Verrucous carcinoma of the scalp.

Verrucous carcinoma is a distinctive form of low-grade squamous cell carcinoma. It typically involves the oral cavity, larynx, esophagus, and skin. Cutaneous lesions typically arise in the genitocrural area and plantar surface of the foot, with rare case reports of verrucous carcinoma arising elsewhere on the body. Human papillomaviruses, predominately types 6 and 11, have been associated with some case reports. We present a case of verrucous carcinoma arising on the scalp with negative human papillomavirus testing in a relatively young patient.

Clioquinol effects on tissue chelatable zinc in mice.

Recent evidence for the involvement of zinc in the formation of beta-amyloid plaques in the brain in Alzheimer's disease has led to the establishment of new therapeutic strategies for the degenerative disorder based on metal chelation. The present experiment was conducted on a membrane-permeable zinc chelator, clioquinol (CQ), that has shown potential in initial studies on a mouse model of Alzheimer's disease [1]. The degree of chelatable zinc in mice treated with CQ, delivered by two different routes, was measured using complementary protocols for identifying chelatable zinc: 6-methoxy-8-quinolyl- p-toluenesulfonamide (TSQ) histofluorescence, and selenite autometalography. Mice injected intraperitoneally with CQ showed a dramatic reduction in chelatable zinc in brain, testis, and pancreas. In contrast, mice given CQ orally showed no significant change in levels of chelatable zinc in these tissues. This suggests that CQ administered orally to patients with Alzheimer's disease should not significantly perturb chelatable zinc levels in key organs and may be used over long periods without adverse endocrinological and reproductive effects related to zinc deficiency. In contrast, CQ injected intraperitoneally may be used not only as a tool for investigating chelatable zinc pools but also in a clinical context. For example, injected CQ could be employed in situations requiring the rapid buffering of excessive chelatable zinc following ischemic episodes or brain trauma. Thus, our findings indicate that CQ has considerable potential as a versatile scientific and clinical tool used for selective modulation of zinc pools.

Histochemical and histofluorescence tracing of chelatable zinc in the developing mouse.

Zinc is an essential element in mammalian development. However, little is known about concentrations of zinc in specific regions/organs in the embryo. We have employed selenite autometallography (AMG) and TSQ histofluoroscence to detect histochemically reactive (chelatable) zinc in whole midsagittal embryos and sections from neonatal mice. Chelatable zinc exhibited a broad distribution, being particularly localized to rapidly proliferating tissues, such as skin and gastrointestinal epithelium. Zinc was also observed in various types of tissues such as bone and liver. In the perinatal central nervous system, zinc was present almost exclusively in choroid plexus. The two methods used demonstrated generally similar distributions with some exceptions, e.g., in liver and blood. The ubiquity of zinc in the embryo, particularly in rapidly proliferating tissues, suggests a widespread role in fetal physiology.

Postnatal regulation of ZnT-1 expression in the mouse brain.

We have characterized the postnatal development of ZnT-1, a putative zinc transporter, in the mouse brain with respect to chelatable zinc in four distinct brain areas: cerebral cortex, hippocampus, olfactory bulb and cerebellum. At birth, both zinc and ZnT-1 immunoreactivity were nearly undetectable. Beginning at the end of the first postnatal week, ZnT-1 expression increased significantly in all areas examined except the cerebellum, which contains virtually no synaptic zinc. Moreover, neurons immunoreactive for ZnT-1 were typically present in areas rich in synaptic zinc, which increased in parallel with ZnT-1. In the cerebellum, in contrast, Purkinje cells exhibited robust immunoreactivity for ZnT-1 only in the second postnatal week. While the parallel development of zinc and ZnT-1 in forebrain regions supports a direct role for synaptic zinc in regulating ZnT-1 expression, ZnT-1 in cerebellar Purkinje cells could indicate that expression of this zinc transporter may also be regulated by a non-synaptic pool of zinc or by other mechanism(s). The striking developmental regulation of ZnT-1 expression together with synaptic zinc indicates that ZnT-1 may play a key role in protecting developing neurons against potentially toxic zinc.