174 Matching Annotations
  1. Feb 2024
  2. Jan 2024
    1. for - healthy eating - Dr. William Li - nutrition - healthy food - inflammation - angiogenesis

      summary - A good interview about human health and healthy diet. William Li begins by talking about angiogenesis as a key aspect of human health - and how pathology of angiogenesis is at the root of many major diseases. - The interviewer then asks Dr. Li about the connection between another keystone disease, and angiogenesis. - Dr. Li then describes some healthy foods and good dietary practices including extra virgin olive oil.

      adjacency - between - angiogenesis - inflammation - Micheal Levine's work - evolutionary biology - adjacency statement - they all seem related, as evolutionary biology has created legacy subsystems within the human body

    2. if a tumor is kind of like a wound it can hijack blood vessels and you got inflammation and now the cancer itself causes some inflammation you're just making it a hell of a lot 00:28:49 easier for that tumor to get a blood supply which means that the cancer is more likely to grow

      for - adjacency - cancer - inflammation - angiogenesis

      adjacency - between - cancer - angiogenesis - inflammation - adjacency statement - if a tumor is kind of like a wound - it can hijack blood vessels - if you have some form of chronic inflammation - and cancer causes inflammation - it makes it easier to access blood supply - making cancer growth more likely

    3. what foods are able to do foods that inhibit angiogenesis

      for - adjacency - food - angiogenesis - cancer

    4. once an avascular or bloodless cancer 00:22:48 is able to get vessels to touch it that moment that touch is that the cancer can grow 16 000 times in two weeks

      for - avascular (bloodless) cancer - angiogenesis creates malignancy - stats - angiogenesis and avascular cancer

      stats - angiogenisis and avascular cancer - During research, the research lab that William Li worked in discovered that once blood vessesl touch a harmless avascular (bloodless) cancer - it transforms it into a deadly, malignant tumor that grows 16,000x in two weeks

    5. cancer without disease

      for - cancer without disease - microscopic cancer

      definition - cancer without disease

      • biologically we are actually all forming cancers in our body all the time
      • because all it takes for our 40 trillion cells to do is
      • to make those little mistakes
      • I told you 10 000 mistakes are fixed every day
      • A few of those sneaking through
      • will turn into a microscopic tumor microscopic cancer
      • and this is called cancer without disease
      • because as tiny little mutant cancer can grow up to the size of the tip of a ballpoint pen
      • and then it's frozen like a pimple can't go any bigger
      • because it doesn't have
        • a blood supply
        • no oxygen
        • no food
        • nothing to feed it and so
      • those little microscopic cancers sit there
      • until another one of our defense systems our immune system wings by like a cop on a beat and sees this abnormal cell sitting on that street corner in a good neighborhood and then says
        • "get in the car we're taking you away"
      • and so our immune system destroys these microscopic cancers
      • but some microscopic cancers are able to hijack our body's regular angiogenesis defense system
      • and selfishly grow blood vessels to feed themselves.
    1. Uncontrolledself-replication in these newer technologies runs a much greater risk: arisk of substantial damage in the physical world.

      As a case in point, the self-replication of misinformation on social media networks has become a substantial physical risk in the early 21st century causing not only swings in elections, but riots, take overs, swings in the stock market (GameStop short squeeze January 2021), and mob killings. It is incredibly difficult to create risk assessments for these sorts of future harms.

      In biology, we see major damage to a wide variety of species as the result of uncontrolled self-replication. We call it cancer.

      We also see programmed processes in biological settings including apoptosis and necrosis as means of avoiding major harms. What might these look like with respect to artificial intelligence?

  3. Dec 2023
    1. Will artificial intelligence create useless class of people? - Yuval Noah Harari

      1:00 "bring the latest findings of science of the public", otherwise the public space "gets filled with conspiracy theories and fake news and whatever".<br /> he fails to mention that ALL his beautiful "scientists" are financially dependent on corporations, who dictate the expected results, and who sabotage "unwanted research".<br /> for example, the pharma industry will NEVER pay money for research of natural cancer cures, or "alternative" covid cures like ivermectin / zinc / vitamin C, because these cures have no patent, so there is no profit motive, and also because the "militant pacifists" want to fix overpopulation this way.<br /> a "scientist" should be someone, who has all freedom to propose hypotheses, which then are tested in experiments (peer review), and compared to real placebo control groups. because that is science, or "the scientific method". everything else is lobbying for "shekel shekel".

