Tiny, wearable patch makes you invisible to mosquitos.

A mosquito can detect the carbon dioxide emanating from a prospective meal from hundreds of feet away. The Kite Patch, a small, non-toxic sticker that you place on your clothing, can jam a mosquito’s CO2 radar. Wear one, the patch’s creators say, and you’ll be effectively invisible to the bloodsuckers for up to 48 hours.

The Kite Patch was developed by Grey Frandsen, Michelle Brown and Torrey Tayanaka of Olfactor Laboratories and, according to the FAQ page at the patch’s website, is based on the findings of researcher Anandasankar Ray and his colleagues at University of California Riverside. If we had to guess, we’d say the FAQ are referring to this study, published by Ray and his team in a June 2011 issue of Nature, in which the researchers identify three groups of chemicals that can which disrupt a mosquito’s carbon dioxide receptors. 


Each group of chemicals works a little differently to confound its target. The first actually mimics carbon dioxide, and could be used to lure mosquitoes away from their human targets and into insect traps; the second prevents the mosquitoes from detecting carbon dioxide altogether; and the third actually switches the CO2-sensing machinery of the mosquitoes into overdrive, overloading the mosquitoes’ senses to the point of confusion.

In a project currently seeking funding on indiegogo, the team hopes to field test the patch in Uganda, “one of the toughest proving grounds there is”:

With your help, large-scale testing in Uganda will simultaneously provide over1,000,000 hours of protection during a large field test for families who are suffering from malaria infection rates of over 60% and allow us to optimize Kite before we begin scaling for global distribution.

The results will help us finalize the formulation and any last product design changes. Once the formulation is finalized we can begin the EPA registration process for the US. Once we have approval in the US, we will be capable of scaling the product for widespread and market-sensitive distribution – especially for those where mosquitoes mean life or death.

The Kite Patch is what’s known in epidemiological circles as as spatial repellant. In a review published last year in Malaria Journal, researchers note that spatial repellants have shown a lot of promise in the fight against disease-transmission by vectors like mosquitoes, but have yet to be incorporated into multi-lateral disease control programs. One reason for this is a lack of epidemiological data supporting their efficacy:

There is a critical need for Phase III community trials integrating simultaneous monitoring of infection incidence with vector population metrics… Such confirmatory studies will require unambiguous entomological measures of repellency versus irritancy and/or knock down effects in reducing vector entry into a given interior space or outside area, as well as reductions in vector biting densities (to include potential redirection to untreated spaces with human hosts) concurrent with reduced pathogen transmission. The challenge arises when designing an impact study to ensure both entomological and parasitological endpoints correlate with true repellency effects.

How rigorous the Kite Patch’s fields tests will actually be remains to be seen, but a project like this has the potential to provide tons of data, while helping the people who need it most. Fingers crossed for progress, everybody.

Source: http://io9.com

Why You Should Eat Breakfast and the Best Times for the Rest of the Day’s Meals.

Keeping track of what you’re supposed to eat to stay healthy can already be overwhelming, but it turns out that when you eat what can also be important for keeping your weight in control and for warding off chronic disease.

It turns out Mom was right: you should eat breakfast. And if you don’t believe Mom, a growing body of studies shows that a good meal in the morning can help your body prepare for the day to come, and lower your risk of heart diseasediabetesand obesity. But what about the rest of the day’s meals? Here’s what nutrition experts say about the best times to eat and why.


Don’t skip breakfast. Reporting in the American Heart Association journal Circulation, Harvard School of Public Health researchers studied the health outcomes of 26,902 male health professionals ages 45 to 82 over a 16-year period. They discovered that the men who skipped breakfast had a 27% higher risk of heart attack or death from heart disease than those who honored the morning meal. According to the scientists, skipping breakfast may make you hungrier and more likely to eat larger meals, which leads to a surge in blood sugar. Such spikes can pave the way for diabetes, high blood pressure and high cholesterol levels, all risk factors that can snowball into a heart attack.

Pass on the pastry. Eating in the morning — and what you eat — is important for setting your blood-sugar pattern for the rest of the day. “If you eat something that is whole grain and has some fat and protein to it, your blood sugar is going to rise slowly and go down slowly. If you eat something refined, like an overly sweet cinnamon roll, that’s the worst thing you can eat,” says Judy Caplan, a registered dietitian nutritionist for the Academy of Nutrition and Dietetics. “You get an insulin [spike], and [then] your blood sugar drops too low so you get hungry again. That’s why people get into a cycle of overeating junk.”

