Showing posts with label medicine. Show all posts
Showing posts with label medicine. Show all posts

Tuesday, October 24, 2017

War on Health: Profits Before Patient Safety


Keep in mind, according to CDC statistics, no one has died from the use of food or dietary supplements, yet now, thanks to the FDA, you’ve got 3x as much regulation for food and dietary supplements as you have for pharmaceutical drugs, despite the fact that pharmaceutical drugs have proved to be one of the top killers of American citizens.

The relationship between physicians and the drug industry doesn’t begin once you have your MD or once you own your private practice; it begins the day you hit medical school. Big Pharma often give medical students gifts on their very first day. These gifts are always “Big Pharma” propaganda disguised as education, or something medical industry related that leaves the hard pressed medical student feeling like, at least someone cares, because we all know how tough medical school is.

But why is it so tough? Why are there intern boot camps?  Why must medical students and residents go through Why is "the private group that oversees physician training in the United States proposed rolling back rules so that young doctors just out of medical school can work shifts as long as 28 hours"? I mean, who wants an exhausted medical student/intern/resident practicing their craft on you when you are at your most vulnerable? Well one answer is that "medical school functions as a highly efficient system of inDOCtrination to ensure that physicians are less likely to question or confront the systems of power."
Professors who have already been indoctrinated to think a particular way ensure discussions are kept "on topic," or within the traditional bounds of acceptable debate that do not challenge power. I personally have lost track of the number of times I have heard a professor say, "That is interesting, but it is just outside of the scope of the discussion we are trying to have." This is a highly efficient and subtle way of controlling thought.

It makes more sense when you consider modern medicine was founded by a robber barons and an oil tycoon in particular, John D. Rockefeller. The conspiracy to limit and eliminate competition from non-drug therapies began with the Abraham Flexner Rockefeller Report on Medical Education of 1910. Abraham Flexner was engaged by John D. Rockefeller to  “evaluate” the effectiveness of therapies taught in medical schools and other institutions of the healing arts. The Flexner report unequivocally recommended the closure of all the homeopathic and naturopathic medical schools, in other words, anyone or any institution who use natural medicines to heal.

Subsequently, federal alphabet agencies--FDA, CDC, etc.-- were created to enforce the allopathic model under the guise of "protecting" the American food and drug supply.   In actuality, these agencies serve the medical industrial complex, not American citizens as you will see in the following documentaries.  The reason is obvious: alternative, mostly inexpensive non-toxic therapies represent a potential loss of billions, if not trillions of dollars to allopathic (drug) medicine and drug companies, not to mention, there is nothing more threatening to elite power than a healthy, robust public.







Links:

Overdosed America: The Broken Promise of American Medicine by John Abramson, M.D.

AIDS, Opium, Diamonds, and Empire: The Deadly Virus of International Greed. by Nancy Turner Banks, M.D.

Treaties and International Agreements


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Friday, April 14, 2017

Natural Cancer Bullets A - Z

There are many silver bullets that you can use to fight cancer. I will post some of these bullets (alphabetically) along with sources and brief explanations over the next several months.


Acai Berries


Source: Fruits from the Açaí Palm.

Brazilian berry destroys cancer cells in lab, UF study shows
Published today in the Journal of Agricultural and Food Chemistry, the study showed extracts from acai (ah-SAH’-ee) berries triggered a self-destruct response in up to 86 percent of leukemia cells tested, said Stephen Talcott, an assistant professor with UF’s Institute of Food and Agricultural Sciences. “Acai berries are already considered one of the richest fruit sources of antioxidants,” Talcott said. “This study was an important step toward learning what people may gain from using beverages, dietary supplements or other products made with the berries.”

Aloe-emodin

Sources: Aloe Vera Plant, Aloe Vera Juice



Aloe-Emodin Induces Apoptosis in T24 Human Bladder Cancer Cells

AE inhibited cell viability, and induced G2/M arrest and apoptosis in T24 cells. AE increased the levels of Wee1 and cdc25c, and may have led to inhibition of the levels of cyclin-dependent kinase 1 and cyclin B1, which cause G2/M arrest. AE induced p53 expression and was accompanied by the induction of p21 and caspase-3 activation, which was associated with apoptosis. In addition, AE was associated with a marked increase in Fas/APO1 receptor and Bax expression but it inhibited Bcl-2 expression.

Anticancer effect of aloe-emodin on cervical cancer cells involves G2/M arrest and induction of differentiation.
Aloe-emodin inhibited the growth of HeLa cells in a dose-dependent manner at concentrations ranging between 2.5 and 40 micromol/L. The flow cytometric analysis showed that HeLa cells were arrested at the G2/M phase. This effect was associated with the decrease in cyclin A and CDK2, and the increase in cyclin B1 and CDK1. More importantly, the ALP activity was found to be increased by aloe-emodin treatment, and accompanied by the inhibition of PCNA expression. In addition, aloe-emodin suppressed the expression of PKCalpha and c-myc.

Aloe-emodin suppresses prostate cancer by targeting the mTOR complex 2
Our results herein are noteworthy in that prostate cancer cell growth is suppressed by aloe-emodin in vivo. Moreover, the low in vivo toxicity and tumor inhibitory activity of aloe-emodin observed in nude mice suggest that aloe-emodin is an effective chemopreventive agent against prostate cancer (Figure 6A and B). In conclusion, we showed here that mTORC2 is closely associated with prostate cancer cell growth. We also provided clear evidence showing that aloe-emodin effectively suppresses anchorage-independent cell growth and in vivo tumor growth in PC3 cancer cell-bearing nude mice by inhibiting Akt activity. Collectively, these findings support the anticancer efficacy of aloe-emodin through its targeting of mTORC2 for the inhibition of prostate cancer progression.
Protein kinase C involvement in aloe-emodin- and emodin-induced apoptosis in lung carcinoma cell
This study demonstrated aloe-emodin- and emodin-induced apoptosis in lung carcinoma cell lines CH27 (human lung squamous carcinoma cell) and H460 (human lung non-small cell carcinoma cell). Aloe-emodin- and emodin-induced apoptosis was characterized by nuclear morphological changes and DNA fragmentation.

