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Stroke is one of the most prevalent chronic illnesses in Canada. Family caregivers can make a significant contribution toward patients’ recovery. Caregivers’ emotions can impact their motivation to engage in empathy-related helping behaviours. The purpose of this study was to examine relationships among functional deficits of post-stroke individuals, family caregivers’ emotions, and caregivers’ ability to empathize with post-stroke individuals. As guided by Davis’s organizational model on empathy, a correlational descriptive methodology was employed. Participants were requested to complete four questionnaires. Study found that caregiver fatigue was the only factor associated with caregiver empathy-related behaviour. Analyses also found that communication deficits had a linkage with caregivers’ negative emotions. Study results will contribute to the current state of the literature on post-stroke care at home by understanding of the impact of caregivers’ psychological experiences on their empathy-related responses toward post-stroke individuals. Recommendations for clinical practice and future research were made based on this study’s results.

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Bakgrund: När en person drabbas av stroke påverkas även anhöriga. I samband med utskrivning får anhöriga ofta bli vårdare för dem i hemmet. Eftersom de strokedrabbade familjemedlemmarna i olika utsträckning påverkats av stroken behöver de stöttning i det dagliga livet. Anhöriga blir nu vårdare till sin strokedrabbade familjemedlem, vilket medför en förändring i deras liv.   Syfte: Syftet med litteraturstudien var att belysa anhörigas levda erfarenhet av att vårda en strokedrabbad familjemedlem i hemmet i en västerländsk kultur. Antonovskys salutogena modell, känsla av sammanhang utgör en teoretisk referensramen i detta arbete. Metod: En systematisk litteraturstudie med en analysmodell inspirerad av Friberg. Resultat: Analysen resulterade i två teman; förändringar i familjerelationen och förändringar i det egna livet. Relationen blev förändrad och rollerna ändrades när en anhörig blev vårdare för sin strokedrabbade familjemedlem i hemmet. För anhörigvårdaren blev det en ökad arbetsbelastning, ekonomin påverkades och ett större ansvar vilade på denne. Detta ledde för många anhörigvårdare till oro, trots detta var det flera anhörigvårdare som kunde känna glädje och såg positivt på tillvaron. Slutsats: Många anhörigvårdare kunde trots den svåra situationen hitta positiva aspekter. När de blev anhörigvårdare till en strokedrabbad familjemedlem förändrades livet. Det ökade ansvaret ledde till trötthet och utmattning. Förändringar skedde både i egna livet, men även i familjerelationen. Därför var det av vikt att anhöriga gjordes delaktiga i vården och gavs stöd av sjukvården.

Since electric power is one the most important necessities for today’s life and industry, its service reliability must be maintained in an extremely high level. Thunderstorms often reduce this quality of service. Since cloud-to-ground lightning strokes are among the most frequent yet least understood causes of service interruption, predicting the geographical and temporal distribution of the lightning strokes can help power system planners and designers improve the protection of new and existing transmission lines. Such a prediction needs a model that is based on physical properties of the phenomenon and acquired data. This approach requires several stages including modelling, simulation, and characterization. Characterization provides metrics for comparison between the physical and simulated data. The distributions of the lightning stroke densities (aka lightning stroke maps (LSMs)) have patterns that are highly nonlinear, nonstationary, and stochastic. Ordinary analyzes and metrics are insufficient to characterize such patterns. Multiscale analysis of these patterns indicates their self-affinity over multiple scales, which is an indication of their multifractality. Consequently, multifractal analysis methods such as the Rényi fractal dimension spectrum are appropriate candidates for characterization of these density maps. This work uses the lightning stroke data collected by Canadian lightning detection network for Manitoba from 1998 to 2006, employs a multifractal analysis of the lightning stroke maps, and investigates the consistency of such a characterization over time. The results indicate that the LSMs of Manitoba have multifractal distributions, both locally and globally. The results also indicate a convergence in statistical distribution for the LSMs and strong sensitivity of the Rényi spectra to the data variations. For modelling such data, multifractal approaches such as diffusion limited aggregation, percolation, or cellular automata are appropriate candidates. This work provides diffusion limited aggregate modelling and simulation for the maps and compares the physical and simulated lightning stroke maps through Rényi spectra, where the results indicate a high similarity, both visually and analytically. Since lightning strokes are global phenomena, the same methods and techniques can be used for LSMs anywhere in the world. In addition, the utilized methods and approaches for analysis and modelling can be used for similarly complicated phenomena.

