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PubMed1988

Dietary calcium intake as a mitigating factor in colon cancer.

A population-based case-control study was conducted in Utah to test the hypothesis that calcium decreases the risk of developing colon cancer. A total of 231 cases and 391 controls were identified and interviewed between 1979 and 1982. A quantitative food frequency instrument was used to ascertain individual dietary intake two years prior to diagnosis for the cases and two years prior to interview for the controls. Calcium, calcium per 1,000 calories, and total dairy product consumption were used as indicators of dietary calcium intake. Categories of dietary intake were determined by the distribution of these variables in the control population. A protective effect was observed for males for intake of calcium (odds ratio (OR) = 0.48), calcium per 1,000 calories (OR = 0.35), and total diary products (OR = 0.49). The magnitude of the protective effect from calcium intake increased after adjusting for intake of calories (OR = 0.41), protein (OR = 0.31), and fat (OR = 0.46). Calcium provided less of a protective effect in females, with the odds ratio for calcium being 0.50, 0.55, and 0.56 after adjusting for calories, protein, and fat, respectively. Risk associated with calories, protein, and fat also increased after adjusting for calcium. Of interest is an odds ratio of 5.30 in males for protein after adjusting for calcium. A biologic mechanism is presented to help explain the role of calcium in the development of colon cancer.

Adult↗
PubMed2002

A strong effect of AT mutational bias on amino acid usage in Buchnera is mitigated at high-expression genes.

The advent of full genome sequences provides exceptionally rich data sets to explore molecular and evolutionary mechanisms that shape divergence among and within genomes. In this study, we use multivariate analysis to determine the processes driving genome-wide patterns of amino usage in the obligate endosymbiont Buchnera and its close free-living relative Escherichia coli. In the AT-rich Buchnera genome, the primary source of variation in amino acid usage differentiates high- and low-expression genes. Amino acids of high-expression Buchnera genes are generally less aromatic and use relatively GC-rich codons, suggesting that selection against aromatic amino acids and against amino acids with AT-rich codons is stronger in high-expression genes. Selection to maintain hydrophobic amino acids in integral membrane proteins is a primary factor driving protein evolution in E. coli but is a secondary factor in Buchnera. In E. coli, gene expression is a secondary force driving amino acid usage, and a correlation with tRNA abundance suggests that translational selection contributes to this effect. Although this and previous studies demonstrate that AT mutational bias and genetic drift influence amino acid usage in Buchnera, this genome-wide analysis argues that selection is sufficient to affect the amino acid content of proteins with different expression and hydropathy levels.

Adenine↗
PubMed2005

Chicken embryo extract mitigates growth and morphological changes in a spontaneously immortalized chicken embryo fibroblast cell line.

The SC-1 spontaneously immortalized chicken embryo fibroblast (CEF) cell line has been established recently. Although this cell line had been in culture for over 3 yr, its growth rate has remained lower than that of primary CEF cells, and the morphology has not been as uniform as observed in primary cells. In the present study, the SC-1 cell line was treated with chicken embryo extract (CEE) to determine whether growth rates could be increased and cell morphology enhanced. The CEE also was tested on primary CEF cells, another spontaneously immortalized CEF cell line (DF-1), and on 2 other nonvirally and nonchemically immortalized CEF cell lines (BCEFi and HCEFi). Results indicated that concentrations of CEE > or = 100 microg/mL inhibited growth of all cells tested. However, addition of 50 microg of CEE/mL enhanced the growth rate and improved the morphology of the SC-1 cells. Addition of CEE to the other immortal or primary CEF cells did not increase the growth rate or change their morphology. Analysis of mRNA expression revealed that SC-1 cells treated with 50 microg of CEE/mL had lower levels of the p16(INK4a) alternate reading frame sequence (ARF) and E2F-1 than untreated SC-1 cells. The increased growth rate and improved morphology of the SC-1 cells achieved with CEE treatment were retained following removal of CEE, and these improvements should aid in increasing the utility of the SC-1 cell line as a cellular/molecular reagent.

Animals↗
PubMed2006

Mitigation of effects of extreme drought during stage III of peach fruit development by summer pruning and fruit thinning.

A water deficit during stage III of fruit growth was established with the aim of determining if it is possible to achieve an improvement in tree water status by summer pruning and fruit thinning. The experiment was set up as a randomized block split-plot design across trials (irrigation) where pruning was assigned to the main plot and fruit thinning to the sub-plots. The irrigation treatments were (1) standard full irrigation (FI), and (2) suppression of irrigation during stage III of fruit growth until leaves visibly withered (LWI); the pruning treatments were (1) experimental summer pruning (EP), and (2) standard summer pruning (CP); and three fruit thinning intensities were applied to facilitate analysis of the effects of the treatments in relation to fruit load. Changes in amount of light intercepted and in tree stem water potential (Psi stem) were evaluated. The EP treatment reduced the amount of light intercepted by the tree. In the FI treatment, there was a significant reduction in fruit growth measured as both water accumulation and dry mass accumulation. Under FI conditions, reductions in fruit load as a result of EP were not accompanied by a significant improvement in Psi stem. In the LWI treatment, EP produced a significant improvement of 0.17 MPa in Psi stem, but there was no improvement in fruit growth compared with CP trees. A reduction in fruit load from 350 (commercial load) to 150 per tree significantly improved Psi stem by 0.3 MPa at the end of stage III of fruit growth. These results indicate that improvements in water status in response to pruning may be insufficient to promote fruit growth if the pruned trees are unable to provide an adequate supply of assimilates to the developing fruits.

