DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA . In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claim 1-20 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
The term “produce significant destruction of subcutaneous lipid-rich cells" in claim 1 and 20 is indefinite. The scope of the claim is unclear. Significant destruction can vary depending on the desired treatment.
Claim 7 recites the limitation “the dermal layer, the subcutaneous layer" in line 2. There is insufficient antecedent basis for this limitation in the claim.
Claim 9 recites the limitation “the epidermal layer, dermal layer, the subcutaneous layer" in line 2. There is insufficient antecedent basis for this limitation in the claim.
Claim 12 recites the limitation “the temperature of said treatment unit" in line 1. There is insufficient antecedent basis for this limitation in the claim.
Claim 13 recites the limitation “the temperature of the epidermis" in line 1-2. There is insufficient antecedent basis for this limitation in the claim.
Claim 14 recites the limitation “the epidermis" in line 2. There is insufficient antecedent basis for this limitation in the claim.
Claim 15 recites the limitation “the temperature of the subcutaneous fat layer" in line 1-2. There is insufficient antecedent basis for this limitation in the claim.
Claim 16 recites the limitation “the temperature of the subcutaneous fat layer” in line 1-2. There is insufficient antecedent basis for this limitation in the claim.
Claim 18 recites the limitation “the temperature of the subcutaneous fat layer” in line 1-2. There is insufficient antecedent basis for this limitation in the claim.
Claim 19 recites the limitation “the epidermis” in line 4. There is insufficient antecedent basis for this limitation in the claim.
Claim 19 recites the limitation “the temperature of the subcutaneous fat layer” in line 7-8. There is insufficient antecedent basis for this limitation in the claim.
Claim 20 recites the limitation “the epidermis” in line 4. There is insufficient antecedent basis for this limitation in the claim.
Claim 20 recites the limitation “the temperature of the subcutaneous fat layer in line 7-8. There is insufficient antecedent basis for this limitation in the claim.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
Claim 1, 4-5, 8-13, 20 are rejected under 35 U.S.C. 102 (a) (1) as being anticipated by DeBenedictis et al. (US 2015/0216719).
Regarding claim 1, DeBenedictis discloses a method of improving one or more skin characteristics in a subject comprising cooling the subject's skin at a target site to a degree that alters adipocyte signaling but does not produce significant destruction of subcutaneous lipid-rich cells, wherein said alteration of adipocyte signaling produces an improvement in one or more skin characteristics (fig.1A. see also [0064] and [0068]).
Regarding claim 4, DeBenedictis discloses the method of claim 1, wherein said cooling does not produce any adverse skin effects ([0064] and [0068]).
Regarding claim 5, DeBenedictis discloses the method of claim 4, wherein said adverse effects are selected from the group consisting of hyper-pigmentation, hypo-pigmentation, unwanted blistering, unwanted scarring, permanent undesirable alterations, and disfiguring scars ([0053], [0079] and [0088]).
Regarding claim 8, DeBenedictis discloses the method of claim 1, wherein said alteration in adipocyte signaling results in an increase in one or more extracellular matrix components selected from the group consisting of collagen, elastin, proteoglycans (e.g., heparan sulfate, keratin sulfate, and chondroitin sulfate), fibrinogen, laminin, fibrin, fibronectin, hyaluronan, hyaluronic acid, versican, aggrecan, lumican, decorin, glypican, tenascins, syndecans, integrins, discoidin domain receptors, perlecan, N-CAM, ICAM, VCAM, focal adhesion kinases, matrix metalloproteases, and Rho-kinases [0103].
Regarding claim 9, DeBenedictis discloses the method of claim 8, wherein said increase in one or more extracellular matrix components occurs in the epidermal layer, dermal layer, the subcutaneous layer, or combinations thereof [0103].
Regarding claim 10, DeBenedictis discloses the method of claim 1, wherein said one or more improved skin characteristics are selected from the group consisting of increased skin thickness, increased new collagen content, increased skin firmness, increased skin smoothness, skin tightening, increased dermal/epidermal hydration, dermal remodeling, and fibrous septae thickening [0059].
