Red RC base and naphthol were the commonest allergens in the 'tie and dye' industry.

Various paraneoplastic dermatoses may be seen in association with underlying visceral, especially gastrointestinal, malignancy. Florid cutaneous papillomatosis describes the sudden appearance of multiple acuminate keratotic papules that morphologically resemble viral warts. It may be seen in association with acanthosis nigricans and/or the sign of Leser Triotalat. We report a 35-year-old male with extensive seborrhoeic keratoses and florid cutaneous papillomatosis. Unusually marked verrucous changes caused disfigurement of the hands and feet. The patient also reported dyspepsia, abdominal distention and weight loss 6 months prior to the development of cutaneous lesions. Gastroscopy revealed a large growth in the stomach. Histopathology of the tumor showed features of adenocarcinoma.

1. Following opioid-induced antinociception in mice, hyperalgesic responses may be observed. The present study was designed to evaluate the effect of different N-methyl-d-aspartate (NMDA) receptor modulators (magnesium, dextromethorphan, d-serine) on the development of morphine-induced hyperalgesia in mice. The tail-flick test was used to assess the effects of morphine alone and in combination with the NMDA receptor modulators. 2. Administration of a single low dose (2 mg/kg) of morphine to mice produced antinociception that was followed by hyperalgesia. 3. Administration of magnesium sulphate (5 mg/kg) and d-serine (10 mg/kg) alone produced a transient antinociceptive response, whereas dextromethorphan (10 mg/kg) alone produced a prolonged antinociceptive response that had a relatively delayed onset after 4 h. 4. When coadministered with morphine, the NMDA receptor blockers magnesium (2 mg/kg) and dextromethorphan (2 and 5 mg/kg) and the NMDA receptor agonist d-serine (2, 5 and 10 mg/kg), maintained the duration of the antinociceptive response to morphine and inhibited the development of the hyperalgesic response. Coadministration of dextromethorphan (10 mg/kg) with morphine produced antinociception at 30-120 min and at 4-24 h. 5. The results of the present study suggest that coadministration of low-dose NMDA receptor antagonists, as well as the NMDA receptor agonist d-serine, with morphine can inhibit morphine-induced hyperalgesia.

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We read with interest the article entitled "Ciproß oxacin breakpoints in enteric fever-time to revise our susceptibility criteria" by Rodrigues et al, [1] published in Jan-Mar 2008 issue of the Indian Journal of Medical Microbiology. The article is thought provoking but certain critical aspects have been overlooked, which if mentioned would be enriching for the various investigators and decision makers in this crucial area.Firstly, this study only mentions the number of nalidixic acid resistant strains isolated in 2005, but does not mention the total number of Salmonella typhi isolates from which they have been characterized. This does not allow us to calculate the prevalence of nalidixic acid resistant strains in a geographical area, which in this study happens to be Mumbai. Secondly, the methodology used in obtaining the results has not been mentioned. The MIC values are known to vary signiÞ cantly with the methodology used.[2] To revise the susceptibility criteria in our country all the centers working on S. typhi should follow same methodology. Thirdly, this study does not comment on the clinical outcome of the cases from which the 96 nalidixic acid resistant strains have been isolated. The increased MIC values of ciproß oxacin in S. typhi in India have been reported since many years, [3,4] but the important issue that has not been adequately addressed in many of these studies is the extent of clinical failure. Fourthly, this article mentions that the attainable AUC of ciproß oxacin is 31.06 μg/mL with 750 mg twice daily dose of ciproß oxacin, which is a satisfactory PK-PD value for the treatment of S. typhi enteric fever. However, there is evidence to suggest that free drug AUC and not the total AUC is more predictive of clinical success. [2] Considering plasma protein binding of approximately 30% for ciproß oxacin, for 750 mg b.d. daily dose, AUC free gets reduced to 22, and at MIC = 0.25µg/mL, AUC free :MIC ratio becomes 88.[5] This implies a dose of 750 mg b.d. daily would also be inadequate, as the recommended AUC free : MIC ratio for gram negative microorganisms is >100.

Myostatin recovered to baseline in both groups. Finally, we demonstrated that GDF-15 caused atrophy of myotubes in vitro (average control myotube diameter was 26.3±9.0 µm versus 22.3±7.5 µm for GDF-15 treated myotubes, equating to 15% myotube atrophy, p= 0.011). Conclusion This data supports the hypothesis that acute muscle loss occurs as a result of an imbalance between drivers of muscle atrophy and hypertrophy. GDF-15 is a potential novel mediator of muscle atrophy in ICUAP, which may become a therapeutic target in patients with ICUAP and other forms of acute muscle wasting.

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