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mothertobehyd

Mothertobe - Best Fertility Specialist In Hyderabad - 0 views

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    Mothertobe fertility clinic is one of the award-winning and top ranked fertility centre in Hyderabad. Find high quality and best fertility specialist in Hyderabad get quick Infertility treatment with higher success rate.
harshitatyagi

Is it moral/ethical to use assisted reproductive technologies (ART) such as in-vitro fe... - 0 views

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    Yes, it is completely fine to opt In-vitro fertilization when suffering from infertility, It is the most popular method accepted all around the globe, and only due to this treatment method many couples have been able to become parents.
harshitatyagi

What are some infertility treatments in Delhi, India? - 0 views

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    If you are struggling with infertility and have no idea what to do or how to resolve the biggest complications, then you need to take the essential step right now and acknowledge what the top infertility treatments as suggested by top fertility experts are: IVF, IUI & ICSI, for more details visit the link.
Nathan Goodyear

Vitamin D and assisted reproductive treatment outcome: a systematic review and meta-ana... - 0 views

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    New meta-analysis suggests vitamin D is key to fertility rates in ART.  At Seasons Wellness, we have long advocated vitamin D in fertility treatment.
harshitatyagi

Success chances with IVF after failed IUI` - 0 views

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    Being the popular form of ART, In-vitro fertilization is a treatment that stands out to combat the infertility challenges when all other treatments fail.
harshitatyagi

Hysteroscopy and Its Role in IVF - 0 views

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    Hysteroscopy is a less-invasive diagnostic procedure in fertility treatments like in vitro fertilization (IVF). The process involves inserting a small, lighted telescope known as a hysteroscope through the vagina and cervix and into the uterus. Lets explore the role of hysteroscopy in IVF, benefits, Risks, procedure etc.
Nathan Goodyear

Exogenous testosterone: a preventable cause of male infertility - Crosnoe - Translation... - 0 views

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    very nice case review and discussion of the treatment of low T and low sperm count in men desiring preservation of fertility.  Clomid and HCG are viable options to increase endogenous Testosterone production, though both work via different mechanisms.
harshitatyagi

How To Tell If You Have Hyperspermia or Hypospermia - 0 views

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    Hyperspermia & Hypospermia are two conditions that are lesser-known but may impact quantity of men's sperm and hence ability to conceive a child. Both conditions have different symptoms, causes, & treatments but share the same outcome, i.e., fertility complications.
harshitatyagi

Penile Yeast Infection in Men, Causes, Symptoms and Treatment - 0 views

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    Penile Yeast infections in men are generally not known due to their lack of awareness. This severe illness can cause a range of infections that will affect hygiene and the fertility rate. And due to increasing cases of infertility in men, it becomes significant to acknowledge cautious infections in men to combat the rising infertility cases.
harshitatyagi

What Is Secondary Infertility? Causes and Effects - 0 views

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    Secondary infertility is the inability to conceive or complete a pregnancy after a previous birth. To be classified as secondary infertility, a previous birth must have occurred without the help of drugs or fertility treatments such as IVF. If you've been trying to get pregnant for a while without success, you may be wondering if something is wrong. Is secondary infertility possible? To know the common sign of Secondary Infertility click on the link.
Nathan Goodyear

Cancer cells metabolically "fertilize" the tumor microenvironment with hydrogen peroxid... - 0 views