  4. Nov 2023
    1. CANCER PREVENTION (prophylactic) – Those that have had genetic tests and know they’re really prone to getting cancer can take Fenbendazole prophylactically. Take one capsule (222 mg) 3 times a week, once a day after a fatty meal. Then no Fenbendazole for four days. Repeat for 10 weeks and then take 10 weeks off; Curcumin (600 mg) one capsule two times a day after breakfast and lunch; CBD oil (25mg) 1-2 drops under the tongue every day before sleep. Continue that regimen indefinitely.

      Fenbendazole cancer prophylaxis protocol.

    2. Inhibition of Glucose uptake in cancer cells. Malignant cells are known to have an enormous glucose uptake. That’s why I tell everybody that has cancer to immediately (a) get on a ketogenic diet, and (b) take High Dose Vitamin C. Note: Cancer cells consume glucose 200 times faster than ordinary cells. If you study cancer you know of the Warburg Effect. This is the aerobic glycolysis effect and it can be seen on PET scans. It’s pretty obvious. Fenbendazole limits cancer cell fueling with sugar by limiting this glucose uptake, decreasing the amount of what are called “glute transporters” (canals that take the glucose into cancer cells from the blood). An enzyme called hexokinase 2 is inhibited as well. This is very important. It helps those tumors to not divide rapidly and prevent sugar from getting in there.

      Sugar (glucose) is the primary fuel for cancer. Fenbendazole limits glucose uptake in cancer cells, limiting growth.

      Also a reason for adopting a ketogenic diet with high dose vitamin c.

    1. there's a microbe in the mouth called fusobacterium nucleotide it over proliferates it's okay to have normally but it over proliferates when 01:28:39 you have bleeding gums gingivitis or periodontitis where it then enters the bloodstream this is called translocation and colonize the colon and the evidence is very good it is a principal cause of 01:28:52 colon cancer colon cancer starts in the mouth incredibly and doesn't get there by swallowing gets her through the bloodstream translocation
      • for:holistic medicine - example - oral microbiome and colon cancer, oral microbiome - colon cancer, bleeding gums - colon cancer, gingivitus - colon cancer, periodontitis - colon cancer, bloodstream translocation, complexity - example - human body - colon cancer - oral microbiome

      • comment

        • colon cancer starts in the mouth!
      • references

        • Oral-Intestinal Microbiota in Colorectal Cancer: Inflammation and Immunosuppression (2022)

          • https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8824753/
          • Abstract
            • It is widely recognized that microbial disorders are involved in the pathogenesis of many malignant tumors.
            • The oral and intestinal tract are two of the overriding microbial habitats in the human body. Although they are anatomically and physiologically continuous, belonging to the openings at both ends of the digestive tract, the oral and intestinal microbiome do not cross talk with each other due to a variety of reasons, including
              • intestinal microbial colonization resistance and
              • chemical barriers in the upper digestive tract.
            • However, this balance can be upset in certain circumstances, such as
              • disruption of colonization resistance of gut microbes,
              • intestinal inflammation, and
              • disruption of the digestive tract chemical barrier.
            • Evidence is now accruing to suggest that the oral microbiome can colonize the gut, leading to dysregulation of the gut microbes.
            • Furthermore, the oral-gut microbes create an
              • intestinal inflammatory and
              • immunosuppressive microenvironment
            • conducive to
              • tumorigenesis and
              • progression of colorectal cancer (CRC).
            • Here, we review
              • the oral to intestinal microbial transmission and
              • the inflammatory and immunosuppressive microenvironment, induced by oral-gut axis microbes in the gut.
            • A superior comprehension of the contribution of the oral-intestinal microbes to CRC provides new insights into the prevention and treatment of CRC in the future.
        • Insights into oral microbiome and colorectal cancer – on the way of searching new perspectives (2023)

