U.S. patent application number 15/765109 was filed with the patent office on 2018-09-27 for treatment systems processes and devices addressing cerebral vasospasm/vasoconstriction.
The applicant listed for this patent is NEURVANA MEDICAL, LLC. Invention is credited to Joshua Benjamin, Pervinder Bhogal, David A Ferrera, Michael Sodermann.
Application Number | 20180271683 15/765109 |
Document ID | / |
Family ID | 58408518 |
Filed Date | 2018-09-27 |
United States Patent
Application |
20180271683 |
Kind Code |
A1 |
Ferrera; David A ; et
al. |
September 27, 2018 |
Treatment Systems Processes and Devices Addressing Cerebral
Vasospasm/Vasoconstriction
Abstract
Endovascular treatment of, for example, delayed cerebral
vasospasm involves the placing of a microcatheter in the affected
vessels followed by the teachings of the instant disclosure, which
is clinically improved with comparison to stow infusion of a
vasodilating compound. Systems, processes and self-expanding
designed stents and stent-like members are featured whereas as
stents and stent-like members are retrieved, nothing is left in the
vessel.
Inventors: |
Ferrera; David A; (Coto De
Caza, CA) ; Benjamin; Joshua; (Mission Viejo, CA)
; Bhogal; Pervinder; (Islington, London, GB) ;
Sodermann; Michael; (Stockholm, SE) |
|
Applicant: |
Name |
City |
State |
Country |
Type |
NEURVANA MEDICAL, LLC |
Tustin |
CA |
US |
|
|
Family ID: |
58408518 |
Appl. No.: |
15/765109 |
Filed: |
May 13, 2016 |
PCT Filed: |
May 13, 2016 |
PCT NO: |
PCT/US2016/032563 |
371 Date: |
April 16, 2018 |
Related U.S. Patent Documents
|
|
|
|
|
|
Application
Number |
Filing Date |
Patent Number |
|
|
62253025 |
Nov 9, 2015 |
|
|
|
62235361 |
Sep 30, 2015 |
|
|
|
62235543 |
Sep 30, 2015 |
|
|
|
Current U.S.
Class: |
1/1 |
Current CPC
Class: |
A61F 2/966 20130101;
A61L 2300/42 20130101; A61L 31/022 20130101; A61F 2/90 20130101;
A61L 31/16 20130101; A61M 2025/0042 20130101; A61F 2002/9528
20130101; A61M 25/09 20130101; A61L 2300/418 20130101; A61F
2210/0014 20130101; A61F 2250/0067 20130101; A61F 2/844 20130101;
A61F 2250/0098 20130101; A61L 2300/416 20130101; A61L 31/146
20130101; A61L 31/18 20130101; A61L 31/148 20130101; A61F 2210/0004
20130101; A61B 6/504 20130101; A61L 33/0011 20130101; A61F
2250/0059 20130101 |
International
Class: |
A61F 2/90 20060101
A61F002/90; A61F 2/966 20060101 A61F002/966; A61M 25/09 20060101
A61M025/09; A61B 6/00 20060101 A61B006/00; A61L 31/02 20060101
A61L031/02; A61L 31/16 20060101 A61L031/16; A61L 31/18 20060101
A61L031/18; A61L 31/14 20060101 A61L031/14 |
Claims
1. A treatment system for cerebral arterial vasospasm which
comprises in combination: a guide catheter effective for
emplacement in the ICA/VCA; Heparin and/or related compounds in
treatment-based aliquots; Imaging, further comprising, angiograms;
At least a microcatheter and microguidewire; At least a retrievable
stent, with radial forced tuned to the application; namely, less
force than a dilatation balloon and, Sheath-means for covering and
advancing the at least a retrievable stent to a target zone, for a
predetermined time interval.
2. The system of claim 1, wherein said at least a retrievable stent
is self-expanding nitinol.
