400 Matching Annotations
  1. Dec 2024
  2. Nov 2024
    1. accumulation of all of that movement of charge is contributing to that electrical phenomenon and therefore in the end what you're doing is talking about a higher level of causation U than the components of the cell

      for - evolutionary biology - Denis Noble - journey from reductionist to non-reductionist - ion channel and cell membrane work - connects to bioelectricity in the entire body

    2. you started from a reductionist camp when you were studying ion channels and cell membranes

      for - Denis Noble - background - early work on ion channels and cell membranes

  3. Oct 2024
  4. Sep 2024
  5. Aug 2024
  6. Jul 2024
  7. Jun 2024
  8. May 2024
    1. there are no genes for any of those membranes all the lipids that form the membranes and the complicated 00:07:27 structures that you can see in a typical cell none of that is coded for in the genome all of that is inherited

      for - key insight - decision-making structures are in the cell membrane, not the genes

      key insight - The codes that enable us to make choices are located in - the membranes of our cells and - their protein channels - There are no genes for - any of those membranes - all the lipids that form the membranes and the complicated structures that you can see in a typical cell - None of that is coded for in the genome - All of that is inherited

    2. a bit of size comparison

      for - size comparison - genome to cell

  9. Apr 2024
  10. Mar 2024
  11. Jan 2024
    1. it's easy for us to look at us and think okay we're 30 trillion human cells give or take we're about 39 trillion bacterial cells at what point do we consider ourselves bacteria or at what point do we consider ourselves 00:07:46 human

      for - question - identity - individual cell vs multicellular organism

      question - identity - individual cell vs multicellular organism - This is a fascinating question as it looks at our evolutionarily composite nature - as a multi-scale competency architecture - Certainly our ordinary consciousness operates as the governance system for the entire population of collaborating cells and microbes - but can we actually directly identify with each individual cell or microbe in this vast integrated collection? - how does Levin's computational boundary of self help to shed light on this question?

    1. Fluorescence Activated Cell Sorting (FACS).  From sorting cells for single cell genomics to identifying the host range of a plasmid; from detecting metabolically active cells in an environmental sample to studying colitogenic-driving intestinal bacteria, FACS can be used in a multitude of applications to study microbial communities (Rinke et al. 2014, Klumper et al. 2015, Kalyuzhnaya et al. 2008, Hatzenpichler et al. 2016, Palm et al. 2014).
  12. Dec 2023
    1. Komórki Purkinjego i móżdżekJak stwierdzono, komputery PC wmóżdżekmają istotne prognozy dotyczące LC ( Schwarz i in., 2015 ). Warto zauważyć, że niższa całkowita liczba komputerów PC lub zmniejszona gęstość komputerów PC to jedne z najbardziej powtarzalnych odkryć neurobiologicznych w ASD (około 75% osób z ASD wykazuje dysfunkcję/zmniejszoną liczbę komputerów PC ; Fatemi i in., 2002 ; Whitney i in., 2009 ;Passarelli i in., 2013 ;Hampson i Blatt, 2015 ). Niektóre dowody wskazują, że liczba komputerów PC zmniejsza się również w przypadku ADHD , ale konieczne są dalsze badania (Rout i in., 2012 ;Passarelli i in., 2013 ). Jak zauważają Rout i in. (2012 ),zmniejszoną liczbę PC można zaobserwować jedynie w podtypie ADHD z dysfunkcją móżdżku, jak wykazano w bardziej globalnej ocenie neuroobrazowania(patrz Durston i in., 2011 ). Obecnie wciąż nie można zrozumieć genetycznych podstaw PC w ASD (Hampson i Blatt, 2015 ). W jednym badaniu przeprowadzonym przez Rout i wsp. (2012 ) wykazano zwiększony poziom przeciwciał przeciwko dekarboksylazie kwasu glutaminowego 65 ( GAD65 ) w surowicy w grupach ASD i ADHD w porównaniu z osobami z grupy kontrolnej (przeciwciała GAD65 nie były obecne u żadnej zdrowej osoby). GAD65 jest ważny w syntezie kwasu γ-aminomasłowego ( GABA ). Następnie myszom nałożono surowicę z grup ASD i ADHDmóżdżek, gdzie przeciwciała reagowały z komputerami PC . Zastosowanie tych przeciwciał ostatecznie doprowadziło do śmierci PC ( Mitoma i in., 2003 ;Rout i in., 2012 ). Zwiększone przeciwciała przeciwko GAD65 mogą zatem przyczyniać się do dysfunkcji PC w ASD i ADHD , ale wymagane są badania na większych próbach. Nieprawidłowe projekcje doprowadzające PC w ASD i być może ADHD do LC mogą prowadzić do dysfunkcji LC -NE. Jednak możliwa jest także sytuacja odwrotna. Jak stwierdzono, LC moduluje asocjacyjną plastyczność synaptyczną móżdżku, co wpływa na odpalanie PC ( Carey i Regehr, 2009 ). Dlatego nieprawidłowe działanie LC -NE może prowadzić do zakłóceń w działaniu komputera .Ostatnią opcją jest to, że wzajemne projekcje między LC i móżdżkiem w obu kierunkach są nieprawidłowe, co również wskazywałoby na dysfunkcję LC-NE i PC/móżdżku

