Galactomyces Ferment Filtrate Potentiates an Anti-Inflammaging System in Keratinocytes
Open accessAbstract
Skincare products play a crucial role in preventing the dry skin induced by various causes. Certain ingredients can help to improve the efficacy of skincare products. Galactomyces ferment filtrate (GFF) is such a functional ingredient. Its use originated from the empirical observation that the hands of sake brewers who deal with yeast fermentation retain a beautiful and youthful appearance. Consequently, skincare products based on GFF are widely used throughout the world. Recent studies have demonstrated that GFF activates an aryl hydrocarbon receptor (AHR) and upregulates the expression of filaggrin, a pivotal endogenous source of natural moisturizing factors, in epidermal keratinocytes. It also activates nuclear factor erythroid-2-related factor 2 (NRF2), the antioxidative master transcription factor, and exhibits potent antioxidative activity against oxidative stress induced by ultraviolet irradiation and proinflammatory cytokines, which also accelerate inflammaging. GFF-mediated NRF2 activation downregulates the expression of CDKN2A, which is known to be overexpressed in senescent keratinocytes. Moreover, GFF enhances epidermal terminal differentiation by upregulating the expression of caspase-14, claudin-1, and claudin-4. It also promotes the synthesis of the antiinflammatory cytokine IL-37 and downregulates the expression of proallergic cytokine IL-33 in keratinocytes. In addition, GFF downregulates the expression of the CXCL14 and IL6R genes, which are involved in inflammaging. These beneficial properties might underpin the potent barrier-protecting and anti-inflammaging effects of GFF-containing skin formulae.
AI snapshot
Written from the paper’s full text.
TL;DR
This review synthesizes evidence that Galactomyces ferment filtrate (GFF), a cosmetic ingredient, acts as a dual agonist of AHR and NRF2 in keratinocytes, upregulating barrier proteins and antioxidative enzymes while downregulating inflammaging-related genes. The authors propose GFF as an antioxidative cosmetic AHR-modulating agent with barrier-protecting and anti-inflammaging properties.
Key findings
- GFF activates AHR, driving nuclear translocation and upregulating filaggrin and loricrin; this is AHR-dependent since knockdown of AHR abrogates filaggrin induction, and GFF counteracts IL-4/IL-13-mediated downregulation of filaggrin and loricrin.
- GFF induces NRF2 nuclear translocation and upregulates GPX2, NQO1, and HMOX1; it ameliorates TNF-α-, UVB-, and IL-13-induced ROS production in keratinocytes. GFF-induced CDKN2A (p16INK4A) downregulation is NRF2-dependent, and AHR knockdown partially ameliorates GFF-NRF2-mediated NQO1 induction.
- GFF upregulates caspase-14 and tight-junction molecules (claudin-1, claudin-4, occludin, ZO-1), enhancing cell–cell attachment and permeability barrier as measured by increased transepithelial electric resistance (TER); claudin-1/4 upregulation appears AHR-independent.
- GFF upregulates antiinflammatory IL-37 in an AHR-dependent manner, which downregulates proallergic IL-33 (cancelled by AHR or IL-37 knockdown), and downregulates CXCL14 and IL6R genes linked to inflammaging.
Methods
This is a narrative review; no primary experiments are reported. It synthesizes prior in vitro studies of GFF-treated human keratinocytes (and some melanocyte/sebocyte data) examining AHR, NRF2, filaggrin, caspase-14, claudins, IL-37/IL-33, CXCL14, and IL6R, alongside referenced clinical trials of GFF-containing moisturizers and of therapeutic AHR-modulating agents (tapinarof, coal tar, glyteer).
Limitations
The authors state that the in-depth cellular mechanisms of GFF activity have not been fully elucidated in keratinocytes, and that the biological significance of GFF in melanocytes and sebocytes remains unclear. Evident from the text: this is a review without new primary data, and several mechanistic claims rest on cited prior studies rather than experiments performed here; the physiological relevance of caspase-14 upregulation is described as uncertain.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
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Cites
Statistics
Claims the paper makes
19 of 50 cited sources checked · 9 supported · 0 flagged · accuracy not yet measured
- Premisecitation
GFF activates the aryl hydrocarbon receptor (AHR).
“Recent studies have demonstrated that GFF activates an aryl hydrocarbon receptor (AHR)”
- Also stated in: § 2. Moisturizers and Their Ingredients · boosted
“it has been demonstrated to operate as a potent antioxidative AHR agonist [10,55,56].”
Quote in the paperSubstantial claim1 of 3 sources checked- cites [10] Furue, M., Uchi, H., Mitoma, C., Hashimoto-Hachiya, A., Chiba, T., Ito, T., Nakahara, T., and Tsuji, G. (2017). Antioxidants for healthy skin: The emerging role of aryl hydrocarbon receptors and nuclear factor-erythroid 2-related factor-2. Nutrients, 9. source
- cites [55] Takei, 2015, Galactomyces fermentation filtrate prevents T helper 2-mediated reduction of filaggrin in an aryl hydrocarbon receptor-dependent manner, Clin. Exp. Dermatol. source
- cites [56] Tsuji, 2019, Antioxidants cinnamaldehyde and Galactomyces fermentation filtrate downregulate senescence marker CDKN2A/p16INK4A via NRF2 activation in keratinocytes, J. Dermatol. Sci. source
- Also stated in: § 2. Moisturizers and Their Ingredients · boosted
- Premisecitation
GFF operates as a potent antioxidative AHR agonist.
“it has been demonstrated to operate as a potent antioxidative AHR agonist [10,55,56].”
