Prenatal viral infection leads to pyramidal cell atrophy and macrocephaly in adulthood: implications for genesis of autism and schizophrenia

We investigated the role of maternal exposure to human influenza virus (H1N1) in C57BL/6 mice on Day 9 of pregnancy on pyramidal and nonpyramidal cell density, pyramidal nuclear area, and overall brain size in Day 0 neonates and 14-week-old progeny and compared them to sham-infected cohorts. Pyramidal cell density increased significantly (p < 0.0038) by 170% in Day 0 infected mice vs. controls. Nonpyramidal cell density decreased by 33% in Day 0 infected progeny vs. controls albeit, nonsignificantly. Pyramidal cell nuclear size decreased significantly (p < 0.0465) by 29% in exposed newborn mice vs. controls. Fourteen-week-old exposed mice continued to show significant increases in both pyramidal and nonpyramidal cell density values vs. controls respectively (p < 0.0085 E1 (exposed group 1), p < 0.0279 E2 (exposed group 2) pyramidal cell density; p < 0.0092 E1, p < 0.0252 E2, nonpyramidal cell density). By the same token, pyramidal cell nuclear size exhibited 37–43% reductions when compared to control values; these were statistically significant vs. controls (p < 0.04 E1, p < 0.0259 E2). Brain and ventricular area measurements in adult exposed mice also showed significant increases and decreases respectively vs. controls. Ventricular brain ratios exhibited 38–50% decreases in exposed mice vs. controls. While the rate of pyramidal cell proliferation per unit area decreased from birth to adulthood in both control and exposed groups, nonpyramidal cell growth rate increased only in the exposed adult mice. These data show for the first time that prenatal exposure of pregnant mice on Day 9 of pregnancy to a sublethal intranasal administration of influenza virus has both short-term and long-lasting deleterious effects on developing brain structure in the progeny as evident by altered pyramidal and nonpyramidal cell density values; atrophy of pyramidal cells despite normal cell proliferation rate and final enlargement of brain. Moreover, abnormal corticogenesis is associated with development of abnormal behavior in the exposed adult mice.     

Effects of Extremely Low Frequency Magnetic Fields on Blood Coagulation in Mice: An Initial Study

OF1 mice were chronically exposed to a 50‐Hz sinusoidal East–West magnetic field 15 µT (rms), in order to evaluate the blood coagulation variations related to the effect of this nonionizing radiation. Mating and pregnancy of ancestors (first generation), and birth, lactation, and development of second‐generation female mice until adulthood took place in the experimental field. A global blood coagulation study of both control and exposed 14‐ to 15‐week‐old and 50‐ to 52‐week‐old, second‐generation females was carried out. Plasma calcium content was determined by atomic absorption spectrophotometry. Different steps of blood coagulation were studied by thromboelastography (TEG) in whole blood (WB), platelet‐rich plasma (PRP), and platelet‐poor plasma (PPP). A significant decrease (approximately 34.5%) of calcium concentration was detected with aging; however, no change was induced by medium‐term or long‐term exposure to extremely low frequency magnetic field (ELF‐MF). Medium‐term exposure could not be related to noticeable changes in global coagulation. However, a great deterioration of fibrin clot formation in mature exposed female mice was detected as a result of the long‐term exposure that was strengthened by aging. These deficiencies seemed to be compensated by the discrete, although statistically not significant, decrease of platelet counts and the significant decrease of blood cells' mean corpuscular volume associated to ELF‐MF exposure of 50‐Hz, 15 µT. Consequently, whole blood TEG values of mature exposed female mice were similar to those from the young control group. In view of the obtained results, further studies on variations associated with ELF‐MF exposure in different coagulation parameters will be necessary.     

Modifications of pyrethroid effects associated with kdr mutation in Anopheles gambiae