      Komurki Purkinego bardziej związane z ASD, ale możliwe że LC NE zaburza działanie komurek purkinjego

    1. Jaka jest behawioralna konsekwencja tej synchronizacji? Prawdopodobieństwo synchronizacji było największe dla sakkad, które znajdowały się w kierunku, który pokrywał się z najmniejszym prawdopodobieństwem CS (CS+180). W przypadku wielu rodzajów zachowań, w tym kondycjonowania powiek oczu, sakkad i ruchów kończyn, strojenie CS komórki P jest prawdopodobnie dostosowane do kierunku działania neuronu jądra [19, 46, 47]. Na przykład w sakkadowych ruchach gałek ocznych analiza wpływu CS na SS i zachowanie sugeruje, że komórki P, które mają dostrojenie CS do błędów punktu końcowego w lewo, rzutują na neurony jądra, które mają dalszy kierunek działania, który pośrednio promuje wytwarzanie sił w lewo [19], korygując w ten sposób te błędy. Oznacza to, że podczas sakkady w kierunku CS+180 zwiększona synchronizacja łączy się z odhamowaniem (pauzą szczytową), aby porwać neurony jądra podczas zwalniania [9], wytwarzając siły w dół, które są wyrównane z CS-on macierzystych komórek P. W rezultacie, efekt synchronizacji limfocytów P, w połączeniu z odhamowaniem jądra, prawdopodobnie wytworzy siły, które sprzeciwiają się kierunkowi ruchu, powodując jego zatrzymanie.

      Hamowanie za pomocą Komurek Purkinjego

    2. Tu Skupiliśmy się na wychylnych ruchach gałek ocznych, ponieważ są one tak krótkie, że wykluczają możliwość sensorycznego sprzężenia zwrotnego, co wymaga od mózgu polegania wyłącznie na swoich wewnętrznych przewidywaniach [13,14,15]. Przewidywania te zależą w dużej mierze od móżdżku [16, 17]. Na przykład szybkość wypalania populacji komórek P, ale nie pojedynczych komórek, przewiduje kierunek i prędkość trwającej sakkady [18, 19]. Jednak, aby sprawdzić synchronizację, musieliśmy jednocześnie rejestrować z wielu komórek P podczas sakkad, coś, co, według naszej wiedzy, nie zostało osiągnięte u żadnego gatunku naczelnych.Informacje, które jeden obszar mózgu przekazuje drugiemu, są zwykle postrzegane przez pryzmat szybkości wypalania. Gdyby jednak neurony wyjściowe mogły zmieniać czas swoich skoków, to poprzez synchronizację zwracałyby uwagę na informacje, które mogą mieć kluczowe znaczenie dla kontroli zachowania. Tutaj donosimy, że w móżdżku populacje komórek Purkinjego, które podzielają preferencję błędu, przekazują do jądra, kiedy spowolnić ruch, zmniejszając szybkość wypalania i tymczasowo synchronizując pozostałe kolce.

