|

6450 Lusk Blvd. Suite E102
San Diego, CA 92121
|
Macrolide Antibiotic / Overviw:
It has been 60 years since the first report of erythromycin in 1952. Over the course of this 60 years the macrolide antibiotics—14- and 16-membered macrolactams—have been followed at intervals by the lincosamides, streptogramins, azalides and now the ketolides.
Erythromycin and other macrolide antibiotics bind to the 50S subunit of the bacterial ribosome and physically prevent the elongation of nascent polypeptide chains.The 50S macrolide-binding site is composed of portions of the 23S rRNA subunit, ribosomal protein L4 and ribosomal protein L22. Bacteria may acquire macrolide resistance when the genes encoding these components sustain mutations that alter the drug binding site.
Polyketides are natural products, many of which have applied potential as pharmaceuticals. Examples of such polyketides include erythromycin (anti-bacterial), Nystatin (anti-fungal), avermectin (anti-parasitic), rapamycin (immunosuppressant) and daunorubicin (anti-tumor). The Gram-positive bacteria of the genus Streptomyces are the main producers of polyketides, and the genetics and biochemistry of polyketide biosynthesis in these organisms are relatively well characterized1.
During earlier work, Shaw had discovered that LKB1 activates a metabolic master switch. The switch, an enzyme known as AMPK, acts like a gas gauge by sensing how much energy a cell has. When a cell has plenty of energy, AMPK remains inactive and the cell carries out its normal processes. If a cell runs on empty, LKB1 turns on AMPK, which puts a damper on cell growth and proliferation. When LKB1 is absent or disabled, cells facing starvation never get the message and simply continue to divide.

Right A Lkb1+/- mouse before and after treatment with rapamycin. Image: Courtesy of Dr. David R. Vera, University of California, San Diego. Press release June 15, 2009,© Salk Institute for Biological Studies.
Polyketide antibiotics of bacterial origin can be grouped into two major categories, type I and type II, based on the compound structures and biosynthetic mechanisms. Type I polyketides are synthesized by large multifunctional enzymes, while type II polyketides are assembled by dissociated enzymes.
Polyketide natural products are known to possess a wealth of pharmacologically important activities, including antimicrobial, antifungal, antiparasitic, antitumor and agrochemical properties. These metabolites are ubiquitous in distribution and have been reported from organisms as diverse as bacteria, fungi, plants, insects, dinoflagellates, mollusks and sponges. The wide spectrum of activity of polyketides makes them economically, clinically and industrially the most sought after molecules.
Many polyketide products are well-known compounds such as Erythromycin A, a broad spectrum macrolide antibiotic, the antihelmintic agent, avermectin or the immunosuppressants: FK506 and rapamycin. Oleandomycin, rifamycin, lovastatin, oxytetracycline and reserveratrol are a few more of the thousands of polyketides discovered so far. Polyketides are usually categorized on the basis of their chemical structures.
Source:
-
Hopwood, D.A. (1997). Genetic contributions to understanding polyketide synthases. Chem. Rev. 97, 2465-2497.
Polyene Macrolide Antibiotics Examples:
|
Avermectin
|
FK-506
|
Oligomycin B
|
Spiramycin
|
|
Amphotericin B
|
Flopristin
|
Oligomycin C
|
Streptogramin A
|
|
Azalide
|
Flucanazole
|
Oxytetracycline
|
Streptovaricin
|
|
Azithromycin
|
Flurithromycin
|
Pentamycin
|
Tilmicosin
|
|
Boromycin
|
Josamycin
|
Perimycin
|
Troleandomycin
|
|
Brefeldin A
|
Kinamycin
|
Pikromycin
|
Tulathromycin
|
|
Candicidin
|
Kitasamycin
|
Polyketide
|
Tylosin
|
|
Calicheamicin
|
Lovastatin
|
Pristinamycin IIA
|
Virginiamycin S1
|
|
Callystatin A
|
Macrocin
|
Pristinamycin IIA
|
|
|
Clarithromycin
|
Mepartricin
|
Rapamycin
|
|
|
Daunorubicin
|
Midecamycin
|
Resveratrol
|
|
|
Dirithromycin
|
Miocamycin
|
Rifamycin B
|
|
|
Echinocandin B
|
Monocerin
|
Roxithromycin
|
|
|
Filipin
|
Mycolactone
|
Roxithromycin
|
|
|
Epthilone B
|
Nargenicin
|
Solithromycin
|
|
|
Erythromycin A
|
Oleandomycin
|
Spiramycin
|
|
|
Fidaxomicin
|
Oligomycin A
|
Streptogramin A
|
|
WANT MORE? Download our entire Antibiotic E-GUIDE BELOW.
Sincerely, Chip Lindgren, Founder & President, A.G. Scientific, Inc.
************************************************************
A.G. Scientific, Inc., an ISO 9001:2008 Company
6450 Lusk Blvd. Ste. E102,
San Diego, CA 92121, Phone +858 452 9925,
Fax +858 452 9926, www.agscientific.com
Personal email: chip@agscientific.com
Corporate email: info@agscientific.com
************************************************************
|