Regarding claim 11, DeBenedictis discloses the method of claim 1, wherein said cooling is performed by applying a treatment unit proximal to the target site (fig.1b).
Regarding claim 12, DeBenedictis discloses the method of claim 11, wherein the temperature of said treatment unit is about -18°C to about 0°C [0073].
Regarding claim 13, DeBenedictis discloses the method of claim 1, wherein said cooling lowers the temperature of the epidermis at the target site to about -15°C to about 5°C [0073].
Regarding claim 20, DeBenedictis discloses a method of improving one or more skin characteristics in a subject comprising: applying a cooling element proximal to a target site on the subject's skin for a period of time sufficient to cool the epidermis at the target site to about -15°C to about 5°C [0058], wherein said cooling results in an alteration of one or more adipocyte signaling events; and removing the cooling element before the temperature of the entire subcutaneous fat layer beneath the target site is decreased to a level that produces significant destruction of subcutaneous lipid-rich cells therein (fig.1A. see also [0064] and [0068]).
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claim 2-3 are rejected under 35 U.S.C. 103 as being unpatentable over DeBenedictis (US 2015/0216719) in view of Anderson at al. (US 2017/0165105).
Regarding claim 2-3, DeBenedictis discloses the method as claimed above. DeBenedictis discloses that systems and methods for affecting a target region of a human subject's body by removing heat from the target region to alter subdermal connective tissue while lipid-rich cells in the subcutaneous layer are not substantially affected [0055]. However, DeBenedictis does not disclose wherein less than 10% of the subcutaneous lipid-rich cells are destroyed and wherein less than 1%, 2%, 3%, 4%, 5%, or 7% of the subcutaneous lipid-rich cells are destroyed.
Anderson teaches a cooling device can be controlled in order to produce the desired cooling of one or more sebaceous glands without permanently and/or reversibly injuring epidermal tissue or subcutaneous adipose tissue [0123]. Anderson teaches that absence of subcutaneous adipose tissue means the adipose cell count, thickness, or volume reduced by less than 10%, 9%, 8%, 7%, 6%, 5%, 4%, 3%, 2%, or 1% [0123]. Therefore, it would have been obvious to one of ordinary skill in the art at the time the application was effectively filed to modify the method as taught by DeBenedictis with a method destroying less than 1%, 2%, 3%, 4%, 5%, 7% or 10% or of the subcutaneous lipid-rich cells as taught by Anderson for the purpose of preventing subcutaneous lipid-rich cells injury when desired.
Claim 6-7 are rejected under 35 U.S.C. 103 as being unpatentable over DeBenedictis (US 2015/0216719) in view Swyer et al. (US 2016/0143771).
Regarding claim 6-7, DeBenedictis discloses the method of claim 1, wherein said alteration in adipocyte signaling results in an increase in expression of one or more cytokines selected from the group consisting of TGF-P, TNF-a, IL-1 P, IL-6, MCP-1, leptin, adiponectin, resistin, acylation-stimulating protein, alpha 1 acid glycoprotein, pentraxin-3, IL-1 receptor antagonist, macrophage migration inhibitor factor, and SAA3 and wherein said increase in expression occurs in the dermal layer, the subcutaneous layer, or both.
Swyer teaches a system and method for cooling/heating that is configured to alter cytokines, hormones, or other levels, such as adiponectin, interleukins, or TNF [0005]. Swyer teaches this heat loss can stimulate the hypothalamus, which through the sympathetic nervous system stimulates white and/or brown adipose tissue to compensate with lipolysis and rapid release of adipocytokines. In the ensuing "cytochrome storm" pro-inflammatory cytokines such as TNF trigger pain, nausea, and vomiting; leptin triggers pain and loss of appetite; the leukotrienes trigger white blood cells and mast cells to release histamines and other mediators cause eye-tearing redness, rhinorrhea, and photophobia ([0037] and [0039]). Therefore, it would have been obvious to one of ordinary skill in the art at the time the application was effectively filed to modify the method as taught by DeBenedictis with a method of cooling results with alter cytokines such as TNF as taught by Swyer since that is a result of the treatment.
Claim 14-19 are rejected under 35 U.S.C. 103 as being unpatentable over DeBenedictis (US 2015/0216719).
