Error-Reduced Digital Elevation Model of the Qinghai-Tibet Plateau using ICESat-2 and Fusion Model.

The Qinghai-Tibet Plateau (QTP) holds significance for investigating Earth's surface processes. However, due to rugged terrain, forest canopy, and snow accumulation, open-access Digital Elevation Models (DEMs) exhibit considerable noise, resulting in low accuracy and pronounced data inconsistency. Furthermore, the glacier regions within the QTP undergo substantial changes, necessitating updates. This study employs a fusion of open-access DEMs and high-accuracy photons from the Ice, Cloud, and land Elevation Satellite-2 (ICESat-2). Additionally, snow cover and canopy heights are considered, and an ensemble learning fusion model is presented to harness the complementary information in the multi-sensor elevation observations. This innovative approach results in the creation of HQTP30, the most accurate representation of the 2021 QTP terrain. Comparative analysis with high-resolution imagery, UAV-derived DEMs, control points, and ICESat-2 highlights the advantages of HQTP30. Notably, in non-glacier regions, HQTP30 achieved a Mean Absolute Error (MAE) of 0.71 m, while in glacier regions, it reduced the MAE by 4.35 m compared to the state-of-the-art Copernicus DEM (COPDEM), demonstrating its versatile applicability.

Copper Difluorocarbene Enables Catalytic Difluoromethylation.

Despite the synthetic versatility of difluorocarbene, its high reactivity severely regulates widespread applications of difluorocarbene in organic synthesis. Here, we report a copper difluorocarbene-involved catalytic coupling, representing a new mode of the difluoromethylation reaction. This method allows difluoromethylation of a wide range of readily available allyl/propargyl electrophiles with NaBH3CN and low-cost difluorocarbene precursor BrCF2CO2K, featuring high cost-efficiency, high stereo- and regioselectivities, and high functional group tolerance, even with complex drug-like molecules. Applying the method led to the efficient synthesis of deuterated difluoromethylated compounds of medicinal interest. The resulting difluoromethylated allyl and allenyl products can serve as versatile synthons for diverse transformations, rendering the approach attractive for synthesizing complex fluorinated structures. Experimental mechanistic studies and computational calculations reveal that the formation of a difluoromethylcopper(I) intermediate through the nucleophilic attack of boron hydride on the copper(I) difluorocarbene is the key step in the reaction.

WWP2 protects against sepsis-induced cardiac injury through inhibiting cardiomyocyte ferroptosis.

Background and Objectives: Cardiac injury plays a critical role in contributing to the mortality associated with sepsis, a condition marked by various forms of programmed cell deaths. Previous studies hinted at the WW domain-containing E3 ubiquitin protein ligase 2 (WWP2) involving in heart failure and endothelial injury. However, the precise implications of WWP2 in sepsis-induced cardiac injury, along with the underlying mechanisms, remain enigmatic. Methods: Sepsis induced cardiac injury were constructed by intraperitoneal injection of lipopolysaccharide. To discover the function of WWP2 during this process, we designed and performed loss/gain-of-function studies with cardiac-specific vectors and WWP2 knockout mice. Combination experiments were performed to investigate the relationship between WWP2 and downstream signaling in septic myocardium injury. Results: The protein level of WWP2 was downregulated in cardiomyocytes during sepsis. Cardiac-specific overexpression of WWP2 protected heart from sepsis induced mitochondrial oxidative stress, programmed cell death and cardiac injury, while knockdown or knockout of WWP2 exacerbated this process. The protective potency of WWP2 was predominantly linked to its ability to suppress cardiomyocyte ferroptosis rather than apoptosis. Mechanistically, our study revealed a direct interaction between WWP2 and acyl-CoA synthetase long-chain family member 4 (FACL4), through which WWP2 facilitated the ubiquitin-dependent degradation of FACL4. Notably, we observed a notable reduction in ferroptosis and cardiac injury within WWP2 knockout mice after FACL4 knockdown during sepsis. Conclusions: WWP2 assumes a critical role in safeguarding the heart against injury induced by sepsis via regulating FACL4 to inhibit LPS-induced cardiomyocytes ferroptosis.