Effects of knockdown resistance (kdr) were investigated in three pyrethroid‐resistant (RR) strains of the Afrotropical mosquito Anopheles gambiae Giles (Diptera: Culicidae): Kou from Burkina Faso, Tola and Yao from Côte d'Ivoire; compared with a standard susceptible (SS) strain from Kisumu, Kenya. The kdr factor was incompletely recessive, conferring 43‐fold resistance ratio at LD₅₀ level and 29‐fold at LD₉₅ level, as determined by topical application tests with Kou strain. When adult mosquitoes were exposed to 0.25% permethrin‐impregnated papers, the 50% and 95% knockdown times (KdT) were 23 and 42 min for SS females, compared with 40 and 62 min for RS (F₁ Kou × Kisumu) females. On 1% permethrin the KdT₅₀ and KdT₉₅ were 11 and 21 min for SS compared with 18 and 33 min for RS females. Following 1 h exposure to permethrin (0.25% or 1%), no significant knockdown of Kou RR females occurred within 24 h. Permethrin irritancy to An. gambiae was assessed by comparing ‘time to first take‐off’ (TO) for females. The standard TO₅₀ and TO₉₅ values for Kisumu SS on untreated paper were 58 and 1044 s, respectively, vs. 3.7 and 16.5 s on 1% permethrin. For Kou RR females the comparable values were 27.3 s for TO₅₀ and 294 s for TO₉₅, with intermediate RS values of 10.1 s for TO₅₀ and 71.9 s for TO₉₅. Thus, TO values for RS were 2.7–4.4 times more than for SS, and those for RR were 7–18 times longer than for SS. Experiments with pyrethroid‐impregnated nets were designed to induce hungry female mosquitoes to pass through holes cut in the netting. Laboratory ‘tunnel tests’ used a bait guinea‐pig to attract mosquitoes through circular holes (5 × 1 cm) in a net screen. With untreated netting, 75–83% of laboratory‐reared females passed through the holes overnight, 63–69% blood‐fed successfully and 9–17% died, with no significant differences between SS and RR genotypes. When the netting was treated with permethrin 250 mg ai/m² the proportions that passed through the holes overnight were only 10% of SS vs. 40–46% of RR (Tola & Kou); mortality rates were 100% of SS compared with 59–82% of RR; bloodmeals were obtained by 9% of Kou RR and 17% of Tola RR, but none of the Kisumu SS females. When the net was treated with deltamethrin 25 mg ai/m² the proportions of An. gambiae that went through the holes and blood‐fed successfully were 3.9% of Kisumu SS and 3.5% of Yaokoffikro field population (94% R). Mortality rates were 97% of Kisumu SS vs. 47% of Yaokoffikro R. Evidently this deltamethrin treatment was sufficient to kill nearly all SS and half of the Yaokoffikro R An. gambiae population despite its high kdr frequency. Experimental huts at Yaokoffikro were used for overnight evaluation of bednets against An. gambiae females. The huts were sealed to prevent egress of mosquitoes released at 20.00 hours and collected at 05.00 hours. Each net was perforated with 225 square holes (2 × 2 cm). A man slept under the net as bait. With untreated nets, only 4–6% of mosquitoes died overnight and bloodmeals were taken by 17% of SS vs. 29% of Yaokoffikro R (P < 0.05). Nets treated with permethrin 500 mg/m² caused mortality rates of 95% Kisumu SS and 45% Yao R (P < 0.001) and blood‐feeding rates were reduced to 1.3% of SS vs. 8.1% of Yao R (P < 0.05). Nets treated with deltamethrin 25 mg/m² caused mortality rates of 91% Kisumu SS and 54% Yao R (P < 0.001) and reduced blood‐feeding rates to zero for SS vs. 2.5% for Yao R (P > 0.05). Pyrethroid‐impregnated bednets in experimental huts and ‘tunnel tests’ gave equivalent results, showing that nets impregnated with permethrin or deltamethrin provided good levels of protection against kdr homozygous strains of An. gambiae (Kou and Tola), and against the field population at Yaokoffikro with 94% kdr frequency. The explanation seems to be that (a) high proportions of kdr females are killed by prolonged contact with pyrethroids through diminished sensitivity to the usual irritant and repellent effects, and (b) relatively few kdr females take advantage of this prolonged contact to ingest a bloodmeal.     

