CO2 in indoor environments: From environmental and health risk to potential renewable carbon source.

In the developed world, individuals spend most of their time indoors. Poor Indoor Air Quality (IAQ) has a wide range of effects on human health. The burden of disease associated with indoor air accounts for millions of premature deaths related to exposure to Indoor Air Pollutants (IAPs). Among them, CO2 is the most common one, and is commonly used as a metric of IAQ. Indoor CO2 concentrations can be significantly higher than outdoors due to human metabolism and activities. Even in presence of ventilation, controlling the CO2 concentration below the Indoor Air Guideline Values (IAGVs) is a challenge, and many indoor environments including schools, offices and transportation exceed the recommended value of 1000 ppmv. This is often accompanied by high concentration of other pollutants, including bio-effluents such as viruses, and the importance of mitigating the transmission of airborne diseases has been highlighted by the COVID-19 pandemic. On the other hand, the relatively high CO2 concentration of indoor environments presents a thermodynamic advantage for direct air capture (DAC) in comparison to atmospheric CO2 concentration. This review aims to describe the issues associated with poor IAQ, and to demonstrate the potential of indoor CO2 DAC to purify indoor air while generating a renewable carbon stream that can replace conventional carbon sources as a building block for chemical production, contributing to the circular economy.

Oviposition dynamics of Aedes aegypti in Central Argentina.

Aedes (Stegomyia) aegypti (L.) (Diptera: Culicidae) is the vector of multiple arboviruses. To evaluate the association between environmental factors and the oviposition activity of Ae. aegypti in Argentina, data on the presence and abundance of eggs were collected using ovitraps, between September of 2018 and May of 2019, in the cities of Villa María, Río Cuarto and Salsipuedes (Córdoba province, Argentina). We analysed the relationships between oviposition and five environmental factors: Temperature, precipitation, vegetation cover, human population density and distance to sites with a potential high density of larval habitats, like cemeteries and trash dumps. Environmental factors' data were collected using satellite image products. The oviposition activity was randomly distributed in three cities. Using generalized linear mixed models, we show that the house where each ovitrap was placed was a source of variability in oviposition, suggesting the relevance of microsite factors and the importance of domestic control actions. Ae. aegypti oviposition was positively correlated with night-time temperature of the previous 3 weeks, and in a context-dependent manner, it was positively correlated with human population density, vegetation cover and precipitation. The consistency and magnitude of these relationships varied between cities, indicating that oviposition is related to a complex system of environmental variables.

Antibody-Mediated Rejection Treatment With Bortezomib in Renal Transplant Recipients: A Single-Center 24-Month Follow-up Case Report.

INTRODUCTION: Antibody-mediated rejection (AMR) is related to a poor prognosis in graft survival, with 27% to 40% of patients experiencing graft loss within the first year. The mechanism of damage in AMR is mediated by donor-specific antibodies (DSA). No standard treatment for AMR exists, and conventional management includes high doses of steroids, plasmapheresis, intravenous immunoglobulin, and either rituximab or bortezomib. Because of the high cost of these medications and the lack of prospective studies to evaluate their efficacy and safety, their routine use is limited. In the following study, we describe the use of bortezomib for the treatment of AMR in 5 renal transplant recipients with a 24-month follow-up and compare this case with the reviewed literature. MATERIAL AND METHODS: Five cases of AMR diagnosed by biopsy are reported, and these patients received bortezomib at a rate of 1.3 mg/m2 on days 1, 4, 8, and 11; plasmapheresis; and 1 patient received 30 g of intravenous immunoglobulin. RESULTS: All patients received his or her first transplant; 4 were from a cadaveric donor, and 1 patient received thymoglobulin at a standard dose. All patients had maintenance therapy based on cyclosporine, mycophenolate mofetil, and prednisone, with an average baseline creatinine level of 1.3 mg/dL. The average days until rejection event were 952 days. DISCUSSION AND CONCLUSION: AMR treatment with bortezomib was effective, showing stable renal function at 24 months. Patients had adequate tolerance for administration. So far, these results contrast with the literature reviewed, so additional studies and follow-up are required for a new evaluation.