The BNIP3 family, a group of death-inducing mitochondrial proteins, includes BNIP3, NIX and BNIP3h. These proteins share structural and functional similarities. BNIP3 causes neuronal cell death in a necrosis-like, caspase-independent manner with mitochondrial dysfunction. We reported that BNIP3 plays a role in delayed neuronal death in stroke models. Over-expression of BNIP3 causes up to 70% neuronal death, while knockdown of BNIP3 only protects 23% neurons from hypoxia. Thus, we hypothesize that other members of the BNIP3 subfamily compensate for the loss of BNIP3. BNIP3 and NIX were highly upregulated in the oxygen and glucose deprivation (OGD)/reoxygenation model, and knockdown of BNIP3 or NIX protected about 20% - 44% of neurons. Knockdown of BNIP3 family reduced neuronal death by 48%. Mitochondrial membrane potential loss, mitochondrial permeability transition pore (MPTP) opening and reactive oxygen species (ROS) production were all significantly attenuated by BNIP3 and/or NIX inhibition. AIF and EndoG were reported involving in caspase-independent cell death in ischemic stroke. We found that AIF was released from mitochondria and translocated into nuclei in neurons after OGD/reoxygenation, while inhibition of BNIP3 blocked AIF and EndoG translocation and prevented neuronal death. Over-expression of BNIP3 and NIX caused AIF translocation and subsequent neuronal death. These data reveal the effects of the BNIP3 family in neuronal death and indicate that AIF and EndoG are two downstream factors in the BNIP3-mediated cell death pathway. Meanwhile, necrostatin-1 (Nec-1), an inhibitor for a caspase-independent necrotic cell death, is able to protect neurons from death in stroke, mechanism of which is unclear. Here, we confirmed that Nec-1 significantly increased survival of neurons in models of stroke in vivo and in vitro. It also attenuated hypoxia or BNIP3-induced mitochondrial dysfunction and prevented mitochondrial release of AIF. Nec-1 did not affect the expression levels of BNIP3 but prevented its integration into mitochondria. These results suggest that Nec-1 protects neurons against ischemia by targeting BNIP3. In summary, this research indicates that the BNIP3 family is one of the regulators of caspase-independent neuronal death in stroke and that Nec-1 is an inhibitor for BNIP3 and a potential therapeutic agent for stroke.

Objective: To develop a score for hematoma expansion prediction, identify predictors of outcome, and validated existing prognostic scores in acute intracerebral hemorrhage (ICH). Methods: Data were obtained from a prospective multicenter ICH cohort. Patients were evaluated with computed tomography (CT) angiography, 24-hour CT, and 3-month outcome. Multivariable regression identified predictors of 24-hour expansion and 3-month outcome and a score was developed for expansion prediction. Existing scores were evaluated in the dataset. Results: The PREDICT Hematoma Expansion Score predicts 24-hour expansion based on number of spots, stroke severity, time from onset, and coagulopathy (c-statistic: 0.803). Prediction was improved over spot sign presence (p<0.001) and clinical variables alone (p=0.002). Existing scores for hematoma expansion and clinical outcome demonstrated reduced discrimination compared with the original reports. Conclusion: The PREDICT Hematoma Expansion Score may aid patient selection for future interventions aimed at reducing expansion however external validation is required. Existing scores demonstrated reduced discrimination.

Objective: To develop a score for hematoma expansion prediction, identify predictors of outcome, and validated existing prognostic scores in acute intracerebral hemorrhage (ICH). Methods: Data were obtained from a prospective multicenter ICH cohort. Patients were evaluated with computed tomography (CT) angiography, 24-hour CT, and 3-month outcome. Multivariable regression identified predictors of 24-hour expansion and 3-month outcome and a score was developed for expansion prediction. Existing scores were evaluated in the dataset. Results: The PREDICT Hematoma Expansion Score predicts 24-hour expansion based on number of spots, stroke severity, time from onset, and coagulopathy (c-statistic: 0.803). Prediction was improved over spot sign presence (p<0.001) and clinical variables alone (p=0.002). Existing scores for hematoma expansion and clinical outcome demonstrated reduced discrimination compared with the original reports. Conclusion: The PREDICT Hematoma Expansion Score may aid patient selection for future interventions aimed at reducing expansion however external validation is required. Existing scores demonstrated reduced discrimination.