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Background@#Pitavastatin is a cholesterol-lowering drug and is widely used clinically. In addition to this effect, pitavastatin has shown the potential to induce apoptosis in cutaneous squamous cell carcinoma (SCC) cells. @*Objective@#The purpose of this study is to investigate the effects and possible action mechanisms of pitavastatin. @*Methods@#SCC cells (SCC12 and SCC13 cells) were treated with pitavastatin, and induction of apoptosis was confirmed by Western blot. To examine whether pitavastatin-induced apoptosis is related to a decrease in the amount of intermediate mediators in the cholesterol synthesis pathway, the changes in pitavastatin-induced apoptosis after supplementation with mevalonate, squalene, geranylgeranyl pyrophosphate (GGPP) and dolichol were investigated. @*Results@#Pitavastatin dose-dependently induced apoptosis of cutaneous SCC cells, but the viability of normal keratinocytes was not affected by pitavastatin at the same concentrations. In supplementation experiments, pitavastatin-induced apoptosis was inhibited by the addition of mevalonate or downstream metabolite GGPP. As a result of examining the effect on intracellular signaling, pitavastatin decreased Yes1 associated transcriptional regulator and Ras homolog family member A and increased Rac family small GTPase 1 and c-Jun Nterminal kinase (JNK) activity. All these effects of pitavastatin on signaling molecules were restored when supplemented with either mevalonate or GGPP. Furthermore, pitavastatininduced apoptosis of cutaneous SCC cells was inhibited by a JNK inhibitor. @*Conclusion@#These results suggest that pitavastatin induces apoptosis of cutaneous SCC cells through GGPP-dependent JNK activation.
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Background@#Pathogenesis of psoriasis is related to dysregulated keratinocyte function and immune responses. Genetic background is one of the most important factors in disease pathogenesis. However, psoriasis-associated genes have not yet been fully identified. Activating transcription factor 3 (ATF3) is a member of the cyclic adenosine monophosphate responsive element-binding protein family of transcription factors, which may regulate epidermal keratinocytes. @*Objective@#We aimed to evaluate the effects of ATF3 on inflammation and differentiation of keratinocytes. @*Methods@#We evaluated the expression of ATF3 in polyinosinic:polycytidylic acid (poly[I:C])-treated keratinocytes. Subsequently, we compared ATF3 levels in psoriatic and normal skin using immunohistochemical staining. To illustrate the role of ATF3, we generated ATF3-overexpressing keratinocytes and ATF3-knockdown keratinocytes using a recombinant adenovirus. We investigated inflammation and differentiation of keratinocytes by measuring the mRNA levels of inflammatory cytokines and differentiation markers. @*Results@#Treatment of keratinocytes with poly(I:C) increased ATF3 expression in a time-dependent manner. Immunohistochemical staining showed that ATF3 expression was increased in the epidermis of psoriatic tissues. When ATF3 was overexpressed in keratinocytes using a recombinant adenovirus, poly(I:C)-induced inflammation was reduced. Conversely, ATF3 knockdown increased poly(I:C)-induced inflammation. Thus, ATF3 overexpression inhibited keratinocyte differentiation, while ATF3 knockdown promoted it. @*Conclusion@#ATF3 may be involved in the pathogenesis of psoriasis by influencing the inflammatory response and differentiation of keratinocytes.
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Background@#Acral melanoma is the most common subtype of melanoma among Koreans, and regional or distant metastasis is an indicator of poor prognosis. Yes-associated protein (YAP), a key effector of the Hippo pathway, is known to induce tumor progression and metastasis in various cancers. @*Objective@#We aimed to analyze the clinical and histopathological characteristics of acral melanoma among Koreans and to evaluate their association with YAP expression. @*Methods@#This retrospective review included 27 patients with acral melanoma. Clinical features including age, sex, lesion site, and stage were obtained from the medical records and images. Biopsy slides of patients with acral melanoma were reviewed, and immunohistochemical staining for YAP was performed. @*Results@#The rate of YAP expression was significantly higher in patients having acral melanoma with regional or distant lymph node (LN) metastasis than in those without metastasis (n=4/5, 80.0% vs. n=2/22, 9.1%; p=0.004). Histopathologically, the rate of YAP expression was higher in patients having acral melanoma with lymphovascular invasion than in those without lymphovascular invasion (n=4/8, 50.0% vs. n=2/19, 10.5%; p=0.044). Among the 27 lesions, 14 (51.9%) were on stress-bearing sites such as the forefoot and heel. However, the rate of YAP expression did not differ significantly between weight-bearing and non-weight-bearing locations (p=0.834). @*Conclusion@#YAP expression is significantly associated with metastasis, especially LN metastasis, in patients with acral melanoma. Therefore, YAP expression may be used as a prognostic factor for LN metastasis and a target for novel treatments in patients with melanoma.
