0198]
of Branham lists “examples of therapeutic agents” and, as such, does not
teach or suggest treating a subject with fluid retention, let alone specifically
measuring the parasympathetic/sympathetic activity ratio to detect a
systemic loss of parasympathetic function in a subject with fluid retention.
Id.
We are not persuaded. In our Prior Decision, we found that Branham
teaches:
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“[A]dministering a pharmacological agent to said subject
sufficient to provide systemic pharmacological modulation of
said subject’s autonomic nervous system to modulate the
parasympathetic activity/sympathetic activity ratio.” For
example, Branham teaches, inter alia, the use of
“parasympathomimetics, cholinergic agonist
parasympathomimetics, cholinesterase inhibitor
parasympathomimetics, sympatholytics, a-blocker
sympatholytics, ß-blocker sympatholytics, sympathomimetics,
and adrenergic agonist sympathomimetics" as therapeutic
agents, all of which are well-known in the art to target and
influence the activity of the sympathetic or parasympathetic
subsystems of the autonomic nervous systems, which include the
recited conditions.

Prior Decision 14 (citing Branham ¶ 200). Branham further teaches that
such active agents can include diuretics, which are well known in the art for
the treatment of fluid retention by removing water from the body. Branham
¶ 198 (see Mayo Clinic, Diuretics, available at: https://www.mayoclinic.org/
diseases-conditions/high-blood-pressure/in-depth/diuretics/art-20048129
(last visited October 19, 2020). We have explained supra why we find that
Kuo or Childre teach measuring the parasympathetic/sympathetic activity
ratio to detect a systemic loss of parasympathetic function. We
consequently affirm the Examiner’s rejection of claim 184.

J. Claim 185 (Appellant’s Group IX): Obviousness over Ivanova and
Kuo or Childre

Issue
Claim 185 recites: “The method according to Claim 149, wherein the
condition is Alzheimer’s [disease].” App. Br. 62. Appellant argues that the
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Examiner erred in finding that Ivanova teaches the limitation in which the
condition is Alzheimer’s disease. App. Br. 24.

Analysis
Appellant repeats the argument that the Examiner has not established
that the cited art teaches or suggests measuring the parasympathetic/
sympathetic activity ratio of a subject with Alzheimer’s to detect that the
subject has a systemic loss of parasympathetic function. App. Br. 24.
We are not persuaded. As we have explained supra, both Kuo and
Childre teach measuring systemic loss of parasympathetic function. We
have also explained why we find that Ivanova teaches the treatment of a loss
of systemic parasympathetic function with Alzheimer’s disease, and why a
person of ordinary skill in the art would have found it obvious to combine
the teachings of Ivanova with those of Kuo or Childre. We consequently
affirm the Examiner’s rejection of claim 185.

J. Claim 176–178: Obviousness over Branham or Watkins, and Kuo or
Childre, and Shapland

Issue
Claim 176 recites:
The method according to Claim 149, wherein measuring the
subject’s parasympathetic/sympathetic activity ratio comprises
measuring one or more indicators of the autonomic nervous
system selected from the group consisting of: amount of T
helper cells, nerve conduction, catecholamine levels, heart rate
variability, action potentials, QT interval, chronotropic
response, inotropic response, vasodilator response, plasma
volume, effective renal plasma volume, effective renal blood
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flow, norepinephrine, and concentrations of rennin-angiotensin-
aldosterone system hormone.