  • reducing oxidative stress with powerful antioxidants, is an important strategy for cancer prevention, as it would suppress one of the key early initiating steps where DNA damage and tumor-stroma metabolic-coupling begins. This would prevent cancer cells from acting as metabolic “parasites
  • Oxidative stress in cancer-associated fibroblasts triggers autophagy and mitophagy, resulting in compartmentalized cellular catabolism, loss of mitochondrial function, and the onset of aerobic glycolysis, in the tumor stroma. As such, cancer-associated fibroblasts produce high-energy nutrients (such as lactate and ketones) that fuel mitochondrial biogenesis and oxidative metabolism in cancer cells. We have termed this new energy-transfer mechanism the “reverse Warburg effect.
  • Then, oxidative stress, in cancer-associated fibroblasts, triggers the activation of two main transcription factors, NFκB and HIF-1α, leading to the onset of inflammation, autophagy, mitophagy and aerobic glycolysis in the tumor microenvironment
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  • oxidative stress and ROS, produced in cancer-associated fibroblasts, has a “bystander effect” on adjacent cancer cells, leading to DNA damage, genomic instability and aneuploidy, which appears to be driving tumor-stroma co-evolution
  • tumor cells produce and secrete hydrogen peroxide, thereby “fertilizing” the tumor microenvironment and driving the “reverse Warburg effect.”
  • This type of stromal metabolism then produces high-energy nutrients (lactate, ketones and glutamine), as well as recycled chemical building blocks (nucleotides, amino acids, fatty acids), to literally “feed” cancer cells
  • loss of stromal caveolin (Cav-1) is sufficient to drive mitochondrial dysfunction with increased glucose uptake in fibroblasts, mimicking the glycolytic phenotype of cancer-associated fibroblasts.
  • oxidative stress initiated in tumor cells is transferred to cancer-associated fibroblasts.
  • Then, cancer-associated fibroblasts show quantitative reductions in mitochondrial activity and compensatory increases in glucose uptake, as well as high ROS production
  • These findings may explain the prognostic value of a loss of stromal Cav-1 as a marker of a “lethal” tumor microenvironment
  • aerobic glycolysis takes place in cancer-associated fibroblasts, rather than in tumor cells, as previously suspected.
  • our results may also explain the “field effect” in cancer biology,5 as hydrogen peroxide secreted by cancer cells, and the propagation of ROS production, from cancer cells to fibroblasts, would create an increasing “mutagenic field” of ROS production, due to the resulting DNA damage
  • Interruption of this process, by addition of catalase (an enzyme that detoxifies hydrogen peroxide) to the tissue culture media, blocks ROS activity in cancer cells and leads to apoptotic cell death in cancer cells
  • In this new paradigm, cancer cells induce oxidative stress in neighboring cancer-associated fibroblasts
  • cancer-associated fibroblasts have the largest increases in glucose uptake
  • cancer cells secrete hydrogen peroxide, which induces ROS production in cancer-associated fibroblasts
  • Then, oxidative stress in cancer-associated fibroblast leads to decreases in functional mitochondrial activity, and a corresponding increase in glucose uptake, to fuel aerobic glycolysis
  • cancer cells show significant increases in mitochondrial activity, and decreases in glucose uptake
  • fibroblasts and cancer cells in co-culture become metabolically coupled, resulting in the development of a “symbiotic” or “parasitic” relationship.
  • cancer-associated fibroblasts undergo aerobic glycolysis (producing lactate), while cancer cells use oxidative mitochondrial metabolism.
  • We have previously shown that oxidative stress in cancer-associated fibroblasts drives a loss of stromal Cav-1, due to its destruction via autophagy/lysosomal degradation
  • a loss of stromal Cav-1 is sufficient to induce further oxidative stress, DNA damage and autophagy, essentially mimicking pseudo-hypoxia and driving mitochondrial dysfunction
  • loss of stromal Cav-1 is a powerful biomarker for identifying breast cancer patients with early tumor recurrence, lymph-node metastasis, drug-resistance and poor clinical outcome
  • this type of metabolism (aerobic glycolysis and autophagy in the tumor stroma) is characteristic of a lethal tumor micro-environment, as it fuels anabolic growth in cancer cells, via the production of high-energy nutrients (such as lactate, ketones and glutamine) and other chemical building blocks
  • the upstream tumor-initiating event appears to be the secretion of hydrogen peroxide
  • one such enzymatically-active protein anti-oxidant that may be of therapeutic use is catalase, as it detoxifies hydrogen peroxide to water
  • numerous studies show that “catalase therapy” in pre-clinical animal models is indeed sufficient to almost completely block tumor recurrence and metastasis
  • by eliminating oxidative stress in cancer cells and the tumor microenvironment,55 we may be able to effectively cut off the tumor's fuel supply, by blocking stromal autophagy and aerobic glycolysis
  • breast cancer patients show systemic evidence of increased oxidative stress and a decreased anti-oxidant defense, which increases with aging and tumor progression.68–70 Chemotherapy and radiation therapy then promote further oxidative stress.69 Unfortunately, “sub-lethal” doses of oxidative stress during cancer therapy may contribute to tumor recurrence and metastasis, via the activation of myofibroblasts.
  • a loss of stromal Cav-1 is associated with the increased expression of gene profiles associated with normal aging, oxidative stress, DNA damage, HIF1/hypoxia, NFκB/inflammation, glycolysis and mitochondrial dysfunction
  • cancer-associated fibroblasts show the largest increases in glucose uptake, while cancer cells show corresponding decreases in glucose uptake, under identical co-culture conditions
  • Thus, increased PET glucose avidity may actually be a surrogate marker for a loss of stromal Cav-1 in human tumors, allowing the rapid detection of a lethal tumor microenvironment.
  • it appears that astrocytes are actually the cell type responsible for the glucose avidity.
  • In the brain, astrocytes are glycolytic and undergo aerobic glycolysis. Thus, astrocytes take up and metabolically process glucose to lactate.7
  • Then, lactate is secreted via a mono-carboxylate transporter, namely MCT4. As a consequence, neurons use lactate as their preferred energy substrate
  • both astrocytes and cancer-associated fibroblasts express MCT4 (which extrudes lactate) and MCT4 is upregulated by oxidative stress in stromal fibroblasts.34
  • In accordance with the idea that cancer-associated fibroblasts take up the bulk of glucose, PET glucose avidity is also now routinely used to measure the extent of fibrosis in a number of human diseases, including interstitial pulmonary fibrosis, postsurgical scars, keloids, arthritis and a variety of collagen-vascular diseases.
  • PET glucose avidity and elevated serum inflammatory markers both correlate with poor prognosis in breast cancers.
  • PET signal over-estimates the actual anatomical size of the tumor, consistent with the idea that PET glucose avidity is really measuring fibrosis and inflammation in the tumor microenvironment.
  • human breast and lung cancer patients can be positively identified by examining their exhaled breath for the presence of hydrogen peroxide.
  • tumor cell production of hydrogen peroxide drives NFκB-activation in adjacent normal cells in culture6 and during metastasis,103 directly implicating the use of antioxidants, NFκB-inhibitors and anti-inflammatory agents, in the treatment of aggressive human cancers.
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    Good description of the communication between cancer cells and fibroblasts.  This theory is termed the "reverse Warburg effect".
harshitatyagi