Hyperuricemia and gout are associated with cancer incidence and mortality: A meta-analysis based on cohort studies

The association between hyperuricemia or gout and cancer risk has been investigated in various published studies, but their results are conflicting. We conducted a meta-analysis to investigate whether hyperuricemia or gout was associated with the cancer incidence and mortality. Linear and nonlinear trend analyses were conducted to explore the dose–response association between them. The pooled relative risk (RR) and 95% confidence interval (CI) were used to evaluate cancer risk. A total of 24 articles (33 independent studies) were eligible for inclusion. When compared participants with the highest SUA (hyperuricemia) levels and those with the lowest SUA levels, the pooled RR was 1.08 (95% CI, 1.04–1.12), it was significantly associated among males but not among females (males, RR = 1.07; 95% CI, 1.03–1.11; females, RR = 1.06; 95% CI, 0.96–1.17). Hyperuricemia increased total cancer mortality (RR = 1.15; 95% CI, 1.05–1.26), but a significant association was observed in females rather than in males (females: RR = 1.26; 95% CI, 1.09–1.45; males, RR = 1.02; 95% CI, 0.80–1.30). Linear relationships of SUA levels with overall cancer incidence (p for nonlinearity = 0.238) and overall cancer mortality (p for nonlinearity = 0.263) were identified. However, 1 mg/dL increment in SUA levels was weakly significant in overall cancer incidence (RR = 1.01; 95% CI, 1.01–1.01) but not associated with overall cancer mortality (RR = 1.01; 95% CI, 0.99–1.03). Gout was significantly associated with increased cancer incidence (RR = 1.19; 95% CI, 1.12–1.25). In conclusion, Hyperuricemia or gout was associated with higher cancer incidence and mortality. Though a potential linear relationship between them was found, we'd better treat this result with caution.     

Telogen elongation in the hair cycle of ob/ob mice

Alopecia impairs the physical and mental health of patients. We have previously shown that 8-week-old ob/ob mice have no reactivity to depilation, which is a stimulus that induces anagen transition in normal mice, while no hair cycle abnormalities have been reported in other studies until mice reach 7 weeks of age. Therefore, we hypothesized that ob/ob mice have abnormalities in hair cycle progression beyond 7 weeks of age. We examined 6- to 24-week-old ob/ob and 6- to 10-week-old normal mice. After acclimation, the dorsal skin was harvested and the hair cycle phase was identified histologically and immunohistochemically. Normal mice showed catagen–telogen and telogen–anagen transitions at 6 and 8–9 weeks old, respectively. In contrast, the anagen–catagen transition was observed in 7-week-old mice and the telogen phase was maintained from 10 to 24 weeks in most ob/ob mice. These results suggests that ob/ob mice are a possible model animal for telogen effluvium.     

Circadian rhythm in QT interval is preserved in mice deficient of potassium channel interacting protein 2

Potassium Channel Interacting Protein 2 (KChIP2) is suggested to be responsible for the circadian rhythm in repolarization duration, ventricular arrhythmias, and sudden cardiac death. We investigated the hypothesis that there is no circadian rhythm in QT interval in the absence of KChIP2. Implanted telemetric devices recorded electrocardiogram continuously for 5 days in conscious wild-type mice (WT, n = 9) and KChIP2^?/? mice (n = 9) in light:dark periods and in complete darkness. QT intervals were determined from all RR intervals and corrected for heart rate (QT₁₀₀ = QT/(RR/100)^1/2). Moreover, QT intervals were determined from complexes within the RR range of mean-RR ± 1% in the individual mouse (QT_mean-RR). We find that RR intervals are 125 ± 5 ms in WT and 123 ± 4 ms in KChIP2^?/? (p = 0.81), and QT intervals are 52 ± 1 and 52 ± 1 ms, respectively(p = 0.89). No ventricular arrhythmias or sudden cardiac deaths were observed. We find similar diurnal (light:dark) and circadian (darkness) rhythms of RR intervals in WT and KChIP2^?/? mice. Circadian rhythms in QT₁₀₀ intervals are present in both groups, but at physiological small amplitudes: 1.6 ± 0.2 and 1.0 ± 0.3 ms in WT and KChIP2^?/?, respectively (p = 0.15). A diurnal rhythm in QT₁₀₀ intervals was only found in WT mice. QT_mean-RR intervals display clear diurnal and circadian rhythms in both WT and KChIP2^?/?. The amplitude of the circadian rhythm in QT_mean-RR is 4.0 ± 0.3 and 3.1 ± 0.5 ms in WT and KChIP2^?/?, respectively (p = 0.16). In conclusion, KChIP2 expression does not appear to underlie the circadian rhythm in repolarization duration.     