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Background@#Fibroblasts produce collagen molecules that support the structure of the skin.The decrease and hypersynthesis of collagen causes skin problems such as skin atrophy, wrinkles and scars. @*Objective@#The purpose of this study is to investigate the mechanism of mitoxantrone on collagen synthesis in fibroblasts. @*Methods@#Cultured fibroblasts were treated with mitoxantrone, and then collagen synthesis was confirmed by reverse transcription-polymerase chain reaction and Western blot. @*Results@#Mitoxantrone inhibited the expression of type I collagen in fibroblasts at both the mRNA and protein levels. In the collagen gel contraction assay, mitoxantrone significantly inhibited gel contraction compared to the control group. Mitoxantrone inhibited transforming growth factor (TGF)-β-induced phosphorylation of SMAD3. Finally, mitoxantrone inhibited the expression of LARP6, an RNA-binding protein that regulates collagen mRNA stability. @*Conclusion@#These results suggest that mitoxantrone reduces collagen synthesis by inhibiting TGF-β/SMAD signaling and LARP6 expression in fibroblasts, which can be developed as a therapeutic agent for diseases caused by collagen hypersynthesis.
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Background@#Skin aging can be divided into intrinsic and extrinsic processes, and occur due to several factors. Although the interest in skin youthfulness is increasing globally, research on facial skin youthfulness and lifestyle is limited. @*Objective@#This study aimed to evaluate the association between facial skin youthfulness and biophysical facial skin parameters in Korean women over 50 years of age. We further investigated lifestyle factors that make people appear younger than their chronological age. @*Methods@#We surveyed the essential information and lifestyle of subjects by questionnaires, and measured the biophysical parameters of the facial skin. We then performed clinical facial assessments, and the values were compared with the chronologic age. The associations between age differences, biophysical parameters, and living habits were evaluated. @*Results@#We identified a positive correlation between age and melanin index (r=0.245, p＜0.001) and erythema index (r=0.119, p=0.002). The melanin index was statistically significantly lower in the group without regular outdoor activities (144.66±43.24 vs. 137.00±55.48, p=0.043). The melanin index and erythema index were the significant differences that defined younger perceived age than chronological age. The perceived age was younger in the group who wore a hat when performing outdoor activities than the group who did not (3.70±1.84 vs. 3.40±1.94, p=0.034). @*Conclusion@#To retain youthful skin, it is essential to reduce sun exposure, as this factor can affect the melanin and erythema indices by inducing photoaging. Therefore, avoiding the sun bia proper methods, such as wearing a hat and sunscreen during outdoor activities, is recommended to maintain skin youthfulness.
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Background@#Alopecia areata (AA) is an autoimmune disease characterized by chronic inflammation, the pathogenesis of which is unknown. Stress is believed to play a role; however, evidence remains insufficient. A recent study showed that substance P (SP) damaged hair follicles by causing neurogenic inflammation, activating perifollicular mast cells, and inducing keratinocyte apoptosis. @*Objective@#We aimed at studying the role of SP in AA pathogenesis. We investigated the SP levels in the lesional scalp tissues and serum. We also studied the effect of SP on the inflammatory response and hair growth in the outer root sheath (ORS) cells. @*Methods@#We compared the serum levels of SP in 58 AA patients and 28 healthy subjects.Then, we checked the expression of SP and SP receptor, neurokinin-1 receptor (NK-1R) in the scalps of AA patients and healthy controls using immunohistochemical staining.Finally, we analyzed the mRNA expression of inflammatory cytokines and hair growthrelated factors in ORS cells. @*Results@#SP and NK-1R expression were markedly higher in the hair follicles and interfollicular epidermis of the scalp lesions of AA patients. However, there was no statistically significant difference in serum SP levels between controls and patients, regardless of the type of alopecia. SP significantly increased the mRNA expression of inflammatory cytokines and decreased hair growth-related growth factors in ORS cells, but the results were not dramatic. @*Conclusion@#SP triggered a localized micro-inflammation in lesional hair follicles, provoked an inf lammatory response, and inhibited hair growth, thereby confirming the pathogenic role of SP in AA.
