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Paraxial propagation through isotropic, homogeneous, linear media exhibits invariance under rotations around the propagation axis, a symmetry described by the su (2) Lie algebra. We explore a family of paraxial beams that exploit this symmetry, constructed as linear superpositions of Laguerre-Gaussian beams (LGBs), serving as optical analogs of generalized SU (2) Lie group coherent states. A single complex parameter controls a smooth transition between Laguerre-Gaussian and Hermite-Gaussian beams (HGBs), producing intermediate beams that blend the characteristics of both families. Our beams exhibit propagation-invariant properties, up to a scaling factor, a highly desirable feature for optical applications. Experimental validation via digital holography demonstrates the practical feasibility of our approach.

Objective: The objective of this study is to characterise available clinical trial information for paediatric obstructive sleep apnea (OSA) and identify opportunities for future research to better treat children with this condition., Methods: A cross-sectional analysis of paediatric OSA clinical trials was conducted using the International Clinical Trials Registry. Criteria for inclusion included sleep apnea trials with participants < 18 years old and an interventional design. We assessed the information available on the database to identify recent trends in research. We used PubMed to examine publication rate. NIH RePORTER was used to characterise funding patterns for trials conducted in the United States., Results: Of 91 trials analysed, 54% of trials were conducted in the United States. The number of paediatric OSA clinical trials has been increasing since 2005. Patients aged 6, 7 and/or 8 were enrolled in 70% of trials, whereas infants under 12 months of age were only represented in approximately 9%. Overall, 31.9% had results reported directly on the registry, while 57% had results published. Median time to trial completion by sponsor for US trials was 3.04 years for NIH-sponsored trials, 1.29 years for industry-sponsored trials, and 1.96 years for non-funded sources. The NIH funded 56% of US trials., Conclusion: Despite a growing interest in paediatric OSA, continued focus on reporting and publishing results in a timely manner is essential to further advance the care of children with OSA. Future research should aim to address the gaps in age representation and focus on early intervention to treat age groups with higher prevalence., (© 2025 John Wiley & Sons Ltd.)

Objective: Seizures can be difficult to control in infants and toddlers. Seizures with periods of apnea and hypoventilation are common following severe traumatic brain injury (TBI). We previously observed that brief apnea with hypoventilation (A&H) in our severe TBI model acutely interrupted seizures. The current study is designed to determine the effect of A&H on subsequent seizures and whether A&H has potential therapeutic implications., Methods: Piglets (1 week or 1 month old) received multifactorial injuries: cortical impact, mass effect, subdural hematoma, subarachnoid hemorrhage, and seizures induced with kainic acid. A&H (1 min apnea, 10 min hypoventilation) was induced either before or after seizure induction, or control piglets received subdural/subarachnoid hematoma and seizure without A&H. In an intensive care unit, piglets were sedated, intubated, and mechanically ventilated, and epidural electroencephalogram was recorded for an average of 18 h after seizure induction., Results: In our severe TBI model, A&H after seizure reduced ipsilateral seizure burden by 80% compared to the same injuries without A&H. In the A&H before seizure induction group, more piglets had exclusively contralateral seizures, although most piglets in all groups had seizures that shifted location throughout the several hours of seizure. After 8-10 h, seizures transitioned to interictal epileptiform discharges regardless of A&H or timing of A&H., Significance: Even brief A&H may alter traumatic seizures. In our preclinical model, we will address the possibility of hypercapnia with normoxia, with controlled intracranial pressure, as a therapeutic option for children with status epilepticus after hemorrhagic TBI., (© 2024 International League Against Epilepsy.)

