Infiltration of CCR2+Ly6Chigh Proinflammatory Monocytes and Neutrophils into the Central Nervous System Is Modulated by Nicotinic Acetylcholine Receptors in a Model of Multiple Sclerosis.

Myeloid cells, including proinflammatory monocytes and neutrophils, have important roles in the pathology of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). These cells infiltrate the CNS in the early stages of disease development and contribute to the inflammatory response that is associated with symptom severity. It is thus crucial to identify and understand new mechanisms that can regulate the CNS infiltration of proinflammatory myeloid cells.

Differential modulation of EAE by α9*- and β2*-nicotinic acetylcholine receptors.

Nicotine is a potent inhibitor of the immune response and is protective against experimental autoimmune encephalomyelitis (EAE). Initial studies suggested that the cholinergic system modulates inflammation via the α7-nicotinic acetylcholine receptor (nAChR) subtype. We recently have shown that effector T cells and myeloid cells constitutively express mRNAs encoding nAChR α9 and β2 subunits and found evidence for immune system roles for non-α7-nAChRs.

Iron deficiency and diffuse nonscarring scalp alopecia in women: more pieces to the puzzle.

The relationship between nonscarring scalp alopecia in women and iron deficiency continues to be a subject of debate. We review the literature regarding the relationship between iron deficiency and nonscarring scalp alopecia and describe iron-dependent genes in the hair follicle bulge region that may be affected by iron deficiency. We conclude with a description of our approach to the diagnosis and treatment of nonscarring alopecia in women with low iron stores.

Phenotypic delineation of Emanuel syndrome (supernumerary derivative 22 syndrome): Clinical features of 63 individuals.

Emanuel syndrome is characterized by multiple congenital anomalies and developmental disability. It is caused by the presence of a supernumerary derivative chromosome that contains material from chromosomes 11 and 22. The origin of this imbalance is 3:1 malsegregation of a parental balanced translocation between chromosomes 11 and 22, which is the most common recurrent reciprocal translocation in humans.