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Background@#Sebocytes are the main cells involved in the pathogenesis of acne by producing lipids and inflammatory cytokines. Although palmitic acid (PA) has been suggested to induce an inflammatory reaction, its effect on sebocytes remains to be elucidated. @*Objective@#In the present study, we investigated whether PA promotes inflammasome-mediated inflammation of sebocytes both in vivo and in vitro. @*Methods@#We intradermally injected PA into the mice ears. And, we treated cultured human sebocytes with PA. Inflammasome-mediated inflammation was verified by immunohistochemistry, Western blot and ELISA. @*Results@#PA-treated mice developed an inflammatory response associated with increased interleukin (IL)-1β expression in the sebaceous glands. When PA was added to cultured human sebocytes, caspase-1 activation and IL-1β secretion were significantly enhanced. In addition, NLRP3 knockdown attenuated IL-1β production by sebocytes stimulated with PA. PA-mediated inflammasome activation required reactive oxygen species. @*Conclusion@#These findings indicate that PA activates the NLRP3 inflammasome before induction of an inflammatory response in sebocytes. Thus, PA may play a role in the inflammation of acne
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Background@#Hormone therapy, which includes tamoxifen and aromatase inhibitors, is the most common adjuvant therapy used for breast cancer. However, only a few studies have reported endocrine therapy induced alopecia. @*Objective@#We investigated the effects of long-term adjuvant hormone therapy on hair in patients with breast cancer, in addition to patients’ concerns and current treatment for hair loss. @*Methods@#Patients completed a questionnaire that included information on self-perceived hair changes after each adjuvant therapy session, distress, and current treatment for hair loss. Using a folliscope, we measured hair density and thickness in each patient and in healthy controls. @*Results@#The study included 93 patients with breast cancer (mean age 51.9±9.8 years). The density and hair thickness were 106.36±21.85 hairs/cm2 and 0.07±0.01 mm in the patient group and 147.86±30.67 hairs/cm2 and 0.07±0.01 mm in the control group (n=98, mean age 52.10±8.40 years), respectively. The mean hair density was significantly lower in the patient group than in the control group; however, no statistically significant intergroup difference was observed in hair thickness. Among 76 patients who perceived hair changes after adjuvant therapy, 71.1% (n=54) were distressed with regard to hair changes. However, only 7.8% of the patients, including two who were treated by dermatologists, currently received treatment for hair changes. @*Conclusion@#Dermatologists should be familiar with hair changes in patients with breast cancer and provide appropriate education to encourage patients to consult dermatologists for hair loss and thinning after breast cancer treatment.
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Background@#Increased sebum secretion is considered the main causative factor in the pathogenesis of acne. There is an unmet pharmacological need for a novel drug that can control sebum production with a favorable adverse effect profile. @*Objective@#To investigate the effect of azidothymidine on lipid synthesis in sebocytes and to identify the underlying mechanism of the inhibitory effect of azidothymidine on insulin-like growth factor (IGF)-1-induced lipid synthesis in sebocytes. @*Methods@#Immortalized human sebocytes were used for the analysis. Thin-layer chromatography (TLC) and Oil Red O staining were performed to evaluate lipid synthesis in the sebocytes. The differentiation, lipid synthesis, mitochondrial biogenesis, and mitophagy in sebocytes were investigated. @*Results@#TLC and Oil Red O staining revealed that azidothymidine reduced IGF-1 induced lipid synthesis in the immortalized human sebocytes. Azidothymidine also reduced IGF-1-induced expression of transcriptional factors and enzymes involved in sebocyte differentiation and lipid synthesis, respectively. Moreover, we found that IGF-1 upregulated the levels of peroxisome proliferator-activated receptor-gamma coactivator-1α, LC-3B, p62, and Parkin, major regulators of mitochondrial biogenesis and mitophagy in immortalized human sebocytes. In contrast, azidothymidine inhibited IGF-1 induced mitochondrial biogenesis and mitophagy in the sebocytes. @*Conclusion@#These results suggest that azidothymidine downregulates IGF-1-induced lipogenesis by dysregulating the quality of mitochondria through suppression of mitochondrial biogenesis and mitophagy in immortalized human sebocytes. Our study provides early evidence that azidothymidine may be an effective candidate for a new pharmacological agent for controlling lipogenesis in sebocytes.