Objective: Tongue-tie, which is also known as ankyloglossia, is a common condition where the lingual frenulum is unusually tight or short. While most literature investigates the impact of tongue-tie on breastfeeding, recent articles have examined its role in speech production in children. However, these have not previously been reviewed systematically. This study aims to determine the impact of tongue-tie on speech outcomes and assess whether frenectomy can improve speech function., Methods: In this systematic review, we conducted a comprehensive search of PubMed/MEDLINE, Cochrane Library, Embase, and speechBITE to analyze primary studies investigating the impact of frenectomy for tongue-tie on speech outcomes. We extracted data regarding patient age, male to female ratio, procedure type, follow-up time, and speech outcomes and ran statistical analyses to determine if frenectomy for tongue-tie leads to improvement in speech issues in pediatric patients. Speech outcomes extracted were subjectively measured based on the interpretation of a speech and language pathologist or parent., Results: Our analysis included 10 studies with an average patient age of 4.10 years, and average cohort size of 22.17 patients. Overall, frenectomy for tongue-tie was associated with an improvement in speech articulation (0.78; 95% CI: 0.64-0.87; P  < .01). Increasing patient age was found to be negatively correlated with post-frenectomy speech outcomes ( P  = .01). However, this relationship disappeared in the adjusted model., Conclusion: Overall, we conclude that frenectomy is a suitable treatment to correct speech issues in select patients with tongue-tie if caught early in childhood. Despite the limited investigations around speech outcomes post-frenectomy, these results are informative to providers treating tongue-tie., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Introduction: The Hypoglossal Nerve Stimulator (HNS) is a novel therapy that has been extensively studied in adults and more recently, it has been incorporated in children with Down Syndrome (DS) with persistent obstructive sleep apnea after adenotonsillectomy and trial of continuous positive airway pressure treatment. This systematic review article aims to examine the existing literature on HNS use in children to explore the benefits, efficacy, and parental experiences., Methods: MEDLINE, Web of Science and EMBASE were searched to include all studies published up to March 2nd, 2023, on the topic of HNS use in pediatric population under 21 years old., Results: A total of 179 studies were initially identified from which 10 articles were consistent with the inclusion criteria. Nine articles addressed outcomes after implantation of the HNS device in children with DS and 1 article explored the parental experiences. Findings were similar across studies where after implantation of HNS, there was marked improvement in polysomnographic outcomes and quality of life scores with high level of compliance., Conclusions: HNS holds promise as an effective treatment option for pediatric patients with DS and persistent OSA after AT and CPAP trials. It significantly improves sleep-disordered breathing, quality of life, and neurocognitive measures, leading to substantial and sustained benefits for these children. While the findings are encouraging, further research is needed to explore the potential of HNS in other pediatric populations without DS and to raise awareness among healthcare providers about this treatment option. Overall, HNS may offer significant long-term benefits for the overall well-being and health of pediatric patients with DS and persistent OSA., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Introduction: A striking pattern in young children after severe TBI is when the entire cortical ribbon displays tissue damage: hemispheric hypodensity (HH). HH is often a result of abusive head trauma (AHT). We previously reported a model of HH in a gyrencephalic species where a combination of injuries consisting of (1) cortical impact, (2) midline shift, (3) subdural hematoma/subarachnoid hemorrhage, (4) traumatic seizures, and (5) brief apnea and hypoventilation resulted in extensive, hypoxic-ischemic-type injury. Importantly, this mechanism closely resembles that seen in children, with relative sparing of the contralateral cortex, thus ruling out a pure asphyxia mechanism. In this model, piglets of similar developmental stage to human toddlers (postnatal day 30, PND30) have extensive hypoxic-ischemic damage to the cortical ribbon with sparing of the contralateral hemisphere and deep gray matter areas. However, piglets of similar developmental stage to human infants (postnatal day 7, PND7) have less hypoxic-ischemic damage that is notably bilateral and patchy. We therefore sought to discover whether the extensive tissue damage observed in PND30 was due to a greater upregulation of matrix metalloproteinases (MMPs)., Materials and Methods: In PND7 or PND30 piglets receiving AHT injuries (cortical impact, midline shift, subdural hematoma/subarachnoid hemorrhage, traumatic seizures, and brief apnea and hypoventilation) or a sham injury, the pattern of albumin extravasation and MMP-9 upregulation throughout the brain was determined via immunohistochemistry, brain tissue adjacent to the cortical impact where the tissue damage spreads was collected for Western blots, and the gelatinase activity was determined over time in peripheral plasma. EEG was recorded, and piglets survived up to 24 h after injury administration., Results: The pattern of albumin extravasation, indicating vasogenic edema, as well as increase in MMP-9, were both present at the same areas of hypoxic-ischemic tissue damage. Evidence from immunohistochemistry, Western blot, and zymogens demonstrate that MMP-2, -3, or -9 are constitutively expressed during immaturity and are not different between developmental stages; however, active forms are upregulated in PND30 but not PND7 after in response to AHT model injuries. Furthermore, peripheral active MMP-9 was downregulated after model injuries in PND7., Conclusions: This differential response to AHT model injuries might confer protection to the PND7 brain. Additionally, we find that immature gyrencephalic species have a greater baseline and array of MMPs than previously demonstrated in rodent species. Treatment with an oral or intravenous broad-spectrum matrix metalloproteinase inhibitor might reduce the extensive spread of injury in PND30, but the exposure to metalloproteinase inhibitors must be acute as to not interfere with the homeostatic role of matrix metalloproteinases in normal postnatal brain development and plasticity as well as post-injury synaptogenesis and tissue repair., (© 2024 The Author(s). Published by S. Karger AG, Basel.)

