Background Mental disorders among refugees have been well explored in several studies. However, longitudinal studies on the impact of the pandemic on refugee populations are widely lacking. This study was designed to examine the impact of the current pandemic on the mental health of Rohingya refugees living in Bangladesh. Method This longitudinal study involved a convenience sample of 732 Rohingya people with pre-existing health problems who lived in the Kutupalong refugee camp in Cox’s Bazar, Bangladesh. The first recruitment was performed on 5 July 2019 (prepandemic visit) and assessed the health status of refugees using the Refugee Health Screener-15 (RHS-15). The follow-up survey was conducted on 10 November 2020, approximately 15 months later, during the pandemic. A total of 342 Rohingya refugees who completed the initial survey participated in the follow-up survey. A newly developed COVID-19 Impact on Quality of Life (COV19-QoL) scale was used alongside the RHS-15 scale during the second survey. Ethical measures were taken in compliance with the current Declaration of Helsinki. The analysis was performed using SPSS 26. Result A total of 342 Rohingya refugees completed this longitudinal survey. The average age of participants was 32.25 ± 14.01 years (SD), and the predominant age group was ≤ 30 years (n = 207, 60.5%). Most of the participants were female (n = 209, 61.1%). A significant increase in stress was noted from the prepandemic to pandemic periods, as determined by the RHS-15 scale (RHS-15 Part I: 22.96 ± 8.43 vs. 46.72 ± 1.87, p < 0.001; and RHS-15 Part II: 4.43 ± 1.59 vs. 6.91 ± 1.49, p < 0.001). The mean COV19-QoL score of the participants was 4.47 ± 0.15 (out of 5), indicating a perceived negative impact of the pandemic in their lives. In the multiple regression analysis, female sex (β = 0.604, p = 0.017) and COV19-QoL score (β = 2.537, p = 0.003) were significantly associated with higher perceived distress among participants. Conclusion Rohingya refugees experienced a significant deterioration of mental health during the COVID-19 pandemic. Alongside other socioeconomic, environmental, and political factors, the pandemic itself might have been a crucial contributor to this negative trend.

Mucus clearance is an important airway innate defense mechanism. Airway-targeted overexpression of the epithelial Na+channel β-subunit [encoded by sodium channel nonvoltage gated 1, beta subunit ( Scnn1b)] in mice [ Scnn1b-transgenic (Tg) mice] increases transepithelial Na+absorption and dehydrates the airway surface, which produces key features of human obstructive lung diseases, including mucus obstruction, inflammation, and air-space enlargement. Because the first Scnn1b-Tg mice were generated on a mixed background, the impact of genetic background on disease phenotype in Scnn1b-Tg mice is unknown. To explore this issue, congenic Scnn1b-Tg mice strains were generated on C57BL/6N, C3H/HeN, BALB/cJ, and FVB/NJ backgrounds. All strains exhibited a two- to threefold increase in tracheal epithelial Na+absorption, and all developed airway mucus obstruction, inflammation, and air-space enlargement. However, there were striking differences in neonatal survival, ranging from 5 to 80% (FVB/NJ<BALB/cJ<C3H/HeN<C57BL/6N), which correlated with the incidence of upper airway mucus plugging and the levels of Muc5b in bronchoalveolar lavage. The strains also exhibited variable Clara cell necrotic degeneration in neonatal intrapulmonary airways and a variable incidence of pulmonary hemorrhage and lung atelectasis. The spontaneous occurrence of a high surviving BALB/cJ line, which exhibited delayed onset of Na+hyperabsorption, provided evidence that: 1) air-space enlargement and postnatal death were only present when Na+hyperabsorption occurred early, and 2) inflammation and mucus obstruction developed whenever Na+hyperabsorption was expressed. In summary, the genetic context and timing of airway innate immune dysfunction critically determines lung disease phenotype. These mouse strains may be useful to identify key modifier genes and pathways.

