Pages that link to "Q36202856"
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The following pages link to Probing the effects of stress mediators on the human hair follicle: substance P holds central position (Q36202856):
Displaying 49 items.
- The neuropeptide galanin is a novel inhibitor of human hair growth (Q24305220) (← links)
- TRP channels in the skin (Q33562177) (← links)
- Hair and stress: A pilot study of hair and cytokine balance alteration in healthy young women under major exam stress (Q33579850) (← links)
- Hormones and the pilosebaceous unit (Q33716944) (← links)
- Laminin-511, inducer of hair growth, is down-regulated and its suppressor in hair growth, laminin-332 up-regulated in chemotherapy-induced alopecia (Q33829487) (← links)
- What causes alopecia areata? (Q33889367) (← links)
- Key role of CRF in the skin stress response system (Q34363640) (← links)
- Mental stress in atopic dermatitis--neuronal plasticity and the cholinergic system are affected in atopic dermatitis and in response to acute experimental mental stress in a randomized controlled pilot study (Q34612102) (← links)
- Tumour necrosis factor alpha, interferon gamma and substance P are novel modulators of extrapituitary prolactin expression in human skin (Q34692078) (← links)
- Chronic restraint stress inhibits hair growth via substance P mediated by reactive oxygen species in mice (Q34700434) (← links)
- Cutaneous Denervation of Psoriasiform Mouse Skin Improves Acanthosis and Inflammation in a Sensory Neuropeptide-Dependent Manner (Q35048297) (← links)
- The itchy scalp--scratching for an explanation. (Q35602011) (← links)
- Human hair follicle organ culture: theory, application and perspectives (Q35748809) (← links)
- Alopecia in IL-10-deficient mouse pups is c-kit-dependent and can be triggered by iron deficiency (Q36447181) (← links)
- Development of alopecia areata is associated with higher central and peripheral hypothalamic-pituitary-adrenal tone in the skin graft induced C3H/HeJ mouse model (Q36858794) (← links)
- Frontal Fibrosing Alopecia and Increased Scalp Sweating: Is Neurogenic Inflammation the Common Link? (Q37005767) (← links)
- An overview of alopecias (Q37604289) (← links)
- Alopecia areata: Animal models illuminate autoimmune pathogenesis and novel immunotherapeutic strategies (Q37720518) (← links)
- The pathogenesis of primary cicatricial alopecias (Q37796446) (← links)
- An Evolutionary Stress-Response Hypothesis for Chronic Widespread Pain (Fibromyalgia Syndrome) (Q37892662) (← links)
- Pathobiology of chemotherapy-induced hair loss (Q38078135) (← links)
- The role of hair follicle immune privilege collapse in alopecia areata: status and perspectives (Q38170254) (← links)
- Tachykinin peptide, substance P, and its receptor NK-1R play an important role in alimentary tract mucosal inflammation during cytotoxic therapy (Q38224991) (← links)
- A primer for studying cell cycle dynamics of the human hair follicle. (Q38812230) (← links)
- Stress-related skin disorders (Q38883601) (← links)
- Drug-induced photosensitivity: new insights into pathomechanisms and clinical variation through basic and applied science (Q38924006) (← links)
- Mesenchymal Stem Cells from Adipose Tissue in Clinical Applications for Dermatological Indications and Skin Aging (Q39100850) (← links)
- Presence of Mast Cells and Mast Cell Degranulation in Scalp Biopsies of Telogen Effluvium (Q41043253) (← links)
- Early stage alopecia areata is associated with inflammation in the upper dermis and damage to the hair follicle infundibulum (Q44606055) (← links)
- The immune system of mouse vibrissae follicles: cellular composition and indications of immune privilege (Q47775048) (← links)
- PPAR-γ Agonists and Their Role in Primary Cicatricial Alopecia. (Q48247479) (← links)
- Calcitonin gene-related peptide (CGRP) may award relative protection from interferon-γ-induced collapse of human hair follicle immune privilege (Q48293523) (← links)
- A Clinical and Biological Guide for Understanding Chemotherapy-Induced Alopecia and Its Prevention. (Q49807125) (← links)
- Inhibitory effect of tianeptine on catagen induction in alopecia areata-like lesions induced by ultrasonic wave stress in mice (Q50235606) (← links)
- Profiling mRNA of the graying human hair follicle constitutes a promising state-of-the-art tool to assess its aging: an exemplary report. (Q52885746) (← links)
- Substance P stimulates endothelin 1 secretion via endothelin-converting enzyme 1 and promotes melanogenesis in human melanocytes. (Q53015367) (← links)
- Efficacy of tofacitinib in treatment of alopecia universalis in two patients. (Q54189934) (← links)
- Corticotropin-releasing hormone stimulates the in situ generation of mast cells from precursors in the human hair follicle mesenchyme. (Q54700834) (← links)
- Proprietary Herbal Extract Downregulates the Gene Expression of IL-1α in HaCaT Cells: Possible Implications Against Nonscarring Alopecia (Q57301416) (← links)
- Immune Privilege Collapse and Alopecia Development: Is Stress a Factor (Q58602752) (← links)
- Autoimmune Disease Induction in a Healthy Human Organ: A Humanized Mouse Model of Alopecia Areata (Q62659504) (← links)
- A neuroendocrinological perspective on human hair follicle pigmentation (Q62659529) (← links)
- Frontal fibrosing alopecia: An update on the hypothesis of pathogenesis and treatment (Q64226671) (← links)
- Neuroendocrine perspectives in alopecia areata: does stress play a role? (Q83811051) (← links)
- An implication for post-transcriptional control: Reciprocal changes of melanocortin receptor type 2 mRNA and protein expression in alopecia areata (Q85115703) (← links)
- Epigallocatechin-3 Gallate Inhibits STAT-1/JAK2/IRF-1/HLA-DR/HLA-B and Reduces CD8 MKG2D Lymphocytes of Alopecia Areata Patients (Q90589637) (← links)
- Alcohol extract from Vernonia anthelmintica willd (L.) seed counteracts stress-induced murine hair follicle growth inhibition (Q92055034) (← links)
- Effects of the selective TrkA agonist gambogic amide on pigmentation and growth of human hair follicles in vitro (Q92982652) (← links)
- T-cell positioning by chemokines in autoimmune skin diseases (Q93049089) (← links)