P&R Labpak - Everything for your laboratory

P&R Labpak - Everything for your laboratory
Our Head Office in St Helens

Tuesday, 30 May 2017

On this day in science – the rubber fire hose was patented

In 1821, a fire hose of cotton web lined with rubber was patented by James Boyd of Boston, Mass. He invented it to replace riveted leather hose. Leather hose had many drawbacks, including drying out, cracking and bursting from excessive pressure. The introduction of rivets (1807), to replace stitching, had allowed higher pressures and greater delivery of water on the fireground. The improved hose now was 40 to 50 feet in length and weighed more than 85 pounds with the couplings. Hose oilers were developed to keep the leather supple and pliable. Various types of oils and other substances were used to keep the hose in shape. By 1871, the Cincinnati Fire Department was using the B.F. Goodrich Company's new rubber hose reinforced with cotton ply.

Indoor fire hose with a fire extinguisher, by Raysonho @ Open Grid Scheduler / Grid Engine (Own work) [CC0], via Wikimedia Commons
Modern fire hoses use a variety of natural and synthetic fabrics and elastomers in their construction. These materials allow the hoses to be stored wet without rotting and to resist the damaging effects of exposure to sunlight and chemicals. Modern hoses are also lighter weight than older designs, and this has helped reduce the physical strain on firefighters. Various devices are becoming more prevalent that remove the air from the interior of fire hose, commonly referred to as fire hose vacuums. This process makes hoses smaller and somewhat rigid, thus allowing more fire hose to be packed or loaded into the same compartment on a fire fighting apparatus.

There are several types of hose designed specifically for the fire service. Those designed to operate under positive pressure are called discharge hoses. They include attack hose, supply hose, relay hose, forestry hose, and booster hose. Those designed to operate under negative pressure are called suction hoses.

For more information visit:-

Monday, 22 May 2017

A guide to the twenty common amino acids

Have you ever thought about what makes up your body? Only 20 amino acids! Take a look at the graphic below, to discover the structure of each of these, plus information on the notation used to represent them.

Source: Compound Interest. Click to enlarge.

Amino acids are organic compounds containing amine (-NH2) and carboxyl (-COOH) functional groups, along with a side chain (R group) specific to each amino acid. The key elements of an amino acid are carbon, hydrogen, oxygen, and nitrogen, although other elements are found in the side chains of certain amino acids. About 500 amino acids are known and can be classified in many ways. They can be classified according to the core structural functional groups' locations as alpha- (α-), beta- (β-), gamma- (γ-) or delta- (δ-) amino acids; other categories relate to polarity, pH level, and side chain group type (aliphatic, acyclic, aromatic, containing hydroxyl or sulfur, etc.). In the form of proteins, amino acid residues form the second-largest component (water is the largest) of human muscles and other tissues. Beyond their role as residues in proteins, amino acids participate in a number of processes such as neurotransmitter transport and biosynthesis.

In biochemistry, amino acids having both the amine and the carboxylic acid groups attached to the first (alpha-) carbon atom have particular importance. They are known as 2-, alpha-, or α-amino acids (generic formula H2NCHRCOOH in most cases, where R is an organic substituent known as a "side chain"); often the term "amino acid" is used to refer specifically to these. They include the 22 proteinogenic ("protein-building") amino acids, which combine into peptide chains ("polypeptides") to form the building-blocks of a vast array of proteins. These are all L-stereoisomers ("left-handed" isomers), although a few D-amino acids ("right-handed") occur in bacterial envelopes, as a neuromodulator (D-serine), and in some antibiotics. 

Twenty of the proteinogenic amino acids are encoded directly by triplet codons in the genetic code and are known as "standard" amino acids. The other two ("non-standard" or "non-canonical") are selenocysteine (present in many noneukaryotes as well as most eukaryotes, but not coded directly by DNA), and pyrrolysine (found only in some archea and one bacterium). Pyrrolysine and selenocysteine are encoded via variant codons; for example, selenocysteine is encoded by stop codon and SECIS element. N-formylmethionine (which is often the initial amino acid of proteins in bacteria, mitochondria, and chloroplasts) is generally considered as a form of methionine rather than as a separate proteinogenic amino acid. Codon–tRNA combinations not found in nature can also be used to "expand" the genetic code and create novel proteins known as alloproteins incorporating non-proteinogenic amino acids.

