Preparation and properties of phase-change materials with enhanced radial thermal conductivities based on anisotropic graphene aerogels.

In this study, anisotropic graphene aerogels are prepared using the heat-flow method. Then, graphene aerogels with nanosilver particles are prepared via a silver mirror reaction. The aerogels are soaked in paraffin wax and the effects on the properties of the wax are investigated. The thermal conductivity of pure paraffin wax is 0.2553 W m-1 K-1. For the prepared PCM, the aerogel content was 0.92 vol%; this increases to 1.2234 W m-1 K-1, which corresponds to a thermal conductivity enhancement efficiency of 582%. The axial thermal conductivity is 1.4953 W m-1 K-1, which corresponds to a thermal conductivity enhancement efficiency of 746%. The graphene aerogels with the nanosilver particles show high phase-change efficiency. Owing to the significant improvements in the axial and thermal conductivities, the radial and axial heat transfer properties show good consistency suitable for practical applications.

Empagliflozin ameliorates vascular calcification in diabetic mice through inhibiting Bhlhe40-dependent NLRP3 inflammasome activation.

Type 2 diabetes mellitus (T2DM) patients exhibit greater susceptibility to vascular calcification (VC), which has a higher risk of death and disability. However, there is no specific drug for VC therapy. NLRP3 inflammasome activation as a hallmark event of medial calcification leads to arterial stiffness, causing vasoconstrictive dysfunction in T2DM. Empagliflozin (EMPA), a sodium-glucose co-transporter 2 inhibitor (SGLT2i), restrains hyperglycemia with definite cardiovascular benefits. Given the anti-inflammatory activity of EMPA, herein we investigated whether EMPA protected against VC in the aorta of T2DM mice by inhibiting NLRP3 inflammasome activation. Since db/db mice receiving a normal diet developed VC at the age of about 20 weeks, we administered EMPA (5, 10, 20 mg·kg-1·d-1, i.g) to 8 week-old db/db mice for 12 weeks. We showed that EMPA intervention dose-dependently ameliorated the calcium deposition, accompanied by reduced expression of RUNX2 and BMP2 proteins in the aortas. We found that EMPA (10 mg·kg-1·d-1 for 6 weeks) also protected against VC in vitamin D3-overloaded mice, suggesting the protective effects independent of metabolism. We showed that EMPA (10 mg·kg-1·d-1) inhibited the abnormal activation of NLRP3 inflammasome in aortic smooth muscle layer of db/db mice. Knockout (KO) of NLRP3 significantly alleviated VC in STZ-induced diabetic mice. The protective effects of EMPA were verified in high glucose (HG)-treated mouse aortic smooth muscle cells (MOVASs). In HG-treated NLRP3 KO MOVASs, EMPA (1 µM) did not cause further improvement. Bioinformatics and Western blot analysis revealed that EMPA significantly increased the expression levels of basic helix-loop-helix family transcription factor e40 (Bhlhe40) in HG-treated MOVASs, which served as a negative transcription factor directly binding to the promotor of Nlrp3. We conclude that EMPA ameliorates VC by inhibiting Bhlhe40-dpendent NLRP3 inflammasome activation. These results might provide potential significance for EMPA in VC therapy of T2DM patients.

Enhancing supercapacitor performance using nanosheet-covered nanotube structures Co3S4/Ni0.96S@CNTs with carbon nanotubes as conductive substrates.

Transition metal sulfides have broad application prospects as supercapacitor electrode materials. However, their poor structural stability and conductivity hinder improvements in their electrochemical performance. Therefore, the introduction of highly conductive carbon nanotubes (CNTs) as sulfide growth substrates is considered to improve the microstructure and electrochemical performance of electrode materials. In this study, a highly conductive CNT solution was sprayed onto a nickel foam current collector, and Co3S4/Ni0.96S was successfully constructed on a CNT conductive substrate using a combination of hydrothermal and electrochemical deposition methods, forming a unique nanosheet-covered nanotube structure Co3S4/Ni0.96S@CNTs. The addition of an appropriate concentration of CNTs can not only serve as a substrate for the growth of Co3S4/Ni0.96S, but also effectively maintain the overall nanosheet structure. Thus, the Co3S4/Ni0.96S@CNTs (2-CSNS@CNTs) have a stable structure and a wide range of electrochemical reaction sites, ensuring excellent conductivity and cycling stability. The electrode material 2-CSNS@CNTs exhibited a specific capacity of 1427.05 C g-1 at 1 A g-1. Additionally, the asymmetric supercapacitor 2-CSNS@CNTs exhibited a high energy density of 53.76 W h kg-1 at 800 W kg-1 and a capacity retention rate of 68.5% at 10 A g-1 after 1000 cycles.

