Induction of autoimmune cholangitis in non‐obese diabetic (NOD).1101 mice following a chemical xenobiotic immunization

Our laboratory has suggested that loss of tolerance to pyruvate dehydrogenase (PDC‐E2) leads to an anti‐mitochondrial antibody response and autoimmune cholangitis, similar to human primary biliary cirrhosis (PBC). We have suggested that this loss of tolerance can be induced either via chemical xenobiotic immunization or exposure to select bacteria. Our work has also highlighted the importance of genetic susceptibility. Using the non‐obese diabetic (NOD) congenic strain 1101 (hereafter referred to as NOD.1101 mice), which has chromosome 3 regions from B6 introgressed onto a NOD background, we exposed animals to 2‐octynoic acid (2OA) coupled to bovine serum albumin (BSA). 2OA has been demonstrated previously by a quantitative structural activity relationship to react as well as or better than lipoic acid to anti‐mitochondrial antibodies. We demonstrate herein that NOD.1101 mice immunized with 2OA‐BSA, but not with BSA alone, develop high titre anti‐mitochondrial antibodies and histological features, including portal infiltrates enriched in CD8⁺ cells and liver granulomas, similar to human PBC. We believe this model will allow the rigorous dissection of early immunogenetic cause of biliary damage.     

Latanoprost-associated recurrent herpes simplex keratitis

PURPOSE/METHOD: We present a case of a patient who developed recurrent epithelial herpes simplex keratitis after starting treatment with latanoprost. Her ophthalmic history was only remarkable for a past episode of herpetic keratitis 21 years previously. RESULTS/CONCLUSIONS: Episodes of herpetic keratitis were under remission only when latanoprost was discontinued. No recurrences of herpes simplex keratitis have been observed since then. Latanoprost usage might be associated with recurrent episodes of herpes simplex keratitis in patients with previous history of ocular herpes simplex virus infection.     

Association of RET codon 691 polymorphism in radiation-induced human thyroid tumours with C-cell hyperplasia in peritumoural tissue

The RET proto-oncogene encodes a protein structurally related to transmembrane receptors with an intracellular tyrosine kinase domain. In human thyroid gland, the RET proto-oncogene is normally expressed in parafollicular C-cells. Thyroid C-cell hyperplasia is associated with inherited medullary thyroid carcinomas and is considered as a pre-neoplastic stage of C-cells disease. It has also been observed in thyroid tissues adjacent to follicular and papillary carcinomas. In order to study the relationship between a misfunctioning of the RET proto-oncogene and the presence of C-cell hyperplasia, we compared a series of thyroid glands presenting sporadic or radiation-associated tumours, as well as samples of unrelated normal thyroid tissues, for alteration in exons 10 and 11 of the gene and for the presence or absence of C-cell hyperplasia. Here we report a significantly higher frequency of C-cell hyperplasia present in peritumoural thyroid tissues of radiation-induced epithelial thyroid tumours, than in peritumoural of sporadic thyroid tumours or in control normal thyroid tissues (P=0.001). A G691S RET polymorphism was present with a higher frequency in radiation-induced epithelial thyroid tumours (55%) than in sporadic tumours (20%) and in control normal thyroid tissues (15%). Interestingly, this polymorphism was associated in the majority (88%) of radiation-induced tumours with a C-cell hyperplasia in the peritumoural tissues. Several explanations for this association are discussed.     

Peripheral multineuritis pointing at systemic sarcoidosis

We report a patient with a peripheral neuropathy as the first symptom of sarcoidosis. The systemic illness was proved by the presence of typic granulomes in the bone marrow. The fact that sarcoidosis is the cause for the neuropathy is supported by the temporary relation and by the good response of all clinical picture to the corticosteroid therapy.Sarcoid neuropathy can rarely be the presenting feature of sarcoidosis.     

山苍子水提物柠檬醛抗哮喘作用的实验研究

目的：研究山苍子水提物柠檬醛的抗哮喘作用及其机理。方法：通过豚鼠氯化乙酰胆碱-磷酸组胺喷雾致喘法、小鼠浓氨水喷雾引咳法、小鼠酚红排泻法观察柠檬醛的平喘、镇咳、祛痰作用，通过观察张力变化研究柠檬醛对豚鼠离体气管环张力的影响及乙酰胆碱对气管收缩的抑制作用。结果：柠檬醛能明显延长氯化乙酰胆碱-磷酸组胺喷雾引起的豚鼠哮喘潜伏期，能延长浓氨水喷雾诱发小鼠咳嗽反应潜伏期，明显减少咳嗽次数。能增加小鼠呼吸道酚红排泌量，能抑制乙酰胆碱对豚鼠离体气管平滑肌的收缩作用，使乙酰胆碱所致气管平滑肌量效曲线右移。结论：柠檬醛气雾剂具有一定的平喘、镇咳和祛痰作用，具有良好的支气管解痉作用。     

Variability of results of cavernous nerve stimulation during radical prostatectomy

PURPOSE: We assess the reliability of intraoperative cavernous nerve stimulation for producing an erectile response during radical prostatectomy. MATERIALS AND METHODS: In 61 patients cavernous nerve function was assessed during radical retropubic prostatectomy using a CaverMap nerve stimulator. Control stimulation was also performed before and after prostatic dissection by placing the nerve stimulator tip on the anterior bladder wall. An increase in penile circumference measured by the device was considered a tumescence response while any measurable detumescence was also categorized. RESULTS: Patient age ranged 43 to 72 years (mean 59.8). Before apical dissection 41% and 46% had tumescence, 31% and 21% had detumescence, and 28% and 33% had no response with stimulation of the neurovascular bundle and anterior bladder wall, respectively. After dissection 42% and 25% had tumescence, 16% and 18% had detumescence, and 42% and 57% had no response with stimulation of the neurovascular bundle and anterior bladder wall, respectively. CONCLUSIONS: A response to neurovascular bundle stimulation using this device does not necessarily correlate with the precise anatomical location of the cavernous nerves. There is considerable background variability related to anesthesia, surgical manipulation and other undefined factors that may cause minor but measurable changes in penile circumference.