Fixed exanthema from systemic tobramycin.

Eye drops contain several ophthalmic medications which can produce allergic reactions. We report the case of a patient with contact dermatitis from neomycin and a probable fixed exanthema after parenteral administration of tobramycin who tolerated topical tobramycin and other aminoglycosides.     

Neurotensin injected into the nucleus accumbens blocks the psychostimulant effects of cocaine but does not attenuate cocaine self-administration in the rat

The neuropeptide neurotensin (NT) has been shown to modulate mesolimbic dopaminergic activity. Neurotensin injected into the VTA produces motor stimulation and release of dopamine in the nucleus accumbens. In contrast, when neurotensin is administered into the nucleus accumbens, it produces neuroleptic-like effects such as attenuation of the locomotor activity elicited by psychostimulants. In the present study, the hypothesis that neurotensin injected into the nucleus accumbens might modulate the psychostimulant and reinforcing actions of cocaine was tested. In experiment one, rats were trained to self-administer cocaine intravenously on an FR5 schedule of reinforcement. Following the establishment of baseline responding, rats were implanted with bilateral cannulae in the nucleus accumbens. One week later, rats were injected into the nucleus accumbens with various doses of neurotensin (4.2, 8.4 and 16.7 μg, total doses bilaterally) immediately prior to the self-administration session. No significant effects were found with any of the doses of neurotensin tested on the self-administration of cocaine. However, in experiment 2, neurotensin at doses of 4.2 and 16.7 μg injected into the nucleus accumbens significantly reduced the locomotor activation induced by an acute injection of cocaine (15 mg/kg i.p.) and a dose of 16.7 μg attenuated the locomotor activation induced by amphetamine (0.75 mg/kg i.p.). Thus, neurotensin in the nucleus accumbens appears to specifically modulate the acute locomotor activating properties of cocaine but not cocaine self-administration. Different mechanisms by which NT interacts with dopamine in the nucleus accumbens may provide a means of selectively altering psychostimulant motor actions without affecting psychostimulant reinforcement.     

Outer membrane proteins of E. coli in the host-pathogen interaction in urinary tract infection.

Outer membrane protein patterns (Omp) of Escherichia coli obtained directly from the urine of bacteriuric patients without passage on artificial culture media (ACM) were studied by polyacrylamide gel electrophoresis (SDS-PAGE) in an effort to determine whether in vivo conditions of growth affected the expression of these bacterial surface structures. Seventeen strains studied showed two distinct Omp patterns: one protein band appeared at the level of porin proteins (40 kDa) in both patterns, but Omp A protein was at the level of 36 kDa in the first pattern and a new protein was observed at 21.5 kDa in the second pattern suggesting that it is a fragment of Omp A. High molecular weight proteins were also observed in most of the strains and this finding was related to lack of free iron when the same strains were grown under iron restricted conditions in vitro. The same strains grown in pooled urine from normal females showed the first pattern mentioned above. Comparative growth on ACM of urinary strains and E. coli strains isolated from blood, feces and wounds showed an increase in the number of porins expressed (from 1 to 2 or 3, with some variability observed between strains). Differences in osmolality between pooled urine and ACM used, plus in vitro studies varying the osmolality of culture media, showed that osmolality accounted for differences in the number of porins expressed: porin expression decreased in urine the ACM of high osmolality, suggesting that the same phenomena occurred in vivo. It is concluded that host factors including low availability of iron and high osmolality present in the urinary tract influence the expression of several E. coli surface proteins. These proteins may relate to the ability of E. coli to colonize and invade the urinary tract by regulating the physiologic and/or metabolic state of the bacterial cell favoring survival of the organism in a hostile environment. Specific immune responses directed against porins could influence the outcome of this host-parasite interaction.     

Carcinoma of the hepaticopancreatic ampullar region: role of US

Hepaticopancreatic ampullar tumors are so called because they are located at the confluence of the bile duct, pancreatic duct, and duodenum. Jaundice is an early sign of the disease and often leads to early diagnosis and favorable prognosis compared with other tumors that occur in this area. Of eight patients who underwent ultrasound (US) in the past 5 years, six (75%) were found to have tumor. The sizes of the tumors ranged from 1.6 to 2 cm. An intraluminal, polypoid mass in the distal part of the common bile duct was seen in four patients. In the other two patients, a sharply delineated mass gave rise to abrupt termination of the distal duct. Improved US resolution, more experience with this modality, and accurate diagnosis of these tumors with US will contribute to improved detection and prompt treatment.     

The role of quinone reductase (NQO1) and quinone chemistry in quercetin cytotoxicity.

The effects of quercetin on viability and proliferation of Chinese Hamster Ovary (CHO) cells and CHO cells overexpressing human quinone reductase (CHO+NQO1) were studied to investigate the involvement of the pro-oxidant quinone chemistry of quercetin. The toxicity of menadione was significantly reduced in CHO+NQO1 cells compared to wild-type CHO cells, validating the NQO1-overexpression in the CHO+NQO1 transfectant. Quercetin inhibited the proliferation of wild-type CHO and CHO+NQO1 cells to a similar extent without affecting cell viability, indicating that NQO1 enrichment of CHO cells did not provide increased protection. On the other hand, inhibition of NQO1 in both types of cells by dicoumarol significantly potentiated the inhibitory effect of quercetin on cell proliferation, revealing the role of NQO1 in cellular protection against quercetin. Altogether, these results can be explained by the hypothesis that both wild-type CHO and CHO+NQO1 cells contain sufficient NQO1 activity for optimal protection against the pro-oxidant effect of quercetin on cell proliferation. The results also point at a cellular NQO1 threshold for optimal protection against quercetin. This NQO1 threshold seems to be in the range of NQO1 activities already present in various tissues.     

A rapid and easy method for multiple endocrine neoplasia type 1 mutation detection using conformation-sensitive gel electrophoresis

Until now, the study of the multiple endocrine neoplasia type 1 (MEN1) gene in patients suspected of having the disease was expensive and laborious due to the large size of the gene. We have optimized the conformation-sensitive gel electrophoresis (CSGE) technique to analyze by four rather simple multiplex PCR reactions, and a single electrophoresis run, the entire coding region of the MEN1 gene, plus the exon–intron boundaries. This improvement of the CSGE technique was confirmed as an effective procedure for screening for the MEN1 gene by detecting ten previously known MEN1 gene mutations and four polymorphisms. The MEN1 gene of 12 patients with unknown mutations was then screened, and an abnormal CSGE profile was identified in 10/12 cases. Subsequent DNA sequencing demonstrated 3 of them to be novel mutations (E45K, 4479delACAG, 6073insC) and 7 to have been previously reported; in the remaining 2 patients, we confirmed the absence of any alteration of the coding sequence of MEN1. Mutation screening of the MEN1 gene using CSGE was demonstrated to be a fast, simple, and inexpensive method to study patients suspected of having MEN1 disease. Received: November 29, 2001 / Accepted: January 28, 2002     

Large deletions of the MECP2 gene detected by gene dosage analysis in patients with Rett syndrome

The original article to which this Erratum refers was published in Human Mutation 23:234–244 Human Mutation(2004) 23(3) 234–244