Tropical spastic paraparesis-like illness occurring in a patient dually infected with HIV-1 and HTLV-II

We describe a 34-year-old man from southern Florida with a history of intravenous drug use, dually infected with human immunodeficiency virus type 1 (HIV-1) and human T-lymphotropic virus type II (HTLV-II), who developed a myelopathy clinically indistinguishable from HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP). This myelopathy was characterized by spastic lower extremity weakness, distal paresthesias, sensory loss with a discrete thoracic level to pinprick, back pain, impotence, and sphincter disturbances. Nerve conduction studies revealed an associated mixed axonal and demyelinative neuropathy. Despite a lack of response to 10 months of zidovudine therapy, the myeloneuropathy improved dramatically 2 years after its onset in the absence of any therapeutic intervention.     

Role of five platelet membrane glycoprotein polymorphisms in branch retinal vein occlusion.

To determine whether polymorphisms of platelet surface glycoprotein associated with arterial thrombosis are risk factors for branch retinal vein occlusion. A case-control study in which 69 patients with branch retinal vein occlusion and 147 controls who attended the eye clinic for nonvascular complications participated. DNA was extracted from whole blood and analyzed for genotyping of platelet glycoprotein polymorphisms by polymerase chain reactions and specific restricted enzymes. No relationship was found between the four platelet glycoprotein polymorphisms i.e. GPIa C807T, VNTR and Kozak of glycoprotein Ibalpha, the HPA-1 of glycoprotein IIIa and the occurrence of branch retinal vein occlusion. The HPA-2 polymorphism was found in 18 out 60 (30%) patients with branch retinal vein occlusion in comparison with 27 out 142 (19%) of controls, with an estimated odds ratio of 1.8 (95% confidence interval, 0.91-3.65). The four platelet glycoprotein polymorphisms are not risk factors for branch retinal vein occlusion and therefore it seems unnecessary to screen those patients for it. A larger study is required, however, to determine whether HPA-2 is a novel risk factor for branch retinal vein occlusion.     

Conserved sequence of the TgsGP gene in Group 1 Trypanosoma brucei gambiense

The trypanosome responsible for the majority of cases of human trypanosomiasis in Africa is Group 1 Trypanosoma brucei gambiense. Currently the most reliable test for the parasite is based on a single gene, which encodes a 47 kDa receptor-like T. b. gambiense-specific glycoprotein, TgsGP, expressed in the flagellar pocket of bloodstream forms. Although TgsGP has been demonstrated in T. b. gambiense throughout its geographic range, similar genes have been demonstrated in other T. brucei sspp. isolates, and there are no data on the extent of sequence variation in TgsGP. Here we have carried out a comparison of TgsGP sequences in a range of Group 1 T. b. gambiense isolates and compared the gene to homologues in other T. brucei sspp. in order to provide information to support the use of this gene as the key identification target for Group 1 T. b. gambiense. We demonstrate that the sequence of TgsGP is well conserved in Group 1 T. b. gambiense across the endemic range of gambian human trypanosomiasis and confirm that this gene is a suitable target for specific detection of this parasite. The TgsGp-like genes in some isolates of T. b. brucei, T. b. rhodesiense and Group 2 T. b. gambiense are closely similar to VSG Tb10.v4.0178, which may be the ancestral gene from which TgsGP was derived.     

Further evidence of dopamine transporter dysregulation in ADHD: a controlled PET imaging study using altropane.

BACKGROUND: The dopamine transporter (DAT) is known to be a key regulator of dopamine, and recent studies of genetics, treatment, and imaging have highlighted the role of DAT in attention-deficit/hyperactivity disorder (ADHD). The findings of in vivo neuroimaging of DAT in ADHD have been somewhat discrepant, however. METHOD: Dopamine transporter binding was measured using a highly selective ligand (C-11 altropane) and positron emission tomography (PET). The sample consisted of 47 well-characterized, treatment-na?ve, nonsmoking, non-comorbid adults with and without ADHD. Additionally, control subjects had few symptoms of ADHD. RESULTS: Results showed significantly increased DAT binding in the right caudate in adults with ADHD compared with matched control subjects without this disorder. CONCLUSIONS: These results confirm abnormal DAT binding in the striatum of adults with ADHD and provide further support that dysregulation of DAT may be an important component of the pathophysiology of ADHD.     

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