Quote in the paperNot a substantial claim1 of 3 sources checked- cites [10] Furue, M., Uchi, H., Mitoma, C., Hashimoto-Hachiya, A., Chiba, T., Ito, T., Nakahara, T., and Tsuji, G. (2017). Antioxidants for healthy skin: The emerging role of aryl hydrocarbon receptors and nuclear factor-erythroid 2-related factor-2. Nutrients, 9. source
Section 4.2.2 describes Galactomyces fermentation filtrate (GFF) as an AHR stimulant. It reports antioxidant activity when GFF is combined with epigallocatechin gallate, but does not describe GFF alone as potently antioxidative or quantify its AHR-agonist potency. (LLM, conf=0.86)
Experimental — accuracy not yet measured - cites [55] Takei, 2015, Galactomyces fermentation filtrate prevents T helper 2-mediated reduction of filaggrin in an aryl hydrocarbon receptor-dependent manner, Clin. Exp. Dermatol. source
- cites [56] Tsuji, 2019, Antioxidants cinnamaldehyde and Galactomyces fermentation filtrate downregulate senescence marker CDKN2A/p16INK4A via NRF2 activation in keratinocytes, J. Dermatol. Sci. source
- Premisecitation
GFF upregulates the expression of the SLPI gene.
“Notably, it is reported that GFF upregulated the expression of the SLPI gene [81].”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [81] Nakajima, A., Sakae, N., Yan, X., Hakozaki, T., Zhao, W., Laughlin, T., and Furue, M. (2022). Transcriptomic analysis of human keratinocytes treated with Galactomyces ferment filtrate, a beneficial cosmetic ingredient. J. Clin. Med., 11. source
- Premisecitation
GFF significantly ameliorates TNF-α-induced production of ROS in human keratinocytes.
“GFF significantly ameliorates both TNF-α-induced [10] and UVB-induced [76] production of ROS in human keratinocytes.”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [10] Furue, M., Uchi, H., Mitoma, C., Hashimoto-Hachiya, A., Chiba, T., Ito, T., Nakahara, T., and Tsuji, G. (2017). Antioxidants for healthy skin: The emerging role of aryl hydrocarbon receptors and nuclear factor-erythroid 2-related factor-2. Nutrients, 9. source
Section 4.2.2 (page unavailable) reports that Galactomyces fermentation filtrate (GFF) and epigallocatechin gallate have synergistic antioxidant activity against TNF-α-induced ROS production. It does not establish that GFF alone significantly reduces that production in human keratinocytes. (LLM, conf=0.83)
Experimental — accuracy not yet measured
- Premisecitation
GFF upregulates IL-37 expression in human keratinocytes in an AHR-dependent fashion.
“Notably, GFF upregulated IL-37 expression in human keratinocytes in an AHR-dependent fashion [116] (Figure 2).”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [116] Tsuji, 2022, Natural compounds tapinarof and Galactomyces ferment filtrate downregulate IL-33 via the AHR/IL-37 axis in human keratinocytes, Front. Immunol. source
- Premisecitation
Mask-induced exacerbation of fluctuations in redness and pore size is ameliorated by topical treatment with GFF.
“Mask-induced exacerbation of fluctuations in redness and pore size is also ameliorated by topical treatment with GFF [54].”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [54] Miyamoto, K., Munakata, Y., Yan, X., Tsuji, G., and Furue, M. (2022). Enhanced fluctuations in facial pore size, redness, and TEWL caused by mask usage are normalized by the application of a moisturizer. J. Clin. Med., 11. source
The Results report that a GFF-containing moisturizer significantly improved mask-related fluctuations in pore size and redness. The Discussion cautions that the study could not determine whether this effect was due to GFF itself or to moisturization, so it does not establish an effect of GFF alone. (LLM, conf=0.86)
Experimental — accuracy not yet measured
- Premisecitation
GFF-induced IL-37 downregulates the expression of IL-33 in keratinocytes.
“The GFF-induced IL-37 is biologically active, because it downregulates the expression of IL-33 in keratinocytes [116].”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [116] Tsuji, 2022, Natural compounds tapinarof and Galactomyces ferment filtrate downregulate IL-33 via the AHR/IL-37 axis in human keratinocytes, Front. Immunol. source
- Premisecitation
The GFF-AHR-IL-37-induced downregulation of IL-33 is canceled by knockdown of either AHR or IL-37.
“Moreover, the GFF-AHR-IL-37-induced downregulation of IL-33 is canceled by the knockdown of either AHR or IL-37 [116].”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [116] Tsuji, 2022, Natural compounds tapinarof and Galactomyces ferment filtrate downregulate IL-33 via the AHR/IL-37 axis in human keratinocytes, Front. Immunol. source
The Results section ('Inhibitory Effect of Tapinarof and GFF Treatment on IL-33 Expression') reports that knockdown of either IL-37 or AHR partially reversed GFF-induced downregulation of IL-33 protein in human keratinocytes. The claim omits 'partially' and therefore overstates the extent of cancellation. Page numbers are not provided in our copy. (LLM, conf=0.90)
Experimental — accuracy not yet measured
- Premisecitation
GFF downregulates the expression of the IL6R gene.
“GFF also downregulated the expression of the IL6R gene for the interleukin-6 receptor [81].”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [81] Nakajima, A., Sakae, N., Yan, X., Hakozaki, T., Zhao, W., Laughlin, T., and Furue, M. (2022). Transcriptomic analysis of human keratinocytes treated with Galactomyces ferment filtrate, a beneficial cosmetic ingredient. J. Clin. Med., 11. source
- Premisecitation
GFF strongly inhibits the expression of the CXCL14 gene in keratinocytes.
“GFF was proved to strongly inhibit the expression of the CXCL14 gene for the chemokine (C-X-C motif) ligand 14 in keratinocytes [81].”
Quote in the paperSubstantial claim1 of 1 sources checked- cites [81] Nakajima, A., Sakae, N., Yan, X., Hakozaki, T., Zhao, W., Laughlin, T., and Furue, M. (2022). Transcriptomic analysis of human keratinocytes treated with Galactomyces ferment filtrate, a beneficial cosmetic ingredient. J. Clin. Med., 11. source
- Premisecitation
GFF upregulates the expression of GPX2, NQO1, and HMOX1.
