strategies directed to preserve phospholipids in the plasma membrane such as the use of dietary docosahexaenoic
acid (C22:6n-3; DHA)5 can have beneficial effects for post-TBI recovery
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Dietary Strategy to Repair Plasma Membrane After Brain Trauma - 0 views
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DHA is the most abundant polyunsaturated fatty acid (PUFA) in the brain
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Curcumin provided in the diet before TBI can reduce oxidative damage and counteract TBI-related cognitive dysfunction.
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Our previous study indicated that n-3 fatty acids supplemented in the diet counteracted learning disability after TBI
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There was a significant group effect on BDNF (F 4,25 = 5.229, P < .01 by ANOVA), and FPI reduced BDNF levels (50% of CTL, P < .01; Figure 1C), which was counteracted by DHA supplementation (90% of CTL, P < .05; Figure 1C). Curcumin also counteracted this reduction of BDNF
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The combination of curcumin and DHA had a trend of greater effects in BDNF (117% of CTL; Figure 1C) compared with DHA or curcumin alone.
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curcumin contributed to enhance the action of DHA, protecting against cognitive impairment, and these effects were associated with elevations in the BDNF receptor signaling
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Our current results show that curcumin contributes to enhance the effects of DHA on TBI by promoting phosphorylation of the BDNF receptor TrkB in the hippocampus.
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previous evidence indicates that curcumin10 and DHA5 counteract TBI-related learning disability by involving BDNF
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The effects of the DHA diet and curcumin on cognitive enhancement were consistent with enhanced elevations in BDNF receptor signaling
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effects of DHA and curcumin up to 2 weeks after TBI because this is the most critical period for the course of injury recovery because the brain is metabolically dysfunctional during this time
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study that finds curcumin + DHA increased cognitive improvement after TBI within 2 weeks. Good discussion of the proposed mechanism--increased BDNF.
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ScienceDirect - Journal of Steroid Biochemistry : Saliva testosterone time-course respo... - 0 views
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Thus it was suggested to collect saliva instead of plasma for the evaluation of testicular secretion of testosterone after hCG administration
Safe and Legal Pot - 4 views
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shared by Nathan Goodyear on 13 Jan 15
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Intravenous Fluid Use in Athletes - 0 views
www.ncbi.nlm.nih.gov/...PMC3435915
IV intravenous fluid nutrition athletes athlete sports medicine sports exercise
shared by Nathan Goodyear on 13 Jan 15
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Treatment of exercise-associated hyponatremia with hypertonic IV infusion to correct plasma sodium levels is also a standard and accepted use of IV fluid infusions
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athletes who present for medical care with hypernatremia who cannot tolerate oral fluids can benefit from IV fluids
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Vaporization of sweat accounts for 80% of heat loss in hot, dry atmospheric conditions. This mechanism of water loss is the major contributor for exercise-associated dehydration
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The rate of water loss can be quantified through measurement of sweat rate
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Pre- and postexercise body weight measurements are the most common means to estimate overall water loss but are condition specific
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It appears that 1% to 2% body weight loss is well tolerated by the exercising athlete
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Dehydration, defined as greater than 2% loss of body weight, can negatively affect performance
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In highly trained endurance athletes, plasma volume and sodium serum concentration were preserved despite a 5% body weight loss
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In Ironman triathletes, dehydration to 5% body weight loss did not correlate with occurrence of medical complications
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hydration should begin hours prior to exercise, especially if known deficits are present, and fluids should be consumed at a slow, steady rate, with 5 to 7 mL/kg taken 4 hours prior to exercise
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Sodium concentration did not produce significant changes in the rate of absorption but was primarily dependent on carbohydrate concentration
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Replacing 150% of body weight loss over 60 minutes has been tolerated without complications
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IV treatment of severe dehydration (>7% body weight loss), exertional heat illness, nausea, emesis, or diarrhea, and in those who cannot ingest oral fluids for other reasons, is clinically indicated
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A recent survey of the National Football League teams revealed that 75% (24 of 32) of the teams utilized IV infusion of fluids for prehydration in at least some otherwise healthy individuals
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In the National Football League, an average of 1.5 L of normal saline was administered approximately 2.5 hours prior to competition
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after 2 hours of exercise, the rectal temperature was 0.6° higher in the group not receiving IV infusion. Also, stroke volume and cardiac output were 11% to 16% lower in the control group versus the IV infusion group.
