A Hybrid Controller with Chedoke-McMaster Stroke Assessment for Robot-Assisted Rehabilitation

See if your therapist has any way to use robotics or if they even know about this stuff.
http://www.sciencedirect.com/science/article/pii/S1877705812026227

Abstract

Amongst the major challenges in post-stroke rehabilitation are the repetitiveness nature of rehabilitation procedure, and the accessibility of therapists for long-term treatment. In manual rehabilitation procedure, the patient is subjected to repetitive mechanical movement of the affected limb by the therapist. In one of the techniques called active-assist exercise, the subject moves his affected limb along a specified trajectory with the therapist guiding the motion. The therapist gives some assistance to the subject to complete the course if deemed necessary and the procedure repeats. The significant advantages of using robots in assisting rehabilitation are its efficiency and it is fatigue free. The robots however need to be developed to have the capability of human therapist in providing the rehabilitation more naturally. In this paper, the work focuses on developing a new framework for the robot controller system. In particular, a low-level controller, which is in the form of force controller based on impedance control theory is discussed. The controller is capable of governing the active-assist exercise through autonomous guidance during the therapeutic procedure based on the Chedoke-McMaster stroke assessment method.

Endonuclease VIII-like 1 (NEIL1) promotes short-term spatial memory retention and protects from ischemic stroke-induced brain dysfunction and death in mice

Another one to talk to your researcher about.
http://www.pnas.org/content/early/2012/08/22/1204156109.short

Abstract

Recent findings suggest that neurons can efficiently repair oxidatively damaged DNA, and that both DNA damage and repair are enhanced by activation of excitatory glutamate receptors. However, in pathological conditions such as ischemic stroke, excessive DNA damage can trigger the death of neurons. Oxidative DNA damage is mainly repaired by base excision repair (BER), a process initiated by DNA glycosylases that recognize and remove damaged DNA bases. Endonuclease VIII-like 1 (NEIL1) is a DNA glycosylase that recognizes a broad range of oxidative lesions. Here, we show that mice lacking NEIL1 exhibit impaired memory retention in a water maze test, but no abnormalities in tests of motor performance, anxiety, or fear conditioning. NEIL1 deficiency results in increased brain damage and a defective functional outcome in a focal ischemia/reperfusion model of stroke. The incision capacity on a 5-hydroxyuracil–containing bubble substrate was lower in the ipsilateral side of ischemic brains and in the mitochondrial lysates of unstressed old NEIL1-deficient mice. These results indicate that NEIL1 plays an important role in learning and memory and in protection of neurons against ischemic injury.

Neuron-Specific Prolyl-4-Hydroxylase Domain 2 Knockout Reduces Brain Injury After Transient Cerebral Ischemia

I'm sure  your researcher can explain how this matches up with other hyperacute therapies and what the plan is going forward.
http://stroke.ahajournals.org/content/early/2012/08/24/STROKEAHA.112.669598.abstract

Abstract

Background and Purpose—Numerous factors involved in the adaptive response to hypoxia, including erythropoietin and vascular endothelial growth factor are transcriptionally regulated by hypoxia-inducible factors (HIFs). During normoxia, prolyl-4-hydroxylase domain (PHD) proteins hydroxylate HIF-α subunits, resulting in their degradation. We investigated the effect of neuronal deletion of PHD2, the most abundant isoform in brain, for stroke outcome.

Methods—We generated neuron-specific Phd2 knockout mice and subjected animals to systemic hypoxia or transient middle cerebral artery occlusion. Infarct volume and cell death were determined by histology. HIF-1α, HIF-2α, and HIF target genes were analyzed by immunoblotting and real-time polymerase chain reaction, respectively.

Results—Neuron-specific ablation of Phd2 significantly increased protein stability of HIF-1α and HIF-2α in the forebrain and enhanced expression of the neuroprotective HIF target genes erythropoietin and vascular endothelial growth factor as well as glucose transporter and glycolysis-related enzymes under hypoxic and ischemic conditions. Mice with Phd2-deficient neurons subjected to transient cerebral ischemia exhibited a strong reduction in infarct size, and cell death of hippocampal CA1 neurons located in the peri-infarct region was dramatically reduced in these mice. Vessel density in forebrain subregions, except for caudate–putamen, was not altered in Phd2-deficient animals.