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Background@#Psoriasis is a chronic inflammatory skin disease. The etiology of psoriasis is not fully understood, but the genetic background is considered to be the most important factor. To date, many psoriasis-related genes have been discovered, but the role of many important genes has not been well understood. @*Objective@#The purpose of this study is to uncover possible roles of MDA5 in psoriasis. @*Methods@#Expression of MDA5 was investigated using immunohistochemistry. Then, MDA5 was overexpressed in keratinocytes using a recombinant adenovirus. @*Results@#As a result of immunohistochemical staining, the expression of MDA5 was significantly increased in the epidermis of psoriasis compared to normal skin. Similarly, the expression of MDA5 was increased in imiquimod-induced psoriasiform dermatitis model. In cultured keratinocytes, toll-like receptor 3 agonist poly(I:C) induced expression of MDA5 at both mRNA and protein levels. When MDA5 was overexpressed using a recombinant adenovirus, poly(I:C)-induced cytokine expression was significantly increased. Finally, MDA5 overexpression significantly inhibited calcium-induced differentiation of keratinocytes. @*Conclusion@#These results suggest that MDA5 increases in psoriasis and negatively regulates keratinocyte differentiation.
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Background@#Hormone therapy, which includes tamoxifen and aromatase inhibitors, is the most common adjuvant therapy used for breast cancer. However, only a few studies have reported endocrine therapy induced alopecia. @*Objective@#We investigated the effects of long-term adjuvant hormone therapy on hair in patients with breast cancer, in addition to patients’ concerns and current treatment for hair loss. @*Methods@#Patients completed a questionnaire that included information on self-perceived hair changes after each adjuvant therapy session, distress, and current treatment for hair loss. Using a folliscope, we measured hair density and thickness in each patient and in healthy controls. @*Results@#The study included 93 patients with breast cancer (mean age 51.9±9.8 years). The density and hair thickness were 106.36±21.85 hairs/cm2 and 0.07±0.01 mm in the patient group and 147.86±30.67 hairs/cm2 and 0.07±0.01 mm in the control group (n=98, mean age 52.10±8.40 years), respectively. The mean hair density was significantly lower in the patient group than in the control group; however, no statistically significant intergroup difference was observed in hair thickness. Among 76 patients who perceived hair changes after adjuvant therapy, 71.1% (n=54) were distressed with regard to hair changes. However, only 7.8% of the patients, including two who were treated by dermatologists, currently received treatment for hair changes. @*Conclusion@#Dermatologists should be familiar with hair changes in patients with breast cancer and provide appropriate education to encourage patients to consult dermatologists for hair loss and thinning after breast cancer treatment.
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Background@#Increased sebum secretion is considered the main causative factor in the pathogenesis of acne. There is an unmet pharmacological need for a novel drug that can control sebum production with a favorable adverse effect profile. @*Objective@#To investigate the effect of azidothymidine on lipid synthesis in sebocytes and to identify the underlying mechanism of the inhibitory effect of azidothymidine on insulin-like growth factor (IGF)-1-induced lipid synthesis in sebocytes. @*Methods@#Immortalized human sebocytes were used for the analysis. Thin-layer chromatography (TLC) and Oil Red O staining were performed to evaluate lipid synthesis in the sebocytes. The differentiation, lipid synthesis, mitochondrial biogenesis, and mitophagy in sebocytes were investigated. @*Results@#TLC and Oil Red O staining revealed that azidothymidine reduced IGF-1 induced lipid synthesis in the immortalized human sebocytes. Azidothymidine also reduced IGF-1-induced expression of transcriptional factors and enzymes involved in sebocyte differentiation and lipid synthesis, respectively. Moreover, we found that IGF-1 upregulated the levels of peroxisome proliferator-activated receptor-gamma coactivator-1α, LC-3B, p62, and Parkin, major regulators of mitochondrial biogenesis and mitophagy in immortalized human sebocytes. In contrast, azidothymidine inhibited IGF-1 induced mitochondrial biogenesis and mitophagy in the sebocytes. @*Conclusion@#These results suggest that azidothymidine downregulates IGF-1-induced lipogenesis by dysregulating the quality of mitochondria through suppression of mitochondrial biogenesis and mitophagy in immortalized human sebocytes. Our study provides early evidence that azidothymidine may be an effective candidate for a new pharmacological agent for controlling lipogenesis in sebocytes.