Disasters↗
PubMed1989

Increased hematocrit mitigates ischemic renal damage in the splenectomized dog.

Splenectomy (SPLX) prevents ischemic acute tubular necrosis (ATN) and peritubular capillary (PTC) congestion. This study attempts to reverse the protective effect of splenectomy in the ischemic model of ATN by increasing hematocrit before inducing ATN. Sham-SPLX, SPLX, and SPLX dogs given packed red cells to elevate hematocrit by 30% (SPLX-high hematocrit) received bilateral renal artery obstruction (RAO) for 120 minutes. Renal function was tested for 6 days post-RAO. Hematocrit in the SPLX-high hematocrit group was greater (p less than .05) than the SPLX-RAO group but did not differ from the non-SPLX group. All groups had different (p less than .05) serum creatinine levels for 48 hours post-RAO, and untreated animals differed from all the others at 144 hours. Serum creatinine was highest in untreated, lowest in SPLX-high hematocrit, and intermediate in noninfused SPLX animals. The same pattern was observed in blood urea nitrogen, creatinine clearance and renal histopathology. Fractional excretion of sodium in the SPLX groups was six times that in the intact animals (p less than .05), irrespective of hematocrit level. We conclude that increased hematocrit is protective in ischemic ATN, and does not promote PTC congestion or ATN in the SPLX animal. In addition, the protective effect of splenectomy may be mediated, in part, by mechanism(s) that alter sodium transport or osmolar excretion.

Acute Kidney Injury↗
PubMed1999

Ineffectiveness of burst suppression therapy in mitigating perioperative cerebrovascular dysfunction. Multicenter Study of Perioperative Ischemia (McSPI) Research Group.

BACKGROUND: Cerebral injury is among the most common and disabling complications of open heart surgery. Attempts to provide neuroprotection have yielded conflicting results. We assessed the potential of propofol-induced burst suppression during open heart surgery to provide cerebral protection as determined by postoperative neuropsychologic function. METHODS: Two hundred twenty-five patients undergoing valve surgery were randomized to receive either sufentanil or sufentanil plus propofol titrated to electroencephalographic burst suppression. Blinded investigators performed neurologic and neuropsychologic testing at baseline, postoperative day (POD) 1 (neurologic testing only), PODs 5-7, and PODs 50-70. Neuropsychologic tests were compared with the results of 40 nonsurgical patients matched for age and education. RESULTS: Electroencephalographic burst suppression was successfully achieved in all 109 propofol patients. However, these patients sustained at least as many adverse neurologic outcomes as the 116 controls: POD 1, 40% versus 25%, P = 0.06; PODs 5-7, -18% versus 8%, P = 0.07; PODs 50-70, -6% versus 6%, P = 0.80. No differences in the incidence of neuropsychologic deficits were detected, with 91% of the propofol patients versus 92% of the control patients being impaired at PODs 5-7, decreasing to 52 and 47%, respectively, by PODs 50-70. No significant differences in the severity of neuropsychologic dysfunction, depression, or anxiety were noted. CONCLUSIONS: Electroencephalographic burst suppression surgery with propofol during cardiac valve replacement did not significantly reduce the incidence or severity of neurologic or neuropsychologic dysfunction. The authors' results suggest that neither cerebral metabolic suppression nor reduction in cerebral blood flow reliably provide neuroprotection during open heart surgery. Other therapeutic approaches must be evaluated to address this important medical problem.

Adult↗
PubMed1996

Radon mitigation at Birch Cliff Public School.

In 1991, Canadian Institute for Radiation Safety (CAIRS) conducted a radon screening program in all Metropolitan Toronto public schools. Birch Cliff Public School had a radon progeny level higher than the action level of 4.16 x 10(-7) Jm-3 (20 mWL). Follow-up radon testing was carried out at the school. Locations on the ground floor and in the basement were tested. All locations on the ground floor had radon progeny levels below the action level. Six locations in the basement had readings above the action level. All cracks and openings in the basement were sealed and a new heating/ventilating (HV) system for the basement was designed and installed. Then, the basement was tested again. Radon progeny levels are now well below the action level with an average of 7.43 x 10(-8) Jm-3 (3.57 mWL). This is about one fifth of the average radon progeny level found in the first stage of follow-up testing.

Air Pollutants, Radioactive↗
PubMed2004

Mobile phones in the hospital: improved mobile communication and mitigation of EMI concerns can lead to an overall benefit to healthcare.

