Sex-Selection Abortion is taken up by the US Congress.


A recent poll shows that 77% of Americans are opposed to sex-selection abortion. This is the real war against women. Sex-selection occurs, for the most part, because couples do not want a little girl. This odious practice is being targeted by the Prenatal Nondescrimination Act. While this act might pass the House, it will probably die in the Democrat-dominated Senate.

The President is indicating that he is against this legislation. He is too far into the pockets of Planned Parenthood to support this legislation.

This act should be passed.  Abortion because the baby is female is horrific.  As David Bass puts it:  “pro-choice ideology claims to place the highest value on women and womanhood. Yet they are forced to accept, as both moral and legal, the aborting of an unborn baby strictly because she is female. To do anything less would violate their core beliefs about the un-personhood of the fetus and the absolute autonomy of the parents (specifically, the mother) in deciding whether to terminate the unborn life.”

Pro-choice advocates want abortion at any cost and for any reason, but sex-selection abortion is what we get when we allow abortion for any reason.  Murdering women because they are women is the ultimate misogyny, and defending it is complicity with such misogyny.  This simple fact of the matter is that pro-choice advocates are not pro-choice, they are pro-abortion.  See the following articles by David Bass at the American Spectator see here, and here.

Update – June 1, 2012 Wall Street Journal reported that the Prenatal Nondiscrimination Act failed to pass the House.

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The First Limbal Stem Cell Transplant with Cultured Limbal Stem Cells from a Cadaver


A genetic condition called “aniridia” results from mutations in the PAX6 gene. Approximately 1/50,000-1/1000,000 babies have aniridia. Aniridia results in the complete absence of an iris, and aniridia patients are unable to adjust to light differences.

Because mutations in the PAX6 gene are dominant, aniridia patients half a 50% chance of passing the aniridia condition to their children.

Fortunately for aniridia patients, limbal stem cells can now be cultured in the laboratory and used in clinical settings (see Di Iorio E, et al., Ocul Surf. 2010;8(3):146-53). A Scottish woman with aniridia has just received on of the first limbal stem cell transplants from a cadaver. These cadaver limbal stem cells were cultured and then transplanted onto the surface of her eye.

This woman, Sylvia Paton, who is 50 years old and from the Scottish town of Corstorphine (a west suburb of Edinburgh), is the first person in the United Kingdom to experience this ground-breaking treatment in February of 2012. Her procedure will hopefully reduce her vision problems and ready her for another procedure whereby her lens will be replaced.

For this procedure, limbal stem cells from a dead donor were cultured in the laboratory. The cells were attached to a membrane and then transplanted onto the surface of the left eye. The operation took a total of three hours.

Before her operation, Mrs. Paton could previously only see dark and light through her eye, but this treatment should repair her cornea, and prepare her for another surgery one year later to remove her cataract.

Dr Ashish Agrawal, the National Health Service consultant ophthalmologist who performed the operation, said: “It is now 12 weeks since the transplant and I am delighted to report that Sylvia is recovering well. Her cornea is clear and I hope that it will continue to maintain clarity. However, this is the first and the major step in the complex visual rehabilitation process and she will require further surgical treatment to restore vision.”

We wish Mrs. Paton well and hope that her vision continues to improve.

Dental Stem Cells for Therapeutic Purposes


Brazilian and American scientists have made induced pluripotent stem cells (iPSCs) from stem cells found in teeth. These adult stem cells are immature enough so that forming iPSCs from that is relatively easy.

Human immature dental pulp stem cells (IDPSCs) are found in dental pulp. Dental pulp is the soft living tissue inside a tooth, and it houses various stem cell populations. These stem cells express a whole cluster of genes normally found in very young and immature cells. Therefore, IDPSCs are “primal” cells that are very young and undifferentiated.

According to Dr. Patricia C.B. Bealtrao-Braga of the National Institute of Science and Technology in Stem and Cell Therapy in Ribeirao Preto, Brazil, human IDPSCs are easily isolated from adult or baby teeth during routine dental visits. IDPSCs are not viewed as foreign by the immune system and can be used in the absence of any drugs that suppress the immune system. They have very valuable cell therapy applications, including the reconstruction of large cranial defects.

Another research project in the Republic of Korea, at the college of Veterinary Medicine, Gyeongsang National University, Republic of Korea have examined a stem cell population from third molars called human dental papilla stem cells (DpaSCs). DpaSCs can form dentin and dental pulp, but they also have biological features that are similar to those of bone marrow-derived mesenchymal stem cells (MSCs).