To ease your body into a more consistent blood-sugar pattern, try some oatmeal, whole-wheat toast with almond butter, or an omelette with spinach and avocado. Caplan’s favorite breakfast is a baked sweet potato with a little bit of cinnamon and a small bit of butter. Who says you have to eat just cereal in the morning?

Fuel up at the right time. In the 1960s, nutritionist Adelle Davis popularized the mantra “Eat breakfast like a king, lunch like a prince and dinner like a pauper.” Why? Fueling up makes sense earlier in the day, when your body needs the most calories for energy. That’s why in many European countries, the largest meal of the day occurs in the afternoon. “Ideally, you want to give yourself fuel before you do harder labor,” says Caplan.

If you’re used to eating a smaller meal for lunch and a larger meal later, you can still fill up with a hearty meal that has significantly fewer calories. “A fairly large meal [that] is full of salad and vegetables [is] big in volume but light in calories,” says Caplan.

Don’t overdo it. Calories get burned up no matter when you eat them, so theoretically it’s O.K. to eat after dark. But if you eat a heavy dinner, you’re not as likely to get rid of those calories before you turn in. “What you don’t burn off is more likely to be stored as fat, as you become less active toward the end of the day,” says Tracy Lockwood, a registered dietitian at F-Factor Nutrition. “Eating too close to bedtime increases your blood sugar and insulin, which causes you to have a hard time falling asleep. Therefore, your last meal should be the lightest of the day and should be eaten at least three hours before you go to sleep.”

There’s another reason that late-night eating, after dinner, isn’t a good idea. In most cases, those visits to the fridge involve sweet treats such as ice cream and other desserts that can send blood sugar soaring right before bed. That can lower levels of the hormone melatonin, which is supposed to help you feel tired and relaxed, so waning levels can make it harder to fall asleep. “A boost of energy coming from your dinner, which may have consisted of pasta, rice or bread, can act as a short-lived stimulant, causing you to feel more awake immediately after a meal,” says Lockwood. “Also, it is not recommended to lie down immediately after a meal, especially a big one, since it increases your chance for acid reflux.”

Keep it light. “If you go to Europe and places where there is not as much obesity as the rest of the world, people eat very late and they’re not necessarily overweight. That’s because they are walking everywhere and they are typically not eating a huge and heavy meal,” says Caplan. “Instead, it may be avocado and toast with a side of soup.”

Source: http://healthland.time.com




Scientists discover the molecule responsible for causing feelings of depression.

Protein receptor is found to release hormones that can cause anxiety and depression

Scientists have used one of the world’s most powerful X-ray machines to identify the molecule responsible for feelings of stress, anxiety and even depression.

The pituitary gland is known to the medical world as a key player in stress and anxiety, as it releases stress chemicals in the blood.

However, scientists have now discovered that the protein receptor CRF1 is responsible for releasing hormones which can cause anxiety and depression over extended periods of time. The protein receptor is found in the brain and controls our response to stress. When it detects stress molecules released by the hypothalamus, it releases these hormones.

The study, conducted by drug company Heptares Therapeutics, was published in the Nature journal on 17 July.

Researchers used a particle accelerator called the Diamond Light Source to understand the structure of CRF1. The X-ray machine’s powerful beams illuminated the protein’s structure, according to the Sunday Times, including a crevice that could become a new target for drug therapy.

The information gained from this study will be used to design small molecule drugs that fit into this new pocket to treat depression.

Speaking to the Sunday Times, Dr Fiona Marshall, Chief Scientific Officer at Heptares Therapeutics, said: “Now we know its shape, we can design a molecule that will lock into this crevice and block it so that CRF1 becomes inactive — ending the biochemical cascade that ends in stress.”

Writing on Diamond’s website, Dr. Andrew Dore, a senior scientist with Heptares added that the structure of the protein receptor “can be used as a template to solve closely related receptors that open up the potential for new drugs to treat a number of major diseases including Type 2 diabetes and osteoporosis”.

Source: http://www.independent.co.uk

Factors Influencing the Effectiveness of Scalp Cooling in the Prevention of Chemotherapy-Induced Alopecia.


