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Collagen

Collagen is a structural protein found in the extracellular matrix of connective tissues throughout the body.
It provides strength, stability, and flexibility to tissues like skin, bone, cartilage, and tendons.
Collagen is the most abundant protein in mammals, comprising up to 30% of the total protein content.
It exists in over 28 different genetic types, with types I, II, and III being the most common.
Collagen plays a crucial role in wound healing, cell signaling, and maintaining tissue integrity.
Reserach into collagen has implications for a wide range of medical applications, including tissue engineering, regenerative medicine, and the treatment of collagen-related disorders.
Understanding the structure, function, and regulation of collagen is an important area of biomedical research.

Most cited protocols related to «Collagen»

Briefly, the two key features of NASH, steatosis and inflammation, were categorized as follows: steatosis was determined by analyzing hepatocellular vesicular steatosis, i.e. macrovesicular steatosis and microvesicular steatosis separately, and by hepatocellular hypertrophy as defined below (Fig. 2). Inflammation was scored by analyzing the amount of inflammatory cell aggregates (Fig. 2). The proposed rodent scoring system is shown in Table 4 and options for its use in diagnosis are shown in S1 Fig. The purpose of this scoring system is however not to derive a single score, but to score the individual features.
Macrovesicular steatosis and microvesicular steatosis were both separately scored and the severity was graded, based on the percentage of the total area affected, into the following categories: 0 (<5%), 1 (5–33%), 2 (34–66%) and 3 (>66%). The difference between macrovesicular and microvesicular steatosis was defined by whether the vacuoles displaced the nucleus to the side (macrovesicular) or not (microvesicular). Similarly, the level of hepatocellular hypertrophy, defined as cellular enlargement more than 1.5 times the normal hepatocyte diameter, was scored, based on the percentage of the total area affected, into the following categories: 0 (<5%), 1 (5–33%), 2 (34–66%) and 3 (>66%). For hepatocellular hypertrophy the evaluation was merely based on abnormal enlargement of the cells, irrespective of rounding of the cells and/or changes in cytoplasm or the number of vacuoles, and is therefore not a substitute of ballooning. The unweight sum of the scores for steatosis (macrovesicular steatosis, microvesicular steatosis and hypertrophy) thus ranged from 0–9. Both steatosis and hypertrophy were evaluated at a 40 to 100× magnification and only the sheets of hepatocytes were taken into account (terminal hepatic venules and portal tracts etc were excluded).
Inflammation was evaluated by counting the number of inflammatory foci per field using a 100 x magnification (view size of 3.1 mm2). A focus was defined a cluster, not a row, of ≥5 inflammatory cells. Five different fields were counted and the average was subsequently scored into the following categories: normal (<0.5 foci), slight (0.5–1.0 foci), moderate (1.0–2.0 foci), severe (>2.0 foci).
Hepatic fibrosis was identified using Sirius Red stained slides at 40 x magnification and evaluated by scoring whether pathologic collagen staining was absent (only in vessels) or collagen staining observed within the liver slide, the latter further defined as mild, moderate or massive. In addition, the percentage of the total area affected was evaluated using using image analysis of surface area on Sirius red stained slides.
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Publication 2014
Blood Vessel Cell-Derived Microparticles Cell Enlargement Cell Nucleus Cells Collagen Cytoplasm Diagnosis Fibrosis, Liver Hepatocyte Hypertrophy Inflammation Liver Nonalcoholic Steatohepatitis Portal System Rodent Steatohepatitis Vacuole Venules
