61 research outputs found

    Shark fossil diversity (Squalomorphii, Squatinomorphii, and Galeomorphii) from the Langhian of Brielas (Lower Tagus Basin, Portugal)

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    The fossiliferous marine Miocene sediments of the Lower Tagus Basin (Portugal) present a great diversity of Chondrichthyes forms. The current study focuses on the fossil sharks from the Langhian Vc unit of the Brielas section, located in the Setúbal Peninsula. A total of 384 isolated fossil teeth were analysed and ascribed to 17 species from the Orders Hexanchiformes, Squaliformes, Squatiniformes, Lamniformes, and Carcharhiniformes. Centrophorus granulosus and Iago angustidens are described for the first time in Portuguese sediments, whereas Pachyscyllium dachiardii and Rhizoprionodon ficheuri represent only their second reported occurrence. Galeorhinus goncalvesi was already known from the Portuguese uppermost Miocene (Alvalade Basin), but it is now recognized in older sediments. Furthermore, the new material seems to include the first reported occurrence of Hexanchus cf. agassizi in Miocene sediments. As a whole, these new findings support the previous palaeoenvironment characterization of a warm infralittoral setting gradually deepening to a circalittoral one, where seasonal upwelling phenomena could have occurred

    Assessing lesion malignancy by scanning small-angle x-ray scattering of breast tissue with microcalcifications

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    Scanning small-angle x-ray scattering (SAXS) measurements were performed on 36 formalin-fixed breast tissue biopsies obtained from two patients. All samples contained microcalcifications of type II, i.e. formed by hydroxyapatite. We demonstrate the feasibility of classifying breast lesions by scanning SAXS of tissues containing microcalcifications with a resolution of 35 mu m x 30 mu m We report a characteristic Bragg peak found around q = 1.725 nm(-1) that occurs primarily for malignant lesions. Such a clear SAXS fingerprint is potentially linked to structural changes of breast tissue and corresponds to dimensions of about 3.7 nm. This material property could be used as an early indicator of malignancy development, as it is readily assessed by SAXS. If this fingerprint is combined with other known SAXS features, which also indicate the level of malignancy, such as lipid spacing and collagen periodicity, it could complement traditional pathology-based analyses. To confirm the SAXS-based classification, a histopathological workup and a gold standard histopathological diagnosis were conducted to determine the malignancy level of the lesions. Our aim is to report this SAXS fingerprint, which is clearly related to malignant breast lesions. However, any further conclusion based on our dataset is limited by the low number of patients and samples. Running a broad study to increase the number of samples and patients is of great importance and relevance for the breast-imaging community

    Nitric oxide infused in the solitary tract nucleus blocks brain glucose retention induced by carotid chemoreceptor stimulation

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    Previous work has shown that the carotid body glomus cells can function as glucose sensors. The activation of these chemoreceptors, and of its afferent nucleus in the brainstem (solitary tract nucleus - STn), induces rapid changes in blood glucose levels and brain glucose retention. Nitric oxide (NO) in STn has been suggested to play a key role in the processing of baroreceptor signaling initiated in the carotid sinus [1]. However, the relationship between changes in NO in STn and carotid body induced glycemic changes has not been studied. Here we investigated in anesthetized rats how changes in brain glucose retention, induced by the local stimulation of carotid body chemoreceptors with sodium cyanide (NaCN), were affected by modulation of NO levels in STn. We found that NO donor sodium nitroprusside (SNP) micro-injected into STn completely blocked the brain glucose retention reflex induced by NaCN chemoreceptor stimulation. In contrast, NOS inhibitor Nω-nitro-l-arginine methyl ester (l-NAME) increased brain glucose retention reflex compared to controls or to SNP rats. Interestingly, carotid body stimulation doubled the expression of nNOS in STn, but had no effect in iNOS. NO in STn could function to terminate brain glucose retention induced by carotid body stimulation. The work indicates that NO and STn play key roles in the regulation of brain glucose retention. © 2011 Elsevier Inc. All rights reserved

    Nicotine and fluoxetine induce arousing effects on sleep-wake cycle in antidepressive doses: A possible mechanism of antidepressant-like effects of nicotine

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    Previous work has shown that the carotid body glomus cells can function as glucose sensors. The activation of these chemoreceptors, and of its afferent nucleus in the brainstem (solitary tract nucleus - STn), induces rapid changes in blood glucose levels and brain glucose retention. Nitric oxide (NO) in STn has been suggested to play a key role in the processing of baroreceptor signaling initiated in the carotid sinus [1]. However, the relationship between changes in NO in STn and carotid body induced glycemic changes has not been studied. Here we investigated in anesthetized rats how changes in brain glucose retention, induced by the local stimulation of carotid body chemoreceptors with sodium cyanide (NaCN), were affected by modulation of NO levels in STn. We found that NO donor sodium nitroprusside (SNP) micro-injected into STn completely blocked the brain glucose retention reflex induced by NaCN chemoreceptor stimulation. In contrast, NOS inhibitor N?-nitro-l-arginine methyl ester (l-NAME) increased brain glucose retention reflex compared to controls or to SNP rats. Interestingly, carotid body stimulation doubled the expression of nNOS in STn, but had no effect in iNOS. NO in STn could function to terminate brain glucose retention induced by carotid body stimulation. The work indicates that NO and STn play key roles in the regulation of brain glucose retention. " 2011 Elsevier Inc. All rights reserved.",,,,,,"10.1016/j.niox.2011.09.003",,,"http://hdl.handle.net/20.500.12104/43150","http://www.scopus.com/inward/record.url?eid=2-s2.0-81755177545&partnerID=40&md5=7da91b1b1ac1f5dad487d85b00687cdd",,,,,,"4",,"Nitric Oxide - Biology and Chemistry",,"38

    Nitric oxide in the commissural nucleus tractus solitarii regulates carotid chemoreception hyperglycemic reflex and c-Fos expression

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    Carotid body chemoreceptors function as glucose sensors and contribute to glucose homeostasis. The nucleus tractus solitarii (NTS) is the first central nervous system (CNS) nuclei for processing of information arising in the carotid body. Here, we microinjected a nitric oxide (NO) donor sodium nitroprusside (SNP), an NO-independent activator of the soluble guanylyl cyclase (sGC) (YC1) or an NO-synthase (NOS) inhibitor Nω-nitro-l- arginine methyl ester (L-NAME) into the commissural NTS (cNTS) before carotid chemoreceptor anoxic stimulation and measured arterial glucose and the expression of Fos-like immunoreactivity (Fos-ir). Male Wistar rats (250-300 g) were anesthetized, and the carotid sinus was vascularly isolated. Either artificial cerebrospinal fluid (aCSF), SNP, YC1 or L-NAME were stereotaxically injected into the cNTS. The SNP and YC1 infused into the cNTS before carotid chemoreceptor stimulation (SNP-2 and YC1-2 groups) similarly increased arterial glucose compared to the aCSF-2 group. By contrast, infusion of L-NAME into the cNTS before carotid chemoreceptor stimulation (L-NAME-2 group) decreased arterial glucose concentration. The number of cNTS Fos-ir neurons, determined in all the groups studied except for YC1 groups, significantly increased in SNP-2 rat when compared to the aCSF-2 or SNP-2 groups. Our findings demonstrate that NO signaling, and the correlative activation of groups of cNTS neurons, plays key roles in the hyperglycemic reflex initiated by carotid chemoreceptor stimulation. © 2013 Elsevier Inc. All rights reserved
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