Character Sweets

Shirokuma (しろくま) and Penguin (ぺんぎん) Japanese-style Confectionery

The sweets are available from AEON stores in Japan for a box of 2 pieces at 380 yen (plus tax).

Apple Strudel

Ingredients

9 oz plain white flour, sifted
2 tbsp oil
salt
1/2 cup warm water

Filling

1 1b 2 oz apples or similar, peeled, sliced
1 oz bread crumbs
1 oz butter
1 oz raisins
1-1/2 oz granulated sugar
1 tsp grounded cinnamon
clarified butter to brush
icing sugar to sprinkle

Method

1. Place the flour, warm water, oil and salt in a bowl and knead until a dough forms, preferably with an electric mixer. Shape into a ball, brush with oil and leave to rest for 1/2 hour.
2. Lay a large cotton cloth on a table and dredge with flour. Put the dough in the centre and sift over a little flour. Pat the dough into a square then roll out into a large rectangle.
3. To stretch the dough, flour your hands and slip them, palms down, under the centre of the dough. Working towards the nearest edge, move your hands apart repeatedly whilst gently stretching and pulling the dough. Move round the table stretching a section of dough at a time until it is thin enough.
4. Cut off the thick borders which will build up around the edges.
5. Spread the filling thick in a strip along the edge nearest to you. Brush the pastry edges with clarified butter.
6. Fold in the side edges of the pastry. Using the cloth to help lift the dough, roll the strudel into a fairly loose roll.
7. Place the strudel seam-side down, onto a large baking tray or into a deep roasting tin. Brush the strudel with cold, clarified butter. Bake for 25 minutes with 200°C. Brush once more with butter.
8. Remove from the oven, sprinkle with icing sugar and serve warm.

Makes 4 servings.

Source: Culinary Austria

Clorox and Lysol Want to Kill Germs — and Each Other

Henry Grabar wrote . . . . . . . . .

Whether you’re wiping down the countertop or injecting them into your veins, Clorox and Lysol are two brands that are virtually interchangeable to American consumers.

Each is more than a century old. Each is a leading name in cleaning wipes and disinfectant sprays. Neither can manufacture and ship enough product to satisfy America’s pandemic-driven demand for cleaning, with sales up two- to threefold over the same period last year, according to Nielsen.

And each has it out for the other. They are the Coke and Pepsi of wipes, the Capulets and Montagues of the toilet bowl.

Just watch the ads: In spot after spot, Lysol is mopping the floor with Clorox. In “Strength Test,” a Lysol wipe holds up a kettlebell and a Clorox wipe breaks. In “Fake It,” Lysol spray kills germs that Clorox wipes cannot. In “Bleach Indicator Test,” Clorox Clean Up turns food brown as observers recoil in horror.

Last year, Clorox sued Lysol parent company Reckitt Benckiser over the campaign, which Clorox vice president Eric Reynolds called “egregious and misleading.” Clorox says the ads are full of lies that have hurt the Oakland-based bleach company and helped its devious rival gain market share. Lysol, whose U.S. headquarters is in New Jersey, grew its sales by double digits in 2018.

But this was only the latest mess in the surprisingly litigious history between America’s two favorite toilet cleaners.

They are the Coke and Pepsi of wipes, the Capulets and Montagues of the toilet bowl.

Two decades ago, it was Clorox coming for Lysol, with a new product called Clorox Disinfecting Spray designed to take down Lysol’s popular and well-established Lysol Disinfectant Spray (spot the difference?). Clorox boasted its product would work on surfaces for 24 hours—even through repeated touching. “The claim made by Clorox is false,” Lysol manager Steve Rosenberg retorted, in Brandweek. Clorox spray wouldn’t work against infectious diarrhea germs, he added.

Lysol’s disinfectants have been the company’s claim to fame since the start of the 20th century. They were advertised to cure the 1918 flu: “Make a better fight again disease than it can make against you and yours,” reads a New York Times ad from 1918. (They were also marketed to women for vaginal douching, in a long-running series of ads that attributed marital discord to women not practicing “complete feminine hygiene.”)

For many decades, there was one mess Lysol couldn’t quite clean: Pinesol, the scented floor soap that took off in the 1930s. As the head of the U.S. Patent and Trademark Office noted in denying Pinesol’s trademark in the 1940s, the “pine” in the name could be slurred to start to sound like “Pysol,” which was awfully close to “Lysol,” which had been trademarked since 1906. Pinesol wouldn’t take no for an answer. Several subsequent lawsuits hammered out the rules around the iconic cleaning fragrance: Pine-Sol had to be spelled with a dash, space, or tree icon between the e and the s. Eventually, Pine-Sol negotiated the right to produce a pump-spray disinfectant—but only if the word “clean” was more prominent than the word “disinfectant.” In return, Lysol got permission to sell Lysol Pine Action Cleaner.

