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An eight-year study report on arsenic contamination in groundwater and health effects in Eruani village, Bangladesh and an approach for its mitigation.

Based on several surveys during 1997-2005 and visits of a medical team to Eruani village, Laksham upazila, Comilla district, Bangladesh, the arsenic contamination situation and consequent clinical manifestations of arsenicosis among the villagers, including dermatology, neuropathy, and obstetric outcome, are reported here. Analysis of biological samples from patients and non-patients showed high body burden of arsenic. Even after eight years of known exposure, village children were still drinking arsenic-contaminated water, and many of them had arsenical skin lesions. There were social problems due to the symptoms of arsenicosis. The last survey established that there is a lack of proper awareness among villagers about different aspects of arsenic toxicity. The viability of different options of safe water, such as dugwells, deep tubewells, rainwater harvesting, and surface water with watershed management in the village, was studied. Finally, based on 19 years of field experience, it was felt that, for any successful mitigation programme, emphasis should be given to creating awareness among villagers about the arsenic problem, role of arsenic-free water, better nutrition from local fruits and vegetables, and, above all, active participation of women along with others in the struggle against the arsenic menace.

Adult↗

Repetitive pulsed-train "off" duration mitigates reductions in root growth rates of Pisum sativum L. induced by 60-Hz electric field.

An investigation was undertaken to define a 60-Hz electric field exposure system which would affect a eukaryotic cell system while mitigating a potential thermal rise. The biological effectiveness of pulsed 60-Hz electric fields on a cell system of defined sensitivity to continuous-wave 60-Hz electric fields was sought. Roots of garden pea (Pisum sativum L.) were exposed to pulsed trains of 60-Hz, 430 V/m electric fields. The "on" time was constant at 1 s and the "off" time varied. The repetitive on:off regimens used were 1:20, 1:50, 1:100, 1:130, 1:200, and 1:300. With continuous or 1:20 pulsed fields the growth response was equivalent (representing a 60% depression in root growth rate). The severity of the growth effect diminished as the off time increased; for the 1:100 regimen, the relative growth rate was depressed by about 30%; for the 1:300 regimen, the relative growth rate was equal to that of the controls.

Electromagnetic Fields↗

Mitigation of cretinism by breast-feeding.

An athyrotic infant had hypothyroidism at 1 year of age. He had grown at an above-average velocity until age 10 months when breast-feeding was discontinued, yet his bone age remained that of a newborn. These observations suggested that breast-feeding had attenuated hypothyroidism by providing significant quantities of thyroid hormones in the milk. To test this hypothesis, thyroxine (T4), 3,5,3'-triiodothyronine (T3), and 3,3,5'-triodothyronine (reverse T3) were measured in breast milk samples collected serially from three months before to four months after delivery. Mean breast milk T4 content fell from 1.4 to 0.7 microgram/dl within 48 hours after delivery, while T3 content rose from 136 to 286 ng/dl. Reverse T3 content remained unchanged. The shift in the T4/T3 ratio after delivery was observed in samples of all five donors; the highest postpartum T4 level was 1.1 microgram/dl and the highest postpartum T3 level was 405 ng/dl. It is concluded that breast-feeding may deliver sufficient thyroid hormones to the athyrotic infant to mitigate severe hypothyroidism and to prevent impaired neurological development.

Breast Feeding↗

[Mitigated neurogenic bladder (author's transl)].

The mitigated neurogenic bladder is gaining increasing significance in the investigation of children suffering from recurrent therapy-resistant infection of the urinary tract or enuresis. It is found in 33 to 48% of these cases and refers to isolated functional disorders of the bladder, which do not correspond to any neurological pattern. Morphological changes, if found, only occur as a result of functional changes. The functional correlations, diagnosis and therapy are discussed together with the description of 3 cases.

Adolescent↗

Approaches that mitigate doxorubicin-induced delayed adverse effects on mitochondrial function in rat hearts; liposome-encapsulated doxorubicin or combination therapy with antioxidant.