Introduction. The success of scalp cooling in preventing or reducing chemotherapy-induced alopecia (CIA) is highly variable between patients and chemotherapy regimens. The outcome of hair preservation is often unpredictable and depends on various factors.

Methods. We performed a structured search of literature published from 1970 to February 2012 for articles that reported on factors influencing the effectiveness of scalp cooling to prevent CIA in patients with cancer.

Results. The literature search identified 192 reports, of which 32 studies were considered relevant. Randomized studies on scalp cooling are scarce and there is little information on the determinants of the result. The effectiveness of scalp cooling for hair preservation depends on dose and type of chemotherapy, with less favorable results at higher doses. Temperature seems to be an important determinant. Various studies suggest that a subcutaneous scalp temperature less than 22°C is required for hair preservation.

Conclusions. The effectiveness of scalp cooling for hair preservation varies by chemotherapy type and dose, and probably by the degree and duration of cooling.

Anti-Epidermal Growth Factor Receptor Therapy in Head and Neck Squamous Cell Carcinoma: Focus on Potential Molecular Mechanisms of Drug Resistance.


Targeted therapy against the epidermal growth factor receptor (EGFR) is one of the most promising molecular therapeutics for head and neck squamous cell carcinoma (HNSCC). EGFR is overexpressed in a wide range of malignancies, including HNSCC, and initiates important signal transduction pathways in HNSCC carcinogenesis. However, primary and acquired resistance are serious problems and are responsible for low single-agent response rate and tumor recurrence. Therefore, an improved understanding of the molecular mechanisms of resistance to EGFR inhibitors may provide valuable indications to identify biomarkers that can be used clinically to predict response to EGFR blockade and to establish new treatment options to overcome resistance. To date, no predictive biomarker for HNSCC is available in the clinic. Therapeutic resistance to anti-EGFR therapy may arise from mechanisms that can compensate for reduced EGFR signaling and/or mechanisms that can modulate EGFR-dependent signaling. In this review, we will summarize some of these molecular mechanisms and describe strategies to overcome that resistance.

  • Source: the Oncologist

AZD1480: A Phase I Study of a Novel JAK2 Inhibitor in Solid Tumors.


Background. AZD1480 is a novel agent that inhibits Janus-associated kinases 1 and 2 (JAK1 and JAK2). The primary objective of this phase I study was to investigate the safety and tolerability of AZD1480 when administered as monotherapy to patients with solid tumors.

Methods. Thirty-eight patients with advanced malignancies were treated at doses of 10–70 mg once daily (QD) and 20–45 mg b.i.d. .

Results. Pharmacokinetic (PK) analysis revealed rapid absorption and elimination with minimal accumulation after repeated QD or b.i.d. dosing. Exposure increased in a dose-dependent manner from 10–50 mg. Maximum plasma concentration (Cmax) was attained ∼1 hour after dose, and t1/2 was ∼5 hours. Pharmacodynamic analysis of circulating granulocytes demonstrated maximum phosphorylated STAT3 (pSTAT3) inhibition 1–2 hours after dose, coincident with Cmax, and greater pSTAT3 inhibition at higher doses. The average pSTAT3 inhibition in granulocytes at the highest dose tested, 70 mg QD, was 56% (standard deviation: ±21%) at steady-state drug levels. Dose-limiting toxicities (DLTs) consisted of pleiotropic neurologic adverse events (AEs), including dizziness, anxiety, ataxia, memory loss, hallucinations, and behavior changes. These AEs were generally reversible with dose reduction or treatment cessation.

Conclusions. Whether the DLTs were due to inhibition of JAK-1/2 or to off-target effects is unknown. The unusual DLTs and the lack of clinical activity led to discontinuation of development.

  • Source: the Oncologist

Trastuzumab-Related Cardiotoxicity in Early Breast Cancer: A Cohort Study.