In 1990, Clorox bought Pine-Sol, and like every previous owner of the trademark, got fed up with the restrictions when it tried to spruce up its new asset. Lysol’s then-owner got a New Jersey state court to issue an injunction against a TV commercial for Pine-Sol, on the grounds that Clorox was leaning too hard into the product’s “disinfectant” properties. (Clorox could sell disinfectant; Pine-Sol could not.) Clorox sued; the brands exchanged more than a million documents during discovery, and the battle went on for five years. Clorox lost, appealed, and lost again in 1997. No Pine-Sol Disinfectant Spray would be produced.

Such disputes are not unusual among the relatively few, big companies that dominate the consumer product goods sector, said Christine Bittar, a business reporter who chronicled the Clorox-Lysol dispute for Brandweek at the time. She recalled one 2001 incident in which Cincinnati-based Procter & Gamble confessed to dumpster-diving for trade secrets outside Unilever’s hair care headquarters in Chicago. “It was like an episode of The Sopranos, but it was these two conservative consumer products companies.” S.C. Johnson & Son sued Clorox over resealable bag ads; Clorox sued P&G over the laundry slogan “whiter is not possible.”

If Lysol and Clorox found themselves stuck on wartime footing, it might have been because the market for established household cleaners has seemed very nearly saturated. Clorox and Lysol are Nos. 1 and 2 in the $600 million U.S. toilet cleaner market, according to Euromonitor International, with the two companies accounting for two-thirds of all sales. When it comes to the larger $6 billion surface cleaning market, the brands are Nos. 1 and 3 (P&G, maker of Mr. Clean, is No. 2).

The porcelain pie is barely any bigger now than it was a decade ago. Between 2012 and 2017, as personal consumption grew by 17 percent, toilet cleaner sales grew by just 3 percent. Surface cleaners grew faster but still lagged behind consumer purchases as a whole.

Clorox does have some good points in its false advertising case against Lysol, not all of which require you to get familiar with case-law precedents like the time Subway sued Quiznos over double-meat sandwich ads. In the “Fake It” commercial, Lysol parent Reckitt compared Clorox wipes with Lysol spray. Apples and oranges. Clorox contends that neither product is even long enough to hold up a kettlebell anyway. (At the moment, I’d sooner use my college diploma to lift a kettlebell than my sweet, sweet surface wipes.)

While that case makes its way through the system, the two brands face a weirder challenge: Right now, both Clorox and Lysol are so oversold that eco-friendly cleaning products, shunned at the start of the pandemic, are flying off the shelves. For the moment, Americans aren’t choosing between Clorox and Lysol. They’re not choosing at all.

Source: Slate

A New Biosensor for the COVID-19 Virus

Karin Weinmann wrote . . . . . . . . .

A team of researchers from Empa, ETH Zurich and Zurich University Hospital has succeeded in developing a novel sensor for detecting the new coronavirus. In future it could be used to measure the concentration of the virus in the environment – for example in places where there are many people or in hospital ventilation systems.

Jing Wang and his team at Empa and ETH Zurich usually work on measuring, analyzing and reducing airborne pollutants such as aerosols and artificially produced nanoparticles. However, the challenge the whole world is currently facing is also changing the goals and strategies in the research laboratories. The new focus: a sensor that can quickly and reliably detect SARS-CoV-2 – the new coronavirus.

But the idea is not quite so far removed from the group’s previous research work: even before the COVID-19 began to spread, first in China and then around the world, Wang and his colleagues were researching sensors that could detect bacteria and viruses in the air. As early as January, the idea of using this basis to further develop the sensor in such a way that it could reliably identify a specific virus was born. The sensor will not necessarily replace the established laboratory tests, but could be used as an alternative method for clinical diagnosis, and more prominently to measure the virus concentration in the air in real time: For example, in busy places like train stations or hospitals.

Fast and reliable tests for the new coronavirus are urgently needed to bring the pandemic under control as soon as possible. Most laboratories use a molecular method called reverse transcription polymerase chain reaction, or RT-PCR for short, to detect viruses in respiratory infections. This is well established and can detect even tiny amount of viruses – but at the same time it can be time consuming and prone to error.

An optical sensor for RNA samples

Jing Wang and his team have developed an alternative test method in the form of an optical biosensor. The sensor combines two different effects to detect the virus safely and reliably: an optical and a thermal one.

The sensor is based on tiny structures of gold, so-called gold nanoislands, on a glass substrate. Artificially produced DNA receptors that match specific RNA sequences of the SARS-CoV-2 are grafted onto the nanoislands. The coronavirus is a so-called RNA virus: Its genome does not consist of a DNA double strand as in living organisms, but of a single RNA strand. The receptors on the sensor are therefore the complementary sequences to the virus’ unique RNA sequences, which can reliably identify the virus.

The technology the researchers use for detection is called LSPR, short for localized surface plasmon resonance. This is an optical phenomenon that occurs in metallic nanostructures: When excited, they modulate the incident light in a specific wavelength range and create a plasmonic near-field around the nanostructure. When molecules bind to the surface, the local refractive index within the excited plasmonic near-field changes. An optical sensor located on the back of the sensor can be used to measure this change and thus determine whether the sample contains the RNA strands in question.