Caspase-1 affects chronic restraint stress-induced depression-like behaviors by modifying GABAergic dysfunction in the hippocampus.

Major depression disorder (MDD) is one of the most common psychiatric disorders and one of the leading causes of disability in worldwide. Both inflammation and GABAergic dysfunction have been implicated in the pathophysiology of MDD. Caspase-1, a classic inflammatory caspase, regulates AMPARs-mediated glutamatergic neurotransmission. However, the role of caspase-1 in chronic stress-induced GABAergic dysfunction remains largely unknown. In this study, we found that serum and hippocampal caspase-1-IL-1ß levels increased significantly in chronic restraint stress (CRS) mice, and a significant negative correlation occurred between levels of caspase-1 and depression-like behaviors. Furthermore, CRS significantly decreased GAD67 mRNA levels and GABAergic neurotransmission accompanied by the reduction of GABA concentration, reduced the amplitude and frequency of mIPSCs inhibitory postsynaptic currents (mIPSCs) and the decreased surface expression of GABAARs γ2 subunit in the hippocampus. Genetic deficiency of caspase-1 not only blocked CRS-induced depression-like behaviors, but also alleviated CRS-induced impairments in GABAergic neurotransmission. Finally, reexpression of caspase-1 in the hippocampus of Caspase-1-/- mice increased susceptibility to stress-induced anxiety- and depression-like behaviors through inhibiting GAD67 expression and GABAARs-mediated synaptic transmission. Our study suggests that CRS dysregulates GABAergic neurotransmission via increasing the levels of caspase-1-mediated neuroinflammation in the hippocampus, ultimately leading to depression-like behaviors. This work illustrates that targeting caspase-1 may provide potential therapeutic benefits to stress-related GABAergic dysfunction in the pathogenesis of MDD.

IL-1ra treatment prevents chronic social defeat stress-induced depression-like behaviors and glutamatergic dysfunction via the upregulation of CREB-BDNF.

BACKGROUND: Proinflammatory cytokines IL-1ß has been proposed to be a key mediator in the pathophysiology of mood-related disorders. However, the IL-1 receptor antagonist (IL-1ra) is a natural antagonist of IL-1 and plays a key role in the regulation of IL-1-mediated inflammation, the effects of IL-1ra in stress-induced depression has not been well elucidated. METHODS: Chronic social defeat stress (CSDS) and lipopolysaccharide (LPS) were used to investigate the effects of IL-1ra. ELISA kit and qPCR were used to detect IL-1ra levels. Golgi staining and electrophysiological recordings were used to investigate glutamatergic neurotransmission in the hippocampus. Immunofluorescence and western blotting were used to analyze CREB-BDNF pathway and synaptic proteins. RESULTS: Serum levels of IL-1ra increased significantly in two animal models of depression, and there was a significant correlation between serum IL-1ra levels and depression-like behaviors. Both CSDS and LPS induced the imbalance of IL-1ra and IL-1ß in the hippocampus. Furthermore, chronic intracerebroventricular (i.c.v.) infusion of IL-1ra not only blocked CSDS-induced depression-like behaviors, but also alleviated CSDS-induced decrease in dendritic spine density and impairments in AMPARs-mediated neurotransmission. Finally, IL-1ra treatment produces antidepressant-like effects through the activation of CREB-BDNF in the hippocampus. LIMITATION: Further studies need to investigate the effect of IL-1ra in the periphery in CSDS-induced depression. CONCLUSION: Our study suggests that the imbalance of IL-1ra and IL-1ß reduces the expression of the CREB-BDNF pathway in the hippocampus, which dysregulates AMPARs-mediated neurotransmission, ultimately leading to depression-like behaviors. IL-1ra could be a new potential candidate for the treatment of mood disorders.

Gallic acid ameliorates dextran sulfate sodium-induced ulcerative colitis in mice via inhibiting NLRP3 inflammasome.