Currently, immunotherapy based on PD-1/PD-L1 pathway blockade has improved survival of non-small cell lung cancer (NSCLC) patients. However, differential responses have been observed by sex, where men appear to respond better than women. Additionally, adverse effects of immunotherapy are mainly observed in women. Studies in some types of hormone-dependent cancer have revealed a role of sex hormones in anti-tumor response, tumor microenvironment and immune evasion. Estrogens mainly promote immune tolerance regulating T-cell function and modifying tumor microenvironment, while androgens attenuate anti-tumor immune responses. The precise mechanism by which sex and sex hormones may modulate immune response to tumor, modify PD-L1 expression in cancer cells and promote immune escape in NSCLC is still unclear, but current data show how sexual differences affect immune therapy response and prognosis. This review provides update information regarding anti-PD-1/PD-L immunotherapeutic efficacy in NSCLC by sex, analyzing potential roles for sex hormones on PD-L1 expression, and discussing a plausible of sex and sex hormones as predictive response factors to immunotherapy., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Rodriguez-Lara, Giovanny, Avila-Costa, Whaley, Rodriguez-Cid, Ordoñez-Librado, Rodriguez-Maldonado and Heredia-Jara.)

Perivascular spaces (PVS) visible on brain MRI signal cerebral small vessel disease (CSVD). The coexistence of PVS with other CSVD manifestations likely increases the risk of adverse neurological outcomes. We related PVS to other CSVD manifestations and brain volumes that are markers of vascular brain injury and neurodegeneration. Framingham Heart Study (FHS) participants with CSVD ratings on brain MRI were included. PVS were rated in the basal ganglia (BG) and centrum semiovale (CSO) into grades I-IV and a category reflecting high burden in single or mixed CSO-BG regions. We related PVS to covert brain infarcts (CBI), white matter hyperintensities (WMH), cerebral microbleeds (CMB), total brain, hippocampal, and cortical gray matter volumes using adjusted multivariable regression analyses. In 2454 participants (mean age 54 ± 12 years), we observed that higher PVS burden in both BG and CSO was related to CMB in lobar and deep brain regions and increased WMH. Greater CSO PVS burden was associated with decreased total cortical gray volumes. PVS are associated with ischemic markers of CSVD and neurodegeneration markers. Further studies should elucidate the causality between PVS and other CSVD manifestations.

Background: Magnetic resonance imaging (MRI) visible perivascular spaces (PVS) are associated with the risk of incident dementia but their association with the early stages of cognitive impairment remains equivocal., Objective: We examined the association between MRI visible PVS and the risk of incident mild cognitive impairment (MCI) in the community-based Framingham Heart Study (FHS)., Methods: FHS participants aged at least 50 years free of stroke, cognitive impairment, and dementia at the time of MRI were included. PVS were rated according to severity in the basal ganglia and centrum semiovale (CSO) using established criteria. Cox regression analyses were used to relate PVS to incident MCI adjusted for demographic and cardiovascular variables., Results: The mean age of the sample (1,314 participants) at MRI was 68 years (SD, 9; 54% women). There were 263 cases of incident MCI over a median 7.4 years follow-up (max, 19.8 years). MCI risk increased with higher PVS severity in the CSO. Relative to persons with the lowest severity rating, persons with the highest severity rating in the CSO had a higher risk of incident MCI (hazard ratio [HR] = 2.55; 95% confidence interval [CI], 1.48-4.37; p = 0.0007). In secondary analysis, this association seemed stronger in women. Risk of incident MCI was nominally higher for participants with the highest severity grade of PVS in the basal ganglia, though not statistically significant relative to the lowest grade (HR = 2.19; 95% CI, 0.78-6.14; p = 0.14)., Conclusions: PVS burden in the CSO may be a risk marker for early cognitive impairment.