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The closed-loop brain stimulation technique plays a key role in neural network information processing and therapies of neurological diseases. Transcranial ultrasound stimulation (TUS) is an established neuromodulation method for the neural oscillation in animals or human. All available TUS systems provide brain stimulation in an open-loop pattern. In this study, we developed a closed-loop transcranial ultrasound stimulation (CLTUS) system for real-time non-invasive neuromodulation in vivo. We used the CLTUS system to modulate the neural activities of the hippocampus of a wild-type mouse based on the phase of the theta rhythm recorded at the ultrasound-targeted location. In addition, we modulated the hippocampus of a temporal lobe epilepsy (TLE) mouse. The ultrasound stimulation increased the absolute power and reduced the relative power of the theta rhythm, which were independent of the specific phase of the theta rhythm. Compared with those of a sham stimulation, the latency of epileptic seizures was significantly increased, while the epileptic seizure duration was significantly decreased under the CLTUS. The above results indicate that the CLTUS can be used to not only modulate the neural oscillation through the theta-phase-specific manipulation of the hippocampus but also effectively inhibit the seizure of a TLE mouse in time. CLTUS has large application potentials for the understanding of the causal relationship of neural circuits as well as for timely, effective, and non-invasive therapies of neurological diseases such as epilepsy and Parkinson's disease.

Epithelial-mesenchymal transition (EMT) is believed to be involved in lung fibrosis process induced by paraquat (PQ); however, the molecular mechanism of this process has not been clearly established. The present study investigated the potential involvement of EMT after PQ poisoning. The expressions of EMT markers, such as E-cadherin and α-smooth muscle actin (α-SMA), at multiple time points after exposure to different concentrations of PQ were evaluated by western blot analysis. Following PQ treatment, EMT induction was observed under microscopy. Related fibrosis genes, including Matrix metalloproteinase 2 (MMP-2), Matrix metalloproteinase 9 (MMP-9), collagens type I (COL I), and type III (COL III), were also evaluated by measuring their mRNA levels using RT-PCR analysis. Signaling pathways were analyzed using selective pharmacological inhibitors for MAPK. Cell migration ability was evaluated by scratch wound and Transwell assays. The data showed that PQ-induced epithelial RLE-6NT cells to develop mesenchymal cell characteristics, as indicated by a significant decrease in the epithelial marker E-cadherin and a significant increase in the extracellular matrix (ECM) marker α-smooth muscle actin in a dose and time-dependent manner. Moreover, PQ-treated RLE-6NT cells had an EMT-like phenotype with elevated expression of MMP-2, MMP-9, and COL I and COL III and enhanced migration ability. Signal pathway analysis revealed that PQ-induced EMT led to ERK-1 and Smad2 phosphorylation through activation of the MAPK pathway. The results of the current study indicate that PQ-induced pulmonary fibrosis occurs via EMT, which is mediated by the MAPK pathway. This implies that the MAPK pathway is a promising therapeutic target in alveolar epithelial cells. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1407-1414, 2016.

Low-intensity pulsed ultrasound stimulation (LIPUS) can inhibit seizures associated with temporal lobe epilepsy (TLE), which is the most common epileptic syndrome in adults and accounts for more than half of the cases of intractable epilepsy. Electroencephalography (EEG) signal analysis is an important method for studying epilepsy. The nonlinear dynamics of epileptic EEG signals can be used as biomarkers for the prediction and diagnosis of epilepsy. However, how ultrasound modulates the nonlinear dynamic characteristics of EEG signals in TLE is still unclear. Here, we used low-intensity pulsed ultrasound to stimulate the CA3 region of kainite (KA)-induced TLE mice, simultaneously recorded local field potentials (LFP) in the stimulation regions before, during, and after LIPUS. The nonlinear characteristics, including complexity, approximate entropy of different frequency bands, and Lyapunov exponent of the LFP, were calculated. Compared with the control group, the experimental group showed that LIPUS inhibited TLE seizure and the complexity, approximate entropy of the delta (0.5–4 Hz) and theta (4–8 Hz) frequency bands, and Lyapunov exponent of the LFP significantly increased in response to ultrasound stimulation. The values before ultrasound stimulation were higher ∼1.87 (complexity), ∼1.39 (approximate entropy of delta frequency bands), ∼1.13 (approximate entropy of theta frequency bands) and ∼1.46 times (Lyapunov exponent) than that after ultrasound stimulation ( p < 0.05). The above results demonstrated that LIPUS can alter nonlinear dynamic characteristics and provide a basis for the application of ultrasound stimulation in the treatment of epilepsy.