      Działanie komórek Purkinjego

  13. Nov 2023
    1. you can train them it has memory you can train it you can take a a trained one and a naive one and fuse them they 00:39:24 they'll fuse together and then the memory sort of propagates and the naive one will now remember you know have the memory that that the other one had um no nerves no no brain um single cell
      • for: Michael Levin - slime mold experiment, question - new theory of consciousness from a single cell

      • question

        • is it possible that a theory can be constructed to explain consciousness from the behavior of a single cell organism such as a slime mold?
  14. Oct 2023
    1. Eukaryotic single-celled organisms appear in the fossil record perhaps by 1.6 BYA (Knoll et al., 2006). Yet for a “boring billion” years of evolutionary history, they remain minor components in bacterial-dominated ecosystems before explosively radiating as large, multicellular species in an Ediacaran and Cambrian MST. Eukaryotes are obviously essential for this MST, as all animals, plants and fungi are eukaryotes. However, the initial appearance of eukaryotic cells seems insufficient for a MST.
      • for: example, example - MET and FET insufficient for MST

      • example: MET and FET insufficient for MST

      • paraphrase

        • Eukaryotic single-celled organisms appear in the fossil record by approx. 1.6 BYA (Knoll et al., 2006).
        • Yet for a “boring billion” years of evolutionary history, they remain minor components in bacterial-dominated ecosystems
          • before explosively radiating as large, multicellular species in
            • an Ediacaran and
            • Cambrian MST.
        • Eukaryotes are obviously essential for this MST, as all
          • animals,
          • plants and
          • fungi
        • are eukaryotes.

        • However, the initial appearance of eukaryotic cells seems insufficient for a MST

    1. Imagine having your own self-contained knowledge manipulator in a portable package the size andshape of an ordinary notebook. How would you use it if it had enough power to outrace yoursenses of sight and hearing, enough capacity to store for later retrieval thousands of page-equivalentsof reference materials, poems, letters, recipes, drawings, animations, musical scores, waveforms,dynamic simulations, and anything else you would like to create, remember, and change?

      Fascinating how Even though we did realized some of this with the mobile phone we still have a system that's so fragmented that it's fundamentally getting in the way of progress

  15. Sep 2023
      • for: superorganism, multi-level superorganism, collective intelligence, individual-collective gestalt, Michael Levin,

      • title: Cell Intelligence in Physiological and Morphological Spaces

      • author: Michael Levin
      • date 2022
      • comment
        • This is a talk on collective intelligence in unconventional spaces
  16. Aug 2023
  17. Jul 2023
    1. the big discovery of the 21st century is that actually just because someone's died and I've given them a Death Note as a physician as an intensive care physician the cells inside the body 00:02:15 have not yet died
      • (cell) life after death
        • cells within the body still remain alive after what a physician would normally deem a person dead.
        • cells (including brain cells) go into a hibernation state for many hours after death.
  18. Jun 2023
  19. May 2023
  20. Apr 2023
  21. Mar 2023
    1. Review coordinated by Life Science Editors.

      Reviewed by: Dr. Helen Pickersgill, Life Science Editors

      Potential Conflicts of Interest: None

      Main point of the paper: By combining multiple stains and antibodies with ultrastructural expansion (light) microscopy in Plasmodium falciparum during the course of mitosis within red blood cells (the asexual blood stage), when it causes the symptoms of malaria, the authors identified new structural features of cell division in this important human parasite.

      Why this is interesting: Imaging the dramatic physical events that occur when cells divide tells us a lot about the biology of the process and is insightful to compare between different eukaryotes, but many organisms are too small to visualise by light microscopy, which is the most versatile imaging technique. So, they used an existing preparation technique to enlarge the parasites, a wide array of dyes and antibodies, and sampled at multiple timepoints so that more intracellular structures could be visualised and their behaviour and potential functions in cell division revealed.

      Background: Expansion microscopy (ExM) has been around since 2015 (doi: 10.1126/science.1260088) and is a fairly simple and affordable technique. It involves physically magnifying a specimen by embedding it in a polyelectrolyte gel that swells up in water enabling super-resolution imaging. It has been previously applied to Plasmodium and other Apicomplexa, but not with so many different labels across different timepoints at this important life-stage.