The antiproliferative activity of aloe-emodin is through p53-dependent and p21-dependent apoptotic pathway in human hepatoma cell lines

The aim of this study is to investigate the anticancer effect of aloe-emodin in two human liver cancer cell lines, Hep G2 and Hep 3B. We observed that aloe-emodin inhibited cell proliferation and induced apoptosis in both examined cell lines, but with different the antiproliferative mechanisms.
Aloe-emodin Is a New Type of Anticancer Agent with Selective Activity against Neuroectodermal Tumors
Here we report that aloe-emodin (AE), a hydroxyanthraquinone present in Aloe vera leaves, has a specific in vitro and in vivo antineuroectodermal tumor activity. The growth of human neuroectodermal tumors is inhibited in mice with severe combined immunodeficiency without any appreciable toxic effects on the animals. The compound does not inhibit the proliferation of normal fibroblasts nor that of hemopoietic progenitor cells. The cytotoxicity mechanism consists of the induction of apoptosis, whereas the selectivity against neuroectodermal tumor cells is founded on a specific energy-dependent pathway of drug incorporation. Taking into account its unique cytotoxicity profile and mode of action, AE might represent a conceptually new lead antitumor drug.
Aloe-emodin induced in vitro G2/M arrest of cell cycle in human promyelocytic leukemia HL-60 cells.
Aloe-emodin inhibited cell proliferation and induced G2/M arrest and apoptosis in HL-60 cells. Investigation of the levels of cyclins B1, E and A by immunoblot analysis showed that cyclin E level was unaffected, whereas cyclin B1 and A levels increased with aloe-emodin in HL-60 cells. Investigation of the levels of cyclin-dependent kinases, Cdk1 and 2, showed increased levels of Cdk1 but the levels of Cdk2 were not effected with aloe-emodin in HL-60 cells. The levels of p27 were increased after HL-60 cells were cotreated with various concentrations of aloe-emodin.
Aloe-emodin-induced apoptosis in human gastric carcinoma cells
The purpose of this study was to investigate the anticancer effect of aloe-emodin, an anthraquinone compound present in the leaves of Aloe vera, on two distinct human gastric carcinoma cell lines, AGS and NCI-N87. We demonstrate that aloe-emodin induced cell death in a dose- and time-dependent manner. Noteworthy is that the AGS cells were generally more sensitive than the NCI-N87 cells. Aloe-emodin caused the release of apoptosis-inducing factor and cytochrome c from mitochondria, followed by the activation of caspase-3, leading to nuclear shrinkage and apoptosis.

Aloe-emodin induces in vitro G2/M arrest and alkaline phosphatase activation in human oral cancer KB cells
Aloe-emodin is a natural anthraquinone compound from the root and rhizome of Rheum palmatum. In this study, KB cells were treated with 2.5, 5, 10, 20, and 40 microM aloe-emodin for 1 to 5 days. The results showed that aloe-emodin inhibited cancer cells in a dose-dependent manner. Treatment with aloe-emodin at 10 to 40 microM resulted in cell cycle arrest at G2/M phase. The alkaline phosphatase (ALP) activity in KB cells increased upon treatment with aloe-emodin when compared to controls. This is one of the first studies to focus on the expression of ALP in human oral carcinomas cells treated with aloe-emodin. These results indicate that aloe-emodin has anti-cancer effect on oral cancer, which may lead to its use in chemotherapy and chemo preventment of oral cancer.

Anandamide

Source: Cannabis


Anandamide May Fight Aggressive Skin Cancer
According to the study’s results, anandamide may be involved in a complex mechanism that includes the CB1 receptor, and possibly GPR55 – a cannabinoid receptor in its own right. Although not much is known about GPR55, it is sometimes referred to as the CB3 receptor, because it responds to both endogenous and plant-derived cannabinoids.
The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation
Anandamide was the first brain metabolite shown to act as a ligand of “central” CB1 cannabinoid receptors. Here we report that the endogenous cannabinoid potently and selectively inhibits the proliferation of human breast cancer cells in vitro. Anandamide dose-dependently inhibited the proliferation of MCF-7 and EFM-19 cells with IC50 values between 0.5 and 1.5 μM and 83–92% maximal inhibition at 5–10 μM. The proliferation of several other nonmammary tumoral cell lines was not affected by 10 μM anandamide. The anti-proliferative effect of anandamide was not due to toxicity or to apoptosis of cells but was accompanied by a reduction of cells in the S phase of the cell cycle. ...These data suggest that anandamide blocks human breast cancer cell proliferation through CB1-like receptor-mediated inhibition of endogenous prolactin action at the level of prolactin receptor.

Anti-proliferative and apoptotic effects of anandamide in human prostatic cancer cell lines
ANA induced a decrease of EGFR levels on LNCaP, DU145, and PC3 prostatic cancer cells by acting through cannabinoid CB1 receptor subtype and this leaded to an inhibition of the EGF-stimulated growth of these cells. Moreover, the G1 arrest of metastatic DU145 and PC3 growth was accompanied by a massive cell death by apoptosis and/or necrosis while LNCaP cells were less sensitive to cytotoxic effects of ANA. The apoptotic/necrotic responses induced by ANA on these prostatic cancer cells were also potentiated by the acidic ceramidase inhibitor, N-oleoylethanolamine and partially inhibited by the specific ceramide synthetase inhibitor, fumonisin B1 indicating that these cytotoxic actions of ANA might be induced via the cellular ceramide production. The potent anti-proliferative and cytotoxic effects of ANA on metastatic prostatic cancer cells might provide basis for the design of new therapeutic agents for effective treatment of recurrent and invasive prostatic cancers.
Cannabinoids, Endocannabinoids and Cancer
Cannabinoids exert a number of interesting effects that are dependent on the cell line or tumor type. Synthetic cannabinoids and the endocannabinoid system are implicated in inhibiting cancer cell proliferation and angiogenesis, reducing tumor growth and metastases, and inducing apoptosis.
Anandamide is an endogenous inhibitor for the migration of tumor cells and T lymphocytes
Cell migration is of paramount importance in physiological processes such as immune surveillance, but also in the pathological processes of tumor cell migration and metastasis development. The factors that regulate this tumor cell migration, most prominently neurotransmitters, have thus been the focus of intense investigation. While the majority of neurotransmitters have a stimulatory effect on cell migration, we herein report the inhibitory effect of the endogenous substance anandamide on both tumor cell and lymphocyte migration. ...Using the specific agonist docosatetraenoylethanolamide (DEA), we have observed that the norepinephrine-induced migration of colon carcinoma cells is inhibited by the CB1-R. The SDF-1–induced migration of CD8+ T lymphocytes was, however, inhibited via the CB2-R, as shown by using the specific agonist JWH 133. Therefore, specific inhibition of tumor cell migration via CB1-R engagement might be a selective tool to prevent metastasis formation without depreciatory effects on the immune system of cancer patients.
The endogenous cannabinoid, anandamide, induces cell death in colorectal carcinoma cells
These findings suggest anandamide may be a useful chemopreventive/therapeutic agent for colorectal cancer as it targets cells that are high expressors of COX-2, and may also be used in the eradication of tumour cells that have become resistant to apoptosis.

