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Background: Adverse psychological states in surgical patients can impact outcomes. This study aimed to evaluate mood disorders and associated factors in general surgery inpatients using the Huaxi Emotional Distress Index (HEI). Methods: This retrospective cross-sectional study analyzed HEI scores of 20,398 adult patients hospitalized for elective surgery at a tertiary hospital in China (2018–2021). Univariable and multivariable logistic regression identified factors linked to moderate/severe mood disturbances. Results: Factors linked to moderate/severe mood disturbances were identified through univariable and multivariable logistic regression. The results showed that 3.7% of the patients had HEI ≥  13, indicating significant emotional issues. The mean age was 52.67 (16.14) years in the group with no/mild distress and 59.65 (16.34) years in the group with moderate/severe distress. Among all the cases included, there were 2,689 cases (13.18%) of gastric and esophageal diseases, 1,437 cases (7.04%) of hepatic diseases, 913 cases (4.47%) of periampullary and pancreatic tumors, 9,150 cases (44.85%) of gallbladder diseases, 2,777 cases (13.61%) of colorectal diseases, and 3,432 cases (16.83%) of other diseases. The male percentage was 45.5 and 54.9% in the two groups, respectively. Older age, male gender, unstable occupations, lower education, and unmarried status were associated with higher risks of mood disturbances (all p  <  0.05). A significant downward trend in adverse emotions was observed with increasing education levels (p  <  0.001). Furthermore, the study found that the inpatients had higher HEI scores prior to the COVID-19 pandemic compared to during the pandemic (p  <  0.001). However, the occurrence of adverse mood states in these patients was not exacerbated by the COVID-19 pandemic. The trend test remained highly significant in the none-adjusted, age-sex adjusted, and fully adjusted models (all p for trend <0.001). Conclusion: The implementation of routine screening in higher education institutions (HEIs) allows for the early identification of surgical inpatients who require psychological intervention. It is recommended that counseling services focus on individuals with lower levels of education and income instability in order to address negative mood states. Furthermore, the potential application of this screening system in other clinical settings could enable earlier psychological interventions for a larger number of patients. [ABSTRACT FROM AUTHOR]

The increasing number of biological applications for black phosphorus (BP) nanomaterials has precipitated considerable concern about their interactions with physiological systems. Here we demonstrate the adsorption of plasma protein onto BP nanomaterials and the subsequent immune perturbation effect on macrophages. Using liquid chromatography tandem mass spectrometry, 75.8% of the proteins bound to BP quantum dots were immune relevant proteins, while that percentage for BP nanosheet–corona complexes is 69.9%. In particular, the protein corona dramatically reshapes BP nanomaterial–corona complexes, influenced cellular uptake, activated the NF-κB pathway and even increased cytokine secretion by 2–4-fold. BP nanomaterials induce immunotoxicity and immune perturbation in macrophages in the presence of a plasma corona. These findings offer important insights into the development of safe and effective BP nanomaterial-based therapies. [ABSTRACT FROM AUTHOR]

This Letter presents the effectiveness of an oxide trench array (OTA) as a passive temperature compensation structure for aluminum nitride on silicon (AlN-on-Si) quasi-surface acoustic wave (SAW) micromechanical resonators over a wide temperature range. Two types of devices, namely, those with OTA and their reference counterparts without OTA, are designed, fabricated, and characterized over a wide temperature range of 360 °C. Experimental results show that the resonator with OTA has a first-order temperature coefficient of frequency (TCf1) at room temperature (20 °C) of 6.66 ppm/°C, which is lower than that of the reference device without OTA by 72% in magnitude. A high turnover temperature of 197 °C is achieved. Furthermore, the second-order temperature stability of the device has also improved. OTA is experimentally demonstrated to be an effective structure for passive temperature compensation, hence paving the way for using AlN-on-Si resonators as ultrasonic sensors or timing devices in ruggedized environments where the large fluctuation in temperature places stringent demands on temperature stability. [ABSTRACT FROM AUTHOR]