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Background@#Psoriasis is a chronic inflammatory skin disease. The etiology of psoriasis is not fully understood, but the genetic background is considered to be the most important factor. To date, many psoriasis-related genes have been discovered, but the role of many important genes has not been well understood. @*Objective@#The purpose of this study is to uncover possible roles of MDA5 in psoriasis. @*Methods@#Expression of MDA5 was investigated using immunohistochemistry. Then, MDA5 was overexpressed in keratinocytes using a recombinant adenovirus. @*Results@#As a result of immunohistochemical staining, the expression of MDA5 was significantly increased in the epidermis of psoriasis compared to normal skin. Similarly, the expression of MDA5 was increased in imiquimod-induced psoriasiform dermatitis model. In cultured keratinocytes, toll-like receptor 3 agonist poly(I:C) induced expression of MDA5 at both mRNA and protein levels. When MDA5 was overexpressed using a recombinant adenovirus, poly(I:C)-induced cytokine expression was significantly increased. Finally, MDA5 overexpression significantly inhibited calcium-induced differentiation of keratinocytes. @*Conclusion@#These results suggest that MDA5 increases in psoriasis and negatively regulates keratinocyte differentiation.
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Background@#Female-pattern hair loss (FPHL) is a common hair loss disorder in women. The various treatments include topical minoxidil and 17α-estradiol, as well as oral anti-androgens. However, the clinical efficacy of 5α -reductase inhibitors remains controversial. @*Objective@#We evaluated the clinical utility of dutasteride in FPHL patients and how dutasteride promotes hair growth. @*Methods@#We evaluated hair follicle density and thickness before and after oral dutasteride treatment in 24 patients with FPHL. We measured β-catenin activity in primary cultures of human dermal papilla cells (DPCs) using the TOP Flash reporter assay and Western blotting. The expression levels of genes promoting hair growth were quantitatively assessed using quantitative polymerase chain reaction (Q-PCR). @*Results@#The mean vertex hair density increased significantly from 67±14 to 76±13/cm2 (p=0.001) and the mean occipital hair density increased from 89±11 to 94±13/cm2 (p=0.012) after dutasteride treatment. However, the mean hair thickness did not increase. When DPCs were treated with dutasteride, TOP Flash activity increased in a dose-dependent manner, and the protein level of non-phosphorylated (active) β-catenin also increased. The mRNA level of vascular endothelial growth factor increased, but the mRNA levels of the keratinocyte growth factor, insulin growth factor-1, and Noggin were not affected by dutasteride. @*Conclusion@#This study shows a novel mechanism of dutasteride in promoting hair growth and provides support for the possible clinical application of 5α-reductase inhibitors for the treatment of FPHL.
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Background@#Psoriasis is a common chronic inflammatory skin disease. The development of psoriasis is dependent on many intercellular events such as innate immunity and T cell-mediated inflammation. Furthermore, genetic factors are strongly implicated in the pathophysiology of psoriasis. Although a variety of susceptible genes are identified, it is likely that many important genes remain undisclosed. @*Objective@#The aim of this study is to investigate the possible role of lysine demethylase 2A (KDM2A) in the pathophysiology of psoriasis. @*Methods@#We examined the expression of KDM2A using a well established imiquimod-induced psoriasiform dermatitis model. @*Results@#Immunohistochemistry analysis showed that expression of KDM2A was increased in imiquimod-induced psoriasiform dermatitis. Consistent with this result, KDM2A level was markedly increased in the epidermis of psoriatic patient. When keratinocytes were stimulated with TLR3 agonist poly(I:C), KDM2A was increased at both the mRNA and protein levels. Poly(I:C) increased the expression of psoriasis-related cytokines including tumor necrosis factor-α, interleukin-8, and CCL20, and KDM2A inhibitor daminozide enhanced the poly(I:C)-induced cytokine expression. Finally, topical co-application of imiquimod and daminozide exacerbated the imiquimod-induced psoriasiform dermatitis. @*Conclusion@#Together, these results suggest that KDM2A is increased to negatively regulate the inflammatory reaction of epidermal keratinocytes in psoriasis.