We constructed all-cause rehospitalization within 30 days of discharge from Medicare claims (34 –36 ). Other variables drawn from Medicare files, included patient age, gender, race, Medicaid status, initial Medicare enrollment due to disability, index hospitalization length of stay and discharge to a skilled nursing facility. Race was categorized into ‘White’, ‘Black’, and ‘Other’ based upon the beneficiary race code. Each patient’s Centers for Medicare and Medicaid Services hierarchical condition category (HCC) score, calculated from all outpatient and inpatient claims over the 12 months prior to the index hospitalization, was included as a risk adjustment measure (38 (link)). Comorbid conditions were identified using Elixhauser methods, incorporating data from the index hospitalization and from all hospitalizations and physician claims during the year prior to the index hospitalization (39 (link)). Of the comorbidities identified using this approach, 17 had frequencies of greater than 5% in the sample and were included as indicators. Comorbidities occurring less often were compiled into an ‘other comorbidity’ indicator and included alcohol/drug abuse, rheumatoid arthritis/collagen vascular disease, chronic blood loss anemia, liver disease, lymphoma, metastatic cancer, solid tumor without metastases, paralysis, psychoses and peptic ulcer disease. We assessed rurality of each patient’s zip code of residence using the US Department of Agriculture’s Rural/Urban Commuting Area (RUCA) Codes, grouped into categories of “urban core areas,” “suburban areas,” “large town areas,” and “small town/isolated rural areas” (40 , 41 ). Index hospital characteristics, including Medicare geographic region, for-profit status and medical school affiliation, were drawn from the Medicare provider of services file corresponding to the patient’s index hospitalization date (42 ). We estimated annual Medicare discharge volume for each hospital by multiplying the number of claims from each hospital in the 5% national sample, by 20. We then grouped hospitals into low, middle and high volume tertiles. About one percent of our sample was missing race data (n=291), and less than 3% were missing hospital medical school affiliation (n=777) and for-profit status (n=777). There were no missing data for other patient-level variables.
Publication 2014
Abuse, Alcohol Anemia Blood Vessel Collagen Collagen Diseases Disabled Persons Gender Hemorrhage Hospitalization Inpatient Liver Diseases Lymphoma Neoplasm Metastasis Outpatients Patient Discharge Patient Readmission Patients Peptic Ulcer Physicians Psychotic Disorders Rheumatoid Arthritis Vascular Diseases
Outbred Ekkwill strain (EK) or EK/AB mixed background zebrafish 6–12 months of age were used for ventricular resection surgeries as described previously4 (link). All transgenic strains were analyzed as hemizygotes; details of their construction are described in the separate Methods section. Animal density was maintained at ~4 fish/liter in all experiments. 4-hydroxytamoxifen (4-HT) (Sigma) dissolved with ethanol (5 mg/ml) was diluted in water to 0.5 mg/ml for intraperitoneal injections. 10% ethanol was used as a vehicle control. EGFP labeling quantification is described in the separate Methods section. Heat-shock experiments were performed as described previously27 (link), using double transgenic hsp70:dnfgfr1; cmlc2:nucDsRed2 or hsp70:dnfgfr1; gata4:EGFP animals. For BrdU incorporation experiments, 2.5 mg/ml BrdU (Sigma) was injected intraperitoneally once daily for 3 days prior to collection. Immunofluorescence, in situ hybridization, and Acid Fuchsin Orange G stains (detecting fibrin and collagen) were performed as described previously4 (link). Primary antibodies used in this study were: anti-Mef2 (rabbit; Santa Cruz Biotechnology), anti-Myosin heavy chain (F59, mouse; Developmental Studies Hybridoma Bank), anti-β-catenin (rabbit; Sigma), anti-zf Raldh2 (rabbit: Abmart), anti-BrdU (rat; Accurate), and anti-GFP (rabbit, used only for co-detection with BrdU; Invitrogen). Secondary antibodies (Invitrogen) used in this study were Alexa Fluor 594 goat anti-rabbit IgG (H+L) for anti-Mef2, Alexa Fluor 594 goat anti-mouse IgG (H+L) for F59, Alexa Fluor 594 goat anti-rat IgG (H+L) for anti-BrdU, and Alexa Fluor 488 goat anti-rabbit IgG (H+L) for anti-GFP. In situ hybridization and immunofluorescence images were taken using a Leica DM6000 microscope with a Retiga-EXi camera (Q-IMAGING), and confocal images were taken using a Leica SP2 or SP5 confocal microscope. Physiology methods are described in the separate Methods section.
Publication 2010
acid-fuchsin afimoxifene ALDH1A2 protein, human Alexa594 alexa fluor 488 Animals Animals, Transgenic anti-IgG Antibodies Bromodeoxyuridine Collagen CTNNB1 protein, human Ethanol Fibrin Fishes Fluorescent Antibody Technique Goat Heart Ventricle Heat-Shock Proteins 70 Heat-Shock Response Hemizygote Hybridomas Injections, Intraperitoneal In Situ Hybridization Mice, House Microscopy Microscopy, Confocal Myosin Heavy Chains Operative Surgical Procedures Orange G physiology Rabbits Staining Strains Zebrafish