Conclusions—Our findings denote that the endogenous adaptive response on hypoxic–ischemic insults in the brain is at least partly dependent on the activity of HIFs and identify PHD2 as the key regulator for the protective hypoxia response. The results suggest that specific inhibition of PHD2 may provide a useful therapeutic strategy to protect brain tissue from ischemic injury.

No. 2 Acupuncture treatment programs for post-stroke motor rehabilitation in community hospitals: study protocol of a multicenter, randomized, controlled trial

I moved this to get it out of the top post.
Why are people even reading this unsupported crap? I have more important posts you should be reading.
 See here for lack of evidence.  Why is the NIH even publishing this stuff?
http://www.ncbi.nlm.nih.gov/pubmed/22587973

Abstract

BACKGROUND:

Stroke is responsible for increasingly high rates of mortality and disability worldwide. Approximately two million people suffer from stroke for the first time in China each year. The high incidence (50%) of post-stroke disability brings a heavy burden to patients and their caregivers. Acupuncture has been widely used in the communities for post-stroke rehabilitation in China.(who cares? Is it effective?, research?) The objective of this trial is to apply our acupuncture research achievement to treatment and evaluation of post-stroke hemiplegic patients in community.

METHODS AND DESIGN:

A multicenter, randomized, controlled trial will be performed in Longhua Hospital and a number of community health service centers in Shanghai. A total of 124 patients (estimated sample size) with post-stroke hemiplegia will be randomly divided into an acupuncture group and a control group. The patients undergoing randomization should be stratified according to National Institutes of Health Stroke Scale score at baseline. Within the acupuncture group, different acupuncture protocols are administered to patients with flaccid paralysis or spastic paralysis based on the Ashworth Scale. Patients in the acupuncture group will also be treated with comprehensive rehabilitation therapy.(dual treatment,which one works?) The control group will be treated with comprehensive rehabilitation therapy only. The primary outcome measures are the Simplified Fugl-Meyer Motor Scale, the Modified Barthel Index, and the Burden of Stroke Scale. Secondary outcome measures are the modified Rankin Scale, the modified Ashworth Scale and the Stroke Scale of Traditional Chinese Medicine. Outcome measures will be performed after 4 and 8 weeks of treatment. The patients will be followed up after 6 months.

DISCUSSION:

The results of this study are expected to demonstrate that our standardized acupuncture protocol for treating and evaluating post-stroke hemiplegic patients will improve motor function and lessen the burden of post-stroke patients within the communities. This will provide the evidence to support successful translation of acupuncture therapy for post-stroke hemiplegic patients in community hospital use.

TRIAL REGISTRATION:

This trial was registered in Chinese Clinical Trial Registry with the registration number ChiCTR-TRC-11001347.