Apigenin

Sources: Parsley, Celery, Coriander, Licorice, Majoram, Oregano, Rosemary, Tarragon, Citrus, Tea and Wheat.


Breast cancer effectively treated with chemical found in celery, parsley, mouse study suggests
Apigenin, a natural substance found in grocery store produce aisles, shows promise as a non-toxic treatment for an aggressive form of human breast cancer, following a new study. Researchers found apigenin shrank a type of breast cancer tumor that is stimulated by progestin, a synthetic hormone given to women to ease symptoms related to menopause.
Apigenin induces apoptosis...in breast cancer cells
Apigenin is a low toxicity and non-mutagenic phytopolyphenol and protein kinase inhibitor. It exhibits anti-proliferating effects on human breast cancer cells. Here we examined several human breast cancer cell lines having different levels of HER2/neu expression and found that apigenin exhibited potent growth-inhibitory activity in HER2/neu-over expressing breast cancer cells but was much less effective for those cells expressing basal levels of HER2/neu
.
Selective growth-inhibitory, cell-cycle deregulatory and apoptotic response of apigenin in normal versus human prostate carcinoma cells
The growth-inhibitory and apoptotic potential of apigenin was also observed in a variety of prostate carcinoma cells representing different stage and androgen responsiveness. Apigenin may be developed as a promising chemopreventive and/or chemotherapeutic agent against prostate cancer.
Signal pathways involved in apigenin inhibition of growth and induction of apoptosis of human anaplastic thyroid cancer cells
Recently we demonstrated that several flavonoids can inhibit the proliferation of certain human thyroid cancer cell lines. Among the flavonoids tested, apigenin and luteolin are the most effective inhibitors of these tumor cell lines. In the present study, we investigated the signal transduction mechanism associated with the growth inhibitory effect of apigenin, using a human anaplastic thyroid carcinoma cell line, ARO.

5,6-Dichloro-ribifuranosylbenzimidazole- and apigenin-induced sensitization of colon cancer cells to TNF--mediated apoptosis

Here we report that inhibition of CK2 in HCT-116 and HT-29 cells with the use of two specific CK2 inhibitors, 5,6-dichloro-ribifuranosylbenzimidazole (DRB) and apigenin, effected a synergistic reduction in cell survival when used in conjunction with TNF-. Furthermore, there was a demonstrable synergistic reduction in colony formation in soft agar with the use of the same combinations.

Induction of apoptosis by apigenin in leukaemia HL-60 cells
The potency of these flavonoids on these features of apoptosis were in the order of: apigenin>quercetin>myricetin>kaempferol in HL-60 cells treated with 60μM flavonoids. These results suggest that flavonoid-induced apoptosis is stimulated by the release of cytochrome c to the cytosol, by procaspase-9 processing, and through a caspase-3-dependent mechanism. The induction of apoptosis by flavonoids may be attributed to their cancer chemopreventive activity. Furthermore, the potency of flavonoids for inducing apoptosis may be dependent on the numbers of hydroxyl groups in the 2-phenyl group and on the absence of the 3-hydroxyl group. This provides new information on the structure–activity relationship of flavonoids.
Arachidonyl Ethanolamide

Source: Cannabis


Arachidonyl ethanolamide induces apoptosis of uterine cervix cancer cells via aberrantly expressed vanilloid receptor-1
The major finding was that AEA induced apoptosis of CxCa cell lines via aberrantly expressed vanilloid receptor-1, whereas AEA binding to the classical CB1 and CB2 cannabinoid receptors mediated a protective effect. Furthermore, unexpectedly, a strong expression of the three forms of AEA receptors was observed in ex vivo CxCa biopsies.
Artemisinin

Sources: wormwood plant


Artemisinin Induces Apoptosis in Human Cancer Cells
Artemisinin is a chemical compound extracted from the wormwood plant, Artemisia annua L. It has been shown to selectively kill cancer cells in vitro and retard the growth of implanted fibrosarcoma tumors in rats. In the present research, we investigated its mechanism of cytotoxicity to cancer cells. ...This rapid induction of apoptosis in cancer cells after treatment with DHA indicates that artemisinin and its analogs may be inexpensive and effective cancer agents.
Effects of artemisinin and its derivatives on growth inhibition and apoptosis of oral cancer cells
Artemisinin is of special biological interest because of its outstanding antimalarial activity. Recently, it was reported that artemisinin has antitumor activity. Its derivatives, artesunate, arteether, and artemeter, also have antitumor activity against melanoma, breast, ovarian, prostate, CNS, and renal cancer cell lines. Recently, monomer, dimer, and trimer derivatives were synthesized from deoxoartemisinin, and the dimers and the trimers were found to have much more potent antitumor activity than the monomers. ...The deoxoartemisinin trimer was found to have greater antitumor effect on tumor cells than other commonly used chemotherapeutic drugs, such as 5-FU, cisplatin, and paclitaxel. Furthermore, the ability of artemisinin and its derivatives to induce apoptosis highlights their potential as chemotherapeutic agents, for many anticancer drugs achieve their antitumor effects by inducing apoptosis in tumor cells.
Transferrin overcomes drug resistance to artemisinin in human small-cell lung carcinoma cells
Multiple drug resistance is a significant problem in small-cell lung cancer (SCLC). Artemisinin (ART) is a natural product used to treat drug-resistant malaria. The drug is effective because the Fe2+ present in infected erythrocytes acts non-enzymatically to convert ART to toxic products. We tested the effects of ART on drug-sensitive (H69) and multi-drug-resistant (H69VP) SCLC cells, pretreated with transferrin (TF) to increase the intracellular Fe2+ level. ...These data indicate the potential use of ART and TF in drug-resistant SCLC.
Dihydroartemisinin induces apoptosis and sensitizes human ovarian cancer cells to carboplatin therapy
The present study was designed to determine the effects of artemisinin (ARS) and its derivatives on human ovarian cancer cells, to evaluate their potential as novel chemotherapeutic agents used alone or in combination with a conventional cancer chemotherapeutic agent, and to investigate their underlying mechanisms of action. Human ovarian cancer cells (A2780 and OVCAR-3), and immortalized non-tumourigenic human ovarian surface epithelial cells (IOSE144), were exposed to four ARS compounds for cytotoxicity testing. The in vitro and in vivo antitumour effects and possible underlying mechanisms of action of dihydroartemisinin (DHA), the most effective compound, were further determined in ovarian cancer cells. ...These effects were also observed in in vivo ovarian A2780 and OVCAR-3 xenograft tumour models. In conclusion, ARS derivatives, particularly DHA, exhibit significant anticancer activity against ovarian cancer cells in vitro and in vivo, with minimal toxicity to non-tumourigenic human OSE cells, indicating that they may be promising therapeutic agents for ovarian cancer, either used alone or in combination with conventional chemotherapy.

