Smart Gait-Aid Glasses for Parkinson's Disease Patients.

Parkinson's disease (PD) is a chronic progressive disease caused by loss of dopaminergic neurons in the substantia nigra, degenerating the nervous system of a patient over time. Freezing of gait (FOG), which is a form of akinesia, is a symptom of PD. Meanwhile, recent studies show that the gait of PD patients experiencing FOG can be significantly improved by providing the regular visual or auditory patterns for the patients. In this paper, we propose a gait-aid system built upon smart glasses. Our system continuously monitors the gait and so on of a PD patient to detect FOG, and upon detection of FOG it projects visual patterns on the glasses as if the patterns were actually on the floor. Conducting experiments involving ten PD patients, we demonstrate that our system achieves the accuracy of 92.86 % in detecting FOG episodes and that it improves the gait speed and stride length of PD patients by 15.3  âˆ¼  37.2% and 18.7   âˆ¼  31.7%, respectively.

Brazilin Isolated from Caesalpinia sappan suppresses nuclear envelope reassembly by inhibiting barrier-to-autointegration factor phosphorylation.

To date, many anticancer drugs have been developed by directly or indirectly targeting microtubules, which are involved in cell division. Although this approach has yielded many anticancer drugs, these drugs produce undesirable side effects. An alternative strategy is needed, and targeting mitotic exit may be one alternative approach. Localization of phosphorylated barrier-to-autointegration factor (BAF) to the chromosomal core region is essential for nuclear envelope compartment relocalization. In this study, we isolated brazilin from Caesalpinia sappan Leguminosae and demonstrated that it inhibited BAF phosphorylation in vitro and in vivo. Moreover, we demonstrated direct binding between brazilin and BAF. The inhibition of BAF phosphorylation induced abnormal nuclear envelope reassembly and cell death, indicating that perturbation of nuclear envelope reassembly could be a novel approach to anticancer therapy. We propose that brazilin isolated from C. sappan may be a new anticancer drug candidate that induces cell death by inhibiting vaccinia-related kinase 1-mediated BAF phosphorylation.

Acute spinal subdural hematoma after vigorous back massage: a case report and review of literature.

STUDY DESIGN: A case report and review of literature. OBJECTIVE: We report on a patient with traumatic spinal subdural hematoma after vigorous back massage while on vacation. SUMMARY OF BACKGROUND DATA: Traumatic spinal subdural hematoma is extremely rare, and to our knowledge, this is the first case reported after violent back massage. We emphasize a high index of suspicion for early recognition and treatment for a good neurological recovery. METHODS: A 41-year-old male was brought to our hospital with severe back pain, motor and sensory impairments of the bilateral lower extremities, and urinary dysfunction after vigorous back massage. Magnetic resonance images revealed an acute spinal subdural hematoma in the thoracolumbar region. After careful monitoring of his neurological status, the patient was successfully managed with conservative treatment. RESULTS: After 2 weeks of hospitalization, complete motor power recovery was achieved with only minor sensory deficit. At a follow-up of more than 12 months, the patient has no residual neurological deficits. CONCLUSION: Spinal subdural hematoma secondary to physical trauma is quite rare. This case brings new information that traumatic spinal subdural hematoma can be caused by violent massage. LEVEL OF EVIDENCE: N/A.

Chronic sleep deprivation-induced proteome changes in astrocytes of the rat hypothalamus.

Sleep deprivation (SD) can influence cognition, memory, and sleep/wake homeostasis and can cause impairments in many physiological processes. Because the homeostatic control of the sleep/wake cycle is closely associated with the hypothalamus, the current study was undertaken to examine proteomic changes occurring in hypothalamic astrocytes following chronic partial SD. After chronic partial SD for 7 days, astrocytes were prepared from rat hypothalamus using a Percoll gradient method, and their proteome profiles were determined by LC-MS/MS. Comparisons of the proteome profiles of hypothalamic astrocytes revealed that chronic partial SD increased (≥1.5-fold) 89 proteins and decreased (≤0.7-fold) 50 proteins; these changes in protein expression were validated by western blot or immunohistochemistry. DAVID and IPA analyses of these proteins suggested that SD may influence gliotransmission and astrocyte activation. PPP2R1A, RTN4, VAMP-2, LGI-1, and SLC17A7 were identified and validated as the main targets of SD in astrocytes. Our results suggest that SD may modulate gliotransmission in the hypothalamus, thereby disturbing sleep/wake homeostasis and increasing susceptibility to neurological disease; however, further studies are required to confirm whether the proteome changes are specific to SD.

In vitro antiproliferative characteristics of flavonoids and diazepam on SNU-C4 colorectal adenocarcinoma cells.

The need for beneficial use of sedatives in oncologic patients is increasing. Therefore, in this study, antiproliferative characteristics of herbal and synthetic sedatives were examined in vitro in SNU-C4 human colorectal adenocarcinoma cells. Apigenin (50% inhibition concentration, IC(50) = 1.8 +/- 0.5 microM) and diazepam (IC(50) = 7.0 +/- 0.5 microM) showed concentration-dependent inhibition of SNU-C4 cancer cell survival. Efficacy of cancer cell survival inhibition by apigenin and diazepam was much lower than that of 5-fluorouracil (5-FU), a known chemotherapeutic drug. However, 10(-6) M concentration of apigenin and diazepam potentiated 5-FU-induced cytotoxicity. In SNU-C4 cells, 10(-6) M concentrations of diazepam, flumazenil (Ro15-1788), Ro5-4864, or PK11195, all ligands for central- or peripheral-type benzodiazepine (BZD) receptors, inhibited cell survival like the flavonoid apigenin (4',5,7-trihydroxyflavone) and fisetin (3,7,3',4'-tetrahydroxyflavone). Also like the plant flavonoids, treatment with 10(-6) M concentration of diazepam for 3 days hardly affect the peripheral-type BZD receptor (PBR) messenger RNA (mRNA) expression and inhibited glucose utilization of SNU-C4 cells. Treatment with flavonoids or diazepam for 6 days upregulated PBR mRNA expression and cell cytotoxicity of SNU-C4 cells. Furthermore, treatment with 10(-6) M concentration of apigenin, a natural sedative material originating from traditional herbs, positively modulated BZD-induced antiproliferative cytotoxicity in SNU-C4 cells. Overall, the in vitro antiproliferative activity on SNU-C4 cancer cells of herbal sedatives, such as apigenin, plus additive enhancement of synthetic BZD- and 5-FU-induced antiproliferative activities, were shown. In conclusion, this study provides experimental basis for advanced trial in the future.

Inhibition of microglial neurotoxicity by ethanol extract of Artemisia asiatica Nakai.

Artemisia asiatica Nakai has been used for the treatment of infections and inflammatory disorders in traditional Oriental medicine. Previously, an ethanol extract of A. asiatica has been shown to exert antioxidative and antiinflammatory activities and to exhibit protective effects against experimentally induced damage in the gastrointestinal system, liver and pancreas. This study examined whether the ethanol extract of A. asiatica affects inflammatory activation of microglia in the central nervous system, and whether the antiinflammatory activity of A. asiatica is related to neuroprotective effects. The extract of A. asiatica inhibited inflammatory activation of mouse microglial cells as determined by the production of nitric oxide and the expression of inducible nitric oxide synthase and inflammatory cytokine. The extract also protected nerve growth factor-differentiated PC12 cells against microglial cytotoxicity, indicating that the ethanol extract of A. asiatica may be neuroprotective by inhibiting microglial neurotoxicity.