The neuropeptide galanin (GAL) is involved in food intake and in fat ingestion. Presumably, these effects are conveyed via the galanin 1 receptor (GALR1). We screened the coding region of GAL (including 444 bp of its promoter region) and GALR1 for mutations using single-strand conformation polymorphism analysis and denaturing HPLC in up to 191 obese children and adolescents and 106 healthy underweight young adults (students). In GAL, we identified 3 novel single nucleotide polymorphisms (SNPs; silent: g.-419T-->C, g.-244G-->A; missense: g.47C-->T: Ala16Val) and one infrequent missense variation (c.253A-->G: Asn85Asp), and in GALR1 2 novel SNPs (silent: c.150C-->T, missense: c.793A-->T: Ile265Phe). To test for an association with obesity, we genotyped 7 SNPs (GAL: g.-244G-->A, g.47C-->T, rs7101947, rs1042577, rs3136540; GALR1: c.150C-->T, c.793A-->T) in up to 322 obese children and adolescents compared with up to 277 healthy underweight and normal weight young adults. Furthermore, we analyzed these SNPs with respect to potential effects on the percentage of energy consumed as fat in obese children and adolescents. Allele and genotype frequencies did not differ among the groups tested. In addition, we performed a pedigree transmission disequilibrium test (PDT) for one SNP (GAL: g.-244G-->A) in 610 (518 independent) obesity-trios (obese child or adolescent and both of its parents). However, the PDT for SNP GAL g.-244G-->A revealed no transmission disequilibrium. We conclude that the analyzed SNPs in GAL and GALR1 do not play a major role in early onset obesity or dietary fat intake in the obese children and adolescents of our study groups.

The human insulin‐responsive glucose transporter 4 gene (GLUT4) has been related to non‐insulin‐dependent diabetes mellitus (NIDDM) in several studies. Obesity is commonly found in patients with NIDDM. Hence, genes involved in NIDDM might also be relevant for obesity. We have analyzed 212 extremely obese children and adolescents, 82 normal‐weight students, and 94 underweight students for two single nucleotide polymorphisms (SNPs: promoter −30G/A; exon 4a: silent 2061T/C) in the vicinity of the GLUT4 by polymerase chain reaction with subsequent restriction fragment length polymorphism analyses (PCR‐RFLP) or single‐strand conformation polymorphism analyses (SSCP). Allele and genotype distributions were similar in all study groups (all p values > 0.05). Hence, we did not detect association of any of the analyzed SNP alleles in the GLUT4 to different weight extremes, so these seem not to be involved in weight regulation in our study groups.

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Longitudinal brainstem involvement in systemic lupus erythematosusSir, Central nervous system (CNS) involvement in systemic lupus erythematosus (SLE) is highly diverse. 1 In their extensive literature review, Jennekens and Kater delineated 16 different CNS syndromes that may be induced by SLE. 1 However, brainstem involvement is extremely rare and has not been included in their modified nomenclature system. So far, small distinct brainstem lesions 2-6 as well as vasculitic brainstem involvement 7,8 have been reported. Here we present a patient with an extensive longitudinal brainstem lesion as a first CNS manifestation of SLE.A 48 year-old female patient presented with a 4-day history of gradual onset diplopia and gait disturbance. She had a medical history of SLE without renal or hepatic involvement and was on 20 mg prednisolone. The diagnosis was established 20 years prior to the current admission on the basis of malar rash, arthritis, photosensitivity, haematological disorder and positive antinuclear antibodies. Examination revealed esotropia and a highfrequency gaze-evoked nystagmus on lateral and upward gaze. The gait was severely ataxic. The remainder of the neurologic examination was unremarkable, in particular, the examination of the lower cranial nerves and the sensory system was normal. The patient was afebrile and normotensive (blood pressure 110/75 mmHg). Antiphospholipid antibodies were negative. Lumbar puncture showed 12 WBC/mm 3 (90% lymphocytes) with normal lactate and glucose levels. A complete