MSCs have been very heavily studied. While these stem cells have remarkable therapeutic capabilities, they have the disadvantage of only being able to grow in culture or a short period of time. After growing in culture for about a week, MSCs tend to go to sleep and not grow anymore.

DPaSCs, however, have a remarkable capacity to grow in culture. Data from work done in the laboratory of Gyu-Jin Ryo has shown they can grow for a longer period of time than MSCs in culture without going to sleep. Therefore, they not only can form a greater number of progeny, but they can also, potentially, form larger tissues and structures.

Based on their increased culture capabilities, DPaSCs can provide a source of stem cells for tooth regeneration and repair and, possibly, a source of cells for a wide variety of regenerative medical applications.

Drug Developers Increase Their Use of Stem Cells


Industries have increased their use of stem cells in research and development and product testing and the industrial use of stem cells will almost certainly increase in the future.

Despite the image of stem cells in the popular imagination as the stalwarts of regenerative medicine, stem cells have revolutionized drug development and testing. James Thomson, director of regenerative biology at the Morgridge Institute for Research in Madison, Wisconsin, and one of the founders of Cellular Dynamics International, also in Madison, said, “I think there are tremendous parallels to the early days of recombinant DNA in this field. I don’t think people appreciated what a broad-ranging tool recombinant DNA was in the middle ’70s.” Thomson also thinks that people also seriously underestimate the tremendous number of hurdles that must be overcome in order to use such technologies in clinical treatments. Stem cells, according to Thomson, are in a similar situation. While the therapeutic use of these cells might eventually come to fruition, “people underappreciate how broadly enabling a research tool it is.”

About two years ago, drug companies began to investigate the use of stem cells in testing and evaluating new drugs. Today, the pharmaceutical industries all over the world are increasingly using stem cell lines to test drug toxicity and identify and evaluate potential new therapies. For example, Thomson’s company, Cellular Dynamics, sells human heart cells called cardiomyocytes, which are made from induced pluripotent stem (iPS) cells. Thomson says that “essentially all the major pharma companies” have purchased these cells for use in their laboratories. The company also produces brain cells and cells that line blood vessels, and is about to release a line of human liver cells.

Cellular Dynamics is not the only company that makes stem cell lines for drug testing. Three years ago, a stem-cell biologist named Stephen Minger left his job in at a United Kingdom university to be the head of General Electric Healthcare’s push into stem cells. This medical-technology company, which is headquartered in Chalfont St. Giles, UK, has been selling human heart cells made from embryonic stem (ES) cells for well over a year, and is due to start selling ES cell-derived liver cells soon.

Minger’s team at GE Healthcare assessed their ES-derived heart muscle cells in a blind trial against a set of unnamed drug compounds to determine if they could determine which compounds were toxic. Once the tests were completed, Minger said that they found that the cells had been affected by those compounds that are known to be toxic. However, the stem cells also identified a problem that had only been discovered after the drugs had reached the market (after they had been approved by the US Food and Drug Administration). According to Minger, “These are compounds which went all the way through animal testing, then went through phase I, II, III and then were licensed in many cases by the FDA.”

Stem cell lines can do more than identify drugs with dangerous side effects’ they can save the industry millions of dollars in wasted development costs. However, they might also be tools for drug development. Cellular Dynamics and GE Healthcare even market their cells from this very purpose. Adam Rosenthal, senior director for strategic and corporate development at iPierian, a biopharmaceutical company based in San Francisco, California, said, “Many of the animal models out there are poor, demonstrating great efficacy in the mouse, but not repeating in man during late-stage clinical trials. Therefore having an in vitro model years before, which can actually recapitulate human disease, would be a huge advantage.

iPierian has a different strategy than other stem cell companies, since it has its own proprietary in-house stem cell lines that it uses. It does not sell those cell lines, but uses them to develop treatments for neurodegenerative diseases; e.g., Alzheimer’s. This same company has recently announced that they are going to move forward with their development of monoclonal antibodies that target the tau proteins thought to be important in the onset of Alzhiemer’s disease. iPierian made this decision based on information that came from stem-cell work.