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Recent evidence suggests the etiology of EAMC is related to muscle fatigue and neuronal excitability
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no correlation between hydration status or electrolyte concentrations with EAMC
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there may be a subset of muscle cramping that is associated with a loss of both body fluid and sodium
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Glycerol is the primary agent for oral hyperhydration
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elevation of plasma volume by 200 to 300 mL via dextran infusion resulted in 15% increase in stroke volume, 4% increase in VO2 max, and an increase in the exercise time to fatigue
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Neither the tonicity nor mode of hydration resulted in improved speed of rehydration, greater fluid retention, or improved performance
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There are beneficial anecdotal reports of EAMC treatment in elite and professional-level athletes with IV hydration during the course of an event
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Plasma volume was better restored during rehydration with IV fluids at preexercise and 5 minutes of exercise. At 15 minutes, there was no difference between IV and oral rehydration
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More rapid restoration of plasma volume was accomplished in the IV treatment group with no advantages over oral rehydration in physiological strain, heat tolerance, ratings of perceived effort, or thermal sensations
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No difference was found in exercise time to exhaustion. IV and oral rehydration methods were equally effective. Heart rates were statistically higher in the oral rehydration group through 75 minutes of exercise, and there were higher increases in norepinephrine plasma concentrations
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No significant differences between the groups were found for time to recovery, number of days with pain, number of days with stiffness, sleep disturbance, fatigue, rectal temperature, and loss of appetite
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The current data suggest that IV rehydration is faster than oral
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There may be physiological benefits of decreased heart rate and norepinephrine in athletes rehydrated via IV route
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Postexercise blood 1 hour and 24 hours showed no differences in circulating myoglobin or creatine kinase
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The use of IV fluid may be beneficial for a subset of fluid sensitive athletes
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this should be reserved for high-level athletes with strong histories of symptoms in well-monitored settings.
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Volume expanders may also be beneficial for some athletes
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shared by wheelchairindia9 on 21 May 15
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Transport Chairs - 0 views
www.wheelchairindia.com/...TRAVEL-WHEELCHAIR
Transportation Wheelchair For Problems of People with Disabilities best transport wheelchairs benefits that transport wheelchairs Transport wheelchairs are machines Transport Wheelchairs Are Less Bulky
shared by wheelchairindia9 on 21 May 15
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Lightweight wheelchairs provide convenience and comfort to the user and caregiver alike and are often built using materials like aluminum and titanium alloy, while foldable wheelchairs allow for easy storage and transport. Merge the two styles, and got a great mobility aid that isn't a pain to lug around. Utilizing small wheels and lighter materials, transport wheelchairs can tip the scale at as little as 19 lbs, ideal for those looking for a highly portable option. Transport chairs also tend to be more affordable and offer the benefit of increased mobility without breaking the bank. This type of lightweight wheelchair is often referred to as a "transfer chair" and is typically used for shorter trips. Since it's geared towards storability and portability, it features four smaller wheels and dispenses with the larger, rear-mounted wheels that characterize standard wheelchairs. Its construction ensures that it's always foldable and portable, but does so at the expense of self-propulsion. Instead, a transport chair is built so that a caregiver can easily push the user. Transport wheelchairs or companion chairs are companion wheelchairs where the purpose is for a companion to push the user. Most transporters have swing-away leg rests, fixed armrests, and side panels. Instead of the usual 'large back - small front' wheels typical of most wheelchairs, light travel chairs have four small wheels providing much easier maneuverability of the chair. Karma Travel Wheelchair KM TV 20.2: Karma Travel Wheelchair KM TV 20.2 - 606 T-6 aircraft-grade aluminum-alloy frame provides incredible strength. Easy-to-fold in three seconds. Karma Travel Wheelchair KM TV 20.2 Features: Type: Travel Wheelchair. T-6 aircraft-grade aluminum. Secure brake improve safety. Padded flip back armrest. PU front caster & rear wheel. Karma Travel Wheelchair KM TV 20.2 Measurements: Weight: 8.9kg. Seat width: 39.5cm. Tyre: PU front casters and rear wheels. Capacity: 100