CCL2-mediated macrophage infiltration in articular tissues plays a pivotal role in the development of the osteoarthritis (OA). miRNAs regulate the onset and progression of diseases via controlling the expression of a series of genes. How the CCL2 gene was regulated by miRNAs was still not fully elucidated. In the present study, we demonstrated that the binding sites of miR-33 in the 3UTR of CCL2 gene were conserved in human, mouse and rat species. By performing gain- or loss-of-function studies, we verified that miR-33 suppressed CCL2 expression in the mRNA and protein levels. We also found that miR-33 suppressed the CCL2 levels in the supernatant of cultured primary mouse chondrocytes. With reporter gene assay, we demonstrated that miR-33 targeted at AAUGCA in the 3UTR of CCL2 gene. In transwell migration assays, we demonstrated that the conditional medium (CM) from miR-33 deficient chondrocytes potentiated the monocyte chemotaxis in a CCL2 dependent manner. Finally, we demonstrated that the level of miR-33 was decreased, whereas the CCL2 level was increased in the articular cartilage from the OA patients compared with the control group. In summary, we identified miR-33 as a novel suppressor of CCL2 in chondrocytes. The miR-33/CCL2 axis in chondrocytes regulates monocyte chemotaxis, providing a potential mechanism of macrophage infiltration in OA. [ABSTRACT FROM AUTHOR]

Obesity is causally linked to osteoarthritis (OA), with the mechanism being not fully elucidated. miRNAs (miRs) are pivotal regulators of various diseases in multiple tissues, including inflammation in the chondrocytes. In the present study, we for the first time identified the expression of miR-26a in mouse chondrocytes. Decreased level of miR- 26a was correlated to increased chronic inflammation in the chondrocytes and circulation in obese mouse model. Mechanistically, we demonstrated that miR-26a attenuated saturated free fatty acid-induced activation of NF-κB (p65) and production of proinflammatory cytokines in chondrocytes. Meanwhile, NF-κB (p65) also suppressed miR- 26a production by directly binding to a predicted NF-κB binding element in the promoter region of miR-26a. Finally, we observed a negative correlation between NF-κB and miR-26a in human patients with osteoarthritis. Thus, we identified a reciprocal inhibition between miR-26a and NF-κB downstream of non-esterified fatty acid (NEFA) signalling in obesity-related chondrocytes. Our findings provide a potential mechanism linking obesity to cartilage inflammation. [ABSTRACT FROM AUTHOR]

Transcription factor 4 (TCF-4) was recently identified as a candidate gene for the cause of type 2 diabetes, although the mechanisms have not been fully elucidated. In the present study, we demonstrated that the TCF-4 transgene in macrophages aggravated high-fat diet (HFD)-induced insulin resistance and chronic inflammation, characterized by the elevation of proinflammatory cytokines in the blood, liver and white adipose tissue, as well as a proinflammatory profile of immune cells in visceral fats in mice. Mechanistically, TCF-4 functioned as a co-activator of p65 to amplify the saturated free fatty acid (FFA)-stimulated promoter activity, mRNA transcription and secretion of proinflammatory cytokines in primary macrophages. Blockage of p65 with a specific interfering RNA or inhibitor could prevent TCF-4-enhanced expression of proinflammatory cytokines in FFA/lipopolysaccharide-treated primary macrophages. The p65 inhibitor could abolish macrophage TCF-4 transgene-aggravated systemic inflammation, glucose intolerance and insulin resistance in HFD-treated mice. In addition, we demonstrated that the mRNA expression of TCF-4 in the peripheral blood monocytes from humans was positively correlated to the levels of interleukin (IL)-1β, tumour necrosis factor α, IL-6 and fasting plasma glucose. In summary, we identified TCF-4 as a co-activator of p65 in the potentiation of proinflammatory cytokine production in macrophages and aggravation of HFD-induced chronic inflammation and insulin resistance in mice. [ABSTRACT FROM AUTHOR]