Protein May Play Part in Future Heart Failure

Talk to your researcher/doctor and have them explain the difference between Galectin-1, useful for stem cells and Galectin-3.
http://www.medpagetoday.com/Cardiology/CHF/34513
Galectin-3 (Gal-3), a marker of cardiac fibrosis, is associated with an increased risk of heart failure and death, researchers found.
Over a mean follow-up of nearly 9 years, those with elevated levels of Gal-3 had a significant 28% (95% CI 1.14 to 1.43, P
. "This collective experimental evidence suggests that Gal-3 may play a causal in cardiac remodeling," the authors stated.
However, adding Gal-3 to clinical factors resulted in only minor improvements in net reclassification. It also did not substantially increase the C-statistic (0.855 to 0.859).
Nonetheless, this is the first time that it's been shown that Gal-3 has a relationship with future heart failure, noted David Morrow, MD, MPH, and Michelle O'Donoghue, MD, MPH, of Brigham and Women's Hospital in Boston, in an accompanying editorial.
Although Gal-3 has been associated with adverse events in those with heart failure, it has not been evaluated as a predictor of incident heart failure in apparently healthy people.
Cardiac fibrosis, of which Gal-3 is a marker, plays an important role in the development of heart failure. Earlier identification of elevated levels of this betagalactoside-binding lectin might offer the opportunity to treat people long before heart failure develops, researchers said.
To fill in the gap, Levy and colleagues evaluated 3,353 participants enrolled in the offspring cohort of the community-based Framingham Heart Study.
The mean age of participants was 59 and 53% of them were women. Overall, Gal-3 levels were higher in women than men (median 14.3 ng/mL versus 13.1 ng/mL, P<0 .05=".05" p="p"> Also, those with higher concentrations of the protein tended to be older and have more cardiovascular risk factors such as high blood pressure, diabetes, previous coronary artery disease, a higher body mass index, and a lower estimated glomerular filtration rate (eGFR; P less than 0.0001, for the trend for all).
When researchers performed a multivariate analysis, only eGFR was dropped from the list of risk factors above, while B-type natriuretic peptide (BNP) was added.
Examining the echocardiographic data, researchers found Gal-3 was significantly associated with positive left ventricular remodeling. Having higher levels of the protein conferred twice the odds of having elevated left ventricular mass, they wrote.
But Gal-3 was not associated with fractional shortening, left ventricular systolic dysfunction, or left atrial size.
Crude heart failure rates progressed in a step-wise fashion with increasing Gal-3 quartiles.
During a mean follow-up period of 8.1 years, 5.1% of patients experienced first heart failure events.
The upper limits for Gal-3 quartiles for men and women were 15.4 ng/ml to 47.7 ng/ml and 16.8 ng/ml to 52.1 ng/ml, respectively. The lower limits were 3.9 ng/ml to 11.1 ng/ml for men and 5.0 ng/ml to 12.0 ng/ml for women.
Among the 25% of people with the highest Gal-3 levels, the annual rate of heart failure was 12 per 1,000 person-years compared with 3 per 1,000 person-years for the 25% of participants with the lowest levels.
Researchers added BNP to the multivariate analysis and found that high Gal-3 levels increased the risk of a first heart failure incident by a significant 23%. However, BNP was associated with a significant 46% increased risk.
There was no difference regarding Gal-3 levels between those with preserved ejection fraction and depressed ejection fraction.
Levy and colleagues suggested that directly modulating that Gal-3 pathway may be beneficial in these patients. They called for more study into how assessment of Gal-3 can help this patient population.
Morrow and O'Donoghue noted that Gal-3 is also sensitive to fibrotic conditions in other areas such as the liver, lungs, and kidneys. For that reason, it may difficult to include the protein in a screening strategy.
Study limitations included the modest number of heart failure events and the possibility that Gal-3 levels are influenced by other conditions. Also, the results may not be generalizable because patients were mostly Caucasian.

Rest at the link.

Rehabilitation of the Upper Extremity after Stroke: A Case Series Evaluating REO Therapy and an Auditory Sensor Feedback for Trunk Control

You'll have to have your therapist explain this one.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3423950/

Abstract

BACKGROUND AND PURPOSE:

Task-related training (TRT) but not resistive exercise (RE) was found to improve the path of the hand of a hemiparetic upper extremity when reaching to targets. Forward movement of the trunk, however, compensated for the poststroke motor impairment. Prior studies also demonstrated that short-term practice of reaching to grasp objects with truncal motion restrained (compared to unrestrained practice) increased elbow extension, lessened compensatory trunk movement, and improved interjoint coordination during performance with the trunk unrestrained.

OBJECTIVE:

To determine the effects of TRT and RE on unrestrained reaching following extended practice in which compensatory truncal motion was limited.

METHODS:

Using a restraining device to reduce movement of the trunk, hemiparetic patients with moderately severe motor impairment were given 12 sessions over 4 weeks of TRT (n = 5) or RE (n = 6). Reaching when the trunk was not restrained to targets located ipsilateral, midline, and contralateral to the impaired arm was tested before and 2 days after training by 3D kinematic analyses.

RESULTS:

After both training protocols, kinematic analysis showed that trunk flexion decreased (P < .01, eta(2) = .53) scapular motion shifted toward protraction (P < .01, eta(2) = .57) and elbow extension increased (P < .04, eta(2) = .39). Only after TRT did the path of the hand straighten (P < .02, eta(2) = .46), deceleration time decrease (P < .03, eta(2) = .44), and, at the difficult ipsilateral target, shoulder flexion increase (P < .03, eta( 2) = .31).

CONCLUSIONS:

Training that restricted compensatory truncal motion during TRT improved the precision of reaching more than during RE. Truncal restraint during rehabilitation of reaching may be an effective therapeutic strategy in patients with moderately severe hemiparetic stroke, especially when combined with TRT.