Many important proteinogenic and non-proteinogenic amino acids have biological functions. For example, in the human brain, glutamate (standard glutamic acid) and gamma-amino-butyric acid ("GABA", non-standard gamma-amino acid) are, respectively, the main excitatory and inhibitory neurotransmitters. Hydroxyproline, a major component of the connective tissue collagen, is synthesised from proline. Glycine is a biosynthetic precursor to porphyrins used in red blood cells. Carnitine is used in lipid transport.

Nine proteinogenic amino acids are called "essential" for humans because they cannot be created from other compounds by the human body and so must be taken in as food. Others may be conditionally essential for certain ages or medical conditions. Essential amino acids may also differ between species.

Because of their biological significance, amino acids are important in nutrition and are commonly used in nutritional supplements, fertilizers, and food technology. Industrial uses include the production of drugs, biodegradable plastics, and chiral catalysts.

For more information visit:-



Tuesday, 16 May 2017

Diesels pollute more than lab tests detect

Because of testing inefficiencies, maintenance inadequacies and other factors, cars, trucks and buses worldwide emit 4.6 million tons more harmful nitrogen oxide (NOx) than standards allow, according to a new study co-authored by University of Colorado Boulder researchers.

The study, published in Nature, shows these excess emissions alone lead to 38,000 premature deaths annually worldwide, including 1,100 deaths in the United States.

The findings reveal major inconsistencies between what vehicles emit during testing and what they emit in the real world - a problem that's far more severe, said the researchers, than the incident in 2015, when federal regulators discovered Volkswagen had been fitting millions of new diesel cars with "defeat devices."

Red Diesel Tank, by Meena Kadri [CC BY 2.0 (http://creativecommons.org/licenses/by/2.0)], via Wikimedia Commons
The devices sense when a vehicle is undergoing testing and reduce emissions to comply with government standards. Excess emissions from defeat devices have been linked to about 50 to 100 U.S. deaths per year, studies show.

"A lot of attention has been paid to defeat devices, but our work emphasizes the existence of a much larger problem," said Daven Henze, an associate professor of mechanical engineering at CU Boulder who, along with postdoctoral researcher Forrest Lacey, contributed to the study. "It shows that in addition to tightening emissions standards, we need to be attaining the standards that already exist in real-world driving conditions."

The research was conducted in partnership with the International Council on Clean Transportation, a Washington, D.C.-based nonprofit organization, and Environmental Health Analytics LLC.

For the paper, the researchers assessed 30 studies of vehicle emissions under real-world driving conditions in 11 major vehicle markets representing 80 percent of new diesel vehicle sales in 2015. Those markets include Australia, Brazil, Canada, China, the European Union, India, Japan, Mexico, Russia, South Korea and the United States.

They found that in 2015, diesel vehicles emitted 13.1 million tons of NOx, a chemical precursor to particulate matter and ozone. Exposure in humans can lead to heart disease, stroke, lung cancer and other health problems. Had the emissions met standards, the vehicles would have emitted closer to 8.6 million tons of NOx.

Heavy-duty vehicles, such as commercial trucks and buses, were by far the largest contributor worldwide, accounting for 76 percent of the total excess NOx emissions.

Henze used computer modeling and NASA satellite data to simulate how particulate matter and ozone levels are, and will be, impacted by excess NOx levels in specific locations. The team then computed the impacts on health, crops and climate.

"The consequences of excess diesel NOx emissions for public health are striking," said Susan Anenberg, co-lead author of the study and co-founder of Environmental Health Analytics LLC.

China suffers the greatest health impact with 31,400 deaths annually attributed to diesel NOx pollution, with 10,700 of those deaths linked to excess NOx emissions beyond certification limits. In Europe, where diesel-passenger cars are common, 28,500 deaths annually are attributed to diesel NOx pollution, with 11,500 of those deaths linked to excess emissions.

The study projects that by 2040, 183,600 people will die prematurely each year due to diesel vehicle NOx emissions unless governments act.

