Air pollution associated with hospital visits for mental and behavioral disorders in Northeast China

BackgroundRelated studies have found that air pollution is an important factor affecting mental and behavioral disorders. Thus, we performed this time-series study to evaluate the relationship between short-term exposure to ambient air pollutants and visits to hospital by patients with mental and behavioral disorders in northeastern China.MethodsWe used quasi-Poisson regression models and generalized additive models to probe the links between air pollution and mental and behavioral disorders. The possible influences were also explored stratified by season, age and gender.ResultsWe found that sulfur dioxide (SO2) had a cumulative effect on mental and behavioral disorders at lag04–lag07 and had the greatest effect at lag07 [Relative risk (RR) = 1.068, 95%CI = 1.021–1.117]. Particulate matter of size 2.5 μm (PM2.5) and SO2 had a cumulative effect on depression and both had the largest effect at lag07 (RR = 1.021, 95%CI = 1.002–1.041; RR = 1.103, 95%CI = 1.032–1.178); SO2 also had a cumulative effect on anxiety disorders, with the largest effect at lag06 (RR = 1.058, 95%CI = 1.009–1.110). In the stratified analysis, people are more susceptible in the cold season compared to the warm season and females and the 18–60-year age group are more sensitive to air pollutants. It is suggested to strengthen management and preventive measures to decrease air pollution exposure.ConclusionThis study found an association between increased concentrations of air pollutants and increased outpatient visits for mental and behavioral disorders. We recommend that preventive and protective measures should be strengthened in an effort to reduce exposure to air pollution in order to maintain physical and mental health

Primary Pulmonary Mucoepidermoid Carcinoma: Histopathological and Moleculargenetic Studies of 26 Cases.

Pulmonary mucoepidermoid carcinoma (PMEC) is an uncommon neoplasm of the lung and the main salivary gland-type lung carcinoma. The aims of this study were to review the clinicopathological and immunohistochemical features of PMEC and characterize the genetic events in PMEC.We reviewed the pathology cases in our hospital and found 34 initially diagnosed PMEC cases, 26 of which were confirmed as PMEC after excluding 8 cases of MEC-like pulmonary carcinoma. The clinicopathological characteristics of the 26 PMEC cases and the 8 cases of MEC-like pulmonary carcinoma were retrospectively reviewed. MAML2 rearrangement was detected by fluorescence In Situ Hybridization (FISH). Immunostains of ALK, calponin, collagen IV, CK7, EGFR, HER2, Ki-67, Muc5Ac, p63, p40, and TTF-1 were performed. DNA was extracted from 23 cases of PMEC. Mutation profiling of the EGFR, KRAS, BRAF, ALK, PIK3CA, PDGFRA, and DDR2 genes were carried out using next-generation sequencing (NGS), Sanger sequencing, and quantitative polymerase chain reaction (QPCR) in 9 successfully amplified cases.Twenty-six cases of PMEC (18 low-grade, 8 high-grade) included 13 men and 13 women aged 12-79 years. Twenty-two cases had a central/endobronchial growth pattern, and 4 cases had a peribronchial growth pattern. Immunohistochemically, CK7, Muc5Ac, p40, and p63 were positive in all cases (26/26);EGFR was positive in 11 cases (11/26); TTF-1, Calponin, HER2 and ALK were negative in all cases (0/26). MAML2 rearrangement was identified in 12 of 18 PMEC cases. No mutations were detected in any of the 7 genes in the 9 cases that qualified for mutation analysis. Twenty-three PMEC patients had follow-up information with a median interval of 32.6 months. Both the 5- and 10-year overall survival rates (OS) were 72.1%, and a high-grade tumor was an adverse prognostic factor in PMEC. There were 8 cases of MEC-like pulmonary carcinoma aged 36-78 years: 2 cases were located in the bronchus, and 6 cases were located in the lung. p63 and TTF-1 were positive in all cases (8/8), p40 was positive in 5 cases (5/8), and ALK was positive in 5 cases (5/8). No cases of MAML2 rearrangement were detected, but there were 5 cases of ALK rearrangement.PMEC is a primary malignant pulmonary tumor with a relatively good prognosis that is historically characterized by the presence of mucous cells and a lack of keratinization. There are distinct differences between PMEC and MEC-like pulmonary carcinoma in tumor location preference, immunophenotype, and molecular genetics, and the differential diagnosis is critical due to the therapeutic and prognostic considerations

VDR Activation Attenuates Renal Tubular Epithelial Cell Ferroptosis by Regulating Nrf2/HO‐1 Signaling Pathway in Diabetic Nephropathy

