gianniskritikos2
Active Member
http://www.today.com/video/today/49001161#49001161
vitamine D news
- Έναρξη μίζας gianniskritikos2
- Ημερομηνία έναρξης
Παρακαλώ συνδεθείτε ή εγγραφείτε για να απενεργοποιήσετε τις διαφημίσεις.
Η d3 έχει πολύ καλές προϋποθέσεις. Αλλά μιλάμε για την ενεργή μορφή της και όχι την απλή d3
Δες και εδώ στο πως βοηθάει
http://www.hairlossgr.com/forum/thread-8039-post-106346.html#pid106346
cool11
http://www.galinos.gr/web/drugs/main/citations/2850
Παρενέργειες σοβαρές δεν βρήκα το μόνο που δεν γνωρίζω είναι πως επειδή έχουμε αρκετούς d3 receptors στο κεφάλι και επειδή ο οργανισμός είναι περίεργο πράγμα, φοβάμαι μήπως δίνοντας του έτοιμη τροφή στην πορεία τεμπελιάσει όπως συμβαίνει και σε αρκετά άλλα και όταν κάποια στιγμή διακόψουμε την calcipotriol μήπως οι υποδοχείς υπολειτουργούν...
Δες και εδώ στο πως βοηθάει
http://www.hairlossgr.com/forum/thread-8039-post-106346.html#pid106346
cool11
http://www.galinos.gr/web/drugs/main/citations/2850
Παρενέργειες σοβαρές δεν βρήκα το μόνο που δεν γνωρίζω είναι πως επειδή έχουμε αρκετούς d3 receptors στο κεφάλι και επειδή ο οργανισμός είναι περίεργο πράγμα, φοβάμαι μήπως δίνοντας του έτοιμη τροφή στην πορεία τεμπελιάσει όπως συμβαίνει και σε αρκετά άλλα και όταν κάποια στιγμή διακόψουμε την calcipotriol μήπως οι υποδοχείς υπολειτουργούν...
Ίσως αλλά αν βοηθάει στα μαλλιά όπως δείχνει τότε με τη διακοπή ανα μήνα θα υποχωρεί και η όποια θετική διαδικασία. Για να δούμε αν όντως έχει αποτέλεσμα ίσως χρήση για 3 μήνες να είναι αρκετή και μετά βλέπουμε.
Πάντως αν κάποιος σκέφτεται να το δοκιμάσει καλύτερα από Οκτώβρη γιατί δεν είναι και ότι καλύτερο να εκθέτουμε το κεφάλι μας στον καλοκαιρινό ήλιο κατά τη χρήση του.
Oral χρήση
Calcitriol has several
actions that might be expected to slow or reverse the
disease process, including immunoregulatory effects
and inhibition of fibroblast growth and collagen synthesis.
A 35-year-old woman with a two-year history of localized scleroderma was given calcitriol for
six months. The initial dose was 0.25 mcg per day for
one week, increased by 0.25 mcg per day each week
until a dosage of 1.25 mcg daily was reached in the
fifth week. Thereafter, 0.5 mcg per day was given for
four months. After six months of treatment, the skin
lesions had almost completely resolved.
Three patients with generalized morphea received 0.5-0.75 mcg calcitriol daily. After 3-7 months
of treatment, joint mobility improved and skin extensibility increased. No adverse effects were seen
Seven children (ages 3-13 years) with linear
scleroderma received 0.25 mcg calcitriol daily for one
week; this was increased every week to a maximum
of 0.5-1.25 mcg per day, depending on body surface
area and response to treatment. Dietary calcium intake was restricted to 600 mg daily. Five of seven
patients showed good-to-excellent improvement of
their lesions. One patient had a partial relapse after
19 months, but responded well to a second course of
therapy. No significant side effects were seen.