6450 Lusk Blvd. Suite E102
San Diego, CA 92121
|
BACKGROUND/OVERVIEW:
Bacteriocidal antibiotics obtained from Streptomyces that inhibit protein synthesis in bacterial ribosomes and are effective against aerobic gram-negative bacilli. This group of antibiotics includes at least eight drugs: amikacin, gentamicin, kanamycin, neomycin, netilmicin, paromomycin, streptomycin, and tobramycin. All of these drugs have the same basic chemical structure.

Figure 1: Structures of 2-deoxystreptamine (2-DOS) aminoglycosides. (A) monosubstituted 2-DOS: apramycin. (B) 4,5-disubstituted 2-DOS: ribostamycin, paromomycin, and lividomycin. (C) 4,6-disubstituted 2-DOS: tobramycin and bekanamycin.
Aminoglycosides are primarily used to combat infections due to aerobic, Gram-negative bacteria. Bacteria that can successfully be combated with aminoglycosides include Pseudomonas, Acinetobacter, and Enterobacter species, among others. Aminoglycosides are also effective against mycobacteria, the bacteria responsible for tuberculosis.
The aminoglycosides can be used against certain Gram-positive bacteria, but are not typically employed because other antibiotics are more effective and have fewer side effects. Aminoglycosides are ineffective against anaerobic bacteria (bacteria that cannot grow in the presence of oxygen), viruses, and fungi. One aminoglycoside, paromomycin, is used against parasitic infection. Like all other antibiotics, aminoglycosides are not effective against influenza, the common cold, or other viral infections.
Aminoglycosides are absorbed very poorly from the gastrointestinal tract. The typical routes of administration are by intramuscular (injection into a muscle) or intravenous injection (injection into a vein), irrigation, topical skin application, or inhalation. If the infection being treated involves the central nervous system, the drug can be injected into the spinal canal. The bactericidal ability of aminoglycosides has not been fully explained.
It is known that the drug attaches to a bacterial cell wall and is drawn into the cell via channels made up of the protein, porin. Once inside the cell, the aminoglycoside attaches to the cell's ribosomes. Ribosomes are the intracellular structures responsible for manufacturing proteins. This attachment either shuts down protein production or causes the cell to produce abnormal, ineffective proteins. The bacterial cell cannot survive with this impediment.
Aminoglycosides have been shown to be toxic to certain cells in the ears and in the kidneys. At the proper dosage and in the presence of gram negative enteric (intestinal) bacteria, aminoglycosides are very effective in treating an infection.
Source: Books. Chambers, Henry F., W. Keith Hadley, and Ernest Jawetz. "Aminoglycosides & Spectinomycin." In Basic and Clinical Pharmacology, edited by Bertram G. Katzung, 7th ed. Stamford: Appleton & Lange, 1998.
AMINOGLYCOSIDE /AMINOGLYSIDIC ANTIBIOTIC EXAMPLES:
|
Amikacin
|
G-418, Sulfate
|
Paromomycin Sulfate
|
|
Apramycin
|
Gentamycin
|
Ribostamycin
|
|
Arbekamycin
|
Hygromycin B
|
Sisomycin
|
|
Bekanamycin
|
Isepamicin
|
Streptoduocin
|
|
Capreomycin
|
Kanamycin
|
Streptomycin
|
|
Dibekacin
|
Kasugamycin
|
Tobramycin
|
|
Dihydrostreptomycin
|
Micronomicin
|
Verdamicin
|
|
Elsamitrucin
|
Neomycin
|
|
|
Fosfomycyin/ Tobramycin
|
Netilmicin
|
|