“In addition to its AHR-stimulating properties, GFF induces nuclear translocation of NRF2 in the cytoplasm (Figure 3) and upregulates the expression of GPX2, NQO1, and HMOX1 [10,56,74,76,77].”
Quote in the paperSubstantial claim2 of 5 sources checked- cites [10] Furue, M., Uchi, H., Mitoma, C., Hashimoto-Hachiya, A., Chiba, T., Ito, T., Nakahara, T., and Tsuji, G. (2017). Antioxidants for healthy skin: The emerging role of aryl hydrocarbon receptors and nuclear factor-erythroid 2-related factor-2. Nutrients, 9. source
Section 4.2.2 describes Galactomyces fermentation filtrate (GFF) as an AHR stimulant and reports antioxidant activity when it is combined with epigallocatechin gallate. Section 3 identifies NQO1 and HO-1 as NRF2-regulated enzymes, but neither section says GFF upregulates GPX2, NQO1, or HMOX1. Searches for GFF with those gene names found no passage establishing the claimed effect. (LLM, conf=0.76)
Experimental — accuracy not yet measured - cites [56] Tsuji, 2019, Antioxidants cinnamaldehyde and Galactomyces fermentation filtrate downregulate senescence marker CDKN2A/p16INK4A via NRF2 activation in keratinocytes, J. Dermatol. Sci. source
- cites [74] Fuyuno, 2018, Perillaldehyde inhibits AHR signaling and activates NRF2 antioxidant pathway in human keratinocytes, Oxid. Med. Cell Longev. source
The Results (section 3.4; page not provided) report that perillaldehyde (PAH) upregulated HO1 expression in human keratinocytes. Our copy does not report an effect of GFF on GPX2, NQO1, or HMOX1; searches for GFF and those genes found no passage addressing the attributed claim. (LLM, conf=0.76)
Experimental — accuracy not yet measured - cites [76] Takei, 2014, Galactomyces ferment filtrate (Pitera) inhibits UVB-induced ROS production by Ahr/NRrf2/Nqo1 signaling, Aesthet, Dermatol.
Not checked in the free run.
- cites [77] Cooper, 2019, Galactomyces ferment filtrate suppresses reactive oxygen species generation and promotes cellular redox balance in human melanocytes via Nrf2-ARE pathway, J. Clin. Cosmet. Dermatol.
Not checked in the free run.
- Premisecitation
Mask usage aggravates intraday fluctuations in facial skin conditions.
“Mask usage aggravates intraday fluctuations in these facial skin conditions [54].”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [54] Miyamoto, K., Munakata, Y., Yan, X., Tsuji, G., and Furue, M. (2022). Enhanced fluctuations in facial pore size, redness, and TEWL caused by mask usage are normalized by the application of a moisturizer. J. Clin. Med., 11. source
- Premisecitation
GFF induces nuclear translocation of NRF2 in keratinocytes.
“In addition to its AHR-stimulating properties, GFF induces nuclear translocation of NRF2 in the cytoplasm (Figure 3) and upregulates the expression of GPX2, NQO1, and HMOX1 [10,56,74,76,77].”
Quote in the paperSubstantial claim2 of 5 sources checked- cites [10] Furue, M., Uchi, H., Mitoma, C., Hashimoto-Hachiya, A., Chiba, T., Ito, T., Nakahara, T., and Tsuji, G. (2017). Antioxidants for healthy skin: The emerging role of aryl hydrocarbon receptors and nuclear factor-erythroid 2-related factor-2. Nutrients, 9. source
Section 3 describes NRF2 translocation to the nucleus generally. Section 4.2.2 describes Galactomyces fermentation filtrate (GFF) as an AHR stimulant and reports antioxidant activity when it is combined with epigallocatechin gallate, but does not say GFF induces NRF2 nuclear translocation in keratinocytes. Searched for GFF, its full name, and NRF2 translocation. (LLM, conf=0.74)
Experimental — accuracy not yet measured - cites [56] Tsuji, 2019, Antioxidants cinnamaldehyde and Galactomyces fermentation filtrate downregulate senescence marker CDKN2A/p16INK4A via NRF2 activation in keratinocytes, J. Dermatol. Sci. source
- cites [74] Fuyuno, 2018, Perillaldehyde inhibits AHR signaling and activates NRF2 antioxidant pathway in human keratinocytes, Oxid. Med. Cell Longev. source
Results §3.4 reports NRF2 translocation from the cytoplasm into the nucleus in keratinocytes stimulated with PAH (perillaldehyde). It does not report this effect for GFF, the agent named in the claim. No page number is available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measured - cites [76] Takei, 2014, Galactomyces ferment filtrate (Pitera) inhibits UVB-induced ROS production by Ahr/NRrf2/Nqo1 signaling, Aesthet, Dermatol.
Not checked in the free run.
- cites [77] Cooper, 2019, Galactomyces ferment filtrate suppresses reactive oxygen species generation and promotes cellular redox balance in human melanocytes via Nrf2-ARE pathway, J. Clin. Cosmet. Dermatol.
Not checked in the free run.
- Findingown data
GFF inhibits IL-13-induced ROS production in keratinocytes.
“IL-13-induced ROS production in keratinocytes is also inhibited by GFF (Figure 4).”
Quote in the paperSubstantial claim - Premisecitation
GFF significantly ameliorates UVB-induced production of ROS in human keratinocytes.
“GFF significantly ameliorates both TNF-α-induced [10] and UVB-induced [76] production of ROS in human keratinocytes.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [76] Takei, 2014, Galactomyces ferment filtrate (Pitera) inhibits UVB-induced ROS production by Ahr/NRrf2/Nqo1 signaling, Aesthet, Dermatol.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Premisecitation
GFF significantly decreases CDKN2A expression in keratinocytes.