Müller cells are the principal glial cells in the retina and they assume many of the functions carried out by astrocytes, oligodendrocytes and ependymal cells in other regions of the central nervous system. Müller cells express growth factors, neurotransmitter transporters and antioxidant agents that could fulfill important roles in preventing excitotoxic damage to retinal neurons. Vertebrate Müller cells are well-defined cells, characterized by a common set of features throughout the phylum. Nevertheless, several major differences have been observed among the Müller cells in distinct vertebrates, such as neurogenesis, the capacity to reprogram fish Müller glia to neurons. Here, the Müller glia of the largest adult mammal in the world, the whale, have been analyzed, and given the difficulties in obtaining cetacean cells for study, these whale glia were analyzed both in primary cultures and as immortalized whale Müller cells. After isolating the retina from the eye of a beached sei whale ( Balaenoptera borealis ), primary Müller cell cultures were established and once the cultures reached confluence, half of the cultures were immortalized with the simian virus 40 (SV40) large T-antigen commonly used to immortalize human cell lines. The primary cell cultures were grown until cells reached senescence. Expression of the principal molecular markers of Müller cells (GFAP, Vimentin and Glutamine synthetase) was studied in both primary and immortalized cells at each culture passage. Proliferation kinetics of the cells were analyzed by time-lapse microscopy: the time between divisions, the time that cells take to divide, and the proportion of dividing cells in the same field. The karyotypes of the primary and immortalized whale Müller cells were also characterized. Our results shown that W21M proliferate more rapidly and they have a stable karyotype. W21M cells display a heterogeneous cell morphology, less motility and a distinctive expression of some typical molecular markers of Müller cells, with an increase in dedifferentiation markers like α-SMA and β-III tubulin, while they preserve their GS expression depending on the culture passage. Here we also discuss the possible influence of the animal's age and size on these cells, and on their senescence., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Pereiro, Beriain, Rodriguez, Roiz-Valle, Ruzafa and Vecino.)

Background: Treatment-resistant schizophrenia is prevalent and difficult to manage, as patients fail multiple antipsychotic trials before being considered as treatment-resistant. Currently clozapine is the only Food and Drug Administration-approved pharmacotherapy for treatment-resistant schizophrenia but remains under-prescribed. The purpose of this study is to investigate recent literature on clozapine in order to identify barriers to prescribing clozapine and categorize the recommended solutions., Methods: We conducted a systematic review following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Using free text and the medical subject headings, we searched MEDLINE/PubMed electronic bibliographic database from 2017 until 2020. Eligible studies included peer-reviewed English language articles with multiple methodologies aiming to identify clozapine barriers in treatment-resistant schizophrenia. We used search terms combining clozapine AND treatment OR treatment-resistant schizophrenia AND barriers AND prescribing OR prescription OR prescriber. We merged search results in a citation manager software, removed duplicates, and screened the remaining articles based on the study eligibility criteria., Results: We retrieved 123 studies, however, only 10 articles exclusively met the study inclusion criteria for full text review. These studies represented 20 countries; 6 were exclusively conducted in the US. The top barriers delineated by the studies include: providers' lack of knowledge and training (n = 7), concern about side effects (n = 8), and poor adherence (n = 7). All studies described more than 1 barrier. Other barriers included prescriber-perceived barriers (n = 4), administrative barriers (n = 5), and other healthcare systems-related barriers (n = 3). Top recommendations to overcome clozapine prescription barriers included improving prescriber clozapine education/training, utilizing interdisciplinary teams and providing integrated care via clozapine clinics, and simplifying blood test monitoring., Conclusion: Clozapine remains under-prescribed for patients with treatment-resistant schizophrenia due to multiple barriers related to the individual prescriber, system of care, and technology. It is recommended that by improving prescriber knowledge and training, use of integrated care, and use of technology that can enable continuous, real-time blood test monitoring, these barriers may be overcome., Competing Interests: The authors have no conflicts of interest to disclose., (Copyright © 2021 the Author(s). Published by Wolters Kluwer Health, Inc.)

Lung cancer incidence and mortality have significantly increased in women worldwide. Lung adenocarcinoma is the most common form of lung cancer globally. This type of lung cancer shows differences by sex, including the mutational burden, behavior, clinical characteristics, and response to treatment. The effect of sex on lung cancer patients' survival is still controversial; however, lung adenocarcinoma is considered a different disease in women and men. Moreover, lung adenocarcinoma is strongly influenced by estrogen and is also different depending on the hormonal status of the patient. Young pre-menopausal women have been explored as an independent group. They presented in more advanced stages at diagnosis, exhibited more aggressive tumors, and showed poor survival compared to men and post-menopausal women, supporting the role of sex hormones in this pathology. Several reports indicate the estrogen's role in lung carcinogenesis and tumor progression. Thus, there are currently some clinical trials testing the efficacy of antihormonal therapy in lung cancer treatment. This mini review shows the updated data about lung cancer in women, its characteristics, the etiological factors that influence carcinogenesis, and the critical role of estrogen in lung cancer and treatment., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Rodriguez-Lara and Avila-Costa.)