Enhanced architecture and implementation of spectrum shaping codes.

Spectral shaping codes are modulation codes widely used in communication and data storage systems. This research enhances the algorithms employed in constructing spectral shaping codes for hardware implementation. We present a parallel scrambling calculation with a time complexity of O(1). Second, in the minimum accumulated signal power (MASP) module, the sine-cosine accumulation needs to be determined by remainder with time complexity O(n2). We offer reduced MASP computations for short bit-width data, ROM storage, and addition pipelines. It can remove the remainder operation, reducing accumulated complexity to O(1). In addition, we present a search algorithm to generate segmented lines to replace the square operations in the MASP module. By employing the search algorithm and shift operations, we can reduce the complexity of the square from O(n2) to O(1). The implementation results reveal that the original and proposed MASPs yield nearly identical spectrum nulls. The encoder-decoder of the spectral shaping codes with proposed approaches consumes just 6% of the hardware resources when carried out with a Spartan6 XC6SLX25.

Late-stage gem-difluoroallylation of phenol in bioactive molecules and peptides with 3,3-difluoroallyl sulfonium salts.

An efficient method for the late-stage selective O-fluoroalkylation of tyrosine residues with a stable yet highly reactive fluoroalkylating reagent, 3,3-difluoroallyl sulfonium salts (DFASs), has been developed. The reaction proceeds in a mild basic aqueous buffer (pH = 11.6) with high efficiency, high biocompatibility, and excellent regio- and chemoselectivity. Various oligopeptides and phenol-containing bioactive molecules, including carbohydrates and nucleosides, could be selectively O-fluoroalkylated. The added vinyl and other functional groups from DFASs can be valuable linkers for successive modification, significantly expanding the chemical space for further bioconjugation. The synthetic utility of this protocol has been demonstrated by the fluorescently labeled anti-cancer drug and the synthesis of O-link type 1,4,7,10-tetraazacyclododecane-N,N',N,N'-tetraacetic acid-tyrosine3-octreotate (DOTA-TATE), showing the prospect of the method in medicinal chemistry and chemical biology.

Synergistic Interfacial Effect of Ru/Co3 O4 Heterojunctions for Boosting Overall Water Splitting.

Low-cost bifunctional electrocatalysts capable of efficiently driving the hydrogen evolution reaction (HER) and oxygen evolution reaction (OER) are needed for the growth of a green hydrogen economy. Herein, a Ru/Co3 O4 heterojunction catalyst rich in oxygen vacancies (VO ) and supported on carbon cloth (RCO-VO @CC) is prepared via a solid phase reaction (SPR) strategy. A RuO2 /Co9 S8 @CC precursor (ROC@CC) is first prepared by loading Co9 S8 nanosheets onto CC, following the addition of RuO2 nanoparticles (NPs). After the SPR process in an Ar atmosphere, Ru/Co3 O4 heterojunctions with abundant VO are formed on the CC. The compositionally optimized RCO-VO @CC electrocatalyst with a Ru content of 0.55 wt.% exhibits very low overpotential values of 11 and 253 mV at 10 mA cm-2 for HER and OER, respectively, in 1 m KOH. Further, a low cell voltage of only 1.49 V is required to achieve a current density of 10 mA cm-2 . Density functional theoretical calculations verify that the outstanding bifunctional electrocatalytic performance originates from synergistic charge transfer between Ru metal and VO -rich Co3 O4 . This work reports a novel approach toward a high-efficiency HER/OER electrocatalyst for energy storage and conversion.

Advances in the study of exosomes in cardiovascular diseases.