SAIL: A 3D rehabilitation system to improve arm function following stroke

Who is going to get these into a clinical setting? The Joint Commission? Hah!
A stroke association? ASA?, NSA? Hah!
Look at that, its for chronic.
http://onlinelibrary.wiley.com/doi/10.1002/pnp.242/abstract

Abstract

Our March/April 2011 issue featured an article describing a 3D robotic and electrical stimulation system known as SAIL (Stimulation Assistance through Iterative Learning). This system was developed at the University of Southampton for rehabilitation of arm movement post stroke. Here, the multidisciplinary team at Southampton present the results of their first study to investigate the efficacy of the system in chronic stroke patients.

This is where the academic document should be;
 http://soton.academia.edu/ZhonglunCai/Papers/676272/Stimulation_Assistance_through_Iterative_Learning_SAIL_A_3D_Stroke_Rehabilitation_System

 More documentation here;
http://ifess.org/proceedings/IFESS2011/IFESS2011_028_Meadmore.pdf

Should a Patient Undergo Rehabilitation After Stroke?

An appalling question to ask. It does degenerate into a commercial.
http://handtutorblog.wordpress.com/2012/08/28/should-a-patient-undergo-rehabilitation-after-stroke/

Henrik S. Jørgensen, MD etal of the Department of Radiology, Bispebjerg Hospital, Copenhagen, Denmark cocnducted a study to determine the value of post stroke rehabilitation.

The objective of the study was  to evaluate the outcome of stroke divided according to both the severity of the initial stroke  and the  initial level of disability.

How to Learn in Your Sleep

The application described is pretty limited but our stroke researchers should be able to find  a way for us to make use of it. Then they could compare this to lucid dreaming efficacy.
http://www.scientificamerican.com/article.cfm?id=how-to-learn-in-your-sleep

A novel walking speed estimation scheme and its application to treadmill control for gait rehabilitation

Now if we just can get someone smart enough to translate this into a stroke protocol.
http://www.jneuroengrehab.com/content/9/1/62/abstract

Abstract (provisional)

Background

Virtual reality (VR) technology along with treadmill training (TT) can effectively provide goal-oriented practice and promote improved motor learning in patients with neurological disorders. Moreover, the VR + TT scheme may enhance cognitive engagement for more effective gait rehabilitation and greater transfer to over ground walking. For this purpose, we developed an individualized treadmill controller with a novel speed estimation scheme using swing foot velocity, which can enable user-driven treadmill walking (UDW) to more closely simulate over ground walking (OGW) during treadmill training. OGW involves a cyclic acceleration-deceleration profile of pelvic velocity that contrasts with typical treadmill-driven walking (TDW), which constrains a person to walk at a preset constant speed. In this study, we investigated the effects of the proposed speed adaptation controller by analyzing the gait kinematics of UDW and TDW, which were compared to those of OGW at three pre-determined velocities.

Methods

Ten healthy subjects were asked to walk in each mode (TDW, UDW, and OGW) at three pre-determined speeds (0.5 m/s, 1.0 m/s, and 1.5 m/s) with real time feedback provided through visual displays. Temporal-spatial gait data and 3D pelvic kinematics were analyzed and comparisons were made between UDW on a treadmill, TDW, and OGW.

Results

The observed step length, cadence, and walk ratio defined as the ratio of stride length to cadence were not significantly different between UDW and TDW. Additionally, the average magnitude of pelvic acceleration peak values along the anterior-posterior direction for each step and the associated standard deviations (variability) were not significantly different between the two modalities. The differences between OGW and UDW and TDW were mainly in swing time and cadence, as have been reported previously (Lee and Hidler, and Wass et. al.). Also, step lengths between OGW and TDW were different for 0.5 m/s and 1.5 m/s gait velocities, and walk ratio between OGS and UDW was different for 1.0 m/s gait velocities.

Conclusions

Our treadmill control scheme implements similar gait biomechanics of TDW, which has been used for repetitive gait training in a small and constrained space as well as controlled and safe environments. These results reveal that users can walk as stably during UDW as TDW and employ similar strategies to maintain walking speed in both UDW and TDW. Furthermore, since UDW can allow a user to actively participate in the virtual reality (VR) applications with variable walking velocity, it can induce more cognitive activities during the training with VR, which may enhance motor learning effects

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.