“In contrast, GFF significantly decreases CDKN2A expression in keratinocytes [56].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [56] Tsuji, 2019, Antioxidants cinnamaldehyde and Galactomyces fermentation filtrate downregulate senescence marker CDKN2A/p16INK4A via NRF2 activation in keratinocytes, J. Dermatol. Sci. source
- Interpretationcitation
The GFF-mediated upregulation of claudin-1 and claudin-4 is independent of AHR activation.
“These results indicate that the GFF-mediated upregulation of claudin-1 and claudin-4 is independent of AHR activation.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [55] Takei, 2015, Galactomyces fermentation filtrate prevents T helper 2-mediated reduction of filaggrin in an aryl hydrocarbon receptor-dependent manner, Clin. Exp. Dermatol. source
- Premisecitation
GFF strongly upregulates the expression of caspase-14 in keratinocytes.
“Notably, the expression of caspase-14 is strongly upregulated in GFF-treated keratinocytes [91] (Figure 2).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [91] Kataoka, 2013, Human keratinocyte caspase-14 expression is altered in human epidermal 3D models by dexamethasone and by natural products used in cosmetics, Arch. Dermatol. Res. source
- Premisecitation
GFF-induced NRF2 activation is observed in melanocytes.
“GFF-induced NRF2 activation is also observed in melanocytes [77] and, probably, in macrophages [86].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [77] Cooper, 2019, Galactomyces ferment filtrate suppresses reactive oxygen species generation and promotes cellular redox balance in human melanocytes via Nrf2-ARE pathway, J. Clin. Cosmet. Dermatol.
Not checked in the free run.
- Premisecitation
Upon GFF stimulation, activated AHR translocates from the cytoplasm into the nucleus in keratinocytes.
“Upon stimulation by GFF, activated AHR translocates into the nucleus from the cytoplasm (Figure 1), where it upregulates the expression of filaggrin [55].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [55] Takei, 2015, Galactomyces fermentation filtrate prevents T helper 2-mediated reduction of filaggrin in an aryl hydrocarbon receptor-dependent manner, Clin. Exp. Dermatol. source
- Interpretationnone given
GFF is a potent dual agonist for AHR and NRF2.
“GFF has since been shown to be a potent dual agonist for AHR and NRF2.”
Quote in the paperNot a substantial claim - Interpretationown data
GFF might ameliorate inflammaging by downregulating the expression of CXCL14 and IL6R.
“GFF might also ameliorate inflammaging by downregulating the expression of CXCL14 and IL6R.”
Quote in the paperSubstantial claim - Interpretationnone given
GFF increases the expression of caspase-14 and claudins, which are involved in epidermal terminal differentiation and tight-junction maturation.
“In addition, GFF increases the expression of caspase-14 and claudins, which are essentially involved in epidermal terminal differentiation and tight-junction maturation.”
Quote in the paperSubstantial claim - Premisecitation
GFF augments the permeability barrier, as assessed by an increase in TER.
“In parallel, GFF also enhances cell–cell attachment in cultured keratinocytes and augments the permeability barrier, as assessed by an increase in TER [100].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [100] Wong, 2011, Up-regulation of tight junction-related proteins and increase of human epidermal keratinocytes barrier function by Saccharomycosis ferment filtrate, J. Cosm. Dermatol. Sci. Appl.
Not checked in the free run.
- Premisecitation
GFF counteracts the IL-4-induced inhibition of loricrin expression.
“In addition to the upregulation of filaggrin, GFF upregulates the expression of loricrin and counteracts the IL-4-induced inhibition of loricrin expression [55].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [55] Takei, 2015, Galactomyces fermentation filtrate prevents T helper 2-mediated reduction of filaggrin in an aryl hydrocarbon receptor-dependent manner, Clin. Exp. Dermatol. source
- Premisecitation
UVB-induced ROS generation in melanocytes is alleviated in the presence of GFF.
“In parallel, UVB-induced ROS generation in melanocytes is alleviated in the presence of GFF [77].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [77] Cooper, 2019, Galactomyces ferment filtrate suppresses reactive oxygen species generation and promotes cellular redox balance in human melanocytes via Nrf2-ARE pathway, J. Clin. Cosmet. Dermatol.
Not checked in the free run.
- Premisecitation
The GFF-induced downregulation of CDKN2A is NRF2-dependent.
“Notably, the GFF-induced downregulation of CDKN2A is also NRF2-dependent.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [56] Tsuji, 2019, Antioxidants cinnamaldehyde and Galactomyces fermentation filtrate downregulate senescence marker CDKN2A/p16INK4A via NRF2 activation in keratinocytes, J. Dermatol. Sci. source
- Premisecitation
GFF-mediated filaggrin upregulation is AHR-dependent, as it is abrogated by AHR knockdown.
“GFF-mediated filaggrin upregulation is AHR-dependent because it is abrogated by the knockdown of AHR [55] (Figure 2).”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [55] Takei, 2015, Galactomyces fermentation filtrate prevents T helper 2-mediated reduction of filaggrin in an aryl hydrocarbon receptor-dependent manner, Clin. Exp. Dermatol. source
- Premisecitation
GFF enhances cell-cell attachment in cultured keratinocytes.
“In parallel, GFF also enhances cell–cell attachment in cultured keratinocytes and augments the permeability barrier, as assessed by an increase in TER [100].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [100] Wong, 2011, Up-regulation of tight junction-related proteins and increase of human epidermal keratinocytes barrier function by Saccharomycosis ferment filtrate, J. Cosm. Dermatol. Sci. Appl.
Not checked in the free run.
- Interpretationreasoning
GFF might be categorized as an antioxidative cosmetic AHR-modulating agent.
“As the biological and functional properties of GFF are similar to those of TAMA, GFF might be categorized as an antioxidative cosmetic AHR-modulating agent.”
Quote in the paperNot a substantial claim - Premisecitation
In GFF-treated melanocytes, the expression of HMOX1 and NQO1 is upregulated in an NRF2-mediated fashion.
