Human Parthenogenesis: The Virgin Birth

Last night on House, M.D., an interesting medical synopsis was proposed: Human Parthenogenesis, or the virgin birth. I think it may have had something to do with the proximity to Christmas and the legend of the virgin birth. This particular scenario, which is greek for "virgin creation", is an asexual form of reproduction found in females where growth and development of offspring occurs without male involvement. In other words, human parthenogenesis is precisely the phenomenon that is proposed in the bible during the birth of Jesus.

Parthenogenesis occurs naturally in some plants, invertebrates, and vertebrates. Although there have been no known cases of naturally-occurring parthenogenesis in wild mammals, it has been induced in the laboratory in a few circumstances [1,2]. Typically, however, parthenogenesis in mammals results in abnormal development because mammals have "imprinted" genetic regions, where certain genes are expressed that come from either the mother or the father. In other words, mammals possess two copies of their genome, one copy inherited from each parent at fertilisation, but gene expression occurs from only set of genomes [3].

That being said, on June 26th 2007 the International Stem Cell Corporation announced they were intentionally creating human stem cells from unfertilized human eggs using parthenogenesis. On December 18th 2007 this group published an article that stated they had successfully used parthenogenesis to produce human stem cells that are homozygous in the "HLA" region of the DNA [4]. In lay terms, this group successfully developed a parthenogenesis technique that can be used to create embryonic stem cells without the use of embryos, in which the "HLA" region (region containing the information about the Histocompatibility Complex, or cell surface markers that can identify your cells from other cells) is similar to the donor. In this way, tissues grown using their technique are not rejected by donors like other forms of tissue transplantation. It is quite a feat, but by no means is it naturally-occuring human parthenogenesis.

In summary, parthenogenesis is a naturally-occuring phenomenon in many species of plants and animals; however, human parthenogenesis has only been performed in the laboratory, under strict experimental circumstances, and has by no means been used to grow an entire human being.


References

1. Pincus G. and Shapiro H., (1940) Further studies on the parthenogenetic activation of rabbit eggs, Proc US Nat Acad Sci, 26:163-5.

2. Kono T., Obata Y., Wu Q., et al., (2004) Birth of parthenogenetic mice that can develop to adulthood, Nature, 428:860-4.

3. Wilkinson L.S., Davies W., Isles A.R., (2007) Genomic imprinting effects on brain development and function, Nat Rev Neurosci, 8(11):832-43.

4. Revazova E.S., et al., (2008) HLA homozygous stem cell lines derived from human parthenogenetic blastocytes, Cloning and Stem Cells, 10(1):11-24.

Is chronic (long-term) use of the nicotine patch safe?

Some of us that have used the nicotine patch in an attempt to quit smoking wonder if long-term use of the nicotine patch is safe? In other words, is there any long-term side effects that may deter chronic use of the nicotine patch? The results may surprise you (and me).

According to Dr. Lawrence Gibson at the Mayo clinic, long-term use of the nicotine patch isn't known to cause any serious side effects. The most common short-term side effects include mild itching, tingling, or burning on the skin at the site of application. The nicotine in the patch contains none of the toxic compounds found in tobacco smoke, including no tar, carbon monoxide, or carcinogens. Although side effects of nicotine include increased heart rate and blood pressure, these effects occur to a much lesser degree because the amount of nicotine in the bloodstream is much lower (nanograms for the patch vs. milligrams for cigarettes).

In another note, chronic use of transdermal nicotine (the patch) has been shown to improve memory and attentional performance in patients with Alzheimer's disease (1-3) as well as age-associated memory impairment (4).

Although these opinions and studies suggest that long-term nicotine use is relatively safe, it is only in comparison to tobacco smoking. Long-term exposure to nicotine has been shown to increase the risk of vascular disease in laboratory animals, specifically causing a significant increase in aortic endothelial cell death (cells that line the vessels) and causing leaky vasculature (5), as well as causing issues with endothelium-dependent arteriolar dilatation (6). These results suggest that long-term nicotine exposure may cause issues with blood pressure regulation, although they have only been examined in pre-clinical (animal model) circumstances.

