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ABSTRACT Endothelial dysfunction/apoptosis is critical to the development of neointima hyperplasia. Our pilot study identified a novel member of the caspase subfamily, caspase 13 (CASP 13), which is induced by oxidized low density lipoprotein (ox-LDL) in endothelial cells, but not in vascular smooth muscle cells. It remains controversial whether CASP 13 is a human or bovine gene. In this study, we collected four human brachial artery segments during arterioveinous fistula graft removal surgeries. By western blot and quantitative RT-PCR analysis, CASP13 expression was elevated at the anastomosis of brachial arteries from patients receiving hemodialysis. Rat carotid artery balloon model is widely used as in vivo atherosclerosis model for studies on neointima formation and especially vascular smooth muscle proliferation. However, most of the balloon injury studies terminated on the 14th day to sacrifice the animals for histological studies. In this study, we employed the ultrasonic device to record the hemodynamic changes in rat carotid artery at different time intervals after balloon injury. The pre-operative mean left carotid artery internal diameter and blood flow of Sprauge Dawley rats was 0.6 ¡Ó 0.07 mm and 28.75 ¡Ó 4.45 cm/sec, respectively. After balloon dilatation, the mean internal diameter of left carotid artery elevated to 0.77 ¡Ó 0.09 mm and 0.71 ¡Ó 0.08 mm on day 7 and day 14, respectively. Besides, the mean blood flow velocity also increased to 47.6 ¡Ó 9.2 cm/sec and 33.4 ¡Ó 10.8 cm/sec on day 7 and day 14, respectively. However, the left carotid artery blood flow velocity returned to 24 ¡Ó 3.5 cm/sec on day 21. The CASP 13 protein expression was found elevated in the balloon injury sites and mainly localized in the endothelial cells. In summary, CASP 13 is detected in endothelial cells in both human and rat atherosclerosis models and may constitute a novel molecular target for vascular diseases.

ABSTRACT Background: Developmental exposure to endocrine disrupting chemical (EDC), such as Bisphenol A (BPA) has been shown to affect the health during early stages in life. Aim: To assess whether developmental low-dose exposure to BPA alters adipocyte distribution and blood lipid levels in Fischer 344 (F344) rats. Method: Pregnant F344 rats were exposed to BPA via their drinking water from gestational day 3.5 throughout lactation. Doses given were one below the current European Food Safety Authority´s preliminary tolerable daily intake (TDI) of 4 µg BPA/kg bw/day, 0.5 [lower dose, Ld] and one equal to the previous TDI; 50 [higher dose, Hd] µg BPA/kg bw/day. Half the offspring was sacrificed at 5, and half at 52 weeks of age. Body weight was registered, and plasma lipid levels were analyzed. Inguinal white adipose tissue (iWAT) was weighed, Oil red O-stained and analyzed histologically. Results: Five-week-old Ld males and females Hd exhibited significantly higher triglyceride levels (31%, p<0.01; 41%,p<0.05, respectively) compared to control. Total cholesterol was borderline significantly increased (9%, p=0.0554) in 5-week-old Ld males, compared with control. Adipocyte cell density in the 5-week-old offspring was significantly increased; Ld female rats had increased cell density compared to control and Hd (22% and 23%,p<0.05, respectively), whereas the cell density of Hd males increased compared to Ld (29%, p<0.05). In the 52-week-old offspring blood lipid levels and iWAT cell density were not significantly affected. Conclusions: Results of the present study supports that developmental low-dose BPA exposure contributes to elevated triglyceride levels in 5-week-old animals.

Diss. (sammanfattning). Uppsala : Sveriges lantbruksuniv., 2003. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2005. / Härtill 5 uppsatser.

Thesis (Ph. D.)--West Virginia University, 1999. / Title from document title page. Document formatted into pages; contains vi, 125 p. : ill. Vita. Includes abstract. Includes bibliographical references (p. 107-122).

Thesis (Ph.D.)--Michigan State University. Dept. of Anthropology, 2008. / Title from PDF t.p. (viewed on July 7, 2009) Includes bibliographical references (p. 127-135). Also issued in print.

Thesis (doctoral)--Karolinska Institutet, Stockholm, 1986. / Extra t.p. with thesis statement inserted. Includes bibliographical references.

Mitofusin 2 (MFN2), an outer mitochondrial membrane protein expressed in virtually all human tissues, is a multi-faceted protein known to affect mitochondrial morphology, metabolism, tethering, and movement as well as overall cell cycle progression. Most intriguing among its characteristics is its ability to bind to Ras and Raf, upstream effectors in the MAPK/ERK pathway. Conditional knockout (cKO) of renal proximal tubule MFN2 in vivo showed a post-ischemic protective effect. While the two day survival of control mice was only 28%, an unexpected 86% of the MFN2 cKO mice were alive at two days post-ischemia. This is likely explained by MFN2's ability to bind and sequester Ras at baseline. Because the MFN2 deficient mice did not sequester as much Ras, renal proximal tubule cells were able to proliferate at a greater rate and restore organ function more quickly. Immunoprecipitation studies confirm a strong interaction between Ras and MFN2 in resting cells but a weaker one immediately following ischemic insult, even in cells replete with MFN2. These results suggest that blocking the MFN2-Ras interaction may be a novel method to treat acute kidney injury. A small peptide mimicking Ras to block MFN2 could be feasible. This should grant ischemic tissue an increased propensity to regenerate healthy cells while leaving non-ischemic tissue completely unaffected. Such a therapeutic agent would be novel in the treatment of acute kidney injury and may have uses in other tissues as well due to MFN2's widespread expression profile.

Made available in DSpace on 2014-06-11T19:23:42Z (GMT). No. of bitstreams: 0 Previous issue date: 2007-07-06Bitstream added on 2014-06-13T19:48:09Z : No. of bitstreams: 1 martins_dg_me_jabo.pdf: 254602 bytes, checksum: f45d1583561d8115c503fe5bb6c3321d (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / Na prática da clínica de pequenos animais, os médicos veterinários são freqüentemente confrontados com o quadro ou com o diagnóstico diferencial da piometra em cadelas, e devem decidir rapidamente sobre a melhor forma de tratamento, pois se trata de uma situação de risco para a vida da paciente. Esta revisão tem como objetivo a descrição dos conceitos práticos e atuais da etiopatogenia da hiperplasia endometrial cística em cadelas, a qual precede o desenvolvimento do quadro de piometra. Abordam-se tanto a classificação quanto os sintomas, os achados clínicos, bem como aspectos diagnósticos dessa síndrome. Com relação ao tratamento, são consideradas tanto a abordagem cirúrgica quanto a medicamentosa, bem como as vantagens e desvantagens de cada opção. / In clinics, pyometra in bitches is one of the most common disorders. Veterinarians must decide about the therapeutical approach and the best way to conduct treatment. So, it is important to know the complex physiopathogeny of this disorder, as well as the concomitant diseases, laboratorial alterations and types of treatment. The aim of this dissertation is to describe the new concepts of the etiopathogenia of the cystic endometrial hyperplasia-pyometra complex in bitches, evaluate the clinical and laboratorial alterations and also the options of the treatments found in animals consulted at the obstetrics department at the Veterinary Hospital Governador Laudo Natel, FCAV-UNESP-Jaboticabal and confront them with the results published in literature and also with cases from other national and international universities. Thus, it was described the classification of clinical signs, diagnosis and therapeutics of this syndrome.