Self-reported gait unsteadiness in mildly impaired neurological patients: an objective assessment through statistical gait analysis

If we had more of these objective measurements maybe we could duplicate  therapies that actually worked and were repeatable.
http://www.jneuroengrehab.com/content/9/1/64/abstract

Abstract (provisional)

Background

Self-reported gait unsteadiness is often a problem in neurological patients without any clinical evidence of ataxia, because it leads to reduced activity and limitations in function. However, in the literature there are only a few papers that address this disorder. The aim of this study is to identify objectively subclinical abnormal gait strategies in these patients.

Methods

Eleven patients affected by self-reported unsteadiness during gait (4 TBI and 7 MS) and ten healthy subjects underwent gait analysis while walking back and forth on a 15-m long corridor. Time-distance parameters, ankle sagittal motion, and muscular activity during gait were acquired by a wearable gait analysis system (Step32, DemItalia, Italy) on a high number of successive strides in the same walk and statistically processed. Both self-selected gait speed and high speed were tested under relatively unconstrained conditions. Non-parametric statistical analysis (Mann--Whitney, Wilcoxon tests) was carried out on the means of the data of the two examined groups.

Results

The main findings, with data adjusted for velocity of progression, show that increased double support and reduced velocity of progression are the main parameters to discriminate patients with self-reported unsteadiness from healthy controls. Muscular intervals of activation showed a significant increase in the activity duration of the Rectus Femoris and Tibialis Anterior in patients with respect to the control group at high speed.

Conclusions

Patients with a subjective sensation of instability, not clinically documented, walk with altered strategies, especially at high gait speed. This is thought to depend on the mechanisms of postural control and coordination. The gait anomalies detected might explain the symptoms reported by the patients and allow for a more focused treatment design. The wearable gait analysis system used for long distance statistical walking assessment was able to detect subtle differences in functional performance monitoring, otherwise not detectable by common clinical examinations.

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.

Stress, a 'Type A' Personality May Boost Stroke Risk

Stressed-out, type A personalities may be more likely to suffer a stroke than their mellow counterparts, a new Spanish study suggests.
Previous research has linked stress to heart disease, but this latest finding, which appears online Aug. 29 in the Journal of Neurology, Neurosurgery and Psychiatry, looked at stress in relation to stroke risk.

http://www.newsday.com/news/health/stress-a-type-a-personality-may-boost-stroke-risk-1.3938013

 The rest is behind a paywall.

This one gives you a little more info.
http://www.nhs.uk/news/2012/08august/Pages/Aggressive-personality-stroke-risk.aspx

Suitability of Nintendo Wii Balance Board for rehabilitation of standing after stroke

Or you could get a 16.95 balance board from Amazon. But that would have no scientific trials proving it worked so if a clinical trial has not been run then it can't work.  A tree falls in the forest, etc.
http://www.ingentaconnect.com/content/maney/ptr/2012/00000017/00000005/art00006
Abstract:
Background: Normal standing requires ongoing postural adjustments while performing a variety of everyday tasks. Reduced muscle strength and dexterity affect the ability to stand after stroke. Biofeedback has been shown to be effective in training lower limb activities in people with stroke. Nintendo Wii, Nintendo Wii Balance Board, and Nintendo Wii Fit Plus are potentially useful devices for providing feedback to train standing after stroke.

Objectives: What specific Nintendo Wii Fit Plus games are suitable for rehabilitation of standing in patients with stroke?

Method: A criteria-based review of the Nintendo Wii Fit Plus was carried out to determine the movements required, feedback provided, demands upon the patient, difficulty of and instruction provided by the Nintendo Wii Fit Plus games in the context of stroke rehabilitation. Seventy-five Nintendo Wii Fit Plus games were reviewed and 20 were included for in-depth review.

Major findings: The games require movements of the centre of mass in different directions, provide feedback in different ways and place additional physical and cognitive demands upon the patient. Only five games are suitable for people who have severely impaired ability to stand. Six games are suitable for people with moderately impaired standing and nine games are suitable only for people with mildly impaired standing ability. Game goals and the position of the patient can be modified to make the games target physiotherapy goals.

Conclusions: Enough suitable games exist to make the Nintendo Wii and Nintendo Wii Fit Plus an appropriate biofeedback device for rehabilitation of standing after stroke.

Roles of the Akt substrate Girdin in cancer progression, angiogenesis and neurogenesis.

