Rapid subduction initiation and magmatism in the Western Pacific driven by internal vertical forces.

Plate tectonics requires the formation of plate boundaries. Particularly important is the enigmatic initiation of subduction: the sliding of one plate below the other, and the primary driver of plate tectonics. A continuous, in situ record of subduction initiation was recovered by the International Ocean Discovery Program Expedition 352, which drilled a segment of the fore-arc of the Izu-Bonin-Mariana subduction system, revealing a distinct magmatic progression with a rapid timescale (approximately 1 million years). Here, using numerical models, we demonstrate that these observations cannot be produced by previously proposed horizontal external forcing. Instead a geodynamic evolution that is dominated by internal, vertical forces produces both the temporal and spatial distribution of magmatic products, and progresses to self-sustained subduction. Such a primarily internally driven initiation event is necessarily whole-plate scale and the rock sequence generated (also found along the Tethyan margin) may be considered as a smoking gun for this type of event.

Acylated ghrelin: a potential marker for fibromyalgia?

BACKGROUND: Fibromyalgia is characterized by chronic widespread pain and sleep disturbances. Overweight and obesity, which lead to metabolic changes, are additional comorbidities that are rarely explored, although they are highly prevalent in patients with fibromyalgia. METHODS: We compared the plasma levels of leptin and acylated ghrelin in 17 women with fibromyalgia (patients) and 16 healthy women (controls) with similar age, anthropometric measurements and levels of physical activity. We also investigated the relationships between these two neuropeptides and sleep and various pain characteristics in patients with fibromyalgia. Anthropometric measurements were recorded, and physical activity levels were assessed using a questionnaire. Pain intensity was measured using visual analogue scales (weekly general and mean pain scores). Sleep was assessed using an accelerometry technique. RESULTS: Compared to the control group, the patient group had increased leptin levels (patients: 22.4 ± 10.6 vs. controls: 13.3 ± 17.9 ng/mL; p < 0.01) and decreased acylated ghrelin levels (patients: 126.7 ± 47.8 vs. controls: 183.3 ± 102.2 pg/mL; p = 0.048). The leptin level was not significantly correlated with any of the variables. Acylated ghrelin level was inversely correlated with the weekly mean pain score (r = -0.67, p < 0.01) and the weekly general pain score (r = -0.67, p < 0.01). Multiple regression analysis revealed that the variations in acylated ghrelin levels accounted for 35% of the weekly general pain and 29% of the weekly mean pain variability. CONCLUSIONS: These findings indicate that the decreased acylated ghrelin levels in women with fibromyalgia are related to pain intensity.

Defective macrophage function in neonates and its impact on unresponsiveness of neonates to polysaccharide antigens.

Neonates do not respond to thymus-independent (TI) antigens (Ag), making them vulnerable to infection with encapsulated bacteria. The antibody (Ab) response of adult and neonatal B cells to TI Ag requires certain cytokines, which are provided by T cells or macrophages (MPhi). Lipopolysaccharide (LPS) failed to induce neonatal MPhi to produce interleukin (IL)-1beta and tumor necrosis factor alpha (TNF-alpha) mRNA and to secrete IL-1beta, IL-12, and TNF-alpha. However, LPS induced neonates to secrete some IL-6 and three- to fivefold more IL-10 than adults. Accordingly, adding adult but not neonatal MPhi could restore the response of purified adult B cells to trinitrophenol (TNP)-LPS, a TI Ag. Increased IL-10 is causally related to decreased IL-1beta and IL-6 production, as IL-10(-/-) neonatal MPhi responded to LPS by secreting more IL-1beta and IL-6 than wild-type (WT) neonatal MPhi. When cultures were supplemented with a neutralizing Ab to IL-10, WT neonatal MPhi secreted increased amounts of IL-6 and allowed neonatal MPhi to promote adult B cells to mount an Ab response against TNP-LPS. Thus, neonates do not respond to TI Ag as a result of the inability of neonatal MPhi to secrete cytokines, such as IL-1beta and IL-6, probably as a result of an excess production of IL-10. This dysregulated cytokine secretion by neonatal MPhi may be a result of a reduction in expression of Toll-like receptor-2 (TLR-2) and TLR-4 and CD14.

Nitric oxide participates in the intestinal pathology associated with murine syngeneic graft-versus-host disease.