      Results: • They imaged 13 subcellular structures (including microtubules, microtubule organising centres, apicoplasts, Golgi and the ER) at multiple timepoints covering the entire asexual blood stage. • Among many results were the following: • They found a central role for the nuclear MTOC in coordinating mitosis and likely in establishing apical-basal polarity early during the asexual cycle. o the MTOC is tethered to the parasite plasma membrane (via cytoplasmic extensions) throughout mitosis. o the cytoplasmic extensions of the MTOC were closely associated (in numbers and positions) with several apical structures including the Golgi and the basal complex. o the MTOC is tethered to the mitochondria and apicoplast during fission and may also regulate their copy numbers. • They performed the first detailed characterization of the short-lived interpolar spindles, previously difficult to visualize, which consist of microtubules connecting duplicated MTOCs as they move to opposite sides of the cell. They found a large variation in their size, which may be how they enable the MTOCs to move without detaching from the plasma membrane. • They were able to study the biogenesis of rhoptries, which secrete proteins required for the parasite to invade host red blood cells, and discovered that: o biogenesis begins earlier than thought and that they associate with MTOCs during the remaining rounds of mitosis. o Rhoptry pairs are likely synthesized independently because over 95% are different sizes and densities.

      Remaining thoughts: • Clearly written and easy to read paper with stunning images. • Comprehensive (including descriptions of when things didn’t work), but remains largely descriptive (of course). • Could be shortened/sharpened to make it more manageable to read without losing the main messages, which are somewhat lost in the text. • A top-level, specialised paper that opens the door for more targeted studies of organelle functions during mitosis and comparisons of these functions with other (higher) eukaryotes. • By identifying key players in mitosis during the asexual blood stage it may reveal candidate therapeutic targets for treating malaria.

  22. Feb 2023
    1. Review coordinated by Life Science Editors

      Reviewed by: Dr. Helen Pickersgill, Life Science Editors

      Potential Conflicts of Interest: None

      Impact Point: Transcription factors may mediate the release of specific genes in extracellular vesicles that could be taken up by other cells and directly influence their behaviour.

      Background: Extracellular vesicles (EVs) are nanoscale, membrane-bound vesicles containing proteins, nucleic acids and lipids that are released by most cell types. Originally thought of as a cell waste disposal mechanism, they have since been rebranded as a means of intercellular communication, both short and long range, (like a cellular postal service), and can, for example, modify gene expression and function in recipient cells via the transfer of specific RNAs (DOI: 10.1038/s41580-020-0251-y). One interesting function for EVs was the recent discovery that antigen presenting cells (APCs) could donate telomeres via EVs to recipient T cells and rescue them from senescence (DOI: 10.1038/s41556-022-00991-z).

      Given EVs contain a wide variety of cargos derived from the secreting cells, which have been extensively profiled (e.g., DOI: 10.1016/j.cell.2020.07.009) they are particularly interesting as sources of biomarkers for diagnosing diseases such as cancer (e.g., DOI: 10.1038/s12276-019-0219-1). We might also be able to use them as stable delivery mechanisms for controlling cell behaviour or targeting therapeutics/diagnostics.

      We know quite a bit about how RNAs and proteins are selected for secretion by EVs (mediated by the autophagy protein LC3: e.g., DOIs: 10.1080/15548627.2020.1756557; 10.1038/s41556-019-0450-y). But little is known about DNA. DNA presents a particular challenge as it is packed up into the nucleus. This is also particularly important to understand in the context of horizontal gene transfer, i.e., passing functional genes between cells.

      Main question: How does a cell ‘select’ specific DNA cargo from the nucleus and enable it to be released by EVs?

      The advance: They discover that a transcription factor (FOXM1) plays a central role in mediating DNA release in EVs.

      Results: • FOXM1 and LC3 (autophagy protein) colocalize and interact in cultured cells (coIP endogenous and exogenous, EMSA, immunostaining and identify an FOXM1-binding domain mutant). • FOXM1, LC3 and DNA colocalise in the cytoplasm in cultured cells, which increases upon starvation-induced autophagy (immunofluorescence). • FOXM1 and LC3 are found in EVs released from cultured cells (Western blot). • 15,544 DNA identified in EVs released from cultured cells (evDNA sequencing), of which 25 overlapped with DNA loci binding FOXM1 (ChIP). • FOXM1-bound nuclear DNA is transported to the cytoplasm upon induction of autophagy and is released in EVs in cultured cells (knock-in tagged chromatin with CRISPR-cas9, IF and PCR). This is dependent on FOXM1 (knock-out in cultured cells).