Eleven scleroderma patients were treated
with 0.25 mcg calcitriol daily during the first week;
calcitriol was increased by 0.25 mcg daily each week
until urinary or serum calcium levels became elevated. The mean final dose was 1.75 mcg per day
and the maximum dose was 2.5 mcg per day. After
treatment periods ranging from six months to three
years, significant improvements in skin thickness and
extensibility were observed. No serious side effects
were seen except for transient hypercalciuria (always
below 350 mg per day), which responded to a temporary reduction in the dosage.21
Thus, most but not all clinical trials have
shown that calcitriol treatment improves the skin
manifestations of scleroderma. However, in addition
to being expensive, calcitriol can cause hypercalcemia, hypercalciuria, and other side effects requiring
frequent monitoring with laboratory tests.
Απ ότι φαίνεται μπορεί να βοηθήσει και στην ίνωση. Αν όντως το καταφέρνει αυτό με τοπική χρήση τότε θα καταπολεμήσουμε μια από τις μεγαλύτερες αιτίες που τίποτα δεν μπορεί να δουλέψει σωστά.
Από sides, θέλει λίγο προσοχή σε μακροχρόνια χρήση στη λήψη ασβεστίου γιατί βοηθάει στην απορρόφησή του.
Πάντως αν κάποιος σκέφτεται να το δοκιμάσει καλύτερα από Οκτώβρη γιατί δεν είναι και ότι καλύτερο να εκθέτουμε το κεφάλι μας στον καλοκαιρινό ήλιο κατά τη χρήση του.
Oral χρήση
Calcitriol has several
actions that might be expected to slow or reverse the
disease process, including immunoregulatory effects
and inhibition of fibroblast growth and collagen synthesis.
A 35-year-old woman with a two-year history of localized scleroderma was given calcitriol for
six months. The initial dose was 0.25 mcg per day for
one week, increased by 0.25 mcg per day each week
until a dosage of 1.25 mcg daily was reached in the
fifth week. Thereafter, 0.5 mcg per day was given for
four months. After six months of treatment, the skin
lesions had almost completely resolved.
Three patients with generalized morphea received 0.5-0.75 mcg calcitriol daily. After 3-7 months
of treatment, joint mobility improved and skin extensibility increased. No adverse effects were seen
Seven children (ages 3-13 years) with linear
scleroderma received 0.25 mcg calcitriol daily for one
week; this was increased every week to a maximum
of 0.5-1.25 mcg per day, depending on body surface
area and response to treatment. Dietary calcium intake was restricted to 600 mg daily. Five of seven
patients showed good-to-excellent improvement of
their lesions. One patient had a partial relapse after
19 months, but responded well to a second course of
therapy. No significant side effects were seen.
Eleven scleroderma patients were treated
with 0.25 mcg calcitriol daily during the first week;
calcitriol was increased by 0.25 mcg daily each week
until urinary or serum calcium levels became elevated. The mean final dose was 1.75 mcg per day
and the maximum dose was 2.5 mcg per day. After
treatment periods ranging from six months to three
years, significant improvements in skin thickness and
extensibility were observed. No serious side effects
were seen except for transient hypercalciuria (always
below 350 mg per day), which responded to a temporary reduction in the dosage.21
Thus, most but not all clinical trials have
shown that calcitriol treatment improves the skin
manifestations of scleroderma. However, in addition
to being expensive, calcitriol can cause hypercalcemia, hypercalciuria, and other side effects requiring
frequent monitoring with laboratory tests.
Απ ότι φαίνεται μπορεί να βοηθήσει και στην ίνωση. Αν όντως το καταφέρνει αυτό με τοπική χρήση τότε θα καταπολεμήσουμε μια από τις μεγαλύτερες αιτίες που τίποτα δεν μπορεί να δουλέψει σωστά.
Από sides, θέλει λίγο προσοχή σε μακροχρόνια χρήση στη λήψη ασβεστίου γιατί βοηθάει στην απορρόφησή του.