This experiment was designed to evaluate whether or not liposomal encapsulated-doxorubicin and combination therapy of free doxorubicin with coenzyme Q10, an antioxidant, mitigate the delayed adverse effects on cardiac muscle mitochondria. Rats aged 7 weeks were divided into the following four groups; rats were injected with doxorubicin or liposomal encapsulated-doxorubicin, total dose 15 mg/kg. The doxorubicin group consisted of two subgroups depending on diet, i.e., standard diet or 0.2% coenzyme Q10 diet. Mitochondria from cardiac muscles were prepared from rats aged 13 and 35 weeks. No significant decrease in the activity of complex I of the mitochondrial electron transport chain was observed in rats aged 13 weeks among the groups, however, significant decreases in the activity in rats aged 35 weeks were observed in the doxorubicin and liposomal doxorubicin groups compared with the corresponding control rats. In contrast, no significant change in complex I activity was observed in rats fed with coenzyme Q10 diet irrespective of doxorubicin treatment. From these results, not liposomal encapsulation of doxorubicin but combination therapy with antioxidant might be expected to reduce the delayed adverse effects of doxorubicin on heart mitochondria.

Animals↗

Does additional treatment with fish oil mitigate the side effects of recombinant human erythropoietin in dialysis patients?

Since fish oil has been reported to reduce platelet aggregability, to reduce blood viscosity by increasing red blood cell deformability and to lower blood pressure, we studied the effect of dietary supplementation with fish oil on the occurrence of adverse effects in patients receiving recombinant human erythropoietin (rHuEPO). In a prospective, randomized, double blind cross-over design we studied the effect of daily ingestion of 3 g fish oil versus 3 g corn oil (placebo) for 5 months, with a wash-out period of 3 months in between. Thirty-two dialysis patients newly treated with rHuEPO participated. rHuEP0 was given using a low and slow dose regimen (25 U/kg twice weekly s.c.). Target Hct was 35%. Blood pressure, red blood cell deformability, plasma viscosity, fatty acid composition of plasma phospholipids, and fibrinogen levels were measured at 0, 5, 8 and 13 months. In both groups a stable target Hct (35%) was reached within 3 months. Blood pressure was not significantly different between the groups at any time point. In 4 patients (2 on fish oil and 2 on placebo) antihypertensives had to be increased to regulate blood pressure adequately, whereas shunt occlusion occurred in one patient on placebo. Despite a significant increase in the omega-3 fatty acid content of plasma phospholipids during ingestion of fish oil, no significant changes in red blood cell deformability were observed. Since hypertension and shunt occlusion occurred at rates comparable to those reported in the literature, long-term ingestion of fish oil does not appear to mitigate the side effects of low and slow dose rHuEPO.

Anemia↗

The threat of biological weapons. Prophylaxis and mitigation of psychological and social consequences.

The microbial world is mysterious, threatening, and frightening to most people. The stressors associated with a biological terrorist attack could create high numbers of acute and potentially chronic psychiatric casualties who must be recognized, diagnosed, and treated to facilitate triage and medical care. Media communications, planning for quarantine and decontamination, and the role of community leaders are important to the mitigation of psychological consequences. Physicians will need to accurately diagnose anxiety, depression, bereavement, and organic brain syndromes to provide treatment, reassurance, and the relief of pain.

Biological Warfare↗

Programs that mitigate the effects of poverty on children.

This article reviews six federally funded in-kind public assistance programs that are intended to mitigate the effects of poverty on low-income children by providing access to basic human necessities such as food, housing, education, and health care. The evidence suggests that, while each program can be improved, these programs do achieve their basic objectives. In general, food stamps, the Special Supplemental Food Program for Women, Infants, and Children (WIC), and school nutrition programs are successful at providing food assistance to low-income children, starting with the prenatal period and continuing through the school years. The Food Stamp Program provides food assistance nationwide to all households solely on the basis of financial need and is central to the food assistance safety net for low-income children. The WIC program has helped reduce the prevalence of iron-deficiency anemia in infants and children and has increased intakes of certain targeted nutrients for program participants. The school nutrition programs provide free or low-cost meals that satisfy the dietary goals of lunches and breakfasts to most school-age children. The Medicaid program has extended health insurance coverage to millions of low-income children. However, many children remain uninsured, and children enrolled in Medicaid do not have the same access to medical care as privately insured children. Relatively little is known about the effects of Medicaid on children's health status. For Head Start, empirical evidence suggests that participating children show enhanced cognitive, social, and physical development in the short term. Studies of the longer-term impacts of Head Start are inconclusive. Although housing assistance improves housing quality and reduces housing costs for recipients, there is a large unmet need for acceptable, affordable housing among poor families. Important gaps remain in our knowledge of the effects of these programs on the well-being of children. Questions regarding a program's effects over time on health and developmental outcomes particularly need more study.