      Significance: Transcription factors display strong DNA binding specificity and so are ideal candidates for directing specific genes into EVs for potential transfer to recipient cells.

      Remaining questions/points: Care needs to be taken with regard to purification of EVs. Are the FOXM1-DNAs in the EVs functional in recipient cells? Is the DNA being actively ‘selected’ for an intercellular signalling purpose or is this just random degradation? Is it all FOXM1 bound DNA that has the potential to be trafficked to EVs or just a subset? Do other transcription factors have the same function or is it specific to this protein/family? Does this mechanism occur in other contexts (e.g., in vivo, under disease conditions).

    1. Review coordinated by Life Science Editors.

      Reviewed by: Dr. Angela Andersen, Life Science Editors

      Potential Conflicts of Interest: Dr. Mill has worked with Life Science Editors on other manuscripts.

      Background: Retinitis pigmentosa (RP) is a group of rare eye diseases that cause vision loss. Symptoms usually start in childhood, and most people eventually lose most of their sight. There is no cure for RP. Mutations in retinitis pigmentosa GTPase regulator (RPGR) cause RP and compromise the renewal of light-sensitive “disc” membranes (specialized cilia) at the outer segment of photoreceptors, resulting in the loss of these cells over time. Evidence suggests that disc formation is similar to the release of ectosomes (small extracellular vesicles) and that both rely on the actin cytoskeleton. Knockdown of RPGR in retinal pigmented epithelium cells showed stronger actin filaments and reduced cilia suggesting that it may regulate nascent photoreceptor disc formation by regulating actin-mediated membrane extension in the retina (Gakovic et al., Human Molecular Genetics, 2011). In addition, RPGR patient iPSC-retinal models displayed phenotypes consistent with abnormal actin regulation (Megaw et al., Nature Communications, 2017; Karam et al., J Personalized Medicine, 2022).

      Question: What function of RPGR is compromised in photoreceptors to cause RP?

      Advance: The authors generated novel Rpgr mutant mice harboring human disease-causing mutations that recapitulate human disease phenotypes: aborted membrane shedding as ectosome-like vesicles, photoreceptor death and visual loss. RPGR is located at the site of disc formation – to test if it plays a role in disc genesis, they engineered a novel reporter mouse to track outer segment turnover. Rhodopsin was tagged with the self-labelling peptide SNAP- Rhodopsin is the major protein component of outer segment discs, and so incubating RhodSNAP retinal slice cultures with SNAP fluorophores results in outer segment labelling. Perturbation of RPGR resulted in a slowed rate of disc formation, leading to shortened outer segments and increased vesicle shedding. To me, the breakthrough is in the last figure: the actin depolymerizing drug Cytochalasin D in PBS was injected intravitreally, and fixed retinas were analyzed 6 hours later by electron microscopy. Cytochalasin D treatment significantly reduced the number of shed vesicles from the base of the outer segment in Rpgr-mutant mice (they now look like wild-type).

      Significance: Nails down the disease-relevant function of RPGR and a molecular mechanism of RP in photoreceptor cells, in vivo, in mice. Pharmacological rescue not only demonstrates the importance of the mechanism to disease but also sheds light on a potential therapeutic avenue for RP.