Hygromycin B| CAS [31282-04-9]| Selection Antibiotic| A.G. Scientific
Sincerely, Chip Lindgren, Founder & President, A.G. Scientific, Inc.
************************************************************
A.G. Scientific, Inc., an ISO 9001:2008 Company
6450 Lusk Blvd. Ste. E102,
San Diego, CA 92121, Phone +858 452 9925,
Fax +858 452 9926, www.agscientific.com
Personal email: chip@agscientific.com
Corporate email: info@agscientific.com
************************************************************
|

6450 Lusk Blvd. Suite E102
San Diego, CA 92121
|
Hologic Agrees to Acquire Gen-Probe for $3.7 Billion
Hologic Inc. (HOLX), a maker of diagnostic, medical and surgical devices, said the $3.7 billion acquisition of Gen-Probe Inc. (GPRO) will bring “double-digit” returns as the company sells new products to overseas markets.
“We’re very confident that this investment will yield a low double-digit return, and that’s significantly greater than our cost of capital,” Hologic Chief Executive Officer Rob Cascella said in an interview.
Chart: Acquisition Details
The deal will bring Gen-Probe’s testing products for blood screening and sexually transmitted diseases to markets in China and Europe where the company currently has little reach, Cascella said. “We look at it as taking world-beating product and putting it through an engine for growth,” Cascella said.
Gen-Probe investors will receive $82.75 a share in the acquisition, the two companies said today in a statement. That’s about 20 percent above San Diego-based Gen-Probe’s closing price on April 27. The deal’s $3.7 billion value includes net debt.
Gen-Probe dominates testing for sexually transmitted diseases with about a 60 percent share of the U.S. market, including tests for chlamydia and gonorrhea, and human papillomavirus, Bloomberg reported last year. It also does about 80 percent of blood-bank screenings in the U.S.
Junaid Husain, an analyst with Dougherty & Co. in Minneapolis, said he was “very, very cautious” about the deal.
“The Gen-Probe business is very mature,” he said in a telephone interview. “They have infectious-disease products and blood-system products at the top end of the product life cycle, so I am just not sure where they are going to get the accelerated growth.”
Shares Fall
Hologic, based in Bedford, Massachusetts fell 10 percent to $19.12 at the close in New York, its biggest one-day decline since May 2010. Gen-Probe gained 19 percent to $81.55.
The deal will add about 20 cents a share to profit in the first year after closing, Hologic said in the statement. “This transaction establishes Hologic as a premier company in STD diagnostics,” Cascella said in the statement.
The agreement would be the largest purchase of a diagnostic equipment or test kit maker in the last year, according to data compiled by Bloomberg. The next largest was Thermo Fisher Scientific Inc. (TMO)’s purchase of Phadia for $3.5 billion last May.
Hologic is paying about 19 times earnings before interest, taxes, depreciation and amortization. That compares with the median of 17 across 15 similar deals over the past decade, the data show.
Strategic Fit
“Strategically this makes all the sense in the world,” said Bill Quirk, an analyst with Piper Jaffray Cos. in Minneapolis. “The two companies have a strong presence in women’s health, but have little overlap and pretty complementary products,” he said in an interview.
Hologic has 500 people in China, where Gen-Probe only has two, Cascella said on a conference call with investors today.
“What we intend to do is leverage the products of Gen- Probe with the existing infrastructure we have,” Cascella said. “What this does is accelerate market penetration of their products with a ready-made distribution channel.”
Gen-Probe Chief Executive Officer Carl Hull was selected in November to replace Hank Nordhoff as chairman. Nordhoff served as president and CEO from 1994 to 2009, then as chairman until he retired.
Hologic also reported today a net loss for the three months ended March 24. The loss of $40.3 million, or 15 cents a share, compared with a net income of $82.4 million, or 31 cents, a year earlier.
Source: Drew Armstrong at Bloomberg in New York at darmstrong17@bloomberg.net

