Miracle-dz/UniFAR-FTUs huggingface dataset:
Adherence and Efficacy of Smoking Cessation Treatment Among Patients with COPD in China

Background Smoking cessation is a key intervention for all smokers with chronic obstructive pulmonary disease (COPD). Poor treatment adherence is a challenge in clinical practice that might contribute to the lower efficacy of medication (eg, oral drug). However, it is unclear what factors will influence adherence among smokers with COPD. Methods This study was based on an open-label randomized controlled trial (RCT) of varenicline and bupropion for smoking cessation among patients with COPD in China. The medication was given for 12 weeks, and visits and assessments were conducted at weeks 0, 1, 2, 4, 6, 9, 12, and 24. We assessed whether the adherence to smoking cessation treatment affects the smoking cessation efficacy and evaluated predictors of adherence. Results A total of 136 participants were recruited from February 2019 to June 2020, and analyzed using the intention-to-treat (ITT) method. In this study, 48.5% (66/136) of the total participants had good adherence to smoking cessation, and good adherence significantly improved the efficacy of smoking cessation (OR=9.60, 95% CI 4.02–22.96, P < 0.001). After adjusting for age, gender, nationality, education, and marital status, we found older age, higher education level, having more previous quitting attempts, stronger self-efficacy and preparation in quitting smoking, recognizing hazards of smoking, longer duration of COPD, and higher St. George’s Respiratory Questionnaire (SGRQ) scores were relevant to good adherence (P < 0.05). Conclusion To our best knowledge, this is the first study to evaluate adherence to smoking cessation treatment among patients with COPD in China. Our study found that good adherence to smoking cessation treatment significantly improved the smoking cessation efficacy, and predictors of adherence were evaluated. We call on the medical community to pay attention to the adherence to smoking cessation among patients with COPD.
Invariant Natural Killer T Cells as Key Players in Host Resistance against Paracoccidioides brasiliensis

Invariant Natural Killer T (iNKT) cells are key players in the immunity to several pathogens; however, their involvement in the resistance to Paracoccidioides brasiliensis infection remains unknown. Using splenocytes from CD1d (CD1d−/−) and iNKT-deficient (Jα18−/−) mice, we found that iNKT cells are the innate source of IFN-γ after P. brasiliensis infection and are required to potentiate macrophage oxidative burst and control fungal growth. To determine whether iNKT cells contribute in vivo to host resistance against P. brasiliensis infection, we infected intratracheally wild-type and Jα18−/− C57BL/6 mouse strains with the virulent Pb18 isolate. iNKT cell deficiency impaired the airway acute inflammatory response, resulting in decreased airway neutrophilia and reduced IFN-γ, KC, and nitric oxide (NO) production. The deficient innate immune response of Jα18−/− mice to Pb18 infection resulted in increased fungal burden in the lungs and spleen. Besides, the activation of iNKT cells in vivo by administration of the exogenous iNKT ligand α-galactosylceramide (α-GalCer) improved host resistance to P. brasiliensis infection. Although the mechanisms responsible for this phenomenon remain to be clarified, α-GalCer treatment boosted the local inflammatory response and reduced pulmonary fungal burden. In conclusion, our study is the first evidence that iNKT cells are important for the protective immunity to P. brasiliensis infection and their activation by an exogenous ligand is sufficient to improve the host resistance to this fungal infection.
Oral Administration of Gintonin Protects the Brains of Mice against Aβ-Induced Alzheimer Disease Pathology: Antioxidant and Anti-Inflammatory Effects