ναι για τοπική χρήση μιλάμε αλλά όχι απλή D3 αλλά calcipotriol
Apoptosis causes inactivation of vitamin D receptor in human hair derma papilla cells and human keratinocyte through VDR ablation
SY Kim1, MY Kim2, BC Park3, MN Kim2 and BJ Kim2 1Department of Convergence Medicine and Pharmaceutical Biosciences, Graduate School, Chung-Ang University, Seoul, Republic of Korea; 2Department of Dermatology, Chung-Ang University College of Medicine, Seoul, Republic of Korea and 3Dankook University College of Medicine, Dankook University, Cheonan, Republic of Korea
Aims: Vitamin D receptor (VDR) is a ligand-dependent transcription factor that mediates regulation of epidermal homeostasis and hair growth. In contrast, VDR ablation hinders the maintenance of normal hair follicle. In recent studies, we found that VDR was decreased in alopecia areata (AA) and alopecia universalis (AU) lesions compared with the non-lesion areas. In this study we investigated the mechanism of VDR in cultured human hair dermal papilla cells (DPCs) and human keratinocytes.
Methods: Cell viability was assessed by MTT assay. We analyzed the expression levels of VDR, β-catenin, Wnt3a, Wnt5a, and Wnt10b by western blot analysis. Also, VDR silencing was conducted using small interfering RNA (siRNA) for VDR in human hair (DPCs) and human keratinocytes. Also, VDR and cleaved caspase-3 expressions were determined using immune-fluorescence assay. (This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2010–0021960).)
Results: We showed that VDR was expressed in human hair dermal papilla cells (DPCs) and human keratinocytes. Lithocholic acid (LCA) is a ligand of the vitamin D receptor (VDR); LCA treatment induced upregulated expression of VDR and enhanced cell proliferation in a dose-dependent manner. We also showed that VDR silencing downregulated protein VDR and β-catenin and attenuated expression levels of the VDR in both cells. Moreover, we found that VDR silencing dramatically decreased the viability, whereas co-administration with LCA significantly restored the viability, which is associated with VDR repression by LCA. Correspondingly, immune-fluorescence analysis showed that VDR silencing activated cleaved caspase-3 in human keratinocytes.
Conclusion: These results indicate that VDR plays a critical role in human hair DPCs and human keratinocyte cell survival.
Dickkopf-1, an inhibitor of Wnt, regulates hair follicle growth degeneration in human hair dermal papilla cells and is associated with downregulation of VDR through DKK1-released inflammatory cytokines
SY Kim1, HM Kim2, TR Kwon1, YS Song1 and BJ Kim2 1Department of Convergence Medicine and Pharmaceutical Biosciences, Graduate School, Chung-Ang University, Seoul, Republic of Korea and 2Department of Dermatology, Chung-Ang University College of Medicine, Seoul, Republic of Korea
Aims: Dickkopf-1 (DKK-1) inhibits canonical Wnt/β-catenin signaling and maintains follicle anagen. In previous study, we found that DKK-1 suppressed the expressions of VDR and β-catenin in dermal papilla cells. This study examined the role of DKK1 in hair growth degeneration in human dermal papilla cells (DPCs).
Methods: Cell proliferation in human DPCs was assessed by MTT assay. We determined the levels of VDR, GSK-3β, and β-catenin by western blot analysis. Also, VDR expression was determined using immune-fluorescence assay in DKK1-treated cells. The role of DKK1 in human DPCs was examined by determining the levels of IL-1β, IL-6, and TNF-α using enzyme-linked immunosorbent assays (ELISA) and the expression levels of VDR, GSK-3β, and β-catenin using reconstruction of living skin equivalents (LSEs). (This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2010–0021960).)
Results: We found that DKK1 did not alter DP cell proliferation in a dose-dependent manner. However, we found that DKK1 treatment reduced the expression of VDR and β-catenin in human DPCs in a time- and dose-dependent manner. As shown by immune-fluorescence analysis, DKK1 attenuated levels of VDR expression at a concentration of 50 ng ml−1. In addition, the LSE system containing human keratinocytes and DPCs showed that DKK1 downregulates VDR and β-catenin, whereas it upregulates GSK-3β. We observed that DKK1-treated cells showed upregulation of TNFR2 expression and enhanced cytokine levels of IL-1β, IL-6, and TNF-α compared with non-treated cells.
Conclusion: In summary, the results of the present study demonstrate that DKK1 reduced expression levels of VDR and β-catenin in DPCs through the cooperative effect of inflammatory cytokines. Therefore, we suggest that DKK1 promotes hair loss through the inflammation factor in human hair DPCs.
