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Deceleration of carcinogenic potential by adaptation with low dose gamma irradiation.

Animals that have been exposed to a very low dose of radiation are known to have many physiological benefits. Very low dose of ionizing radiation also induces mechanisms whereby cell or tissue become better fit to cope with subsequent exposures of high doses. This phenomenon of low dose radiation is termed 'adaptive response'. This response has been reported to be true in many biological systems and confirmed by experiments on chromosomal and chromatid aberrations, micronucleus formation, sister chromatid exchange tests, DNA mutation and cell survival study and using many other biological end points, although there are quite a few exceptions. The adaptation induced by low doses of radiation has been attributed to the induction of an efficient chromosome break repair mechanism at molecular and biochemical level. It is also substantiated in whole animal systems. When mice are initially conditioned with very small adapting doses, incidence of a challenging dose induced thymic lymphoma is recorded, with delayed latency and reduced frequency. Similarly, appearance of a transplanted barcl-95 thymic tumor has been delayed when mice are preconditioned with a small dose of radiation. Appearance and development of a tumour following transplantation of in vitro irradiated barcl-95 tumour cells with a small dose of 1 cGy are also delayed and volume of the tumour is reduced. Latency period of radiation-induced leukemia is modified by prior treatment with an adapting dose of radiation. Neoplastic transformation of several human cultured cells is also significantly decreased by prior low dose exposure of radiation compared to non-exposed cells. These results indicate that an earlier exposure to a small dose of radiation also reduces the radiation-induced carcinogenesis. Various aspects of molecular mechanism underlying the radio-adaptation have been explained. However, the mechanism underlying the inhibition of carcinogenesis by low dose radiation is yet to be fully resolved.

Adaptation, Physiological↗

Deceleration energy and change in velocity on impact: key factors in fatal versus potentially survivable motor vehicle crash (mvc) aortic injuries (AI): the role of associated injuries as determinants of outcome.

OBJECTIVE: To examine the difference in force mechanisms between fatal and potentially survivable MVC aortic injuries (AI) compared to non-AI severe thoracic injuries (ST). METHODS: Of 324 autopsied MVC driver or front seat passenger fatalities (1997-2000), there were 43 fatal AI (36 scene deaths, 7 hospital deaths) and 5 additional AI survivors. RESULTS: Of the 48 AI, there was only a 42% survival for those reaching hospital alive. 80% of AI survivors had isthmus lesions and all had no or minimal brain injury (GCS >= 13), no cardiac injury and only 20% ribs 1-4 fx or shock; of AI non-survivors reaching hospital alive, 67% had GCS <= 12, 50% cardiac injury, 83% ribs 1-4 fx and 83% shock; AI scene deaths had 78% severe brain injury, 56% cardiac injury, 69% lung injury and 78% ribs 1-4 fx. Quantifying forces in AI scene mortality: the Instantaneous Velocity on Impact of the subject vehicle (delta V1) and the Impact Energy Dissipated (IE) on the subject vehicle (V1) in joules demonstrated a linear regression in fatal car MVC AIs: Energy dissipated (joules) = -56.65 x (delta V1)(2) + 15972 x delta V1 - 454661, r(2) = 0.83. However, for 27 patients with non-AI but severe thoracic (ST) injury (AIS>=3), the relationship of IE to delta V1 had a linear regression of Energy dissipated (joules) = -5.0787 x (delta V1)(2) + 4282.1 x delta V1 - 57182 1, r(2) = 0.84, with the slope difference between the regression for AI scene deaths and that of ST and AI survivors being significant (p<0.05). Based on these relationships, a Critical Zone limited by MVC Impact Energy level of 336000 joules and a delta V1 of 64 kph appears to be the limit of potential survivability in MVCs producing aortic injuries. All AI above these thresholds died. In contrast, ST had greater use of seatbelts (AI 10% vs all ST 60%) and airbags (AI 50% vs all ST 72%), and an 83% survival. CONCLUSION: The data suggest different mechanisms of force delivery and injury patterns in fatal vs potentially survivable AI, and vs ST MVCs. They suggest that an approach to improving vehicle safety measures for AI may involve better safety devices and mechanisms for reducing that fraction of Impact Energy dissipated on V1 for a given delta V1 which is focused on the upper portion of the subject's thoracic cage between the levels of ribs1-8.

Acceleration↗

Saline amnioinfusion for relief of variable decelerations.

Fetal distress due to oligohydramnios can be treated with saline amnioinfusion. The technique is easily learned by physicians who know how to use intrauterine pressure catheters. Therapeutic and prophylactic indications for saline amnioinfusion include oligohydramnios, thick meconium-stained amniotic fluid, and fetal distress. Family physicians can use this new procedure to actively manage labor.

Adult↗