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References: Hair growth and hair loss

Ann Surg. 1993 Apr;217(4):391-6.
Fetal wound healing. The ontogeny of scar formation in the non-human primate.

Lorenz HP, Whitby DJ, Longaker MT, Adzick NS.

Department of Surgery, University of California, San Francisco.

OBJECTIVE: This study determined how scar formation develops in a non-human primate model of fetal skin repair. SUMMARY BACKGROUND DATA: A transition from healing scarlessly to healing with scar formation characterizes skin repair in rat and sheep fetuses. New knowledge of the regulatory processes occurring in the fetal wound at the initial stages of scar formation may provide insights into the early mechanisms of scar formation. METHODS: Full-thickness wounds were made in fetal rhesus monkey lips from 75 through 114 days gestation (n = 6, term = 165 days). Wounds were harvested at 14 days postwounding and processed for histology (hematoxylin & eosin, Masson's trichrome) as well as immunohistochemistry (human type I or type III collagen). RESULTS: Wounds healed with complete restoration of normal tissue architecture in the 75-day gestation fetus. However in the 85-100 day gestation fetuses, wounds healed with an absence of hair follicles and sebaceous glands, but the dermal collagen pattern remained reticular and similar to that in unwounded dermis. At 107 days, a thin scar was present in the wound, thereby demonstrating a transition to scar formation between 100 and 107 days gestation (early 3rd trimester) in the non-human primate. CONCLUSIONS: In the non-human primate fetus, a transition from scarless repair to adult-type repair with scar formation occurs in the early third trimester. These data provide insight into the transition process; the ontogeny of scar formation is characterized initially by wounds healing without the presence of epidermal appendages but with a normal reticular dermal collagen pattern, which we term the "transition wound."

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8466310&dopt=Abstract

Neurosci Lett. 1993 Jan 4;149(1):51-5.
Inward potassium rectifier current in type I vestibular hair cells isolated from guinea pig.

Griguer C, Sans A, Valmier J, Lehouelleur J.

Laboratoires de Neurophysiologie cellulaire et sensorielle, INSERM U-254, Universite Montpellier II, France.

Large inward current activated by hyperpolarization was studied using whole cell patch clamp technique in type I vestibular hair cells of guinea pig. Near the resting membrane potential, at an holding potential of -60 mV (HP -60), this current increased with hyperpolarizing steps and showed time-dependent decay for steps below -80 mV. This current was progressively inactivated at more negative holding potential and was totally abolished at HP -90 mV. The underlying conductance was a K+ conductance as indicated by: (i) its dependence on the external potassium concentration; (ii) its tail currents, which reversed at about -90 mV in solutions with a normal gradient for K+ ions. Pharmacological studies revealed that external application of 4-aminopyridine (5 mM) reversibly blocked (95%) the total inward current, while external application of tetraethylammonium (10 mM) or cesium (2 mM) did not significantly affect the amplitude of this current. This potassium inward rectifier current could contribute to restoration of the resting membrane potential during negative stimulations.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8469379&dopt=Abstract

Carcinogenesis. 1993 Jun;14(6):1101-5.
Genetic heterogeneity of the excision repair defect associated with trichothiodystrophy.

Stefanini M, Lagomarsini P, Giliani S, Nardo T, Botta E, Peserico A, Kleijer WJ, Lehmann AR, Sarasin A.

Istituto di Genetica Biochimica ed Evoluzionistica CNR, Pavia, Italy.

Trichothiodystrophy (TTD) is a rare autosomal recessive disease characterized by brittle hair with reduced sulfur content, mental and physical retardation, a peculiar face and ichthyosis. Photosensitivity has been reported in approximately 20% of the cases in the literature. DNA repair investigations demonstrated that clinical photosensitivity is usually associated with an enhancement of the cellular UV-sensitivity and that the repair defect is in the same gene as in patients from group D of xeroderma pigmentosum (XP). In this paper we describe the characterization of 13 further TTD patients; a defect in the nucleotide-excision repair was observed in fibroblast strains from 10 patients, confirming that TTD is frequently associated with DNA repair defects. Genetic analysis based on complementation studies demonstrated the presence of the XP-D defect in seven repair-defective TTD cases, indicating definitively that the concurrence of TTD with XP-D is not a sporadic or casual event. However, three further cell strains (TTD4VI and TTD6VI from two French siblings and TTD1BR from an English patient) showed restoration of normal UV-induced DNA repair synthesis after fusion with XP or TTD cells belonging to XP group D. These observations, which give the first indication that TTD is associated with repair defects behaving differently in the functional test of complementation, suggest some kind of causal connection between defective excision-repair factors and clinical features diagnostic for TTD. A peculiar aspect of TTD in which repair deficiencies are not related to an increased susceptibility to cancer is confirmed also in all the repair-defective TTD patients investigated in this paper.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8508495&dopt=Abstract

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