Apoptosis causes inactivation of vitamin D receptor in human hair derma papilla cells and human keratinocyte through VDR ablation
SY Kim1, MY Kim2, BC Park3, MN Kim2 and BJ Kim2 1Department of Convergence Medicine and Pharmaceutical Biosciences, Graduate School, Chung-Ang University, Seoul, Republic of Korea; 2Department of Dermatology, Chung-Ang University College of Medicine, Seoul, Republic of Korea and 3Dankook University College of Medicine, Dankook University, Cheonan, Republic of Korea
Aims: Vitamin D receptor (VDR) is a ligand-dependent transcription factor that mediates regulation of epidermal homeostasis and hair growth. In contrast, VDR ablation hinders the maintenance of normal hair follicle. In recent studies, we found that VDR was decreased in alopecia areata (AA) and alopecia universalis (AU) lesions compared with the non-lesion areas. In this study we investigated the mechanism of VDR in cultured human hair dermal papilla cells (DPCs) and human keratinocytes.
Methods: Cell viability was assessed by MTT assay. We analyzed the expression levels of VDR, β-catenin, Wnt3a, Wnt5a, and Wnt10b by western blot analysis. Also, VDR silencing was conducted using small interfering RNA (siRNA) for VDR in human hair (DPCs) and human keratinocytes. Also, VDR and cleaved caspase-3 expressions were determined using immune-fluorescence assay. (This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2010–0021960).)
Results: We showed that VDR was expressed in human hair dermal papilla cells (DPCs) and human keratinocytes. Lithocholic acid (LCA) is a ligand of the vitamin D receptor (VDR); LCA treatment induced upregulated expression of VDR and enhanced cell proliferation in a dose-dependent manner. We also showed that VDR silencing downregulated protein VDR and β-catenin and attenuated expression levels of the VDR in both cells. Moreover, we found that VDR silencing dramatically decreased the viability, whereas co-administration with LCA significantly restored the viability, which is associated with VDR repression by LCA. Correspondingly, immune-fluorescence analysis showed that VDR silencing activated cleaved caspase-3 in human keratinocytes.
Conclusion: These results indicate that VDR plays a critical role in human hair DPCs and human keratinocyte cell survival.
Dickkopf-1, an inhibitor of Wnt, regulates hair follicle growth degeneration in human hair dermal papilla cells and is associated with downregulation of VDR through DKK1-released inflammatory cytokines
SY Kim1, HM Kim2, TR Kwon1, YS Song1 and BJ Kim2 1Department of Convergence Medicine and Pharmaceutical Biosciences, Graduate School, Chung-Ang University, Seoul, Republic of Korea and 2Department of Dermatology, Chung-Ang University College of Medicine, Seoul, Republic of Korea
Aims: Dickkopf-1 (DKK-1) inhibits canonical Wnt/β-catenin signaling and maintains follicle anagen. In previous study, we found that DKK-1 suppressed the expressions of VDR and β-catenin in dermal papilla cells. This study examined the role of DKK1 in hair growth degeneration in human dermal papilla cells (DPCs).
Methods: Cell proliferation in human DPCs was assessed by MTT assay. We determined the levels of VDR, GSK-3β, and β-catenin by western blot analysis. Also, VDR expression was determined using immune-fluorescence assay in DKK1-treated cells. The role of DKK1 in human DPCs was examined by determining the levels of IL-1β, IL-6, and TNF-α using enzyme-linked immunosorbent assays (ELISA) and the expression levels of VDR, GSK-3β, and β-catenin using reconstruction of living skin equivalents (LSEs). (This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2010–0021960).)
Results: We found that DKK1 did not alter DP cell proliferation in a dose-dependent manner. However, we found that DKK1 treatment reduced the expression of VDR and β-catenin in human DPCs in a time- and dose-dependent manner. As shown by immune-fluorescence analysis, DKK1 attenuated levels of VDR expression at a concentration of 50 ng ml−1. In addition, the LSE system containing human keratinocytes and DPCs showed that DKK1 downregulates VDR and β-catenin, whereas it upregulates GSK-3β. We observed that DKK1-treated cells showed upregulation of TNFR2 expression and enhanced cytokine levels of IL-1β, IL-6, and TNF-α compared with non-treated cells.
