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Nathan Goodyear

Adenoid cystic carcinoma: current therapy and potential therapeutic advances based on genomic profiling - 0 views

www.ncbi.nlm.nih.gov/...PMC4741919

adenoid cystic carcinoma

shared by Nathan Goodyear on 03 Oct 18 - No Cached
  • Cisplatin and 5-FU or CAP (cisplatin, doxorubicin, and cyclophosphamide) regimens can be used for combination chemotherapy
  • patients with advanced salivary gland malignancy treated with the CAP regimen achieved partial response (PR) or stable disease (SD) rates of 67% (8 out of 12 patients)
  • Agents commonly given as monotherapy for treating ACC are cisplatin, mitoxantrone, epirubicin, vinorelbine, paclitaxel, and gemcitabine. However, few of these agents have shown efficacy
  • ...23 more annotations...
  • single agent mitoxantrone or vinorelbine were recommended as reasonable choices
  • ACC is subdivided into 3 histological groups based on solid components of the tumor including cribriform, tubular, and solid
  • Cribriform and tubular ACCs usually exhibit a more indolent course, whereas the solid subtype is associated with worse prognosis
  • ACC consists of two different cell types: inner luminal epithelial cells and outer myoepithelial cells
  • epithelial cells express c-kit, cox-2 and Bcl-2
  • myoepithelial cells express EGFR and MYB
  • a balanced translocation of the v-myb avian myeloblastosis viral oncogene homolog-nuclear factor I/B (MYB-NFIB) is considered to be a signature molecular event of ACC oncogenesis
  • As a transcription factor, MYB is known to modulate multiple genetic downstream targets involved in oncogenesis, such as cox-2, c-kit, Bcl-2 and BclX
  • Various signaling cascades are essential for cancer cells to survive and grow. The PI3K/Akt/mTOR pathway is one of them
  • This pathway regulates cell survival and growth and is upregulated in many cancers
  • Mutations in genes associated with DNA repair are frequently found in familial cancer syndromes, such as hereditary breast-ovarian cancer syndrome (HBOC), hereditary non-polyposis colorectal cancer (HNPCC, also called Lynch syndrome) and Li-Fraumeni syndrome [30, 31]. These mutations were also reported in non-hereditary cancers
  • 70% of ACC samples (58 of 84) were found to have genetic alterations in the MYB/MYC pathway, indicating that changes in this pathway are crucial in ACC pathogenesis
  • The second most frequently mutated pathway was involved in chromatin remodeling (epigenetic modification), a pathway that includes multiple histone related proteins, and was altered in 44% of samples
  • C-kit
  • VEGF, iNOS and NF-κB were noted to be highly expressed in ACC cells as compared to normal salivary gland cells
  • members of the SOX family, such as SOX 4 and SOX10, are overexpressed in ACC
  • FABP7 (Fatty acid binding protein 7) and AQP1 (Aquaporin 1) tend to be overexpressed in ACC cell lines
  • considerable variability in HER2 overexpression ranging from 0–58% in patients with ACC
  • the study with cetuximab and concurrent chemoradiation or chemotherapy showed the highest ORR (total 43%, 9.5% CR and 33% PR), but this regimen was only given to the EGFR positive patients
  • Cancer immunotherapy can be classified into 3 major groups. Active immunization using anti-tumor vaccines to induce and recruit T cells, passive immunization based on monoclonal antibodies, and adoptive cell transfer to expand tumor-reactive autologous T cells ex vivo and then reintroduce these cells into the same individual
  • LAK cells showed cytotoxicity against ACC cells
  • cytokine-induced cell apoptosis and the cytotoxic effect of the LAK cells contributed to tumor regression
  • molecular finding of the MYB-NFIB fusion gene has the greatest potential to target what appears to be a fundamental event in disease pathogenesis
  • Nathan Goodyear on 03 Oct 18
     
    good review of adenoid cystic carcinoma
Nathan Goodyear

Inborn-like errors of metabolism are determinants of breast cancer risk, clinical response and survival: a study of human biochemical individuality - 0 views