Heat increases reliability

However, it is important that only those RNA strands that match exactly the DNA receptor on the sensor are captured. This is where a second effect comes into play on the sensor: the plasmonic photothermal (PPT) effect. If the same nanostructure on the sensor is excited with a laser of a certain wavelength, it produces localized heat.

And how does that help reliability? As already mentioned, the genome of the virus consists of only a single strand of RNA. If this strand finds its complementary counterpart, the two combine to form a double strand – a process called hybridization. The counterpart – when a double strand splits into single strands – is called melting or denaturation. This happens at a certain temperature, the melting temperature. However, if the ambient temperature is much lower than the melting temperature, strands that are not complementary to each other can also connect. This could lead to false test results. If the ambient temperature is only slightly lower than the melting temperature, only complementary strands can join. And this is exactly the result of the increased ambient temperature, which is caused by the PPT effect.

To demonstrate how reliably the new sensor detects the current COVID-19 virus, the researchers tested it with a very closely related virus: SARS-CoV. This is the virus that broke out in 2003 and triggered the SARS pandemic. The two viruses – SARS-CoV and SARS-CoV2 – differ only slightly in their RNA. And validation was successful: “Tests showed that the sensor can clearly distinguish between the very similar RNA sequences of the two viruses,” explains Jing Wang. And the results are ready in a matter of minutes.

At the moment, however, the sensor is not yet ready to measure the corona virus concentration in the air, for example in Zurich’s main railway station. A number of developmental steps are still needed to do this – for example, a system that draws in the air, concentrates the aerosols in it and releases the RNA from the viruses. “This still needs development work,” says Wang. But once the sensor is ready, the principle could be applied to other viruses and help to detect and stop epidemics at an early stage.

Source: Empa

Work-related Stress Linked to Increased Risk for Peripheral Artery Disease

People who reported work-related stress were more likely to be hospitalized for peripheral artery disease compared to those who did not report work-related stress, according to new research published today in the Journal of the American Heart Association, an open access journal of the American Heart Association. The article appears in a special spotlight issue exploring different aspects of the complex relationships between psychosocial factors and cardiovascular health.

Peripheral artery disease, or PAD, is a cardiovascular disease that occurs when cholesterol or other fatty substances in the blood build up in the blood vessels away from the heart, usually the legs, impeding blood flow. Symptoms often include leg pain while walking. Left untreated, peripheral artery disease increases the likelihood of heart disease and stroke. Worldwide, peripheral artery disease affects more than 200 million people, including more than 8.5 million in the United States. Despite the considerable burden of peripheral artery disease, the evidence on specific risk factors, including potential primary preventive targets, for this disease is scarce, according to researchers.

Work-related stress, or job strain, refers to psychological and social stress at work, often from high expectations combined with lower levels of personal control. Previous studies have linked work-related stress to other forms of atherosclerotic disease; however, few have specifically analyzed its effects on peripheral artery disease. This study focused on the relationship between work-related stress and hospital treatment for peripheral artery disease.

The researchers evaluated the records of 139,000 men and women (36.4% men; average age of study participants range 39-49) participating in 11 separate studies from 1985-2008 in Finland, Sweden, Denmark and the United Kingdom. Participants included in the analysis had no previous history of peripheral artery disease when the respective studies began. Individual information for each participant included age, sex, BMI, smoker or nonsmoker, alcohol consumption, physical activity level, diabetes status, socioeconomic position, data on hospitalizations and the questionnaire on work-related stress.

During an average 12.8 years of follow up, 667 people (0.2 to 1.8% of participants) were hospitalized for peripheral artery disease. Researchers found that people with work-related stress were 1.4 times as likely as those without work-related stress to have a record of peripheral artery disease in the hospitalization register, after adjusting for age, sex and lifestyle variables.

“Our findings suggest that work-related stress may be a risk factor for peripheral artery disease in a similar way as it is for heart disease and stroke,” said lead study author Katriina Heikkilä, Ph.D., senior researcher at the Karolinska Institute, Stockholm.

Stress is associated with increased inflammation and higher blood glucose levels. So, although there is limited evidence linking work-related stress to heart disease, stress could be contributing to complications and exacerbations of peripheral artery disease.

The investigators measured work-related stress based on participants’ ratings of statements to describe psychosocial aspects of their job. This information was compared to records on peripheral artery disease hospitalizations across nearly 13 years of hospital records.

Overall, nearly one-fourth of participants with no previous hospitalization for peripheral artery disease reported work-related stress at the beginning of the 11 studies.

Researchers noted increased risk among men, those with high socioeconomic position and smokers, but noted such subgroup analysis was limited by the small number of people with peripheral artery disease.

Limitations of this study are that it included hospital-treated peripheral artery disease only, which means that the results cannot be generalized to less severe forms of the disease. Also, certain health information, such as blood pressure and cholesterol levels, was unavailable.

Source: American Heart Association

---

Today’s Comic