  23. Jan 2023
  24. Dec 2022
    1. There are a number of ways in which a cell can move from one point in space to another.
      • Axoneme
      • Cell crawling via the remodelling of the actin cytoskeleton.
  25. Nov 2022
  26. Oct 2022
  27. Sep 2022
  28. Aug 2022
    1. Developmental cell death eliminates half of the neurons initially generated in the mammalian brain, and occurs perinatally in many species. It is possible that the timing of neuronal cell death is developmentally programmed, and only coincidentally associated with birth. Alternatively, birth may play a role in shaping cell death. To test these competing hypotheses, we experimentally advanced or delayed birth by 1 d in mice (within the normal range of gestation for the species) and examined effects on the temporal pattern and magnitude (amount) of neuronal cell death, using immunohistochemical detection of activated caspase-3 as a cell death marker. In order to detect effects of subtle changes in birth timing, we focused on brain areas that exhibit sharp postnatal peaks in cell death. We find that advancing birth advances peak cell death, supporting the hypothesis that birth triggers cell death. However, a delay of birth does not delay cell death. Thus, birth can advance cell death, but if postponed, a developmental program governs. Advancing or delaying birth also caused region-specific changes in the overall magnitude of cell death. Our findings shed light on the long-standing question of what controls the timing and magnitude of developmental neuronal cell death, and position birth as an orchestrator of brain development. Because humans across the world now routinely alter birth timing, these findings may have implications for current obstetric practices.
    1. This means that neurons in small children are prepared to commit suicide through apoptosis if they are not used. In the case of a crisis, such as lack of oxygen, the apoptosis program starts up and the cells die and disappear. Instead of being treated with adult drugs, newborn infants must be given treatment specifically designed for them, but research on newborn infants involves many special difficulties and unique infant medicines with low-frequency use are not interesting for pharmaceutical companies.
    1. Neuronal cell death occurs extensively during development and pathology, where it is especially important because of the limited capacity of adult neurons to proliferate or be replaced. The concept of cell death used to be simple as there were just two or three types, so we just had to work out which type was involved in our particular pathology and then block it. However, we now know that there are at least a dozen ways for neurons to die, that blocking a particular mechanism of cell death may not prevent the cell from dying, and that non-neuronal cells also contribute to neuronal death. We review here the mechanisms of neuronal death by intrinsic and extrinsic apoptosis, oncosis, necroptosis, parthanatos, ferroptosis, sarmoptosis, autophagic cell death, autosis, autolysis, paraptosis, pyroptosis, phagoptosis, and mitochondrial permeability transition. We next explore the mechanisms of neuronal death during development, and those induced by axotomy, aberrant cell-cycle reentry, glutamate (excitoxicity and oxytosis), loss of connected neurons, aggregated proteins and the unfolded protein response, oxidants, inflammation, and microglia. We then reassess which forms of cell death occur in stroke and Alzheimer’s disease, two of the most important pathologies involving neuronal cell death. We also discuss why it has been so difficult to pinpoint the type of neuronal death involved, if and why the mechanism of neuronal death matters, the molecular overlap and interplay between death subroutines, and the therapeutic implications of these multiple overlapping forms of neuronal death.
  29. Jun 2022
  30. May 2022
    1. What to Do About Teenage Cell Phone AddictionAddiction, Mental Health, Self Esteem, Treatment<img width="845" height="321" src="https://bnitreatment.com/wp-content/uploads/2021/09/teenage-cell-phone-addiction-845x321.jpg" class="wp-image-30300 avia-img-lazy-loading-not-30300 attachment-entry_with_sidebar size-entry_with_sidebar wp-post-image" alt="teenage cell phone addiction" /> Table of Contents Teenage cell phone addiction disrupts family time, social time, and study time.What is Teenage Cell Phone Addiction?What Are Signs of Teen Cell Phone Addiction SymptomsThe Impact of Teen Social Media Addiction on Mental HealthWhat Do You Do If Your Teenage Is Addicted to Their PhoneBNI Treatment Centers Helps Teens with Mental Health Disorders Teenage cell phone addiction disrupts family time, social time, and study time. For a teen, having a cell phone is like being a kid in a candy store. With app stores offering a never-ending array of options, it is easy to see how teens get addicted to their phones. By design, software companies have found ways to draw people into their digital products, including teens. Social media apps, and there are many, gobble up the most time among teens. Teens are on these social apps for several hours a day. Data show that teens spend about 3 hours a day on social media. An astounding 20% of teens are on these social platforms for more than 5 hours a day. On average, teens are on their phones about 7 hours