The authors say emission certification tests, both prior to sale and by vehicle owners, could be more accurate if they were to simulate a broader variety of speeds, driving styles and ambient temperatures. Some European countries now use portable testing devices that track emissions of a car in motion.

"Tighter vehicle emission standards coupled with measures to improve real-world compliance could prevent hundreds of thousands of early deaths from air pollution-related diseases each year," said Anenberg.

For more information, visit:-








Tuesday, 9 May 2017

On this day in science history: the Hindenburg Zeppelin arrived at Lakehurst, New Jersey, USA

In 1936, the Hindenburg Zeppelin arrived at Lakehurst, New Jersey, USA, from Germany marking the beginning of a regular transatlantic passenger service. The flight, carrying 51 passengers and 56 crew, took 61 hours.

Hindenburg at Lakehurst, by U.S. Department of the Navy. Bureau of Aeronautics. Naval Aircraft Factory, Philadelphia, Pennsylvania (USA). [Public domain], via Wikimedia Commons
The Hindenburg was a large German commercial passenger-carrying rigid airship, the lead ship of the Hindenburg class, the longest class of flying machine and the largest airship by envelope volume. It was designed and built by the Zeppelin Company (Luftschiffbau Zeppelin GmbH) on the shores of Lake Constance in Friedrichshafen and was operated by the German Zeppelin Airline Company (Deutsche Zeppelin-Reederei). The Hindenburg had a duralumin structure, incorporating 15 Ferris wheel-like bulkheads along its length, with 16 cotton gas bags fitted between them. The bulkheads were braced to each other by longitudinal girders placed around their circumferences. The airship's outer skin was of cotton doped with a mixture of reflective materials intended to protect the gas bags within from radiation, both ultraviolet (which would damage them) and infrared (which might cause them to overheat). The gas cells were made by a new method pioneered by Goodyear using multiple layers of gelatinized latex rather than the previous goldbeater's skins. In 1931 the Zeppelin Company purchased 5,000 kg (11,000 lb) of duralumin salvaged from the wreckage of the October 1930 crash of the British airship R101, which might have been re-cast and used in the construction of the Hindenburg.

The interior furnishings of the Hindenburg were designed by Fritz August Breuhaus, whose design experience included Pullman coaches, ocean liners, and warships of the German Navy. The upper "A" Deck contained small passenger quarters in the middle flanked by large public rooms: a dining room to port and a lounge and writing room to starboard. Paintings on the dining room walls portrayed the Graf Zeppelin's trips to South America. A stylized world map covered the wall of the lounge. Long slanted windows ran the length of both decks. The passengers were expected to spend most of their time in the public areas, rather than their cramped cabins.

The lower "B" Deck contained washrooms, a mess hall for the crew, and a smoking lounge. Harold G. Dick, an American representative from the Goodyear Zeppelin Company, recalled "The only entrance to the smoking room, which was pressurized to prevent the admission of any leaking hydrogen, was via the bar, which had a swiveling air lock door, and all departing passengers were scrutinized by the bar steward to make sure they were not carrying out a lit cigarette or pipe."

Helium was initially selected for the Hindenburg’s lifting gas because it was the safest to use in airships, as it is not flammable. One proposed measure to save helium was to make double-gas cells for 14 of the 16 gas cells; an inner hydrogen cell would be protected by an outer cell filled with helium, with vertical ducting to the dorsal area of the envelope to permit separate filling and venting of the inner hydrogen cells. At the time, however, helium was also relatively rare and extremely expensive as the gas was only available in industrial quantities from distillation plants at certain oil fields in the United States. Hydrogen, by comparison, could be cheaply produced by any industrialized nation and being lighter than helium also provided more lift. Because of its expense and rarity, American rigid airships using helium were forced to conserve the gas at all costs and this hampered their operation.