We report experimental evidence on second-movers' behavior in the investment game (also known as the trust game) when there exists endowment heterogeneity. Using a within-subject analysis, we investigate whether or not second-movers exhibit some taste for inequality aversion by returning a larger (smaller) share of the available funds to first-movers who are initially endowed with a lesser (larger) endowment, respectively. Our data suggest that second-movers do not take into consideration the level of endowments when making their decisions as their behavior is consistent across distribution of endowments; i.e., they return the same proportion of the available funds regardless of the endowments. We indeed find that some second-movers have a tendency to return what they have received from first-movers. In our data, there is also a substantial proportion of second-movers who are selfish and return nothing. (JEL Codes: C72, C91, D3, D63)., Competing Interests: The author has declared that no competing interests exist.

Lung cancer (LC) is the leading cause of cancer death in men worldwide and has significantly increased in women. Differences in non-small cell lung cancer (NSCLC) behavior, prognosis, and response to treatment have been reported by sex and hormonal status, with premenopausal women presenting the worst prognosis compared to postmenopausal women and men. Additionally, the use of hormonal replacement therapy significantly increases NSCLC mortality; supporting the role of estrogen signaling in the pathogenesis of LC. The mechanisms by which estrogen promotes lung carcinogenesis have not been fully elucidated. Estrogen, through its receptor, can stimulate LC cell proliferation, death resistance, angiogenesis, migration and metastasis. Estrogen also induces expression of pro-inflammatory proteins and ligands that promote tumor evasion, suggesting that estrogen might modify the microenvironment and anti-tumor immune response. Recent reports have shown an interaction between the epidermal growth factor receptor (EGFR) pathway and estrogen signaling in lung adenocarcinoma, whence, combined treatment based on tyrosine kinase inhibitors (TKIs) and antiestrogen therapy is beginning to be evaluated. This review focuses on the differences in NSCLC behavior by sex and hormonal status, highlighting the role of estrogen and its receptors in lung carcinogenesis and LC prognosis. Due to the importance of estrogen in NSCLC development and progression we finally discuss the potential of antiestrogen therapy in LC treatment and show the results from preclinical and clinical trials., Competing Interests: Conflicts of Interest: The authors have no conflicts of interest to declare.

Purpose: This study was designed to investigate whether estradiol is related to the expression of the chemokine receptor CXCR4 and its activation in lung adenocarcinoma in vitro, since lung adenocarcinomas from premenopausal women have shown high levels of CXCR4, and this expression has been associated with worse prognosis and poor survival., Methods: The effect of 17-β-estradiol (E2) (0.03 nM-10 nM) on CXCR4 expression was analyzed in lung adenocarcinoma cell lines (SK-LU-1, H1435, H23, A549) by immunofluorescence after 24 and 72-h poststimulation. Tamoxifen treatment was applied to corroborate the estrogenic effect. The wound-healing assay was performed to investigate whether E2 treatment increased CXCR4/CXL12 pathway activity. A549 and SK-LU-1 cells were stimulated with E2, CXCL12, and CXCL12 combined with E2. Tamoxifen and AMD3100 were applied to corroborate estrogen and chemokine pathway activation., Results: Estradiol stimulated significantly CXCR4 overexpression in all the cell lines analyzed in a dose- and a time-dependent manner. Tamoxifen treatment inhibited the CXCR4 overexpression observed in estrogen-treated groups, demonstrating that estrogen strongly influences CXCR4 expression in lung adenocarcinoma cells. Cells treated with E2, CXCL12 and E2 combined with CXCL12 exhibited significant cell migration, which was suppressed when tamoxifen and AMD3100 were present., Conclusion: Overexpression of CXCR4 induced by estrogen and the activity of CXCL12/CXCR4 pathway could be a new mechanism by which this hormone supports tumor progression and metastasis. These findings may partly explain the worse prognosis observed in premenopausal women and suggest considering the role of estrogen in lung cancer for the design of more specific treatment schemes.