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Publication 2010
Bath Calcium Calcium Sulfate, Anhydrous Collagen Collagen Type I Dentin Enzymes Hydrolysis Hydroxyproline Matrix Metalloproteinases Pellets, Drug Peptide Fragments Sodium Hydroxide Vacuum Zinc
Sodium bisulfite treatment on DNA and subsequent real-time PCR (MethyLight [30] (link)) was validated and performed as previously described [31] (link). We quantified DNA methylation in 5 CIMP-specific promoters (CACNA1G, IGF2, NEUROG1, RUNX3 and SOCS1) and 11 other CpG islands [CDKN2A (p16), CHFR, CRABP1, HIC1, IGFBP3, MGMT, MINT1, MINT31, MLH1, p14 (CDKN2A/ARF), and WRN]. COL2A1 (the collagen 2A1 gene) was used to normalize for the amount of template bisulfite-converted DNA [31] (link). Primers and probes were previously described [15] (link), [27] (link), except for IGFBP3, p14 and WRN: IGFBP3-F, 5′-GTT TCG GGC GTG AGT ACG A-3′ (Genbank No. M35878, nucleotide Nos. 1692-1710); IGFBP3-R, GAA TCG ACG CAAACA CGA CTA C(nucleotide Nos. 1789-1810) and IGFBP3-probe, 6FAM-TCG GTT GTT TAG GGC GAA GTA CGG G-BHQ-1(nucleotide Nos. 1760-1784) (bisulfite-converted nucleotides are highlighted by bold face and italics); P14 (CDKN2A/ARF)-F, 5′- TTG GAG GCG GCG AGA ATA T-3′ (Genbank No. L41934, nucleotide Nos. 238-256); P14-R, 5′- CCC CGT AAA CCG CGAAAT A-3′ (nucleotide Nos. 332-350); P14-probe, 6FAM-5′- CGG TTC GTC GCG AGT GAG GGT T-3′ –BHQ-1 (nucleotide Nos. 299-320); WRN-F, 5′-GTA TCG TTC GCG GCG TTT AT-3′ (Genbank No. AY442327, nucleotide Nos. 1827-1846); WRN-R, 5′-ACG AAA CCG ATA TCC GAA ATC A -3′ (nucleotide Nos. 1887-1908) and WRN-probe, 6FAM-TTTTTTTTG CGG TCG TTG CGG G-BHQ-(nucleotide Nos. 1855-1876). The PCR condition was initial denaturation at 95°C for 10 min followed by 45 cycles of 95°C for 15 sec and 60°C for 1 min. A standard curve was made for each PCR plate by duplicated PCR amplifications for COL2A1 on bisulfite-converted human genomic DNA at 4 different concentrations (in a 5-fold dilution series). The percentage of methylated reference (PMR, i.e., degree of methylation) at a specific locus was calculated by dividing the GENE:COL2A1 ratio of template amounts in a sample by the GENE:COL2A1 ratio of template amounts in SssI-treated human genomic DNA (presumably fully methylated) and multiplying this value by 100. Methylation positivity was set as PMR≥4 as previously validated [31] (link).
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Publication 2008
CDKN2A Gene Collagen CpG Islands CRABP1 protein, human DNA Methylation Face Genes Genome, Human hydrogen sulfite IGFBP3 protein, human insulin-like growth factor 2, human Methylation MLH1 protein, human NEUROG1 protein, human Nucleotides O(6)-Methylguanine-DNA Methyltransferase Oligonucleotide Primers Real-Time Polymerase Chain Reaction sodium bisulfite Technique, Dilution

Most recents protocols related to «Collagen»

Example 14

Variables tested include: concentration of HA, concentration of zinc oxide, concentration of titanium dioxide, addition of vitamin C, and serum preparation method.

FIGS. 94A-94C are tables summarizing embodiments of cosmetic serums of the present disclosure with varying additives and concentrations of components suitable for protection against ultraviolet radiation (UV). Table 33 provides an embodiment of a hydrating serum of the present disclosure with vitamin C.

TABLE 33
Embodiment of Hydrating serum of
the present disclosure with vitamin C
% Silk Solution  1.0% w/v
(60 minute boil, 25 kDA)
Hyaluronic Acid 0.75% w/v
(sodium hyaluronate)
Lemongrass Oil20 uL/15 mL
silk solution
Sodium Ascorbyl Phosphate  6 g
Lactic Acid1.2 mL

A serum of the present disclosure can be made with from about 0.25% to about 10% sodium hyaluronate (increasing % results in more viscous serum). 0.5% to about 10% silk solutions can be used to prepare a serum of the present disclosure. A serum of the present disclosure can be clear and have a yellow tinted color. A serum of the present disclosure can have a pH=6. A serum of the present disclosure can have a lubricious texture that is rubbed in easily without residue.