Metabolic Syndrome, a Real Barrier for Living Kidney Donor Transplant.

INTRODUCTION: Renal transplantation is the optimal renal replacement therapy. In Mexico, most of the kidney transplants are from living donors. It is essential to identify conditions that increase the risk of developing chronic kidney disease (CKD) in donors, such as metabolic syndrome (MS). MATERIALS AND METHODS: In retrospect from January 2008 to December 2018, the donation protocols for renal transplantation of the Hospital Central Sur Alta Especialidad "Picacho" were reviewed, classifying all the cases of donors by nephrectomy or no nephrectomy and describing the demographic characteristics, prevalence of metabolic diseases, and cause of rejection of the protocol. RESULTS: A total of 178 donors were studied: 82 women (46%), 96 men (54%), mean age of 42 years, average body mass index (BMI) 27.9 kg/m2, glomerular filtration rate (GFR) by Chronic Kidney Disease Epidemiology Collaboration 99 mL/min, 59 patients with grade I and II obesity (BMI ≥ 30 kg/m2), and 1 patient with morbid obesity (BMI ≥ 40 kg/m2). A total of 39 patients (22%) underwent nephrectomy and 139 (78%) did not. The following characteristics and alterations were found: Of the 139 patients who did not undergo nephrectomy, 91 had metabolic disorders, 20 had low GFR, 21 had albuminuria, and 4 recipients received cadaveric transplants, 3 due to critical conditions of the recipient. The metabolic alterations in the rejected donors were as follows: MS 54 (59%), prediabetes 55 (39%), newly diagnosed hypertension 70 (76%), diabetes mellitus 20 (14%), obesity 47 (51.6%), dyslipidemia 76 (83%), hyperuricemia 17 (12%). DISCUSSION: The prevalence of MS in apparently healthy donors is similar to that of other studies in Mexico. Both MS and its components are independently associated with an increased risk of cardiovascular disease and CKD. It has been shown that these donors have a greater degree of glomerular and interstitial fibrosis; therefore, diagnosis, prevention, and timely treatment in this group are important.

Pathophysiology of beta2-glycoprotein I in antiphospholipid syndrome.

Since beta(2)-glycoprotein I (beta(2)GPI) was described as the major antigenic target for antiphospholipid antibodies, many studies have focused their attention to the physiological role of beta(2)GPI and anti-beta(2)GPI antibodies on autoimmune-mediated thrombosis. Studies reporting the physiological role of beta(2)GPI have been numerous, but the exact mechanism of action(s) has yet to be completely determined. beta(2)GPI's epitopes for anti-beta(2)GPI autoantibodies have been characterized, however, not all of the heterogeneous anti-beta(2)GPI antibodies are pathogenic. The pathophysiologic role of beta(2)GPI has been reported in the fields of coagulation, fibrinolysis, angiogenesis, and atherosclerosis. Our understanding of the impact of beta(2)GPI, its metabolites and autoantibodies to beta(2)GPI on these physiological functions may contribute to the development of better therapeutic strategies to treat and prevent autoimmune-mediated atherothrombotic vascular disease.

Regulatory T Cells in children with intestinal parasite infection.

Chronic intestinal parasite infection can induce both persistent immune activation and defective responsiveness of T cells. This study aimed to assess the number and function of T regulatory (Treg) cells in children with intestinal parasite infection. We have studied the peripheral blood from 93 children, 53 of them parasitized with protozoa, helminths, or both; the remainder were non parasitized, healthy controls. The number and function of CD4(+) CD25(high) and CD4(+) Foxp3(+) cells were similar in parasitized and control children. In contrast, there was a significant increase in the levels of CD3(+) CD69(+), CD4(+) CTLA-4(+), and CD8(+) CD28(-) T cells in helminth infected children. Moreover, some of these patients showed a diminished response to CD3/CD28 stimulation in comparison with the control children. Our data strongly suggest that whilst Treg cells are not affected by intestinal parasite infection, CD3(+) CD69(+), CD4(+) CTLA-4(+) and CD8(+) CD28(-) lymphocytes may play an important, but as yet undetermined role in the diminished immune competence observed in parasitized children.

