Three-dimensional longitudinal changes in craniofacial growth in untreated hemifacial microsomia patients with cone-beam computed tomography.

Introduction: The purpose of this study was to evaluate the concept that the affected and contralateral sides do not grow at the same rate in patients with hemifacial microsomia. Changes in the cranial base, maxilla, mandible, and occlusal plane were evaluated on 3-dimensional images from cone-beam computed tomography data in untreated patients.

Methods: Six patients were classified as having mandibular Pruzansky/Kaban type I, IIA, or IIB hemifacial microsomia.

Regulation of hair regrowth in alopecic site of IFN-gamma-/- mice by macrophages infiltrating into allograft in IFN-gamma+/+ mice.

We previously demonstrated that around 6 weeks of age, most of the interferon-gamma (IFN-gamma)-/- C57BL/6 mice began to lose morphogenesis-derived hairs in their dorsal and occipital areas and that hair regrowth in the alopecic site was induced by intraperitoneal (i.p.) injection of IFN-gamma and allogeneic Meth A cells.

Induction of hair regrowth in the alopecia site of IFN-gamma knockout mice by allografting and IFN-gamma injection into the transplantation site.

We previously demonstrated that around 6 weeks of age most of the interferon-gamma (IFN-gamma)(-/-) but none of the IFN-gamma(+/+) C57BL/6 mice began to lose hair in their dorsal or occipital areas or both and that a single s.c. injection of IFN-gamma into IFN-gamma(-/-) mice at 3 but not at 8 weeks of age (or later) could protect all the mice from alopecia.

Cellular origin of IFN-gamma essential for hair cycle in normal skin.

Hair growth abnormalities in mice usually are accompanied by histologic abnormalities as well. Recently, however, we reported a mouse model in which an arrest of the hair cycle and diffuse shedding of the hair without pathologic features induced alopecia in interferon-gamma(-/-) (IFN-gamma(-/-)) C57BL/6 (B6) mice. Here, we explored the cellular origin of IFN-gamma.

Alopecia of IFN-gamma knockout mouse as a model for disturbance of the hair cycle: a unique arrest of the hair cycle at the anagen phase accompanied by mitosis.

Interferon-gamma(-/-) (IFN-gamma(-/-)) and IFN-gamma(+/+) C57BL/6 mice (3 weeks of age) completed the production of morphogenesis-derived hair. Around 6 weeks of age, however, most of the IFN-gamma(-/-) but none of the IFN-gamma(+/+) mice began to lose hairs in the dorsal and occipital areas in the absence of inflammatory reactions, and the alopecia was sustained for at least several 10-week periods of observation. A single subcutaneous injection of IFN-gamma to IFN-gamma(-/-) mice at 3, but not 4, 5, or 8 weeks of age could protect all the mice from alopecia, revealing that the lack of IFN-gamma around 3 weeks of age is directly responsible for the alopecia.