Concentration of HA:

Hyaluronic acid (Sodium Hyaluronate) was tested as an ingredient in the UV silk serum due to its hygroscopic properties and widely accepted use in cosmetic products to promote hydration of skin. 1%, 2.5% and 5% HA solutions were tested. With increasing HA %, the serum became more viscous and gel like. 1% HA was not feasible for the UV serum due to the fact that the UV additives (zinc oxide, titanium dioxide) are not water soluble and need to be dispersed. 1% HA was not viscous enough for dispersion and the UV additives precipitated out. 2.5% gave the best consistency based on preferred feel, texture and viscosity and was able to disperse the UV additives. 5% was a very thick, viscous serum.

Concentration of Mineral Filters: Zinc Oxide and Titanium Dioxide:

Zinc oxide and titanium dioxide were explored as UV additives that are considered safe. These additives mechanically protect from UV radiation by forming a physical reflective barrier on the skin. Both are not soluble in water and must be dispersed for the current aqueous solution. Zinc oxide concentration varied from 2.5%, 3.75%, 5%, 5.625%, 10%, 12% and 15%. Titanium dioxide concentrations varied from 1.25%, 1.875%, 3%, 5% and 10%. Increasing the concentration of UV additives resulted in minor increases of white residue and how well dispersed the additives were, however if mixed well enough the effects were negligible. Zinc oxide and titanium dioxide were mixed together into serums in order to achieve broad spectrum protection. Zinc oxide is a broad spectrum UV additive capable of protecting against long and short UV A and UV B rays. However titanium dioxide is better at UV B protection and often added with zinc oxides for best broad spectrum protection. Combinations included 3.75%/1.25% ZnO/TiO2, 5.625%/1.875% ZnO/TiO2, 12%/3% ZnO/TiO2, 15%/5% ZnO/TiO2. The 3.75%/1.25% ZnO/TiO2 resulted in spf 5 and the 5.625%/1.875% ZnO/TiO2 produced spf 8.

Vitamin C:

Sodium ascorbyl phosphate was used as a vitamin C source. Formulations were created with the vitamin C concentration equal to that in the silk gel (0.67%). Formulations were also created with 20% sodium ascorbyl phosphate which is soluble in water.

Serum Preparation:

The vitamin C (sodium ascorbyl phosphate) must first be dissolved in water. Sodium hyaluronate is then added to the water, mixed vigorously and left to fully dissolve. The result is a viscous liquid (depending on HA %). The viscosity of the HA solution allows even dispersion of the zinc oxide and titanium dioxide and therefore HA must be mixed before addition of UV additives. The zinc oxide and titanium dioxide are then added to the solution and mixed vigorously with the use of an electric blender. Silk solution is then added and mixed to complete the serum formulation.

Chemical Filters:

A UV serum of the present disclosure can include one, or a combination of two or more, of these active chemical filter ingredients: oxybenzone, avobenzone, octisalate, octocrylene, homosalate and octinoxate. A UV serum of the present disclosure can also include a combination of zinc oxide with chemical filters.

In an embodiment, a UV serum of the present disclosure can be applied approximately 15 minutes before sun exposure to all skin exposed to sun, and can be reapplied at least every 2 hours. In an embodiment, a UV serum of the present disclosure includes water, zinc oxide, sodium hyaluronate, titanium dioxide, silk, and vitamin C or a vitamin C derivative such as sodium ascorbyl phosphate. In an embodiment, a UV serum of the present disclosure protects skin and seals in moisture with the power of silk protein. In an embodiment, a UV serum of the present disclosure improves skin tone, promotes collagen production and diminishes the appearance of wrinkles and fine lines with the antioxidant abilities of vitamin C. In an embodiment, a UV serum of the present disclosure delivers moisture for immediate and long-term hydration throughout the day with concentrated hyaluronic acid. In an embodiment, a UV serum of the present disclosure helps prevent sunburn with the combined action of zinc oxide and titanium dioxide. In an embodiment, a UV serum of the present disclosure is designed to protect, hydrate, and diminish fine lines while shielding skin from harsh UVA and UVB rays. In an embodiment, the silk protein in a UV serum of the present disclosure stabilizes and protects skin while sealing in moisture, without the use of harsh chemical preservatives or synthetic additives. In an embodiment, the vitamin C/derivative in a UV serum of the present disclosure acts as a powerful antioxidant that supports skin rejuvenation. In an embodiment, the sodium hyaluronate in a UV serum of the present disclosure nourishes the skin and delivers moisture for long-lasting hydration. In an embodiment, the zinc oxide and titanium dioxide in a UV serum of the present disclosure shields skin from harmful UVA and UVB rays. The silk protein stabilization matrix in a UV serum of the present disclosure protects the active ingredients from the air, to deliver their full benefits without the use of harsh chemicals or preservatives. The silk matrix also traps moisture within the skin furthering the hydrating effect of the sodium hyaluronate.