www.ncbi.nlm.nih.gov/...PMC6114970

cancer metabolism breast cancer glutamine glutamate aspartate oncogenes

shared by Nathan Goodyear on 24 Sep 18 - No Cached
  • We now recognize that human cancers evolve in an environment of metabolic stress. Rapidly proliferating tumor cells deprived of adequate oxygen, nutrients, hormones and growth factors up-regulate pathways that address these deficiencies to overcome hypoxia (HIF), vascular insufficiency (VEGF), growth factor deprivation (EGFR, HER2) and the loss of hormonal support (ER, PR, AR) all to enhance survival and proliferation
  • RAS, PI3K, TP53 and MYC
  • The results suggest that breast cancer could be preceded by systemic subclinical disturbances in glucose-insulin homeostasis characterized by mild, likely asymptomatic, IEM-like biochemical changes
  • ...16 more annotations...
  • The process would include variable periods of hyperinsulinemia with the consequent systemic MYC activation of glycolysis, glutaminolysis, structural lipidogenesis and further exacerbation of hypoglycemia, the result of MYC's known role as an inhibitor of liver gluconeogenesis
  • The metabolic changes we describe in breast cancer arise in concert with IEM-like changes in oxidative phosphorylation as detected by increased values of the ratio lactate/pyruvate (Supplementary Table 2A, 2B) characteristic of Ox/Phos deficiency [25]. In our study, 76% (70/92) of the European breast cancer patients had lactate/pyruvate ratios values higher than the normal value of 25.8
  • four-fold higher frequency of cancer (including breast) in patients with energy metabolism disorders
  • growing recognition that cancer cells differ from their normal counterparts in their use of nutrients, synthesis of biomolecules and generation of energy
  • glutamine concentrations in the cancer patients were reduced to nearly 1/8 of the levels observed in the normal population
  • blood concentrations of aspartate (p = 1.7e-67, FDR = 8.3e-67) (Figure ​(Figure1E)1E) and glutamate (p = 6.4e-96, FDR = 6.2e-95) (Figure ​(Figure1F)1F) were nearly 10 fold higher than the normal ranges of 0–5 μM/L and 40 μM/L, respectively
  • glutamine consumption associated with parallel increases in glutamate and aspartate (Figure ​(Figure1A1A red arrows) is considered a hallmark of MYC-driven “glutaminolysis”
  • Gln/Glu ratio inversely correlates with i- late stage metabolic syndrome and with ii- increased chance of death
  • changes in glutamine consumption, reflected by the Gln/Glu ratio could provide a metabolic link between breast cancer initiation and diabetes, reflective of a systemic metabolic reprogramming from glucose to glutamine as the preferred source of precursors for biosynthetic reactions and cellular energy
  • lower Gln/Glu ratios inversely correlated with insulin resistance and the risk of diabetes
  • the metabolic dependencies of cancer characterized by excessive glycolysis, glutaminolysis and malignant lipidogenesis, previously considered a consequence of local tumor DNA aberration [23] could, instead, represent a systemic biochemical aberration that predates and very likely promotes tumorigenesis
  • these metabolic disturbances would be expected to remain extant after therapeutic interventions
  • accumulation of very long chain acylcarnitines such as C14:1-OH (p = 0.0, FDR = 0.0), C16 (p = 0.0, FDR = 0.0), C18 (p = 0.0, FDR = 0.0) and C18:1 (p = 1.73e-322, FDR = 1.16-321) and lipids containing VLCFA (lysoPC a C28:0) (p = 1.14-e95, FDR = 1.65e-95) in the blood of breast and colon cancer patients
  • Among the most powerful metabolic equations for MYC-activation is that which links the widely used MYC-driven desaturation marker ratio of SFA/MUFA to the MYC glutaminolysis-associated ratio of (Asp/Gln)
  • liver dysfunction shares many features with both IEM and cancer suggesting a role for hepatic dysfunction in carcinogenesis
  • cancer “conscripts” the human genome to meet its needs under conditions of systemic metabolic stress
  • Nathan Goodyear on 24 Sep 18
     
    Breast cancer is a metabolic disease.  Now, where have I heard that cancer is a metabolic disease?
Nathan Goodyear

Communication between genomic and non-genomic signaling events coordinate steroid hormone actions - 0 views

www.ncbi.nlm.nih.gov/...PMC5864526

genomic signaling cancer hormones non-genomic signaling

shared by Nathan Goodyear on 10 Apr 21 - No Cached
  • 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
  • ...25 more annotations...
  • 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
      Nathan Goodyear on 10 Apr 21
       
