Cavernous haemangioma presenting as an orbital mass after enucleation for a choroidal melanoma: case report.

A patient presented with an ipsilateral orbital mass four years after enucleation for a choroidal malignant melanoma. Clinical examination revealed a darkly coloured mass suggestive of recurrent melanoma. CT scanning indicated a locally extensive tumour. Management was by excision without resort to orbital exenteration. Pathological examination revealed a cavernous haemangioma. The natural history of this tumour is discussed.     

乳酸脱氢酶实验检测细胞新陈代谢的实验研究

目的 探索LDH实验检测细胞活力的可行性。方法 原代培养骨髓细胞和软骨细胞，用LDH实验测定上述两组细胞的活力，并与镜下活体观察到细胞的生长状况相比较。与目前比较成熟的测定细胞活力的MTS实验的测得的值相比较。结果 LDH实验对上述两组细胞的活力的测定结果与镜下活体观察到的结果相符合。与MTS实验的测得的结果经统计学处理无显著差异。结论 LDH实验可用于细胞活力的直接测定，而对活细胞的生存、繁殖无影响。     

Carboplatin desensitization.

BACKGROUND: IgE-mediated carboplatin hypersensitivity reactions occur in up to 30% of patients receiving this agent for chemotherapy of solid tumors, thus limiting therapeutic options. OBJECTIVE: To describe our experience with intravenous carboplatin desensitization regimens, which culminated in a standardized, successful protocol for safe administration. METHODS: Eight consecutive patients with ovarian cancer who had experienced severe anaphylactic reactions to carboplatin were referred to our hospital. Intradermal skin testing was performed by raising a 3-mm bleb by injection of undiluted carboplatin at 10 mg/mL, and the wheal size was read at 20 minutes. The outcomes of the various desensitization regimens were documented prospectively, and the experience gained was used to develop a standardized protocol for administration. RESULTS: All patients had positive intradermal skin test results. The first 3 patients were treated with short (90 minutes to 6 hours) desensitization protocols, and all protocols failed on the first or second infusions. These 3 and a subsequent 5 patients were given intravenous carboplatin according to a protocol of gradual dose escalation over a 4-log dose range given during a 4-day period, with subsequent 3-weekly infusions given more rapidly by omitting the most dilute log dose on each occasion. All patients tolerated the longer infusion protocol without event, and all but 1 patient experienced appropriate tumor marker response. CONCLUSIONS: Short carboplatin desensitization protocols (less than 6 hours) have an unacceptable failure rate in patients with carboplatin allergy, but longer infusion times (days) are well tolerated without recurrence of the allergic reaction and with good tumor response. In cases where carboplatin is the optimal therapeutic agent, clinicians should not be deterred by an anaphylactic reaction to it or by failure of shorter desensitization regimens.     

Mutations in the Ca(2+)-sensing receptor gene cause autosomal dominant and sporadic hypoparathyroidism

Parathyroid hormone secretion is negatively regulated by a 7- transmembrane domain, G-protein coupled Ca(2+)-sensing receptor. We hypothesized that activating mutations in this receptor might cause autosomal dominant hypoparathyroidism (ADHP). Consistent with this hypothesis, we identified, in two families with ADHP, heterozygous missense mutations in the Ca(2+)-sensing receptor gene that cosegregated with the disorder. None of 50 normal controls had either mutation. We also identified a de novo, missense Ca(2+)-sensing receptor mutation in a child with severe sporadic hypoparathyroidism. The amino acid substitution in one ADHP family affected the N-terminal, extracellular domain of the receptor. The other mutations involved the transmembrane region. Unlike patients with acquired hypoparathyroidism, patients with these mutations had hypercalciuria even at low serum calcium concentrations. Their greater hypercalciuria presumably reflected activation of Ca(2+)-sensing receptors in kidney cells, where the receptor negatively regulates calcium reabsorption. This augmented hypercalciuria increases the risk of renal complications and thus has implications for the choice of therapy.      

Exploring young men's drinking using the AUDIT questionnaire.

This paper reports the findings of an AUDIT questionnaire administered to a sample of young (16-24-year-old) white males. Of the sample, 65% were drinking at potentially harmful levels. Averaging 45 U/week, 18-21 years was the age of highest alcohol consumption. Compared with 16-17- and 22-24-year-olds, this group recorded the highest proportion of hazardous drinkers and most negative consequences of drinking.     

Dibenzo[a,l]pyrene-induced DNA adduction, tumorigenicity, and Ki-ras oncogene mutations in strain A/J mouse lung

Dibenzo[a,l]pyrene (DB[a,l]P), an environmental polycyclic aromatic hydrocarbon, is the most potent carcinogen ever tested in mouse skin and rat mammary gland. In this study, DB[a,l]P was examined for DNA adduction, tumorigenicity, and induction of Ki-ras oncogene mutations in tumor DNA in strain A/J mouse lung. Groups of mice received a single i.p. injection of 0.3, 1.5, 3.0, or 6.0 mg/kg DB[a,l]P in tricaprylin. Following treatment, DNA adducts were measured at times between 1 and 28 days, while tumors were counted at 250 days and analyzed for the occurrence of point mutations in codons 12 and 61 of the Ki-ras oncogene. DB[a,l]P in strain A/J mouse lung induced six major and four minor DNA adducts. Maximal levels of adduction occurred between 5 and 10 days after injection followed by a gradual decrease. DB[a,l]P-DNA adducts in lung tissue were derived from both anti- and syn-11,12- dihydroxy-13,14-epoxy- 11,12,13,14-tetrahydrodibenzo[a,l]pyrene (DB[a,l]PDE) and both deoxyadenosine (dAdo) and deoxyguanosine (dGuo) residues in DNA as revealed by cochromatography. The major adduct was identified as a product of the reaction of an anti-DB[a,l]PDE with dAdo in DNA. DB[a,l]P induced significant numbers of lung adenomas in a dose- dependent manner, with the highest dose (6.0 mg/kg) yielding 16.1 adenomas/mouse. In tricaprylin-treated control animals, there were 0.67 adenomas/mouse. Based on the administered dose, DB[a,l]P was more active than other environmental carcinogens including benzo[a]pyrene. As a function of time-integrated DNA adduct levels, DB[a,l]P induced lung adenomas with about the same potency as other PAHs, suggesting that the adducts formed by DB[a,l]P are similar in carcinogenic potency to other PAHs in the strain A/J mouse lung model. Analysis of the Ki- ras mutation spectrum in DB[a,l]P-induced lung tumors revealed the predominant mutations to be G-->T transversions in the first base of codon 12, A-->G transitions in the second base of codon 12, and A-->T transversions in the second or third base of codon 61, concordant with the DNA adduct profile.