“The expression of the antioxidative enzymes HMOX1 and NQO1 is upregulated in GFF-treated melanocytes in an NRF2-mediated fashion [77].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [77] Cooper, 2019, Galactomyces ferment filtrate suppresses reactive oxygen species generation and promotes cellular redox balance in human melanocytes via Nrf2-ARE pathway, J. Clin. Cosmet. Dermatol.
Not checked in the free run.
- Premisecitation
GFF upregulates the expression of filaggrin in epidermal keratinocytes.
“upregulates the expression of filaggrin, a pivotal endogenous source of natural moisturizing factors, in epidermal keratinocytes.”
- Also stated in: § 3. Activation of AHR-Filaggrin Axis by GFF · plain
“where it upregulates the expression of filaggrin [55].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [55] Takei, 2015, Galactomyces fermentation filtrate prevents T helper 2-mediated reduction of filaggrin in an aryl hydrocarbon receptor-dependent manner, Clin. Exp. Dermatol. source
- Also stated in: § 3. Activation of AHR-Filaggrin Axis by GFF · plain
- Premisecitation
GFF counteracts the IL-4- and IL-13-mediated downregulation of filaggrin expression.
“Notably, GFF is capable of counteracting the IL-4- and IL-13-mediated downregulation of filaggrin expression [55].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [55] Takei, 2015, Galactomyces fermentation filtrate prevents T helper 2-mediated reduction of filaggrin in an aryl hydrocarbon receptor-dependent manner, Clin. Exp. Dermatol. source
- Premisecitation
GFF upregulates the expression of loricrin.
“In addition to the upregulation of filaggrin, GFF upregulates the expression of loricrin and counteracts the IL-4-induced inhibition of loricrin expression [55].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [55] Takei, 2015, Galactomyces fermentation filtrate prevents T helper 2-mediated reduction of filaggrin in an aryl hydrocarbon receptor-dependent manner, Clin. Exp. Dermatol. source
- Interpretationreasoning
GFF-mediated downregulation of CXCL14 and IL6R might contribute to retardation of the progress of inflammaging in keratinocytes.
“Thus, GFF-mediated downregulation of CXCL14 and IL6R might contribute to a retardation of the progress of inflammaging in keratinocytes.”
Quote in the paperSubstantial claim
- May combine two claims. 9
- Classified as probably not a substantial claim. 1
May combine two claims.
PremisecitationTopical application of GFF PiteraTM improves intraday fluctuations in facial redness, skin roughness, and hair pore size.
“Clinical trials have also shown that the topical application of GFF Pitera™ improves intraday fluctuations in facial redness, skin roughness, and hair pore size [46].”
Quote in the paperNot a substantial claim1 of 1 sources checked- cites [46] Miyamoto, K., Dissanayake, B., Omotezako, T., Takemura, M., Tsuji, G., and Furue, M. (2021). Daily fluctuation of facial pore area, roughness and redness among young Japanese women; Beneficial effects of Galactomyces ferment filtrate containing antioxidative skin care formula. J. Clin. Med., 10. source
Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.
PremisecitationGFF-containing moisturizers increase skin hydration and reduce TEWL.
“GFF-containing moisturizers are capable of increasing skin hydration and reducing TEWL [46,54].”
Quote in the paperNot a substantial claim2 of 2 sources checked- cites [46] Miyamoto, K., Dissanayake, B., Omotezako, T., Takemura, M., Tsuji, G., and Furue, M. (2021). Daily fluctuation of facial pore area, roughness and redness among young Japanese women; Beneficial effects of Galactomyces ferment filtrate containing antioxidative skin care formula. J. Clin. Med., 10. source
The Discussion reports that the GFF-formulated product increased skin hydration in the study, and the Clinical Study Protocol describes measuring hydration at the cheek. Our copy does not report that the product reduced transepidermal water loss (TEWL); the TEWL mention found is in a reference title, not a finding of this study. (LLM, conf=0.88)
Experimental — accuracy not yet measured - cites [54] Miyamoto, K., Munakata, Y., Yan, X., Tsuji, G., and Furue, M. (2022). Enhanced fluctuations in facial pore size, redness, and TEWL caused by mask usage are normalized by the application of a moisturizer. J. Clin. Med., 11. source
May combine two claims.
PremisecitationGFF increases the expression of claudin-1, claudin-4, occludin, and ZO-1 in keratinocytes.
“Notably, GFF increases the expression of claudin-1, claudin-4, occludin, and ZO-1 in keratinocytes [55,81,100] (Figure 2).”
Quote in the paperSubstantial claim1 of 3 sources checked- cites [55] Takei, 2015, Galactomyces fermentation filtrate prevents T helper 2-mediated reduction of filaggrin in an aryl hydrocarbon receptor-dependent manner, Clin. Exp. Dermatol. source
- cites [81] Nakajima, A., Sakae, N., Yan, X., Hakozaki, T., Zhao, W., Laughlin, T., and Furue, M. (2022). Transcriptomic analysis of human keratinocytes treated with Galactomyces ferment filtrate, a beneficial cosmetic ingredient. J. Clin. Med., 11. source
The Results report that all three GFF lots significantly increased CLDN1 and CLDN4 gene expression in human keratinocytes (section 3; page unavailable). The paper does not report increased expression of occludin or ZO-1, so it supports only two of the four molecules named. (LLM, conf=0.90)
Experimental — accuracy not yet measured - cites [100] Wong, 2011, Up-regulation of tight junction-related proteins and increase of human epidermal keratinocytes barrier function by Saccharomycosis ferment filtrate, J. Cosm. Dermatol. Sci. Appl. source
Not checked in the free run.
May combine two claims.
PremisecitationGFF activates the AHR-NRF2 signaling pathway, because AHR knockdown partially ameliorates the GFF-NRF2-mediated induction of NQO1.