Vanadium (V) is a transition metal often adhered to particulate matter and released into the atmosphere as vanadium pentoxide (V2O5) by the burning of fossil fuels. This air pollutant causes adverse effects in the immune system. Lymphocytosis and splenomegaly have been reported with increased white pulp in mice after V inhalation. The effect of V on the immune system as related to sex has been poorly investigated. This study sought to determine if V inhalation (a) produced lymphoproliferation that could explain the changes previously observed in the spleen and in peripheral blood lymphocyte counts and (b) whether any observed effects differed due to gender. Immunohistochemical analyses of Ki-67, a specific proliferation marker, was made in the spleens of CD-1 male and female mice exposed for 1 h, twice a week, over a 12-week period to V2O5 (at 1.4 mg V2O5/m(3)) by whole-body inhalation; similar analyses were performed on spleens of control mice exposed to vehicle (filtered air). The results showed that in male mice there was a significant increase in percentage of Ki-67 immunopositive lymphocytes starting from the second week and until the end of the exposure. The Ki-67 signal was cytoplasmic and nuclear in the exposed males, while in controls the signal was only nuclear. In female mice, V inhalation singificantly increased the percentage of proliferating lymphocytes only after 1 week of exposure. Ki-67 signal was observed only in the nucleus of lymphocytes from the control and exposed females. The results here help to explain the splenomegaly and lymphocytosis observed previously in male mice and support the lymphoproliferative effect induced by V. Lastly, the finding that there was a sex difference in the effect of vanadium on lymphocyte proliferation suggests a role for sex hormones in potential protection against V immunotoxicity; however, further studies are needed to support this hypothesis.

Particulate matter air pollution has considerably increased during the last decades; vanadium is a transition element adhered to this particulate matter, and the combustion of fossil fuels is the main source in the atmosphere. It has been reported that air pollution and specifically vanadium exposure increases the probability of suffering arrhythmias; however the biological mechanism of such a relationship remains unknown. It has been established that a diminished presence of N-Cadherin alters the Connexin-43 arrangement, and the consequent altered presence of these proteins predisposes to ventricular heart rate problems. We analyzed myocardial histology and the expression of N-Cadherin and Connexin-43 by immunohistochemistry in mouse that inhaled vanadium. Our results showed a significant and progressive reduction in both N-Cadherin and Connexin-43, as well as the presence of meganucleus; myofibrils disruption, and clumping in the exposed groups were also observed. Our findings add more information about a possible explanation for the arrythmogenic effect observed in dwellers of cities with high particulate matter atmospheric pollution.

This paper provides experimental evidence on the relationship between social preferences and cognitive abilities, which we measure using the Cognitive Reflection Test (CRT). We elicit social preferences by way of 24 dictatorial situations, in which the Dictator's choice sets include (i) standard Dictator games, where increasing the Dictator's payoff yields a loss for the Recipient, (ii) efficient Dictator games, where increasing the Dictator's payoff also increases that the Recipient's; as well as other situations in which (iii) either the Dictator's or (iv) the Recipient's monetary payoff is held constant. We partition our subject pool into three groups: reflective (scoring 2 or more in the CRT), impulsive (opting twice or more for the "intuitive" but wrong answers in the CRT) and the remainder. We find that impulsive Dictators show a marked inequity aversion attitude, especially in standard Dictator Games. By contrast, reflective Dictators show lower distributional concerns, except for the situations in which the Dictators' payoff is held constant. In this case, reflective Dictators give significantly more.

Background and Aims: Studies have reported differences in lung cancer behavior between sex and hormonal status that suggest a role of estrogens and estrogen receptor beta (ERβ) in lung carcinogenesis. In some types of hormone-dependent cancer, estrogens may regulate CXCL12/CXCR4 expression through ERβ signaling. High expression of CXCL12/CXCR4 is associated with poor prognosis in lung cancer because it promotes tumor growth and metastasis. Therefore, in this study we investigated whether lung adenocarcinoma tissues from pre- and postmenopausal women and from men exhibit different ERβ, CXCR4/CXCL12 expression and whether this expression is associated with clinicopathological features., Methods: Sixty primary tumor samples of lung adenocarcinoma from pre- and postmenopausal women and from men were collected for this study. Thirty samples of healthy lung tissue adjacent to the tumor site were used as controls. ERβ and CXCL12/CXCR4 expression was analyzed by immunohistochemistry. Expression of these proteins was measured by digital image software and compared between sex and hormonal status., Results: Lung adenocarcinomas overexpressed ERβ, CXCR4 and CXCL12 compared to normal lung. Moreover, lung adenocarcinomas from premenopausal women exhibited higher signals for ERβ, CXCL12 and CXCR4 compared to postmenopausal women and to men, who showed lower signals for these proteins. A multivariate analysis revealed a strong association between the immunoreactivity level of ERβ, CXCL12/CXCR4 and both sex and hormonal status, but not with tumor stage and smoking., Conclusion: These results demonstrated that ERβ and CXCL12/CXCR4 expression in lung adenocarcinoma depends on sex and hormonal status, which may partly explain the sex and hormonal differences in lung cancer behavior., (Copyright © 2014 IMSS. Published by Elsevier Inc. All rights reserved.)