          • https://www.frontiersin.org/articles/10.3389/fcimb.2023.1159822/full
          • Abstract
            • Microbiome is a keystone polymicrobial community that coexist with human body in a beneficial relationship.
            • These microorganisms enable the human body to maintain homeostasis and take part in mechanisms of defense against infection and in the absorption of nutrients.
            • Even though microbiome is involved in physiologic processes that are beneficial to host health, it may also cause serious detrimental issues.
            • Additionally, it has been proven that bacteria can migrate to other human body compartments and colonize them even although significant structural differences with the area of origin exist.
            • Such migrations have been clearly observed when the causes of genesis and progression of colorectal cancer (CRC) have been investigated.
            • It has been demonstrated that the oral microbiome is capable of penetrating into the large intestine and cause impairments leading to dysbiosis and stimulation of cancerogenic processes.
            • The main actors of such events seem to be oral pathogenic bacteria belonging to the red and orange complex (regarding classification of bacteria in the context of periodontal diseases), such as
              • Porphyromonas gingivalis and
              • Fusobacterium nucleatum respectively,
            • which are characterized by significant amount of cancerogenic virulence factors.
            • Further examination of oral microbiome and its impact on CRC may be crucial on early detection of this disease and would allow its use as a precise non-invasive biomarker.
    1. this is a cancer uh approach that we work on which is to not to kill those cells but to force them to re reconnect to their neighbors and when they reconnect to the 00:31:24 neighbors they once again become part of the collective that's working on making nice skin nice muscle they stop being metastatic and they they go back
      • for: quote - Michael Levin, quote - MET of individuality, quote - memory wipe, quote - cancer therapy - MET of individuality

      • quote: Michael Levin

        • this is a cancer approach that we work on which is to not to kill those cells but to force them to re reconnect to their neighbors and when they reconnect to the neighbors they once again become part of the collective that's working on making nice skin nice muscle they stop being metastatic and they they go back
      • comment

        • Michael refers to cancer as a "memory wipe" where they have forgotten the normative programmed narrative of bodily / collective / multicellular unity
    2. when we work on cancer what you see is that when when 00:30:18 individual cells electrically disconnect from the rest of the body they their cognitive light cone shrinks they're back to their amoeba tiny little e gos and as far as they're concerned the rest of the body is just environment to them
      • for: MET of individuality - examples of breakdown - cancer

      • paraphrase

        • cancer is an example of when some part of the evolutionary program that coheres multicellularity into a cohesive whole goes faulty
          • then some subset of cells lose their coherence programming / story / narrative, the unity is lost and that cellular subset no longer identifies as part of the higher order collective individual, but return to a much more evolutionarily primitive state of pre-MET of individuality
        • this means that the MET individuality coherence program has weaknesses that can cause groups of cells to lose sight of the unifying logic and return to the primitive state
        • cancer demonstrates that these primitive programs still exist in all cells in our bodies and when the regulating coherence program is faulty, they can return to these more primitive states
  5. Sep 2023
    1. Defections from large-scale anatomical goals, such as those that occur due to an inappropriate reduction of gap junctional connectivity [74], present as cancer, cause reversions of cell behavior to ancient unicellular concerns which lead to metastasis and over-proliferation as the cells treat the rest of the body as external environment.
      • fresh perspective

        • cancer can be interpreted as a breakdown in the bodies multiscale competency architecture causing cancerous cells to lose their higher level synchronizing signals and revert to their more evolutionarily primitive forms as individuals that see the body as simply an external environment
      • adjacency between

        • gap junction coupling
        • cancer
        • healthy tissue coherence
        • multiscale competency architecture
      • adjacency statement
        • gap junction coupling appears to be an evolutionary means of cohering individuals together to form a larger group
        • hence, they seem to play a critical role in the continued evolution of more complex multicellular organisms
        • their pathologies within multicellular beings destroy multicellular structures and create disease, reverting the organism, or competent multicellular structures of the organism such as tissues and organs back to individualistic behavior, as in cancers
  6. Aug 2023
  7. Jun 2023
  8. May 2023
  9. Apr 2023
    1. 成人癌症通常是大腸癌、肝癌、肺癌等,這些發生在上皮組織的癌症(carcinoma),通常是經過長時間累積基因變異與細胞損壞才會發生;至於兒童癌症,主要是中胚層癌或胚胎型癌,例如腦瘤、軟組織瘤及骨癌等,不是經由體細胞基因變異累積,通常很早就發病。

      成人癌症:上皮組織 兒童癌症:胚胎型癌、中胚層癌

  10. Mar 2023
  11. Feb 2023
  12. Jan 2023
  13. Nov 2022
    1. phytoncides, antibacterial and antimicrobial substances that trees and other plants release into the air to help them fight diseases and harmful organisms. When humans breathe in these substances—typically by spending time in nature—their health can improve. Across several studies, phytoncides have been shown to boost immune function, increase anticancer protein production, reduce stress hormones, improve mood, and help people relax. 