Regarding claim 14-19, DeBenedictis discloses a system that selectively cool tissue at different depth for various ranges based on target tissue and/or desired result [0058]. The duration of the freeze event and temperature of the tissue can be selected to achieve a desired thickened resilient epidermis ([0081], [0092], [0106]. The applicator 104 can periodically or continuously remove heat from the target tissue to keep a volume of target tissue frozen for a suitable length of time to elicit a desired response [0080]. However, DeBenedictis does not disclose wherein said cooling is discontinued after the temperature of the epidermis at the target site has been at a temperature of about -15°C to about 5°C for about 10 minutes to about 25 minutes; the method of claim 1, wherein said cooling does not lower the temperature of the subcutaneous fat layer 7 mm below the target site below about 3°C; wherein said cooling is discontinued after the temperature of the subcutaneous fat layer 7 mm below the target site has been at a temperature of about 3°C to about 30°C for about 10 minutes to about 25 minutes; a method of improving one or more skin characteristics in a subject comprising: applying a cooling element proximal to a target site on the subject's skin for a period of time sufficient to cool the epidermis at the target site to about -15°C to about 5°C, wherein said cooling results in an alteration of one or more adipocyte signaling events; and removing the cooling element before the temperature of the subcutaneous fat layer about 7 mm below the target site decreases below a temperature of +3C. However, it would have been obvious to one having ordinary skill in the art at the time the application was effectively filed have a method of cooling is discontinued after the desired temperature, duration and depth in order to achieve the desired treatment and furthermore since it has been held that where the general conditions of a claim are disclosed in the prior art, discovering the optimum or workable ranges involves only routine skill in the art. In re Aller, 105 USPQ 233.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claim 1-19 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1-16 of U.S. Patent No. US 11,446,175. Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of US 11,446,175 anticipate the claims of the application. Accordingly, the application claims are not patentably distinct from the patent claims. Here, the more specific patent claims encompass the broader application claims. Following the rationale in In re Goodman cited in the preceding paragraph, where applicant has once been granted a patent containing a claim for the specific narrow invention, applicant may not obtain a second patent with a claim for the generic or broader invention without first submitting an appropriate terminal disclaimer.
Claim 1-120 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim 1-16 of U.S. Patent No. US 12102557. Although the claims at issue are not identical, they are not patentably distinct from each other because the claims of US 11,446,175 anticipate the claims of the application. Accordingly, the application claims are not patentably distinct from the patent claims. Here, the more specific patent claims encompass the broader application claims. Following the rationale in In re Goodman cited in the preceding paragraph, where applicant has once been granted a patent containing a claim for the specific narrow invention, applicant may not obtain a second patent with a claim for the generic or broader invention without first submitting an appropriate terminal disclaimer.
18/821,021
US 11,446,175
1. A method of improving one or more skin characteristics in a subject comprising cooling the subject's skin at a target site to a degree that alters adipocyte signaling but does not produce significant destruction of subcutaneous lipid-rich cells, wherein said alteration of adipocyte signaling produces an improvement in one or more skin characteristics.
1. A method of improving one or more skin characteristics in a subject comprising: cooling the subject's skin at a target site with a treatment unit to lower the temperature of the epidermis at the target site to about −15° C. to about 5° C., and discontinuing cooling when the temperature of the epidermis at the target site has been at a temperature of about −15° C. to about 5° C. for about 10 minutes to about 25 minutes such that adipocyte signaling is altered but less than 10% of subcutaneous lipid-rich cells are destroyed, wherein said alteration of adipocyte signaling produces an improvement in one or more skin characteristics.
3. The method of claim 2, wherein less than 1%, 2%, 3%, 4%, 5%, or 7% of the subcutaneous lipid-rich cells are destroyed.
2. The method of claim 1, wherein less than 1%, 2%, 3%, 4%, 5%, or 7% of the subcutaneous lipid-rich cells are destroyed.