The study was aimed at analyzing the protective effects of gintonin in an amyloid beta- (Aβ-) induced Alzheimer's disease (AD) mouse model. For the development of the Aβ-induced AD mouse model, the amyloid-β (Aβ1-42) peptide was stereotaxically injected into the brains of mice. Subsequently, gintonin was administered at a dose of 100 mg/kg/day/per oral (p.o) for four weeks daily, and its effects were evaluated by using western blotting, fluorescence analysis of brain sections, biochemical tests, and memory-related behavioral evaluations. To elucidate the effects of gintonin at the mechanistic level, the activation of endogenous antioxidant mechanisms, as well as the activation of astrocytes, microglia, and proinflammatory mediators such as nuclear factor erythroid 2-related factor 2 (NRF-2) and heme oxygenase-1 (HO-1), was evaluated. In addition, microglial cells (BV-2 cells) were used to analyze the effects of gintonin on microglial activation and signaling mechanisms. Collectively, the results suggested that gintonin reduced elevated oxidative stress by improving the expression of NRF-2 and HO-1 and thereby reducing the generation of reactive oxygen species (ROS) and lipid peroxidation (LPO). Moreover, gintonin significantly suppressed activated microglial cells and inflammatory mediators in the brains of Aβ-injected mice. Our findings also indicated improved synaptic and memory functions in the brains of Aβ-injected mice after treatment with gintonin. These results suggest that gintonin may be effective for relieving AD symptoms by regulating oxidative stress and inflammatory processes in a mouse model of AD. Collectively, the findings of this preclinical study highlight and endorse the potential, multitargeted protective effects of gintonin against AD-associated oxidative damage, neuroinflammation, cognitive impairment, and neurodegeneration.
Exercise alleviates cardiac remodelling in diabetic cardiomyopathy via the miR-486a-5p-Mst1 pathway

Objective(s): Physical exercise has emerged as an effective therapy to mitigate cardiac remodelling in diabetic cardiomyopathy (DCM). The results of our previous studies revealed mammalian sterile 20-like kinase 1 (Mst1) is a key regulator of the progression of DCM. However, the precise molecular mechanism of physical exercise-induced cardiac protection and its association with Mst1 inhibition remain unclear. Materials and Methods: Wildtype and Mst1 transgenic mice were challenged with streptozotocin (STZ) to induce experimental diabetes and were divided into sedentary and exercise groups. The DCM phenotype was evaluated by echocardiography, Masson’s trichrome staining, TUNEL and immunoblotting analyses. The exercise-regulated miRNAs targeting Mst1 were predicted by bioinformatic analysis and later confirmed by RT-qPCR, immunoblotting, and dual-luciferase reporter assays. In addition, cultured neonatal mouse cardiomyocytes were subjected to simulate diabetes to elucidate the underlying mechanisms. Results: Compared to the sedentary diabetic control, physical exercise inhibited Mst1 and alleviated cardiac remodelling in mice with DCM, as evidenced by decreases in the left ventricular end-systolic internal dimension (LVESD) and left ventricular end-diastolic internal dimension (LVEDD), increases in the left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS), attenuation of collagen deposition, and the suppression of apoptosis. Bioinformatic analysis and apoptosis assessments revealed exercise exerted protective effects against DCM through miR-486a-5p release. Moreover, luciferase reporter assays confirmed miR-486a-5p directly suppressed the expression of Mst1, thereby inhibiting the apoptosis of cardiomyocytes subjected to high glucose treatment. Conclusion: Physical exercise inhibits cardiac remodelling in DCM, and the mechanism is associated with miR-486a-5p release-induced Mst1 inhibition.
Binge-Like Ethanol Drinking Increases Otx2, Wnt1, and Mdk Gene Expression in the Ventral Tegmental Area of Adult Mice

Alcohol use disorder is associated with pathophysiological changes in the dopaminergic system. Orthodenticle homeobox 2 (OTX2) is a transcription factor important for the development of dopaminergic neurons residing in the ventral tegmental area (VTA), a critical region of the brain involved in drug reinforcement. Previous studies have demonstrated that ethanol exposure during embryonic development reduces Otx2 mRNA levels in the central nervous system. We hypothesized that levels of OTX2 would be altered by binge-like ethanol consumption in adult animals. To test this, Otx2 mRNA and protein levels in the mouse VTA were measured by quantitative real-time PCR and western blotting, respectively, after mice drank ethanol for 4 days in a procedure that elicits binge levels of ethanol consumption (drinking in the dark). Expression of known and putative OTX2 transcriptional target genes (Sema3c, Wnt1, and Mdk) were also measured in the VTA after ethanol drinking. Otx2 mRNA and protein levels were elevated in the VTA 24 hours after the fourth drinking session and there was a corresponding increase in the expression of Mdk transcript. Interestingly, Wnt1 transcript was elevated in the VTA immediately after the fourth drinking session but returned to control levels 24 hours later. We next investigated if viral-mediated reduction of Otx2 in the mouse VTA would alter ethanol or sucrose intake. Lentiviral vectors expressing a shRNA targeting Otx2 or a control shRNA were injected into the VTA and mice were tested in the drinking in the dark protocol for ethanol and sucrose drinking. Reducing levels of OTX2 in the VTA did not alter ethanol or sucrose consumption. One limitation is that the extent of OTX2 reduction may not have been sufficient. Although OTX2 in the VTA may not play a role in binge-like drinking in adult mice, OTX2 could contribute to ethanol-induced transcriptional changes in this region.
A checklist of vascular plants of Ewe-Adakplame Relic Forest in Benin, West Africa