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Natural Cancer Bullets A - Z

Natural cancer bullets A - Z continued:


β-Elemene

Source: Ginger Root


Antitumor effect of β-elemene in non-small-cell lung cancer cells is mediated via induction of cell cycle arrest and apoptotic cell death
Beta-elemene is a novel anticancer drug, which was extracted from the ginger plant. However, the mechanism of action of beta-elemene in non-small-cell lung cancer (NSCLC) remains unknown. Here we show that beta-elemene had differential inhibitory effects on cell growth between NSCLC cell lines and lung fibroblast and bronchial epithelial cell lines. ...These data indicate that the effect of beta-elemene on lung cancer cell death may be through a mitochondrial release of the cytochrome c-mediated apoptotic pathway.

Elemene displays anti-cancer ability on laryngeal cancer cells in vitro and in vivo
Elemene inhibited the growth of HEp-2 cells in vitro in a dose- and time-dependent manner with an IC50 of 346.5 μM (24 h incubation). Increased apoptosis was observed in elemene-administered cells. Elemene is suspected to enhance caspase-3 activity, and thus inhibit protein expression of eIFs (4E, 4G), bFGF, and VEGF. In vivo, the growth of HEp-2 cell-transplanted tumors in nude mice was inhibited by intraperitoneal injection of elemene. Compared with control groups, elemene significantly inhibited the protein expression of eIFs (4E and 4G), bFGF, and VEGF and decreased the MVD. Conclusions: Elemene inhibits the growth of HEp-2 cells in vitro and in vivo. These data provide useful information for further clinical study on the treatment of LSCC by elemene.

Antiproliferative effect of β-elemene in chemoresistant ovarian carcinoma cells

In this study, we show that beta-elemene inhibited the proliferation of cisplatin-resistant human ovarian cancer cells and their parental cells, but had only a marginal effect in human ovary cells, indicating differential inhibitory effects on cell growth between ovarian cancer cells and normal ovary cells.
Effect of Local Arterial Infusion of β_elemene on Breast Cancer Tissue Inhibition and Cell Apoptosis and Proliferation
The effect of local arterial infusion of β_elemene on breast cancer tissue inhibition and cell apoptosis and proliferation was observed.
N-(beta-Elemene-13-yl)tryptophan methyl ester induces apoptosis in human leukemia cells
Beta-elemene is an active component of herb medicine Curcuma Wenyujin and N-(beta-elemene-13-yl)tryptophan methyl ester (ETME) was synthesized for increasing its antitumor activity. ETME induced apoptosis in human leukemia HL-60 and NB4 cells at concentrations less than 40 microM. The apoptosis induction ability of ETME was associated with the production of hydrogen peroxide (H(2)O(2)), the decrease of mitochondrial membrane potential, and the activation of caspase-3 that was blocked by catalase. ETME in combination with arsenic trioxide (As(2)O(3)), an agent used to treat acute promyelocytic leukemia, synergistically induced apoptosis in both cell lines by enhanced production of H(2)O(2). These data suggest that ETME induces apoptosis and synergizes with As(2)O(3) in leukemia cells through a H(2)O(2)-dependent pathway.

ß-Glucan

Foods: Mushrooms, Grains & Yeast.
Mushrooms: Shiitake (Lentinula edodes), Reishi (Ganoderma lucidum & Ganoderma tsugae), Maitake (Grifola frondosa), Oyster Mushroom (Pleurotus ostreatus), Cauliflower Mushroom (Sparassis). Grains: Oats, Barley.


Fights cancer and eases the effects of radiation.

NOTE: Literally all of the listed mushrooms above have other important anti-cancer effects not necessarily specified here


ß-Glucan...Uses Antibodies to Target Tumors for Cytotoxic Recognition by Leukocyte Complement Receptor Type 3

ß-Glucans were identified 36 years ago as a biologic response modifier that stimulated tumor rejection. In vitro studies have shown that ß-glucans bind to a lectin domain within complement receptor type 3 (CR3; known also as Mac-1, CD11b/CD18, or Mß2-integrin, that functions as an adhesion molecule and a receptor for factor I-cleaved C3b, i.e., iC3b) resulting in the priming of this iC3b receptor for cytotoxicity of iC3b-opsonized target cells. This investigation explored mechanisms of tumor therapy with soluble ß-glucan in mice. Normal mouse sera were shown to contain low levels of Abs reactive with syngeneic or allogeneic tumor lines that activated complement, depositing C3 onto tumors. Implanted tumors became coated with IgM, IgG, and C3, and the absent C3 deposition on tumors in SCID mice was reconstituted with IgM or IgG isolated from normal sera. Therapy of mice with glucan- or mannan-rich soluble polysaccharides exhibiting high affinity for CR3 caused a 57–90% reduction in tumor weight. In young mice with lower levels of tumor-reactive Abs, the effectiveness of ß-glucan was enhanced by administration of a tumor-specific mAb, and in SCID mice, an absent response to ß-glucan was reconstituted with normal IgM or IgG. The requirement for C3 on tumors and CR3 on leukocytes was highlighted by therapy failures in C3- or CR3-deficient mice. Thus, the tumoricidal function of CR3-binding polysaccharides such as ß-glucan in vivo is defined by natural and elicited Abs that direct iC3b deposition onto neoplastic cells, making them targets for circulating leukocytes bearing polysaccharide-primed CR3. Therapy fails when tumors lack iC3b, but can be restored by tumor-specific Abs that deposit iC3b onto the tumors.