So, in summary, long-term nicotine exposure via the patch may cause some vascular issues down the road, but for the most part it is relatively safe and non-carcinogenic.

References:

1. Howe, M. and Price, I. (2001) Effects of transdermal nicotine on learning, memory, verbal fluency, concentration, and general health in a healthy sample at risk for dementia. Int Psychogeriatr 13:465-475.

2. Jones G.M.M., Sahakian B.J., Levy R. Warburton D.M., Gray J.A. (1992) Effects of acute subcutaneous nicotine on attention, information processing and short-term memory in Alzheimer's disease. Psychopharmacology 108:485-494.

3. Newhouse P., Potter A., Kelton M., Corwin J. (2001) Nicotinic treatment of Alzheimer's disease. Biol Psychiatry 49:268-278.

4. White H.K. and Levin E.D. (2004) Chronic transdermal nicotine patch treatment effects on cognitive performance in age-associated memory impairment. 171(4):465-471.

5. Lin S.J., Hong C.Y., Chang M.S., Chiang B.N., Chien S. (1992) Long-term nicotine exposure increases aortic endothelial cell death and enhances transendothelial macromolecular transport in rats. Arterioscler Thromb 12(11):1305-12.

6. Mayhan W.G. and Sharpe G.M. (1999) Chronic exposure to nicotine alters endothelium-dependent arteriolar dilatation: effect of superoxide dismutase. J Appl Physiol 86: 1126-1134.

Famous subject H.M. dies at age 82

Henry G. Molaison, 82, of Windsor Locks, CT died on Tuesday. He is known in the medical and scientific literatures as “the amnesic patient, H.M.” He was born in Manchester, CT and graduated from East Hartford High School. In 1953, he underwent an experimental brain operation at the Hartford Hospital to relieve his seizure disorder. Immediately after the operation, Mr. Molaison showed a profound amnesia, which became the topic of intense scientific study for more than five decades. From age 27 on, he was unable to establish new memories for events in his everyday life and to acquire general information about the world in which he lived. His memory impairment was “pure” and not accompanied by intellectual or personality disorders. For this reason, and because the operation has not been repeated, he is the most widely studied and famous case in the neuroscience literature of the 20th and 21st centuries. Mr. Molaison’s contributions to knowledge about memory have been groundbreaking, and researchers worldwide are in his debt. Burial will be private.

Brief History of HM (from Wikipedia):

HM suffered from intractable epilepsy that has been often—though inconclusively—attributed to a bicycle accident at the age of nine. He suffered from partial seizures for many years, and then several tonic-clonic seizures following his sixteenth birthday. In 1953, HM was referred to William Scoville, a surgeon at Hartford Hospital, for treatment.

Scoville localized HM's epilepsy to his left and right medial temporal lobes (MTLs) and suggested surgical resection of the MTLs as a treatment. On September 1, 1953, Scoville removed parts of HM's MTL on both sides of his brain. HM lost approximately two-thirds of his hippocampus, parahippocampal gyrus, and amygdala. His hippocampus appears entirely nonfunctional because the remaining 2 cm of hippocampal tissue appears atrophic and because the entire entorhinal cortex, which forms the major sensory input to the hippocampus, was destroyed. Some of his anterolateral temporal cortex was also destroyed.

After the surgery he suffered from severe anterograde amnesia: although his working memory and procedural memory were intact, he could not commit new events to long-term memory. According to some scientists (e.g., Schmolck, Kensinger, Corkin, & Squire, 2002), HM is impaired in his ability to form new semantic knowledge but researchers argue over the extent of this impairment. He also suffered moderate retrograde amnesia, and could not remember most events in the 3–4 -day period before surgery, and some events up to 11 years before, meaning that his amnesia was temporally graded. However, his ability to form long-term procedural memories was still intact; thus he could, as an example, learn new motor skills, despite not being able to remember learning them.

The case was first reported in a paper by Scoville and Brenda Milner in 1957.