Physiological Effects of Slot Play in Women

The purpose of this study is to describe the physiological responses occurring during slot gambling in 23 females with problematic and non-problematic gambling backgrounds in two sites: at a casino using their own money and at a casino laboratory without wagering money. Using the National Opinion Research Center Diagnostic Screen (NODS), 12 women were not-at-risk gamblers and 11 were at-risk, problem, or pathological gamblers. Blood pressure (BP), heart rate (HR), respiratory rate (RR), skin conductance (SC), and skin temperature (ST) were measured for 5 min before gambling (baseline), 10 min while gambling, and 5 min after gambling (recovery). In the casino, SBP (p = .001), DBP (p = .031), HR (p = .030), and RR (p = 004) rose during gambling and fell during recovery; ST rose throughout the study (p = .006). There were no differences between subjects based on NODS score. A total of 12 subjects were also studied in the laboratory. SBP (p = .004), DBP (p = .000); HR (p = .023); RR (p = .000) and SC (p = .002) rose during gambling and fell during recovery; ST rose throughout the study (p = .006). There were no significant differences by location. The observed effects suggest that females find slot play physiologically arousing, with or without financial stakes, because physiological changes were consistent with an arousal response.     

Effects of prenatal exposure to 50 Hz magnetic fields on development in mice: II. Postnatal development and behavior

To investigate the potential of magnetic fields to act as a behavioral teratogen, pregnant CD1 mice were exposed or sham-exposed for all of gestation to a 50 Hz/20 mT magnetic field. Maturation of offspring was assessed using a range of standard developmental indices (eye opening, pinna detachment, hair coat, tooth eruption, sexual maturity, and weight) and simple reflexive behaviors (air righting, surface righting, forepaw grasp, cliff avoidance, and negative geotaxis). Activity and coordination levels were explored in juvenile and adult mice using an open field arena, a head-dip board, an accelerating Rotarod, and a residential activity wheel. All assessments were carried out without knowledge of exposure condition. Results from 168 sham-exposed mice from 21 litters and from 184 exposed mice from 23 litters were compared using survival analysis techniques and multivariate regression methods. Three possible field-dependent effects were found: Exposed animals performed the air righting reflex earlier (P < 0.01); exposed males (but not females) were significantly lighter in weight (P = 0.008) at 30 days of age; and exposed animals remained on a Rota-rod for less time as juveniles (P = 0.03). Some of these results have not been reported in other studies and may reflect spurious statistical significance, although some effect of magnetic field exposure cannot be ruled out. Overall, these results suggest that prenatal exposure to a 50 Hz magnetic field does not engender any gross impairments in the postnatal development or behavior of mice. This does not preclude such exposure affecting more subtle aspects of behavior. Published 1994 by Wiley-Liss, Inc.     

Heart Rate Variability During 24 Hours in Asthmatic Children

The autonomic circadian rhythm plays an important role in asthma. In recent years it has become possible to evaluate autonomic nervous function (ANF) using analysis of heart rate variability (HRV). We analyzed the HRV in the 24h period following the state without an asthma attack in order to study the relationship between asthma and ANF. The HRV was analyzed in 94 asthmatic children (ages 5–15 years). These subjects were divided into groups according to the severity of their asthma. After recording a 24h ambulatory electrocardiograph (AECG), the HRV was analyzed by a computer. Evaluation of the HRV was carried out using time-domain and frequency-domain analyses. The ANF of asthma subjects was decreased in comparison to the normal group. The severity of asthma had a significant effect on the %RR50 (the proportion of cycles during which the difference is > 50 ms), the SD (standard deviation; mean of standard deviation of all normal RR intervals for all 5-minute periods), the low-frequency (LF) band (0.04 to 0.15 Hz), and the high-frequency (HF) band (0.15 to 0.4 Hz) (%RR50: F = 4.31, p = 0.01; SD: F=3.48, p = 0.03; LF: F=3.67, p = 0.02; HF: F=3.41, p = 0.03). These values were lowest in the severe asthma group. With regard to the therapy grouping, the index that exhibited a significant difference was the NNA (mean of normal-to-normal RR intervals over 24h) (F = 4.43, p = 0.01) In conclusion, even in the normal condition in which the patient is free of an asthma attack, the ANF of asthma sufferers differs from that of normal children. It is possible that the different ANF of asthma sufferers is related to the severity of the asthma. (Chronobiology International, 14(6), 597–606, 1997)     

Duration of exposure to environmental carcinogens affects DNA-adduct level in human lymphocytes

Background and objective: An important issue in human biomonitoring is determining how exposure duration affects the kinetics of molecular biomarkers. In this study we compare the influence of exposure variables on DNA adducts.