      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
Nathan Goodyear

Activity and expression of progesterone metabolizing 5α-reductase, 20α-hydroxysteroid oxidoreductase and 3α(β)-hydroxysteroid oxidoreductases in tumorigenic (MCF-7, MDA-MB-231, T-47D) and nontumorigenic (MCF-10A) human breast cancer cells - 0 views

www.ncbi.nlm.nih.gov/...PMC154104

progesterone metabolites breast cancer 5alpha-reductase 5-alpha pregnene 5-alpha pregnenes 4-pregnene 4-pregnenes

shared by Nathan Goodyear on 30 Jan 14 - No Cached
  • Exposure of human breast cell lines (MCF-7, MCF-10A, and ZR-75-1) to 5α-pregnanes results in changes associated with neoplasia, including increased proliferation and decreased attachment [1], depolymerization of F-actin [2] and decreases in adhesion plaque-associated vinculin
  • Exposure to 4-pregnenes results, in general, in opposite (anti-cancer-like) effects
  • 5αR1 has been detected in various androgen-independent organs, such as the liver and brain
  • ...10 more annotations...
  • 5αR2 has been found predominantly in androgen-dependent organs, such as epididymis and prostate
  • The 5α-pregnanes:4-pregnenes ratio was about 8-fold higher in tumorous than in nontumorous breast tissue after an 8-hour incubation with [14C]progesterone
  • Studies with breast cell lines, showing that 5α-pregnanes stimulate proliferation and decrease attachment of cells
  • both tissue and breast cell line studies suggest that an elevated level of progesterone 5α-reductase activity may be an indicator of breast tumorigenesis, regardless of presence or absence of ER and/or PR
  • 5αR1 is the main isoform expressed in human breast carcinomas [29] and that 5αR2 may not be associated with risk of breast cancer
  • the differences in 5α-pregnane production between the cells is due primarily to a difference in 5αR1 expression
  • As in the case of 5α-reductase activity, the presence or absence of ER and PR do not appear to be related to 5α-reductase expression.
  • the conversion of progesterone to the cancer promoting 5α-pregnanes is significantly higher in the human tumorigenic breast cell lines
  • lthough both 5αR1 and 5αR2 are expressed by these cells, the elevated 5α-reductase activity appears to be the result of significantly greater expression of 5αR1
  • Changes in progesterone metabolizing enzyme expression (resulting in enzyme activity changes) may be responsible for promoting breast cancer progression due to increased production of tumor-promoting 5α-pregnanes and decreased production of anti-cancer 20α – and 3α-4-pregnenes
  • Nathan Goodyear on 30 Jan 14
     
    balance of enzyme production between 5alpha-reductase and 20alpha-hydroxysteroid oxidoreductase and 3alpha(beta)-hydroxysteroid oxidoreductase play role in carcinogenesis and proliferation in the balance of production of progesterone metabolites. The 5alpha pregnenes are pro carcinogenic  and the 4-pregnenes are anti carcinogenic.
Nathan Goodyear

Relative Expression of Progesterone Receptors A and B in Endometrioid Cancers of the Endometrium - 0 views

cancerres.aacrjournals.org/...4576.long

progesterone receptor progesterone receptors A B PR-A PR-B endometrial cancer uterine progesterone receptor receptors

shared by Nathan Goodyear on 26 Nov 12 - No Cached
  • Nathan Goodyear on 26 Nov 12
     
    Balance of progesterone receptors A and B in the development of endometrial cancer.
Nathan Goodyear

Israeli Study Shows New Cannabis Treatment Kills Cancer Cells - 0 views

contenthub.gcintelligence.com/s-treatment-kills-cancer-cells

cancer medical cannabis chemotherapy

shared by Nathan Goodyear on 28 Nov 23 - No Cached
  • Nathan Goodyear on 28 Nov 23
     
    Just a PR, but worth a mention. I will track down this study if able
Nathan Goodyear

The dialectic role of progesterone. [Maturitas. 2009] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...19171445

progesterone metabolite metabolites. hormone hormones receptor PR-A PR-B

shared by Nathan Goodyear on 30 Jan 14 - No Cached
  • Nathan Goodyear on 30 Jan 14
     
    knowledge of progesterone and its metabolites are important in the use of hormones.  As the authors concluded here: "natural steroids should not be disparaged...an update on endocrinological knowledge and experience is rather mandatory for gynecologists".  There in lies the problem.  The IOM has shown that the average physician practices at a level of 17 years behind the current scientific knowledge and the environment created by medical governing bodies discourages questions, so as to protect the system.
Nathan Goodyear

Immunohistochemical Expression of Estrogen and Progesterone Receptors in Human Colorectal Adenoma and Carcinoma Using Specified Automated Cellular Image Analysis System: A Clinicopathological Study - 0 views

www.omjournal.org/fultext_PDF.aspx

estrogen progesterone receptors colon cancer

shared by Nathan Goodyear on 19 Nov 13 - No Cached
  • Nathan Goodyear on 19 Nov 13
     
