New legislation will soon place further curbs on tobacco smoking in South Africa – and these laws will also now extend to e-cigarettes. In South Africa, lung cancer is the third most common cancer among men and seventh for women. More than two-thirds of lung cancer patients are diagnosed at an advanced stage, resulting in poorer outcomes for treatment.
The proposed laws impose harsher penalties against smoking in smoke-free zones, being punishable with a fine or up to three months imprisonment. More areas would be designated smoke-free zones, essentially ending the smoking sections currently set aside for restaurants and bars. This would also extend to the homes of people who employ domestic workers – the employers would not be able to smoke while those workers are present.
Smoking would also be banned in homes used for teaching, tutoring and commercial childcare. Shared residences would also have smoking banned in common areas, as would smoking in vehicles with occupants under the age of 18.
Cigarette packaging will also be targeted, with a move to plain packaging with graphic health warnings. It will no longer be legal to sell cigarettes through vending machines, nor display cigarettes at the point of sale. Sweets and toys resembling cigarettes would also be banned – however, the sugar ‘cigarettes’ that many may remember from their youth are already banned.
Vaping and e-cigarette products will also be liable to the same legislation, and are also soon to have an excise tax levied upon them.
A team of Japanese researchers have shown that low concentrations of cetylpyridinium chloride, used in certain mouthwashes, has an antiviral effect on SARS-CoV-2. Their findings were published in the journal Scientific Reports.
SARS-CoV-2 is transmitted via aerosols, which are spread from the oral and nasal cavities. In addition to infecting the cells of the respiratory tract, SARS-CoV-2 is also known to infect the cells of the lining of the mouth and the salivary glands.
Store-bought mouthwashes contain a number of antibiotic and antiviral components, such as cetylpyridinium chloride (CPC), which has been shown to reduce the oral viral load of SARS-CoV-2, chiefly by disrupting the virus’s lipid envelope. While there are other chemicals with similar effects, CPC has the advantage of being tasteless and odourless.
The researchers, led by Professor Kyoko Hida at Hokkaido University, were interested in studying the effects of CPC in Japanese mouthwashes, which typically contain a fraction of the CPC compared to previously tested mouthwashes. They tested the effects of CPC on cell cultures that express trans-membrane protease serine 2 (TMPRSS2), which is required for SARS-CoV-2 entry into the cell.
They found that, within 10 minutes of application, 30–50 µg/mL of CPC inhibited the infectivity and capability for cell entry of SARS-CoV-2. Interestingly, commercially available mouthwashes that contain CPC performed better than CPC alone. They also showed that saliva did not alter the effects of CPC. Testing with the original, alpha, beta and gamma variants of SARS-CoV-2 showed similar effetcts of CPC.
This study shows that low concentrations of CPC in commercial mouthwash suppress the infectivity of four variants of SARS-CoV-2. The authors have already begun assessing the effect on CPC-containing mouthwashes on viral loads in saliva of COVID patients. Future work will also focus on fully understanding the mechanism of effect, as lower concentrations of CPC do not disrupt lipid membranes.
A recent discovery has revealed that the adult brain has far greater potential to recover from inherited blindness than previously believed, with important implications for visually impaired people. The paper appears in Current Biology.
The research team was examining treatment for Leber congenital amaurosis (LCA), a group of inherited retinal diseases distinguished by severe visual impairment at birth. The condition, caused by mutations in any of over two dozen genes, results in degeneration or dysfunction in the retina’s photoreceptors.
Administering chemical compounds that target the retina, called synthetic retinoids, can restore a notable amount of vision in children with LCA. The UCI team wanted to find out if the treatment could make a difference for adults who have the condition.
“Frankly, we were blown away by how much the treatment rescued brain circuits involved in vision,” said corresponding author Sunil Gandhi, professor of neurobiology and behaviour. “Seeing involves more than intact and functioning retinae. It starts in the eye, which sends signals throughout the brain. It’s in the central circuits of the brain where visual perception actually arises.” Until now, scientists believed that the brain must receive those signals in childhood so that central circuits could wire themselves correctly.
The researchers were surprised by what they found in rodent models of LCA. “The central visual pathway signalling was significantly restored in adults, especially the circuits that deal with information coming from both eyes,” Prof Gandhi said. “Immediately after the treatment, the signals coming from the opposite-side eye, which is the dominant pathway in the mouse, activated two times more neurons in the brain. What was even more mind-blowing was that the signals coming from the same-side eye pathway activated five-fold more neurons in the brain after the treatment and this impressive effect was long-lasting. The restoration of visual function at the level of the brain was much greater than expected from the improvements we saw at the level of the retinae. The fact that this treatment works so well in the central visual pathway in adulthood supports a new concept, which is that there is latent potential for vision that is just waiting to be triggered.”
The finding opens exciting research possibilities. “Whenever you have a discovery that breaks with your expectations about the possibility for the brain to adapt and rewire, it teaches you a broader concept,” Prof Gandhi said. “This new paradigm could aid in the development of retinoid therapies to more completely rescue the central visual pathway of adults with this condition.”
