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AimThe aim of this study was to investigate whether Dectin-1 influences the immune-inflammatory response in A. fumigatus keratitis by modulating macrophage polarization.Methods1. The models of 1-day, 3-day, and 5-day of fungal keratitis were established in SPF C57BL/6 mice after stimulation by A. fumigatus. Dectin-1 agonist (curdlan) and antagonist (laminaran) were injected separately in the mouse subconjunctivae for 1 day in the established mouse model of A. fumigatus keratitis; PBS was used as the control. Inflammation of the mouse cornea was observed under a slit lamp to obtain a clinical score. 2. The expression of M1 (TNF-α, INOS, IL-6, IL-12) and M2 (Arg-1, IL-10, Fizz-1, Ym-1) cytokine-encoding mRNAs was quantified by RT-PCR. 3. Changes in the number of macrophages and expression of M1 and M2 macrophages in mouse corneas detected by immunofluorescence and flow cytometry. 4. Pre-treatment of RAW264.7 cells with MAPK cell signaling pathway inhibitors SB203580 (p38 inhibitor, 10µM), U0126 (ERK inhibitor, 20µM), SP600125 (JNK inhibitor, 10µM) and DMSO separately for 2 h, and stimulated by A. fumigatus for 12 h. Changes in the mRNA expression of M1 and M2 cytokines in the macrophages were quantified by RT-PCR.Results1. With curdlan pre-treatment, mouse corneal inflammation worsened, and the clinical score increased after infection. In contrast, in the laminaran pre-treated group, corneal inflammation was alleviated and the clinical score decreased significantly compared to the PBS group after infection. 2. Compared with the control group, the expression levels of macrophage phenotype-related M1 and M2 cytokine mRNAs increased significantly 1, 3, and 5 days after A. fumigatus infected the corneas of mice. 3. With curdlan pre-treatment, the expression of mRNAs encoding M1 cytokines increased, while those encoding M2 cytokines decreased in the cornea compared to the PBS group. In contrast, after infection, mRNA levels for M1 cytokines decreased significantly and those for M2 cytokines increased in the cornea of the laminaran pre-treated group compared to the PBS group. 4. The number of macrophages in the corneal stroma of mice in the curdlan pretreatment group increased significantly compared with the PBS group, while in the laminaran pretreatment group this number decreased significantly. 5. The results of flow cytometry showed that after 3 days of mouse corneal A. fumigatus infection, the number of macrophages in the mouse A. fumigatus model in the curdlan pretreatment group was increased (10.4%) and the number of macrophages in the mouse A. fumigatus model in the laminaran pretreatment group (6.31%), when compared with the AF+FBS group (7.91%). The proportion of M1-type macrophages was increased in the curdlan pretreated group (55.6%) compared to the AF+FBS group (51.2%), the proportion of laminaran pretreatment group had a decreased proportion of M1-type macrophages (46.8%); while M2-type macrophages were the opposite of M1-type: the proportion of M2-type macrophages was 49.2% in the AF+FBS group, the proportion of M2-type macrophages was decreased in the curdlan pretreatment group (44.0%), and the proportion of M2-type macrophages was increased in the laminaran pretreatment group (53.5%). 6. Expression of M1 and M2 cytokine-encoding mRNAs decreased and increased, respectively, after infection, in the RAW264.7 cells pre-treated with MAPK pathway inhibitors, compared to the control.ConclusionIn a mouse model of A. fumigatus keratitis, Dectin-1 can affect macrophage recruitment and polarization, may regulate macrophage phenotype-associated factor changes through the MAPK signaling pathway.

Objective To investigate the ocular clinical features and diagnostic and therapeutic protocol of patients with endogenous endophthalmitis (EE) secondary to Klebsiella pneumoniae liver abscess (KPLA). Methods Six patients (seven eyes) with EE secondary to KPLA who attended our hospital from January 2019 to December 2020 were enrolled and analyzed in terms of clinical manifestation, examination findings, treatment regimen, and prognosis. Results All six patients were male, among whom five had pyrexia. All patients had impaired vision, and at initial diagnosis, there were four patients (five eyes) with no light perception, one patient (one eye) with manual vision, and one case (one eye) with light perception. All patients had the typical clinical manifestations of endophthalmitis such as impaired vision, conjunctival congestion and edema, ocular swelling and pain, and inflammatory response in the anterior chamber, and postoperative microbial culture of intraocular fluid showed positive Klebsiella pneumoniae. At the last visit, four patients (four eyes) had loss of vision, one patient (one eye) did not cooperate in vision check, and one patient (two eyes) was lost to follow-up. Conclusion EE secondary to KPLA is highly destructive to eyeball structure and visual function, and patients with KPLA who develop systemic symptoms (such as fever) or ocular discomfort (such as loss of vision, eye redness, and eye pain) should attend the outpatient service of ophthalmology department and receive regular follow-up examination to be alert to the development of endophthalmitis.