Syngeneic graft-versus-host disease (SGVHD) develops following lethal irradiation, reconstitution with syngeneic bone marrow, and treatment with a short course of cyclosporin A (CsA) therapy. The disease is characterized by the development of a T helper cell type 1-like cytokine response [interleukin (IL)-12, interferon-gamma (IFN-gamma), and tumor necrosis factor alpha], and macrophage activation is central to development of the syndrome. It has been shown that nitric oxide (NO) participates significantly in the development of allogeneic GVHD. Studies were initiated to determine if NO participates in the pathology associated with SGVHD. Significant increases in inducible NO synthase (iNOS) mRNA and circulating NO were found in the tissues of SGVHD versus control animals. Treatment of SGVHD animals with the iNOS inhibitor aminoguanidine (AG) reversed the pathology associated with this disease. Furthermore, AG treatment reduced the production of IL-12 and IFN-gamma mRNA in the colons of CsA-treated mice. These studies demonstrate that NO participates in the pathological processes that are associated with the development of murine SGVHD.

Induction of syngeneic graft-versus-host disease in LPS hyporesponsive C3H/HeJ mice.

Syngeneic GVHD (SGVHD) develops following syngeneic bone marrow transplantation and treatment with cyclosporine A. Previous studies have demonstrated a role for IL-12, IFN-gamma, and TNF-alpha in the development of murine SGVHD. Macrophages can be activated to secrete IL-12 and TNF-alpha via a T-cell-dependent or T-cell-independent pathway (LPS or bacterial products). Studies were designed to determine if LPS participated in the development of SGVHD in C3H/HeN (LPS-responsive) and C3H/HeJ (LPS-hyporesponsive) mice. C3H/HeJ and C3H/HeN mice had similar levels of disease induction and pathology. Following induction of SGVHD, treatment of C3H/HeN, but not C3H/HeJ, mice with a sublethal dose of LPS resulted in mortality. However, neutralization of IL-12 abrogated the development of disease in C3H/HeJ mice, demonstrating that activated macrophages and their products participated in the development of SGVHD in these animals. These data suggested that LPS responsiveness was not a predisposing factor for SGVHD induction.

A Lower Mantle Source for Central European Volcanism.

Cenozoic rifting and volcanism in Europe have been associated with either passive or active mantle upwellings. Tomographic images show a low velocity structure between 660- and 2000-kilometer depth, which we propose to represent a lower mantle upwelling under central Europe that may feed smaller upper-mantle plumes. The position of the rift zones in the foreland of the Alpine belts and the relatively weak volcanism compared to other regions with plume-associated volcanism are probably the result of the past and present subduction under southern Europe.

Lactate and free fatty acids after subarachnoid hemorrhage.

The hypothesis that lactate and free fatty acids (FFA) are elevated in the first minutes after subarachnoid hemorrhage (SAH) is tested. Adult rats were subjected to an endovascular SAH through the right internal carotid artery while under anesthesia. The brains were frozen in-situ at 15, 30, 60 min, and 24 h post-hemorrhage. Regional measures of tissue lactic acid and FFA were made in the hippocampi, ipsilateral cortex, contralateral cortex, and cerebellum. Lactic acid levels were significantly elevated from sham animals in each region within the first hour (p<0.0001 cerebellum, right, and contralateral cortex, p<0.01 hippocampus), but did not change significantly over the first hour. At 24 h post-hemorrhage, there was no significant difference in the lactic acid levels from controls. Similarly, total FFA were significantly higher in each region as compared to sham operated controls within the first hour (p<0.001 cerebellum, p<0.05 hippocampus, p<0.05 contralateral cortex, p<0.0001 ipsilateral cortex). By 24 h, there was no significant difference in FFA levels from shams. The data indicate that aerobic metabolism fails and cellular damage with degradation of cell membranes occurs in the first minutes after SAH, and lasts for at least 1 h. However, this process is stabilized within 24 h in our model. Although the largest effect was seen in the ipsilateral cortex, all areas of the brain were effected.

Tissue culture of wild-type, interspecific genome/plastome hybrids and plastome mutants of evening primrose (Oenothera): controlled morphogenesis and transformation.

A favourable combination of genetic features in the genus Oenothera offers access to fundamental biological aspects that are not readily approached with other materials. We have developed protocols for cell and tissue culture as well as for transformation, in order to establish the basis for a comprehensive cell and molecular biology of Euoenothera species, their genome/plastome hybrids and plastome mutants. Regeneration of plants from excised seedling parts (roots, hypocotyl, cotyledons, shoot tips) and leaf explants was optimal on NT medium containing 1 mg ⋅ l-1 6-benzylaminopurine and 3 mg ⋅ l-1 α-naphtalene acetic acid. This medium also proved to be efficient in the propagation of various wild-type genotypes, interspecific hybrids and plastome mutants. Using Ti-based approaches we also succeeded in generating transgenic Oenothera plants with relatively high efficiency.