Sincerely, Chip Lindgren, Founder & President, A.G. Scientific, Inc.
************************************************************
A.G. Scientific, Inc., an ISO 9001:2008 Company
6450 Lusk Blvd. Ste. E102,
San Diego, CA 92121, Phone +858 452 9925,
Fax +858 452 9926, www.agscientific.com
Personal email: chip@agscientific.com
Corporate email: info@agscientific.com
************************************************************
|

6450 Lusk Blvd. Suite E102
San Diego, CA 92121
|
- CAS #: 33069-62-4
- Chemical Name: Taxol, Baccatin III N-benzyl-β-phenylisoserine ester
- Chemical Formula: C47H51NO14
- Appearance: White Crystalline Powder
- Merck Index: 12.7117.1996
- Molecular Weight: 853.9
- Solubility: Soluble in DMSO, Ethanol, Methanol; Clear colorless solution at 10 mg/ml DMSO and 10 mg/ml methanol
- Storage Temp: -20°C
- Melting Point: 215-217°C
Paclitaxel, Taxus brevifolia, commonly known as the Pacific yew, is a member of the yew family (Taxaceae). It is a small, slow growing evergreen tree native to the northwestern United States (Wheeler et al., 1992). In 1971, a natural product called taxol that was isolated from T. brevifolia. Taxol has been found to be a mitotic inhibitor used for cancer chemotherapy.
Taxol is derived from the bark of the Pacific yew which is a potentially limited source (Wheeler et al., 1992). This limitation has been overcome by combined efforts of pharmaceutical, agricultural, and governmental agencies (Foa et al., l994). Using analytical methods, the needles and stems of the Taxus species are examined for 10-deacetylbaccatin III, a related compound that could be converted to taxol through a semi-synthetic route (Witherup et al., 1990). The concentration of taxol is less in the tips of the branches than at the base of the trunk because branch tips have more taxol in the phloem tissue, and the inner bark is thinner. Concentrations were generally lower in the needles than in the bark. Concentrations of taxol in the bark increased from May through August while the concentration in the needles changed little during that time (Vance et al., 1994)
Taxol's mechanism of antitumor activity is unique because it promotes microtubule assembly and stabilizes the microtubules, thus preventing mitosis (Huizing et al., 1995). Taxol does this by reversibly and specifically binding to the B subunit of tubulin, forming microtubule polymers leading to growth arrest in the G2/M phase of the cell cycle (Gotaskie and Andreassi, 1994). This makes taxol unique in comparison to vincristine and vinblastine which cause microtubule disassembly (Gatzemeier et al., 1995). Additionally, recent evidence indicates that the microtubule system is essential to the release of various cytokines and modulation of cytokine release may play a major role in the drug's antitumor activity (Smith et al., 1995).
Due to taxol's antimitotic activity, it is a useful cytotoxic drug in treating several classic refractory tumors including head and neck cancer, small cell and non-small cell lung cancer and most notably breast and ovarian carcinomas. It may also slow the course of melanoma. Response rates to taxol treatment varies among cancers. Advanced drug refractory ovarian cancer responds at a 19-36% rate, previously treated metastatic breast cancer at 27-62%, and various lung cancers at 21-37%. Taxol has also been shown to produce complete tumor remission in some cases (Guchelaar et al., 1994).
In addition, taxol plus radiation treatment has an additive but not synergistic effect as shown in an experiment using a cervical carcinoma line (Minarik and Hall, 1994). Elderly patients aged more than 60 years did not differ with respect to administered dose intensity, number of cycles of therapy administered, or the occurrence of serious or mild toxicities (Bichner et al., 1993). Thus, elderly patients receiving taxol can be treated as aggressively as younger patients. Clinically, taxol treatment is a possible adjunct to radiation.
Sources: Maria Costello and Kelly Kellmel