“GFF is also known to activate the AHR–NRF2 signaling pathway, because knockdown of AHR partially ameliorates the GFF-NRF2-mediated induction of NQO1 [76].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [76] Takei, 2014, Galactomyces ferment filtrate (Pitera) inhibits UVB-induced ROS production by Ahr/NRrf2/Nqo1 signaling, Aesthet, Dermatol.
Not checked in the free run.
May combine two claims.
PremisecitationGFF upregulates the expression of the antioxidative enzyme GPX2 in keratinocytes, and this upregulation is abrogated by NRF2 knockdown.
“GFF upregulates the expression of the antioxidative enzyme GPX2 in keratinocytes, which is abrogated by NRF2 knockdown [56].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [56] Tsuji, 2019, Antioxidants cinnamaldehyde and Galactomyces fermentation filtrate downregulate senescence marker CDKN2A/p16INK4A via NRF2 activation in keratinocytes, J. Dermatol. Sci. source
May combine two claims.
InterpretationreasoningThe GFF-AHR axis upregulates filaggrin production and induces antiinflammatory IL-37, with subsequent downregulation of proallergic IL-33.
“The GFF–AHR axis upregulates filaggrin production and induces the expression of antiinflammatory IL-37, with subsequent downregulation of the expression of proallergic IL-33.”
Quote in the paperSubstantial claimMay combine two claims.
InterpretationreasoningGFF is a functional moisturizing ingredient with TAMA-like activity.
“Considering its active AHR-stimulating potency, GFF is a functional moisturizing ingredient with TAMA-like activity.”
Quote in the paperSubstantial claimMay combine two claims.
InterpretationreasoningThe GFF-NRF2 axis provides a potent antioxidative effect and is probably beneficial in preventing inflammaging, partly through downregulation of CDKN2A.
“The GFF–NRF2 axis provides a potent antioxidative effect and is probably beneficial in preventing inflammaging, partly through the downregulation of CDKN2A.”
Quote in the paperSubstantial claim- Rests on an assumption: The molecular effects of GFF observed in cultured keratinocytes translate to clinical benefits in human skin, including anti-inflammaging and anti-aging.
May combine two claims.
PremisecitationAHR knockdown partially downregulates occludin expression but does not affect claudin-1 or claudin-4 expression.
“The knockdown of AHR partially downregulates the expression of occludin, whereas it does not affect the expression of claudin-1 or claudin-4 [55].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [55] Takei, 2015, Galactomyces fermentation filtrate prevents T helper 2-mediated reduction of filaggrin in an aryl hydrocarbon receptor-dependent manner, Clin. Exp. Dermatol. source
The paper relies on this without support.
The molecular effects of GFF observed in cultured keratinocytes translate to clinical benefits in human skin, including anti-inflammaging and anti-aging.
“Considering its antioxidative, barrier-protecting, and anti-inflammaging/antisenescence properties, GFF can be considered a potent cosmetic agent for preventing and repairing skin damage caused by various external and internal insults, and for maintaining healthy, youthful-appearing skin by retarding skin aging.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
GFF accelerates the production of the anti-inflammatory cytokine IL-37 in epidermal keratinocytes and contributes to anti-inflammaging.
“GFF also accelerates the production of the anti-inflammatory cytokine IL-37 in epidermal keratinocytes and contributes to anti-inflammaging [9,22].”
From Significant Reversal of Facial Wrinkle, Pigmented Spot and Roughness by Daily Application of Galactomyces Ferment Filtrate-Containing Skin Products for 12 Months—An 11-Year Longitudinal Skin Aging Rejuvenation Study (2023) · cites this paper as [9]
Section 8 reports that GFF upregulates anti-inflammatory IL-37 in human keratinocytes and that the induced IL-37 downregulates IL-33. The paper describes GFF’s anti-inflammaging effects as possible, however, and does not establish that IL-37 production itself contributes to them. (LLM, conf=0.85)
Experimental — accuracy not yet measuredGFF potentiates the anti-inflammaging system in epidermal keratinocytes.
“It also potentiates the anti-inflammaging system in epidermal keratinocytes [9].”
GFF activates aryl hydrocarbon receptor and enhances the expression of filaggrin, which is an essential source of natural moisturizing factors.
“GFF is known to activate aryl hydrocarbon receptor and enhance the expression of filaggrin, which is an essential source of natural moisturizing factors [5,9].”