There is a growing trend in hospitals throughout the world to incorporate mobile phones and other wireless technology to offer more efficient, cost effective, and higher quality healthcare. Misunderstanding of mobile phone systems, electromagnetic interference with medical devices, and available management solutions, however, has led to a wide range of inconsistent hospital policies. Recent reviews and commentaries on the subject have provided inconsistent and in some cases factually incorrect information that confuses the issue. At one extreme, unmanaged use of mobile phones in areas where life-critical medical devices are in operation can result in atypical situations that may place patients at risk. At the other extreme, overly-restrictive policies based upon speculation may deny benefits by acting as an obstacle to technology. Overly-restrictive policies may also not address growing and legitimate communication needs of patients and visitors in times of crisis. While it may not be feasible for hospitals to manage every mobile phone handset that is randomly brought into their facility without certain limits on use in areas where life-critical devices are commonly in operation, restrictions are not usually necessary throughout the entire facility. Restrictive policies are also better facilitated when easily accessible areas are designated where mobile phone use is encouraged. Controlled mobile phone systems for use by doctors and staff for hospital-specific communication, by contrast, can operate compatibly throughout the entire hospital facility with appropriate system design and management, even in sensitive areas, and such systems have already been deployed in a number of hospitals throughout the U.S.

Cell Phone↗
PubMed1998

Adenosine endogenously released during early reperfusion mitigates postischemic myocardial dysfunction by inhibiting platelet adhesion.

The purpose of this study was to investigate platelet effects on postischemic heart function in conjunction with adenosine effects on intracoronary platelet adhesion. Homologous platelets were infused into the coronaries of isolated guinea pig hearts, either during low-flow ischemia or during reperfusion, and external heart work (EHW) and intracoronary platelet adhesion were determined. In most experiments, thrombin was added to the perfusate. The influence of endogenous adenosine was studied by use of the uptake blocker dipyridamole and the unspecific adenosine-receptor blocker theophylline, the A1-receptor blocker 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), and the A2-receptor blocker 3,7-dimethyl-1-propargylxanthine (DMPX). The importance of nitric oxide and prostaglandin I2 (PGI2) was tested by using nitro-L-arginine (NOLAG) and indomethacin, respectively. When platelets were applied with thrombin during low-flow ischemia, EHW recovered to only 63 +/- 4% of the preischemic value, as compared with 89 +/- 3% without platelets (p < 0.05). Despite thrombin, platelets incurred no significant functional loss when applied in the first minute of reperfusion (but again in the fifth minute); however, when theophylline was also present, recovery of EHW amounted to only 42 +/- 12%. Intracoronary adhesion of platelets was negligible without thrombin, and highest during low-flow ischemia with thrombin (35 +/- 3% of the applied number). No adhesion occurred during the first minute of reperfusion, whereas in the fifth minute, adhesion was again 20.8 +/- 4%. Dipyridamole increased adenosine release and attenuated adhesion at this time. Theophylline increased adhesion in the first minute of reperfusion (33 +/- 6.4%), whereas NOLAG and indomethacin proved to be ineffective. DPCPX and DMPX each increased platelet retention during the first minute of reperfusion, their effects being additive. Intracoronary adhesion of platelets induced by thrombin in isolated hearts can reduce postischemic recovery of heart function. During reperfusion, but not during low-flow, endogenous adenosine can prevent platelet adhesion and loss of myocardial function, an action mediated both by A1- and A2-receptor-dependent mechanisms.

Adenosine↗
PubMed1999

Pathogenesis and pharmacological strategies for mitigating secondary damage in acute spinal cord injury.

OBJECTIVE: Experimental models and clinical observations of acute spinal cord injury (SCI) support the concepts of primary and secondary injury, in which the initial mechanical insult is succeeded by a series of deleterious events that promote progressive tissue damage and ischemia. Whereas the primary injury is fated by the circumstances of the trauma, the outcome of the secondary injury may be amenable to therapeutic modulation. This article reviews the pathogenetic determinants of these two phases of injury and summarizes the pharmacological manipulations that may restore neurological function after SCI. METHODS: Experimental models of SCI and their inherent limitations in simulating human SCI are surveyed. The pathogenesis of primary and secondary injury, as well as the theoretical bases of neurological recovery, are examined in detail. The effects of glucocorticoids, lazeroids, gangliosides, opiate antagonists, calcium channel blockers, glutamate receptor antagonists, antioxidants, free radical scavengers, and other pharmacological agents in both animal models and human trials are summarized. Practical limitations to inducing neural regeneration are also addressed. RESULTS: The molecular events that mediate the pathogenesis of SCI are logical targets for pharmacological manipulation and include glutamate accumulation, aberrant calcium fluxes, free radical formation, lipid peroxidation, and generation of arachidonic acid metabolites. Enhancement of neural regeneration and plasticity comprise other possible strategies. CONCLUSION: Pharmacological agents must be given within a narrow window of opportunity to be effective. Although many therapeutic agents show potential promise in animal models, only methylprednisolone has been shown in large, randomized, double-blinded human studies to enhance the functional recovery of neural elements after acute SCI. Future therapy is likely to involve various combinations of these agents.

Acute Disease↗