Author: Dr Anayo Unachukwu, MBBS, LLM
Man is a net product of biology and society. His biology is pretty primordial and sluggish to changes hence he struggles with optimal adaptation to his dynamic environment. It is unsurprising that he is constantly behind the curve, given the epochal changes that are attendant to post modernism. Post modernism has largely informed a parallel discourse to that which exists within public and private institutions and bodies. This discourse has gained increased traction in the 20th and 21st century, given the haemorrhage of trust from professional relationships. As O’ Neil aptly puts it, ‘loss of trust’ is in short, a cliché of our times.[1] The public outcry that attended this breach of trust has led to several layers of professional regulations, inspections of private and public institutions; and latterly the low level of tolerance of risk in more affluent societies. However Maynard opines that the attraction of trust as the determinant of human exchange is that it is potentially more cost-effective than the alternative.[2]
With the advent of information age, the already fragile relationship between the public on one hand and professional bodies and institutions on the other has seen further entropy and perturbation. This level of instability in the relationship was largely informed by marked reduction in information asymmetry that hitherto existed in professional relationships. The nature of these relationships is now undermined by concerns about their efficiency and the consequent need for external performance management.[3] Doctor/patient relationship is unique because of the element of information asymmetry.[4] Not anymore, the public believes that, given the reduced information asymmetry, doctors no longer know the best. The net effect is a further distrust and uncertainty about the intentions of public and private bodies on matters affecting the greater good of the society.
It is within this backdrop that most scientific debates are conducted in the media. The sceptre of scepticism is brought to the fore by the public in navigating very complex debate. This is unsurprising, given that prehistoric man has always been adept in heuristic pursuits as rough and ready guides in making sense of it all when challenged with novel situation.
The debate on Cannabis (Marijuana)-is controversial, but unsurprising, given the heat rather than light it generates-has remained greatly polarising. Like wars, the first casualty is truth. Given Cannabis chequered history, an honest scientific discourse would hardly make the rounds due to the frontloaded emotions integral to the debate. Man being a product of sluggish biology and environment will recourse to heuristic generalisations where nuanced debate is called for.
Most clinicians in mental health-who have seen lives blighted by early childhood exposure to cannabis-are most appalled, given the way the debate on Cannabis is conducted.
Cannabis has over 70 different cannabinoid chemicals[5]. The most active being Δ 9-Tetrahydrocannabinol.This very particular chemical is largely responsible for most of the cognitive[6], emotional and psychomotor impairments associated with the use of the drug.
To further compound the discourse on Cannabis, is the difficulty in predicting with any reasonable degree of accuracy as regards to who will develop mental illness with early exposure to Cannabis in childhood. Given the paucity of scientific knowledge on this, scientific community could only resort to heuristic speculation based on epidemiological data-demographics. However, this issue is more complex, given that genetics and heredity are not in the habit of playing according to linear rules.
It is pertinent to note that a counterpoint to Δ 9-Tetrahydrocannabinol is another active chemical Cannabidiol (CBD) has anxiolytic[7] and possibly antipsychotic[8] properties. However, it is difficult to know the precise ratio of these two active ingredients in Cannabis couriered and consumed on the street.
I am not for a moment advocating that the drug war as we know it-started by Richard Nixon-is the way forward. There should be an honest debate across both opposing aisles on a practical and pragmatic solution to protect the vulnerable in our society. Was it not Ghandhi that said that you can’t shake hands with clenched fists?
[1] O’ Neil O. A question of Trust BBC Reith Lectures 2002. Cambridge: CambridgeUniversity Press, 2002.
[2] Maynard A., Bloor K. Trust and performance management in the medical marketplace; Journal of The Royal Society of Medicine vol. 96 November 2003.
[3] Ibid.
[4] Not anymore, cf Scitovsky T. The benefits of asymmetry markets. J Econ Perspect 1990; 4 135-48. He notes that this is beneficial and it is a by-product of specialisation.
[5] Celia JA Morgan et al (2010). Cannabidiol Attenuates the Appetitive Effects of Δ 9-Tetrahydrocannabinol in Human Smoking Their Chosen Cannabis, Neuropsychopharmacology, 1879-1885.
[6] D’ Souza et al (2004). The psychomimetic effects of intravenous Δ 9-Tetrahydrocannabinol in healthy individuals: implication for psychosis. Neuropsychopharmacology 29: 1558-1572.
