Influence of 100% and 40% oxygen on penumbral blood flow, oxygen level, and T2*-weighted MRI in a rat stroke model

Accurate imaging of the ischemic penumbra is a prerequisite for acute clinical stroke research. T2* magnetic resonance imaging (MRI) combined with an oxygen challenge (OC) is being developed to detect penumbra based on changes in blood deoxyhemoglobin. However, inducing OC with 100% O2 induces sinus artefacts on human scans and influences cerebral blood flow (CBF), which can affect T2* signal. Therefore, we investigated replacing 100% O2 OC with 40% O2 OC (5 minutes 40% O2 versus 100% O2) and determined the effects on blood pressure (BP), CBF, tissue pO2, and T2* signal change in presumed penumbra in a rat stroke model. Probes implanted into penumbra and contralateral cortex simultaneously recorded pO2 and CBF during 40% O2 (n=6) or 100% O2 (n=8) OC. In a separate MRI study, T2* signal change to 40% O2 (n=6) and 100% O2 (n=5) OC was compared. Oxygen challenge (40% and 100% O2) increased BP by 8.2% and 18.1%, penumbra CBF by 5% and 15%, and penumbra pO2 levels by 80% and 144%, respectively. T2* signal significantly increased by 4.56%±1.61% and 8.65%±3.66% in penumbra compared with 2.98%±1.56% and 2.79%±0.66% in contralateral cortex and 1.09%±0.82% and −0.32%±0.67% in ischemic core, respectively. For diagnostic imaging, 40% O2 OC could provide sufficient T2* signal change to detect penumbra with limited influence in BP and CBF

The influence of gender on ‘tissue at risk’ in acute stroke: A diffusion-weighted magnetic resonance imaging study in a rat model of focal cerebral ischaemia

This is the first study to assess the influence of sex on the evolution of ischaemic injury and penumbra. Permanent middle cerebral artery occlusion was induced in male (n = 9) and female (n = 10) Sprague-Dawley rats. Diffusion-weighted imaging was acquired over 4 h and infarct determined from T2 images at 24 h post-permanent middle cerebral artery occlusion. Penumbra was determined retrospectively from serial apparent diffusion coefficient lesions and T2-defined infarct. Apparent diffusion coefficient lesion volume was significantly smaller in females from 0.5 to 4 h post permanent middle cerebral artery occlusion as was infarct volume. Penumbral volume, and its loss over time, was not significantly different despite the sex difference in acute and final lesion volumes

Assessing the above-ground biomass of a complex tropical\ud rainforest using a canopy crane

Current estimates of the total biomass in tropical rainforests vary considerably; this is due in large part\ud to the different approaches that are used to calculate biomass. In this study we have used a canopy crane to measure the tree architectures in a 1 ha plot of complex mesophyll vine forest at Cape Tribulation, Australia. Methods were developed to measure and calculate the crown and stem biomass of six major species of tree and palm (Alstonia scholaris (Apocynaceae), Cleistanthus myrianthus (Euphorbiaceae), Endiandra microneura (Lauraceae), Myristica\ud insipida (Myristicaceae), Acmena graveolens (Myrtaceae), Normanbya normanbyi (Arecaceae)) using the unique access provided by the crane. This has allowed the first non-destructive biomass estimate to be carried out for a\ud forest of this type. Allometric equations which relate tree biomass to the measured variable ‘diameter at breast\ud height’ were developed for the six species, and a general equation was also developed for trees on the plot. The\ud general equation was similar in form to equations developed for tropical rainforests in Brazil and New Guinea.The\ud species equations were applied at the level of families, the generalized equation was applied to the remaining species which allowed the biomass of a total of 680 trees to be calculated. This has provided a current estimate of 270 t ha-1 above-ground biomass at the Australian Canopy Crane site; a value comparable to lowland rainforests in Panama and French Guiana. Using the same tree database seven alternative allometric equations (literature equations for tropical rainforests) were used to calculate the site biomass, the range was large (252–446 t ha-1) with only three equations providing estimates within 34 t ha-1 (12.5%) of the site value. Our use of multiple species-specific allometric equations has provided a site estimate only slightly larger (1%) than that obtained using allometric equations developed specifically for tropical wet rainforests. We have demonstrated that it is possible to nondestructively measure the biomass in a complex forest using an on-site canopy crane. In conjunction the development of crown maps and a detailed tree architecture database allows changes in forest structure to be followed\ud quantitatively

T-Cell Expression and Release of Kidney Injury Molecule-1 in Response to Glucose Variations Initiates Kidney Injury in Early Diabetes

Half of the mortality in diabetes is seen in individuals 1c 66.1 [12.3] mmol/mol; diabetes duration 10.7 ± 5.2 years; and BMI 24.5 [5.3] kg/m2) and 10-year historical uACR, HbA1c, and random blood glucose concentrations collected retrospectively. Glucose fluctuations in the absence of diabetes were also compared with streptozotocin diabetes in apolipoprotein E/ mice. Kidney biopsies were used to examine infiltration of KIM-1–expressing T cells in DKD and compared with other chronic kidney disease. Individuals at high risk for DKD had persistent elevations in uACR defined by area under the curve (AUC; uACR AUC0–10yrs, 29.7 ± 8.8 vs. 4.5 ± 0.5; P 2 higher estimated glomerular filtration rates (modified Schwartz equation; Padj + T cells. These findings were confirmed in a murine model of glycemic variability both in the presence and absence of diabetes. KIM-1+ T cells were also infiltrating kidney biopsies from individuals with DKD. Healthy primary human proximal tubule epithelial cells exposed to plasma from high-risk youth with diabetesshowedelevatedcollagenIVandsodium–glucose cotransporter 2 expression, alleviated with KIM-1 blockade. Taken together, these studies suggest that glycemic variations confer risk for DKD in diabetes via increased CD8+ T-cell production of KIM-1.</p