The aim of this study was to determine whether neural tissue is present in the bone 'dust' given off during temporal bone drilling. Bone 'dust' from three temporal bone dissections was collected and examined. Evidence of neural tissue was present in two out of the three specimens. Neural tissue is present in the bone dust given off during temporal bone drilling. This poses the question as to the risk of prion transmission during such dissection.
Biliary atresia leads to cirrhosis in the vast majority of patients and constitutes
the first cause of paediatric liver transplantation. Animal models allow us to
understand the molecular basis and natural history of diseases. The aim of this study
is to describe a surgically created animal model of biliary atresia with emphasis in
long-term liver function. Forty-two 3-week-old Sprague- Dawley rats were randomly
divided into two groups: bile duct ligature (BDL) and control. The animals were
sacrificed on the 2nd, 4th, and 6th postoperative
weeks. Blood samples were collected for liver function analysis. The spleen to body
weight ratio was determined. Histopathological examination of liver tissue was
performed by hematoxylin-eosin and Sirius red staining. Collagen quantification was
determined by using colorimetric digital image analysis and was expressed as a
percentage of total liver tissue area. Quantitative real-time polymerase chain
reaction was performed to analyse gene expression levels of transforming growth
factor-β1 (Tgfb1) and apeline (Apln) genes.
Statistical analysis was performed where P<0.05 was considered significant.
Animals from BDL group developed increasing cholestasis with clinical and laboratory
features. Splenomegaly was detected at 4th and 6th week
(P<0.05). Histological evaluation of the liver showed ductular reaction,
portal fibrosis and bile plugs. Collagen area to total liver tissue area had a median
of 2.5% in the control group and 6.5 %, 14.3 % and 37.7 % in BDL rats at
2nd, 4th and 6th weeks, respectively
(P<0.001). Tgfb1 mRNA expression level was significantly
higher at 6th week (P<0.001) in BDL group when compared to control.
Apln mRNA expression level was significantly higher at
4th and 6th week (P<0.001) and showed a positive
linear correlation (r = 0.975, P<0.05) in BDL group when compared to control.
Bile duct ligature in young rats is an animal model that recreates clinical,
laboratory, histological and molecular findings of biliary atresia. Bile duct
ligature constitutes a good animal model to investigate therapeutic approaches for
modifying the progression of liver fibrosis in biliary atresia.
Purpose Biliary atresia precedes liver cirrhosis and liver transplantation. Amniotic membrane (AM) promotes tissue regeneration, inhibits fibrosis, and reduces inflammation. Here, we test amniotic membrane potential as a therapeutic tool against cholestatic liver fibrosis. Methods Three groups of rats were used: sham surgery (SS), bile duct ligature (BDL), and bile duct ligature plus human amniotic membrane (BDL + AM). After surgery, animals were sacrificed at different weeks. Biochemical and histopathological analyses of liver tissue were performed. Collagen was expressed as a percentage of total liver tissue area. qPCR was performed to analyse gene expression levels of transforming growth factor-β1 (Tgfb1) and apelin (Apln). Statistical analysis performed considered p < 0.05 was significant. Results Groups undergoing BDL developed cholestasis. Biochemical markers from BDL + AM group improved compared to BDL group. Ductular reaction, portal fibrosis, and bile plugs were markedly reduced in the BDL + AM group compared to BDL group. Collagen area in BDL + AM group was statistically decreased compared to BDL group. Finally, expression levels of both Apln and Tgfb1 mRNA were statistically downregulated in BDL + AM group versus BDL group. Conclusion AM significantly reduces liver fibrosis in a surgical animal model of cholestasis. Our results suggest that AM may be useful as a therapeutic tool in liver cirrhosis.
We present the case of a 53‐year‐old Caucasian woman with seven basal cell carcinomas and one malignant melanoma in situ along her back overlying her spine, which was irradiated in 1968 for ankylosing spondylitis. These lesions developed between 1997 and 1999. She has no other known risk factors for cutaneous malignancy, in particular no history of excessive sun exposure. She has skin type 2. Molecular studies of glutathione S‐transferase and cytochrome P450 status showed her genotype not to constitute an overall increased inherited susceptibility. We therefore postulate that all her skin cancers have arisen as a consequence of her radiotherapy. To our knowledge this is the first case of multiple basal cell carcinoma in addition to a malignant melanoma following radiotherapy for benign disease.
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