      I always feel better during and after a forest walk.

  14. Aug 2022
  15. Jun 2022
  16. May 2022
    1. DICER1 syndrome encompasses a variety of benign and malignant manifestations including multinodular goitre

      Gene: DICER1 PMCID: PMC8451242 PMID: 34552563 Pathogenic Inheritance Pattern: Autosomal Dominant MultipleDiseaseEntities Disease Entity: DICER1 syndrome, multinodular goitre, cystic nephroma, anaplastic renal sarcoma, Wilms tumour, differentiated thyroid carcinoma, gynandroblastoma, ciliary body medulloepithelioma, embryonal rhabdomyosarcoma, pineoblastoma, pituitary blastoma, kidney cyst, pulmonary cyst, Sertoli-Leydig Cell Tumor. Mutation: Germline MultipleGeneVariants Variant & Clinvar IDs: c.3452_3453del (485534), c.316del (no ClinVar ID), c.171_172insAC (no ClinVar ID), c.3434del (no ClinVar ID), c.988C>T (933007), c.5388dup (no ClinVar ID) Zygosity: None provided. Case: At time of operation, the goitre patients living in Denmark were ages 21, 12, 21, 8, 14, and 16. Four underwent total thyroidectomies, and two underwent partial thyroidectomies. The patient originally aged 21 previously had a kidney cyst at age 14 and a pulmonary cyst at an unknown age. The patient aged 14 at time of partial thyroidectomy later manifested a Sertoli-Leydig Cell Tumor at age 15. All six patients were female. CasePresentingHPO: None provided. CasePreviousTesting: thyroidectomy gnomAD: ENSG00000100697.10, https://gnomad.broadinstitute.org/gene/ENSG00000100697 Mutation Type: Frameshift, Nonsense

    1. DICER1 syndrome is a rare genetic disorder that predisposes individuals to multiple cancer types.

      GeneName: DICER1 PMID: 29762508 HGNCID: N/A Inheritance Pattern: Autosomal dominant Disease Entity: Cancer Mutation: Germline Zygosity: Heterozygosity Variant: Unregistered Family Information: 12% of children with pleuropulmonary blastomas have cystic nephromas Case: 11 year old patient with Hodgkin lymphoma with DICER1 mutation in 2016.

    2. GeneName: DICER1 syndrome (pleuropulmonary blastoma familial tumor susceptibility syndrome), PMID (PubMed ID): 29762508, HGNCID: 17098, Inheritance pattern: autosomal-dominant disease, Disease entity: Plueropulomary Blastoma, Mutation: Somatic, Zygosity: heterozygous, Variant: multiple variants, Family information: NA, Case: young children, CasePresentingHPO: N/A, CasePreviousTesting: N/A, Gnomade #: N/A , Mutation type: deletion

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

      GeneName: DICER1 PMID: 33552988 HGNCID: Unavailable Inheritance Pattern: Autosomal Dominant with reduced penetrance Disease Entity: Cystic nephroma, familial pleuropulmonary blastoma (PPB), ovarian Sertoli-Leydig cell tumor (SLCT), cervix embryonal rhabdomyosarcoma, multinodular goiter, Wilms' Tumor, Ciliary body medulloepithelioma, nasal chondromesenchymal hamartoma, differentiated thyroid carcinoma, pituitary blastoma, pineoblastoma, sarcomas of different sites. Mutation: germline mutation Zygosity: heterozygous Variant: ClinVar ID not listed Family Information: No family cases listed Case: No specific case mentioned gnomAD: N/A Mutation Type: Frameshift, Nonsense mutation

  17. Apr 2022
    1. DICER1 syndrome is a rare genetic disorder that predisposes individuals to multiple cancer

      GeneName: DICER1 PMID: 29762508 HGNCID: Can't find Inheritance: Autosomal Dominant Disease Entities: Endocrine and Reproductive Tumors Mutation: Somatic and germline Zygosity: Heterozygous Mutant: Can't find Family: Can't find