Yeast ß-Glucan Amplifies Phagocyte Killing of iC3b-Opsonized Tumor Cells

Anti-tumor mAbs hold promise for cancer therapy, but are relatively inefficient. Therefore, there is a need for agents that might amplify the effectiveness of these mAbs. One such agent is -glucan, a polysaccharide produced by fungi, yeast, and grains, but not mammalian cells. -Glucans are bound by C receptor 3 (CR3) and, in concert with target-associated complement fragment iC3b, elicit phagocytosis and killing of yeast. -Glucans may also promote killing of iC3b-opsonized tumor cells engendered by administration of anti-tumor mAbs. In this study, we report that tumor-bearing mice treated with a combination of -glucan and an anti-tumor mAb show almost complete cessation of tumor growth.

Chemosensitization of Carmustine with Maitake β-Glucan on Androgen-Independent Prostatic Cancer Cells
This study demonstrates a sensitized cytotoxic effect of BCNU with β-glucan in PC-3 cells, which was associated with a drastic (~80%) inactivation of Gly-I. Therefore, the BCNU/β-glucan combination may help to improve current treatment efficacy by targeting Gly-I, which appears to be critically involved in prostate cancer viability.

Beta glucan induces proliferation and activation of monocytes in peripheral blood of patients with advanced breast cancer

Glucans are glucose polymers that constitute a structural part of fungal cell wall. They can stimulate the innate immunity by activation of monocytes/macrophages. In human studies it has been shown that beta glucan has an immunomodulatory effect and can increase the efficacy of the biological therapies in cancer patients. In this prospective clinical trial we assessed in vivo effects of short term oral beta glucan administration on peripheral blood monocytes and their expression of activation markers in patients with advanced breast cancer. ...Oral beta glucan administration seems to stimulate proliferation and activation of peripheral blood monocytes in vivo in patients with advanced breast cancer.

ß-Hydroxyisovalerylshikonin


Source: Lithospermum (herbs).


ß-Hydroxyisovalerylshikonin Inhibits the Cell Growth of Various Cancer Cell Lines and Induces Apoptosis in Leukemia HL–60 Cells
ß-Hydroxyisovalerylshikonin (ß-HIVS), which was isolated from the plant, Lithosper-mium radix, inhibited the growth of various lines of cancer cells derived from human solid, tumors at low concentrations between 10-8 and 10-6 M. When HL-60 cells were treated with 10-6 M ß-HIVS for 3 h, characteristic features of apoptosis, such as DNA fragmentation, nuclear fragmentation, and activation of caspase-3–like activity, were observed.

β-Hydroxyisovalerylshikonin and Cisplatin Act Synergistically to Inhibit Growth and to Induce Apoptosis of Human Lung Cancer DMS114 Cells

beta-Hydroxyisovalerylshikonin (beta-HIVS) and cisplatin (CDDP) had a synergistic growth-inhibitory effect on cultured human small-cell lung carcinoma DMS114 cells, as well as on human leukemia U937 and epidermoid carcinoma A431 cells, while beta-HIVS and CDDP alone at the same respective concentrations had little effect.

Betulin

Source: The bark of Red Alder trees & White Birch trees, and the mushroom Chaga that grows on White Birch.


Anti-Cancer Effect of Betulin on a Human Lung Cancer Cell Line
Betulin is a representative compound of Betula platyphylla, a tree species belonging to the Betulaceae family. In this investigation, we revealed that betulin showed anticancer activity on human lung cancer A549 cells by inducing apoptosis and changes in protein expression profiles were observed.

Betulinic Acid Inhibits Prostate Cancer Growth

Betulinic acid is a pentacyclic triterpene natural product initially identified as a melanoma-specific cytotoxic agent that exhibits low toxicity in animal models. Subsequent studies show that betulinic acid induces apoptosis and antiangiogenic responses in tumors derived from multiple tissues;
Betulinic acid induces apoptosis in human neuroblastoma cell lines
Neuroblastoma has long been recognized to show spontaneous regression during fetal development and in the majority of stage 4s infants
Apoptotic activity of betulinic acid derivatives on murine melanoma B16 cell line
Exposure of B16 cells to betulinic acid, 23-hydroxybetulinic acid and 3-oxo-23-hydroxybetulinic acid caused a rapid increase in reactive oxidative species production and a concomitant dissipation of mitochondrial membrane potential in a dose- and time-dependent manner, which resulted in cell apoptosis, as demonstrated by fluorescence microscopy, gel electrophoresis and flow-cytometric analysis. Cell cycle analysis further demonstrated that both 3-oxo-23-hydroxybetulinic acid and 23-hydroxybetulinic acid dramatically increased DNA fragmentation at the expense of G1 cells at doses as low as 12.5 and 25 microg/ml, respectively, thereby showing their potent apoptotic properties. Our results showed that hydroxylation at the C3 position of betulinic acid is likely to enhance the apoptotic activity of betulinic acid derivatives (23-hydroxybetulinic acid and 3-oxo-23-hydroxybetulinic acid) on murine melanoma B16 cells.

Betulinic acid: A new cytotoxic compound against malignant head and neck cancer cells

In two HNSCC cell lines betulinic acid induced apoptosis, which was characterized by a dose-dependent reduction in cell numbers, emergence of apoptotic cells, and an increase in caspase activity. Western blot analysis of the expression of various Bcl-2 family members in betulinic acid–treated cells showed, surprisingly, a suppression of the expression of the proapoptotic protein Bax but no changes in Mcl-1 or Bcl-2 expression.

Blueberries


Evidence for anti-cancer properties of blueberries: a mini-review.
Blueberries are amongst the most commonly consumed berries in the United States. Berries in general are rich in phenolic compounds, which are known for their high antioxidant capacity. Specifically, evidence from in vitro, in vivo and a few clinical studies suggest that blueberries and their active constituents show promise as effective anti-cancer agents, both in the form of functional foods and as nutritional supplements. Some of the mechanisms by which blueberries have been shown to prevent carcinogenesis include inhibition of the production of pro-inflammatory molecules, oxidative stress and products of oxidative stress such as DNA damage, inhibition of cancer cell proliferation and increased apoptosis. This review will focus on the preclinical and clinical evidence that supports blueberries as an anti-cancer fruit, as well as expressing the need for more preclinical studies and the conduction of clinical studies with respect to the cancer preventive ability of blueberries.