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Adenoid cystic carcinoma: current therapy and potential therapeutic advances based on g... - 0 views
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Cisplatin and 5-FU or CAP (cisplatin, doxorubicin, and cyclophosphamide) regimens can be used for combination chemotherapy
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patients with advanced salivary gland malignancy treated with the CAP regimen achieved partial response (PR) or stable disease (SD) rates of 67% (8 out of 12 patients)
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Agents commonly given as monotherapy for treating ACC are cisplatin, mitoxantrone, epirubicin, vinorelbine, paclitaxel, and gemcitabine. However, few of these agents have shown efficacy
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single agent mitoxantrone or vinorelbine were recommended as reasonable choices
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ACC is subdivided into 3 histological groups based on solid components of the tumor including cribriform, tubular, and solid
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Cribriform and tubular ACCs usually exhibit a more indolent course, whereas the solid subtype is associated with worse prognosis
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ACC consists of two different cell types: inner luminal epithelial cells and outer myoepithelial cells
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epithelial cells express c-kit, cox-2 and Bcl-2
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myoepithelial cells express EGFR and MYB
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a balanced translocation of the v-myb avian myeloblastosis viral oncogene homolog-nuclear factor I/B (MYB-NFIB) is considered to be a signature molecular event of ACC oncogenesis
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As a transcription factor, MYB is known to modulate multiple genetic downstream targets involved in oncogenesis, such as cox-2, c-kit, Bcl-2 and BclX
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Various signaling cascades are essential for cancer cells to survive and grow. The PI3K/Akt/mTOR pathway is one of them
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This pathway regulates cell survival and growth and is upregulated in many cancers
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Mutations in genes associated with DNA repair are frequently found in familial cancer syndromes, such as hereditary breast-ovarian cancer syndrome (HBOC), hereditary non-polyposis colorectal cancer (HNPCC, also called Lynch syndrome) and Li-Fraumeni syndrome [30, 31]. These mutations were also reported in non-hereditary cancers
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70% of ACC samples (58 of 84) were found to have genetic alterations in the MYB/MYC pathway, indicating that changes in this pathway are crucial in ACC pathogenesis
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The second most frequently mutated pathway was involved in chromatin remodeling (epigenetic modification), a pathway that includes multiple histone related proteins, and was altered in 44% of samples
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C-kit
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VEGF, iNOS and NF-κB were noted to be highly expressed in ACC cells as compared to normal salivary gland cells
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members of the SOX family, such as SOX 4 and SOX10, are overexpressed in ACC
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FABP7 (Fatty acid binding protein 7) and AQP1 (Aquaporin 1) tend to be overexpressed in ACC cell lines
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considerable variability in HER2 overexpression ranging from 0–58% in patients with ACC
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the study with cetuximab and concurrent chemoradiation or chemotherapy showed the highest ORR (total 43%, 9.5% CR and 33% PR), but this regimen was only given to the EGFR positive patients
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Cancer immunotherapy can be classified into 3 major groups. Active immunization using anti-tumor vaccines to induce and recruit T cells, passive immunization based on monoclonal antibodies, and adoptive cell transfer to expand tumor-reactive autologous T cells ex vivo and then reintroduce these cells into the same individual
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LAK cells showed cytotoxicity against ACC cells
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cytokine-induced cell apoptosis and the cytotoxic effect of the LAK cells contributed to tumor regression
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molecular finding of the MYB-NFIB fusion gene has the greatest potential to target what appears to be a fundamental event in disease pathogenesis
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shared by Nathan Goodyear on 26 Aug 14
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Clinical experience with intravenous administration of ascorbic acid: achievable levels... - 0 views
www.ncbi.nlm.nih.gov/...PMC3751545
IV vitamin C dosing ascorbic acid inflammation disease cancer IV vitamin C intravenous vitamin C IV intravenous vitamin C vitamin C CRP therapy treatment alternative
shared by Nathan Goodyear on 26 Aug 14
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Patients with higher tumor markers are likely to have higher tumor burden, higher oxidative stress and, therefore, are more likely to have lower post IVC plasma levels.