Primary antiphospholipid syndrome: a low-grade auto-inflammatory disease?

OBJECTIVE: To test the inflammation and immune activation hypothesis in primary thrombotic APS (PAPS) and to identify clinical and laboratory factors related to inflammation and immune activation. METHODS: PAPS (n = 41) patients were compared with patients with inherited thrombophilia (IT, n = 44) and controls (CTR, n = 39). IgG aCL, IgG anti-beta2-glycoprotein I (beta(2)GPI), high-sensitivity CRP (hs-CRP), serum amyloid A (SAA), CRP bound to oxidized low-density lipoprotein-beta(2)GPI complex (CRP-oxLDL-beta(2)GPI) (as inflammatory markers) neopterin (NPT), soluble CD14 (sCD14) (as immune activation markers) were measured by ELISA. RESULTS: After correction for confounders, PAPS showed higher plasma levels of hs-CRP (P = 0.0004), SAA (P < 0.01), CRP-oxLDL-beta(2)GPI (P = 0.0004), NPT (P < 0.0001) and sCD14 (P = 0.007) than IT and CTR. Two regression models were applied to the PAPS group: in the first, IgG aCL and IgG beta(2)GPI were included amongst the independent variables and in the second they were excluded. In the first model, SAA (as the dependent variable) independently related to thrombosis number (P = 0.003); NPT (as the dependent variable) independently related to thrombosis type (arterial, P = 0.03) and number (P = 0.04); sCD14 (as the dependent variable) independently related to IgG beta(2)GPI (P = 0.0001), age (0.001) and arterial thrombosis (P = 0.01); CRP-oxLDL-beta(2)GPI (as the dependent variable) independently related to IgG beta(2)GPI (P = 0.0001). In the second model, sCD14 and NPT independently related to each other (P = 0.002) (this was noted also in the IT group, P < 0.0001) and CRP-oxLDL-beta(2)GPI independently predicted SAA (P = 0.002). CONCLUSION: Low-grade inflammation and immune activation occur in thrombotic PAPS and relate to clinical features and aPL levels.

Autoimmune-mediated atherothrombosis.

Autoimmune vascular inflammation and oxidative stress (lipid peroxidation) are common in systemic autoimmune diseases and contribute to the oxidative modification of low-density lipoprotein (oxLDL) and oxLDL/beta2GPI complex formation. Circulating oxLDL/beta2GPI complexes have been detected in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). The presence of antibodies to oxLDL/beta2GPI complexes indicates that these complexes are immunogenic, and the coexistence of complexes and antibodies has pointed to an active proatherogenic role in the development of autoimmune vascular complications. Immunohistochemical staining of atherosclerotic lesions suggest that these complexes are formed in the arterial wall and released into circulation. The in vitro macrophage uptake of oxLDL/beta2GPI complexes was significantly increased in the presence of antiphospholipid antibodies, either beta2GPI-dependent anticardiolipin or anti-beta2GPI antibodies, suggesting that macrophage Fcgamma receptors are involved in lipid intracellular influx and foam cell formation. These findings provide an explanation for the accelerated development of atherosclerosis seen in SLE and APS. The presence of circulating oxLDL/beta2GPI complexes and IgG antibodies to these complexes indicate significant vascular injury and oxidative stress as well as an active role in autoimmune-mediated atherothrombosis.

Autoimmune diseases and infections: controversial issues.