Conclusion: In summary, the results of the present study demonstrate that DKK1 reduced expression levels of VDR and β-catenin in DPCs through the cooperative effect of inflammatory cytokines. Therefore, we suggest that DKK1 promotes hair loss through the inflammation factor in human hair DPCs.
Komis
Active Member
Να κανω μια σημειωση,μιας και τα παραπανω αρθρα του Gomi ειναι στα αγγλικα και καποιος δεν το προσεξε.
Το πρωτο αρθρο αφορα τη καλσιτριολη ενω το δευτερο τη καλσιποτριολη.
Βρηκε κανεις σκευασμα για αγορα?
Το μονο που βρηκα ειναι το Dovonex.H τιμη του ξεκιναει απο 55$.
Το DOVOBET απο την αλλη περιεχει και κορτικοειδη οποτε μαλλον το αφηνουμε στην ακρη.
Το πρωτο αρθρο αφορα τη καλσιτριολη ενω το δευτερο τη καλσιποτριολη.
Βρηκε κανεις σκευασμα για αγορα?
Το μονο που βρηκα ειναι το Dovonex.H τιμη του ξεκιναει απο 55$.
Το DOVOBET απο την αλλη περιεχει και κορτικοειδη οποτε μαλλον το αφηνουμε στην ακρη.
Παρακαλώ συνδεθείτε ή εγγραφείτε για να απενεργοποιήσετε τις διαφημίσεις.
Λίγο παλιό θέμα, αλλά εξακολουθεί να παρουσιάζει ενδιαφέρον μιας και δεν υπάρχουν έρευνες πάνω στην αλληλεπίδραση των ανδρογόνων υποδοχέων στους υποδοχείς της βιταμίνης d, εκτός από την παρακάτω που αφορά κύτταρα του προστάτη.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3089062/
Investigation of the mechanism revealed that the vitamin D receptor (VDR), which mediates the effects of 1α(OH)D5, is downregulated in LNCaP-AI cells compared to LNCaP in the presence of androgens, whereas AWD restored VDR expression. Since LNCaP-AI cells expressed higher AR compared to LNCaP and AWD decreased AR, this indicated an inverse relationship between VDR and AR. Further, AR stimulation (by increased androgen) suppressed VDR, while AR downregulation (by ARsiRNA) stimulated VDR levels and sensitized LNCaP-AI cells to 1α(OH)D5 similar to AWD.
Οπότε μιας και ο vdr receptor παίζει σημαντικό ρόλο στην φυσιολογική λειτουργία των μαλλιών μιας και ελέγχει σε μεγάλο ποσοστό το wnt pathway και μιας και λίγο πολύ οι περισσότεροι το καλοκαίρι με τον ήλιο έχουμε προβλήματα, ίσως αξίζει να το δούμε λίγο περισσότερο
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1876678/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3089062/
Investigation of the mechanism revealed that the vitamin D receptor (VDR), which mediates the effects of 1α(OH)D5, is downregulated in LNCaP-AI cells compared to LNCaP in the presence of androgens, whereas AWD restored VDR expression. Since LNCaP-AI cells expressed higher AR compared to LNCaP and AWD decreased AR, this indicated an inverse relationship between VDR and AR. Further, AR stimulation (by increased androgen) suppressed VDR, while AR downregulation (by ARsiRNA) stimulated VDR levels and sensitized LNCaP-AI cells to 1α(OH)D5 similar to AWD.
Οπότε μιας και ο vdr receptor παίζει σημαντικό ρόλο στην φυσιολογική λειτουργία των μαλλιών μιας και ελέγχει σε μεγάλο ποσοστό το wnt pathway και μιας και λίγο πολύ οι περισσότεροι το καλοκαίρι με τον ήλιο έχουμε προβλήματα, ίσως αξίζει να το δούμε λίγο περισσότερο
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1876678/
Τελευταία επεξεργασία:
SinsemillaGR
New Member
Γκομι δεν το λεω απο τεμπελια. Αλλα μπορεις να μεταφρασεις γιατι δεν καταλαβαινω τις ορολογιες?