3. The system of claim 2, wherein said at least a retrievable stent
is self-expanding and at least one of open and closed celled,
whereby the radial force is less traumatic than vasospasm inducing
alternatives, such as dilatation balloons which damage the
extra-cellular matrix (ECM).
4. The system of claim 3, wherein said at least a retrievable stent
is self-expanding and at least of open and closed celled, whereby
the radial force is less traumatic than vasospasm inducing
alternatives, and the stents/stent-like members being retrieved,
nothing is left in the vessel.
5. The system of claim 4, whereby said at least a retrievable
stent-means is self-expanding, and further comprising Ca+-channel
blockers for use in the MC during stent deployment, as needed.
6. The system of claim 5, wherein at least a retrievable
stent-means is removable, said devices having at least a drug
covering or coating selected from the group of Everolimus;
Paclitaxel; Sirolimus; Corolimus and any related compounds, salts,
moieties which potentially reduce risk of thrombosis, lumen loss
and related challenges.
7. A Kit, comprising, in combination: At least a guide catheter
system; At least a self-expanding sheath and retrievable
stenting-means; Further comprising an elongated structure ranging
from approximately 20 cm to at least about 50 cm in length, the
radial force designed to stretch but not damage the ECM; A
plurality of cells being smaller cells disposed about the
stenting-means, whereby radial force is maintained within a range
that does not cause the vessel to recoil or vasoconstrict, and;
Digital and hard copy instructions for use, imaging and electronic
links to databases for patients, care-givers and related
procedures.
8. The Kit of claim 14, further comprising: Instructions to
maintain the retrievable stenting means in situ for at least about
5, 7, 10 or more minutes.
9. The Kit of claim 14, further comprising: Instructions to
maintain the retrievable stenting means in situ for enough time to
stretch but not damage the ECM.
10. An improved vessel patency system, which comprises, in
combination: a stent-means/device for deployment in intracranial
arteries experiencing vasospasm, in order to expand vessels to
their optimal diameter and remain patent after the device is
re-sheathed.
11. The improved vessel patency system of claim 10, further
comprising: the stent-means/device being self-expanding nitinol
with small cells.
12. The improved vessel patency system of claim 11, further
comprising: said stent-means/device being self-expanding nitinol
which adduces optimum control and radial force to
mitigate/extenuate or prevent vasoconstriction/vasospasm, without
damaging the ECM.
13. The improved vessel patency system of claim 19, further
comprising: a device ranging from approximately 2-6 mm in diameter
and from at least about 20 cm to approximately 50 cm in length.
14. The system of claim 13, used for patients' refractory to
standard medical treatment.
15. The system of claim 13, whereby an adjustable clot retriever is
included with or substituted or the stent-means device.
16. The system of claim 15, whereby an adjustable clot retriever is
optionally included.
17. The system of claim 16, whereby smooth vascular muscles are
stretched, but no harm to the ECM occurs.
18. The system of claim 15, whereby smooth vascular muscles are
stretched, but no harm to the ECM occurs.
Description
BACKGROUND OF THE DISCLOSURES
[0001] The present disclosures related to therapy and systems for
treating the neurovascular system, in particular the present
inventions relate to endovascular devices for neurovascular
invention designed to impact, extenuate, mitigate or prevent
vasospasm/vasoconstriction.
[0002] The present inventions relate to systems for treating issues
in the brain and related vasculature from injury, insult or
trauma--often related or secondary to stroke, including acute
conditions related to intracranial bleeding and related insults and
injury, both from rupture of aneurysms and attempts to treat
them.
[0003] This includes both (PCHV) Post-hemorrhagic cerebral
aneurysm, DCV (see below) and those related conditions from
ischemic and hemorrhagic stroke wherein vasoconstriction is a
modifiable risk factor.
[0004] Intracranial aneurysms which rupture, and/or those which are
treated with traditional endovascular coiling or neurosurgical
clipping methodologies often result in the most feared sequelae of
subarachnoid hemorrhage, namely Delayed Cerebral Vasospasm
(DCV).