4. The method of claim 1, wherein said cooling does not produce any adverse skin effects
3. The method of claim 1, wherein said cooling does not produce any adverse skin effects.
5. The method of claim 4, wherein said adverse effects are selected from the group consisting of hyper-pigmentation, hypo-pigmentation, unwanted blistering, unwanted scarring, permanent undesirable alterations, and disfiguring scars.
4. The method of claim 3, wherein said adverse effects are selected from the group consisting of hyper-pigmentation, hypo-pigmentation, unwanted blistering, unwanted scarring, permanent undesirable alterations, and disfiguring scars.
6. The method of claim 1, wherein said alteration in adipocyte signaling results in an increase in expression of one or more cytokines selected from the group consisting of TGF-β, TNF-α, IL-1β, IL-6, MCP-1, leptin, adiponectin, resistin, acylation-stimulating protein, alpha 1 acid glycoprotein, pentraxin-3, IL-1 receptor antagonist, macrophage migration inhibitor factor, and SAA3.
5. The method of claim 1, wherein said alteration in adipocyte signaling results in an increase in expression of one or more cytokines selected from the group consisting of TGF-β, TNF-α, IL-1β, IL-6, MCP-1, leptin, adiponectin, resistin, acylation-stimulating protein, alpha 1 acid glycoprotein, pentraxin-3, IL-1 receptor antagonist, macrophage migration inhibitor factor, and SAA3.
7. The method of claim 6, wherein said increase in expression occurs in the dermal layer, the subcutaneous layer, or both.
6. The method of claim 5, wherein said increase in expression occurs in the dermal layer, the subcutaneous layer, or both.
8. The method of claim 1, wherein said alteration in adipocyte signaling results in an increase in one or more extracellular matrix components selected from the group consisting of collagen, elastin, proteoglycans (e.g., heparan sulfate, keratin sulfate, and chondroitin sulfate), fibrinogen, laminin, fibrin, fibronectin, hyaluronan, hyaluronic acid, versican, aggrecan, lumican, decorin, glypican, tenascins, syndecans, integrins, discoidin domain receptors, perlecan, N-CAM, ICAM, VCAM, focal adhesion kinases, matrix metalloproteases, and Rho-kinases.
7. The method of claim 1, wherein said alteration in adipocyte signaling results in an increase in one or more extracellular matrix components selected from the group consisting of collagen, elastin, proteoglycans (e.g., heparan sulfate, keratin sulfate, and chondroitin sulfate), fibrinogen, laminin, fibrin, fibronectin, hyaluronan, hyaluronic acid, versican, aggrecan, lumican, decorin, glypican, tenascins, syndecans, integrins, discoidin domain receptors, perlecan, N-CAM, ICAM, VCAM, focal adhesion kinases, matrix metalloproteases, and Rho-kinases.
9. The method of claim 8, wherein said increase in one or more extracellular matrix components occurs in the epidermal layer, dermal layer, the subcutaneous layer, or combinations thereof.
8. The method of claim 7, wherein said increase in one or more extracellular matrix components occurs in the epidermal layer, dermal layer, the subcutaneous layer, or combinations thereof.
10. The method of claim 1, wherein said one or more improved skin characteristics are selected from the group consisting of increased skin thickness, increased new collagen content, increased skin firmness, increased skin smoothness, skin tightening, increased dermal/epidermal hydration, dermal remodeling, and fibrous septae thickening.
9. The method of claim 1, wherein said one or more improved skin characteristics are selected from the group consisting of increased skin thickness, increased new collagen content, increased skin firmness, increased skin smoothness, skin tightening, increased dermal/epidermal hydration, dermal remodeling, and fibrous septae thickening.
11. The method of claim 1, wherein said cooling is performed by applying a treatment unit proximal to the target site.
10. The method of claim 1, wherein said cooling is performed by applying a treatment unit proximal to the target site.
12. The method of claim 11, wherein the temperature of said treatment unit is about -18ºC to about 0ºC.
11. The method of claim 10, wherein the temperature of said treatment unit is about −18° C. to about 0° C.
14. The method of claim 11, wherein said cooling is discontinued after the temperature of the epidermis at the target site has been at a temperature of about -15ºC to about 5ºC for about 10 minutes to about 25 minutes.