The etiology and pathogenesis of certain types of disease remain controversial and stand like a bridge that crosses infectious, autoimmune and autoinflammatory pathways. Infection, for example, may initiate a disease, although it is the genetic regulation in the host, the interplay between virus or bacteria persistence and autoimmunity that produces the later phases of disease, the antigenic determinants responsible for inducing autoimmune disease, and the pathogenetic effector mechanisms. Infections agents cause pericarditis, but in 85% of cases it is "idiopathic". It has also been shown that persistent Clamydia pneumoniae, Porphyromonas gingivalis, and Helicobacter pylori infections cause host immunity and promote atherogenesis. A number of infectious agents have been suggested as potential triggers for primary biliary cirrhosis. Infections and vaccinations have also been linked to the pathogenesis of fibromyalgia syndrome, a common, chronic syndrome of widespread pain. Many factors are also responsible for fever of unknown origin such as: infections, autoimmunity disease, etc. However, it is difficult to determine a direct correlation between the infections agents in such a large group of diseases. The aim of this review is to analyze some of the controversies about the role of infections in autoimmune diseases.

Atherogenic oxidized low-density lipoprotein/beta2-glycoprotein I (oxLDL/beta2GPI) complexes in patients with systemic lupus erythematosus and antiphospholipid syndrome.

Oxidized low-density lipoprotein (oxLDL) interacts in vitro with beta2-glycoprotein I (beta2GPI) via LDL-derived specific ligands forming oxLDL/beta2GPI complexes. Circulating oxLDL/beta2GPI complexes have been demonstrated in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). Autoimmune vascular inflammation and oxidative stress contribute to oxLDL/beta2GPI complex formation. Immunohistochemical staining of atherosclerotic lesions suggest that these complexes are formed in the arterial wall and released into circulation. The demonstration of antibodies to oxLDL/beta2GPI complexes indicates that these complexes are immunogenic, and the coexistence of complexes and antibodies suggest an active pro-thrombotic/pro-atherogenic role in the development of autoimmune vascular complications. Circulating oxLDL/beta2GPI complexes can be measured by ELISA using a monoclonal antibody specific to complexed human beta2GPI to capture beta2GPI bound to oxLDL. An enzyme-conjugated monoclonal antibody to human Apo B 100 allows the specific detection of oxLDL/beta2GPI complexes. OxLDL/beta2GPI complexes were common in SLE and APS patients suggesting an underlying process of inflammation and oxidation. Using oxLDL/beta2GPI complexes as capture antigen, antibodies to oxLDL/beta2GPI can be measured by ELISA. Serum levels of IgG anti-oxLDL/beta2GPI antibodies were significantly higher in SLE patients with APS compared to SLE controls without APS. Further, high titers of these IgG antibodies were observed in APS patients with a history of arterial thrombosis. The presence of circulating oxLDL/beta2GPI complexes and IgG antibodies to these complexes indicates significant vascular injury and oxidative stress as well as an active role in autoimmune-mediated atherothrombosis.

Antibodies against beta2-glycoprotein I complexed with an oxidised lipoprotein relate to intima thickening of carotid arteries in primary antiphospholipid syndrome.

To explore whether antibodies against beta2-glycoprotein I (beta2GPI) complexed to 7-ketocholesteryl-9-carboxynonanoate (oxLig-1) and to oxidised low-density lipoproteins (oxLDL) relate to paraoxonase activity (PONa) and/or intima media thickness (IMT) of carotid arteries in primary antiphospholipid syndrome (PAPS). As many as 29 thrombotic patients with PAPS, 10 subjects with idiopathic antiphospholipid antibodies (aPL) without thrombosis, 17 thrombotic patients with inherited thrombophilia and 23 healthy controls were investigated. The following were measured in all participants: beta2GPI-oxLDL complexes, IgG anti-beta2GPI-oxLig-1, IgG anti-beta2GPI-oxLDL antibodies (ELISA), PONa, (para-nitrophenol method), IMT of common carotid (CC) artery, carotid bifurcation (B), internal carotid (IC) by high resolution sonography. Beta2GPI-oxLDL complex was highest in the control group (p < 0.01), whereas, IgG anti-beta2GPI-oxLig1 and IgG anti-beta2GPI-oxLDL were highest in PAPS (p < 0.0001). In healthy controls, beta2GPI-oxLDL complexes positively correlated to IMT of the IC (p = 0.007) and negatively to PONa after correction for age (p < 0.03). PONa inversely correlated with age (p = 0.008). In PAPS, IgG anti-beta2GPI-oxLig-1 independently predicted PONa (p = 0.02) and IMT of B (p = 0.003), CC, (p = 0.03) and of IC (p = 0.04). In PAPS, PONa inversely correlated to the IMT of B, CC and IC (p = 0.01, 0.02 and 0.003, respectively). IgG anti-beta2GPI-oxLig-1 may be involved in PAPS related atherogenesis via decreased PON activity.