[0005] Since DCV constitutes the leading cause of morbidity in
patients admitted to tertiary care hospitals, it would be expected
that advances in the devices and approaches which have occurred,
for example, in endovascular coiling and related techniques would
have been used to address this ongoing clinical need.
Unfortunately, prior to the advent of the instant teachings this
has not been the case to the extent that practitioners need it to
be to achieve optimal clinical outcomes.
OBJECTIVES OF THE DISCLOSURES AND SUMMARIES
[0006] Briefly stated, in patients refractory to standard medical
treatment, endovascular treatment of, for example, delayed cerebral
vasospasm involves the placing of a microcatheter in the affected
vessels followed by the teachings of the instant disclosure, which
is believed to be clinically improved with prior existing
approaches such as balloon dilatation (or dilatation with a
COMANECI.RTM. brand of device by Rapid Medical of Israel or
similar) and in comparison to slow infusion of a vasodilating
compound. Systems, processes and self-expanding designed stents and
stent-like members are featured and highlighted. The stents and
stent-like members being recovered and retrieved, nothing is left
in the vessel.
[0007] It is respectfully proposed that the traumatic nature of
balloon dilatation, owing to the paucity of ability to control
radial force, militates strongly for a solution to vasospasm, which
is more atraumatic. Likewise, it is optimal to avoid arterial
rupture secondary to over dilation of the vessel, dissection and
related sequelae.
[0008] Similarly, it is respectfully submitted that local infusion
of calcium channel blockers, such as Nimodipine causes blood
pressures to drop (not good risk for vasospasm patients), is not
effective in all patients and is temporary.
[0009] Heparin and/or related compounds in treatment-based
aliquots, imaging, comprising angiograms, at least a microcatheter
and microguidewire, at least a retrievable self-expanding stent,
with radial forced tuned to the application, and sheath-means or
covering and advancing the at least a retrievable stent to a target
zone, for a predetermined time interval.
BRIEF DESCRIPTION OF THE FIGURES
[0010] FIG. 1 shows an angiogram with ostensive vasospasm issues;
and.
[0011] FIG. 2 shows a completion angiogram according to the instant
teachings;
[0012] FIG. 3 similarly shows a severely impacted vessel including
vasospasm;
[0013] FIG. 4 shows the follow-up shot wherein the vessel is
stabilized by aspects of teachings of the present invention, namely
deployment of the objects of the present invention;
[0014] FIG. 5 shows that a vessel in spasm, even with nimodipine,
can clearly seen to be blocked;
[0015] FIG. 6 also between the arrows shows ho the system of the
present invention leads the vessels from a first vasospasmed state
to a second patent state;
[0016] FIG. 7 shows an exemplary stenting-means, have a
multiplicity of smaller cells which works in conjunction with an
elongated system; and
[0017] FIG. 8 likewise shows an exemplary stenting-means, have a
multiplicity of smaller cells which worn in conjunction with an
elongated system to adduce desired levels of radial force.
EXEMPLARY ISSUE BEING ADDRESSED BY THE DISCLOSURES
Delayed Cerebral Vasospasm Secondary to Acute Sub-arachnoid
Haemorrhage
Background
[0018] Sub-Arachnoid Haemorrhage, Delayed Cerebral Vasospasm and
Delayed Cerebral Injury
[0019] Sub-arachnoid haemorrhage (SAH) is a life threatening
condition with an incidence of approximately 7-10 per 100000
patient years. The diagnosis relies upon a high clinical index of
suspicion and performing the necessary investigations that include
initially a Computed Tomography (CT) scan of the head alongside CT
angiography of the intracranial vessels followed by a delayed
lumbar puncture if the CT scan is negative but suspicion is
high.
[0020] Of all the causes of subarachnoid haemorrhage ruptured
aneurysm arising from the circle of Willis accounts for
approximately 85%. Of the remaining 15% that are not attributable
to saccular aneurysms, 2/3 are caused by non-aneurysmal SAH and the
remaining 5% are cased by a variety of rare conditions.
