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The Humanicsxian: November 09: Issue 06
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University of Helsinki Faculty of Medicine

Poetry of Neurology

We are more than our neurons or their combinations, co-relations, conjunctions, functions and interactions, that are conducted through their gap junctions, synapses or action potentials. We are more than the cells, tissues, organs, systems, DNAs, RNAs, genes etc and their ultimate unification into a whole mechanism and system of magnificence.

We are an infinity unfolding itself in the name of the human mind which, through the physiology of what on appearance is a human physique, it becomes, dreams, imagines, creates, loves and does human: the most astonishing of all things, that we find on this Universe.

All we have to do is to look at its unity off the billion plus expressions of its self and wonder about its endless expressive diversity off the same self in billion plus instances to realise that this human mind is magnificent a thing for the purpose of which the neurology is given to it as the most sophisticated, most elaborately engineered, most complexity-strewn an architecture, a most awe-inspiring bio-chemico-genetico-mechanism, that we humans will ever see in this Universe; nothing else will ever surpass this magnificence.

















And it all begins with the book of genome, that has already been written, that will have all the tools to keep on writing the future of a human physiology and with that begins the human life and soon the Cardiology is formed and follows neurology: the duo or the two in one or the one in two: for they, neither ends nor begins alone but, rather, both just clasp, grasp, sew, knit, cut, run, crisscross, bind, bend, blend and flow in, out, between and through the human physiology in such an 'infinity of subtle, intricate and sublime artistry', that the entire creation of this Universe does not have a parallel to show next to it. And with this Cardiology and Neurology the human becomes more than a physiology: it becomes a human mind and that has not been written out, unlike the genome, which has been, and, here is, where the entire life of this human mind is, as if it has got infinity of white papers bundled into a beautiful blank book, that no one can know how to write but that human mind alone does and this is where humanity is, this is what humanity is and this is how humanity is and this why we publish The Humanion to write a Beautiful Book out of those blank white pages of that book, where genome alone can never write a single word unless The Sanctum Mayakardium and The High Neuranium join forces to make 'one': the one, that is exactly like the heart with two atria; or the one, that is exactly like the brain with two hemispheres: it is two in one and one in two. And here is to this awe, to Humanity: Munayem Mayenin


|| Unravelling the Network of Brain Tumour Genetics ||



|| Wednesday: September 06: 2023 || ά. A new map of the network of genetic changes, that drive the development of brain tumours, has been presented by UCL researchers. The genetic map, published in ‘Brain’, is comparable to a map of the London Underground, where different genetic features, responsible for driving brain tumours are like stations connected by tracks.

Mapping the genetic changes should enable more accurate prediction of survival than standard diagnostic approaches. Brain tumours are a common cause of death worldwide, with around 5,500 deaths due to brain tumours in the UK each year. However, the wide diversity of genetic changes, that enable tumour cells to grow, has made them remarkably difficult to treat. Identifying effective treatments requires an understanding of the variable and, highly individual, relation between tumour genetics, patient outcomes and disease mechanisms. Because this diversity is due to the interaction between multiple genetic changes in tumour development, it is ideally captured as a network.

Just as the shortest path from a given station to another is best found by analysing the whole network of stations and tracks, the shortest path from normal to abnormal cells in an individual patient is best found by identifying the whole network of possible genetic changes, leading to brain tumour development.

In the largest Study of its kind, applying network analysis to tumour genetic data from 4,023 patients with brain tumours, drawn over 14 years across 12 countries, researchers at the UCL Queen Square Institute of Neurology, have shown a new map of the network of individual tumour genetic changes in patients with glioma, amongst the hardest brain tumours to treat.

Derived from data, routinely collected, during clinical care, the map is demonstrated to enable more accurate prediction of individual patient survival than the ‘gold-standard’ diagnostic labels, adopted by the World Health Organisation.  Since the approach does not require new tests, it offers an efficient path to improved, more personalised care without any increase to healthcare costs.

Lead Author, Dr James Ruffle, UCL Queen Square Institute of Neurology, said, ‘The treatment of brain tumours is in desperate need of innovation: outcomes have hardly changed over the past 30 years. A critical step is gaining an understanding of tumour genetic diversity, which we show here to be accessible but, only to data and mathematical models of great size and complexity. A radical change of approach is needed, and we now have the computational tools to bring it into reality.”