Oxidized low-density lipoprotein and beta2-glycoprotein I in patients with systemic lupus erythematosus and increased carotid intima-media thickness: implications in autoimmune-mediated atherosclerosis.

Oxidative stress and LDL modification (oxLDL) are early pro-atherogenic events. OxLDL binds beta2GPI producing immunogenic oxLDL/beta2GPI complexes. Antibodies to these complexes have been associated with arterial thrombosis in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). Circulating oxLDL/beta2GPI complexes, IgG and IgM antibodies to these complexes were measured by ELISA in 30 SLE patients asymptomatic for cardiovascular disease (mean age 31 years) and 27 age/sex matched healthy controls. Carotid intima-media thickness (IMT) was measured by ultrasound in all patients and controls. Forty-seven percent of SLE presented plaques (median IMT of 0.65 +/- 0.12 mm) while only 7% of the controls had plaques (median IMT of 0.50 +/- 0.04 mm, P < 0.001). Median optical density (OD450nm) for oxLDL/beta2GPI complexes in SLE was 0.244 +/- 0.07, higher than controls (0.174 +/- 0.09, P < 0.001). Median OD for IgG anti-oxLDL/beta2GPI antibodies was also higher in SLE (0.297 +/- 0.26) compared to controls (0.194 +/- 0.07, P < 0.001) while the median OD for IgM antibodies in SLE (0.444 +/- 0.46) was not different than controls (0.326 +/- 0.22, P = 0.267). There was no correlation between IMT and oxLDL/beta2GPI complexes, IgG or IgM antibodies, possibly reflecting the complex interrelationship between these serologic elements and tissue factors in the arterial wall. These results support the hypothesis that oxLDL/beta2GPI complexes and IgG (not IgM) anti-oxLDL/beta2GPI antibodies contribute to the development of autoimmune-mediated atherosclerosis.

Oxidized LDL/beta2-glycoprotein I complexes: new aspects in atherosclerosis.

beta2-glycoprotein I (beta2GPI) is a major antigenic target for antiphospholipid antibodies. Oxidized low-density lipoprotein (oxLDL) is the principal lipoprotein found in atherosclerotic lesions, and it colocalizes with beta2GPI and immunoreactive lymphocytes. oxLDL/beta2GPI complexes appeared in the blood circulation of patients with diseases, such as systemic lupus erythematosus (SLE), antiphospholipid syndrome (APS), systemic sclerosis, diabetes mellitus and chronic renal diseases. Thus, the complexes may be associated with systemic and chronic inflammation of the vasculature. IgG anti-oxLDL/beta2GPI complexes autoantibodies and their immune complexes were detected only in SLE/APS patients and in its animal model and were strongly associated with arterial thrombosis. The oxLDL/beta2GPI complexes were internalized by macrophages via IgG anti-beta2GPI antibody-mediated phagocytosis. In contrast, IgM anti-oxLDL antibodies derived from hyperlipidemic mice reduced the incidence of atherosclerosis. The distribution patterns of IgG and IgM anti-oxLDL antibodies in patients suggest the different roles of these antibodies.

The smart life.