14. The method of claim 13, wherein said cooling is discontinued after the temperature of the subcutaneous fat layer 7 mm below the target site has been at a temperature of about 3° C. to about 30° C. for about 10 minutes to about 25 minutes.
15. The method of claim 1, wherein said cooling does not lower the temperature of the subcutaneous fat layer 7 mm below the target site below about 3ºC.
15. The method of claim 1, wherein said cooling is discontinued before the temperature of the subcutaneous fat layer 7 mm below the target site falls below 3° C.
19. A method of improving one or more skin characteristics in a subject comprising: applying a cooling element proximal to a target site on the subject's skin for a period of time sufficient to cool the epidermis at the target site to about -15ºC to about 5ºC, wherein said cooling results in an alteration of one or more adipocyte signaling events; and removing the cooling element before the temperature of the subcutaneous fat layer about 7 mm below the target site decreases below a temperature of +3C.
16. A method of improving one or more skin characteristics in a subject comprising: applying a cooling element proximal to a target site on the subject's skin for a period of time sufficient to cool the epidermis at the target site to about −15° C. to about 5° C., wherein said cooling results in an alteration of one or more adipocyte signaling events; and removing the cooling element before the temperature of the subcutaneous fat layer about 7 mm below the target site decreases below a temperature of 3° C.
18/821,021
US 12,102,557
1. A method of improving one or more skin characteristics in a subject comprising cooling the subject's skin at a target site to a degree that alters adipocyte signaling but does not produce significant destruction of subcutaneous lipid-rich cells, wherein said alteration of adipocyte signaling produces an improvement in one or more skin characteristics.
1. A method of decreasing skin laxity in a subject comprising: cooling the subject's skin at a target site with a treatment unit to lower the temperature of the epidermis at the target site to about −15° Celsius (C) to about 5° C.; and discontinuing cooling before a subcutaneous fat layer 7 mm below the target site decreases below a temperature of about 3° C. such that adipocyte signaling is altered but less than 10% of subcutaneous lipid-rich cells are destroyed, wherein said alteration of adipocyte signaling decreases skin laxity of the subject's skin.
3. The method of claim 2, wherein less than 1%, 2%, 3%, 4%, 5%, or 7% of the subcutaneous lipid-rich cells are destroyed.
2. The method of claim 1, wherein less than 1%, 2%, 3%, 4%, 5%, or 7% of the subcutaneous lipid-rich cells are destroyed.
4. The method of claim 1, wherein said cooling does not produce any adverse skin effects
3. The method of claim 1, wherein said cooling does not produce any adverse skin effects.
5. The method of claim 4, wherein said adverse effects are selected from the group consisting of hyper-pigmentation, hypo-pigmentation, unwanted blistering, unwanted scarring, permanent undesirable alterations, and disfiguring scars.
4. The method of claim 3, wherein said adverse effects are selected from the group consisting of hyper-pigmentation, hypo-pigmentation, unwanted blistering, unwanted scarring, permanent undesirable alterations, and disfiguring scars.
6. The method of claim 1, wherein said alteration in adipocyte signaling results in an increase in expression of one or more cytokines selected from the group consisting of TGF-β, TNF-α, IL-1β, IL-6, MCP-1, leptin, adiponectin, resistin, acylation-stimulating protein, alpha 1 acid glycoprotein, pentraxin-3, IL-1 receptor antagonist, macrophage migration inhibitor factor, and SAA3.
5. The method of claim 1, wherein said alteration in adipocyte signaling results in an increase in expression of one or more cytokines selected from the group consisting of TGF-β, TNF-α, IL-1β, IL-6, MCP-1, leptin, adiponectin, resistin, acylation-stimulating protein, alpha 1 acid glycoprotein, pentraxin-3, IL-1 receptor antagonist, macrophage migration inhibitor factor, and SAA3.
7. The method of claim 6, wherein said increase in expression occurs in the dermal layer, the subcutaneous layer, or both.
6. The method of claim 5, wherein said increase in expression occurs in the dermal layer, the subcutaneous layer, or both.