The  research teams’ work was funded by Wellcome, the Medical Research Council, and the NIHR UCLH Biomedical Research Centre. :::ω::: 

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|| New Approach to Screening Has Potential to Extend Survival in Glioblastoma Brain Cancer ||



|| Sunday: September 04: 2023 || ά. A new form of screening may improve survival rates among people with a fast-growing type of brain tumour by helping identify those most likely to benefit from certain treatments. Innovative pre-clinical research in mouse-models has shown that a molecular imaging technique can show the presence of protein PD-L1 in glioblastomas, the most common type of cancerous brain tumour in adults.

Alongside other measures, tests to detect high levels of PD-L1 could help direct treatment decisions, potentially, leading to better patient outcomes. Currently, scientists assess PD-L1 expression levels by carrying out immunohistochemistry on samples of tissue, taken from the patient during surgery, which is the first-line treatment for glioblastoma. However, this technique is subject to human error and is not standardised globally for these patients or this particular tumour. It can be difficult to quantify the results.

Researchers at the Institute of Cancer Research have now shown that a non-invasive imaging technique, called, immuno-positron emission tomography:Immuno-PET, could be a better approach.

The research has been published in the journal Cancers. It was largely funded by the ICR, which is both a research institute and a charity, and partially, funded by the Cancer Research UK Convergence Science Centre at the ICR, Imperial College London and the National Science Centre in Poland.

Glioblastoma starts as a growth of cells in the brain. It grows quickly and, typically, spreads within the brain, making it very difficult to treat effectively. No cure is yet available, and patients, who, initially, respond to treatment tend to experience relapse. The average survival time is just 12–18 months, with only 05% of patients surviving more than five years.

In recent years, immunotherapy has shown potential as a treatment for glioblastoma. In particular, researchers have been testing drugs, called, immune checkpoint inhibitors, which prevent other proteins from dampening the body’s immune response. The results to date have been mixed, suggesting that the treatment is only likely to be effective for a sub-set of patients.

The ICR’s team successfully used NOTA-maleinide to link ZPD-L1 affibody molecules to fluorine-18 and gallium-68 radionuclides. Affibodies are small proteins, created to bind strongly to target proteins, in this case, PD-L1. This procedure created 18F-AIF-NOTA-ZPD-L1 and 68Ga-NOTA-ZPD-L1, which, with high specificity, recognise PD-L1 on tumour cells and in their micro-environment.

The researchers chose to use affibodies rather than antibodies because their much smaller size means that they clear the body far more quickly, minimising the radiation dose for patients and preventing delays to surgery. Using affibodies, at the same time, makes it possible to get high-quality images just one hour after injection. In comparison, when antibodies are used, the images are usually only retrieved after 48 hours.

The researchers demonstrated that these radio-labelled affibodies could be used to assess the expression level of PD-L1 in tumours in mice. PET scans showed that, although, there was some uptake of the radio-tracer in healthy tissue, the brain tumours were clearly visualised with high tumour-to-background contrast.

Then, the researchers looked into 36 samples from people with newly diagnosed glioblastoma. They noted PD-L1-positive membrane staining in 39 per cent of the samples. A separate analysis of 161 human glioblastoma samples confirmed that tumours with a mesenchymal signature, which is linked to a better response to immune checkpoint inhibitors, had a significantly elevated expression level of PD-L1 compared with other glioblastoma sub-types.

This supports the thinking that healthcare professionals could use Immuno-PET to identify the patients most likely to benefit from immune checkpoint inhibitors. The researchers hope that this work will lead to better outcomes for the 30–49% of patients with the mesenchymal sub-type of glioblastoma.

They are now working on a clinical trial in Poland, that builds on the foundations, laid by this pre-clinical research and expect to present data from that trial in the near future. Dr Gabriela Kramer-Marek, the Group Leader in Pre-clinical Molecular Imaging at ICR, said, ‘’It has been really exciting to see the journey from lab to clinic. We are currently running a clinical trial in people, which was only possible because of this promising pre-clinical work.

The trial was the first ever to use Immuno-PET to evaluate PD-L1 in people with primary glioblastoma and, we hope to see images, that clearly show the presence of PD-L1 in these brain tumours. The treatment for glioblastoma has not changed for decades. Although, we still do not have a cure, I believe that this new screening approach could definitely change patient outcomes.”