[0021] The early prognosis of patients with aneurysmal SAH is most
closely correlated to three variables: [0022] 1. The neurological
condition of the patient on admission. [0023] 2. The age of the
patient [0024] 3. The amount of blood on the initial CT scan.
[0025] Of these variables, the initial neurological condition of
the patient at admission, especially the level of consciousness, is
the most important determinant and the causes of an early acute
deterioration in the status of the patient can be due to a variety
of different factors such as hydrocephalus, early re-bleeding, or
intra-cerebral haematoma.
[0026] The goal of treatment for aneurysmal subarachnoid
haemorrhage is to prevent re-bleeding of the aneurysm, which has
been estimated at between 35-40% in the first 4 weeks. This can be
done via two well-established methods--endovascular coiling of the
aneurysm or neurosurgical clipping of the aneurysm. After the
results of the International Subarachnoid Aneurysm Trial (ISAT) [8]
endovascular coiling has gained widespread acceptance and the
choice between coiling or clipping is often decided following a
multi-disciplinary team meeting between the neurosurgeons and
interventional neuroradiologists. The procedure is performed as
soon as possible after the admission of the patient. These
treatments are effective in securing the aneurysm and preventing
early re-rupture of the aneurysm however, delayed consequences of
the initial subarachnoid haemorrhage can have a devastating effect
on the clinical outcome of patients. The most feared delayed
sequelae of subarachnoid haemorrhage are Delayed Cerebral Vasospasm
(DCV) and Delayed Cerebral Injury (DCI). Other terms such as
Delayed Ischaemic Neurological Deficit (DIND, DID) are also used in
the literature as synonyms.
[0027] Delayed cerebral vasospasm is the leading cause of morbidity
and mortality in patients who have ruptured intracranial aneurysm
and who are admitted to tertiary care hospitals. Delayed cerebral
vasospasm typically occurs between 3-21 days after the initial
insult and may last for 12-16 days. At day 7 post-ictus up to 70%
of patients will demonstrate angiographic evidence of cerebral
arterial vasospasm and approximately 30% of patients will go on to
develop neurological deficits, termed `symptomatic vasospasm`
Angiography done during this time will often reveal diffuse
vasoconstriction of the major intracranial vessels that frequently
involves the terminal internal carotid artery with some evidence
that points towards the location of the blood being closely related
to the site of vascular vasospasm and the development of delayed
cerebral vasospasm and ischaemia within this territory
[0028] To date the only drug of proven benefit that is routinely
used in the prevention of delayed cerebral vasospasm secondary to
subarachnoid haemorrhage is Nimodipine, a dihydropyridine L-Type
voltage gated calcium channel antagonist. This is given orally 60
mg every 4 hours for 21 days. Allen et al. were the first to
publish their findings in the New England Journal of Medicine with
further studies also demonstrating the protective effects of this
medication. However, the exact mechanism as to how calcium channel
antagonists prevent or relieve vasospasm is not clearly understood
and the evidence about efficacy and dosage is based on a single
large trial. It is important to note that without the data from
this single large trial the advantage of nimodipine in these
patients cannot be statistically seen. Therefore, the use of
nimodipine is not without question.
[0029] In patients that develop cerebral vasospasm there is a risk
of infarction that can be widespread. Therefore, in order to
prevent infarctions from developing medical treatment is optimised
to attempt to maintain perfusion. This involves increasing the
blood pressure, normally between 160-200 mmHg (if the patient has
had the aneurysm treated), haemodilution and hypervolaemia. Despite
this some patients continue to deteriorate and in these patients
endovascular treatment options are used.
