A 70 Year Old Male with Left-Sided Flaccidity Following Right Hemorrhagic Cerebrovascular Accident: A Case Study

Background and Purpose: Cerebrovascular accidents (CVAs) are a common medical issue addressed by physical therapists. This case study examines the effectiveness of one rehabilitation plan in an inpatient rehabilitation setting, and explores potential improvements in the method of intervention for patients following a CVA. Case Description: This patient was a 70-year-old male admitted to an inpatient rehabilitation facility following a right CVA resulting in left-sided flaccidity of upper and lower extremities. He underwent therapy in this facility for five weeks. Interventions: Conventional therapy interventions were used with this patient. The interventions consisted of a combination of strengthening, gait training, balance activities, wheelchair mobility, and patient education. The goal of physical therapy was to improve the patient’s function and independence by the time of discharge. Outcomes: The patient achieved significant gains in his mobility and transfer abilities, as well as his activity tolerance. Discussion: While the patient and his family were satisfied with the improvements gained in therapy, additional intervention and examination options may have been beneficial. The use of a fatigue scale and virtual reality-based therapy are discussed as potential beneficial additions to the original rehabilitation process. These additions may have the potential to improve outcomes and overall therapy experience for clients in the future

An Electromyographic and Motion Analysis of Forward and Backward Walking

Backward walking is a common intervention in the rehabilitation of lower extremity injuries. Despite its popularity, there is limited research available on the EMG activity during backward walking at an incline when compared to forward walking. In this study, we recorded EMG activity in four muscles of the lower extremity and utilized motion analysis to evaluate the knee range of motion when walking forward and backward on a treadmill at 0 and 15 percent grade inclines. Overall, our results indicated a greater increase in muscle activity during backward walking than forward walking. Walking backward at a 15 percent grade incline showed the largest increase in muscle activity with the vastus lateralis showing increase of 609%, vastus medialis increasing 339%, semitendinosus increasing 189%, and biceps femoris increasing 172% when compared with forward walking at a 0 percent grade. Our results showed the degree of knee flexion to be the greatest during backward walking at a 15 percent grade (70.2 degrees of knee flexion), followed by forward walking at a 15 percent grade (68.4 degrees of knee flexion), forward walking at 0 percent grade (67.4 degrees of knee flexion) and finally backward walking at 0 percent grade (57.5 degrees of knee flexion). We conclude that both backward and forward walking at an incline can be beneficial for lower extremity rehabilitation

Flow Cytometry for Identification of PRDM1-eYFP Transgenic Mice

The goal of this study was to determine if flow cytometry could be used to identify transgene carrier mice [B6.Cg-Tg(Prdm1-EYFP)1Mnz/J] by their expression of the enhanced yellow fluorescent protein (eYFP) in peripheral blood lymphocytes. In these mice, eYFP expression is under the control of the Prdm1 gene promoter. Littermates were identified as being either wild type or transgene carriers using a polymerase chain reaction (PCR) analysis of tail tissue. Peripheral blood leukocytes were isolated from each of the mice, and both the percent and mean fluorescence intensity (MFI) were determined for eYFP expression by lymphocytes. We found that blood lymphocytes from eYFP transgene carrier mice contained an average of 1.54% eYFP+ cells. In contrast, wild type animals contained significantly fewer (P \u3c 0.05) with an average of 0.18%. The percent eYFP- and eYFP+ data ranges did not overlap. The average MFI values for these groups were also significantly different, but their data ranges overlapped. The PCR process performed in our laboratory required approximately 20 hours over three days to complete with an estimated per animal cost of $16.00. In contrast, the flow cytometry procedure required approximately six hours within one day to complete with an estimated per animal cost of$7.85. We conclude that flow cytometry is an adequate and less costly method for identifying eYFP transgene carrier mice

Schlafen 3 knockout mice display gender-specific differences in weight gain, food efficiency, and expression of markers of intestinal epithelial differentiation, metabolism, and immune cell function

Self-renewal and differentiation are essential for intestinal epithelium absorptive functioning and adaptation to pathological states such as short gut syndrome, ulcers, and inflammatory bowel disease. The rodent Slfn3 and its human analog Slfn12 are critical in regulating intestinal epithelial differentiation. We sought to characterize intestinal function in Slfn3 knockout (KO) mice. Male and female pair-fed Slfn3KO mice gained less weight with decreased food efficiency than wild type (WT) mice, with more pronounced effects in females. RNA sequencing performed on intestinal mucosa of Slfn3KO and WT mice showed gene ontology decreases in cell adhesion molecule signaling, tumor necrosis factor receptor binding, and adaptive immune cell proliferation/functioning genes in Slfn3KO mice, with greater effects in females. qPCR analysis of fatty acid metabolism genes, Pla2g4c, Pla2g2f, and Cyp3c55 revealed an increase in Pla2g4c, and a decrease in Pla2g2f in Slfn3KO females. Additionally, adipogenesis genes, Fabp4 and Lpl were decreased and ketogenesis gene Hmgcs2 was increased in female Slfn3KO mice. Sequencing did not reveal significant changes in differentiation markers, so qPCR was utilized. Slfn3KO tended to have decreased expression of intestinal differentiation markers sucrase isomaltase, dipeptidyl peptidase 4, villin 1, and glucose transporter 1 (Glut1) vs. WT males, although these trends did not achieve statistical significance unless data from several markers was pooled. Differentiation markers, Glut2 and sodium-glucose transporter 1 (SGLT1), did show statistically significant sex-dependent differences. Glut2 mRNA was reduced in Slfn3KO females, while SGLT1 increased in Slfn3KO males. Notch2 and Cdx2 were only increased in female Slfn3KO mice. Although Slfn3KO mice gain less weight and decreased food efficiency, their biochemical phenotype is more subtle and suggests a complex interplay between gender effects, Slfn3, and another regulatory pathway yet to be identified that compensates for the chronic loss of Slfn3