Objective To investigate the effect of the sodium-glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin on renal function and renin-angiotensin-aldosterone system (RAAS) in elderly patients with early diabetic kidney disease (DKD). Methods A total of 97 elderly patients with type 2 diabetes mellitus (T2DM) who attended our hospital from September 1, 2019 to August 1, 2021 were enrolled, and according to urinary albumin-to-creatinine ratio (UACR), they were divided into normal UACR group and early DKD group. A random number table was further used to determine whether each patient in the above two groups was treated with dapagliflozin. Finally, all patients were divided into normal-UACR dapagliflozin group (group A), normal-UACR control group (group B), early-DKD dapagliflozin group (group C), and early-DKD control group (group D), and these four groups were compared in terms of the changes in related clinical indices at 1 year after treatment. Results After 1 year of treatment, group A had significant changes in body mass index (BMI), systolic blood pressure, diastolic blood pressure, UACR, annualized relapse rate (ARR), fasting blood glucose, and fasting insulin (t=2.098-7.122,P

Nitrogen (N) can enhance the biomass and feeding quality of forage crops and advance the growth of the herbivorous livestock industry. Investigating the N fertilizer dynamics in the soil–crop–livestock system is important for resource-use efficiency and environmental safety. By using the 15N-labeled technology and the in vitro incubation technique, an experiment was conducted in the North China Plain (NCP) in 2015–2016 to quantify the migration and distribution of N fertilizer in the soil–forage triticale (X Triticosecale Wittmack)–dairy cow system. The results showed that 34.1–37.3% of the applied N fertilizer was absorbed by forage triticale, in which 35.9–39.6% N accumulated in the stems and 60.4–64.1% accumulated in the leaves. In addition, 36.3–39.1% of the applied N fertilizer remained in the 0–100 cm soil layer, in which 81.8–91.3% was distributed in the 0–40 cm soil layer. The remaining 24.6–26.8% of the applied N fertilizer was lost in various ways and 28.1–31.3% of the N fertilizer could be utilized by dairy cows. When N fertilizer was applied between 0–225 kg N ha−1, the increased application of N fertilizer improved the biomass yield from 14.0 to 17.5 t ha−1 and enhanced the N content of the forage triticale from 1.3% to 1.4%; however, it did not significantly affect the distribution rate of N fertilizer in the soil–forage triticale–dairy cow system. The optimum N fertilizer application rate for forage triticale is less than 225 kg N ha–1 to maintain high-efficient N use in the soil–crop–livestock system and reduce the environmental risks in the NCP. Our results quantified the N fertilizer dynamics in the soil–forage triticale–dairy cow system and provided a significant reference for guiding rational strategies of forage triticale cultivation. [ABSTRACT FROM AUTHOR]

Diabetic cardiomyopathy (DCM) is defined as ventricular dysfunction occurring independently of a recognized cause such as hypertension or coronary artery disease. Liver X receptor [alpha] (LXR[alpha]), a subtype of ligand-activated transcription factors LXRs, has been considered as a potential pharmacological target in the pathogenesis of cardiovascular and metabolic diseases. However, the potential mechanism of how LXR[alpha] is regulated in cardiomyocytes is still unclear. This study investigated the effect of activating LXR[alpha] with GW3965 on cardiomyocyte apoptosis and its upstream regulator in glucose-induced H9C2 cells. Our data indicated that GW3965 up-regulated the expression of LXR[alpha], inhibited cardiomyocyte apoptosis, and altered the apoptosis-related proteins in glucose-induced H9C2 cells. In addition, GW3965 restored the mitochondrial membrane potential level and decreased the ROS production induced by glucose. Moreover, LXR[alpha] was confirmed as a direct target of microRNA-1 (miR-1) that was involved in cardiomyocyte apoptosis of DCM, and overexpression of miR-1 abrogated the inhibiting effect of GW3965 on glucose-induced apoptosis in H9C2 cells. This study highlights an important role of LXR[alpha] in the development of DCM and brings new insights into the complex mechanisms involved in the pathogenesis of DCM. Key words: diabetic cardiomyopathy, liver X receptor [alpha], microRNA-1, apoptosis, reactive oxygen species. La cardiomyopathie diabétique (CMD) est définie comme un dysfonctionnement ventriculaire qui survient indépendamment d'une cause reconnue comme l'hypertension ou la coronaropathie. Le récepteur nucléaire LXR[alpha] (<>), un sous-type des facteurs de transcription activés par les ligands LXR, a été considéré comme cible pharmacologique potentielle dans la pathogenèse des maladies cardiovasculaires et métaboliques. Cependant, le possible mécanisme par lequel le LXR[alpha] est régulé dans les cardiomyocytes n'est toujours pas clair. Cette étude visait à examiner l'effet de l'activation du LXR[alpha] par le GW3965 sur l'apoptose des cardiomyocytes et sur ses régulateurs en amont chez les cellules H9C2 traitées au glucose. Les données ont révélé que le GW3965 régulait à la hausse l'expression du LXR[alpha], inhibait l'apoptose des cardiomyocytes et modifiait l'expression des protéines liées à l'apoptose chez les cellules H9C2 traitées au glucose. De plus, le GW3965 rétablissait le potentiel membranaire mitochondrial et diminuait la production de DRO induite par le glucose. En outre, puisque le LXR[alpha] s'est avéré une cible directe du microARN-1 (miR-1) impliqué dans l'apoptose des cardiomyocytes dans la CMD, la surexpression de miR-1 abolissait l'effet inhibiteur du GW3965 sur l'apoptose induite par le glucose chez les cellules H9C2. Cette étude souligne le rôle important du LXR[alpha] dans le développement de la CMD et apporte de nouvelles connaissances pour mieux comprendre les mécanismes complexes impliqués dans la pathogenèse de la CMD. [Traduit par la Rédaction] Mots-clés: cardiomyopathie diabétique, LXR [alpha], microARN-1, apoptose, dérivés réactifs de l'oxygène., Introduction There is a growing amount of data showing that patients with diabetes mellitus (DM) display a high risk of developing heart failure, independent from other risk factors such as [...]