Background: Ulcerative colitis (UC) is a chronic recurrent inflammatory bowel disease (IBD). The conventional drugs for UC may induce severe side effects. Herbal medicine is considered as a complementary and alternative choice for UC. Purpose: This study aims to estimate the effect of natural polyphenol gallic acid (GA) on the NLRP3 inflammasome with dextran sulfate sodium (DSS)-induced colitis in mice. Study design: The body weights and symptoms of BALB/c mice were recorded. Histological evaluation, ELISA, q-PCR, immunohistochemistry, and western blotting were carried out to observe the morphology, cytokine contents, mRNA expressions, and protein expressions, respectively. Lipopolysaccharide (LPS)-induced RAW264.7 macrophage was used to probe GA's effect on relative protein expression. Results: GA attenuated weight loss (p < 0.05), relieved symptoms, and ameliorated colonic morphological injury (p < 0.05) in mice with colitis induced by DSS. GA also lowered the contents of TNF-α, IL-1ß, IL-18, IL-33, and IFN-γ in the serum and colon of mice, which were elevated by DSS, downregulated protein, and mRNA expressions of the NLRP3 pathway in the colon tissue. Furthermore, GA downregulated the expressions of NLRP3 (p < 0.05), iNOS (p < 0.01), COX2 (p < 0.01), and P-p65 (p < 0.05), and suppressed NO release (p < 0.001) in LPS-induced RAW264.7 cells. Conclusion: GA ameliorated DSS-induced UC in mice via inhibiting the NLRP3 inflammasome. These findings furnish evidence for the anti-inflammatory effect of herbal medicines containing GA on UC.

Water-Driven Synthesis of Deep-Blue Perovskite Colloidal Quantum Wells for Electroluminescent Devices.

Perovskite colloidal quantum wells (QWs) are promising to realize narrow deep-blue emission, but the poor optical performance and stability suppress their practical application. Here, we creatively propose a water-driven synthesis strategy to obtain size-homogenized and strongly confined deep-blue CsPbBr3 QWs, corresponding to three monolayers, which emit at the deep-blue wavelength of 456 nm. The water controls the orientation and distribution of the ligands on the surface of the nanocrystals, thus inducing orientated growth through the Ostwald ripening process by phagocytizing unstable nanocrystals to form well-crystallized QWs. These QWs present remarkable stability and high photoluminescence quantum yield of 94 %. Furthermore, we have prepared light-emitting diodes based on the QWs via the all-solution fabrication strategy, achieving an external quantum efficiency of 1 % and luminance of 2946 cd m-2 , demonstrating state-of-the-art brightness for perovskite QW-based LEDs.

Oleoylethanolamide alleviates hyperlipidaemia-mediated vascular calcification via attenuating mitochondrial DNA stress triggered autophagy-dependent ferroptosis by activating PPARα.

Vascular calcification, a prevalent pathological alteration in metabolic syndromes, is tightly related with cardiometabolic risk events. Ferroptosis, a newly iron-dependent programmed cell death, induced by palmitic acid (PA), the major saturated free fatty acid in hyperlipidemia, is a vital mechanism of vascular calcification. Recent studies reported that ferroptosis is a distinctive type of cell death dependent on autophagy, with the lipotoxicity of PA on cell viability being closely linked with autophagy. Oleoylethanolamide (OEA), an endogenous bioactive mediator of lipid homeostasis, exerts vascular protection against intimal calcification, atherosclerosis; however, its beneficial effect on vascular smooth muscle cell (VSMC)-associated medial calcification has not been investigated. Our aim was to characterize the effect of OEA on vascular calcification and ferroptosis of VSMCs under hyperlipidaemia/PA exposure. In vivo, vascular calcification model was induced in rats by high-fat diet and vitamin D3 plus nicotine; in vitro, VSMCs ferroptosis was induced by PA or plus ß-glycerophosphate mimicking vascular calcification. The calcium deposition in hyperlipidaemia-mediated rat thoracic aortas, the PA-induced ferroptosis and subsequent calcium deposition in VSMCs, were suppressed by OEA treatment. Additionally, CGAS-STING1-induced ferritinophagy, the main molecular mechanism of PA-triggered ferroptosis of VSMCs, was activated by mitochondrial DNA damage; however, early administration of OEA alleviated these phenomena. Intriguingly, overexpression of peroxisome proliferator activated receptor alpha (PPARα) contributed to a decrease in PA-induced ferroptosis, whereas PPARɑ knockdown inhibited the OEA-mediated anti-ferroptotic effects. Collectively, our study demonstrated that OEA serves as a prospective candidate for the prevention and treatment of vascular calcification in metabolic abnormality syndromes.

Modulating the Site Density of Mo Single Atoms to Catch Adventitious O Atoms for Efficient H2 O2 Oxidation with Light.