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STAT3 signal transduction through interleukin-22 in oral squamous cell carcinoma
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Takei, K., Mitoma, C., Hashimoto‐Hachiya, A., Takahara, M., Tsuji, G., Nakahara, T., & Furue, M. (2015) · Clinical and Experimental Dermatology · doi:10.1111/ced.12635 · Cited by 45 · see citing works
Self-citationStudy of Skin Barrier Function in Psoriasis: The Impact of Emollients
Maroto-Morales, D., Montero‐Vílchez, T., & Arias‐Santiago, S. (2021) · Life · doi:10.3390/life11070651 · Cited by 44 · see citing works
Furue, M., Hashimoto‐Hachiya, A., & Tsuji, G. (2018) · Acta Dermato Venereologica · doi:10.2340/00015555-3003 · Cited by 43 · see citing works
Self-citationLueangarun, S., Tragulplaingam, P., Sugkraroek, S., & Tempark, T. (2019) · Dermatologic Therapy · doi:10.1111/dth.13090 · Cited by 42 · see citing works
Mitamura, Y., Murai, M., Mitoma, C., & Furue, M. (2018) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2018/2475047 · Cited by 40 · see citing works
Self-citationCaspase-14—From Biomolecular Basics to Clinical Approach. A Review of Available Data
Markiewicz, A., Sigorski, D., Markiewicz, M., Owczarczyk-Saczonek, A. B., & Placek, W. J. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22115575 · Cited by 40 · see citing works
Jett, J. E., McLaughlin, M., Lee, M. S., Parish, L. C., DuBois, J. C., Raoof, T. J., Tabolt, G., Wilson, T., Somerville, M. C., DellaMaestra, W., et al. (2021) · American Journal of Clinical Dermatology · doi:10.1007/s40257-021-00641-4 · Cited by 40 · see citing works
Frailty and cytokines in preclinical models: Comparisons with humans
Heinze-Milne, S., Banga, S., & Howlett, S. E. (2022) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2022.111706 · Cited by 38 · see citing works
Reciprocal regulation of permeability through a cultured keratinocyte sheet by IFN-γ and IL-4
Kobayashi, J., Inai, T., Morita, K., Moroi, Y., Urabe, K., Shibata, Y., & Furue, M. (2004) · Cytokine · doi:10.1016/j.cyto.2004.08.003 · Cited by 37 · see citing works
Self-citationTanaka, Y., Uchi, H., Hashimoto‐Hachiya, A., & Furue, M. (2018) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2018/9298052 · Cited by 36 · see citing works
Self-citationHasegawa, T., Feng, Z., Yan, Z., Ngo, K. H., Hosoi, J., & Demehri, S. (2019) · Journal of Investigative Dermatology · doi:10.1016/j.jid.2019.11.017 · Cited by 33 · see citing works
The Potential Role of Impaired Notch Signalling in Atopic Dermatitis
Melnik, B. C. (2015) · Acta Dermato Venereologica · doi:10.2340/00015555-1898 · Cited by 32 · see citing works
Identification of genes associated with endometrial cell ageing
Kawamura, T., Tomari, H., Onoyama, I., Araki, H., Yasunaga, M., Lin, C., Kawamura, K., Yokota, N., Yoshida, S., Yagi, H., et al. (2020) · Molecular Human Reproduction · doi:10.1093/molehr/gaaa078 · Cited by 32 · see citing works
Activation of the OVOL1-OVOL2 Axis in the Hair Bulb and in Pilomatricoma
Ito, T., Tsuji, G., Ohno, F., Uchi, H., Nakahara, T., Hashimoto‐Hachiya, A., Yoshida, Y., Yamamoto, O., Oda, Y., & Furue, M. (2016) · American Journal Of Pathology · doi:10.1016/j.ajpath.2015.12.013 · Cited by 31 · see citing works
Self-citationDi, T., Zhai, C., Zhao, J., Wang, Y., Chen, Z., & Li, P. (2021) · International Immunopharmacology · doi:10.1016/j.intimp.2021.107900 · Cited by 30 · see citing works
Miyamoto, K., Inoue, Y., Hsueh, K., Liang, Z., Yan, X., Yoshii, T., & Furue, M. (2011) · Journal of Dermatological Science · doi:10.1016/j.jdermsci.2011.09.009 · Cited by 29 · see citing works
Self-citationMiyamoto, K., Dissanayake, B., Omotezako, T., Takemura, M., Tsuji, G., & Furue, M. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10112502 · Cited by 28 · see citing works
Self-citationSwindell, W. R., Bojanowski, K., & Chaudhuri, R. K. (2019) · Journal of Investigative Dermatology · doi:10.1016/j.jid.2019.07.715 · Cited by 25 · see citing works
Lee, Y., Lim, H.-W., Ryu, I. W., Huang, Y.-H., Park, M., Chi, Y. M., & Lim, C. (2020) · BioMed Research International · doi:10.1155/2020/1759067 · Cited by 24 · see citing works
Hashimoto-Hachiya, A., Tsuji, G., & Furue, M. (2019) · Journal of Dermatological Science · doi:10.1016/j.jdermsci.2019.09.002 · Cited by 23 · see citing works
Self-citationTsuji, G., Hashimoto-Hachiya, A., Matsuda-Taniguchi, T., Takai-Yumine, A., Takemura, M., Yan, X., Furue, M., & Nakahara, T. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.745997 · Cited by 22 · see citing works
Self-citationSkeate, J. G., Porras, T. B., Woodham, A. W., Jang, J. K., Taylor, J. R., Brand, H. E., Kelly, T. J., Jung, J. U., Silva, D. M. D., Yuan, W., et al. (2015) · Journal of General Virology · doi:10.1099/jgv.0.000341 · Cited by 21 · see citing works
Aryl Hydrocarbon Receptor Activation Downregulates IL-33 Expression in Keratinocytes via Ovo-Like 1
Tsuji, G., Hashimoto‐Hachiya, A., Vu, Y. H., Miake, S., Takemura, M., Mitamura, Y., Ito, T., Murata, M., Furue, M., & Nakahara, T. (2020) · Journal of Clinical Medicine · doi:10.3390/jcm9030891 · Cited by 21 · see citing works
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Schleusener, J., Salazar, A., von Hagen, J., Lademann, J. M., & Darvin, M. E. (2021) · Molecules · doi:10.3390/molecules26061649 · Cited by 20 · see citing works
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Self-citationFurue, M., Uchi, H., Mitoma, C., Hashimoto‐Hachiya, A., Tanaka, Y., Ito, T., & Tsuji, G. (2019) · Giornale Italiano di Dermatologia e Venereologia · doi:10.23736/s0392-0488.18.06132-1 · Cited by 19 · see citing works
Self-citationYang, R., Spaulding, S. C., Choudhary, V., Chen, X., & Bollag, W. B. (2020) · Experimental Dermatology · doi:10.1111/exd.14080 · Cited by 18 · see citing works
Ding, W., Fan, L., Tian, Y., & He, C. (2021) · Molecular Biology Reports · doi:10.1007/s11033-021-06918-5 · Cited by 17 · see citing works
Kataoka, S., Hattori, K., Date, A., & Tamura, H. (2013) · Archives of Dermatological Research · doi:10.1007/s00403-013-1359-0 · Cited by 16 · see citing works
Pang, J.-H., Wong, W.-R., Hakozaki, T., Yoshii, T., & Chen, T.-Y. (2011) · Journal of Cosmetics, Dermatological Sciences and Applications · doi:10.4236/jcdsa.2011.11003 · Cited by 15 · see citing works
Miyamoto, K., Munakata, Y., Yan, X., Tsuji, G., & Furue, M. (2022) · Journal of Clinical Medicine · doi:10.3390/jcm11082121 · Cited by 14 · see citing works
Self-citationYan, Y., Furumura, M., Numata, S., Teye, K., Karashima, T., Ohyama, B., Tanida, N., & Hashimoto, T. (2014) · Experimental Dermatology · doi:10.1111/exd.12571 · Cited by 12 · see citing works
Revival of AHR Agonist for the Treatment of Atopic Dermatitis: Tapinarof
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Self-citationTsai, H.-H., Chen, Y., Lee, W.-R., Hu, C., Hakozaki, T., Yoshii, T., & Shen, S. (2006) · Journal of Dermatological Science · doi:10.1016/j.jdermsci.2006.01.009 · Cited by 11 · see citing works
Current Topical Strategies for Skin-Aging and Inflammaging Treatment: Science versus Fiction.