Abstract Diabetic nephropathy (DN) is a serious microvascular complication of diabetes. Ferroptosis, a new form of cell death, plays a crucial role in the pathogenesis of DN. Renal tubular injury triggered by ferroptosis might be essential in this process. Numerous studies demonstrate that the vitamin D receptor (VDR) exerts beneficial effects by suppressing ferroptosis. However, the underlying mechanism has not been fully elucidated. Thus, they verified the nephroprotective effect of VDR activation and explored the mechanism by which VDR activation suppressed ferroptosis in db/db mice and high glucose‐cultured proximal tubular epithelial cells (PTECs). Paricalcitol (PAR) is a VDR agonist that can mitigate kidney injury and prevent renal dysfunction. PAR treatment could inhibit ferroptosis of PTECs through decreasing iron content, increasing glutathione (GSH) levels, reducing malondialdehyde (MDA) generation, decreasing the expression of positive ferroptosis mediator transferrin receptor 1 (TFR‐1), and enhancing the expression of negative ferroptosis mediators including ferritin heavy chain (FTH‐1), glutathione peroxidase 4 (GPX4), and cystine/glutamate antiporter solute carrier family 7 member 11 (SLC7A11). Mechanistically, VDR activation upregulated the NFE2‐related factor 2/heme oxygenase‐1 (Nrf2/HO‐1) signaling pathway to suppress ferroptosis in PTECs. These findings suggested that VDR activation inhibited ferroptosis of PTECs in DN via modulating the Nrf2/HO‐1 signaling pathway

Tailorable copper-bearing titanium alloys with remarkable strength and ductility fabricated by spark plasma sintering for biomedical applications

Titanium and Ti-based alloys are widely used metallic biomaterials, however, the surgical infections related to bacteria always occur on the implants. Developing the antibacterial titanium alloys has been studied as one of the most effective methods to lower the inflammatory response. The addition of Cu element to Ti matrix can produce strong antibacterial properties. Here, the antibacterial Ti-xCu alloys (x = 3, 5, and 7 wt%) were fabricated by powder metallurgy (PM) technique using spark plasma sintering (SPS) route. The effects of Cu addition, SPS temperature, and post-heat treatment on microstructure and tensile properties of Ti–Cu alloys were investigated. The strengthening and deformation mechanisms were also discussed. The microstructures of PM Ti–Cu alloy consisting of α-Ti and Ti2Cu phases are fine and homogenous as well as free of porosity. With the increasing Cu addition, the yield and tensile strengths of Ti–Cu alloys increase, but the elongation decreases. The precipitation of Ti2Cu phases contributes the most increments of yield strength, and can also act as the barriers to pile up the dislocations during the plastic deformation, improving the work hardening rate and tensile strength. PM Ti–Cu alloys possess a good tensile strength of 575–810 MPa, and an excellent elongation of 11%–29%. The optimized tensile properties of PM Ti–5Cu alloys are comparable and even superior to those of Ti and other Ti-based alloys produced by traditional methods. Further, insights for the design and processing of PM Ti–Cu alloys with ample shaping freedom fabricated by SPS method are generalized and discussed

Overall survival of the 23 PMEC patients with follow-up.

<p>(A) OS according to age. (B) OS according to growth pattern. (C) OS according to tumor diameter. (D) OS according to tumor grade. (E) OS according to Ki-67 labeling index. (F) OS according to surgical resection.</p

List of various antibody markers in the present study.

<p>List of various antibody markers in the present study.</p

Immunostains of PMEC.

<p>(A) Muc5AC highlighted the partial mucous cells within the tumors (x150). (B) p63 was positive in both intermediate and epidermoid cells (x150). (C) TTF-1 was negative in all three cells (x150). (D) ALK was negative (x150). (E) Ki-67 was positive in the nucleus in a low-grade tumor, and the labeling index is 2% (x150). (F) Ki-67 was positive in the nucleus in the dedifferentiation area, and the labeling index is about80% (x150).</p

List of 16 exons of 7 genes in the present study.

<p>List of 16 exons of 7 genes in the present study.</p

Microscopic images of MEC-like pulmonary carcinoma.

<p>(A) Case 1 showing solid nests in the left upper corner and mucin-filled cysts and mucous cells on the right side (H&E, x75). (B) Case 2 showing many mucous cells in the solid nests (H&E, x150). (C) Case 3 showing a cribriform-like structure with mucous cells (H&E, x150). (D) Case 4 was a mucoepidermoid carcinoma-like adenosquamous carcinoma (H&E, x150) (the illustration in the lower right corner clearly shows keratinization).</p

Microscopic images of primary pulmonary mucoepidermoid carcinoma.

<p>(A) Cross-section of the lobe bronchus demonstrating primary pulmonary mucoepidermoid carcinoma with an endobronchial growth pattern (H&E, lower power). (B) The same case with solid nests and a cystic component that comprises the tumor with hyalinization stroma, foci of calcification, and mucus in the cystic component (H&E, x75). (C) The tumor was composed of mucous, intermediate, and epidermoid cells without keratinization (H&E, x150). (D) Another primary pulmonary mucoepidermoid carcinoma case showing dedifferentiation with severe nuclear atypia, necrosis, and salient mitotic figures (right side) and the upper left corner showing the typical mucoepidermoid carcinoma area (H&E, x150).</p