Circulating bacterial lipopolysaccharide-induced inflammation reduces flow in brain-irrigating arteries independently from cerebrovascular prostaglandin production

International audienceBrain dysfunction is a frequent complication of the systemic inflammatory response to bacterial infection or sepsis. In the present work, the effects of intravenous bacterial lipopolysaccharide (LPS) administration on cere-bral arterial blood flow were assessed with time-of-flight (TOF)-based magnetic resonance angiography (MRA) in mice. Cerebral expression of the transcription factors nuclear factor-kappaB (NF-jB) and c-Fos and that of enzymes synthesizing vasoactive mediators, such as pros-taglandins and nitric oxide, known to be increased under inflammatory conditions, were studied in the same animals. Time-resolved TOF MRA revealed no differences in blood flow in the internal carotids upstream of the circle of Willis, but indicated lower flow in its lateral parts as well as in the middle and anterior cerebral arteries after intravenous LPS injection as compared to saline administration. Although LPS did not increase c-Fos expression in ventral forebrain structures of these animals, it did induce NF-jB in meningeal blood vessels. LPS also increased cerebral expression of cyclooxygenase-2 and prostaglandin E syn-thase mRNAs, but de novo expression occurred in veins rather than in arteries. In conclusion, our work indicates that LPS-induced systemic inflammation does not necessarily affect filling of the circle of the Willis from the periphery, but that circulating LPS alters outflow from the circle of Willis to the middle and anterior cerebral arteries. These modifications in arterial flow were not related to increased cerebral synthesis of prostaglandins, but may instead be the consequence of the action of circulating prostaglandins and other vasoactive mediators on brain-irrigating arteries during systemic inflammation

Особенности процесса трещинообразования в массиве при управлении его газодинамикой

Исследован процесс сдерживания перехода угля из потенциально устойчивого состояния в стадию бурного разрушения. Ей, как правило, предшествует некоторый промежуток времени относительного затишья. Особенно важно улавливать этот момент среди массы различных откликов массива на ведение горных работ. Одним из вариантов управления развитием и релаксацией системы трещин может служить физико-химическая обработка.The inhibition process of coal transition from the potentially stable state in the stage of stormy destruction is investigation. As a rule, to it is preceded some interval of relative time calm. It is especially important to catch this moment among mass of different responses of array on the conduct of mountain works. Physical and chemical treatment can serve as one of control variants the development and relaxation of the cracks system

Immune-to-brain communication. A functional neuroanatomical approach.

Hans Seyle constateerde als student medicijnen in de jaren dertig al dat ziektes met uiteenlopende oorzaken vaak vergezeld gaan van dezelfde symptomen, zoals een verhoogde lichaamstemperatuur als mede een gebrek aan eetlust en ambitie. Het is echter pas kort geleden dat de factoren verantwoordelijk voor deze symptomen zijn ontdekt. Toediening van cytokines, oorspronkelijk beschreven als boodschapper molekulen tussen witte bloedcellen, zoals interleukine-1B, interleukine-6 en tumor necrois factor, heeft koorts, anorexie, afgifte van cortisol of corticosterone en depressie-achtige veranderingen in gedrag tot gevolg. Deze symptomen hebben naar alle waarschijnlijkheid een belangrijke rol gespeeld in het overleven van infecties gedurende de evolutie, omdat uit dierexperimenteel ondezoek blijkt dat het tegengaan van koorts of anorexie sterfte na een bacteriële infectie verhoogt. .... Zie: Samenvatting

Inflammation and Depression: A Nervous Plea for Psychiatry to Not Become Immune to Interpretation

The possibility that inflammation plays a causal role in major depression is an important claim in the emerging field of immunopsychiatry and has generated hope for new treatments. The aims of the present review are first to provide some historical background and to consider the evidence in favor of the claim that inflammation is causally involved in major depression. The second part discusses some of the possibilities allowed for by the use of broad ‘umbrella’ concepts, such as inflammation and stress, in terms of proposing new working hypotheses and potential mechanisms. The third part reviews proposed biomarkers of inflammation and depression and the final part addresses how elements discussed in the preceding sections are used in immunopsychiatry. The ‘umbrella’ concepts of inflammation and stress, as well as insufficiently-met criteria based inferences and reverse inferences are being used to some extent in immunopsychiatry. The field is therefore encouraged to specify concepts and constructs, as well as to consider potential alternative interpretations and explanations for findings obtained. The hope is that pointing out some of the potential problems will allow for a clearer picture of immunopsychiatry’s current strengths and limitations and help the field mature

Cytokines in the Brain and Neuroinflammation: We Didn’t Starve the Fire!

In spite of the brain-protecting tissues of the skull, meninges, and blood-brain barrier, some forms of injury to or infection of the CNS can give rise to cerebral cytokine production and action and result in drastic changes in brain function and behavior. Interestingly, peripheral infection-induced systemic inflammation can also be accompanied by increased cerebral cytokine production. Furthermore, it has been recently proposed that some forms of psychological stress may have similar CNS effects. Different conditions of cerebral cytokine production and action will be reviewed here against the background of neuroinflammation. Within this context, it is important to both deepen our understanding along already taken paths as well as to explore new ways in which neural functioning can be modified by cytokines. This, in turn, should enable us to put forward different modes of cerebral cytokine production and action in relation to distinct forms of neuroinflammation