Effect of Anthocyanin Fractions from Selected Cultivars of Georgia-Grown Blueberries on Apoptosis and Phase II Enzymes

The response correlated positively with dose. The QR activity was lower in all cells treated with an anthocyanin fraction from Tifblue, Powderblue, Brightblue, and Brightwell cultivars than in control cells (P < 0.05). The activity decreased gradually when treated with increased concentrations of anthocyanin fractions (50−150 μg/mL) in the Tifblue and Powderblue cultivars. The GST activity was lower (P < 0.05) in cells treated with anthocyanin fractions from all of the cultivars and at all concentrations. These results indicated that apoptosis was confirmed in HT-29 cells when treated with anthocyanins from blueberry cultivars at 50−150 μg/mL concentrations, but these same concentrations decrease QR and GST activities rather than induce them.
Availability of blueberry phenolics for microbial metabolism in the colon and the potential inflammatory implications
Blueberries are a rich source of phenylpropanoid-derived phytochemicals, widely studied for their potential health benefits. Of particular interest for colonic health are the lower molecular weight phenolic acids and their derivatives, as these are the predominant phenolic compounds detected in the colon. Blueberries contained a wide variety of phenolic acids, the majority of which (3371.14 ± 422.30 mg/kg compared to 205.06 ± 45.34 mg/kg for the free phenolic acids) were attached to other plant cell-wall components and therefore, likely to become available in the colon. Cytokine-induced stimulation of the inflammatory pathways in colon cells was four-fold up-regulated in the presence of the free phenolic acid fraction. Incubation of the bound phenolic acids with human faecal slurries resulted in qualitative and quantitative differences in the phenolic compounds recovered. The metabolites obtained by incubation with faecal slurries from one volunteer significantly decreased (1.67 ± 0.69 ng/cm3) prostanoid production, whereas an increase (10.78 ± 5.54 ng/cm3) was obtained with faecal slurries from another volunteer. These results suggest that any potential protective effect of blueberry phenolics as anti-inflammatory agents in the colon is a likely result of microbial metabolism. Studies addressing a wide-range of well-characterised human volunteers will be required before such health claims can be fully established.

Broccoli

Relatives: Romanesco, Broccoflower, Cauliflower, Kale, Raab, Brussel Sprouts, Cabbage, Collards and Kohl Rabi.




Natural Compound in Broccoli Slows Breast Cancer Stem Cells
In lab studies, when breast cancer cells were exposed to sulforaphane extract from broccoli, the growth of cancer stems cells slowed down and tumors shrank. The researchers speculate about the possible use of sulforaphane extract to prevent as well as treat breast cancer, someday.
Broccoli Sprouts contain 3X the amount of Sulforaphane Glucosinolate
Johns Hopkins University researchers found that young broccoli sprouts, in particular, contained high concentrations of SGS. The scientists believe that SGS boosts the body's own antioxidant defense system, including Phase 2 detoxification enzymes, which promote long-lasting antioxidant activity in the body.

Diindolylmethane (DIM)
At the University of California at Berkeley, the Chairman of the Nutritional Sciences Department and the Director of the National Institutes of Health Cancer Research Program were studying the biological properties of Diindolylmethane (DIM), a naturally occurring compound found in Brassica vegetables (broccoli, cauliflower, cabbage, kale, brussels sprouts), when they made a remarkable discovery: DIM is a potent activator of the immune response system. They patented their discovery and ActivaMune was launched as a first-in-class nutritional supplement to enhance the immune system and support multiple organs throughout the body: breast, prostate, cardiovascular, vision, skin and colon health. ActivaMune's unique and patented formula combines multiple nutrients for maximum effectiveness: Diindolylmethane (DIM), Sulforaphane, Selenium, Lycopene, Lutein, Zeaxanthin, Calcium and Vitamins C, D3 & E.

Surprising Discovery Reveals How Broccoli Fights Cancer


Broccoli — and to an even greater degree broccoli sprouts — has gained a reputation as a potent cancer-fighter, and recent research sheds new light on the actual mechanics behind its chemoprotective abilities.

One of the compounds in broccoli known to have anti-cancer activity is sulforaphane, a naturally occurring organic sulfur.

Studies have shown sulforaphane supports normal cell function and division while causing apoptosis (programmed cell death) in colon,1 prostate,2 breast3 and tobacco-induced lung cancer4 cells, and reducing the number of cancerous liver tumors in mice.5

Three servings of broccoli per week may reduce your risk of prostate cancer by more than 60 percent.6 Now, Oregon State University (OSU) researchers believe they've discovered yet another way sulforaphane works to protect you against cancer.


Read more...

Wednesday, April 12, 2017

Second Opinion from Doctor Results in Different Diagnosis 88% of Time



Science Daily clearly takes point of view of the Medical Industrial Complex (MIC)--profit before patients--that the value of second opinions are demonstrated in a study, whereas I see this from the highly skeptical-of-the-deeply-rooted-MIC point of view that it can't be trusted 88% of the time. We don't know whether the first or second opinion is right or wrong. What about a third opinion? Would that opinion disagree with the first and the second?
Many patients come to Mayo Clinic for a second opinion or diagnosis confirmation before treatment for a complex condition. In a new study, Mayo Clinic reports that as many as 88 percent of those patients go home with a new or refined diagnosis — changing their care plan and potentially their lives. Conversely, only 12 percent receive confirmation that the original diagnosis was complete and correct.
We take it for granted that the Mayo Clinic is right because, well, they're the Mayo Clinic, the poster child for the MIC, this vast networked system that we've been indoctrinated to believe in since birth.
It's not that the MIC is all bad, or hasn't saved many lives and improved the quality of many others.  It's the fact that the opposite is also true, it has destroyed and ruined lives, possibly in equal measure   and we're made to believe there are no other viable options. 
We are not saying that there are no useful or helpful things within the MIC. It has saved many of our lives or the lives of people we love. We are not anti healthcare or science, but are rather exposing the reality that many of us are dependent on the MIC while we are simultaneously trying to change it and ultimately build alternatives to it. Many of us don’t want to have to turn to the MIC, yet have few other viable options. And still many of us are fighting for access to current (or better) services within the MIC. There are no easy answers and the contradictions we are living in are often painful and unjust. Similar to our work to resist and challenge capitalism or to create alternatives to the police and prisons, resisting and challenging the MIC is rife with complexity and there is so much we need that we don’t have yet.