Coordination environment and site density have great impacts on the catalytic performance for single atoms (SAs). Herein, the site density of Mo-SAs on red polymeric carbon nitrides (RPCN) is modulated via a local carbonization strategy to controllably catch adventitious O atoms from open environment. The addition of melamine derivants with hydrocarbyl chains induces local carbonization during RPCN pyrolysis. These local carbonization regions bring abundant graphitic N3C to anchor Mo-SAs, and most of Mo-SAs catch the O atoms in air, forming the O2 -covered Mo-N3 coordination. The dopants of carbon source with different structures and amounts can modulate the site density of Mo-SAs, therefore controlling the amounts of coordinated O atoms. Furthermore, coordinated O atoms around Mo-SAs construct the catalytic environment with Lewis base and gather photo-generated electrons under light. Such O-covered Mo-SAs endow RPCN materials (Mo-RPCN) with a strong ability for hydrogen abstraction, leading to the 99.51% ratio (28.8 mmol min-1  g-1 ) rate for thioanisole conversion with H2 O2 assisted advance oxidation technology. This work brings a new sight on the coordinated atoms dominant oxidation process.

FYCO1 regulates migration, invasion, and invadopodia formation in HeLa cells through CDC42/N-WASP/Arp2/3 signaling pathway.

FYCO1, an autophagy adaptor, plays an essential role in the trafficking toward the plus-end of microtubules and the fusion of autophagosomes. Autophagic dysfunction is involved in numerous disease states, including cancers. Previous studies have implicated FYCO1 as one of the critical genes involved in the adenoma to carcinoma transition, but the biological function and mechanism of FYCO1 in carcinogenesis remain unclear. This study aims to elucidate the role and mechanism of up- and downregulation of FYCO1 in mediating tumor effects in HeLa cells. Functionally, FYCO1 promotes cellular migration, invasion, epithelial-mesenchymal transition, invadopodia formation, and matrix degradation, which are detected through wound healing, transwell, immunofluorescence, and Western blot approaches. Interestingly, the data show that although FYCO1 does not affect HeLa cell proliferation, cell cycle distribution, nor vessels' formation, FYCO1 can block the apoptotic function. FYCO1 inhibits cleavage of PARP, caspase3, and caspase9 and increases Bcl-2/Bax ratio. Then, we used CK666, an Arp2/3 specific inhibitor, to confirm that FYCO1 may promote the migration and invasion of HeLa cells through the CDC42/N-WASP/Arp2/3 signaling pathway. Taken together, these results provide a new insight that FYCO1, an autophagy adaptor, may also be a new regulator of tumor metastasis.

Degradation mechanisms of perovskite nanocrystals in color-converted InGaN micro-light-emitting diodes.

The metal halide perovskite nanocrystals (NCs) have attracted much attention because of their excellent optical properties and potential for application in optoelectronic devices. However, their photo- and thermostability are still practical challenges and need further optimization. Here, we have studied the degradation behaviors of CsPbI3 NCs utilized as optical conversion layer in InGaN based blue micro-LEDs in situ. Furthermore, the effects of temperature and light irradiation on perovskite NCs were investigated respectively. The results indicate that both blue light irradiation and high temperature can cause the increased nonradiative recombination rate, resulting in the degradation of perovskite NCs and reduction of the photoluminescence quantum yield (PLQY). Especially in high-temperature condition, both the single-exciton nonradiative recombination rate and the biexciton nonradiative recombination rate are increased, causing the significant reduction of PLQY of perovskite NCs in high temperature environment than blue light irradiation. Our work provides a detailed insight about the correlation between the light irradiation and temperature consequences for CsPbI3 NCs and may help to pave the way toward optoelectronic device applications.

Lightweight Deep Learning Model for Marketing Strategy Optimization and Characteristic Analysis.

The business model of traditional market is declining day by day, and people's consumption cognition has risen to a new level with the leap in science and technology. Enterprises need to adjust and optimize their marketing strategies in time according to the new consumption characteristics, so as to smoothly adapt to the environmental changes in the Internet age. This paper briefly analyzes the relationship between sales development and psychology and constructs a fusion model that can predict preferences with the help of neural network structure of the deep learning method. Describe user portraits and characteristics, analyze users' purchasing behavior and credit literacy, and push related products combined with a hash algorithm to achieve accurate e-commerce marketing purposes. The results show that (1) the model constructed in this paper and five different models are used for multi-modal recognition analysis: the accuracy is 79.56%, the recall rate is 77.43%, F1 is 0.785, and the error value can be reduced to about 0.18 by epoch iteration; the model is superior and has great use value. (2) Using the model to extract user attribute features and predict certain preferences, 13 topics and weight ratios are obtained for users of a certain platform, and the portrait model of each user is constructed. (3) According to the portrait optimization, 8 different marketing strategies are obtained, and the marketing effect is remarkable, fluctuating between 69% and 82%, and the income situation is also satisfactory. The final model design is reasonable and the data performance is good, which provides an intelligent and efficient dynamic strategy service for enterprises.