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BACKGROUND: Alopecia areata (AA), a chronic, relapsing hair-loss disorder, is considered to be a T-cell-mediated autoimmune disease. Cold-inducible RNA-binding protein (CIRP) belongs to a family of cold-shock proteins that respond to cold stress, and has been identified as a damage-associated molecular pattern (DAMP) molecule that triggers the inflammatory response. Recent studies have shown that high-mobility group box 1, another DAMP molecule, is elevated in serum and scalp tissue of AA patients, suggesting a relationship between DAMP molecules and the pathogenesis of AA. OBJECTIVE: To investigate the clinical significance of serum CIRP levels in AA. METHODS: The serum levels of CIRP were compared between 68 patients with AA and 20 healthy controls. Additionally, the correlation between CIRP level and various clinical parameters was evaluated. RESULTS: The serum CIRP levels were significantly higher in AA patients compared to healthy subjects. Moreover, there was an association between the serum CIRP level and clinical characteristics, such as disease duration and disease activity. However, there was no significant difference in the serum CIRP level among the clinical types of AA (AA multiplex, alopecia totalis, and alopecia universalis). CONCLUSION: These results suggest that CIRP may play a significant role in the pathogenesis of AA and could be a potential biologic marker for monitoring the disease activity of AA.
Subject(s)
Humans , Alopecia Areata , Alopecia , Autoimmune Diseases , Biomarkers , Healthy Volunteers , Inflammation , RNA-Binding Proteins , ScalpABSTRACT
The authors would like to change the corresponding author of the article.
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Hair graying is an obvious sign of human aging. Although graying has been investigated extensively, the mechanism remains unclear. Here, we reviewed previous studies on the mechanism of graying and seek to offer some new insights. The traditional view is that hair graying is caused by exhaustion of the pigmentary potential of the melanocytes of hair bulbs. Melanocyte dysfunction may be attributable to the effects of toxic reactive oxygen species on melanocyte nuclei and mitochondria. A recent study suggests that bulge melanocyte stem cells (MSCs) are the key cells in play. Graying may be caused by defective MSC self-maintenance, not by any deficiency in bulbar melanocytes. Our previous study suggested that graying may be principally attributable to active hair growth. Active hair growth may produce oxidative or genotoxic stress in hair bulge. These internal stress may cause eventually depletion of MSC in the hair follicles. Taken together, hair graying may be caused by MSC depletion by genotoxic stress in the hair bulge. Hair graying may also be sometimes caused by dysfunction of the melanocytes by oxidative stress in the hair bulb. In addition, hair graying may be attributable to MSC depletion by active hair growth.
Subject(s)
Humans , Aging , DNA Damage , Hair Follicle , Hair , Melanocytes , Mitochondria , Oxidative Stress , Reactive Oxygen Species , Rivers , Stem CellsABSTRACT
BACKGROUND: Skin hydration is a common problem both in elderly and young people as dry skin may cause irritation, dermatological disorders, and wrinkles. While both genetic and environmental factors seem to influence skin hydration, thorough genetic studies on skin hydration have not yet been conducted. OBJECTIVE: We used a genome-wide association study (GWAS) to explore the genetic elements underlying skin hydration by regulating epidermal differentiation and skin barrier function. METHODS: A GWAS was conducted to investigate the genetic factors influencing skin hydration in 100 Korean females along with molecular studies of genes in human epidermal keratinocytes for functional study in vitro. RESULTS: Among several single nucleotide polymorphisms identified in GWAS, we focused on Single Stranded DNA Binding Protein 3 (SSBP3) which is associated with DNA replication and DNA damage repair. To better understand the role of SSBP3 in skin cells, we introduced a calcium-induced differentiation keratinocyte culture system model and found that SSBP3 was upregulated in keratinocytes in a differentiation dependent manner. When SSBP3 was overexpressed using a recombinant adenovirus, the expression of differentiation-related genes such as loricrin and involucrin was markedly increased. CONCLUSION: Taken together, our results suggest that genetic variants in the intronic region of SSBP3 could be determinants in skin hydration of Korean females. SSBP3 represents a new candidate gene to evaluate the molecular basis of the hydration ability in individuals.