Methods: DNA adducts were analysed by 32P-postlabelling in lympho/monocytes of 677 Caucasian subjects.

Results: After correction for other variables, DNA adducts increased depending on the length of occupational and smoke exposures. Higher DNA adducts were detected in workers with more than 14 years of exposure than in workers with shorter exposures (RR?=?1.19, p?=?0.049) and in smokers with more than 10 years of exposure than in smokers with shorter exposure (RR?=?1.21, p <0.001).

Conclusions: Exposure length is the primary factor affecting DNA-adduct level in lympho/monocytes both in smokers and in occupationally exposed subjects.     

Adverse ffects of covert iridovirus infection on life history and demographic parameters of Aedes aegypti

Abstract Sublethal viral infections can cause changes in the body size and demography of insect vectors, with important consequences for population dynamics and the probability that individual mosquitoes will transmit disease. This study examined the effects of covert (sublethal) infection by Invertebrate iridescent virus 6 (IIV‐6) on the demography of female Aedes aegypti and the relationship between key life history parameters in covertly infected female insects compared with healthy (control) insects or non‐infected mosquitoes that had survived exposure to virus inoculum without becoming infected. Of the female mosquitoes that emerged following exposure to virus inoculum and were offered blood meals, 29% (43/150) proved positive for covert IIV‐6 infection. The net reproductive rate (R₀) of covertly infected females was 50% lower for infected females compared to control mosquitoes, whereas non‐infected exposed females had an R₀ approximately 15% lower than that of controls. Reproduction caused a significant decrease of about 13 days in mosquito longevity compared to females that did not reproduce (P < 0.001). Infected females lived 5–8 days less than non‐infected exposed females or controls, respectively (P = 0.028). Infected females and non‐infected exposed females both had significantly shorter wings than control insects (P < 0.001). There was a significant positive correlation between wing length and longevity in covertly infected female mosquitoes but not in control or non‐infected exposed mosquitoes. Longer lived females produced more eggs in all treatments. There were no significant correlations between body size and fecundity or the production of offspring. There was also no correlation between fecundity and fertility, suggesting that sperm inactivation was a more likely cause of decreased fertility in older mosquitoes than sperm depletion. We conclude that covert infection by iridescent virus is likely to reduce the vectorial capacity of this mosquito.     

Lowering Effect of Phenolic Glycosides on the Rise in Postprandial Glucose in Mice

Glycosides were screened for their lowering effect on the postprandial blood glucose rise in vivo. The effect of phlorizin and other phenolic glycosides on the postprandial blood glucose response to glucose ingestion was evaluated in Std ddY mice. When phlorizin was simultaneously added, the peak blood glucose level was significantly decreased by 51% (p < 0.01) compared to vehicles following glucose ingestion by mice, while the blood insulin responses were generally similar. Screening experiments were conducted with different classes of phenolic glycosides added to a glucose solution. Reductions of 40–52% (p < 0.05) were observed in vehicles containing arbutin, 4-hydroxyphenyl-α-d-glucopyranoside (hydroquinone-α-glucoside) or glycyrrhizin, and of only 15–31% (not significant) in vehicles containing neohesperidin dihydrochalcone, glycyrrhetinic acid monoglucuronide, or 3,4-dimethoxyphenyl-β-d-glucopyranoside. No lowering effect was observed in vehicles containing salicin. Since glycyrrhizin, arbutin, and hydroquinone-α-glucoside blunted to varying degrees the postprandial blood glucose rise following glucose ingestion, they may be useful adjuvants for the treatment of diabetic subjects.     

Effects of exposure to electromagnetic field from 915 MHz radiofrequency identification system on circulating blood cells in the healthy adult rat

