ERK1/2-CEBPB Axis-Regulated hBD1 Enhances Anti-Tuberculosis Capacity in Alveolar Type II Epithelial Cells.

Tuberculosis, caused by Mycobacterium tuberculosis (Mtb), remains a global health crisis with substantial morbidity and mortality rates. Type II alveolar epithelial cells (AEC-II) play a critical role in the pulmonary immune response against Mtb infection by secreting effector molecules such as antimicrobial peptides (AMPs). Here, human ß-defensin 1 (hBD1), an important AMP produced by AEC-II, has been demonstrated to exert potent anti-tuberculosis activity. HBD1 overexpression effectively inhibited Mtb proliferation in AEC-II, while mice lacking hBD1 exhibited susceptibility to Mtb and increased lung tissue inflammation. Mechanistically, in A549 cells infected with Mtb, STAT1 negatively regulated hBD1 transcription, while CEBPB was the primary transcription factor upregulating hBD1 expression. Furthermore, we revealed that the ERK1/2 signaling pathway activated by Mtb infection led to CEBPB phosphorylation and nuclear translocation, which subsequently promoted hBD1 expression. Our findings suggest that the ERK1/2-CEBPB-hBD1 regulatory axis can be a potential therapeutic target for anti-tuberculosis therapy aimed at enhancing the immune response of AEC-II cells.

Protocol for estimating the impact of climate change on economic growth and inequality under climate policies.

The impact of climate change on economic inequality has attracted increasing attention from both government and academia. Here, we present a protocol for estimating both the impact of climate change on economic growth and economic growth inequality under multiple climate policies. We describe steps for constructing an uncertainty analysis framework, collecting and pre-processing data, and estimating the climate-economic response. We then detail procedures of predicting climate policy impact and calculating inter-country economic growth inequality. For complete details on the use and execution of this protocol, please refer to Tang et al. (2023).1.

Mitigating climate change to alleviate economic inequality under the Paris Agreement.

Understanding the implications of global climate governance is critical for achieving sustainable economic development, given that the economic impacts of climate change and policies are disproportionately distributed across regions. We estimate the updated damage functions and construct an uncertainty analysis framework to assess whether stringent climate policies entail economic benefits in terms of growth and inequality. The findings show that although climate policies slow the pace of economic growth, the benefits of avoided damage may overweight policy costs in the long run. Moreover, pursuing the 1.5°C goal slows economic catch-up of poor countries in the short to medium term relative to 2°C, but improves global inequality in the long run. This situation may, however, change when moving to a fast-growing and fossil-fueled world, in which inequalities gradually decline but start to rise after 2065. This study highlights the importance of synergizing the stringent 1.5°C goal with economic inequality alleviation.

Autohydrolysis prior to poplar chemi-mechanical pulping: Impact of surface lignin on subsequent alkali impregnation.

Chemi-mechanical pulping, a typical high-yield pulping method, combined with autohydrolysis pretreatment prior to pulping is an efficient and value-added utilization method for biomass in pulp and paper industry. This study investigated the surface lignin changes of poplar sapwood chips in autohydrolysis pretreatment and their effect on the subsequent alkali impregnation for chemi-mechanical pulping. The results showed that the surface lignin content went up with the increase of autohydrolysis intensity, and that the existence of the surface lignin had nearly no impact on the subsequent alkali impregnation in making chemi-mechanical pulps (CMPs) compared to the volume porosity, which was validated by using the stepwise regression analysis. It can be further concluded that autohydrolysis can facilitate the subsequent alkali impregnation of the autohydrolyzed sapwood chips in making CMP, which would be of significance for the combination of biomass refinery and pulp and paper industry.

Prenatal Lipopolysaccharide Exposure Promotes Dyslipidemia in the Male Offspring Rats.

Inflammation is critical to the pathogenesis of cardiovascular diseases (CVDs). We have uncovered intrauterine inflammation induced by lipopolysaccharide (LPS) increases CVDs in adult offspring rats. The present study aimed to explore the role of prenatal exposure to LPS on the lipid profiles in male offspring rats and to further assess their susceptibility to high fat diet (HFD). Maternal LPS (0.79 mg/kg) exposure produced a significant increase in serum and hepatic levels of total cholesterol, triglycerides, low-density lipoprotein cholesterol, aspartate amino transferase as well as liver morphological abnormalities in 8-week-old offspring rats. Meanwhile, disturbed gene expressions involved in hepatic lipid metabolism and related signaling pathways were found, especially the up-regulated very-low density lipoprotein receptor (VLDLR) and down-regulated transmembrane 7 superfamily member 2 (TM7SF2). Following HFD treatment, however, the lipid profile shifts and liver dysfunction were exacerbated compared to the offsprings treated with prenatal LPS exposure alone. Compared with that in control offsprings, the hepatic mitochondria (Mt) in offspring rats solely treated with HFD exhibited remarkably higher ATP level, enforced Complex IV expression and a sharp reduction of its activity, whereas the offsprings from LPS-treated dams showed the loss of ATP content, diminished membrane potential, decline in protein expression and activity of mitochondrial respiratory complex IV, increased level of MtDNA deletion as well. Furthermore, treatment with HFD deteriorated these mitochondrial disorders in the prenatally LPS-exposed offspring rats. Taken together, maternal LPS exposure reinforces dyslipidemia in response to a HFD in adult offsprings, which should be associated with mitochondrial abnormalities and disturbed gene expressions of cholesterol metabolism.

Value of the pudendal nerves terminal motor latency measurements in the diagnosis of occult stress urinary incontinence.

BACKGROUND: Occult stress urinary incontinence may lead to de novo stress urinary incontinence after pelvic floor repair surgery. A measurement of pudendal nerve terminal motor latency can reflect the integrity of the nerves. We aimed to explore the value of pudendal nerve terminal motor latency in the diagnosis of occult stress urinary incontinence in pelvic organ prolapse patients. METHODS: Ten patients with stress urinary incontinence (SUI group), 10 with SUI and uterine or vaginal prolapse (POP + SUI group) and 10 with uncomplicated uterine or vaginal prolapse (POP group) were evaluated for their pudendal nerve terminal motor latency using a keypoint electromyogram. RESULTS: The amplitude of positive waves was between 0.1 and 0.2 mV. The nerve terminal motor latency was between 1.44 and 2.38 ms. There was no significant difference in the wave amplitudes of pudendal nerve evoked action potential among the three different groups (P > 0.05). The pudendal nerve latency of the SUI group, POP + SUI group and POP group were (2.9 ± 0.7) seconds, (2.8 ± 0.7) seconds and (1.9 ± 0.5) seconds respectively. The difference between the SUI group and POP + SUI group was not statistically significant (P > 0.05), whereas the difference between the SUI and POP groups and between the POP + SUI and POP groups were statistically significant (P < 0.05). There was a positive correlation between pudendal nerve latency and the severity of SUI; the correlation coefficient was 0.720 (P < 0.01). CONCLUSIONS: Patients with SUI may have some nerve demyelination injuries in the pudendal nerve but the damage might not involve the nerve axons. The measurement of pudendal nerve latency may be useful for the diagnosis of SUI in POP patients.