[0030] In patients refractory to standard medical treatment
endovascular treatment of delayed cerebral vasospasm involves the
placing of a microcatheter in the affected vessels followed by the
slow infusion of a vasodilating compound, normally over the course
of 5-30 minutes. Numerous different agents have been used including
papaverine, as well as calcium channel antagonists verapamil,
nimodipine and nicardipine. All these agents have demonstrated an
affect on the cerebral vasospasm and it is believed that agents
with longer half-lives may offer a more sustained and long-lasting
effect. It is important to note that there is no level 1 evidence
to support the use of any of the aforementioned agents, although
numerous smaller trials have demonstrated improvement with
different agents used in different institutions.
[0031] Alternatively, the spastic vessels can be dilated
mechanically using balloons. There are numerous publications on
this technique going back as far as 1984. Improvements in vessel
diameters as well as neurological deficits were observed in most
studies following balloon angioplasty and successful treatment
translated into a reduced incidence of delayed cerebral ischaemia
on radiographic imaging in several studies. However, balloon
angioplasty is not without risk and vessel rupture and death have
been reported.
[0032] The exact cause for delayed cerebral vasospasm and delayed
cerebral injury is not completely understood, however as outlined
above the prevention or early treatment of cerebral vasospasm seems
to improve patient outcome. The present inventors have addressed
this issue and offer for consideration systems of devices effective
for the same.
DETAILED DESCRIPTION OF DISCLOSED EMBODIMENTS
[0033] The present inventors have discovered effective ways to
impact vasospasm, and improved devices to do so and create better
clinical outcomes.
[0034] As briefly summarized above, despite rapid advancement in
the minimally invasive and neurovascular fields, there does not
seem to be a synergistic leveraging of techniques and devices to
make outcomes best for patients--given the number of tools.
[0035] Lessons learned from open and closed cell stenting in the
brain, for example U.S. Pat. Nos. 8,088,140; 8,197,493 each
expressly incorporated by reference above, need to be used to
overcome those issues, which balloon dilatation and pharmacology
cannot address adequately in terms of vasospasm.
[0036] Turning to FIG. 1, an angiogram shows that within the target
brain area vessels are subject to vasospasm, as known to those
skilled in the art.
[0037] FIG. 2 shows the follow-up shot wherein the vessel is
stabilized by aspects of teaching of the present invention;
[0038] FIG. 3 similarly shows a severely impacted vessel including
vasospasm;
[0039] FIG. 4 shows the follow-up shot wherein the vessel is
stabilized by aspects of teachings of the present invention, namely
deployment of the objects of the present invention;
[0040] FIG. 5 shows that a vessel in vasospasm, even with
nimodipine, which can clearly be seen to be blocked;
[0041] FIG. 6 also shows by way of the arrow how the system of the
present invention leads the vessels from a first vasospasmed state
to a second patent state.
[0042] FIG. 7 and FIG. 8 demonstrate what has been discovered,
unexpectedly mitigating or preventing vasospasm, namely longer
stents with many smaller cells and radial force which can be tuned
for this application. Referring now to FIG. 7, as discussed the
nature of the stent/device/stenting-means has a specifically
designed cell structure which includes many cells generally of an
open variety, whereby an extended length (e.g. At least about 50
cm) allows for trackability and flexibility, balanced with a proper
amount of control for deployment.
[0043] Referring now also to FIG. 8, self-expanding nitinol
stenting-means is shown with small cells which deliver optimum
control and radial force for the treatment of disease. Artisans
understand that having access with longer stents having smaller
cells and radial force tuned to the neurovascular need undergirds
much of the instant solution. Since this problem was discovered and
overcome by the instant teachings, others may now continue to
advance the science of prevention of vasospasms.
Exemplary Indication
[0044] The instant teachings uniquely add tools to the
practitioner's arsenal for treating--for example, a cerebral
arterial vasospasm secondary to subarachnoid hemorrhage, trauma or
other conditions. Artisans understand that this method applies to
related methods of treatment.
[0045] The Procedure for those skilled in the art includes, for
example the following steps. Artisans understand swapping steps and
substitutions and additions are all within the scope of the list
below, which comprises merely guidance as to one approach for
performing according to the present invention:
[0046] A guiding catheter should be placed in the Internal Carotid
Artery or Vertebral Artery.