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Patent 2024
Acids Antioxidants Ascorbic Acid avobenzone Collagen Electricity Feelings Figs Furuncles homosalate Hyaluronic acid Minerals octinoxate octisalate octocrylene oxybenzone Pharmaceutical Preservatives Proteins Radiation Rejuvenation SERPINA3 protein, human Serum Serum Proteins Silk Skin Skin Pigmentation sodium ascorbyl phosphate Sodium Hyaluronate Strains Sunburn titanium dioxide Viscosity Vitamin A Vitamins west indian lemongrass oil Zinc Oxide

Example 6

Exemplary capsule shell and matrix compositions useful for producing Liquisoft capsules as described herein are shown in Table 8. Composition components are set forth by weight percentage of the total weight of the composition. Such compositions may be encapsulated using rotary die encapsulation as described herein.

Formula 10 was revised to increase the amount of water to 20%, resulting in Formula 11. Formula 11 was encapsulated, but was further revised to reduce the viscosity. Hence, Formula 12 was developed whereby the amount of water was increased to 22% and the total amount of gelatin was limited to 31% resulting in a viscosity of approximately 4300 cP. Formula 12 was used for GMP batch manufacturing to evaluate the combination product.

TABLE 8
Exemplary Liquisoft Composition
Capsule Shell Formulation
ComponentFormula 11Formula 12
Gelatin, 250 Bloom
Gelatin, 150 Bloom22.7 18.9 
Gelatin, 100 Bloom9.78.1
Gelatin Hydrolysate5.05.1
Hydrolyzed Collagen
Powdered Cellulose
Maltitol16.3 16.3 
Glycerol19.7 23.3 
Xylitol5.02.5
Mannitol
Sucralose0.20.2
Citric Acid0.50.5
Glycine
Flavors0.50.5
Water20.2 24.8 
TOTAL100%100%
VISCOSITY13,226 cP4,341 cP

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Patent 2024
Capsule Cellulose Citric Acid Collagen Flavor Enhancers Gelatins Glycerin Glycine maltitol Mannitol sucralose Viscosity Xylitol
Not available on PMC !

Example 5

10 women were surveyed using The Yale Visual Analogue Scale before and after using the vaginal care composition. The women rated their experience on dryness and pain from 0-10 (0 being no dryness/no pain; 10 being most dry/most painful).

The following inclusion and exclusion criteria were used in selecting the subjects: Perimenopausal and menopausal women, women showing symptoms of vulvovaginal dryness, women showing symptoms of painful sex due to dryness or atrophy, women with no treatments of symptoms for the past year, women with no use of estrogen based devices, and women with no use of vaginal Hyaluronic acid (HA), collagen, platelet-rich plasma (prp), carboxytherapy in the past year were included in the study. In contrast, women who received treatments for vaginal dryness or pain symptoms for past year, women who used estrogens locally, women who used vaginal HA, collagen, prp, or carboxytherapy in the past year were excluded from the study.

The subjects intra-vaginally applied intra-vaginal capsules comprising 5 mg exosomes, mg L-carnosine, and 75 mg magnesium citrate twice a week for 60 days.

Results: Women included in the study reported a significant decrease in vaginal dryness (FIG. 3A) and vaginal pain (FIG. 3B) when they used the vaginal care composition for 60 days.

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Patent 2024
Administration, Intravaginal Atrophy Capsule Carnosine Collagen Day Care, Medical Estrogens Exosomes Hyaluronic acid Magnesium magnesium citrate Medical Devices Menopause Pain Platelet-Rich Plasma Vagina Visual Analog Pain Scale Woman
Not available on PMC !

