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BACKGROUND: Ecological disasters create dramatic changes as man-made and natural ecosystems adapt to their effects. In 2017, Hurricanes Irma and María devastated Puerto Rico. Public focus after such traumatic ecological events often neglects pre-existing community dynamics, heterogeneity of lived experience, and complexity of decision-making in the disaster context. We intended to better understand the lived experience of this ecological trauma in communities across ecosystems in Puerto Rico and among those displaced to Florida. METHOD: We used the Critical Medical Ecological (CME) framework to assess the relative contribution of ecological dimensions on lived experience across community levels and time. We used qualitative methods with emic coding and etic mapping of salient constructs to the ecological model. In total, 96 people participated in 23 discussion encounters. Two people coded interviews in Spanish using Dedoose. We identified common themes in sequential order mapped to elements of the CME to approximate the participants' temporal experience. RESULTS: Codes applied to the period of the hurricane's landfall, traverse, and exit were markedly distinct from the other two periods (before and after) examined in this study: the experience of the hurricane's strike was highly personal and, at this level, reflected a mix of sociocultural, biological, and abiotic factors. After the hurricanes, social and community factors re-emerged while new risks and conditions arose that were biological (e.g., leptospirosis, no food or water) or abiotic (e.g., unusable roads/bridges, structures destroyed), but created ongoing stressors and social needs for communities. As we found, the dynamics of the social and household landscape sometimes involved the decision to leave Puerto Rico altogether, or forced people to continually face and adapt to the ongoing collapse in basic services that were only slowly and differentially restored. CONCLUSION: Lived experience across each stage of the hurricanes differed substantially from one another. Communities disrupted by ecological disaster are also frequently entangled within global economic and political histories and dependencies that could preclude recovery. Island nations are especially vulnerable to both climate-induced ecological change and political-economic exploitation. The ongoing health effect of the hurricane remains palpable in many communities of Puerto Rico and among the diaspora in Florida.

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BACKGROUND: Two devastating sequential hurricanes impacted Puerto Rico during September of 2017. The hurricanes were traumatic and created social and ecological upheaval throughout Puerto Rico, and subsequently in communities of Central Florida where affected Puerto Ricans migrated. The 2017 hurricane season exposed and exacerbated previous long-standing socio-political, economic, environmental, and health crises, generating a humanitarian emergency in the country. The consequences of these human-ecological disasters destroyed much of Puerto Rico's residential and environmental infrastructure, displacing thousands of people and resulting in an unprecedented migration to the United States. We report on the lived experience of the investigator team and partnership in conducting community-based formative research subsequent to this disaster, research that aimed to identify salient issues relating to the impact of Hurricanes Irma and María on Puerto Rican communities both in Puerto Rico and in Central Florida. DISCUSSION: The challenges faced during the conduct of this research include but are not limited to (1) emotional distress of participants and team members, (2) access to affected populations, and (3) precarious environmental factors, such as unstable infrastructure. To address these challenges, the researchers applied a Critical Medical Ecological paradigm along with qualitative methods to assist constructing explanatory models while obtaining internally-valid (from the community perspective), cathartic narrative accounts of the lived experience of hurricane survivors. The experience of the research team may help inform other investigators conducting applied research during a humanitarian crisis. CONCLUSION: Lessons learned in this research included: (1) usefulness of applying the Critical Medical Ecological model in the development of the project, (2) incorporating participation and methods that prioritize authenticity, (3) understanding the trauma experience and using study methods sensitive to it, and (4) innovating with best approaches to conduct the study given the challenges in post-hurricane Puerto Rico. These lessons could provide new insights on how to conduct in-depth participatory health research with community members who have been traumatized and - often - displaced. This research also demonstrates the value of pre-existing partnerships, critical consciousness in the field team, and medical ecological modeling as experiential for organizing complex, inter-related, multi-level variables that explain community and individual impact of environmental disasters.

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OBJECTIVE: To explore whether the IFNL3/4 rs12979860 genotype may influence serum levels or production of interferon-inducible protein-10 (IP-10) by peripheral blood mononuclear cells from patients with systemic lupus erythematosus (SLE). METHODS: Sixty-six patients with SLE and 22 healthy blood donors (controls) were included. The IFNL3/4 rs12979860 polymorphism was genotyped by real-time polymerase chain reaction. IP-10 levels in sera supernatants of IFNα stimulated peripheral blood mononuclear cells were measured by enzime-linked immunosorbent assay. RESULTS: Allelic frequencies were CC (29%), CT (52%) and TT (20%) in SLE, and CC (32%), CT (41%) and TT (27%) in healthy controls. Median serum IP-10 levels were higher in SLE patients than in controls (190.8 versus 118.1 pg/ml; p < 0.001), particularly in those with high disease activity (278.5 versus 177.2 pg/ml; p = 0.037). However, serum IP-10 levels were not influenced by IFNL3/4 genotypes. Higher IP-10 production by peripheral blood mononuclear cells was found in both SLE patients (median 519.3 versus 207.6 pg/ml; p = 0.012) and controls (median 454.0 versus 201.7 pg/ml; p = 0.034) carrying the IFNL3/4 C allele compared with carriers of the T allele. CONCLUSIONS: Although IFNL3/4 rs12979860 allele C does not appear to influence serum IP-10 levels in SLE, it plays an important role in the production of IP-10 by peripheral blood mononuclear cells after IFNα stimulation.