How Infertility Affects Mental Health - 0 views

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    Couples experiencing infertility also deal with mental health related stress while trying to conceive. If you or your partner is experiencing any mental health related issue in your pregnancy journey, top fertility experts can help
harshitatyagi

What is the Procedure of IVF with Donor Embryos... - 0 views

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    The embryo is the combined form of a matured egg and sperm. It is generally known as the most critical stage of IVF treatment. Despite that, successful embryo implantation only decides the achievement of pregnancy, and when it fails, it obstructs the entire IVF process. It extensively occurs when a couple fails to develop a healthy embryo using their eggs and sperm because of poor health conditions.
Nathan Goodyear

A randomized, controlled trial comparing the efficacy and safety of aqueous subcutaneou... - 0 views

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    Bioidentical progesterone used in IVF.  This is not new, the SQ administration is.  So, physicians cry against BHRT, yet bioidentical progesterone has been used for years in the treatment of infertility.
harshitatyagi

When should IVF be done? - 0 views

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    The most generic question that interrupts every couple's mind is when the IVF process should be done. Is it done when one fails to conceive, or is it done when one suffers from secondary infertility.
Nathan Goodyear

The preconception Mediterranean dietary pattern in couples undergoing in vitro fertiliz... - 0 views

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    mediterranean diet improves conception rates in couples undergoing IVF/ICSI.
trungtamnamkhoa

Penis enlargement due to where? Cause And Treatment - 1 views

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    The body of the white pimples is a common feature of boys entering puberty. Understanding their nature will help you no longer worry. White pimples on the penis and pores, squeezing out with a white core. Do these acne affect fertility? This top concern in many young people will be answered right after.
Nathan Goodyear

Thyroid hormone treatment among pregnant women with subclinical hypothyroidism: US nati... - 0 views