Abstract Covering 560.14 hectares in the south-east of Benin, the Ewe-Adakplame Relic Forest (EARF) is a micro-refugium that shows insular characteristics within the Dahomey Gap. It is probably one of the last remnants of tropical rain forest that would have survived the late Holocene dry period. Based on intensive field investigations through 25 plots (10 × 50 m size) and matching of herbarium specimens, a checklist of 185 species of vascular plant belonging to 54 families and 142 genera is presented for this forest. In addition to the name for each taxon, we described the life form following Raunkiaer’s definitions, chorology as well as threats to habitat. The Rubiaceae family was the richest (20 species) followed by the Fabaceae (15 species). Life forms showed the preponderance of phanerophytes (88%). The Chorological spectrum was dominated by Guineo-Congolean species (66%). Species richness estimated were 200.52 ± 9.2808 for Bootstrap; 217.62 ± 14.5972; 224.16 ± 15.3725 and 242.67 respectively for Chao, Jacknife1 and Jacknife2. Bootstrap appears to be the estimation closer to the field records. In Benin, EARF is home for Rinorea species described as West African forest bio-indicators and single location for Nesogordonia papaverifera, Mansonia altissima, Englerophytum oblanceolatum, Octolobus spectabilis, Vitex micrantha and most of Drypeteae tribe species (Drypetes aframensis, Drypetes afzelii, Drypetes gilgiana and Drypetes leonensis) recorded in Benin. Our results provides baseline information for further in-depth analysis of vegetation history in Benin by raising the question on the past floristic connection of the Dahomey gap and community engagement in conservation.
Bilobalide Enhances AMPK Activity to Improve Liver Injury and Metabolic Disorders in STZ-Induced Diabetes in Immature Rats via Regulating HMGB1/TLR4/NF-κB Signaling Pathway

This study was aimed at examining the effect and underlying mechanisms of bilobalide (BB) on hepatic injury in streptozotocin- (STZ-) induced diabetes mellitus (DM) in immature rats. Immature rats (one day old) were randomly divided into five groups: group I, control nondiabetic rats; group II, STZ-induced, untreated diabetic rats; groups III/IV/V, STZ-induced and BB-treated diabetic rats, which were intraperitoneally injected with BB (2.5 mg/kg, 5 mg/kg, or 10 mg/kg) after 3 days followed by STZ treatment. We observed that BB improved the histopathological changes and maintained normal glucose metabolism, blood lipid, and liver function indicators, such as fasting blood glucose, obesity index, HbA1c, HOMA-IR, fast serum insulin, adiponectin, total cholesterol (TC), triglyceride (TG), high-density lipoprotein (HDL), low-density lipoprotein (LDL), aspartate transaminase (AST), and alanine transaminase (ALT) in STZ-induced DM in immature rats by a biochemical analyzer or ELISA. Meanwhile, Western blot analysis showed that in STZ-induced DM immature rats, BB decreased the expression of apoptosis-related proteins Bax, cleaved caspase-3, and cleaved caspase-9 while enhancing the Bcl-2 expression; BB downregulated the expression of ACC related to fat anabolism, while upregulating the expression of CPT-1 related to fat catabolism. Strikingly, treatment with BB significantly increased the expression of AMPKα1 as well as inhibited HMGB1, TLR4, and p-P65 expression in hepatic tissues of immature DM rats. AMPK inhibitor (compound C, CC) cotreated with BB undermined the protective effect of BB on the liver injury. The results of the present study suggested BB may have a significant role in alleviating liver damage in the STZ-induced immature DM rats.
Effects of hot-melt extruded nano-copper on the Cu bioavailability and growth of broiler chickens