We investigated whether exposure to the 915 MHz radiofrequency identification (RFID) signal affected circulating blood cells in rats. Sprague–Dawley rats were exposed to RFID at a whole‐body specific absorption rate of 2 W/kg for 8 h per day, 5 days per week, for 2 weeks. Complete blood counts were performed after RFID exposure, and the CD4⁺/CD8⁺ ratio was determined by flow cytometry. The number of red blood cells (RBCs) and the values of hemoglobin, hematocrit, and RBC indices were increased in the RFID‐exposed group compared with those in the cage‐control and sham‐exposed groups (P < 0.05). However, the RBCs and platelet numbers were within normal physiologic response ranges. The number of white blood cells, including lymphocytes, was decreased in RFID‐exposed rats. However, there was no statistically significant difference between the sham‐exposed and RFID‐exposed groups in terms of T‐cell counts or CD4⁺/CD8⁺ ratio (P > 0.05). Although the number of circulating blood cells was significantly altered by RFID exposure at a whole‐body specific absorption rate of 2 W/kg for 2 weeks, these changes do not necessarily indicate that RFID exposure is harmful, as they were within the normal physiological response range. Bioelectromagnetics. 39:68–76, 2018. © 2017 Wiley Periodicals, Inc.     

Can sleep quality and wellbeing be improved by changing the indoor lighting in the homes of healthy,elderly citizens?

The study investigated the effect of bright blue-enriched versus blue-suppressed indoor light on sleep and wellbeing of healthy participants over 65 years. Twenty-nine participants in 20 private houses in a uniform settlement in Copenhagen were exposed to two light epochs of 3 weeks with blue-enriched (280 lux) and 3 weeks blue-suppressed (240 lux) indoor light or vice versa from 8 to 13 pm in a randomized cross-over design. The first light epoch was in October, the second in November and the two light epochs were separated by one week. Participants were examined at baseline and at the end of each light epoch. The experimental indoor light was well tolerated by the majority of the participants. Sleep duration was 7.44 (95% CI 7.14–7.74) hours during blue-enriched conditions and 7.31 (95% CI 7.01–7.62) hours during blue-suppressed conditions (p?=?0.289). Neither rest hours, chromatic pupillometry, nor saliva melatonin profile showed significant changes between blue-enriched and blue-suppressed epochs. Baseline Pittsburgh Sleep Quality Index (PSQI) was significantly worse in females; 7.62 (95% CI 5.13–10.0) versus 4.06 (95% CI 2.64–5.49) in males, p?=?0.009. For females, PSQI improved significantly during blue-enriched light exposure (p?=?0.007); no significant changes were found for males. The subjective grading of indoor light quality doubled from participants habitual indoor light to the bright experimental light, while it was stable between light epochs, although there were clear differences between blue-enriched and blue-suppressed electrical light conditions imposed. Even though the study was carried out in the late autumn at northern latitude, the only significant difference in Actiwatch-measured total blue light exposure was from 8 to 9 am, because contributions from blue-enriched, bright indoor light were superseded by contributions from daylight.     

Effects of Maternal Exposure to Imazalil on Behavioral Development in F1‐Generation Mice

Female mice were exposed maternally to imazalil through diet to provide levels of 0 (control), 0.0006, 0.0018, and 0.0054% during gestation and lactation periods, and selected reproductive and neurobehavioral parameters were measured in F₁ generation. There was no adverse effect of imazalil on litter size, litter weight, or sex ratio at birth. With respect to behavioral developmental parameters, surface righting on postnatal day 4 of male offspring was delayed significantly in a dose‐related manner (p < 0.05). Regarding exploratory behavior in the F₁ generation, movement time was significantly long (p = 0.0206) in the low‐dose group of males at 8 weeks of age. Spontaneous behavior examination in males indicated that movement time increased but in females decreased in the low‐dose groups in the F₁ generation. The dose levels of imazalil in the present study produced some adverse effects in neurobehavioral parameters in mice.     

Effect of Helicobacter pylori eradication on gastric precancerous lesions: A systematic review and meta-analysis

Background

The question of whether eradication of Helicobacter pylori (Hp) can reverse gastric precancerous lesions, including intestinal metaplasia, remains uncertain, leading to ongoing debate. Therefore, a meta-analysis was performed to evaluate the effect of Hp eradication on gastric precancerous lesions.

Materials and Methods

PubMed, Embase, Cochrane Library, Web of Science, Scopus database, and ClinicalTrials.gov were systematically searched from inception to April 2023 for studies that explored the impact of Hp eradication on gastric precancerous lesions. Risk ratios (RRs) and their 95% confidence intervals (95% CIs) were selected as the effect size. We used the random-effects model to assess pooled data. We also performed quality assessments, subgroup analyses, and sensitivity analyses.