    2. The DICER1 gene, located on chromosome 14, position q32.13, encodes the endoribonuclease Dicer protein of the ribonuclease III family

      GeneName: Dicer1 PMID (PubMedID): 29782508 HGNCID= Unavailable Inheritance Pattern: Autosomal Dominant Disease Entity: cancer, multinodular goiter, pleuropulmonary blastoma, cystic nephroma, and ovarian Sertoli-Leydig Cell Tumor Mutation: germline or somatic Zygosity: causes loss of heterozygosity Variant: unregistered Family: those that have the mutation almost always pass it on.

    3. DICER1 syndrome is a rare genetic disorder that predisposes individuals to multiple cancer types

      GeneName: DICER1 PMID (PubMed ID): 29762508 HGNCID: Unavailable Inheritance Pattern: Autosomal Dominant Disease Entity: cancer, rare genetic disorder, pleuroplumonary blastomas, cystic nephroma, rhabdomyosarcoma, multinodular goiter, thyroid cancer, overian Sertoli-Leydig cell tumors, and other meoplasias Mutations: Germline mutations or Somatic mutations Zygosity: Heterozygosity Variant: unregistered Family Information: Cystic nephromas has been reported in approximately 12% of children with pleuripulmonary blastomas or those with a family member with cystic nephroma. Patient with two DICER1 mutations and several of his family members shared these mutations. All members developed a least one type of tumor with differing origins. The patient was an 11-year old boy with a rare Hodgkin lymphoma with DICER1 in 2016. (c.5299delC and c.4616C>T).

    4. DICER1 syndrome is a rare genetic disorder that predisposes individuals to multiple cancer types.

      GeneName = DICER1 PMID = 29762508 HGNCID = Can't find Inheritance pattern = Autosomal dominant Disease entity = cancer, multinodular goiter, pleuropulmonary blastoma, cystic nephroma, ovarian Sertoli-Leydig cell tumor Mutation = germline OR somatic Zygosity = causes loss of heterozygosity Variant = unregistered Family = those with the mutation almost always passed it on

    1. The DICER1 syndrome is an autosomal dominant tumor‐predisposi-tion disorder associated with pleuropulmonary blastoma, a rare pediatric lung cancer

      GeneName:DICER1 PMID (PubMed ID): PMCID: PMC6418698 PMID: 30672147 HGNCID: NOT LISTED<br /> Inheritance Pattern: Autosomal Dominant Disease Entity: Cancer; benign and malignant tumors including pleuropulmonary blastoma, cystic nephroma, Sertoli-Leydig cell tumors, multinodular goiter, Thryoid cancer, rhabdomyosarcoma, and pineoblastoma. Mutation: Somatic missense variation Mutation type: missense Zygosity: None stated Variant: unregistered…. Family Information: Characterize germline variants in familial early-onset clorectal cancer patients; The observation of germline DICER1 variation with uterine corpus endometrial carcinoma merits additional investigation. CasePresentingHPOs: uterine and rectal cancers in germline mutation

    1. DICER1 syndrome is a cancer-predisposing disorder caused by pathogenic variants in the DICER1 gene

      Gene: DICER1 PMCID: PMC7859642 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: Germline Zygosity: Heterozygosity most common Variant: ClinVarID not available Family Information: No mention of disease within family Case: No case specified GnomAD: N/A Mutation Type: Nonsense or Frameshift

    1. ReconfigBehSci on Twitter: "RT @tylerblack32: Ghouls BEFORE COVID: 🤮🤮🤮🤮🤮🤮 ‘Only 0.2% of cancer deaths occur in children! <0.003% will die of cancer! Only about 0.16%…’ / Twitter. (n.d.). Retrieved 7 February 2022, from https://twitter.com/SciBeh/status/1490254426719899655