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Obesity and emphysema are associated with low-grade systemic inflammation and oxidant stress. Assuming that the oxidant stress induced by emphysema would be decreased by obesity, we analyzed the oxidant/antioxidant state in a rat model combining both diseases simultaneously. Obesity was induced using sucrose, while emphysema by exposure to tobacco smoke. End-points evaluated were: body weight, abdominal fat, plasma dyslipidemia and malondialdehyde (MDA), insulin and glucose AUC, activities of Mn-superoxide dismutase (Mn-SOD), glutathione reductase (GR), glutathione transferase (GST) and glutathione peroxidase (GPx); lung MnSOD and 3-nitrotyrosine (3-NT) immunostaining, and expression of αV and ß6 integrin subunits. In rats with obesity, the body weight, abdominal fat, plasma triglyceride levels, glucose AUC, insulin levels, GST activity, and αV and ß6 integrin expressions were amplified. The rats with emphysema had lower values of body weight, abdominal fat, plasma insulin, triglycerides and glucose AUC but higher values of plasma MDA, GPx activity, and the lung expression of the αV and ß6 integrins. The combination of obesity and emphysema compared to either condition alone led to diminished body weight, abdominal fat, plasma insulin MDA levels, GPx and GST activities, and αV and ß6 integrin expressions; these parameters were all previously increased by obesity. Immunostaining for MnSOD augmented in all experimental groups, but the staining for 3-NT only increased in rats treated with tobacco alone or combined with sucrose. Results showed that obesity reduces oxidant stress and integrin expression, increasing antioxidant enzyme activities; these changes seem to partly contribute to a protective mechanism of obesity against emphysema development.

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Obesity is characterized by hypertrophy of adipose tissue and chronic obstructive pulmonary disease (COPD) by lung damage; both diseases are associated with systemic low-grade inflammation. There are no animal models combining obesity and COPD; therefore, these diseases were induced simultaneously in rats to analyze their effects on the expression of inflammatory mediators and enzymes involved in lung tissue remodeling. Obesity was induced with sucrose (30%) for 4 months concomitant with tobacco smoke exposure (20 cigarettes/day, 5 days/wk) for the last 2 months. Were evaluated: body weight, abdominal fat, dyslipidemia, glucose tolerance test (GTT), histology, inflammatory mediators with qPCR and enzyme-linked immunosorbent assay, matrix metalloproteinases (MMP-2), MMP-9, MMP-12, TIMP-1 and TIMP-2 through qRT-PCR, and MMP-2 and MMP-9 by gelatin zymography. The rats on a sucrose diet exhibited increased body weight, abdominal fat, triglycerides, GTT, and plasma levels of insulin, adiponectin, leptin, resistin, IL-6, IL-1ß, tumor necrosis factor-α (TNF-α) and IFN-γ, upregulated lung IL-6, IL-1ß, TNF-α and IFN-γ, showing hyperplastic bronchial and alveolar epithelium. The animals exposed to sucrose and tobacco smoke exhibited decreased body weight, abdominal fat and plasma levels of leptin, resistin, IL-1ß and IFN-γ, reducing inflammation but showing emphysematous lesions. Expression of gelatinases and MMP-12 augmented in the rats exposed to tobacco smoke alone or combined with sucrose. Zymography showed prominent gelatinases activity in all the experimental groups. These results suggest that simultaneous exposure to sucrose and tobacco smoke decreases inflammation but results in emphysematous lesions similar to those observed with tobacco smoke exposure, suggesting that obesity does not confer any protective effect against lung damage.

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Kramecyne is a new peroxide, it was isolated from Krameria cytisoides, methanol extract, and this plant was mostly found in North and South America. This compound showed potent anti-inflammatory activity; however, the mechanisms by which this compound exerts its anti-inflammatory effect are not well understood. In this study, we examined the effects of kramecyne on inflammatory responses in mouse lipopolysaccharide- (LPS-) induced peritoneal macrophages. Our findings indicate that kramecyne inhibits LPS-induced production of tumor necrosis factor (TNF- α ) and interleukin- (IL-) 6. During the inflammatory process, levels of cyclooxygenase- (COX-) 2, nitric oxide synthase (iNOS), and nitric oxide (NO) increased in mouse peritoneal macrophages; however, kramecyne suppressed them significantly. These results provide novel insights into the anti-inflammatory actions and support its potential use in the treatment of inflammatory diseases.

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Exposure to silica induces granulomatous lung inflammation evolving to fibrosis through yet unclear pathogenic mechanisms. We examined the expression of extracellular matrix remodeling molecules: collagenase 3, gelatinases A and B, and TIMP-1 and TIMP-2 in experimental lung silicosis. Rats were instilled with 50 mg of silica and sacrificed after 15 and 60 d. At 60 d a significant increase in lung collagen content was found (170.2 +/- 34.4 versus 88.2 +/- 20.8 microgram/mg in controls, p = 0.01). Gelatin zymography of bronchoalveolar lavage fluid (BALF) from 15 and 60 d revealed bands of progelatinase A and progelatinase B, and lung tissue zymograms showed in addition, the active gelatinase A form at 15 d. By in situ hybridization and immunohistochemistry, early silicotic granulomas exhibited intense staining for all matrix metalloproteinases (MMPs) and TIMPs assayed. Labeling was restricted inside granulomas and surrounding areas. Late silicotic granulomas at 60 d showed lower MMP expression than did early lesions, and in highly fibrotic nodules scarce signal was usually found. TIMP-1 and TIMP-2 showed a moderate reduction in 60-d silicotic nodules. These findings suggest that an imbalance in the expression of MMPs and TIMPs may be implicated in extracellular matrix remodeling and basement membrane disruption during experimental lung silicosis.

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