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Our data also showed that cancer patients with metastasis tend to have lower post-IVC vitamin C levels than those without metastasis
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Lower peak plasma concentrations are obtained in cancer patients than in healthy subjects. Cancer patients who are deficient in vitamin C prior to therapy tend to achieve lower plasma levels post infusion.
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Patients with higher inflammation or tumor burdens, as measured by CRP levels or tumor antigen levels, tend to show lower peak plasma ascorbate levels after IVC.
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Patients with metastatic tumors tend to achieve lower post infusion plasma ascorbate levels than those with localized tumors.
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Meta-analyses of clinical studies involving cancer and vitamins also conclude that antioxidant supplementation does not interfere with the efficacy of chemotherapeutic regiments
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Most of the prostate cancer patients studied, 75±19% (95% confidence), showed reductions in PSA levels during the course of their IVC therapy
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Laboratory studies suggest that, at high concentrations, ascorbate does not interfere with chemotherapy or irradiation and may enhance efficacy in some situations
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Cameron and Pauling observed fourfold survival times in terminal cancer patients treated with intravenous ascorbate infusions followed by oral supplementation
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The inflammatory microenvironment of cancer cells leads to increasing oxidative stress, which apparently depletes vitamin C, resulting in lower plasma ascorbate concentrations in blood samples post IVC infusion. Another explanation for this finding may be that cancers are themselves more metabolically active in their uptake of vitamin C, causing subjects to absorb more of the vitamin, and as a results show lower plasma ascorbate concentrations in blood post IVC infusion.
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patients with severely elevated CRP levels attain plasma ascorbate concentrations after IVC infusions that are only 65% of those attained for subjects with normal CRP levels
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The finding of decreased plasma ascorbate levels in cancer patients may relate to the molecular structure of ascorbic acid; in particular, the similarity of its oxidized form, dihydroascorbic acid, to glucose
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Since tumor have increased requirement for glucose [67], transport of dehydroascorbate into the cancer cells via glucose transport molecules and ascorbate through sodium-dependent transporter may be elevated
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Increased accumulation of ascorbic acid in the tumor site was supported by measurements of the level of ascorbic acid in tumors in animal experiments
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patients with advanced malignancies may have lower level of ascorbic acid in tissue, creating a higher demand for the vitamin C
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IVC therapy appears to reduce CRP levels in cancer patients.
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CRP concentrations directly correlate with disease activity in many cases and can contribute to disease progression through a range of pro-inflammatory properties.
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Being an exquisitely sensitive marker of systemic inflammation and tissue damage, CRP is very useful in screening for organic disease and monitoring treatment responses
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ncreases in CRP concentrations have been associated with poorer prognosis of survival in cancer patients, particularly with advance disease independent of tumor stage
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Regarding inflammation, 73±13% of subjects (95% confidence) showed a reduction in CRP levels during therapy. This was an even more dramatic 86±13% (95% confidence) in subjects who started therapy with CRP levels above 10 mg/L
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patients treated by IVC with follow-up several year showed that suppression of inflammation in cancer patients by high-dose IVC is feasible and potentially beneficial
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Inflammation is a marker of high cancer risk, and poor treatment outcome
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The subjects with highly elevated CRP concentrations have a three-fold elevation “all-cause” mortality risk and a twenty-eight fold increase in cancer mortality risk
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cancer patients may need higher doses to achieve a given plasma concentration.
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patients with lower vitamin C levels may see more distribution of intravenously administered ascorbate into tissues and thus attain less in plasma.
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When treating patients with IVC, the first treatment likely serves to replenish depleted tissue stores, if those subjects were vitamin C deficient at the beginning of the treatment. Then, in subsequent treatments, with increasing doses, higher plasma concentrations can be attained. On-going treatments serve to progressively reduce oxidative stress in cancer patients.
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large doses given intravenously may result in maximum plasma concentrations of roughly 30 mM, a level that has been shown to be sufficient for preferential cytotoxicity against cancer cells
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oral intake of vitamin C exceeded 200 mg administered once daily, it was difficult to increase plasma and tissue concentrations above roughly 200 μM.
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Great review on the use of IV vitamin C in cancer and to reduce inflammation. The article does a great job of discussing the mechanism of vitamin C therapy in cancer as well as the proposed reasons for low vitamin C in cancer patients. The study also highlights the obstacles to rise in vitamin C levels post IV vitamin C in cancer patients.
