Hypoxemia exerts detrimental effects on the choroid plexuses and cerebrospinal fluid system in rats.

Background: Hypoxemia can cause secondary acute brain injury, but the mechanisms behind it are not entirely clear and could involve disturbances in the brain extracellular fluids. We aimed to explore the effects of hypoxemia on the choroid plexus (CPs) and cerebrospinal fluid (CSF) system in rats.

Methods: Male Sprague Dawley rats were kept in O control in vivo cabinet with either 21% (normoxia) or 8% O (hypoxemia) for up to 48 h.

Low oxygen in inspired air causes severe cerebrocortical hypoxia and cell death in the cerebral cortex of awake rats.

Type 1 respiratory failure (T1RF) is associated with secondary acute brain injury (sABI). The underlying mechanisms of sABI could include injury to brain cells mediated either by hypoxia or by lung injury-triggered inflammation. To elucidate to what extent T1RF causes hypoxia and a consequent hypoxic injury in the brain in the absence of lung injury, we exposed healthy, conscious Sprague-Dawley rats to 48 h long low partial pressure of O in inspired air (PiO) (7.

Budd-Chiari syndrome associated with coeliac disease: case report and literature review.

We report a case of Budd-Chiari syndrome occurring in a patient with coeliac disease, who presented with symptoms of increased abdominal girth, right upper quadrant pain and shortness of breath for three weeks prior to admission. Initial assessment revealed the presence of moderate ascites, hepatosplenomegaly and right-sided pleural effusion. Further diagnostic work-up established a diagnosis of chronic Budd-Chiari syndrome.

The Role of Activated Microglia and Resident Macrophages in the Neurovascular Unit during Cerebral Ischemia: Is the Jury Still Out?

Paracrine signaling in the neurovascular unit (NVU) is aimed to adjust the supply of oxygen and nutrients to metabolic demands of the brain in a feed-forward manner. Cerebral ischemia (CI) severely disrupts this homeostatic mechanism and also causes activation of microglia and resident macrophages in the brain. Contradictory data exist on the time pattern of microglial activation and polarization during CI, on molecular mechanisms that trigger them and on effects of microglia-derived cytokines on brain cells.

Differential cytokine expression by brain microglia/macrophages in primary culture after oxygen glucose deprivation and their protective effects on astrocytes during anoxia.

Background: Activation of microglia/macrophages following cerebral ischemia may be beneficial or detrimental for the survival of brain cells, an ambiguity in effects that has been explained by findings that ischemia can induce transformation of resting monocytes/macrophages into two different inflammation-related phenotypes, termed M1 and M2. The extent to which this differentiation depends on paracrine signaling from other brain cells is not clear. This study explored if oxygen glucose deprivation (OGD) can trigger expression of phenotype-specific markers in rat microglia/macrophages in primary culture, in absence/low abundance of other brain cells.