Eassa, H. A., Eltokhy, M. A., Fayyaz, H. A., Khalifa, M. K. A., Shawky, S., Helal, N. A., Eassa, H. A., Youssef, S. F., Latz, I. K., & Nounou, M. I. (2020) · PubMed · Cited by 11 · see citing works
Nakajima, A., Sakae, N., Yan, X., Hakozaki, T., Zhao, W., Laughlin, T., & Furue, M. (2022) · Journal of Clinical Medicine · doi:10.3390/jcm11164645 · Cited by 9 · see citing works
Self-citation(2019) · PubMed · Cited by 8 · see citing works
Influence of Characteristics of Oily Vehicle on Skin Penetration of Ufenamate
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Cooper, J. K. W., Koshoffer, A., Kadekaro, A. L., Hakozaki, T., & Re, B. (2019) · Journal of Clinical and Cosmetic Dermatology · doi:10.16966/2576-2826.138 · Cited by 4 · see citing works
Lee, J., Kim, H.-J., & Yi, J. Y. (2016) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2016.11.053 · Cited by 2 · see citing works
Flagged first, then by citations
1 of the 125 references couldn’t be matched to a known paper.
Research works printed but not linked: 1
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Cited by
Sorted by citations
Rusiñol, L., & Puig, L. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25158437 · Cited by 17 · see citing works
Prinsepia utilis Royle polysaccharides promote skin barrier repair through the Claudin family
Wang, B., Wang, F., Qu, L., Ma, H., Cheng, Y., Wu, X., Liu, J., & He, L. (2024) · Skin Research and Technology · doi:10.1111/srt.13848 · Cited by 13 · see citing works
Miyamoto, K., Inoue, Y., Yan, X., Yagi, S., Suda, S., & Furue, M. (2023) · Journal of Clinical Medicine · doi:10.3390/jcm12031168 · Cited by 9 · see citing works
Self-citationFusco, A., Perfetto, B., Savio, V., Chiaromonte, A., Torelli, G., Donnarumma, G., & Baroni, A. (2023) · Journal of Fungi · doi:10.3390/jof9121153 · Cited by 10 · see citing works
Potential Role of IL-37 in Atopic Dermatitis
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Ki, H., Baek, J. S., Hawkes, H.-J. K., Kim, Y. S., & Hwang, K. Y. (2023) · Foods · doi:10.3390/foods12112107 · Cited by 6 · see citing works
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Self-citationMiyamoto, K., Munakata, Y., Fujii, K., Lei, C., Yang, L., Sudarsana, S., & Furue, M. (2024) · Journal of Cosmetics Dermatological Sciences and Applications · doi:10.4236/jcdsa.2024.141002 · Cited by 3 · see citing works
Self-citationNakamizo, S., Yan, X., & Kabashima, K. (2024) · Journal of Dermatological Science · doi:10.1016/j.jdermsci.2024.03.011 · Cited by 1 · see citing works
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Self-citationAHR: The Overlooked Mediator in Skincare─Bridging Environmental Sensing and Skin Physiology
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The efficacy of pumpkin (Cucurbita sp.) on inflammaging
Novianri, C., & Wahyuniari, I. A. I. (2023) · Indonesia Journal of Biomedical Science · doi:10.15562/ijbs.v17i2.482
Sasa veitchii extract mitigates disruption of skin barrier function in a mouse model of dry skin
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Skincare for All Ages: The Science, Advances and Future of Skincare from Infancy to Adulthood
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Keratinocytes: Dynamic Gatekeepers and Immune Regulators of the Skin
Xue, M., Wang, H., Han, S., & MARCH, L. M. (2026) · Frontiers in Bioscience-Landmark · doi:10.31083/fbl50528 · Cited by 1 · see citing works
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- Authors
- Yan, X., Tsuji, G., Hashimoto-Hachiya, A., & Furue, M.
- Affiliations
- Procter & Gamble Japan K.K. (Japan) (JP)
- Kyushu University (JP)
- Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan
- Corresponding author
- Yan, Xianghong
- Venue
- Journal of Clinical Medicine
- Publisher
- MDPI AG
- Published
- 2022-10-27
- Volume
- 11
- Issue
- 21
- Pages
- 6338
- ISSN
- 2077-0383 (ISSN-L)
- PMC
- PMC9657190
- OpenAlex
- W4307703865
- Cited by
- 20
- References
- 125
- Citations by year
- 2026: 6 · 2025: 1 · 2024: 7 · 2023: 6
- FWCI
- 0.62
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Journal of Clinical Medicine (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
- Keywords
- inflammaging, keratinocytes, aryl hydrocarbon receptor, Nrf2, filaggrin, natural moisturizing factor, oxidative stress, UV damage, CDKN2A, cellular senescence, terminal differentiation, CASP14, claudins, IL-37, IL-33, IL-6 receptor, CXCL14, skin barrier, skin care ingredients, dry skin
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-31.
Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-31.
Cited sources are checked by gpt-6-sol.
Statistics and arithmetic are recomputed, not judged.
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