The Smart Life is an approach conceptualized from a frame of prevention, focused on youth, and aimed toward fostering independent and productive life styles. Currently, the focal concern is on African American youths, ages 12 through 18, who reside in rural areas of North Central Florida. Implemented through seminars, the Smart Life approach is grounded in theory and practice. It is built on grass roots efforts directed toward enlightening youths about the ways to improve their future through formulating goal-directed plans, and awakening their abilities to realize healthy and productive lives. The theoretical framework encompasses both Erik Erikson's psychoanalytic theory of identity development and the life cycle, as it accentuates the psychosocial nature of identify formation during adolescence, and Albert Bandura's social learning theoretical formulations specific to self-efficacy in terms of perceived self-competence.The seminars, held in various community-based settings, cover several areas. The issue to identity is always addressed. Discussions include: the meaning of being an African American, information on the history and global locations of people of African descent, and encouragement to make attachments. The other 4 critical areas that The Smart Life seminars focus on include the prevention of: crime and violence, early sexual experiences and pregnancy, alcohol and drug use and abuse, and school failure.

Logical responses to youth who run away from home: implications for psychiatric mental health nursing.

1. Runaway youths do not fit into a typical profile; they are adolescents of every race, ethnic group, and religious orientation; they are representative of every socioeconomic status and geographic location in America. 2. Psychosocial events including physical and sexual abuse are common antecedents to runaway behaviors. 3. Implications for psychiatric mental health nursing practice include working with community programs focused on reducing runaway episodes; implementing preventive measures focused on strengthening parenting and problem-solving skills for reducing conflict with families with adolescent children; and promoting responsible sexuality through adequate and responsible sex education and counseling.

Clinical significance of immunoglobulin A versus immunoglobulins G and M anti-cardiolipin antibodies in patients with systemic lupus erythematosus. Correlation with thrombosis, thrombocytopenia, and recurrent abortion.

Serum levels of immunoglobulins (Ig) A, G, and M anti-cardiolipin (aCL) antibodies were determined by enzyme-linked immunosorbent assay in a group of selected systemic lupus erythematosus female patients. Patients were divided into three groups based on their clinical history of thrombosis with or without thrombocytopenia (group I), thrombocytopenia alone (group II), and neither of these (group III). After the aCL antibody levels were determined, the patients' obstetric histories of pregnancies and abortions were reviewed. A high incidence of one or more abortions was seen only in group I patients. A high prevalence of elevated levels of IgA and IgG (but not IgM) aCL antibodies was observed in group I patients. However, among the patients in group II, only the levels of IgA aCL antibodies were increased. In both groups, the addition of the IgA aCL determination--to the classical IgG and IgM aCL assays--increased the prevalence of positive reactors in 31.6%. These results indicate that high levels of IgA aCL antibodies correlated better with thrombocytopenia than either IgG or IgM. Also, the importance of including the determination of IgA aCL antibodies to assess properly the risk of thrombosis, thrombocytopenia, and recurrent abortions in systemic lupus erythematosus patients is demonstrated.

Reduction of intra-oral demineralization of enamel after single exposures to sodium fluoride.

Studies demonstrated the effects of single rinses with low concentrations of NaF on the intra-oral demineralization of enamel. Blocks of bovine enamel were covered with Streptococcus mutans IB1600, mounted in palatal appliances, and worn in the mouths of volunteers for specified times. Subjects rinsed with solutions of NaF, with or without sucrose. Demineralization was determined as changes in iodide penetrability (delta Ip) of the enamel, while the pH and F of the streptococcal plaque, and enamel F, were determined with ion-specific electrodes. Delta Ip was reduced by about 80% (from 14.5 +/- 2.7 to 2.8 +/- 2.3 units) when 250 micrograms F/mL was added to the sucrose rinse. Corresponding plaque pH's were 4.1 +/- 0.5 and 4.2 +/- 0.3, consistent with a lack of effect on bacterial acidogenesis. Protection against mineral loss was concentration-dependent. Administration of sucrose at different times after NaF revealed that the effect of F persisted for at least 60 min. Analyses of plaque F demonstrated an initial elevation and concentration within the cells, followed by a drop to stable, baseline values. Enamel F increased slowly to almost 500 micrograms/g enamel after 105 min. The protective effect of F appeared to be manifested in two stages, the first related to a high plaque F and the second to F that became incorporated into the enamel. Analysis of the data suggested that F was transferred from plaque to enamel during the experimental period.