Sincerely, Chip Lindgren, Founder & President, A.G. Scientific, Inc.
************************************************************
A.G. Scientific, Inc., an ISO 9001:2008 Company
6450 Lusk Blvd. Ste. E102,
San Diego, CA 92121, Phone +858 452 9925,
Fax +858 452 9926, www.agscientific.com
Personal email: chip@agscientific.com
Corporate email: info@agscientific.com
************************************************************
|

6450 Lusk Blvd. Suite E102
San Diego, CA 92121
|
Piperlonguminine is a potential novel therapeutic agent for Alzheimer’s disease. Extracellular deposits of Aβ in senile plaques of the cerebral cortex are known to be hallmarks of Alzheimer’s disease. Recent studies show that a mix of piperlonguminine and dihydropiperlonguminine significantly inhibit the expression of Amyloid Precursor Protein (APP). The decreased production of the peptide Amyloid β (Aβ) in SK-N-SH cells is a beneficial effect to Alzheimer’s Disease.

Perperamides, including Piperlonguminine, exhibit promising activity against both Gram-positive and Gram-negative bacteria and Candida species. At experimental levels, Peperlonguminine also shows low toxicity in Vero cells and macrophages. The mechanism of this antimicrobial action is still unknown, however, this potent activity against Bacillus subtilis and Candida tropicalis warrants further investigation.
Piperlonguminine shows in vivo antitumor effects agains sarcoma 180 without showing any significant in vitro cytotoxic effect. In addition, many Piperlonguminine analogs are effective in treating various human cancer cell lines. Many similar spice components have been targeted as potential anticancer solutions, and Piperlonguminie is no exception.
REFERENCES: 1. Hong-Shun, Q., Pei, L., et al. Chinese J. Of Phys. 52(3):160-168,2009. 2. Silva,R.S., Endo E.H., et al. Molecules, 14:1171-1182, 2009. 3. Bezerra, D.P.,Pessoa, C., et al.J.Appl. Toxicol. Jul;28(5):599-607,208;4. Rama Subba Rao, V., Suresh, G.,et al. Med. Chem. Res.21:38-46,2012.
Sincerely, Chip Lindgren, Founder & President, A.G. Scientific, Inc.
************************************************************
A.G. Scientific, Inc., an ISO 9001:2008 Company
6450 Lusk Blvd. Ste. E102,
San Diego, CA 92121, Phone +858 452 9925,
Fax +858 452 9926, www.agscientific.com
Personal email: chip@agscientific.com
Corporate email: info@agscientific.com
************************************************************
|

6450 Lusk Blvd. Suite E102
San Diego, CA 92121
|
Veratramine is a teratogenic steroid alkaloid found in plants of the genus Veratrum. The Veratrum genus is one of coarse, highly poisonous herbs, also known as corn lilies. It is their toxic characteristic that has made them an interesting target for research in a variety of areas, including cancer research and cardiovascular research, and the full extent of its applications is still being studied.