    ER and PR are suggested to play role in colon cancer.  The question is do they play a role in carcinogenesis or does the expression of the receptors indicate something else i.e. attempt at differentiation through progesterone.  Also, what receptors are involver here: ER alpha or beta.  Likewise for the progesterone receptors
Nathan Goodyear

Membrane 5α-pregnane-3,20-dione (5αP) receptors in MCF-7 and MCF-10A breast cancer cells are up-regulated by estradiol and 5αP and down-regulated by the progesterone metabolites, 3α-dihydroprogesterone and 20α-dihydroprogesterone, with associated changes - 0 views

www.sciencedirect.com/...S0960076005003420

breast cancer progesterone metabolites progesterone metabolites hormone hormones

shared by Nathan Goodyear on 18 Jun 14 - No Cached
  • Nathan Goodyear on 18 Jun 14
     
    Very interesting study.  In ER/PR + breast cancer cells, Estradiol and 5alpha-dihydroprogestorone increase the membrane expression of 5alpha-dihydroprogesterone receptors.  This has a pro-growth, pro-metastatic potential.  In contrast, the metabolites 3alpha-dihdroprogesterone and 20alpha-HP inhibit the same membrane receptor expression thus giving an antigrowth, anti-metastatic potential.
Nathan Goodyear

The latest weapon against cancer is ... a keto diet? | Cold Spring Harbor Laboratory - 0 views

www.cshl.edu/-against-cancer-is-a-keto-diet

dexamethasone DEXA ketogenic ferroptosis ketogenic diet cachexia cancer corticosterone

shared by Nathan Goodyear on 31 Dec 23 - No Cached
  • Nathan Goodyear on 31 Dec 23
     
    PR piece for the publication.
Nathan Goodyear

Plasma prolactin and breast cancer risk: a meta- analysis | Scientific Reports - 0 views

www.nature.com/...srep25998

prolactin breast cancer cancer

shared by Nathan Goodyear on 19 Sep 18 - No Cached
  • Nathan Goodyear on 19 Sep 18
     
    prolactin associated wtih ER+/PR+
Nathan Goodyear

Ki-67 is a prognostic parameter in breast cancer patients: results of a large population-based cohort of a cancer registry - 0 views

www.ncbi.nlm.nih.gov/...PMC3669503

ki-67 cancer breast cancer

shared by Nathan Goodyear on 06 Sep 18 - No Cached
  • A wide range of techniques is available to assess tumor cell proliferation such as calculating mitotic figures in stained tissue segments, flow cytometric analysis to determine the proportion of cells being in the S phase of the cell cycle, examination of thymidine-labeling index, proliferating cell nuclear antigen (PCNA), or cyclins E and D
  • Ki-67 is a nuclear protein being associated with cellular proliferation and was originally identified by Gerdes et al.
  • Ki-67 nuclear antigen is expressed in certain phases of the cell cycle namely S, G1, G2, and M phases, but is nonexisting in G0
  • ...11 more annotations...
  • Ki-67 is also expressed at low levels (<3 % of cells) in ER-negative cells, but not in ER-positive cells
  • A meta-analysis involving 12,155 patients demonstrated that the Ki-67 positivity confers a higher risk of recurrence and a worse survival rate in patients with early breast cancer.
  • high levels of Ki-67 are associated with worse prognoses
  • Ki-67 was associated with worse survival rates
  • associated with proliferation
  • higher tumor stages and higher nodal status were associated with higher Ki-67 quartiles indicating that the more aggressive the tumor is the higher is the percentage of cells positively stained for Ki-67
  • Previous studies were able to demonstrate that a prognostic model, the IHC 4 score, using ER, PR, HER2, and Ki-67 provides similar prognostic information to that in the 21-gene Genomic Health recurrence score
  • ER status has been largely identified as being inversely correlated with Ki-67, with the higher rates of ER positivity shown in the lowest proliferating tumors
  • high levels of Ki-67 are associated with HER2/-neu positivity according to former studies
  • higher values of Ki-67-labeling index were associated with adverse prognostic factors
  • Ki-67-labeling index was associated with larger tumors, higher tumor grade, peritumoral vascular invasion, and HER-2 positivity
  • Nathan Goodyear on 06 Sep 18
     
     Increased disease free survival and overall survival in people with breast cancer with ki-67 <15%
indiacardiacsurg

Dr Rajiv Parakh India Evaluated Women Exhibit More Advanced Disease - 0 views

www.freeprnow.com/...-exhibit-more-advanced-disease

Dr Rajiv Parakh India best vascular surgeon in Medanta hospital Gurgaon Dr Rajiv Parakh vascular surgeon in Medanta

shared by indiacardiacsurg on 12 Oct 21 - No Cached
  • indiacardiacsurg on 12 Oct 21
     