Lee Rubin, co-founder of iPierian and director of translational medicine at the Harvard Stem Cell Institute in Cambridge, Massachusetts, says that there is debate within industry if stem cells serve as appropriate model systems to study certain diseases. This is particularly the case with particularly non-genetic or late-onset disorders or conditions that result from pathological interactions between different tissues. Rubin has used stem cells in his research to model a disease called spinal muscular atrophy, which is actually a group of early onset genetic disorders. Rubin makes it clear that the only way to definitively demonstrate that stem cells are a superior model system from drug discovery is to show that the drugs developed from stem cell-based models works in people. Rubin put it this way, “That’s a long-term project. That’s the ultimate test.”

Thomson notes that stem cells will almost certainly find even wider uses than drug-development work. “What human ES cells and iPS cells now do is give you access to the basic building blocks of the human body, just for basic study. We will understand the human body at a much greater detail because of these cells.” How stem cells will be used are not clear, but Thomson added, “But I do think it will profoundly change human medicine.”

The Notch Signaling Pathway


Because stem cell differentiation is controlled by signal transduction pathways, some of my readers have suggested that I discuss particular signal transduction pathways. In the previous post, the Notch signaling pathway was mentioned, and this provides a good reason to introduce my readers to it.

To think of signal transduction, one should consider the popular board game, Mouse Trap. When your game icon lands on the mouse trap spot on the game board, you turn a crank, and this crank rotates a vertical gear that is connected to a gear. Once that gear turns, it pushes lever that is braced with a rubber band until it snaps back and hits a swinging boot. The boot kicks over a bucket, which sends a marble down a rickety staircase. At the bottom of the staircase, the marble enters a chute and eventually taps a vertical pole. At the top of this pole is an open hand (palm-up) that supports another marble. The movement of the pole, caused by the tapping of its base by the first marble knocks the second marble free and it falls through a hole in its platform into a bathtub, and then through a hole in the tub onto one end of a seesaw. The propulsion of the seesaw launches a plastic diver on the other end into a round tub that is on the same base as the barbed pole that supports the mouse cage. The tub’s movement shakes the cage free from the top of the pole and the cage falls to trap the mouse.

This machine that traps the mouse is very similar to signal transduction in cells. The signal to catch the mouse (turning the crank), is far removed from the cage that eventually catches the mouse. Also, the act of catching the mouse (the dropping of the mouse cage), requires the prior execution of many other causally linked steps.

Notch signaling begins with a cell surface protein called Notch. Notch has a large region of the protein outside the cell and a small part of it that intersects the cell membrane, and another region that extends into the cell interior. All three of these domains of the Notch protein play an essential role in the function of Notch.

To turn the crank of this mouse trap, Notch must bind to its receptor. The Notch receptor can be a member of the DSL (Delta, Serrate and Lag-2) gene family.  The receptor is found on the surface of another cell. The binding of Notch to its receptor is the action that “turns the crank” on this mouse trap. Notch binding changes the structure of Notch, and it is clipped into two unequal halves by an enzyme that clips proteins at specific sites (the gamma-secretase). The Notch protein is now broken into a portion that remains anchored in the cell membrane, and another regions that remains inside the cell. This portion of the Notch protein is called “Intracellular Notch” or ICN (Wang MM.Int J Biochem Cell Biol.2011 Nov;43(11):1550-62 & D’Souza B, Miyamoto A, Weinmaster G. Oncogene. 2008 Sep 1;27(38):5148-67).

With the cleavage of Notch, the boot has knocked over the bucket and the marble has moved down the rickety staircase to the chute. ICN is able to enter the cell nucleus. There are proteins in the cytoplasm that can bind to ICN and prevent it from doing so, but we will not discuss them at this time (see van Tetering G, Vooijs M. Curr Mol Med. 2011 Jun;11(4):255-69).

Once in the nucleus, ICN teams up with another protein to activate the express of particular genes. Therefore, what began at the cell surface with the binding of the Notch protein by its receptor had culminated in the changes in gene expression in the nucleus. The other proteins that work together with ICN are members of the “CSL” gene family. CSL stands for “CBF1/RBP-Jκ/Suppressor of Hairless/LAG-1.” When ICN combines with CSL the two proteins are converted from inactive proteins into a complex that actives the synthesis of messenger RNAs for specific genes. This rattles the pole that brings the cage down on the mouse’s head (see Kovall RA. Oncogene. 2008 Sep 1;27(38):5099-109).

What are the target genes of Notch signaling? Great question, but the answer is frustrating, since it depends on the cell type. In developing pancreas, once of the target genes of Notch signaling is PTF1a, but in other cell types and tissues, other genes are activated.