Adolescent↗

"Not as bad as it could have been": assessing and mitigating harm during research interviews on sensitive topics.

Research on sensitive subjects such as perinatal loss places participants at particular risk for psychological distress. Although authors have discussed strategies for minimizing distress during interview research, less is known about the ways participants communicate and investigators respond to psychological pain incurred during the interview itself. Therefore, we describe both verbal and nonverbal indicators of distress during a phenomenological study on perinatal loss. We also offer suggestions for interviewers on ways to minimize participants' discomfort. We believe this account will help other researchers identify and reduce respondent distress during their own research.

Adaptation, Psychological↗

Bioeffects induced by exposure to microwaves are mitigated by superposition of ELF noise.

We have previously demonstrated that microwave fields, amplitude modulated (AM) by an extremely low-frequency (ELF) sine wave, can induce a nearly twofold enhancement in the activity of ornithine decarboxylase (ODC) in L929 cells at SAR levels of the order of 2.5 W/kg. Similar, although less pronounced, effects were also observed from exposure to a typical digital cellular phone test signal of the same power level, burst modulated at 50 Hz. We have also shown that ODC enhancement in L929 cells produced by exposure to ELF fields can be inhibited by superposition of ELF noise. In the present study, we explore the possibility that similar inhibition techniques can be used to suppress the microwave response. We concurrently exposed L929 cells to 60 Hz AM microwave fields or a 50 Hz burst-modulated DAMPS (Digital Advanced Mobile Phone System) digital cellular phone field at levels known to produce ODC enhancement, together with band-limited 30-100 Hz ELF noise with root mean square amplitude of up to 10 microT. All exposures were carried out for 8 h, which was previously found to yield the peak microwave response. In both cases, the ODC enhancement was found to decrease exponentially as a function of the noise root mean square amplitude. With 60 Hz AM microwaves, complete inhibition was obtained with noise levels at or above 2 microT. With the DAMPS digital cellular phone signal, complete inhibition occurred with noise levels at or above 5 microT. These results suggest a possible practical means to inhibit biological effects from exposure to both ELF and microwave fields.

Animals↗

Temporally incoherent magnetic fields mitigate the response of biological systems to temporally coherent magnetic fields.

We have previously demonstrated that a weak, extremely-low-frequency magnetic field must be coherent for some minimum length of time (approximately 10 s) in order to affect the specific activity of ornithine decarboxylase (ODC) in L929 mouse cells. In this study we explore whether or not the superposition of an incoherent (noise) magnetic field can block the bioeffect of a coherent 60 Hz magnetic field, since the sum of the two fields is incoherent. An experimental test of this idea was conducted using as a biological marker the twofold enhancement of ODC activity found in L929 murine cells after exposure to a 60 Hz, 10 microT rms magnetic field. We superimposed an incoherent magnetic noise field, containing frequencies from 30 to 90 Hz, whose rms amplitude was comparable to that of the 60 Hz field. Under these conditions the ODC activity observed after exposure was equal to control levels. It is concluded that the superposition of incoherent magnetic fields can block the enhancement of ODC activity by a coherent magnetic field if the strength of the incoherent field is equal to or greater than that of the coherent field. When the superimposed, incoherent noise field was reduced in strength, the enhancement of ODC activity by the coherent field increased. Full ODC enhancement was obtained when the rms value of the applied EM noise was less than one-tenth that of the coherent field. These results are discussed in relation to the question of cellular detection of weak EM fields in the presence of endogenous thermal noise fields.

Animals↗

Astrocyte-induced regulatory T cells mitigate CNS autoimmunity.