    "It was interesting to see that females were less likely to present with a history of coronary disease," the best vascular surgeon in Medanta hospital Gurgaon said. "That is a finding that is counterintuitive because the vascular disease is in truth a systemic disorder; consequently any patient with PAD has a high probability of concomitant CAD. Email id- dr.rajivparakh@indiacardiacsurgerysite.com Call for Appointment- +91-9370586696
Nathan Goodyear

RU486 exerts antiestrogenic activities through a novel progesterone receptor A form-mediated mechanism. - 0 views

www.jbc.org/...11945.full.pdf+html

progesterone receptor progesterone receptor A PR-A estrogen receptor estrogen receptor progesterone

shared by Nathan Goodyear on 24 Nov 12 - No Cached
  • Nathan Goodyear on 24 Nov 12
     
    Progesterone receptor A inhibits estrogen receptors.
spineneuro

Disposable Spinal Rod Strain Sensor Earns High Kyphosis Surgery Success Rate - 0 views

www.briefingwire.com/...-kyphosis-surgery-success-rate

Kyphosis Kyphosis Treatment India Best Kyphosis Treatment Cost India Top 10 Kyphosis Specialists of India Kyphosis Surgery Success Rate Best of 5 hospitals for Kyphosis surgery India

shared by spineneuro on 16 Oct 21 - No Cached
  • spineneuro on 16 Oct 21
     
    Kyphosis, also known as hyperkyphosis, is a high curvature of the spine. As our backs have a natural curve to them of approximately 20 to 45 ranges, hyperkyphosis exists when the curve within the lower back is more than a 50-degree angle. Contact Us International Helpline Number : +91-9325887033 Email id: enquiry@spineandneurosurgeryhospitalindia.com
spineneuro

Dr. Vidyadhara S Provide A Better Way to Get Rid Of Severe Back Pain - 0 views

www.briefingwire.com/...to-get-rid-of-severe-back-pain

Best spine surgeon in Manipal hospital Dr. Vidyadhara S Manipal hospital

shared by spineneuro on 15 Aug 22 - No Cached
  • spineneuro on 15 Aug 22
     
    Dr. Vidyadhara S is the leading choice for spine care in India. Dr. Vidyadhara S has a patient satisfaction score of 96 and a patient recommendation score of 97 out of 100.
spineneuro

Top Surgeons for VBT Surgery Shows Success As Treatment for Scoliosis - 0 views

www.briefingwire.com/...ess-as-treatment-for-scoliosis

VBT surgery VBT surgery surgeons VBT surgery Hospitals VBT Surgery Cost

shared by spineneuro on 16 Feb 22 - No Cached
  • spineneuro on 16 Feb 22
     
    Top surgeons for VBT surgery and his team performed a retrospective review of 29 consecutive patients with 2-5 years follow-ups. Successful outcomes were described via a curve of much less than 30 degrees in patients who reached skeletal maturity and had not received a PSF. For More Info International Helpline Number : +91-9325887033 Email id: enquiry@spineandneurosurgeryhospitalindia.com
indiacardiacsurg

Dr Rajiv Parakh Talk about 3 Things You Can Do Today to Prevent Apoplexy - 0 views

www.briefingwire.com/...n-do-today-to-prevent-apoplexy

Dr. Rajiv Parakh Vascular Surgeon Medanta Gurugram Top Endovascular Surgeon

shared by indiacardiacsurg on 29 Mar 22 - No Cached
  • indiacardiacsurg on 29 Mar 22
     
    Vascular Surgeon in Medanta Gurugram explains "Living a sedentary way of life and consuming the wrong forms of meals puts people at a more risk of having apoplexy." The expert goes on to say that eating a healthy diet and getting sufficient workout routines are two of the most important things people can do to save apoplexy.
spineneuro

Leading the Way: Dr. Vipul Gupta's Pioneering Efforts in Interventional Neurology - 0 views

www.briefingwire.com/...ts-in-interventional-neurology

Dr. Vipul Gupta Top Interventional neurologist in Artemis Hospital Gurgaon

shared by spineneuro on 19 Apr 23 - No Cached
  • spineneuro on 19 Apr 23
     
    Dr. Vipul Gupta is a professional in each open cerebrovascular surgical treatment further to minimally invasive endovascular neurosurgery and is taken into consideration one of just a few neurosurgeons within the country with a dual-skilled in every specialty.
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