SARAH MORLOCKE - FILE#072303-0008 [22:57:04]
Subject shows extremely rapid and uncontrolled ossification of skeletal frame. The body produces 'flares' and 'flanges' of dense spun bone material, which is extruded from existing bones and pushed through the flesh to be discarded. Samples show much higher levels of calcium phosphorous and trace minerals evident in extruded samples than normally found in the human body.
Investigation of chondrocyte metabolism, which forms part of the complex spatial organization of the growth plate, is essential for identifying and manipulating the pathways of normal and abnormal development of bone. The effects of chemical signals, cytokines, systemic hormones and growth factors on cell proliferation and differentiation were studied. Tools such as cell lines stably expressing hormone receptors have been developed. Chondrocytes in situ may deviate from their original state of differentiation therefore a set of markers of differentiation, including cell morphology, specific matrix protein synthesis and enzyme activities has been defined. Specific mutations in growth factor receptors which cause abnormal chondrocyte differentiation have been evaluated. In addition, involvement of various hormones and their receptors in the aetiology of the mutation have been studied. All of these studies intended to elucidate the normal growth plate development.
Calcification of bone is a complex process in which a calcium-phosphate mineral phase is deposited in a highly ordered fashion within the organic matrix. Apart from the availability of calcium and phosphorus, requirements for normal mineralization include: 1) adequate metabolic and transport function of chondrocytes and osteoblasts to regulate the concentration of calcium phosphorus and other ions at the calcification sites; 2) the presence of collagen with unique type, number and distribution of cross-links, distinct patterns of hydroxylation and glycosylation and abundant phosphate content, which collective facilitate deposition of mineral at gaps (or "hole zones") between the distal ends of collagen molecules; 3) a low concentration of mineralization inhibitors (such as pyrophosphates and proteoglycans) in bone matrix; and 4) maintenance of an appropriate pH of approximately 7.6 for deposition of calcium-phosphorus complexes.
The abnormal mineralization in the hypophosphatemic disorders, is due most likely to phosphopenia at calcification sites and, in some cases, paracrine inhibitory factors, which result in accumulation of unmineralized osteoid, a sine qua non for the diagnosis of osteomalacia. Since the resultant abundant osteoid is not unique, however, establishing the diagnosis of osteomalacia histopathologically requires demonstration that abnormal mineralization, and not increased production, underlies the pathological abnormality. Concordance of these events is manifest by an increase in the bone forming surface covered by incompletely mineralized osteoid, an increase in osteoid volume and thickness and a decrease in the mineralization front (the percentage of osteoid-covered bone-forming surface undergoing calcification) or the mineral apposition rate.
The inadequate cartilage mineralization in rickets is confined to the maturation zone of cartilage wherein the height of the cell columns is increased and the cells are closely packed and irregularly aligned. Moreover, calcification in the interstitial regions of this hypertrophic zone is defective. These changes result in increased thickness of the epiphyseal plate, accompanied by an increase in transverse diameter that often extends beyond the ends of the bone and causes characteristic cupping or flaring. Longitudinal bone growth, which determines the size and shape of the body frame, proceeds at a rate distinct from those of muscle and other tissues and is controlled by specific mechanisms. The epiphyseal growth plate of the long bones is of utmost importance in the process of bone elongation and growth. From the practical viewpoint, irregular metabolism in the growth plate area is associated with dwarfism and tibial dyschondroplasia. The traditional approach has not so far resulted in feasible protocols to reduce the occurrence of abnormal bone growth substantially.
Given the random nature of the extruded growths, it is noted that the subject has not yet suffered anything greater than superficial injury from her growths. Considering that the bones do not follow any specific pattern, a rudimentary or unconscious control of the growth must be existent to prevent such an incidence. Subject also shows no kidney or liver damage, which would be consistent with the advanced ossification and reabsorption of the calcium phosphates. This indicates that all mineral absorption returns to the development of new bones. Subject also displays a rapid or quantum healing rate, which prevents permanent tissue and nerve damage from bone extraction.
TREATMENTS - DISCARDED
CHEMICAL INHIBITERS OF OSSIFICATION: Using a combination of drugs, we can inhibit the growth of bones tissue by a factor of two or three. Leeching out the needed mineral components and directly interfering with the growth triggers in the subject's system. The disadvantages are that there is no telling what reaction the X factor would have on the system, with a danger of internal damage.
BONE SHEATHING: By artificially sheathing the skeletal frame with nanite bundles, we can absorb the excess minerals and retard all bone growth beyond a programmed limit. Nano-bundles would be converters, changing over minerals into bio-energy needed to sustain limits. Of course, this would require extensive surgery to implant control centres on the skeletal frame, and would eliminate the possibility of the subject ever using mutation on any level.
TREATMENT - IN TRIAL
LIMITED NANO-GROWTH INHIBITERS: We can implant a control chip in the spinal column that will serve as an internal monitor of the skeletal integrity. Using the data, we can selectively choose which growths to encourage to grow by placing bioterminal nanopackets into the area and terminating growths in unwanted areas. The resulting increased material would allow for faster and more directed ossification, leading to shorter withdrawal times. The packets would be absorbed into the body and broken down as their limited power expires. The treatment offers no real negatives, save for time requirements that would be inherent in monitoring and packet injection.