Veratramine was found to significantly inhibit the hedgehog signaling pathway in NIH/3T3 cells in a study involving several different kinds of steroidal alkaloids. The hedgehog signaling pathway has been found to be a vital force behind tumor self renewal in some types of tumor-initiating cells, and inhibition of the pathway is being targeted as a possible treatment for those types of cancers.
Veratramine also produces a characteristic excitatory action on the central nervous system, accompanied by changes in serotonin content in the hypothalamus. Results indicate that Veratramine may be a serotonin agonist, a mechanism that would explain Veratramine’s action in the experiment. A different study showed that Veratramine prevents or abolishes the cardioaccelerator action of epinephrine in doses which do not negate its vasopressor effect.
REFERENCES: 1. Tang J,eta l. Phytother Res. 24(6):821-6(2010). 2. Izumi K, et al. Brain Res Bull. 3(3);237-10(1978). 3. Krayer O. Exp Biol Med 70(4):631-32(1949).
Sincerely, Chip Lindgren, Founder & President, A.G. Scientific, Inc.
************************************************************
A.G. Scientific, Inc., an ISO 9001:2008 Company
6450 Lusk Blvd. Ste. E102,
San Diego, CA 92121, Phone +858 452 9925,
Fax +858 452 9926, www.agscientific.com
Personal email: chip@agscientific.com
Corporate email: info@agscientific.com
************************************************************
|

6450 Lusk Blvd. Suite E102
San Diego, CA 92121
|
Poly ADP Ribose Polymerase (PARP) Inhibitors are a group of compounds used in the treatment of cancer. They are unique in their ability to specifically target cancerous cells. PARP proteins are responsible for repairing single-strand breaks in DNA, and when inhibited result in double strand breaks during the raid DNA replication that is characteristic of cancers. This collection of double strand breaks will then cause the death of the cancerous cell. Normal, healthy cells, however, undergo replication slowly enough that the DNA may be repaired by other mechanisms such as through homologous repair, allowing them to survive the PARP inhibition.

Certain cancers in particular are much more dependent on PARP than regular cells, making them good targets for chemotherapeutic cancer therapy by PARP inhibitors. For example, PARP inhibitors are especially effective in the case of cancers caused by BRCA mutations. BRCA1 and BRCA2 are responsible for proteins that help in DNA repair themselves, and mutated forms of these genes can cause some types of cancer by letting errors in DNA amass. In cancer cells where this is the case, inhibiting PARP in combination with the innate initial strain on cell repair thanks to the nature of the BRCA mutations causes cell death.
NEW PARP INHIBITORS
1. Iniparib: PAPR Inhbitor that is being studied as a treatment for pancreatic cancer.

2. Olaparib: Found to have strong potential against breast, ovarian, and colorectal cancer.

3. Veliparib: A good candidate for treating metastic melanoma, as well as breast cancer.

REFERENCES: 1.Piskunova TS, Yuorva MN, et al. Curr. Gerontol. Geriatr. Res. 754190 (2008). 2. Hall JM, Lee MK, et al. Science. 250:1684-89(1990). 3.Fogelman DR., Wolff RA., et al. Anticancer Res. (4): 1417-20 (2011). 4. Fong PC, Boss DS, et al. N. Engl. J. Med. 361(2):123-34 (2009). 5.Isakoff SJ, Overmoyer NM, et al. J. Clin. Oncol. 28:15s (2010).
Sincerely, Chip Lindgren, Founder & President, A.G. Scientific, Inc.
************************************************************
A.G. Scientific, Inc., an ISO 9001:2008 Company
6450 Lusk Blvd. Ste. E102,
San Diego, CA 92121, Phone +858 452 9925,
Fax +858 452 9926, www.agscientific.com
Personal email: chip@agscientific.com
Corporate email: info@agscientific.com
************************************************************
|

