Effects of nurse-led lower extremity strength training on knee function recovery in patients who underwent total knee replacement.

AIMS AND OBJECTIVES: To examine the effects of lower extremity muscle strength training on knee function recovery and quality of life in patients who underwent total knee replacement. BACKGROUND: Patients with knee osteoarthritis after surgery experience decreased knee function that impacts their quality of life. However, patients typically lack a long-term, home-based and continuous leg exercise training method and rarely have studies explored the effects of exercise training on knee function recovery and quality of life. DESIGN: A experimental and longitudinal study design. METHODS: The simple randomised sampling (based on patients' admission priority order) was used to collect participant data. Outcome measurements included the Knee Injury and Osteoarthritis Outcome Score. Participants were randomised to receive and starting lower extremity muscle strength training before surgery (training group, n = 100) or to receive usual care (nontraining group, n = 100). Data were collected and followed up with the patients before surgery (T1) and at 2 weeks (T2), 1 month (T3), 2 months (T4) and 3 months (T5) after discharge. RESULTS: The Knee Injury and Osteoarthritis Outcome Score subscale scores showed that both groups of patients experienced knee function and quality of life decreases 2 weeks after total knee replacement, but all subscale scores gradually increased from the first month to the third month after total knee replacement. Both groups and times were significantly different, but the training group's knee function and quality of life recovered earlier and better than the nontraining group does. CONCLUSIONS: This study confirmed that lower extremity muscle strength training helps to improve quality of life and knee function in patients who undergo total knee replacement. Healthcare staff should include this training in presurgical nursing care and in patients' discharge plans as a continuous, daily rehabilitation activity at home. RELEVANCE TO CLINICAL PRACTICE: When patients are diagnosed with knee osteoarthritis and undergo surgery, a presurgical exercise education and discussion of knee function rehabilitation should be part of standard care.

Roles of PTEN-induced putative kinase 1 and dynamin-related protein 1 in transient global ischemia-induced hippocampal neuronal injury.

Recent studies showed that increased mitochondrial fission is an early event of cell death during cerebral ischemia and dynamin-related protein 1 (Drp1) plays an important role in mitochondrial fission, which may be regulated by PTEN-induced putative kinase 1 (PINK1), a mitochondrial serine/threonine-protein kinase thought to protect cells from stress-induced mitochondrial dysfunction and regulate mitochondrial fission. However, the roles of PINK1 and Drp1 in hippocampal injury caused by transient global ischemia (TGI) remain unknown. We therefore tested the hypothesis that TGI may induce PINK1 causing downregulation of Drp1 phosphorylation to enhance hippocampal neuronal survival, thus functioning as an endogenous neuroprotective mechanism. We found progressively increased PINK1 expression in the hippocampal CA1 subfield1-48 h following TGI, reaching the maximal level at 4 h. Despite lack of changes in the expression level of total Drp1 and phosphor-Drp1 at Ser637, TGI induced a time-dependent increase of Drp1 phosphorlation at Ser616 that peaked after 24 h. Notably, PINK1-siRNA increased p-Drp1(Ser616) protein level in hippocampal CA1 subfield 24 h after TGI. The PINK1 siRNA also aggravated the TGI-induced oxidative DNA damage with an increased 8-hydroxy-deoxyguanosine (8-OHdG) content in hippocampal CA1 subfield. Furthermore, PINK1 siRNA also augmented TGI-induced apoptosis as evidenced by the increased numbers of TUNEL-positive staining and enhanced DNA fragmentation. These findings indicated that PINK1 is an endogenous protective mediator vital for neuronal survival under ischemic insult through regulating Drp1 phosphorylation at Ser616.

A robust graph-based segmentation method for breast tumors in ultrasound images.

OBJECTIVES: This paper introduces a new graph-based method for segmenting breast tumors in US images. BACKGROUND AND MOTIVATION: Segmentation for breast tumors in ultrasound (US) images is crucial for computer-aided diagnosis system, but it has always been a difficult task due to the defects inherent in the US images, such as speckles and low contrast. METHODS: The proposed segmentation algorithm constructed a graph using improved neighborhood models. In addition, taking advantages of local statistics, a new pair-wise region comparison predicate that was insensitive to noises was proposed to determine the mergence of any two of adjacent subregions. RESULTS AND CONCLUSION: Experimental results have shown that the proposed method could improve the segmentation accuracy by 1.5-5.6% in comparison with three often used segmentation methods, and should be capable of segmenting breast tumors in US images.

Activation of calcium/calmodulin-dependent protein kinase IV and peroxisome proliferator-activated receptor γ coactivator-1α signaling pathway protects against neuronal injury and promotes mitochondrial biogenesis in the hippocampal CA1 subfield after transient global ischemia.