per day. Smartphone addiction is very real. When teens use the apps, they will receive a dopamine hit that gets logged in the brain’s reward system. This leads to the teen spending ever more time on their phones, as the behavior gets continually reinforced. Keep reading to learn more about teen cell phone addiction and what can be done to curb the problem. What is Teenage Cell Phone Addiction? There is ample research showing how smartphone overuse, especially social media, impacts the brain. In fact, it can cause the same brain chemical responses as a drug. When a teen sees new likes, positive comments, or new followers on their feeds, they receive a burst of dopamine. Similar to a drug’s high, as social app use escalates, the more engagement they crave. The time spent engaging on social feeds will increase more and more as this reward cycle takes hold. The teen may put off other activities they once enjoyed in exchange for spending more time on their phones. Homework is not completed, which affects the teen’s grades. Sleep is forfeited, which impacts their health in many ways. In person social time is traded off for engaging with strangers on their social media feeds. All of these adverse effects caused by excess cell phone use can lead to mental health issues. Anxiety can result due to the time wasted on the phone. This causes stress because the teen now lacks time to complete their schoolwork or chores. Too much time online also results in depression, mainly because the teen begins to feel lonely. What Are Signs of Teen Cell Phone Addiction Symptoms As with other behavioral addictions, there will be certain signs the teen displays. Signs of a teenage cell phone addiction might include: Teen cannot carry on a live conversation. Teen is always scrolling and clicking around on their phone. Teen is not able to be without their phone, even for a few minutes. Teen shows signs of depression the more they are on their phone. Teen becomes obsessed with selfies and their social feels. Teen is having sleep problems. Teen’s grades drop, due to reduced time for studying or homework. Parents might want to think about having a digital time out, where all phones are shelved for a day or a weekend. Taking a break from the cell phones will do the whole family a lot of good. The Impact of Teen Social Media Addiction on Mental Health During the teen years, the brain is still under construction. The teen brain is more vulnerable to things that could lead to an addiction, like video games and social media. A recent study explains how the reward system in the teenage brain works. Call Our Parent Hotline (888) 522-1504 It shows the same type of dopamine release in response to social media likes as one might have to a drug. The study also points out that the teen will show “withdrawal” symptoms, like irritability and anxiety. This happens when they are not allowed to use their cell phone or social media. But anxiety and depression in themselves can be a result of too much cell phone use. Studies show that teens that spend large amounts of time on social platforms suffer from higher levels of mental health issues. This is due to the time spent on social apps, which can fuel low self-esteem, body dysmorphia, and bullying. Also, excess time on smartphones means a lack of in person contact with friends and family. Face-to-face time is traded off for huge amounts of time chatting online with strangers. These interactions are shallow and do not lead to any real human connection. Over time, this can result in feelings of loneliness and depression. What Do You Do If Your Teenage Is Addicted to Their Phone Parent Guidelines to Reduce Teenager Cell Phone Addiction Parents can help limit their teen’s cell phone use in several ways. It is likely a waste of time to forbid them to be on their phones, but you can set rules. Remind the teen that having a phone is a privilege, not a right, and that you are paying for it. Of course, guidelines for a 13 year-old will be different from that of a 17 year-old. Consider these tips for parents: Set limits on time for phone use. Set up screen-free periods during the day, with a place for the phone to be stored during that time. Tell the teen the phone will be shut off if their grades drop. Have your teen shut down their cell phone at a certain time each night. Keep communication open and bring up any concerns if you think they might be bullied on social media. Have clear consequences should the teen break your cell phone rules. Suggest your teen take breaks from their cell phone to enjoy an outdoor activity. Teach the teen about online predators. Limit the types of social media platforms they can use. Because social media isn’t going anywhere, it is best for parents to take the offense and partner with their teen to help them negotiate the challenges and emotional landmines together. Learning ways to reduce the chances for teenage cell phone addiction can help your teen avoid risks to mental health. BNI Treatment Centers Helps Teens with Mental Health Disorders BNI Treatment Centers provides the intensive treatment and support needed for teens with depression or anxiety disorders. Teens who struggle with mental health issues related to smartphone addiction are guided toward making better use of their time. For more details about our program, call BNI today at (888) 522-1504.