Clonidine-induced diuresis and its relation to endogenous opioid peptides

Para estudar a diurese induzida por clonidina, esta substância foi administrada, por via intraperitoneal, em ratos. Intenso efeito diurético foi observado com doses entre 0,025 e 1,25 mg/kg, além de excreçäo aumentada de íons sódio e potássio. Esse efeito diurético foi intensamente inibido pela administraçäo prévia de ioimbina (bloqueador de receptores alfa-dois adrenérgicos) ou N-metil-nalorfina (bloqueador de receptores) opióides que penetra mal o sistema nervoso central). Por outro lado, seu efeito diurético foi aumentado, pela administraçäo prévia de naloxona, um bloqueador de receptores opióides mi. É provável que a ativaçäo de receptores alfa-dois adrenérgicos pela clonidina possa induzir a liberaçäo de substâncias endógenas opióides que causem diurese através da ativaçäo de receptores periféricos com baixa afinidade por naloxona

Effects of anesthetics on the incidence and duration of reperfusion arrhythmias in isolated rat heart.

The present study was carried out to evaluate the effect of anesthetics on reperfusion arrhythmias. Male Wistar rats (200-300 g) were injected ip with heparin (200 IU), followed by anesthesia with thiopental (40 mg/kg), pentobarbital (30 mg/kg), urethane (1.2 g/kg), either, or halothane and sacrificed by decapitation. The isolated heart (5 to 8 per group) was perfused with Locke solution by the Langendorff method and the left coronary artery was ligated for 10 min. The incidence of reperfusion arrhythmias (100%) was similar in hearts of control and previously anesthetized rats, but the duration of the arrhythmias was significantly increased by anesthesia (5-fold with thiopental, 15-fold with pentobarbital, ether and halothane, and 30-fold with urethane). In hearts taken from unanesthetized rats and perfused with Locke solution containing anesthetics (5-7 per group), the duration of reperfusion arrhythmias decreased with thiopental (0.23 +/- 0.15 min), did not change with pentobarbital (1.14 +/- 0.26 min) and increased with urethane (16.10 +/- 5.60 min). Our results show that anesthetics alter the duration of reperfusion arrhythmias in the isolated rat heart.

Effects of anesthetics on the incidence and duration of reperfusion arrhythmias in isolated rat heart

The present study was carried out to evaluate the effect of anesthetics on reperfusion arrhythmias. Male Wistar rats (200-300 g) were injected ip with heparin (200 IU), followed by anesthesia with thiopental (40 mg/kg), pentobarbital (30 mg/kg), urethane (1.2 g/kg), either, or halothane and sacrificed by decapitation. The isolated heart (5 to 8 per group) was perfused with Locke solution by the Langendorff method and the left coronary artery was ligated for 10 min. The incidence of reperfusion arrhythmias (100 per cent ) was similar in hearts of control and previously anesthetized rats, but the duration of the arrhythmias was significantly increased by anesthesia (5-fold with thiopental, 15-fold with pentobarbital, ether and halothane, and 30-fold with urethane). In hearts taken from unanesthetized rats and perfused with Locke solution containing anesthetics (5-7 per group), the duration of reperfusion arrhythmias decreased with thiopental (0.23 +/- 0.15 min), did not change with pentobarbital (1.14 +/- 0.26 min) and increased with urethane (16.10 +/- 5.60 min). Our results show that anesthetics alter the duration of reperfusion arrhythmias in the isolated rat heart

Analgesia induzida por xilazina: influência de antagonistas opiodérgicos e da desmedulaçäo adrenal / Xylazine-induced analgesia: influence of opioidergic antagonists and adrenal demedullation

Um efeito analgésico, dose-dependente, da xilazina foi observado em ratos, usando uma modificaçäo do teste nociceptivo de retirada da cauda ao estímulo térmico. O efeito foi inibido por administraçäo intraperitoneal de ioimbina, nalaxona e N-metilnalorfina. Ratos submetidos à desmedulaçäo adrenal bilateral, 48 h e 144 h após a cirurgia, também apresentaram significativa reduçäo no efeito analgésico induzido por xilazina. Os resultados sugerem a participaçäo de mecanismos opioidérgicos no efeito analgésico da xilazina. A semelhança do efeito inibitório da N-metilnalorfina, que näo atravessa a barreira hematoencefálica e da desmedulaçäo adrenal bilateral sobre a analgesia induzida por xilazina (2,5 mg/kg), sugere que haja a participaçäo de mecanismos controladores da dor a nível periférico, que podem ser acionados por peptídeos opióides endógenos, liberados pelas adrenais