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shared by Nathan Goodyear on 18 May 17
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Long Course Hyperbaric Oxygen Stimulates Neurogenesis and Attenuates Inflammation after... - 0 views
www.hindawi.com/...512978
hbot hyperbaric hyperbaric therapy brain MPO stroke neurogenesis BDNF brain derived neurotrophic factor
shared by Nathan Goodyear on 18 May 17
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animal study finds that HBOT reduced stroke infarct size, increased neurogenesis, increased BDNF, and reduced MPO.
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shared by Nathan Goodyear on 02 Aug 17
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The Risk of Fluoroquinolone-induced Tendinopathy and Tendon Rupture - 0 views
www.ncbi.nlm.nih.gov/...PMC2921747
flouroquinolones ciprofloxacin levoquin tendinitis tendinopathy Tendon rupture
shared by Nathan Goodyear on 02 Aug 17
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Achilles tendinitis or rupture is among the most serious side effects associated with FQ use
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The large body of data provided by clinical reports, histopathological examination, and experimental studies provides cogent evidence supporting a direct link between FQ use and tendonitis/tendon rupture
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Risk factors associated with FQ-induced tendon disorders include age greater than 60 years, corticosteroid therapy, renal failure, diabetes mellitus, and a history of musculoskeletal disorders
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The average age of FQ-induced tendinopathy is 64 years, with a male-to-female ratio of 2:1, and a 27-percent incidence of bilateral involvement
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Although more than 95 percent of cases of tendinitis/rupture secondary to FQ involve the Achilles tendon, other reported sites of tendon involvement include the quadriceps, peroneus brevis, and rotator cuff
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FQs demonstrate a 3.8-fold greater risk for development of Achilles tendinitis/rupture
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a large population-based case control analysis, patients treated with FQs exhibited a substantially increased risk of developing tendon disorders overall (1.7-fold), tendon rupture (1.3-fold), and ATR (4.1-fold)
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patients taking FQs with concurrent exposure to corticosteroids were found to experience a compounding effect on the risk of tendon rupture, specifically a 46-fold greater predisposition
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Some authors have recommended that patients with a history of Achilles tendinitis and advanced age should not be prescribed FQ antibiotics
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Approximately 50 percent of patients will recover within 30 days, with 25 percent of patients having symptoms persistent for longer than two months
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The mean latency period between the start of FQ treatment and occurrence of tendinopathy has been reported to be a few hours to months, with a median onset of 6 days
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The exact pathophysiology of FQ-induced tendinopathy remains elusive
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it is possible that FQs have a direct cytotoxic effect on enzymes found in mammalian musculoskeletal tissue
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It has been theorized that FQs disproportionately affect human tendons that have a limited capacity for repair, such as in older patients or structural compromise (i.e., pre-existing tendinopathy or trauma)
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histopathological findings are similar to those observed in overuse conditions in athletes
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Treatment with a FQ should be discontinued and physical therapy initiated
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treatment should include rest and decreasing the physical load on the tendon.
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Approximately 85 percent of patients present in less than one month
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Because rupture can occur even late in the course of treatment or after discontinuation of FQ use, patients receiving a FQ should be counseled to seek medical attention immediately if symptoms, such as redness, pain, swelling, and stiffness, develop
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FQs should be used cautiously in patients with risk factors associated with tendinitis, such as advanced age, history of tendon rupture, corticosteroid use, and/or acute or chronic renal dysfunction
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Great review of the link between flouroquinolones and Tendinitis and Tendon rupture. Yes, there is a direct link.