We need angiogenesis and neurogenesis and Akt to help cell migration.  Have Akt lasso those newborn neurons and drag them to the correct spot.
http://w3serv.nagoya-u.ac.jp/coemed/en/meetings/meetings/international/dr-masahide-takahashi-1/
The serine/threonine kinase Akt is involved in a variety of cellular processes including cell proliferation, survival and gene expression. Akt has also been shown to be required for cell migration in different organisms. However, the mechanism by which Akt functions to promote cell migration is not fully understood. We identified a new Akt substrate, Girdin (girders of actin filament) which is an actin-binding protein, and found that Girdin is essential for the integrity of the actin cytoskeleton and cell migration. Girdin is expressed in immature endothelial cells, neuronal cells and some types of cancer cells, such as breast cancer and glioblastoma. Akt phosphorylates serine at position 1416 in Girdin, and phosphorylated Girdin accumulates at the leading edge of migrating cells. Cells expressing mutant Girdin, in which serine 1416 was replaced with alanine, exhibited limited migration and lamellipodia formation. Girdin-deficient mice exhibited neuronal migration defect which results in hypoplasia of the olfactory bulb and granule cell dispersion in the dentate gyrus. In addition, we obtained evidence that Akt-mediated phosphorylation of Girdin promotes VEGF-dependent migration and capillary formation of endothelial cells. Depletion of Girdin also resulted in severe impairment of cancer cell migration and invasion. A significant observation is that Girdin is dispensable for cell migratory events during embryonic development. Our findings suggest that Girdin and its interacting proteins are potential pharmaceutical targets for cancer therapies and pathological angiogenesis, including tumor angiogenesis.

Neurocognitive effects of multivitamin supplementation on the steady state visually evoked potential (SSVEP) measure of brain activity in elderly women

We as survivors will need better cognition in order to direct our neurogenesis and neuroplasticity efforts. Get your researcher involved in testing this in survivors. You do want to get Smarter After Stroke, don't you? I couldn't resist Peter.
http://www.sciencedirect.com/science/article/pii/S003193841200282X

Abstract

Objective

Growing evidence suggests that dietary supplementation with selected micronutrients and nutraceuticals may have the potential to improve cognition in older adults. Fewer studies have investigated the effects of these substances on brain activity.

Methods

This study was a randomised, double-blind, placebo-controlled trial, conducted to explore the effects of 16 weeks supplementation with a combined multivitamin, mineral and herbal formula on the steady state visually evoked potential (SSVEP) measure of brain electrical activity. Participants were elderly women aged between 64 and 79 years, with subjective memory complaints. Baseline and post-treatment SSVEP data was obtained for 22 participants in the multivitamin group and 19 in the placebo group. A spatial working memory delayed response task (DRT) was performed during the recording of the SSVEP.

Results

The results revealed that when compared to placebo, multivitamin supplementation delayed SSVEP latency during retrieval, interpreted as an increase in inhibitory neural processes. Behavioural performance on the DRT was not improved by the multivitamin, however improved performance accuracy was associated with increased midline central SSVEP latency. There were no multivitamin-related effects on SSVEP amplitude.

Conclusion

These findings indicate that in the elderly, multivitamin supplementation may enhance neural efficiency during memory retrieval.

---

Highlights

► The SSVEP was examined before and after 16 weeks multivitamin or placebo treatment. ► The multivitamin increased SSVEP latency during spatial working memory performance. ► Increased latency was interpreted as an increase in inhibitory neural processes. ► Multivitamin supplementation may influence cognition by enhancing neural efficiency.

Downregulation of PMCA2 or PMCA3 reorganizes Ca2+ handling systems in differentiating PC12 cells

I liked the longer neurites. Who is going to translate this to a stroke protocol?
http://www.sciencedirect.com/science/article/pii/S0143416012001583

Abstract

Changes in PMCA2 and PMCA3 expression during neuronal development are tightly linked to structural and functional modifications in Ca²⁺ handling machinery. Using antisense strategy we obtained stably transfected PC12 lines with reduced level of PMCA2 or PMCA3, which were then subjected to dibutyryl-cAMP differentiation. Reduced level of neuron-specific PMCAs led to acceleration of differentiation and formation of longer neurites than in control PC12 line. Treatment with dibutyryl-cAMP was associated with retraction of growth cones and intensified formation of varicosities. In PMCA2-reduced cells development of apoptosis and DNA laddering were detected. Higher amounts of constitutive isoforms PMCA1 and PMCA4, their putative extended location to gaps left after partial removal of PMCA2 or PMCA3, together with increased SERCA may indicate the induction of compensatory mechanism in modified cells. Functional studies showed altered expression of certain types of VDCCs in PMCA-reduced cells, which correlated with their higher contribution to Ca²⁺ influx. The cell response to PMCAs suppression suggests the interplay between transcription level of two opposite calcium-transporting systems i.e. voltage- and store depletion-activated channels facilitating Ca²⁺ influx and calcium pumps responsible for Ca²⁺ clearance, as well highlights the role of both neuron-specific PMCA isoforms in the control of PC12 cells differentiation.