There is an elaborate interplay between genes, sex, the environment during growth, and age and how they influence variation in longevity, according to a study published in the journal Science. These findings are an important step in understanding why some people live longer than others and provide a basis for future studies to improve a healthy lifespan.
Robert Williams, PhD, at the University of Tennessee Health Science Center (UTHSC), along with Johan Auwerx, MD, PhD, at the École Polytechnique Fédérale de Lausanne (EPFL) in Switzerland, began a program in 2016 to define genetic factors involved in agieng and lifespan. “Finding common molecular pathways that control differences in rate of aging is critical to our understanding of how individuals differ in their health and lifespan,” Dr Williams said. “Such insights may help us work out ways to intervene rationally.”
Drs Williams and Auwerx received DNA of over 12 000 mice from the National Institute of Aging. Each of the 27 574 genetically heterogeneous mice studied is a full sibling, sharing half its genetic inheritance with each other mouse in the programme, and each has a known lifespan, making them an ideal system to study.
The research team analysed the genes of over 3 000 mice, all of them genetic brothers or sisters which were allowed to live until their natural death. Comparing their DNA to lifespan, the researchers defined stretches of DNA in genomes that affect longevity. The results show the DNA segments, or loci, associated with longevity are largely sex-specific, with females having a region in chromosome 3 that affects lifespan. When the males who died early due to non-aging-related reasons were removed from the analysis, additional genetic signals started to emerge, suggesting some genetic variations only affect lifespan after a certain age.
In addition to finding genetic determinants of longevity, the researchers explored other contributors. In general, bigger mice die younger. The researchers found that some, but not all, of the genetic effects on longevity are through effects on growth. One of the non-genetic effects may be how early access to food affects growth. They observed that mice from smaller litters tended to be heavier adults and live shorter lives. Mice from larger litters that had to share their mother’s milk with more siblings, grew more slowly and lived longer on average. The researchers corroborated these trends of early growth versus longevity in large human datasets with hundreds of thousands of participants.
Beyond characterising how longevity is affected, the researchers worked to find genes most likely to play a role in longevity determination. They measured the effect of DNA variation on how genes are expressed and compared their analyses with multiple human and non-human databases. From this they nominated a few genes likely to modulate aging rates. They then tested the effects of manipulating these genes in roundworms and found that a subset of gene perturbations did in fact affect the lifespan. The results of this study will be a rich resource of aging genes that will hopefully guide the design of therapies that not only extend lifespan, but also healthspan.
Red blood cells, platelets and T cells. Source: CC0
In a surprising discovery published in Science Advances, turning off the two proteins that regulate iron uptake results in not only anaemia but also in neutrophil levels plummeting. Iron deficiency, a known defence mechanism against infectious pathogens, can therefore a double-edged sword, as it simultaneously curbs the defensive power of this important arm of the innate immune system.
Iron is an indispensable component, needed for the blood pigment haemoglobin. The iron supply to the cells is controlled by the two proteins IRP-1 and IRP-2. If the cell lacks iron, IRP-1 and IRP-2 crank up the production of the various iron transporter proteins that take iron into the cell. IRP-1 and IRP-2 also ensure that an equally dangerous excess of iron does not occur.
IRP-1 and IRP-2 are essential for survival: mice lacking both control proteins during embryonic development die while still in the womb. But what happens when IRP-1 and IRP-2 fail in adult mice? A team led by Bruno Galy at the German Cancer Research Center (DKFZ) has now investigated this by shutting down IRP production in mice.
As the researchers had expected, the most striking change after IRPs were switched off was a pronounced decrease in red blood cells. Due to the lack of haemoglobin, these erythrocytes reached only a minimal size.
However, the researchers were surprised to see that white blood cells also decreased, mainly due to a deficiency of neutrophils, which account for up to two-thirds of white blood cells in humans.
The neutrophil decline was not caused by a mass die-off but a developmental blockade in the haematopoietic system: the precursor cells in the bone marrow no longer develop into mature neutrophils – an iron-dependent process. Other types of white blood cells, such as monocytes, were unaffected by the IRP-dependent developmental blockade.
Iron limitation is a double-edged sword
“This strong iron dependence of neutrophils was previously unknown. It possibly affects the immune defence against bacterial pathogens,” said senior author Bruno Galy. Yet iron deficiency is one of the body’s defence strategies in bacterial infections since many pathogens are dependent on iron. The body hoards the metal in certain cells to cut off access for pathogens, limiting their ability to replicate.
Galy is involved with another study also in Science Advances, which shows that iron deficiency in blood serum, as typically occurs with infections, leads to a decrease in neutrophils in mice and limits the ability of these immune cells to fight bacteria. “Iron deficiency apparently modulates the innate immune system. It suppresses the maturation of neutrophils and also throttles their defensive power,” commented Bruno Galy. “The limitation of available iron is apparently a double-edged sword: On the one hand, the body thereby prevents bacteria from spreading. On the other hand, the function of an important arm of the innate immune system suffers.”
Inflammation often leads to anaemia, as can be experienced by cancer patients. The researchers next want to investigate whether iron deficiency in chronic inflammation also impairs immune function.