[7] Crippa JA et al (2004). Effects of cannabidiol (CBD) on regional cerebral blood flow, Neuropsychopharmacology 29: 417-429.
[8] Zaurdi AW et al (2006). Cannabidiol monotherapy for treatment-resistant schizophrenia. J Psychopharmacol 20: 683-686.
PUT IT IN CONTEXT OF CANCER CELL MOVEMENT
The contraction of skeletal muscle is triggered by nerve impulses, which stimulate the release of Ca2+ from the sarcoplasmic reticuluma specialized network of internal membranes, similar to the endoplasmic reticulum, that stores high concentrations of Ca2+ ions. The release of Ca2+ from the sarcoplasmic reticulum increases the concentration of Ca2+ in the cytosol from approximately 10-7 to 10-5 M. The increased Ca2+ concentration signals muscle contraction via the action of two accessory proteins bound to the actin filaments: tropomyosin and troponin (Figure 11.25). Tropomyosin is a fibrous protein that binds lengthwise along the groove of actin filaments. In striated muscle, each tropomyosin molecule is bound to troponin, which is a complex of three polypeptides: troponin C (Ca2+-binding), troponin I (inhibitory), and troponin T (tropomyosin-binding). When the concentration of Ca2+ is low, the complex of the troponins with tropomyosin blocks the interaction of actin and myosin, so the muscle does not contract. At high concentrations, Ca2+ binding to troponin C shifts the position of the complex, relieving this inhibition and allowing contraction to proceed.
Figure 11.25
Association of tropomyosin and troponins with actin filaments. (A) Tropomyosin binds lengthwise along actin filaments and, in striated muscle, is associated with a complex of three troponins: troponin I (TnI), troponin C (TnC), and troponin T (TnT). In (more ) Contractile Assemblies of Actin and Myosin in Nonmuscle Cells
Contractile assemblies of actin and myosin, resembling small-scale versions of muscle fibers, are present also in nonmuscle cells. As in muscle, the actin filaments in these contractile assemblies are interdigitated with bipolar filaments of myosin II, consisting of 15 to 20 myosin II molecules, which produce contraction by sliding the actin filaments relative to one another (Figure 11.26). The actin filaments in contractile bundles in nonmuscle cells are also associated with tropomyosin, which facilitates their interaction with myosin II, probably by competing with filamin for binding sites on actin.
Figure 11.26
Contractile assemblies in nonmuscle cells. Bipolar filaments of myosin II produce contraction by sliding actin filaments in opposite directions. Two examples of contractile assemblies in nonmuscle cells, stress fibers and adhesion belts, were discussed earlier with respect to attachment of the actin cytoskeleton to regions of cell-substrate and cell-cell contacts (see Figures 11.13 and 11.14). The contraction of stress fibers produces tension across the cell, allowing the cell to pull on a substrate (e.g., the extracellular matrix) to which it is anchored. The contraction of adhesion belts alters the shape of epithelial cell sheets: a process that is particularly important during embryonic development, when sheets of epithelial cells fold into structures such as tubes.
The most dramatic example of actin-myosin contraction in nonmuscle cells, however, is provided by cytokinesisthe division of a cell into two following mitosis (Figure 11.27). Toward the end of mitosis in animal cells, a contractile ring consisting of actin filaments and myosin II assembles just underneath the plasma membrane. Its contraction pulls the plasma membrane progressively inward, constricting the center of the cell and pinching it in two. Interestingly, the thickness of the contractile ring remains constant as it contracts, implying that actin filaments disassemble as contraction proceeds. The ring then disperses completely following cell division.
Figure 11.27
Cytokinesis. Following completion of mitosis (nuclear division), a contractile ring consisting of actin filaments and myosin II divides the cell in two.
http://www.ncbi.nlm.nih.gov/books/NBK9961/
This is good. I don’t recall seeing it in the original comment. I am very aware of the actin myosin troponin connection in heart and in skeletal muscle, and I did know about the nonmuscle work. I won’t deal with it now, and I have been working with Aviral now online for 2 hours.
I have had a considerable background from way back in atomic orbital theory, physical chemistry, organic chemistry, and the equilibrium necessary for cations and anions. Despite the calcium role in contraction, I would not discount hypomagnesemia in having a disease role because of the intracellular-extracellular connection. The description you pasted reminds me also of a lecture given a few years ago by the Nobel Laureate that year on the mechanism of cell division.