Vanadium is a transition metal released into the atmosphere, as air-suspended particles, as a result of the combustion of fossil fuels and some metallurgic industry activities. Air-suspended particle pollution causes inflammation-related processes such as thrombosis and other cardiovascular events. Our aim was to evaluate the effect of vanadium pentoxide (V2O5) on endothelial cells since they are key participants in the pathogenesis of several cardiovascular and inflammatory diseases. Cell adhesion, the expression of adhesion molecules and oxidative stress, as well as proliferation, morphology and cell death of human umbilical vein endothelial cells (HUVECs) exposed to V2O5, were evaluated. Vanadium pentoxide at a 3.12 µg cm(-2) concentration induced an enhanced adhesion of the U937 macrophage cell line to HUVECs, owing to an increased expression of late adhesion molecules. HUVECs exposed to V2O5 showed an increase in ROS and nitric oxide production, and a diminished proliferation. These changes in vanadium-treated HUVECs were accompanied by severe morphological changes and apoptotic cell death. Vanadium pentoxide induced serious endothelial cell damage, probably related to the increased cardiovascular morbidity and mortality observed in individuals living in highly air-polluted areas., (Copyright © 2011 John Wiley & Sons, Ltd.)

There is an increased concern about the health effects that air-suspended particles have on human health which have been dissected in animal models. Using CD-1 mouse, we explore the effects that vanadium inhalation produce in different tissues and organs. Our findings support the systemic effects of air pollution. In this paper, we describe our findings in different organs in our conditions and contrast our results with the literature.

Nasal epithelium is a source for identifying atmospheric pollution impact. Antioxidants play a relevant role in the protection of the cells from environmental injury, but scarce information is available about the interaction of endogenous antioxidants and genotoxic damage in nasal epithelium from urban populations highly exposed to traffic-generated air pollutants. An immunocytochemical and genotoxic evaluation was implemented in nasal cell epithelium in a population chronically exposed to atmospheric pollution from autumn 2004 to autumn 2005. Superoxide dismutase (SOD) and Catalase (CAT) were evaluated in nasal scrapings by morphometry and genotoxicity by comet assay. An increase in DNA damage correlates with a decrease in SOD and CAT in nasal cells during autumn and the inverse result was observed during summer (R = 0.88). Not only should exogenous antioxidant supplements be encouraged, but also a healthy diet to strengthen intracellular defenses against oxidative stress induced by exposure to air pollutants., (Copyright © 2010 John Wiley & Sons, Ltd.)

Air pollution by suspended particles has become a worldwide health problem. The main sources of these particles are fossils and additives combustion. Mn enters the body through inhalation, but part of the particles accesses contact with tongue's posterior surface where lingual tonsils and lingual papillae are placed. We decided to explore in a mouse model, the impact that the deposit of inhaled Mn has on the tongue's surface. Atrophy of the lingual tonsil, filiform papillae, as well as the swelling of taste buds in fungiform papillae, were the predominant changes. Ferropenic anemia is associated with the changes described and could be related to the interference of Mn in iron metabolism and riboflavin absorption. More research should be done to explore the participation of suspended particles trapped in the oral cavity in toxicology of Mn or other inhaled pollutants.

An increased incidence in ischemic and thromboembolic events in the population of cities with rising air suspended particle pollution has suggested the interaction of some of the components of these particles in the coagulation system. A previous report from our laboratory identified thrombocytosis as a consequence of the subacute and chronic inhalation of vanadium. With this preceding information we decided to evaluate the effects of this element in the spleen and bone marrow in a mouse experimental model. CD-1 male mice inhaled V2O5 0.02 M for one hour twice a week for twelve weeks. The spleen and bone marrow were processed for light microscopy. The increase in quantity and size of megakaryocytes (MKs) in the exposed group in both organs was striking. Also, modifications in the cytoplasm, granule content and nuclear ultrastructure were evident. Our results indicate the influence of vanadium on megakaryopoyesis, an effect which could be the onset of the thrombocytosis previously reported by our group. The modifications in MKs described here suggest that inhaled vanadium could induce megakaryocytic proliferation, which may result in increased production of platelets and increased risk for thromboembolic events.