We are asking, why we have so few options when it comes to our healthcare needs? And why insurance and pharmaceutical companies get to call the shots on the kind of care we receive—or don’t? Why don’t we talk more about the ways that forced medicalization has become part of our prison system? Or how non-western and alternative healing practices are often no less ableist than western medical practices? We are asking, what could “health,” “wellness,” “care,” “accessibility” and “sustainability” look like in practice, outside of theory? We are revealing where and how the MIC is already in our lives in ways we might not have thought of before. We are urging us all to connect the MIC to our political work, because healing, wellness, care, “health” and disability are part of whatever liberatory work we are engaged in.

Links:

Medical Industrial Complex Visual
The Medical Industrial Complex is an enormous system with tentacles that reach beyond simply doctors, nurses, clinics, and hospitals. It is a system about profit, first and foremost, rather than “health,” well being and care. Its roots run deep and its history and present are connected to everything including eugenics, capitalism, colonization, slavery, immigration, war, prisons, and reproductive oppression. It is not just a major piece of the history of ableism, but all systems of oppression.

Read more...

Thursday, February 02, 2012

Bioethicists Conclude Human Life is About as Sacred as Weeds.

Is nothing sacred anymore? Does anything matter? Is there any intrinsic value to life? Apparently not, according to two nihilistic American bioethicists in an online article in the Journal of Medical Ethics. That's right. Humanity has no innate value, no purpose, no meaning. And unfortunately, these two prominent bioethicists are not alone in their thinking. So, what makes killing wrong? Well, according to these "experts", human life is only valuable if is productive. Hmmm...if I remember correctly, this kind of utilitarian thinking was the same kind of rationale used by Nazi Germany.

“[I]f killing were wrong just because it is causing death or the loss of life, then the same principle would apply with the same strength to pulling weeds out of a garden. If it is not immoral to weed a garden, then life as such cannot really be sacred, and killing as such cannot be morally wrong.”
Take Bill "reduce the population with vaccines" Gates , for instance, with his 500,000 shares , of   Monsanto stock. Developer/producer of GMO seeds/foods, and all types of poisons like DDT/agent orange, and who spreads their toxic GMO seeds in order to sue non-corporate farmers with patent infringement.  Read Monsanto: Harvest of fear.
“The world today has 6.8 billion people… that’s headed up to about 9 billion. Now, if we do a really great job on new vaccines, health care, reproductive health services, we could lower that by perhaps 10 or 15 percent.” -- Bill Gates
As it is, a significant portion of the developed world's population believe in nothing greater than themselves, which tends to make the dehumanization of others fairly simple. What exactly is dehumanization? Basically, valuing human life about as much as you value the weeds in your garden. It's viewing people as statistics, commodities, or as interchangeable. This, I would argue is a direct result of our ever increasing acquisitive society.

Consumption has replaced production, and everything and everyone is a consumer item. The brutal underlying values of a casino/"free" market consumerist society are inherently nihilistic, in that nothing we do, nothing we create, nothing we love has meaning. Thus, 'we the weeds people' are essentially disposable, like dirty Pampers.

Related Links:

Executive order 13139: President Clinton signed this order authorizing the Department of Defense to administer "new investigational drugs" to troops ---- with or without their consent ---- to protect them from biological, chemical or radiological agents during military actions.

Executive Order 13544,  whose goal is to severely limit private and organic farming

Public Law 105-85 Use of human subjects for testing of biological or chemical agents

S 510, the Food Safety Modernization Act precludes the public’s right to grow, own, trade, transport, share, feed and eat each and every food that nature makes. In other words, consolidated corporate control of your food.

Bill Gates, China jointly developing nuclear reactor

Codex Alimentarius is a collection of internationally recognized standards, codes of practice, guidelines and other recommendations relating to foods, food production, and food safety.

Read more...

Thursday, March 18, 2010

Big Pharma or Us?

Generic drugs make up 70% of all prescriptions, and according to House Energy and Commerce Committee chairman Henry Waxman, "in the last decade alone, generic drugs have saved consumers, businesses and state and federal governments $734 billion." Despite that savings, the cost of drugs continues to escalate. In large part this is due to what is regarded as the future of health care: biotechnology drugs, or "biologics".

Simply put, biologics are protein based drugs made from living organisms - hamster ovaries, mare's urine, pig intestines, blood - grown inside living cells, as opposed to chemicals, normally showing better efficacy and safety than conventional drugs. Used to treat everything from cancer to multiple sclerosis to psoriasis, biologics currently make up about 20% of the pharmaceutical market - predicted to make up half the market by 2015 - and are the fastest-growing class of medicines, with more than $40 billion in annual sales in the United States.

However, the FDA has no authority to approve lower-cost, generic versions, biosimilars or “follow-on biologics” (“FOBs”) so, these drugs very rarely face competition from generic copies. FOBs (generic form of biologics) could save patients, insurers and our government anywhere from $67 billion to $108 billion during the first decade, and between $236 billion to $378 billion over the next two decades according to the Generic Pharmaceutical Association.

The contentious issue here is the length of time that brand names can hold a monopoly before the FDA can approve the entry of generic competitors. Competition from generic drugs has substantially reduced prescription drug prices and overall prescription drug expenditures, increased access to therapeutic drugs for more Americans, and hastened the pace of innovation.

The provision in proposed health care legislation would allow pharmaceutical companies to extend monopolies to 12-years exclusivity once the product is licensed by the FDA. Even after 12 years, this legislation would allow a pharmaceutical company to extend market protection for its biologic by making minor modifications to the drug to effect dosing, for example.

Generic brand medications only make up for 17 percent of all profits, and generic prescription companies are more focused on the hit that consumers will take financially if longer terms of exclusivity are given to brand-names and biologics. Brand names and biologics, however, are more focused on their profits.
So, why do biologics need a 12-year instead of a 5-year monopoly?