BACKGROUND: Cardiovascular disease (CVD) has been the leading cause of death worldwide for many years. In recent years, exosomes have gained extensive attention in the cardiovascular system due to their excellent biocompatibility. Studies have extensively researched miRNAs in exosomes and found that they play critical roles in various physiological and pathological processes in the cardiovascular system. These processes include promoting or inhibiting inflammatory responses, promoting angiogenesis, participating in cell proliferation and migration, and promoting pathological progression such as fibrosis. AIM OF REVIEW: This systematic review examines the role of exosomes in various cardiovascular diseases such as atherosclerosis, myocardial infarction, ischemia-reperfusion injury, heart failure and cardiomyopathy. It also presents the latest treatment and prevention methods utilizing exosomes. The study aims to provide new insights and approaches for preventing and treating cardiovascular diseases by exploring the relationship between exosomes and these conditions. Furthermore, the review emphasizes the potential clinical use of exosomes as biomarkers for diagnosing cardiovascular diseases. KEY SCIENTIFIC CONCEPTS OF REVIEW: Exosomes are nanoscale vesicles surrounded by lipid bilayers that are secreted by most cells in the body. They are heterogeneous, varying in size and composition, with a diameter typically ranging from 40 to 160 nm. Exosomes serve as a means of information communication between cells, carrying various biologically active substances, including lipids, proteins, and small RNAs such as miRNAs and lncRNAs. As a result, they participate in both physiological and pathological processes within the body.

Atorvastatin rescues vascular endothelial injury in hypertension by WWP2-mediated ubiquitination and degradation of ATP5A.

As a widely used lipid-lowering drug in clinical practice, atorvastatin is widely recognized for its role in protecting vascular endothelium in the cardiovascular system. However, a clear mechanistic understanding of its action is lacking. Here, we found that atorvastatin counteracted angiotensin II-induced vascular endothelial injury in mice with hypertension. Mechanistically, atorvastatin up-regulated WWP2, a E6AP C-terminus (HECT)-type E3 ubiquitin ligase with an essential role in regulating protein ubiquitination and various biological processes, thereby rescuing vascular endothelial injury. By ubiquitinating ATP5A (ATP synthase mitochondrial F1 complex subunit alpha), WWP2 degraded ATP5A via the proteasome pathway, stabilizing Bcl-2/Bax in the mitochondrial pathway of apoptosis. Moreover, atorvastatin further ameliorated death of vascular endothelial cells and improved vascular endothelial functions under WWP2 overexpression, whereas WWP2 knockout abrogated these beneficial effects of atorvastatin. Furthermore, we generated endothelial cell-specific WWP2 knockout mice, and this WWP2-mediated mechanism was faithfully recapitulated in vivo. Thus, we propose that activation of a WWP2-dependent pathway that is pathologically repressed in damaged vascular endothelium under hypertension is a major mechanism of atorvastatin. Our findings are also pertinent to develop novel therapeutic strategies for vascular endothelial injury-related cardiovascular diseases.

Nickel-Catalyzed Selective C(sp2 )-F Bond Alkylation of Industrially Relevant Hydrofluoroolefin HFO-1234yf.

The selective transition-metal catalyzed C-F bond functionalization of inexpensive industrial fluorochemicals represents one of the most attractive approaches to valuable fluorinated compounds. However, the selective C(sp2 )-F bond carbofunctionalization of refrigerant hydrofluoroolefins (HFOs) remains challenging. Here, we report a nickel-catalyzed selective C(sp2 )-F bond alkylation of HFO-1234yf with alkylzinc reagents. The resulting 2-trifluoromethylalkenes can serve as a versatile synthon for diversified transformations, including the anti-Markovnikov type hydroalkylation and the synthesis of bioactive molecule analogues. Mechanistic studies reveal that lithium salt is essential to promote the oxidative addition of Ni0 (Ln ) to the C-F bond; the less electron-rich N-based ligands, such as bipyridine and pyridine-oxazoline, feature comparable or even higher oxidative addition rates than the electron-rich phosphine ligands; the strong σ-donating phosphine ligands, such as PMe3 , are detrimental to transmetallation, but the less electron-rich and bulky N-based ligands, such as pyridine-oxazoline, facilitate transmetallation and reductive elimination to form the final product.