6450 Lusk Blvd. Suite E102
San Diego, CA 92121
|
STAUPRIMIDE FAQs - PRODUCT #: S-2092

WHAT IS STAUPRIMIDE? Staurprimde is a semi-synthetic analog of the staurosporine family of indolocarbazoles. The study conducted by Zhu, et al (2009) found Stauprimide increases efficiency of directed Embryonic Stem Cells (ESC) differentiation. Stauprimide promoted induction of Sox17 / Sox 7 cells in both mouse and human ESC , and also helped induce extensive endoderm differentiation markers in the mouse ESC. Early stauprimide treatment was found to enhance later differentiation of the cells toward hepatic and pancreatic lineages. Additionally the study shows Staurpimide binds NME2, impairing nuclear localization of NME2, down-regulating c-Myc. Research indicates, this down-regulation of c-Myc may facilitate ESC exit from the pluripotent state, enabling differentiation.
- Alternative Names: N-Benzol-7-oxostaurosporine; Spd, EMT Inducer
- Chemical Formula: C35H28N4O5
- Molecular Weight: 584.6
- CAS #: 154589-96-5
- Effective Concentration: (EC50 = 0.3 µM)
- Appearance: White solid/powder, color range of yellow to white.
- Solubility: DMSO (20mg/ml); may also be soluble in Ethanol, DMF, Methanol. Poor solubility in water. Rapid stirring, sonication, or warming via water bath may aid in solubilzing the product.
- Storage: Store at -20C recommended, solutions -20C. Protect from light.
LITERATURE REFERENCES
- A small molecule primes embryonic stem cells for differentiation. Zhu S, Wurdak H, Wang J, Lyssiotis CA, Peters EC, Cho CY, Wu X, Schultz PG.
- Using Small Molecules to Great Effect in Stem Cell Differentiation; Kenneth S. Zaret; Cell Stem Cell, Volume 4, Issue 5, 8 May 2009, Pages 373-374
- LIF/STAT3 controls ES cell self-renewal and pluripotency by a Myc-dependent mechanism, Cartwright et al., 2005, P. Cartwright, C. McLean, A. Sheppard, D. Rivett, K. Jones, S. Dalton, Development, 132 (2005), pp. 885–896
- An extended transcriptional network for pluripotency of embryonic stem cells, Kim et al., 2008, J. Kim, J. Chu, X. Shen, J. Wang, S.H. Orkin, Cell, 132 (2008), pp. 1049–1061
Sincerely, Chip Lindgren, Founder & President, A.G. Scientific, Inc.
************************************************************
A.G. Scientific, Inc., an ISO 9001:2008 Company
6450 Lusk Blvd. Ste. E102,
San Diego, CA 92121, Phone +858 452 9925,
Fax +858 452 9926, www.agscientific.com
Personal email: chip@agscientific.com
Corporate email: info@agscientific.com
************************************************************
|

6450 Lusk Blvd. Suite E102
San Diego, CA 92121
|
A large new epidemiological study appears to provide further evidence that regular intake of fiber from fruits, vegetables and whole grains is associated with a reduced risk of developing breast cancer in women. The study examined data from 16 prospective studies in what is called a meta-analysis. The results showed that women who consumed the most fiber in their diets had a lower risk of breast regardless of other risk factors, such as smoking, alcohol consumption, obesity, and menopausal status. Fiber obtained from cereals provided the greatest risk reduction. In addition to containing fiber, fruits, vegetables and whole grains contain an abundance of other cancer-fighting compounds and should be part of a healthy diet.
There are a number of possible ways in which dietary fiber could reduce women’s breast cancer risk. Fiber can bind with toxins, carcinogens and estrogens in the digestive tract and prevent their absorption by the body. Whole grain foods, which are high cereal fiber, are also rich in various nutrients such as polyphenols and flavanoids that have been shown to reduce tumor growth and the development of tumor blood vessels (angiogenesis).