Role of RAGE and its ligand HMGB1 in the development of COPD.

Smoking is a well-established risk factor for chronic obstructive pulmonary disease (COPD). Chronic lung inflammation continues even after smoking cessation and leads to COPD progression. To date, anti-inflammatory therapies are ineffective in improving pulmonary function and COPD symptoms, and new molecular targets are urgently needed to deal with this challenge. The receptor for advanced glycation end-products (RAGE) was shown to be relevant in COPD pathogenesis, since it is both a genetic determinant of low lung function and a determinant of COPD susceptibility. Moreover, RAGE is involved in the physiological response to cigarette smoke exposure. Since innate and acquired immunity plays an essential role in the development of chronic inflammation and emphysema in COPD, here we summarized the roles of RAGE and its ligand HMGB1 in COPD immunity.

Identification and functional analysis of two GJA8 variants in Chinese families with eye anomalies.

In this study, we report on two different GJA8 variants related to congenital eye anomalies in two unrelated families, respectively. GJA8 (or Cx50) encoding a transmembrane protein to form lens connexons has been known as a common causative gene in congenital cataracts and its variants have recently been reported related to a wide phenotypic spectrum of eye defects. We identified two GJA8 variants, c.134G>T (p.Try45Leu, W45L) detected in a cataract family by Sanger sequencing and c.281G>A (p.Gly94Glu, G94E) found in a family with severe eye malformations including microphthalmia by whole-exome sequencing. These two variants were absent in healthy population and predicted deleterious by bioinformatic analysis. Furthermore, we compared the expression in cell lines between these mutants and the wildtype to explore their potential mechanism. Cell counting kit-8 assay showed that overexpression of either W45L or G94E decreased cell viability compared with wild-type Cx50 and the control. A lower protein level in W45L found by western blotting and fewer punctate fluorescent signals showed by fluorescence microscopy suggested that W45L may have less protein expression. A higher G94E protein level and abundant dotted distribution indicated that G94E may cause aberrant protein degradation and accumulation. Such results from in vitro assays confirmed the impact of these two variants and gave us a hint about their different pathogenic roles in different phenotypes. In conclusion, our study is the first to have the functional analysis of two GJA8 variants c.134G>T and c.281G>A in Chinese pedigrees and explore the impact of these variants, which can help in prenatal diagnosis and genetic counseling as well in basic studies on GJA8.

Ultrastructural visualization of chromatin in cancer pathogenesis using a simple small-molecule fluorescent probe.

Imaging chromatin organization at the molecular-scale resolution remains an important endeavor in basic and translational research. Stochastic optical reconstruction microscopy (STORM) is a powerful superresolution imaging technique to visualize nanoscale molecular organization down to the resolution of ~20 to 30 nm. Despite the substantial progress in imaging chromatin organization in cells and model systems, its routine application on assessing pathological tissue remains limited. It is, in part, hampered by the lack of simple labels that consistently generates high-quality STORM images on the highly processed clinical tissue. We developed a fast, simple, and robust small-molecule fluorescent probe-cyanine 5-conjugated Hoechst-for routine superresolution imaging of nanoscale nuclear architecture on clinical tissue. We demonstrated the biological and clinical significance of imaging superresolved chromatin structure in cancer development and its potential clinical utility for cancer risk stratification.

Identification and functional study of FOXC1 variants in Chinese families with glaucoma.

This study aimed to identify the disease-causing gene of three Chinese families with glaucoma. Whole exome sequencing was performed on the probands and detected three different variants (c.405C>A (p.Cys135Ter), c.851G>T (p.Ser284Ile), and c.392C>T (p.Ser131Leu)) in FOXC1 as a causative gene of glaucoma, and Sanger sequencing was performed for verification and cosegregation analysis. Three in silico tools all predicted these two missense variants to be probably disease-causing. Western blot analysis, immunofluorescence, and dual-luciferase assay were further used to evaluate the effect of FOXC1 missense variants, and demonstrated that the two variants resulted in decreased transactivation activity of FOXC1 although the variants had no effect on the protein amount and the nucleus subcellar localization of FOXC1 compared with the wild type, which implies that both of two variants may be probably pathogenic. In this study, we reported two novel FOXC1 variants as well as a reported variant and the phenotypes associated to these variants, which expands the spectrum and relevant phenotypes of FOXC1 variants. Additionally, the functional analysis of FOXC1 variants provides further insight into the possible pathogenesis of anterior segment anomaly related to FOXC1.