Abstract This study was aimed to investigate the Cu bioavailability, growth response, digestibility of nutrients, and blood metabolites of broiler chicks fed CuSO4 in nano or common forms. A total of 720 broiler chickens were distributed between eight treatments according to a completely randomized design. There were 8 treatments and 6 replicates in each treatment with 15 birds/replicate. The treatments were divided into common copper sulfate at the doses of 16 ppm, 40 ppm, 80 ppm, and 120 ppm (INO) and hot-melt extruded copper sulfate at the doses of 16 ppm, 40 ppm, 80 ppm, and 120 ppm (HME-Cu). The experiment was operated for 35 days in 2 phases (phase 1, d 0 to 14; and phase 2, d 15 to 35). No significant differences were shown in growth performance, feed intake, FCR, and nutrient digestibility among the treatments. The concentration of Cu in the serum was increased in the HME-Cu broilers compared with the INO broilers at phase 2. A linear increase was observed in the concentration of Cu in the liver in broilers fed INO diets, however, no significant differences were observed by the supplementation of HME-Cu levels. The linear increase was detected in the content of Cu in excreta in the INO and HME-Cu treatments by increasing the dietary Cu content. The HME-Cu treatments showed a lower Cu concentration in the excreta compared with the INO treatments. The higher bioavailability of Cu in HME form can decrease the recommended dose of Cu in broiler diets.
Remnant gastric cancer: An ordinary primary adenocarcinoma or a tumor with its own pattern?

BACKGROUND Remnant gastric cancer (RGC) is defined as a tumor that develops in the stomach after a previous gastrectomy and is generally associated with a worse prognosis. However, there little information available regarding RGCs and their prognostic factors and survival. AIM To evaluate the clinicopathological characteristics and prognosis of RGC after previous gastrectomy for benign disease. METHODS Patients who underwent curative resection for primary gastric cancer (GC) at our institute between 2009 and 2019 were retrospectively evaluated. All RGC resections with histological diagnosis of gastric adenocarcinoma were enrolled in this study. Primary proximal GC (PGC) who underwent total gastrectomy was selected as the comparison group. Clinical and pathological data were collected from a prospective medical database. RESULTS A total of 41 patients with RGC and 120 PGC were included. Older age (P = 0.001), lower body mass index (P = 0.006), hemoglobin level (P < 0.001), and number of resected lymph nodes resected (LN) (P < 0.001) were associated with the RGC group. Lauren type, pathological tumor-node-metastasis, and perioperative morbimortality were similar between RGC and PGC. There was no difference in disease-free survival (P = 0.592) and overall survival (P = 0.930) between groups. LN status was the only independent factor related to survival. CONCLUSION RGC had similar clinicopathological characteristics to PGC. Despite the lower number of resected LN, RGC had a similar prognosis.
Ketogenic Diet Suppressed T-Regulatory Cells and Promoted Cardiac Fibrosis via Reducing Mitochondria-Associated Membranes and Inhibiting Mitochondrial Function

Ketogenic diet (KD) is popular in diabetic patients but its cardiac safety and efficiency on the heart are unknown. The aim of the present study is to determine the effects and the underlined mechanisms of KD on cardiac function in diabetic cardiomyopathy (DCM). We used db/db mice to model DCM, and different diets (regular or KD) were used. Cardiac function and interstitial fibrosis were determined. T-regulatory cell (Treg) number and functions were evaluated. The effects of ketone body (KB) on fatty acid (FA) and glucose metabolism, mitochondria-associated endoplasmic reticulum membranes (MAMs), and mitochondrial respiration were assessed. The mechanisms via which KB regulated MAMs and Tregs were addressed. KD improved metabolic indices in db/db mice. However, KD impaired cardiac diastolic function and exacerbated ventricular fibrosis. Proportions of circulatory CD4+CD25+Foxp3+ cells in whole blood cells and serum levels of IL-4 and IL-10 were reduced in mice fed with KD. KB suppressed the differentiation to Tregs from naive CD4+ T cells. Cultured medium from KB-treated Tregs synergically activated cardiac fibroblasts. Meanwhile, KB inhibited Treg proliferation and productions of IL-4 and IL-10. Treg MAMs, mitochondrial respiration and respiratory complexes, and FA synthesis and oxidation were all suppressed by KB while glycolytic levels were increased. L-carnitine reversed Treg proliferation and function inhibited by KB. Proportions of ST2L+ cells in Tregs were reduced by KB, as well as the production of ST2L ligand, IL-33. Reinforcement expressions of ST2L in Tregs counteracted the reductions in MAMs, mitochondrial respiration, and Treg proliferations and productions of Treg cytokines IL-4 and IL-10. Therefore, despite the improvement of metabolic indices, KD impaired Treg expansion and function and promoted cardiac fibroblast activation and interstitial fibrosis. This could be mainly mediated by the suppression of MAMs and fatty acid metabolism inhibition via blunting IL-33/ST2L signaling.
Genome-wide investigation of the AP2/ERF superfamily and their expression under salt stress in Chinese willow (Salix matsudana)