      Parent Guidelines to Reduce Teenager addicted to Cell Phone

      Parents can help limit their teen’s cell phone use in several ways. It is likely a waste of time to forbid them to be on their phones, but you can set rules.

    1. DICER1 syndrome is a rare genetic condition predisposing to hereditary cancer and caused by variants in the DICER1

      GeneName: DICER1 PMCID: PMC7859642 HGNCID: Unavailable Inheritance Pattern: Autosomal dominant. Disease Entity: Familial pleuropulmonary blastoma (PPB), cervix embryonal rhabdomyosarcoma, multinodular goiter, nasal chondromesenchymal hemartoma, Ciliary body medulloepithelioma, Sertoli-Leydig Cell Tumor (SLCT), differentiated thyroid carcinoma, pituitary blastoma, pineoblastoma, cystic nephroma, Wilm's tumor and sarcomas of different sites including, amongst others, the uterine cervix, kidney and brain. Mutation: Germline Zygosity: Heterozygose Variant: No ClinVarID present. Family Information: No family outline Case: No specified information of patients included. CasePresentingHPO's: n/a CasePrevious Testing: n/a gnomAD: n/a Mutation Type: nonsense, frameshift, or splice affected.

  31. Apr 2022
    1. DICER1 syndrome is a rare genetic condition predisposing to hereditary cancer and caused by variants in the DICER1 gene.

      Gene Name: DICER1 PMID:33552988 HGNCID: Unavailable Inheritance Pattern:Autosomal Dominant Disease Entity: familial pleuropulmonary blastoma (PPB),cystic nephroma, ovarian Sertoli-Leydig cell tumor (SLCT), multinodular goiter, cervix embryonal rhabdomyosarcoma, Wilms’ tumor, nasal chondromesenchymal hamartoma, ciliary body medulloepithelioma, differentiated thyroid carcinoma, pituitary blastoma, pineoblastoma, and sarcomas of different sites. Mutation: Nonsense, Frameshift<br /> Zygosity: Heterosygosity Variant:No ClinVar ID present Family Information:no diseases mentioned in family Case: no specified case in this article gnomAD: n/a Mutation type: Nonsense. frameshift

    1. Payne, R. P., Longet, S., Austin, J. A., Skelly, D. T., Dejnirattisai, W., Adele, S., Meardon, N., Faustini, S., Al-Taei, S., Moore, S. C., Tipton, T., Hering, L. M., Angyal, A., Brown, R., Nicols, A. R., Gillson, N., Dobson, S. L., Amini, A., Supasa, P., … Zawia, A. A. T. (2021). Immunogenicity of standard and extended dosing intervals of BNT162b2 mRNA vaccine. Cell, 184(23), 5699-5714.e11. https://doi.org/10.1016/j.cell.2021.10.011

    1. Edward Nirenberg 🇺🇦 [@ENirenberg]. (2021, November 30). This is also not limited to the vaccine- any infection we encounter will do the same thing. It’s how we evolved to get around a massive genetic and bioenergetic challenge and it’s brilliant and it’s happening all the time regardless of any vaccines we get. [Tweet]. Twitter. https://twitter.com/ENirenberg/status/1465698637434933254

  32. Mar 2022
    1. Eric Topol. (2022, February 28). A multimodal #AI study of ~54 million blood cells from Covid patients @YaleMedicine for predicting mortality risk highlights protective T cell role (not TH17), poor outcomes of granulocytes, monocytes, and has 83% accuracy https://nature.com/articles/s41587-021-01186-x @NatureBiotech @KrishnaswamyLab https://t.co/V32Kq0Q5ez [Tweet]. @EricTopol. https://twitter.com/EricTopol/status/1498373229097799680

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    1. start:使内容在单元格左侧对齐, center:使内容在单元格居中对齐, end:使内容在单元格右侧对齐,
    1. Townsend, L., Dyer, A. H., Naughton, A., Kiersey, R., Holden, D., Gardiner, M., Dowds, J., O’Brien, K., Bannan, C., Nadarajan, P., Dunne, J., Martin-Loeches, I., Fallon, P. G., Bergin, C., O’Farrelly, C., Cheallaigh, C. N., Bourke, N. M., & Conlon, N. (2021). Longitudinal Analysis of COVID-19 Patients Shows Age-Associated T Cell Changes Independent of Ongoing Ill-Health. Frontiers in Immunology, 12. https://www.frontiersin.org/article/10.3389/fimmu.2021.676932

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    1. Heitmann, J. S., Bilich, T., Tandler, C., Nelde, A., Maringer, Y., Marconato, M., Reusch, J., Jäger, S., Denk, M., Richter, M., Anton, L., Weber, L. M., Roerden, M., Bauer, J., Rieth, J., Wacker, M., Hörber, S., Peter, A., Meisner, C., … Walz, J. S. (2021). A COVID-19 peptide vaccine for the induction of SARS-CoV-2 T cell immunity. Nature, 1–9. https://doi.org/10.1038/s41586-021-04232-5

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  38. Sep 2021