  18. Mar 2022
    1. Valter Longo, PhD has been studying an aspect of fasting and autophagy that is fascinating enough, I wanted to include it in it’s own section. One area of his research focuses on how fasting induces differential stress resistance to make chemotherapy far more effective. In a food scarce environment, normal cells become more resistant to oxidative stress, but cancer cells don’t. Remember, cancer cells are broken cells. Something went wrong with them and they are replicating out of control. Being broken means they don’t retain all the typical functions and protective mechanisms of normal cells, like antioxidant generation. That’s one of the reasons cancer cells switch their metabolism from oxidative phosphorylation to glycolysis even in the presence of oxygen. It’s known as the Warburg effect. There are many theories on why this happens, but one is because cancer cells are more sensitive to the reactive oxygen species created during normal metabolism. Eating creates an environment where cancer cells thrive and normal cells are stressed. Cancer cells need an environment rich with sugar, growth factors (like IGF-1) and amino acids like glutamine. For normal cells, metabolism creates reactive oxygen species and triggers an immune response to deal with all the pathogens riding along on top of your meals. However, when you fast, normal cells become 1000 times more resistant to reactive oxygen species, but cancer cells do not. This same starvation-protection also makes normal cells far more resistant to chemotherapy drugs.

      So fasting helps protect healthy cells and weakens cancerous ones. That's cool. But then it says cacer clles need sugar, growth factors like [[IGF-1]] and amino acids like glutamine. The [[Carnivore Diet]] is going to increse IGF-1 and amino acid levels but should starve the cancer cells of sugar. Given Dr Clemens' success treating cancer with the [[PKD]] protocol I'm inferring that it's the triad that needs to be inn place and if sugar is missing then the other factors being elevated eoesn't matter that much.

  19. Feb 2022
    1. People like to say to and about cancer patients: "How brave."  And "What a brave fight."  And he/she "fought cancer valiantly."   Holy mother of god.    There is no bravery.  There is only fear.  There is only pain. If we could escape this by retreating - all of us would.  Seriously, show me a coward's way out, and I will take it.   We are not brave.  We are struggling to survive. 
  20. Jan 2022
    1. Fernandez-Castaneda, A., Lu, P., Geraghty, A. C., Song, E., Lee, M.-H., Wood, J., Yalcin, B., Taylor, K. R., Dutton, S., Acosta-Alvarez, L., Ni, L., Contreras-Esquivel, D., Gehlhausen, J. R., Klein, J., Lucas, C., Mao, T., Silva, J., Pena-Hernandez, M., Tabachnikova, A., … Monje, M. (2022). Mild respiratory SARS-CoV-2 infection can cause multi-lineage cellular dysregulation and myelin loss in the brain (p. 2022.01.07.475453). https://doi.org/10.1101/2022.01.07.475453

  21. Dec 2021
    1. US28-mediated activation of MAPKs and of PLCβ was also shown to mediate activation of the cAMP response element binding protein (CREB) in HEK-293 cells and COS-7 cells transiently transfected with US28 [31,38], a transcription factor linked to a broad range of cellular processes, such as cell proliferation, differentiation, survival, angiogenesis, immune response, migration and invasion [83] (Figure 2). Although this has not been proven in the context of HCMV infection, in HEK-293 cells transiently transfected with US28, this activation of CREB by US28 has also been reported to stimulate the major immediate early gene promoter/enhancer (MIE) [84], thus playing a key role in the activation and replication of HCMV, but also in HCMV reactivation from latency

      CREB stimulates the major immediate early gene promoter/enhancer, and it plays a key role in the activation and replication of HCMV.

  22. Nov 2021
  23. Oct 2021
  24. Aug 2021
    1. When I began to understand that attitude doesn’t have anything to do with survival, I felt myself coming up out of deep water. I didn’t cause my cancer by having a bad attitude, and I wasn’t going to cure it by having a good one.And then Coscarelli told me the whole truth about cancer. If you’re ready, I will tell it to you.Cancer occurs when a group of cells divide in rapid and abnormal ways. Treatments are successful if they interfere with that process.That’s it, that’s the whole equation.Everyone with cancer has a different experience, and different beliefs about what will help. I feel strongly that these beliefs should be respected—including the feelings of those who decide not to have any treatment at all. It’s sadism to learn that someone is dangerously ill and to impose upon her your own set of unproven assumptions, especially ones that blame the patient for getting sick in the first place.

      Attitude doesn't have anything to do with healing Cancer.