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    Thyroid therapy in women with subclinical hypothyroidism found to have improved pregnancy rates (lower pregnancy loss).
Nathan Goodyear

Communication between genomic and non-genomic signaling events coordinate steroid hormo... - 0 views

  • steroid hormones typically interact with their cognate receptor in the cytoplasm for AR, glucocorticoid receptor (GR) and PR, but may also bind receptor in the nucleus as appears to often be the case for ERα and ERβ
  • This ligand binding results in a conformational change in the cytoplasmic NRs that leads to the dissociation of HSPs, translocation of the ligand-bound receptor to the nucleus
  • In the nucleus, the ligand-bound receptor dimerizes and then binds to DNA at specific HREs to regulate gene transcription
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  • some steroid hormone-induced nuclear events can occur in minutes
  • the genomic effects of steroid hormones take longer, with changes in gene expression occurring on the timescale of hours
  • Classical steroid hormone signaling occurs when hormone binds nuclear receptors (NR) in the cytoplasm, setting off a chain of genomic events that results in, among other changes, dimerization and translocation to the nucleus where the ligand-bound receptor forms a complex with coregulators to modulate gene transcription through direct interactions with a hormone response element (HRE)
  • NRs have been found at the plasma membrane of cells, where they can propagate signal transduction often through kinase pathways
  • Membrane-localized ER, PR and AR have been reported to modulate the activity of MAPK/ERK, phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt), nitric oxide (NO), PKC, calcium flux and increase inositol triphosphate (IP3) levels to promote cell processes including autophagy, proliferation, apoptosis, survival, differentiation, and vasodilation
  • ERα36, a 36kDa truncated form of ERα that lacks the transcriptional activation domains of the full-length protein. Membrane-localized ERα36 can activate pathways including protein kinase C (PKC) and/or mitogen activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) to promote the progression of various cancers
  • G protein-coupled receptor 30 (GPR30), also referred to as G protein-coupled estrogen receptor (GPER), is a membrane-localized receptor that has been observed to respond to estrogen to activate rapid signaling
  • hormone-responsive G protein coupled receptor is Zip9, which androgens can activate
  • GPRC6A is another G protein-coupled membrane receptor that is responsive to androgen
  • androgen-mediated non-genomic signaling through this GPCR can modulate male fertility, hormone secretion and prostate cancer progression
  • non-NR proteins located at the cell surface can bind to steroid hormones and respond by eliciting rapid signaling events
  • Estrogens have been shown to induce rapid (i.e. seconds) calcium flux via membrane-localized ER (mER)
  • ER-calcium dynamics lead to activation of kinase pathways such as MAPK/ERK which can result in cellular effects like migration and proliferation
  • 17β-estradiol (E2) has been reported to promote angiogenesis through the activation of GPER
  • Membrane NRs may also mediate rapid signaling through crosstalk with growth factor receptors (GFR)
  • A similar crosstalk occurs between the receptor tyrosine kinase insulin-related growth factor-1 receptor (IGF-IR) and ERα. Not only does IGF-IR activate ERα, but inhibition of IGF-IR downregulates estrogen-mediated ERα activity, suggesting that IGF-IR is essential for maximal ERα signaling
    • Nathan Goodyear
       
      This is a bombshell that shatters the current right brain approach to ER. It completely shatters the concept of eat sugar, whatever you want, with cancer treatment in ER+ or hormonally responsive cancer!
  • Further, ER activates IGF-IR pathways including MAPK
  • GPER is involved in the transactivation of the EGFR independent of classical ER
  • tight interconnection between genomic and non-genomic effects of NRs.
  • non-genomic pathways can also lead to genomic effects
  • androgen-bound AR associates with the kinase Src at the plasma membrane, activating Src which then leads to a signaling cascade through MAPK/ERK
  • However, Src can also increase the expression of AR target genes by the ligand-independent transactivation of AR
  • extranuclear steroid hormone actions can potentially reprogram nuclear NR events
  • estrogen modulated the expression of several genes including endothelial nitric oxide synthase (eNOS) via rapid signaling pathways
  • epigenetic changes can then mediate genomic events in uterine tissue and breast cancer cells
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