Gene expression profiling and network analysis of peripheral blood monocytes in a chronic model of allergic asthma

The Aspergillus fumigatus mouse model of asthma mimics the characteristics of human fungal asthma, including local and systemic inflammation. Monocyte/macrophage lineage cells direct innate immune responses and guide adaptive responses. To identify gene expression changes in peripheral blood monocytes in the context of fungal allergy, mice were exposed to systemic and intranasal inoculations of fungal antigen (sensitized), and naïve and sensitized animals were challenged intratracheally with live A. fumigatus conidia. Microarray analysis of blood monocytes from allergic versus non-allergic mice showed ≥ twofold modulation of 45 genes. Ingenuity pathway analysis revealed a network of these genes involved in antigen presentation, inflammation, and immune cell trafficking. These data show that allergen sensitization and challenge affects gene expression in peripheral monocytes.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/79085/1/j.1348-0421.2010.00242.x.pd

Schlafen 12 Interaction with SerpinB12 and Deubiquitylases Drives Human Enterocyte Differentiation

Background/Aims: Human enterocytic differentiation is altered during development, fasting, adaptation, and bariatric surgery, but its intracellular control remains unclear. We hypothesized that Schlafen 12 (SLFN12) regulates enterocyte differentiation. Methods: We used laser capture dissection of epithelium, qRT-PCR, and immunohistochemistry to evaluate SLFN12 expression in biopsies of control and fasting human duodenal mucosa, and viral overexpression and siRNA to trace the SLFN12 pathway in human Caco-2 and HIEC6 intestinal epithelial cells. Results: Fasting human duodenal mucosa expressed less SLFN12 mRNA and protein, accompanied by decreases in enterocytic markers like sucrase-isomaltase. SLFN12 overexpression increased Caco-2 sucrase-isomaltase promoter activity, mRNA, and protein independently of proliferation, and activated the SLFN12 putative promoter. SLFN12 coprecipitated Serpin B12 (SERPB12). An inactivating SLFN12 point mutation prevented both SERPB12 binding and sucrase-isomaltase induction. SERPB12 overexpression also induced sucrase-isomaltase, while reducing SERPB12 prevented the SLFN12 effect on sucrase-isomaltase. Sucrase-isomaltase induction by both SLFN12 and SERPB12 was attenuated by reducing UCHL5 or USP14, and blocked by reducing both. SERPB12 stimulated USP14 but not UCHL5 activity. SERPB12 coprecipitated USP14 but not UCHL5. Moreover, SLFN12 increased protein levels of the sucrase-isomaltase-promoter-binding transcription factor cdx2 without altering Cdx2 mRNA. This was prevented by reducing UCHL5 and USP14. We further validated this pathway in vitro and in vivo. SLFN12 or SERPB12 overexpression induced sucrase-isomaltase in human non-malignant HIEC-6 enterocytes. Conclusions: SLFN12 regulates human enterocytic differentiation by a pathway involving SERPB12, the deubiquitylases, and Cdx2. This pathway may be targeted to manipulate human enterocytic differentiation in mucosal atrophy, short gut or obesity

Regulatory iNKT cells lack PLZF expression and control Treg cell and macrophage homeostasis in adipose tissue

iNKT cells are CD1d-restricted lipid-sensing innate T cells that express the transcription factor PLZF. iNKT cells accumulate in adipose tissue, where they are anti-inflammatory, but the factors that contribute to their anti-inflammatory nature, and their targets in adipose tissue are unknown. Here we report that adipose tissue iNKT cells have a unique transcriptional program and produce interleukin 2 (IL-2) and IL-10. Unlike other iNKT cells, they lack PLZF, but express the transcription factor E4BP4, which controls their IL-10 production. Adipose iNKT cells are a tissue resident population that induces an anti-inflammatory phenotype in macrophages and, through production of IL-2, controls the number, proliferation and suppressor function of adipose regulatory T (Treg) cells. Thus, adipose tissue iNKT cells are unique regulators of immune homeostasis in this tissue