Background. Concerns have been raised about the cardiac safety profile of trastuzumab for the adjuvant treatment of early stage breast cancer in clinical practice. We assessed trastuzumab-related cardiotoxicity and its predictors in a large cohort of Italian women. Methods. Through a record linkage between four regional health care databases, we identified the rate of severe cardiac adverse events among women treated with trastuzumab for early breast cancer in Lombardy. The cumulative risk of cardiotoxicity was estimated using the Kaplan-Meier method, and independent predictors were assessed using the Cox model. Results. Of 2,046 trastuzumab users, 53 (2.6%) experienced at least one hospitalization for a cardiac event, and there were two cardiac deaths. The cumulative risk of cardiotoxicity increased up to 2 years after starting treatment, reaching a plateau at 2.8%. The risk was low (0.2%) among young women, whereas the incidence was approximately 10% in women aged ≥70 years, irrespective of cardiovascular risk factors. Age and history of cardiac disease were strong predictors of cardiotoxicity, with a hazard ratio of 11.3 (95% confidence interval [CI]: 3.5–36.6) for women aged ≥70 years as compared with those <50 years of age. Hazard ratio was 4.4 (95% CI: 2.1–9.5) for women with a history of cardiac disease compared with those without a history of cardiac disease. Conclusions. Cardiotoxicity of trastuzumab varies considerably across subgroups of patients. The long-term safety profile was less favorable than in the largest clinical trial. Strategies to reduce cardiotoxicity in high-risk women should be investigated.

  • Source: the Oncologist

Genomic Alterations in Advanced Esophageal Cancer May Lead to Subtype-Specific Therapies.


The development of targeted agents for metastatic esophageal or gastroesophageal junction (GEJ) tumors has been limited when compared with that for other common tumors. To date, the anti-human epidermal growth factor receptor-2 (HER-2) antibody, trastuzumab, in combination with chemotherapy, is the only approved novel agent for these cancers, and its use is limited to the small population of patients whose tumors overexpress HER-2. Despite recent progress in the field, median overall survival remains only 8–12 months for patients with stage IV esophageal or GEJ cancer. In this article, we examine the molecular aberrations thought to drive the development and spread of esophageal cancer and identify promising targets for specific tumor inhibition. Data from clinical studies of targeted agents are reviewed, including epidermal growth factor receptor antibodies, tyrosine kinase inhibitors, HER-2, and vascular endothelial growth factor-directed therapy. Current and future targets include MET, fibroblast growth factor receptor, and immune-based therapies. Evidence from trials to date suggests that molecularly unselected patient cohorts derive minimal benefit from most target-specific agents, suggesting that future collaborative investigation should focus on preselected molecular subgroups of patients with this challenging heterogeneous disease.

  • Source: the Oncologist

Neoadjuvant Doxorubicin/Cyclophosphamide Followed by Ixabepilone or Paclitaxel in Early Stage Breast Cancer and Evaluation of βIII-Tubulin Expression as a Predictive Marker.

Abstract Background. This randomized phase II trial was designed to compare the rate of pathologic complete response (pCR) induced by neoadjuvant cyclophosphamide plus doxorubicin (AC) followed by ixabepilone or paclitaxel in women with early stage breast cancer (BC). Expression of βIII-tubulin as a predictive marker was also evaluated. Patients and Methods. Women with untreated, histologically confirmed primary invasive breast adenocarcinoma received four cycles of AC followed by 1:1 randomization to either ixabepilone 40 mg/m2 (3-hour infusion) every 3 weeks for four cycles (n = 148) or weekly paclitaxel 80 mg/m2 (1-hour infusion) for 12 weeks (n = 147). All patients underwent a core needle biopsy of the primary cancer for molecular marker analysis prior to chemotherapy. βIII-Tubulin expression was assessed using immunohistochemistry. Results. There was no significant difference in the rate of pCR in the ixabepilone treatment arm (24.3%; 90% confidence interval [CI], 18.6–30.8) and the paclitaxel treatment arm (25.2%; 90% CI, 19.4–31.7). βIII-Tubulin-positive patients obtained higher pCR rates compared with βIII-tubulin-negative patients in both treatment arms; however, βIII-tubulin expression was not significantly associated with a differential response to ixabepilone or paclitaxel. The safety profiles of both regimens were generally similar, although neutropenia occurred more frequently in the ixabepilone arm (grade 3/4: 41.3% vs. 8.4%). The most common nonhematologic toxicity was peripheral neuropathy. Conclusions. Neoadjuvant treatment of early stage BC with AC followed by ixabepilone every 3 weeks or weekly paclitaxel was well tolerated with no significant difference in efficacy. Higher response rates were observed among βIII-tubulin-positive patients.

  • Source: the Oncologist