Cation: A PET scan, showing glioblastoma in a mouse-model: Credit: Pre-clinical Molecular Imaging Team at ICR, using the Albira PET:SPECT:CT Bruker System :::ω:::

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|| Alzheimer’s Disease: New Study Links Changes in Brain Immune Cells to the Condition ||


|| Wednesday: August 30: 2023 || ά. Immune cells in the brains Alzheimer’s Disease appear to behave differently than those, who are of the same age and with healthy brains for their age, according to an analysis of the concerned cells’ gene activity. The finding suggests that it might be possible to treat Alzheimer’s by altering the behaviour of these cells. According to Dr Katherine Prater, an expert in neuroinflammation and an acting instructor in neurology at the University of Washington School of Medicine.

“If, we can determine what they are doing, we might be able to change their behaviour with treatments, that might prevent or slow this disease.” Dr Prater said. Dr Prater and her co-researchers at the University of Washing Medicine:UWM, Fred Hutchinson Cancer Centre, Arizona State University and University of North Carolina at Chapel Hill reported their findings on May 29 in the journal Nature Aging.

“Now that we have determined the genetic profiles of these microglia, we can try to find out exactly what they are doing and, hopefully, identify ways to change their behaviours, that may be contributing to Alzheimer’s disease.” Neuroscientist Dr Katherine Prater said. In the Study, the researchers looked at immune cells, called, microglia, which play a variety of essential roles in the brain.

They promote brain development and learning by stimulating new connections between and among brain cells and pruning connections, that are no longer need. They perform routine housekeeping chores, such as clearing away dead cells and unwanted debris. And they protect the brain from infection by engulfing microbes and releasing chemical signals, which help orchestrate the body’s immune response. 

Their role in Alzheimer’s Disease, however, is less clear. For example, they appear to protect the brain by clearing out amyloid deposits, the toxic protein clumps, that form in the brains of people suffering from the disease but, they, may, also, contribute to an inflammatory process seen in Alzheimer’s, which leads to the death of brain cells.

To better understand what these cells do, the researchers examined the genes, that were active in microglia taken from the brains Alzheimer’s sufferers and from those, who did not have the disease. Because genes control a cell’s behaviour, knowing which ones are active can help know what a cell is likely tp be doing.

To identify which genes were active, the scientists took advantage of the fact that when a gene is activated, the instructions encoded in its DNA sequence are copied, or transcribed, into a related molecule or RNA. Therefore, by sequencing the RNA in a cell’s nucleus, using single-nucleus RNA sequencing technique, it is possible to know which genes are active in different cells.

In their Study, the researchers studied microglia from the brains of 12 people, who died with Alzheimer’s and 10 who did not have this disease. They found that populations of microglia in both sets of brains were diverse, with the populations falling into 10 subpopulations, each of which, based on gene activity, likely exhibit different characteristics and behaviours.

Although the microglia populations were similar in both sets of brains, the mix was different, with some populations being more prevalent in the brains affected by Alzheimer’s. The differences could be attributed to the cells' contributing to the destruction of brain cells, seen with Alzheimer’s, or they could result from the destruction caused by the disease, Dr Prater said.

“At this point, we can’t say whether the microglia are causing the pathology or whether the pathology is causing these microglia to alter their behaviour.” She said. Among the cell populations, that were more prevalent in the brains, affected by Alzheimer’s were cells, that appear to be in a pre-inflammatory state. Those cells may have an impaired ability to perform the house-cleaning tasks microglia typically do. There were, also, fewer protective cells, that are thought to promote healthy aging.

“Now that we have determined the genetic profiles of these microglia, we can try to find out exactly what they are doing and, hopefully, identify ways to change their behaviours, that may be contributing to Alzheimer’s Disease.” Dr Prater said.

Caption: Photomicrograph of microglia in green from a brain, affected by Alzheimer’s Disease. shows enlarged lysosomes in pink, a sign that the cell’s house-keeping duties have been disrupted: Lexi Cochoit, UW Neuroinflammation Lab: University of Washington Medicine :::ω:::

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Year Ninth: Day 67: Wednesday: November 29: 2023: The Humanion: We Are One











Life's Laurel Is You In One-Line-Poetry A Heaven-Bound Propagated Ray Of Light Off The Eye Of The Book Of Life: Love For You Are Only Once






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|| All copyrights @ The Humanion: London: England: United Kingdom || Contact: The Humanion: editor at || Regine Humanics Foundation Ltd: elleesium at || Editor-In-Chief: Munayem Mayenin || First Published: September 24: 2015 ||
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