Diabetic mellitus, vascular calcification and hypoxia: A complex and neglected tripartite relationship.

DM (diabetic mellitus) and its common vascular complications VC (vascular calcification), are increasingly harmful to human health. In recent years, the research on the relationship between DM and VC is also deepening. Hypoxia, as one of the pathogenic factors of many disease models, is also closely related to the occurrence of DM and VC. There are some studies on the role of hypoxia in the pathogenesis of DM and VC respectively, but no one has made an in-depth summary of the systematic connection between hypoxia, DM and VC. Therefore, what we want to review in this article are the relationship between DM, VC and hypoxia, respectively, as well as the role of hypoxia in the development of DM and VC, which has little concern but is a novel and potentially target that may provide some new ideas for the prevention and treatment of DM, VC, especially diabetic VC.

A Facile Probe for Fluorescence Turn-on and Simultaneous Naked-Eyes Discrimination of H2S and biothiols (Cys and GSH) and Its Application.

Hydrogen sulfide and biothiol molecules such as Cys and GSH acted important roles in many physiological processes. To simultaneously detect and distinguish them was quite necessary by a suitable fluorescent probe. A novel chemosensor 4-(4-(benzo[d]thiazol-2-yl)-2-methoxyphenoxy)-7-nitrobenzo[c][1,2,5]oxadiazole (BMNO) was designed to detect H2S/Cys/GSH using the combination of nitrobenzofurazan (NBD) and benzothiazole fluorophores linked by a facile ether bond. The probe BMNO was developed for simultaneous identification of H2S, Cys and GSH. Noticeably, the color changes (from colorless to light purple, light orange and light yellow) of probe BMNO solutions for sensing H2S, Cys and GSH could be observed by naked eyes, respectively. The probe BMNO exhibited high selectivity and sensitivity for H2S, Cys and GSH showing distinct optical signal with detection limit as low as 0.15 µM, 0.03 µM and 0.14 µM, respectively. The sensing mechanism was clarified by spectrum analysis and some controlled experiments. In addition, these outstanding properties of probe BMNO enabled its practical applications in detection H2S in beer, and in cell imaging for Cys and GSH as well.

Talaromyces marneffei and nontuberculous mycobacteria co-infection in HIV-negative patients.

To describe the clinical features and the risk factors for nontuberculous mycobacteria (NTM) and Talaromyces marneffei (TM) co-infections in HIV-negative patients. A multicenter retrospective study in 13 hospitals, and a systematic literature review were performed of original articles published in English related to TM/NTM co-infections. HIV-negative patients with TM and NTM co-infections comprised Group 1; TM-only infection Group 2; NTM-only infection Group 3; and healthy volunteers Group 4. Univariate logistic analysis was used to estimate the potential risk factors of TM/NTM co-infections. A total of 22 cases of TM and NTM co-infections were enrolled. Of these, 17 patients (77.3%) had a missed diagnosis of one of the TM or NTM pathogens. The anti-IFN-γ autoantibodies (AIGAs) titer, white blood cell (WBC), neutrophil counts (N), erythrocyte sedimentation rate (ESR), C reactive protein (CRP), globulin, and immunoglobulin G (IgG) levels of Group 1 were higher than those of the other groups, whereas the levels of CD4+T cells was lower than those of other groups. There was a significant negative correlation between the AIGA titers and the number of CD4+T cells (P < 0.05). Factors including the ratio of the actual values to the cut-off values of AIGAs, WBC, N, HGB, CD4+T cells, IgG, IgM, IgA, serum globulin, ESR, and CRP were taken as potential risk factors for TM and NTM co-infection. Most patients with TM and NTM co-infection had a missed diagnosis of one of the TM or NTM pathogens. The levels of AIGAs, WBC, N, ESR, and CRP in TM and NTM co-infections were remarkably higher than in mono-infection. High-titer AIGAs may be a potential risk factor and susceptibility factor for co-infection of TM and NTM in HIV-negative hosts.