AP2/ERF transcription factors (TFs) play indispensable roles in plant growth, development, and especially in various abiotic stresses responses. The AP2/ERF TF family has been discovered and classified in more than 50 species. However, little is known about the AP2/ERF gene family of Chinese willow (Salix matsudana), which is a tetraploid ornamental tree species that is widely planted and is also considered as a species that can improve the soil salinity of coastal beaches. In this study, 364 AP2/ERF genes of Salix matsudana (SmAP2/ERF) were identified depending on the recently produced whole genome sequencing data of Salix matsudana. These genes were renamed according to the chromosomal location of the SmAP2/ERF genes. The SmAP2/ERF genes included three major subfamilies: AP2 (55 members), ERF (301 members), and RAV (six members) and two Soloist genes. Genes’ structure and conserved motifs were analyzed in SmAP2/ERF family members, and introns were not found in most genes of the ERF subfamily, some unique motifs were found to be important for the function of SmAP2/ERF genes. Syntenic relationships between the SmAP2/ERF genes and AP2/ERF genes from Populus trichocarpa and Salix purpurea showed that Salix matsudana is genetically more closely related to Populus trichocarpa than to Salix purpurea. Evolution analysis on paralog gene pairs suggested that progenitor of S. matsudana originated from hybridization between two different diploid salix germplasms and underwent genome duplication not more than 10 Mya. RNA sequencing results demonstrated the differential expression patterns of some SmAP2/ERF genes under salt stress and this information can help reveal the mechanism of salt tolerance regulation in Salix matsudana.
Responding to the 2018–2020 Ebola Virus Outbreak in the Democratic Republic of the Congo: Rethinking Humanitarian Approaches

Abstract The Democratic Republic of Congo (DRC) presents a challenging context in which to respond to public health crises. Its 2018–2020 Ebola outbreak was the second largest in history. Lessons were known from the previous West African outbreak. Chief among these was the recognition that local action and involvement are key to establishing effective epidemic-response. It remains unclear whether and how this was achieved in DRC’s Ebola response. Additionally, there is a lack of scholarship on how to build resilience (the ability to adapt or transform under pressure) in crisis-response. In this article, we critically review literature to examine evidence on whether and how communities were involved, trust built, and resilience strengthened through adaptation or transformation of DRC’s 2018–2020 Ebola response measures. Overall, we found limited evidence that the response adapted to engage and involve local actors and institutions or respond to locally expressed concerns. When adaptations occurred, they were shaped by national and international actors rather than enabling local actors to develop locally trusted initiatives. Communities were “engaged” to understand their perceptions but were not involved in decision-making or shaping responses. Few studies documented how trust was built or analyzed power dynamics between different groups in DRC. Yet, both these elements appear to be critical in building effective, resilient responses. These failures occurred because there was no willingness by the national government or international agencies to concede decision-making power to local people. Emergency humanitarian response is entrenched in highly medicalized, military style command and control approaches which have no space for decentralizing decision-making to “non-experts”. To transform humanitarian responses, international responders can no longer be regarded as “experts” who own the knowledge and control the response. To successfully tackle future humanitarian crises requires a transformation of international humanitarian and emergency response systems such that they are led, or shaped, through inclusive, equitable collaboration with local actors.
First report of Meloidogyne incognita infecting Cannabis sativa in Alabama

Abstract Hemp (Cannabis sativa L.) is a new crop in Alabama. In 2019, symptomatic plants with stunted growth, poor root development, and numerous galls were observed in hemp plants grown in Geneva County, AL. After harvest, soil samples were collected from areas with the symptomatic plants and root-knot nematode (Meloidogyne spp.) were found in the soil. Based on morphological features and the polymerase chain reactions using species-specific primers, it was identified as Meloidogyne incognita. Further, a host differential test in a greenhouse assay confirmed it to be M. incognita race 3. The pathogenicity of the nematode to the hemp was confirmed by a modified version of Koch’s postulates. To our knowledge, this is the first report of M. incognita infecting Cannabis sativa in Alabama.