Results

Fifteen studies were included. Compared with placebo, Hp eradication could significantly prevent the progression of gastric precancerous lesions (RR = 0.87, 95% CI: 0.81–0.94, p < 0.01) and reverse them (RR = 1.32, 95% CI: 1.17–1.50, p < 0.01). Then, specific precancerous lesions were further explored. The progression of intestinal metaplasia was significantly prevented by Hp eradication compared to placebo or no treatment (RR = 0.80, 95% CI: 0.69–0.94, p < 0.01). Moreover, compared with placebo or no treatment, Hp eradication also improved chronic atrophic gastritis (RR = 1.84, 95% CI: 1.30–2.61, p < 0.01) and intestinal metaplasia (RR = 1.41, 95% CI: 1.15–1.73, p < 0.01). However, in terms of preventing dysplasia progression (RR = 0.86, 95% CI: 0.37–2.00) and improving dysplasia (RR = 0.89, 95% CI: 0.47–1.70), Hp eradication had no advantage compared to placebo or no treatment.

Conclusions

Hp eradication therapy could prevent the progression of gastric precancerous lesions and reverse them. Notably, intestinal metaplasia can be reversed, but this may only be appropriate for patients with epigenetic alterations and milder lesions.     

Factors associated with blood zinc,chromium, and lead concentrations in residents of the Nam Pong River in Thailand

This cross-sectional analytical study aimed to determine the blood levels of zinc (B-Zn), chromium (B-Cr), and lead (B-Pb) and to identify the factors influencing these levels in the blood of residents of the Nam Pong River. Quantitative data collection was utilized, and systematic random sampling was conducted to obtain 420 samples for measuring serum heavy metals, including B-Zn, B-Cr, and B-Pb. Multiple regression analysis was used to identify factors influencing the accumulation of heavy metals in the population, reported mean differences, 95% confidence intervals, and p values. The average levels of heavy metals were 74.38 ± 14.00 µg/dL (95% confidence interval [CI]: 73.03–75.72) for zinc, 0.28 ± 0.23 µg/L (95% CI: 0.26–0.30) for chromium, and 2.80 ± 1.60 µg/dL (95% CI: 2.64–2.95) for lead, which all were within normal limits. Factors influencing zinc levels included occupational exposure (batteries) (mean diff = 11.56; 95% CI: 1.81–21.32, p value = 0.02) and consumption of fish from the river exceeding 300 grams/meal or three times/week (mean diff = 4.68; 95% CI: 0.09–9.45, p value = 0.05). Factors influencing chromium levels included a history of past illness (mean diff = 0.19; 95% CI: 0.05–0.34, p value = 0.01) and dust/chemical exposure from industry (mean diff = 0.05; 95% CI: 0.00–0.11, p value = 0.05). Factors influencing lead concentrations included gender (mean diff = 1.82; 95% CI: 0.26–1.98, p value = 0.001), smoking (mean diff = 1.03; 95% CI: 0.60–1.45, p value < 0.001), and occupational exposure (garage) (mean diff = 1.11; 95% CI: 0.27–1.94, p value = 0.01).     

Impact of maternal lifestyle factors on newborn HPRT mutant frequencies and molecular spectrum — Initial results from the Prenatal Exposures and Preeclampsia Prevention (PEPP) Study