Vanadium (V) derivatives are well-known environmental pollutants and its toxicity has been related with oxidative stress. Toxicity after vanadium inhalation on the substantia nigra, corpus striatum, hippocampus and ependymal epithelium was reported previously. The purpose of this study was to analyse the role of matrix metalloproteinases 2 (MMP-2) and 9 (MMP-9) in the changes observed in brain tissue after chronic V inhalation. Mice were exposed to vaporized, vanadium pentoxide 0.02 m in deionized water for 1 h twice a week, and killed at 1 h, 1, 2 and 4 weeks after exposure. The brain was removed and the olfactory bulb, prefrontal cortex, striatum and hippocampus were dissected and the MMP content was obtained by zymography. The results showed that MMP-9 increased in all the structures at the end of the exposure, although in the hippocampus this increment was evident after 1 week of exposure. When MMP-2 was analysed in the olfactory bulb and prefrontal cortex it remained unchanged throughout the whole exposure, while in the hippocampus it increased at week 4, while in the striatum MMP-2 increased from the second week only, through the whole experiment. These results demonstrate that V increased MMPs in different structures of the CNS and this change might be associated with the previously reported modifications, such as dendritic spine loss and neuronal cell death. The modifications in MMPs could be related with blood-brain barrier (BBB) disruption which was reported previously. Oxidative stress might also be involved in the activation of these gelatinases as part of the different mechanisms which take place in V toxicity in the CNS., (Copyright 2007 John Wiley & Sons, Ltd.)

Vanadium, an important air pollutant derived from fuel product combustion, aggravates respiratory diseases and impairs cardiovascular function. In contrast, its effects on immune response are conflicting. The aim of our work was to determine if spleens of vanadium-exposed CD1 mice showed histological lesions that might result in immune response malfunction. One hundred and twelve CD-1 male mice were placed in an acrylic box and inhaled 0.02 M vanadium pentoxide (V2O5); actual concentration in chamber approximately 1.4 mg V2O5/m(3)) for 1 hr/d, twice a week, for 12 wk. Control mice inhaled only vehicle. Eight mice were sacrificed prior to the exposures. Eight control and eight V2O5-exposed mice were sacrificed 24 hr after the second exposure of each week until the 12-wk study was over. Another 8 mice that completed the 12-wk regimen were immunized with recombinant Hepatitis B surface antigen (HBsAg; three times over an 8-wk period) before sacrifice and analyses of their levels of anti-HBsAg antibody (HBSAb) using ELISA. In all studies, at sacrifice, blood samples were obtained by direct heart puncture and the spleen was removed, weighed and processed for H-E staining and quantitation of CD19 cells. The results indicated that the spleen weight of V2O5-exposed animals peaked at 9 wk (546 +/- 45 vs. 274 +/- 27 mg, p < 0.0001) and thereafter progressively decreased (321 +/- 39 mg at 12 wk, p < 0.001; control spleen = 298 +/- 35 mg). Spleens of V2O5-exposed animals showed an increased number of very large and non-clearly delimited germinal centers (that contained more lymphocytes and megakaryocytes) compared to those of control mice. In addition, their red pulp was poorly delimited and had an increase in CD19+ cells within hyperplasic germinal nodes. The mean HBsAb levels in immunized control mice were greater than that in the exposed hosts (i.e., OD = 0.39 +/- 0.03 vs. 0.11 +/- 0.05, p < 0.01). HBsAb avidity dropped to a value of 40 in V2O5-exposed animals vs. 86 in controls (p < 0.0001). We conclude that the chronic inhalation of V2O5, a frequent particle (PM(2.5)) component, induces histological changes and functional damage to the spleen, each of which appear to result in severe effects on the humoral immune response.

Purpose: To investigate the clinical use of a commercially available gating system for minimizing respiratory-induced anatomic motion over a range of treatment sites., Methods and Materials: The gating system consists of a reflective marker placed on the patient's anterior surface. The motion of the marker is tracked using a camera interfaced to a computer. Gated intervals were defined that limited the motion of the diaphragm to less than 1 cm during free breathing. Patients underwent a computed tomography virtual simulation using a breath-hold technique. At the time of treatment, verification of patient position and gating interval were performed using electronic portal imaging., Results: Between September 2000 and January 2002, 136 patients were simulated with respiratory gating. Of these, 108 patients were treated to 110 sites for a total of 2301 treatment sessions. Ninety-seven percent of patients completed their entire course of therapy with gated treatment delivery., Conclusions: Respiratory gating is a practical and achievable solution for minimizing respiratory-induced target motion during both simulation and treatment. With proper patient selection and training, it can be successfully implemented in a clinical radiation therapy department.