Delayed neuronal cell death occurs in the vulnerable CA1 subfield of the hippocampus after transient global ischemia (TGI). We demonstrated previously, based on an experimental model of TGI, that the significantly increased content of oxidized proteins in hippocampal CA1 neuron was observed as early as 30 min after TGI, followed by augmentation of PGC-1α expression at 1 hr, as well as up-regulation of mitochondrial uncoupling protein 2 (UCP2) and superoxide dismutases 2 (SOD2). Using the same animal model, the present study investigated the role of calcium/calmodulin-dependent protein kinase IV (CaMKIV) and PGC-1α in delayed neuronal cell death and mitochondrial biogenesis in the hippocampus. In Sprague-Dawley rats, significantly increased expression of nuclear CaMKIV was noted in the hippocampal CA1 subfield as early as 15 min after TGI. In addition, the index of mitochondrial biogenesis, including a mitochondrial DNA-encoded polypeptide, cytochrome c oxidase subunit 1 (COX1), and mitochondrial number significantly increased in the hippocampal CA1 subfield 4 hr after TGI. Application bilaterally into the hippocampal CA1 subfield of an inhibitor of CaMKIV, KN-93, 30 min before TGI attenuated both CaMKIV and PGC-1α expression, followed by down-regulation of UCP2 and SOD2, decrease of COX1 expression and mitochondrial number, heightened protein oxidation, and enhanced hippocampal CA1 neuronal damage. This study provides correlative evidence for the neuroprotective cascade of CaMKIV/PGC-1α which implicates at least in part the mitochondrial antioxidants UCP2 and SOD2 as well as mitochondrial biogenesis in ischemic brain injury.

Protective effects of peroxisome proliferator-activated receptors gamma coactivator-1alpha against neuronal cell death in the hippocampal CA1 subfield after transient global ischemia.

Peroxisome proliferator-activated receptors gamma coactivator-1alpha (PGC-1alpha) may regulate the mitochondrial antioxidant defense system under many neuropathological settings. However, the exact role of PGC-1alpha in ischemic brain damage is still under debate. Based on an experimental model of transient global ischemia (TGI), this study evaluated the hypothesis that the activation of PGC-1alpha signaling pathway protects hippocampal CA1 neurons against delayed neuronal death after TGI. In Sprague-Dawley rats, significantly increased content of oxidized proteins in the hippocampal CA1 tissue was observed as early as 30 min after TGI, followed by augmentation of PGC-1alpha expression at 1 hr. Expression of uncoupling protein 2 (UCP2) and superoxide dismutases 2 (SOD2) in the hippocampal CA1 neurons was upregulated 4-48 hr after TGI. In addition, knock-down of PGC-1alpha expression by pretreatment with a specific antisense oligodeoxynucleotide in the hippocampal CA1 subfield downregulated the expression of UCP2 and SOD2 with resultant exacerbation of oxidative stress and augmentation of delayed neuronal cell death in the hippocampus after TGI. Overall, our results indicate that PGC-1alpha is induced by cerebral ischemia leading to upregulation of UCP2 and SOD2, thereby providing a neuroprotective effect against ischemic brain injury in the hippocampus by ameliorating oxidative stress.

Effects of rosiglitazone on global ischemia-induced hippocampal injury and expression of mitochondrial uncoupling protein 2.

We investigate the effect of rosiglitazone, a ligand for peroxisome proliferator-activated receptor-gamma (PPARgamma) with anti-inflammatory and anti-oxidative actions, on hippocampal injury and its roles in mitochondrial uncoupling protein 2 (UCP2) expression caused by transient global ischemia (TGI) in rats. Increased UCP2 expression was observed in mitochondria of hippocampal CA1 2-24h after TGI/reperfusion, with maximal expression levels at 6-18h. Administration of rosiglitazone to hippocampus 30min prior to the onset of TGI further enhanced mitochondrial UCP2 expression 2-6h following TGI/reperfusion. Rats subjected to TGI/reperfusion displayed a significant increase in lipid peroxidation, based on increased malondialdehyde (MDA) levels, in hippocampal CA1 mitochondria 2-6 h after reperfusion. Rosiglitazone significantly attenuated TGI/reperfusion-induced lipid peroxidation and suppressed hippocampal CA1 neuronal death based on the surviving neuronal counts. In conclusion, our results provide correlative evidence for the "PPARgamma-->UCP2-->neuroprotection" cascade in ischemic brain injury.

Modulation of somatosensory evoked potentials during wake-sleep states and spike-wave discharges in the rat.

STUDY OBJECTIVE: To clarify the cortical evoked responses in the primary somatosensory cortex of the rat under states of waking, slow-wave sleep (SWS), paradoxical sleep (PS), and spike-wave discharges (SWDs), which are associated with absence seizure. DESIGN: Somatosensory evoked potentials (SEPs) in response to single- and paired-pulse stimulations under waking, SWS, PS, and SWDs were compared. SEPs to a single-pulse stimulus with regard to cortical spikes of sleep spindles and SWDs were also evaluated. PARTICIPANTS: Twenty Long Evans rats. INTERVENTIONS: Single- and paired-pulse innocuous electrical stimulations were applied to the tail of rats with chronically implanted electrodes in the primary somatosensory cortex and neck muscle under waking, SWS, PS, and SWDs. MEASUREMENTS AND RESULTS: SEPs displayed distinct patterns under waking/PS and SWS/SWDs. The short-latency P1-N1 wave of the SEP was severely impeded during SWDs but not in other states. Reduction of the P1-N1 magnitude to the second stimulus of the paired-pulse stimulus for interstimulus intervals of < or = 300 milliseconds appeared in waking and PS states, but the decrease occurred only at particular interstimulus intervals under SWS. Interestingly, augmentation was found under SWDs. Moreover, cyclic augmentation of the P1-N1 magnitude was associated with spindle spikes, but cyclic reduction was observed with SWD spikes. CONCLUSION: Changes in SEPs are not only behavior dependent, but also phase locked onto ongoing brain activity. Distinct short-term plasticity of SEPs during sleep spindles or SWDs may merit further studies for seizure control and tactile information processing.