8. The method of claim 1, wherein said alteration in adipocyte signaling results in an increase in one or more extracellular matrix components selected from the group consisting of collagen, elastin, proteoglycans (e.g., heparan sulfate, keratin sulfate, and chondroitin sulfate), fibrinogen, laminin, fibrin, fibronectin, hyaluronan, hyaluronic acid, versican, aggrecan, lumican, decorin, glypican, tenascins, syndecans, integrins, discoidin domain receptors, perlecan, N-CAM, ICAM, VCAM, focal adhesion kinases, matrix metalloproteases, and Rho-kinases.
7. The method of claim 1, wherein said alteration in adipocyte signaling results in an increase in one or more extracellular matrix components selected from the group consisting of collagen, elastin, proteoglycans (e.g., heparan sulfate, keratin sulfate, and chondroitin sulfate), fibrinogen, laminin, fibrin, fibronectin, hyaluronan, hyaluronic acid, versican, aggrecan, lumican, decorin, glypican, tenascins, syndecans, integrins, discoidin domain receptors, perlecan, N-CAM, ICAM, VCAM, focal adhesion kinases, matrix metalloproteases, and Rho-kinases.
9. The method of claim 8, wherein said increase in one or more extracellular matrix components occurs in the epidermal layer, dermal layer, the subcutaneous layer, or combinations thereof.
8. The method of claim 7, wherein said increase in one or more extracellular matrix components occurs in the epidermal layer, dermal layer, the subcutaneous layer, or combinations thereof.
10. The method of claim 1, wherein said one or more improved skin characteristics are selected from the group consisting of increased skin thickness, increased new collagen content, increased skin firmness, increased skin smoothness, skin tightening, increased dermal/epidermal hydration, dermal remodeling, and fibrous septae thickening.
9. The method of claim 1, wherein said one or more improved skin characteristics are selected from the group consisting of increased skin thickness, increased new collagen content, increased skin firmness, increased skin smoothness, skin tightening, increased dermal/epidermal hydration, dermal remodeling, and fibrous septae thickening.
11. The method of claim 1, wherein said cooling is performed by applying a treatment unit proximal to the target site.
10. The method of claim 1, wherein said cooling is performed by applying a treatment unit proximal to the target site.
12. The method of claim 11, wherein the temperature of said treatment unit is about -18ºC to about 0ºC.
11. The method of claim 10, wherein the temperature of said treatment unit is about −18° C. to about 0° C.
19. A method of improving one or more skin characteristics in a subject comprising: applying a cooling element proximal to a target site on the subject's skin for a period of time sufficient to cool the epidermis at the target site to about -15ºC to about 5ºC, wherein said cooling results in an alteration of one or more adipocyte signaling events; and removing the cooling element before the temperature of the subcutaneous fat layer about 7 mm below the target site decreases below a temperature of +3C.
12. A method of decreasing skin laxity in a subject comprising: applying a cooling element proximal to a target site on the subject's skin for a period of time sufficient to cool the epidermis at the target site to about −15° C. to about 5° C., wherein said cooling results in an alteration of one or more adipocyte signaling events; and removing the cooling element before the temperature of the subcutaneous fat layer about 7 mm below the target site decreases below a temperature of +3° C.
20. A method of improving one or more skin characteristics in a subject comprising: applying a cooling element proximal to a target site on the subject's skin for a period of time sufficient to cool the epidermis at the target site to about -15ºC to about 5ºC, wherein said cooling results in an alteration of one or more adipocyte signaling events; and removing the cooling element before the temperature of the entire subcutaneous fat layer beneath the target site is decreased to a level that produces significant destruction of subcutaneous lipid-rich cells therein.
13. A method of decreasing skin laxity in a subject comprising: applying a cooling element proximal to a target site on the subject's skin for a period of time sufficient to cool the epidermis at the target site to about −15° C. to about 5° C., wherein said cooling results in an alteration of one or more adipocyte signaling events; and removing the cooling element when the temperature of the epidermis at the target site has been at a temperature of about −15° C. to about 5° C. for about 10 minutes to about 25 minutes such that adipocyte signaling is altered but less than 10% of subcutaneous lipid-rich cells are destroyed.
Conclusion
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/TIGIST S DEMIE/Examiner, Art Unit 3794
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