Tumour angiogenesis has classically been inhibited by anti-angiogenic agents that affect ECs directly. Alternative anti-tumour angiogenesis strategies target other cell types in tumours (mural and stromal cells, haematopoietic cells and tumour cells), which stimulate angiogenesis indirectly. The yellow boxes show agents (such as VEGF inhibitors, metronomic chemotherapy and other compounds) that target endothelial (progenitor) cells (EPCs); they inhibit (lymph)angiogenesis (a), induce vessel regression (a) and normalization (b), and block recruitment of EPCs (c). The red boxes show agents (such as PDGF inhibitors) that target mural and stromal cells and destabilize vessels (d), reduce the release of pro-angiogenic factors or progenitor cytokines, and lower the interstitial fluid pressure (IFP), which improves drug delivery (e). The green boxes indicate agents (such as VEGFR-1 inhibitors, chemokine antagonists and so on) that target haematopoietic cells and reduce the infiltration of pro-angiogenic bone-marrow-derived precursors and mature leukocytes (c,f), and stimulate the release of endogenous angiogenesis inhibitors in dendritic cells (g). The blue boxes show agents targeting cancer cells (chemotherapy, radiation, tumour-cell-targeted biologicals) that improve drug delivery by decompressing tumour vessels (h) and decrease the release of (lymph)angiogenic factors (i); some anti-angiogenic agents are also cytotoxic for tumour cells (j). BV, blood vessel; CAF, carcinoma-activated fibroblast; CC, cancer cell; DC, dendritic cell; LV, lymph vessel; Ly, lymphocyte; Ma, macrophage; PC, pericyte; MC, mast cells.
Source: Angiogenesis in life, disease and medicine, Peter Carmeliet, Nature 438, 932-936(15 December 2005).
Other anti-cancer substances found in whole grains include carotenoids, vitamin E, fatty acids, and phytoestrogens, among others. It is thought that phytoestrogens, plant-derived substances that are chemically similar to estrogen, may protect against hormone-dependent cancers like breast cancer, although the data on this topic is inconsistent. Fruit fiber contains citrus pectin, which has been shown in studies in mice to inhibit tumor growth, angiogenesis and the spread (metastasis) of cancer cells.
Sincerely, Chip Lindgren, Founder & President, A.G. Scientific, Inc.
************************************************************
A.G. Scientific, Inc., an ISO 9001:2008 Company
6450 Lusk Blvd. Ste. E102,
San Diego, CA 92121, Phone +858 452 9925,
Fax +858 452 9926, www.agscientific.com
Personal email: chip@agscientific.com
Corporate email: info@agscientific.com
************************************************************
|

6450 Lusk Blvd. Suite E102
San Diego, CA 92121
|
UCSD Jacobs Medical Center breaks ground – Monday April 9th
The groundbreaking ceremony for UCSD Jacobs Medical Center. The project, originally announced in 2010, will focus on cancer treatment, advanced surgery, and maternity & infant care. The Jacobs Medical Center is just one of a number of projects UCSD has completed or are under development. Last year the Sulpizio Cardiovascular Center opened, and next year UCSD plans to break ground on the Altman Clinical and Translational Research Institute, which will develop and test new medicines and treatments.

According to Dr. Mark Talamini, chair of the university’s Department of Surgery, The Jacobs Medical Center will add bed space to accommodate more patients from around the country and beyond, allowing UCSD to recruit top researchers and physicians. UC San Diego has consistently ranked among the top 10 research universities in R&D obligations, and reported over $960 million in funding for 2011.
The Jacobs Medical center is estimated to cost $670 million dollars, and was made possible in part by a $75 million donation from Qualcomm founder Irwin Jacobs and his wife Joan. The new center will open in phases beginning in 2015 thru 2016.
Sincerely, Chip Lindgren, Founder & President, A.G. Scientific, Inc.
************************************************************
A.G. Scientific, Inc., an ISO 9001:2008 Company
6450 Lusk Blvd. Ste. E102,
San Diego, CA 92121, Phone +858 452 9925,
Fax +858 452 9926, www.agscientific.com
Personal email: chip@agscientific.com
Corporate email: info@agscientific.com
************************************************************