Epidemiological studies have demonstrated associations between maternal tobacco smoke exposure and consumption of alcohol during pregnancy and increased risk of pediatric malignancies, particularly infant leukemias. Molecular evidence also suggests that somatic mutational events occurring during fetal hematopoiesis in utero can contribute to this process. As part of an ongoing multi-endpoint biomarker study of 2000 mothers and newborns, the HPRT T-lymphocyte cloning assay was used to determine mutant frequencies (M_f) in umbilical cord blood samples from an initial group of 60 neonates born to a sociodemographically diverse cohort of mothers characterized with respect to age, ethnicity, socioeconomic status, and cigarette smoke and alcohol exposure. Non-zero M_f (N=47) ranged from 0.19 to 5.62×10⁻⁶, median 0.70×10⁻⁶, mean±SD 0.98±0.95×10⁻⁶. No significant difference in M_f was observed between female and male newborns. Multivariable Poisson regression analysis revealed that increased HPRT M_f were significantly associated with maternal consumption of alcohol at the beginning [Relative Rate (RR)=1.84, 95% CI=0.99–3.40, P=0.052) and during pregnancy (RR=2.99, 95% CI=1.14–7.84, P=0.026). No independent effect of self-reported active maternal cigarette smoking, either at the beginning or throughout pregnancy, nor maternal passive exposure to cigarette smoke was observed. Although based on limited initial data, this is the first report of a positive association between maternal alcohol consumption during pregnancy and HPRT M_f in human newborns. In addition, the spectrum of mutations at the HPRT locus was determined in 33 mutant clones derived from 19 newborns of mothers with no self-reported exposure to tobacco smoke and 14 newborns of mothers exposed passively or actively to cigarette smoke. In the unexposed group, alterations leading to specific exon 2–3 deletions, presumably as a result of illegitimate V(D)J recombinase activity, were found in five of the 19 mutants (26.3%); in the passively exposed group, two exon 2–3 deletions were present among the seven mutants (28.6%); and in the actively exposed group, six of the seven mutants (85.7%) were exon 2–3 deletions. Although no overall increase in HPRT M_f was observed and the number of mutant clones examined was small, these initial results point to an increase in V(D)J recombinase-associated HPRT gene exon 2–3 deletions in cord blood T-lymphocytes in newborns of actively smoking mothers relative to unexposed mothers (P=0.011). Together, these results add to growing molecular evidence that in utero exposures to genotoxicants result in detectable transplacental mutagenic effects in human newborns.     

Infectivity and Immunogenicity of Irradiated Babesia rodhaini*

SYNOPSIS. Babesia rodhaini-parasitized mouse blood exposed to varied doses of γ radiation up to 30 kRad was inoculated into mice. Mice inoculated with nonirradiated B. rodhaini developed progressive infections and died 7–11 days postinoculation. Mice infected with B. rodhaini-parasitized blood exposed to doses up to and including 22 kRad developed progressive parasitemias which were delayed in comparison to mice inoculated with non-irradiated B. rodhaini. Some mice receiving parasitized blood irradiated at 26 kRad did not develop progressive parasitemias. Progressive infections were prevented by exposure to irradiation at 30 kRad. The results of 2 separate experiments revealed that one inoculation of parasitized blood exposed to 30 kRad or higher apparently stimulated a resistance to a challenge infection with nonirradiated parasitized blood. While 20 of 20 control mice died as a result of challenging infections, 9 of 28 mice previously exposed to irradiated parasitized blood survived. The injection of irradiated nonparasitized blood did not produce a discernible acquired resistance to B. rodhaini. Presumably the irradiated parasitized blood was responsible for the development of acquired resistance to B. rodhaini.     

Effects of 1800 MHz GSM-like exposure on the gonadal function and hematological parameters of male mice

The aim of this study was to evaluate the possible effects of in vivo 1800 MHz GSM-like exposure on male reproduction. In five separate experiments, male NMRI mice (35-41 g) were exposed (11-12 mice each) to 1800 MHz GSM-like radiation. The average power density was 100 microW/cm2, the estimated SAR was 0.018-0.023 W/kg. The animals were exposed ten times (over two weeks on workdays) and the duration of exposure was 2 h/day. On the day of the last treatment, mice were anesthetized with i.p. pentobarbital, and blood samples were taken for hematology, serum chemistry and serum testosterone (T) determinations (ELISA). Testicles, epididymes, adrenals, prostates and pituitary glands were removed for histology. One testicle of each animal was used for culture of Leydig cells. The cells were cultured for 48 h in the presence or absence of human chorionic gonadotropin (hCG) to evaluate the in vitro steroidogenic response of Leydig cells. In the exposed animals red blood cell count (RBC: 8.59+/-0.10 T/l, n=37) and volume of packed red cells (VPRC: 42.29+/-0.43%, n=37) were significantly higher (p<0.01) compared with the controls (RBC: 8.12+/-0.08 T/l, n=36; VPRC: 39.76+/-0.36%, n=36). The serum testosterone level of the exposed animals (7.85+/-1.08 ng/ml, n=56) was also significantly elevated (p<0.05) compared to the controls (5.12+/-0.79, n=52), while the in vitro steroidogenic capacity of the Leydig cells was unaltered. No significant differences in the other investigated variables were found between controls and exposed mice. Our results indicate that the applied GSM-like microwave exposure may induce slight, but statistically significant alterations in some hematological and endocrine parameters of male mice within the physiological range. Further investigations are required to establish the biological significance of these phenomena.