Despite a U.S. ban on the export of helium under the Helium Control Act of 1927, the Germans designed the airship to use the far safer gas in the belief that they could convince the US government to license its export. When the designers learned that the National Munitions Control Board would refuse to lift the export ban, they were forced to re-engineer the Hindenburg to use hydrogen for lift. Despite the danger of using flammable hydrogen, no alternative lighter-than-air gases could provide sufficient lift. One beneficial side effect of employing hydrogen was that more passenger cabins could be added. The Germans' long history of flying hydrogen-filled passenger airships without a single injury or fatality engendered a widely held belief they had mastered the safe use of hydrogen. The Hindenburg's first season performance appeared to demonstrate this, however the airship was destroyed by fire 14 months later on May 6, 1937, at the end of the first North American transatlantic journey of its second season of service. Thirty-six people died in the accident, which occurred while landing at Lakehurst. This was the last of the great airship disasters; it was preceded by the crashes of the British R38 in 1921 (44 dead), the US airship Roma in 1922 (34 dead), the French Dixmude in 1923 (52 dead), the British R101 in 1930 (48 dead), and the US Akron in 1933 (73 dead).


For more information visit:-


Tuesday, 2 May 2017

Mice with missing lipid-modifying enzyme heal better after heart attack

Two immune responses are important for recovery after a heart attack - an acute inflammatory response that attracts leukocyte immune cells to remove dead tissue, followed by a resolving response that allows healing.

The human heart by Patrick J. Lynch, medical illustrator (Patrick J. Lynch, medical illustrator) [CC BY 2.5 (http://creativecommons.org/licenses/by/2.5)], via Wikimedia Commons
Failure of the resolving response can allow a persistent, low-grade nonresolving inflammation, which can lead to progressive acute or chronic heart failure. Despite medical advances, 2 to 17 percent of patients die within one year after a heart attack due to failure to resolve inflammation. More than 50 percent die within five years.

Using a mouse heart attack model, Ganesh Halade, Ph.D., and his University of Alabama at Birmingham colleagues have shown that knocking out one particular lipid-modifying enzyme, along with a short-term dietary excess of a certain lipid, can improve post-heart attack healing and clear inflammation. Halade, an assistant professor in the UAB Department of Medicine, hopes that future physicians will be able to use knowledge from studies like his to boost healing in patients after heart attacks and prevent heart failure.

"Our goal is healing, and we are reaching that goal," he said of efforts in the UAB Division of Cardiovascular Medicine.

Why are lipids and lipid-modifying enzymes important in inflammation and resolving inflammation? Three key lipid modifying enzymes in the body change the lipids into various signaling agents. Some of these signaling agents regulate the triggering of inflammation, and others promote the reparative pathway.

The lipids modified by the enzymes are two types of essential fatty acids that come from food, since mammals cannot synthesize them. One is n-6 or omega-6 fatty acids, and the other type is n-3 or omega-3 fatty acids. The balance of these two types is important.

The Mediterranean diet, with a near balance of omega-3 and omega-6 fatty acids, promotes heart health. The Western diet, with large amounts of omega-6 fatty acids that greatly exceed the levels of omega-3 fatty acids, can lead to heart disease.

The three main lipid-modifying enzymes compete with each other to modify whatever fatty acids are available from the diet. So, Halade and colleagues asked, what will happen if we knock out one of the key enzymes, the 12/15 lipoxygenase?

They reasoned that this would increase the metabolites produced by the other two main enzymes, cyclooxygenase and cytochrome P450 because they no longer had to compete with 12/15 lipoxygenase for lipids to modify. This might be a benefit because those signaling lipids produced through the cyclooxygenase and cytochrome P450 pathways were already known to lead to major resolution promotion factors for post-heart attack healing.

The UAB researchers found that knocking out the 12/15 lipoxygenase and feeding the mice a short-term excess of polyunsaturated fatty acids led to increased leukocyte clearance after experimental heart attack, meaning less chronic inflammation. It also improved heart function, increased the levels of bioactive lipids during the reparative phase of healing, and led to higher levels of reparative cytokine markers. Additionally, the heart muscle showed less of the fibrosis that is a factor in heart failure.

Besides congestive heart failure, persistent inflammation aggravates a vicious cycle in many cardiovascular diseases, including atherogenesis, atheroprogression, atherosclerosis and peripheral artery disease.

Halade says further mechanistic studies are warranted to develop novel targets for treatment and to find therapies that support the onset of left ventricle healing and prevent heart failure pathology.

For more information visit:-