    1. https://nooshu.com/blog/2021/05/12/weve-spotted-something-on-your-scan/

      The waiting and not knowing is one of the worst parts. Even reading updates into August is difficult. I was hoping that the surgery would have taken place already.

      Hoping the best for you and your family Matt.

  25. Jul 2021
  26. Jun 2021
    1. Luisa: I wanted Northwestern. I had my eye set on Northwestern. I don't know what it was about Northwestern that called to me, but I wanted Northwestern. That's what I wanted, and it wasn't unachievable. One of my friends got into Brown University and she had worse grades than I did, so I was like, "Northwestern's going to be easy. I got this." I wanted to be an oncologist—yes, an oncologist, cancer. I don't know why [Chuckles]. I don't know. Human tragedy, I wanted to save people. That's been my thing. I want to save people. I want to make people better. So [Pause] I killed myself in school. 4.6 GPA. I had all these extracurriculars.

      Time in the US, Higher Education, Dreaming About

    2. Thank God for Cook County Hospital [Chuckles]. They don't charge you a thing, but she got the medical treatment that she needed. She had brain surgery. They removed the tumor and she had to be in therapy for a few years in order to gain … she couldn't talk. She didn't have movement in half of her face, so she couldn't speak because her tongue was numb on one side, so she had to have physical therapy. I went with her a couple times because I had to translate. Sometimes they didn't have people who would translate for my mother. At this point, I had already learned English, but she had to practice every single day. Still to this day, there are a few words that she cannot say.

      Time in the US, Illness

    3. since my mom … my mom at the time, we did not know she had a tumor in the back of her brain. Right where her brain stem is, she had a huge tumor there and we had no idea. Nobody knew. She doesn't remember a lot of this. I don't know if it's because of the emotional trauma or because of the tumor, but once we got to Chicago, it was evident that something was wrong with my mother and she started going to the doctor.

      Time in the US, Illness

  27. May 2021
    1. I worked on a recent project to sketch out for a centre-right German think-tank how a European data commons might work. I tried to steer it away from property rights and towards what you’d get if you started with the commons and then worked back to what data could be harnessed, and to which collective purposes. This is eminently do-able, and pushes you towards two distinct areas; groups of people who are served poorly or not at all by current data regimes, and existing cooperatives, unions and mutual societies who could collect and process their members’ data to improve collective bargaining, or licence access to it to generate revenue and boost affiliate membership. Viewing personal data as a collective asset points towards all sorts of currently under-provided public goods (I briefly describe several, on p. 74 here – yes, oddly enough, this stuff got shoved into an annex).

      Apparently lots of reading to catch up on here.

      I definitely like the idea of starting with the commons and working backwards, not only with respect to data, but with respect to most natural resources. This should be the primary goal of governments and the goal should be to prevent private individuals and corporations from privatizing profits and socializing the losses.

      Think of an individual organism in analogy to a country or even personkind. What do we call a group of cells that grows without check and consumes all the resources? (A cancer). The organism needs each cell and group of cells to work together for the common good. We can't have a group of cis-gender white men aggregating all the power and resources for themselves at the cost of the rest otherwise they're just a cancer on humanity.

  28. Apr 2021
  29. Mar 2021
  30. Feb 2021
    1. Dr. Tara C. Smith. (2021, January 23). A reminder: Especially among the elderly, some individuals will die shortly after receipt of the vaccine. What we need to understand is the background rate of such deaths. Are they higher then in the vaccinated population? We didn’t see that in the trials. Some data from @RtAVM. https://t.co/LJe9k1WJQC [Tweet]. @aetiology. https://twitter.com/aetiology/status/1352810672359428097

  31. Nov 2020
    1. Tumor suppressor genes

      These are genes that slow down cell division, repair DNA errors, and/or tell cells to terminate. If these Tumor Suppressor Genes fail to function properly, they go rouge and become cancer cells.

  32. Oct 2020
    1. How this phenomenon translates into absolute, rather than relative, risk, however, is a bit thorny. A large study published in 2018, for instance, found that among women who had children between 34 and 47, 2.2 percent developed breast cancer within three to seven years after they gave birth (among women who never had children, the rate was 1.9 percent). Over all, according to the American Cancer Society, women between 40 and 49 have a 1.5 percent chance of developing breast cancer.

      The rates here are so low as to be nearly negligible on their face. Why bother reporting it?