The answer is, of course, profit, and not just a little profit...a lot of profit. According to the pharmaceutical trade association, the average research and development costs are approximately the same for biologics as they are for conventional drugs. Not only that, generics face higher than normal barriers to entering the market. The FTC recently released a report entitled, “Follow-on Biologic Drug Competition” which addressed questions that have arisen about whether the price of biologics might be reduced by competition if there were a statutory process to encourage biosimilars or FOBs to enter and compete with pioneer (brand name) biologics once a pioneer drug’s patents have expired. The FTC did not recommend biologics any years of exclusivity protection.
Based on these findings, the Report concludes that patent protection and market-based pricing will promote competition by FOBs, as well as spur biologic innovation. It states that legislation to put a process in place for the abbreviated FDA approval of FOBs is likely to be an efficient way to bring FOBs to market, because of the time and cost savings it would provide.

In addition, the Report states that the 12- to 14-year regulatory exclusivity period is too long to promote innovation by these firms, particularly since they likely will retain substantial market share after FOB entry. The Report concludes that special procedures to resolve patent issues between pioneer and FOB manufacturers before FDA approval, which are not needed,
could undermine patent incentives and harm consumers. Finally, the Report states that FOB manufacturers are unlikely to need additional incentives – such as a 180-day marketing exclusivity period – to develop interchangeable FOB products.
Links:

Act and Myth of Exclusivity Incentive

Competition Counts

Frequently Asked Questions About Therapeutic Biological Products

Emerging Health Care Competition and Consumer Issues

See How Pay-for-Delay Settlements Make Consumers and the Federal Government Pay More for Much Needed Drugs: Hearing Before the H. Subcomm. on Commerce, Trade, and Consumer Protection, Comm. on Energy and Commerce.

Read more...

Thursday, September 24, 2009

Shutting Down the Pain Gate Before it Shuts You Down

Dr. Rollin Gallagher, Director of the Center for Pain Medicine, Research and Policy and clinical professor of psychiatry at the University of Pennsylvania and Director of Pain Medicine at the Philadelphia VA Medical Center currently studies the treatment of pain in injured troops on the battlefield.
Pain management is no different on the battlefield today than it was during the Civil War…an injection of Morphine which provides short-term relief but does not do anything to prevent the pain from continuing long-term.

This new method of pain management Dr. Rollin Gallagher is studying not only stops the pain but it also prevents neural pathways of pain to be created, therefore addressing the chronic permanent pain many times associated with injury. This method works by placing a catheter right next to the nerves that transmit the pain information from the area of injury to the brain -- the soldier pushes a button that continuously dribbles medicine right on that nerve to paralyze the specific nerve connected to the place of injury. This new method of pain management prevents the pain signal from getting into the spinal cord where it makes those changes in the neural pathways leading to chronic severe nerve pain.
How pain works?
When injured, a signal immediately goes from the injured tissue into the nerves to your spinal cord and then it is relayed through a set of relay stations in your spinal cord to two parts of your brain, one part of the brains says it’s in my left arm and it’s bad or not so bad and the other part of the brain says this hurts and I hate it...the suffering part.
Then the brain sends a message back down to the spinal cord or the descending control mechanism that say this is really important or this is not so important.
Then you have a reaction around the tissue involved in the injury and have inflammatory cells getting activated and the inflammatory process.
Then either healing begins, if the area is stabilized or if it’s a disease process or a disease process that interferes with healing or continue to do something to activate the injury then healing won’t begin. The longer the pain goes untreated such as the actual stimulus doesn’t heal up properly then your going to have changes in the mechanics of the muscles involved in the area of injury that will continue to send signals from the periphery.
More importantly you may have changes in the spinal cord and brain that then permanently activate the pain causing Chronic Regional Pain Syndrome, where just moving, blowing on the area actually activates the pain system. In addition, from not using the area the person gets bone absorption, contractures (a shortening or distortion of muscular or connective tissue due to spasm, scar, or paralysis of the antagonist of the contracting muscle) and other problems that create new neural pathways of pain.
Studies are suggesting that early exposure (babies or children) to pain that is not controlled actually enables an overgrowth of the pain neuron system in the spinal cord so there may be people who are more reactive to the same level of stimulus based on what happened to them earlier on in life.

Read more...

Tuesday, July 28, 2009

Money Driven Medicine

Increasingly, over the last century, the history of U.S. health care has been shaped by corporate interests' and market forces have splintered our health care system. As it is, $1 out of every $3 is wasted on redundant or ineffective treatments, and in ten years, health care costs will double. Costly and inefficient, our health care system ranks very low amongst industrialized nations.

-Health care spending is 4.3 times the amount spent on national defense

-U.S. health care spending reached $2.4 trillion last year/ est. $4.3 trillion in 2017

-U.S. spends 6 times more per capita to administer our health care system than its peer Western European nations

-We spend more on health care for nearly 46 million uninsured Americans than other industrialized nations who provide health insurance for all their citizens.

-Electronic medical records still are not a reality.

-20 percent of Americans visit an Emergency Room each year

-64 percent of U.S. residents are overweight (30 pounds over their proper weight)

-Health care expenditures continue to increase annually at twice the rate of inflation

-Our government currently pays more than 50 percent of all health care costs in America.

-80% of health care dollars are currently spent on patients who are chronically ill.
Market forces do not keep prices down in the health care market as they do in other markets. Normally, consumers have the power to bring prices down as producers compete with each other, because in other markets, consumers can afford to wait until prices fall to what they are willing to pay. Not so when it comes to health care. Sick people cannot wait for prices to fall. They can't comparison shop. They have no choices.

Money-Driven Medicine is a new documentary based on Maggie Mahar's book Money-Driven Medicine: The Real Reason Health Care Costs So Much

Healthbeat is Maggie Mahar's blog.

Read more...

Monday, February 05, 2007

List of Unsolved Problems


If you have nothing better to do, you might want to try tackling some of the following unsolved problems in various subjects:













* Unsolved problems in biology
* Unsolved problems in chemistry
* Unsolved problems in cognitive science
* Unsolved problems in computer science
* Unsolved problems in economics
* Unsolved problems in Egyptology
* Unsolved problems in linguistics
* Unsolved problems in mathematics
* Unsolved problems in medicine
* Unsolved problems in neuroscience
* Unsolved problems in philosophy
* Unsolved problems in physics
* Unsolved problems in Sinology

Read more...
Iraq Deaths Estimator
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