Example 6

IL-17RA inhibition was also shown to be effective in a CIA model when dosing was initiated after the onset of clinical signs (i.e. therapeutic dosing protocol) in a wild-type and TNFR p55/p75 KO model. Treatment was initiated approximately 6-7 days post collagen introduction in both models. FIG. 10 shows that therapeutic treatment with anti-IL-17RA mAb stabilized mean clinical scores in both wild-type mice. FIG. 11 shows that therapeutic treatment with anti-IL-17RA mAb stabilized mean clinical scores in TNFR p55/p75 KO models. Mice were treated with either an anti-IL-17RA mAb, anti-IL-1R mAb, or control Ig on a Monday, Wednesday and Friday schedule for 2 weeks post randomization into therapeutic treatment groups. These data are representative of 2 independent experiments performed in both WT and TNFR p55/p75 KO CIA models. Administering anti-IL-17RA mAbs showed a reduced clinical score as compared to control IgG in CIA induced wild-type mice. Surprisingly, the similar efficacy of anti-IL-17RA mAbs in the TNF p55/p75 KO model stabilized CIA independently of TNF signaling. This data suggests anti-IL-17RA antigen binding protein therapy may pick up non-responders to anti-TNF therapies. Combination therapy of an anti-IL-17RA antigen binding protein with anti-TNF therapies may be more beneficial than either alone.

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Patent 2024
Antigens Binding Proteins Collagen Combined Modality Therapy Group Therapy IL17RA protein, human Monoclonal Antibodies Mus Proteins Psychological Inhibition Receptors, Interleukin-17 Receptors, Tumor Necrosis Factor, Type II

Example 5

Exemplary capsule shell and matrix compositions useful for producing Liquisoft capsules as described herein are shown in Table 7. Composition components are set forth by weight percentage of the total weight of the composition. Such compositions may be encapsulated using rotary die encapsulation as described herein.

The composition of Formulas 8, 9, and 10 included increased amounts of 100 Bloom gelatin to minimize shell toughness. As seen in Table 7, increased amounts of 100 Bloom gelatin resulted in decreased viscosity but encapsulation was unsuccessful. Formula 10 was revised further.

TABLE 7
Exemplary Liquisoft Composition
Capsule Shell Formulation
ComponentFormula 8Formula 9Formula 10
Gelatin, 250 Bloom
Gelatin, 150 Bloom14.218.719.8
Gelatin, 100 Bloom14.212.513.1
Gelatin Hydrolysate 4.9 4.9 5.2
Hydrolyzed Collagen
Powdered Cellulose
Maltitol15.716.718.8
Glycerol18.920.220.6
Xylitol 0.5 0.5 5.2
Mannitol
Sucralose 0.5 0.5 0.2
Citric Acid 0.5 0.2 0.5
Glycine
Flavors
Water30.625.816.6
TOTAL100%100%100%
VISCOSITY2,628 cP1,899 cP8,376 cP

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Patent 2024
Capsule Cellulose Citric Acid Collagen Flavor Enhancers Gelatins Glycerin Glycine maltitol Mannitol sucralose Viscosity Vision Xylitol

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More about "Collagen"

Collagen is a ubiquitous structural protein found throughout the human body, particularly in the extracellular matrix of connective tissues like skin, bone, cartilage, and tendons.
This essential biomolecule provides strength, stability, and flexibility to these tissues, playing a crucial role in wound healing, cell signaling, and maintaining tissue integrity.
Collagen is the most abundant protein in mammals, comprising up to 30% of the total protein content.
There are over 28 different genetic types of collagen, with types I, II, and III being the most common.
Understanding the structure, function, and regulation of this versatile protein is a key area of biomedical research, with implications for a wide range of medical applications, including tissue engineering, regenerative medicine, and the treatment of collagen-related disorders.
Researchers investigating collagen often utilize various cell culture techniques and reagents, such as Fetal Bovine Serum (FBS), Penicillin/Streptomycin, and DMEM media, to maintain and study collagen-producing cells.
Additionally, molecular biology tools like the TRIzol reagent and RNeasy Mini Kit are commonly employed to extract and analyze collagen-related gene expression.
Imaging software like Image-Pro Plus 6.0 and Image-Pro Plus can be used to visualize and quantify collagen structures.
By leveraging the insights gained from the MeSH term description and the metadescription, researchers can optimize their collagen studies using innovative AI-driven platforms like PubCompare.ai.
This tool can help locate relevant protocols from the literature, preprints, and patents, and provide AI-driven comparisons to identify the best protocols and products, enhancing the reproducibility and accuracy of their collagen research.