In embryonic stem cells and other stem cells as well, the Notch signaling pathway plays a vital role in the differentiation of these cells into various cell types. Notch signaling is also an important component of the pathology of organ failure in many organs and is also a central pathway involved in the onset and maintenance of several different types of cancers.  Understanding its function and how to regulate it is crucial.

Stem Cell Research Provides New Insights into Insulin Production


Insulin is a protein hormone made by the beta cells of the pancreatic islets. It signals to the liver, skeletal muscles, and fat tissue to take up glucose and store it as glycogen (a polymer of glucose), or to convert it into fat. Insulin also induces the uptake of amino acids by muscles and the liver to form protein. This makes insulin one of the most important anabolic (building) hormones in the body.

Without sufficient quantities of insulin, blood sugar levels soar, since cells do not have the signal to take up sugar. Large quantities of sugar are quite damaging to cells and tissues, and the accumulating damage causes blindness, kidney failure, heart failure, circulatory and peripheral nerve troubles and other ailments.

This pathological condition is known as diabetes mellitus, and treatment of it requires routine injections of insulin. In order to actually treat insulin, we must somehow replace the deleted or damaged beta cells. Stem care cell treatment can potentially do this, but the details are still being worked out.

Danish stem cell scientists have provided some insights into ways to convert stem cells into pancreatic beta cells. By examining pancreatic development in mice, Palle Serup and his research group discovered a new gene called “Mind Bomb-1” that plays a role in pancreatic beta cell formation.

Accord to Dr., Serup, “To get stem cells to develop into insulin-producing beta cells, it is necessary tp know what signaling mechanisms normally control the creation of beta cells during fetal development. This is what our new research results can contribute. When we know the signaling paths, we can copy then in test tubes and thus in time convert stem cells to beta cells.” Dr. Serup is a member of the Danish Stem Cell Center or DanStem at the University of Copenhagen.

In a collaboration with researchers at DanStem, the Danish Hagedorn Research Institute, and other international partners in Japan, Germany, South Korea and the United States, these new findings were published in the April edition of the Proceedings of the National Academy of Sciences.

Previous work has established that during the early hours of the development of the pancreas, a signaling pathway that utilizes the “Notch” protein prevents pancreatic cells from differentiating into endocrine (hormone-making) cells and promotes the continued growth and proliferation of a kind of generic, all-purpose pancreas precursor cell. These all-purpose pancreatic precursor cells are called multipotent progenitor cells or MPCs, and they express two genes: Nkx6-1, and Ptf1.

A bit later, Nkx6 and Ptf1a start to antagonize each other such that cells that express Nkx6 cannot express and Ptf1 and Ptf1-expressing cells cannot express Nkx6. This antagonism between these two genes segregates the developing pancreas into two domains. The bit that is furthest away from the ductal system expresses Ptf1a+ and form “acinar progenitors.” The acinar cells are the clusters that make all the digestive enzymes released by the pancreas the bicarbonate ions. The portion of the developing pancreas that is closet to the ductal system expresses Nkx6-1, and makes the pancreatic duct and β-cell progenitors (see Russ HA, Efrat S. Pediatr Endocrinol Rev. 2011 Dec;9(2):590-7).

This sounds simple, but there are still several gaps that have yet to be filled in. For example, the signals that regulate patterning of the incipient pancreas and cause the segregation of the cells from one end to the other. Also, what dictates the formation of β-cell progenitors as opposed to ductal cells is also presently unknown.

In this present article, Serup and his colleagues discovered that deleting Mind Bomb-1 activity from the developing pancreas preventing the segregation of MPCs into Nkx6-expressing and Ptf1a-expressing cells. Instead the Nkx6-1-expressing cells were replaced by Ptf1-expressing cells. This prevented the formation of beta cells.

Interestingly, Serup and his team found that once the Notch protein acts early during pancreatic development, it actually acts again to help establish the segregated pancreas with Nkx6-1-expressing cells at one end and Ptf1a-expressing cells at the other. This shows that Notch is not only necessary early on, but also later for beta cell formation.

According the Serup, “Our research contributes knowledge about the next step in development and the signaling involved in the communication between cells – an area that has not been extensively described. This new knowledge about the ability of the so-called “Notch” signaling first to inhibit and then to stimulate the creation of hormone-producing cells is crucially important to being able to control stem cells better when working with them in test tubes.”