Although astrocytes presumably participate in maintaining the immune privilege of the central nervous system (CNS), the mechanisms behind their immunoregulatory properties are still largely undefined. In this study, we describe the development of regulatory T cells upon contact with astrocytes. Rat T cells pre-incubated with astrocytes completely lost the ability to proliferate in response to mitogenic stimuli. The cells were blocked in G0/G1 phase of the cell cycle, expressed less IL-2R, and produced significantly lower amounts of interferon-gamma (IFN-gamma), but not interleukin-2 (IL-2), IL-10, or tumor necrosis factor (TNF). These anergic cells completely prevented mitogen-induced growth of normal T lymphocytes, as well as CNS antigen-driven proliferation of autoreactive T cells. The suppressive activity resided in both CD4+ and CD8+ T-cell compartments. Heat-sensitive soluble T-cell factors, not including transforming growth factor-beta (TGF-beta) or IL-10, were solely responsible for the observed suppression, as well as for the transfer of suppressive activity to normal T cells. The administration of astrocyte-induced regulatory T cells markedly alleviated CNS inflammation and clinical symptoms of CNS autoimmunity in rats with experimental allergic encephalomyelitis. Finally, the cells with suppressive properties were readily generated from human lymphocytes after contact with astrocytes. Taken together, these data indicate that astrocyte-induced regulatory T cells might represent an important mechanism for self-limitation of excessive inflammation in the brain.

Animals↗

Overexpression of GRP78 mitigates stress induction of glucose regulated proteins and blocks secretion of selective proteins in Chinese hamster ovary cells.

GRP78 is a resident protein of the endoplasmic reticulum (ER) and a member of the glucose regulated protein (GRP) family. Many secretion incompetent proteins are found in stable association with GRP78 and are retained in the ER. Some proteins which are destined for secretion transiently associate with GRP78. To further increase our understanding of the role of GRP78 in secretion, we have stably overexpressed GRP78 in Chinese hamster ovary (CHO) cells and examined the effect on protein secretion and the stress response. GRP78 overexpressing cells treated with tunicamycin or A23187 exhibited a reduced induction of endogenous GRP78 and GRP94 mRNAs compared to wild-type CHO cells. This suggests that GRP78 overexpression either alleviates the stress or is directly involved in signaling stress-induced expression of GRPs. Transient expression of secreted proteins was used to measure secretion efficiency in the GRP78 overexpressing cells. Secretion of von Willebrand factor and a mutant form of factor VIII, two proteins which transiently associate with GRP78, was reduced by GRP78 overexpression. In contrast, secretion of M-CSF, which was not detected in association with GRP78, was unaffected. This indicates that elevated levels of GRP78 may increase stable association and decrease the secretion efficiency of proteins which normally transiently associate with GRP78. These results indicate that one function of GRP78 is selective protein retention in the ER.

Adenosine↗

Metallothionein I and II mitigate age-dependent secondary brain injury.

Both the immediate insult and delayed apoptosis contribute to functional deficits after brain injury. Secondary, delayed apoptotic death is more rapid in immature than in adult CNS neurons, suggesting the presence of age-dependent protective factors. To understand the molecular pathobiology of secondary injury in the context of brain development, we identified changes in expression of oxidative stress response genes during postnatal development and target deprivation-induced neurodegeneration. The antioxidants metallothionein I and II (MT I/II) were increased markedly in the thalamus of adult C57BL/6 mice compared to mice <15 days old. Target deprivation generates reactive oxygen species that mediate neuronal apoptosis in the central nervous system; thus the more rapid apoptosis observed in the immature brain might be due to lower levels of MT I/II. We tested this hypothesis by documenting neuronal loss after target-deprivation injury. MT I/II-deficient adult mice experienced greater thalamic neuron loss at 96 hr after cortical injury compared to that in controls (80 +/- 2% vs. 57 +/- 4%, P < 0.01), but not greater overall neuronal loss (84 +/- 4% vs. 79 +/- 3%, MT I/II-deficient vs. controls). Ten-day-old MT I/II-deficient mice, however, experienced both faster onset of secondary neuronal death (30 vs. 48 hr) and greater overall neuronal loss (88 +/- 2% vs. 69 +/- 4%, P = 0.02). MT I/II are thus inhibitors of age-dependent secondary brain injury, and the low levels of MT I/II in immature brains explains, in part, the enhanced susceptibility of the young brain to neuronal loss after injury. These findings have implications for the development of age-specific therapeutic strategies to enhance recovery after brain injury.

Age Factors↗