[0047] Heparinization to double ACT-level.
[0048] A diagnostic angiogram is performed in order to visualize
the location and extent of the arterial spasm and exclude other
pathologies that may be contraindications to the treatment.
[0049] The MCA, ACerA or PCerA is catherized to the M2, A2 or P2
segment with a microcatheter (MC) and microguidewire. In case this
is not necessary or cannot be safely done the tip of the MC may be
placed in the M1, A1 or P1.
[0050] The microguidewire is removed.
[0051] The temporary stent is inserted in the MC and advanced to
the tip of the MC.
[0052] The temporary stent is kept in place while the MC is
withdrawn to the level of the proximal end of the stent. The stent
is thus deployed without being advanced or retracted.
[0053] Control angiography through the guiding catheter.
[0054] The temporary stent is kept in place for 3-10 minutes.
[0055] Resheathing of the temporary stent by advancing the MC while
the stent is kept immobile.
[0056] Retraction of the MC to the ICA or Vert Art with the stent
still inside.
[0057] Control angiography through the guiding catheter.
[0058] The procedure may be repeated in the same or other
vessels.
[0059] Nimodipine (Ca+-channel blockers) can be given in the MC
during the stent deployment.
[0060] Unless otherwise indicated, all numbers expressing
quantities of ingredients, properties such as molecular weight,
reaction conditions, and so forth used in the specification and
claims are to be understood as being modified in all instances by
the term "about." Accordingly, unless indicated to the contrary,
the numerical parameters set forth in the specification and
attached claims are approximations that may vary depending upon the
desired properties sought to be obtained by the present invention.
At the very least, and not as an attempt to limit the application
of the doctrine of equivalents to the scope of the claims, each
numerical parameter should at least be construed in light of the
number of reported significant digits and by applying ordinary
rounding techniques. Notwithstanding that the numerical ranges and
parameters setting forth the broad scope of the invention are
approximations, the numerical values set forth in the specific
examples are reported as precisely as possible. Any numerical
value, however, inherently contains certain errors necessarily
resulting from the standard deviation found in their respective
testing measurements.
[0061] The terms "a," "an," "the" and similar referents used in the
context of describing the invention (especially in the context of
the following claims) are to be construed to cover both the
singular and the plural, unless otherwise indicated herein or
clearly contradicted by context. Recitation of ranges of values
herein is merely intended to serve as a shorthand method of
referring individually to each separate value falling within the
range. Unless otherwise indicated herein, each individual value is
incorporated into the specification as if it were individually
recited herein. All methods described herein can be performed in
any suitable order unless otherwise indicated herein or otherwise
clearly contradicted by context. The use of any and all examples,
or exemplary language (e.g., "such as") provided herein is intended
merely to better illuminate the invention and does not pose a
limitation on the scope of the invention otherwise claimed. No
language in the specification should be construed as indicating any
non-claimed element essential to the practice of the invention.
[0062] Groupings of alternative elements or embodiments of the
invention disclosed herein are not to be construed as limitations.
Each group member may be referred to and claimed individually or in
any combination with other members of the group or other elements
found herein. It is anticipated that one or more members of a group
may be included in, or deleted from, a group for reasons of
convenience and/or patentability. When any such inclusion or
deletion occurs, the specification is deemed to contain the group
as modified thus fulfilling the written description of all Markush
groups used in the appended claims.
[0063] Certain embodiments of this invention are described herein,
including the best mode known to the inventors for carrying out the
invention. Of course, variations on these described embodiments
will become apparent to those of ordinary skill in the art upon
reading the foregoing description. The inventor expects skilled
artisans to employ such variations as appropriate, and the
inventors intend for the invention to be practiced otherwise than
specifically described herein. Accordingly, this invention includes
all modifications and equivalents of the subject matter recited in
the claims appended hereto as permitted by applicable law.