Perfusion Augmentation in Acute Stroke Using Mechanical Counter-Pulsation–Phase IIa

I wonder if this got farther, ask your doctor, you may need it for your next stroke. Have them compare it to leg compressions.
http://stroke.ahajournals.org/content/39/10/2760.short

Abstract

Background and Purpose— External counterpulsation (ECP) improves coronary perfusion, increases left ventricular stroke volume similar to intraaortic balloon counterpulsation, and recruits arterial collaterals within ischemic territories. We sought to determine ECPs effect on middle cerebral artery (MCA) blood flow augmentation in normal controls as a first step to support future clinical trials in acute stroke.

Methods— Healthy volunteers were recruited and screened for exclusions. Bilateral 2-MHz pulsed wave transcranial Doppler (TCD) probes were mounted by head frame, and baseline M1 MCA TCD measurements were obtained. ECP was then initiated using standard procedures for 30 minutes, and TCD readings were repeated at 5 and 20 minutes. Physiological correlates associated with ECP-TCD waveform morphology were identified, and measurable criteria for TCD assessment of ECP arterial mean flow velocity (MFV) augmentation were constructed.

Results— Five subjects were enrolled in the study. Preprocedural M1 MCA TCD measurements were within normal limits. Onset of ECP counterpulsation produced an immediate change in TCD waveform configuration with the appearance of a second upstroke at the dicrotic notch, labeled peak diastolic augmented velocity (PDAV). Although end-diastolic velocities did not increase, both R-MCA and L-MCA PDAVs were significantly higher than baseline end-diastolic values (P less than 0.05 Wilcoxon rank-sum test) at 5 and 20 minutes. Augmented MFVs (aMFVs) were also significantly higher than baseline MFV in the R-MCA and L-MCA at both 5 and 20 minutes (P less than 0.05).

Conclusions— ECP induces marked changes in cerebral arterial waveforms and augmented peak diastolic and mean MCA flow velocities on TCD in 5 healthy subjects.

Severe Diet Doesn’t Prolong Life, at Least in Monkeys

A new York Times article  with a couple of items on cardiovascular risk.
http://www.nytimes.com/2012/08/30/science/low-calorie-diet-doesnt-prolong-life-study-of-monkeys-finds.html?_r=1

Which Diseases/Conditions Are Connected?

I was disappointed that the connection list didn't include either stroke or heart disease, or CV - cardiovascular. But look for connections to your other diseases/conditions. It doesn't look like they covered any brain problems; Alzheimers, Huntingtons, Parkinsons
https://www.23andme.com/curetogether_connections/

Do you suffer from asthma as well as allergies? Is your insomnia coupled with chronic pain? It turns out that two (or more) is company when it comes to diseases and symptoms. But which conditions are most strongly connected to each other?

This graph shows connections* between conditions reported by members of CureTogether, a free resource for patients to share information about diseases and treatments. Connections are only shown if they are stronger than would be expected by chance based on how common the two conditions are.

Into the possible - The Daily Motivator

I received this from work, daily inspirational postings from Ralph Marston. The first line applies to us except we need to adjust it vastly upwards - maybe millions of failures.
http://greatday.com/
Even after a thousand failed attempts, success is possible. In fact, each disappointing result brings you closer to the result you intend to achieve.
Your past may be filled with failure and disappointment, or it may be filled with achievement and joy. But no matter how it has been, it doesn’t have to hold you back right now.

Read more: http://greatday.com/#ixzz24wgYoPzC

Taxonomy of roles played by organizational agents involved into the post-stroke rehabilitation process within a rehabilitation hospital in the Careflow project.

Look at this carefully, it seems to suggest that physiatrists only have a peripheral role and I'm assuming that the apex is the survivor who has to direct everything.
http://www.hcklab.org/research/computerized-clinical-guidelines/careflow-systems.htm

I think this is a poor representation of what is and what should be.