App. Br. 60–61.
Claim 177 recites: “The method according to Claim 176, wherein the
one or more indicators comprises heart rate variability and the measuring
comprises measuring low HRV frequency peak (LF), high HRV frequency
peak (HF), the HRV LF/HF ratio or a combination thereof.” App. Br. 61.
Claim 178 recites: “The method according to Claim 149, wherein
measuring the subject’s parasympathetic/sympathetic activity ratio
comprises detecting nerve cell or axon activity in the subject.” App. Br. 61.
The Examiner states that Shapland is cited to more explicitly teach a
wide variety of methods to check the functioning of the parasympathetic
nervous system including heart rate variability, volume of pressure changes,
direct neural measurements, etc. Adv. Act. 10 (citing Shapland col. 1, ll. 54
et seq.).
We have explained supra how both Kuo and Childre teach the
limitation reciting “measuring the subject’s parasympathetic/sympathetic
activity ratio comprises measuring one or more indicators of the autonomic
nervous system selected from the group consisting of … heart rate
variability….,” as recited in claim 176. Furthermore, we have explained
how both Kuo and Childre explicitly teach measuring “heart rate variability
and the measuring comprises measuring low HRV frequency peak (LF),
high HRV frequency peak (HF), the HRV LF/HF ratio or a combination
thereof.” See, e.g., Kuo ¶ 29; Childre col. 8, ll. 56–62.
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Shapland teaches:
The present invention relates to a system for monitoring the
autonomic neural tone of a patient and taking preventative or
curative actions in an implanted device upon the occurrence of
altered levels of the autonomic neural tone. The autonomic
neural tone is detected by several methods including heart rate
variability, the derivative of the volume or pressure changes in
the heart, systolic time intervals, ventricular electrical
parameters, and direct neural activity measurements.
Shapland col. 1, ll. 54–62 (emphases added). Shapland thus teaches
measurements of both heart rate variability and direct neural activity as a
means of measuring “autonomic neural tone,” i.e., the relative activity levels
of parasympathetic and sympathetic divisions of the autonomic nervous
system. See id. at col. 2, ll. 42–44.
In summary, we find that the combined cited prior art teaches or
suggests all of the limitations of claims 176–178, and we affirm the
Examiner’s rejection of the claims.

K. Claim 173–178: Obviousness over Ivanova, Kuo or Childre, and
Shapland

Claims 173–175 depend, directly or ultimately, from independent
claim 142, and otherwise mirror the language of claims 176–178 supra,
which depend, directly or ultimately, from claim 149. Appellant argues that
Shapland does not remedy these deficiencies of the prior cited art.
We have explained our reasoning supra as to why we find that the
combined cited prior art teaches each and every limitation of claims 142 and
claims 176–78. We consequently affirm the Examiner’s rejection of these
claims.
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L. Claim 173–178: Obviousness over Ivanova, Kuo or Childre, and
Shapland

Claims 173–175 depend, directly or ultimately, from independent
claim 142. Appellant essentially repeats the arguments presented supra. We
have already explained why we find that the combination of Cohen and Kuo
or Childre teaches independent claim 142, and how Kuo or Childre, and
Shapland, teach the limitations of claims 173–175 (and essentially identical
claims 176–178). We consequently affirm the Examiner’s rejection of the
claims.

DECISION
The Examiner’s rejection of claims 142, 147–149, 154–156, 159–163,
167–179, 181, 182, 184, and 185 as unpatentable under 35 U.S.C. § 103(a)
is affirmed.
The Examiner’s rejection of claims 180 and 183 as unpatentable under
35 U.S.C. § 103(a) is reversed.
No time period for taking any subsequent action in connection with
this appeal may be extended under 37 C.F.R. § 1.136(a)(1). See 37 C.F.R.
§ 1.136(a)(1)(iv).

AFFIRMED-IN-PART

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Claims
Rejected
35
U.S.C.
§
Reference(s)/Basis Affirmed Reversed
149, 154, 155,
160–163, 168,
170, 172 176–
179, 184
103(a) Branham, Kuo,
Childre

149, 154, 155,
160–163, 168,
170, 172 176–
179, 184

149, 154, 155,
160–163, 168,
170, 172, 176–
179, 183
103(a) Watkins, Kuo, Childre 149, 154, 155,
160–163, 168,
170, 172, 176–
179,  
183
149, 154, 155,
160–163, 168,
170, 172, 176–
179, 183
103(a)  Rezai, Kuo, Childre 149, 154, 155,
160–163, 168,
170, 172, 176–
179 
183
142, 147–149,
154–156, 159–
163, 167–185
103(a) Ivanova, Kuo, Childre 142, 147–149,
154–156, 159–
163, 167–179,
181, 182, 184,
185
180, 183
142, 147, 148,
156, 159, 167,
169, 171, 173–
175, 180, 181
103(a) Cohen, Kuo, Childre 142, 147, 148,
156, 159, 167,
169, 171, 173–
175
180, 181
176–178 103(a) Branham, Watkins,
Rezai, Kuo, Childre,
Shapland

176–178
173–178 103(a) Ivanova, Kuo, Childre,
Shapland

173–178
173–175 103(a) Cohen, Kuo, Childre,
Shapland

173–175
Overall
Outcome
    142, 147–149,
154–156, 159–
163, 167–179,
180, 183
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181, 182, 184,
185