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Frontiers | Microbiome-Derived Lipopolysaccharide Enriched in the Perinuclear Region of... - 0 views
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lipopolysaccharides (LPS), either alone or in combination, have indicated that when compared, bacterial LPSs exhibit the strongest induction of pro-inflammatory signaling in human neuronal–glial cells in primary coculture of any single inducer, and different LPS extracts from different gastrointestinal (GI)-tract resident Gram-negative bacteria appeared to have different pro-inflammatory potential
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powerful inducer of the NF-κB
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In both neocortex and hippocampus, LPS has been detected to range from a ~7- to ~21-fold increase abundance in AD brain
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Major Gram-negative bacilli of the human GI-tract, such as the abundant B. fragilis and Escherichia coli (E. coli), are capable of discharging a remarkably complex assortment of pro-inflammatory neurotoxins
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(i) bacterial amyloids (10, 21); (ii) endotoxins and exotoxins (5, 12); (iii) LPS (12, 18); and (iv) small non-coding RNAs (sncRNAs)
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integral components of the outer leaflet of the outer membrane of Gram-negative bacteria, LPS
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LPS, the major molecular component of the outer membrane of Gram-negative bacteria normally serves as a physical barrier providing the bacteria protection from its surroundings
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LPS is also recognized by the immune system as a marker for the detection of bacterial pathogen invasion and responsible for the development of inflammatory response is perhaps the most potent stimulator and trigger of inflammation known
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AD-affected brains have remarkably large loads of bacterial-derived toxins compared to controls. The transfer of noxious, pro-inflammatory molecules from the GI-tract microbiome to the CNS may be increasingly important during the course of aging when both the GI-tract and blood–brain barriers become significantly more permeable
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first evidence of a perinuclear association of LPS with AD brain cell nuclei
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LPS-mediated stimulation of chronic inflammation, beta-amyloid accumulation, and episodic memory decline in murine models of AD (39, 40) and a biophysical association of LPS with amyloid deposits and blood vessels in human AD patients
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Strong adherence of LPS to the nuclear periphery has recently been shown to inhibit nuclear maturation and function that may impair or block export of mRNA signals from brain cell nuclei, a highly active organelle with extremely high rates of transcription, mRNA processing, and export into the cytoplasm
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LPS may be further injurious to the nuclear membrane just as LPS contributes to cerebrovascular endothelial cell membrane injury
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high intake of dietary fiber is a strong inhibitor of B. fragilis abundance and proliferation in the intact human GI-tract and as such is a potent inhibitor of the neurotoxic B. fragilis-derived amyloids, LPS, enterotoxins, and sncRNAs.
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GI-tract microbiome-derived LPS may be an important initiator and/or significant contributor to inflammatory degeneration in the AD CNS
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LPS has been recently localized to the same anatomical regions involved in AD-type neuropathology
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a known pro-inflammatory transcription factor complex that triggers the expression of pathogenic pathways involved in neurodegenerative inflammation
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pro-inflammatory amyloids, endo- and exotoxins, LPSs, and sncRNAs but also serve as potent sources of membrane-disrupting agents
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Incidence of low-triiodothyronine syndrome in patients with septic shock - 0 views
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In the course of different disease states, the levels of T3, T4, and TSH decrease
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euthyroid sick syndrome
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low T3 can contribute to associated organ dysfunction
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proportionally associated with disease severity and survival
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nonthyroidal illness syndrome
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Patients with persistent deterioration of hormone levels (T3, T4) during the study period had higher mortality than those who normalized the function of the thyroid axis
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LT3S in patients with septic shock is part of the pathophysiology of this disease and/or an associated organ (endocrine-metabolic) failure and not just an adaptive phenomenon
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substitution treatment with synthetic thyroid hormones could modify the hemodynamic symptoms of septic patients, contributing in part to the decrease in their morbidity and mortality
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Share Trading Course - Admission Open. - 0 views
www.diigo.com/...2ju9
intradayTrading share Training stock Market technical Analysis price Action CandalstickTrading
shared by snfilms on 23 Sep 20
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মোবাইলে চাকরি খুজবেন, নাকি ইনকাম করবেন ? শেয়ার ট্রেডিং শিখতে যোগাযোগ করুন #snfpa 9051355050 Trainer: Sanjib Nath
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Share Trading Course Admission - 0 views
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শেয়ার ট্রেডিং কোর্স | Join #snfpa to learn #shareTrading and start making regular income. Diwali discount ends on 30-Nov. Contact 9051355050 for admission and inquiries. #Trainer Sanjib Nath
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Share Trading Course at SNFPA - 0 views
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বাড়ি বসে ইনকাম | Join #snfpa Share Trading Training (classroom/online) and start making money. Contact us at 9051355050 for detail.
Course Content - #40952: Moderate Sedation - NetCE - 0 views