Moreover, any combination of the above-described elements in all
possible variations thereof is encompassed by the invention unless
otherwise indicated herein or otherwise clearly contradicted by
context.
[0064] Specific embodiments disclosed herein may be further limited
in the claims using consisting of or consisting essentially of
language. When used in the claims, whether as filed or added per
amendment, the transition term "consisting of" excludes any
element, step, or ingredient not specified in the claims. The
transition term "consisting essentially of" limits the scope of a
claim to the specified materials or steps and those that do not
materially affect the basic and novel characteristic(s).
Embodiments of the invention so claimed are inherently or expressly
described and enabled herein.
[0065] As one skilled in the art would recognize as necessary or
best-suited for performance of the methods of the invention, a
computer system or machines of the invention include one or more
processors (e.g., a central processing unit (CPU) a graphics
processing unit (GPU) or both), a main memory and a static memory,
which communicate with each other via a bus.
[0066] A processor may be provided by one or more processors
including, for example, one or more of a single core or multi-core
processor (e.g., AMD Phenom II X2, Intel Core Duo, AMD Phenom II
X4, Intel Core i5, Intel Core I & Extreme Edition 980X, or
Intel Xeon E7-2820).
[0067] An I/O mechanism may include a video display unit (e.g., a
liquid crystal display (LCD) or a cathode ray tube (CRT)), an
alphanumeric input device (e.g., a keyboard), a cursor control
device (e.g., a mouse), a disk drive unit, a signal generation
device (e.g., a speaker), an accelerometer, a microphone, a
cellular radio frequency antenna, and network interface device
(e.g., a network interface card (NIC), Wi-Fi card, cellular modem,
data jack, Ethernet port, modem jack, HDMI port, mini-HDMI port,
USB port), touchscreen (e.g., CRT, LCD, LED, AMOLED, Super AMOLED),
pointing device, trackpad, light (e.g., LED), light/image
projection device, or a combination thereof.
[0068] Memory according to the invention refers to a non-transitory
memory which is provided by one or more tangible devices which
preferably include one or more machine-readable medium on which is
stored one or more sets of instructions (e.g., software) embodying
any one or more of the methodologies or functions described herein.
The software may also reside, completely or at least partially,
within the main memory, processor, or both during execution thereof
by a computer within system, the main memory and the processor also
constituting machine-readable media. The software may further be
transmitted or received over a network via the network interface
device.
[0069] While the machine-readable medium can in an exemplary
embodiment be a single medium, the term "machine-readable medium"
should be taken to include a single medium or multiple media (e.g.,
a centralized or distributed database, and/or associated caches and
servers) that store the one or more sets of instructions. The term
"machine-readable medium" shall also be taken to include any medium
that is capable of storing, encoding or carrying a set of
instructions for execution by the machine and that cause the
machine to perform any one or more of the methodologies of the
present invention. Memory may be, for example, one or more of a
hard disk drive, solid state drive (SSD), an optical disc, flash
memory, zip disk, tape drive, "cloud" storage location, or a
combination thereof. In certain embodiments, a device of the
invention includes a tangible, non-transitory computer readable
medium for memory. Exemplary devices for use as memory include
semiconductor memory devices, (e.g., EPROM, EEPROM, solid state
drive (SSD), and flash memory devices e.g., SD, micro SD, SDXC,
SDIO, SDHC cards); magnetic disks, (e.g., internal hard disks or
removable disks); and optical disks (e.g., CD and DVD disks).
[0070] Furthermore, numerous references have been made to patents
and printed publications throughout this specification. Each of the
above-cited references and printed publications are individually
incorporated herein by reference in their entirety.
[0071] In closing, it is to be understood that the embodiments of
the invention disclosed herein are illustrative of the principles
of the present invention. Other modifications that may be employed
are within the scope of the invention. Thus, by way of example, but
not of limitation, alternative configurations of the present
invention may be utilized in accordance with the teachings herein.
Accordingly, the present invention is not limited to that precisely
as shown and described.
* * * * *