The role of SMURFs in non-cancerous diseases.

The ubiquitin-proteasome system is a crucial mechanism for regulating protein levels in cells, with substrate-specific E3 ubiquitin ligases serving as an integral component of this system. Among these ligases are SMAD-specific E3 ubiquitin-protein ligase 1 (SMURF1) and SMAD-specific E3 ubiquitin-protein ligase 2 (SMURF2), which belong to the neural precursor cell-expressed developmentally downregulated 4 (NEDD4) subfamily of Homologous to E6-AP COOH terminus (HECT)-type E3 ligases. As E3 ligases, SMURFs have critical functions in regulating the stability of multiple proteins, thereby maintaining physiological processes such as cell migration, proliferation, and apoptosis. The occurrence of many diseases is attributed to abnormal cell physiology and an imbalance in cell homeostasis. It is noteworthy that SMURFs play pivotal roles in disease progression, with the regulatory functions being complex and either facilitative or inhibitory. In this review, we elucidate the mechanisms by which SMURF1 and SMURF2 can regulate disease progression in non-cancerous diseases. These significant findings offer potential novel therapeutic targets for various diseases and new avenues for research on SMURF proteins.

Biocatalytic Fluoroalkylation Using Fluorinated S-Adenosyl-l-methionine Cofactors.

Modification of organic molecules with fluorine functionalities offers a critical approach to develop new pharmaceuticals. Here, we report a multienzyme strategy for biocatalytic fluoroalkylation using S-adenosyl-l-methionine (SAM)-dependent methyltransferases (MTs) and fluorinated SAM cofactors prepared from ATP and fluorinated l-methionine analogues by an engineered human methionine adenosyltransferase hMAT2AI322A. This work introduces the first example of biocatalytic 3,3-difluoroallylation. Importantly, this strategy can be applied to late-stage site-selective fluoroalkylation of complex molecule vancomycin with conversions up to 99%.

A novel criterion of metabolically healthy obesity could effectively identify individuals with low cardiovascular risk among Chinese cohort.

Background and objective: Obesity has become a serious public health problem and brings a heavy burden of cardiovascular disease. Metabolically healthy obesity (MHO) is defined as individuals with obesity with no or only minor metabolic complications. Whether individuals with MHO have a lower cardiovascular risk remains controversial. In this study, a new criterion was used to define MHO and assess its predictive value for cardiovascular events and death. At the same time, the new criterion and the traditional criterion are compared to analyze the differences between different diagnostic criteria. Methods: A prospective cohort was established in northeast rural China from 2012 to 2013. Follow-up was conducted in 2015 and 2018 to investigate the incidence of cardiovascular events and survival. Subjects were grouped according to the metabolic health and obesity status. Kaplan-Meier curves were drawn to describe the cumulative risk of endpoint events in the four groups. Cox regression analysis model was constructed to evaluate the risk of endpoint events. Analysis of variance and post hoc analyses were used to calculate and compare differences in metabolic markers between MHO subjects diagnosed by novel and traditional criteria. Results: A total of 9345 participants 35 years of age or older without a history of cardiovascular disease were included in this study. After a median follow-up of 4.66 years, the data showed that participants in the MHO group had no significant increase in the risk of composite cardiovascular events and stroke, but had a 162% increase in the risk of coronary heart disease (HR: 2.62; 95%CI: 1.21-5.67). However, when using conventional criteria for metabolic health, mMHO group had a 52% increase in combined CVD risk (HR: 1.52; 95%CI: 1.14-2.03). By comparing the differences of metabolic indicators between MHO subjects diagnosed by the two criteria, MHO subjects diagnosed by the new criterion had higher WC, WHR, TG, FPG, and lower HDL-C levels except for lower blood pressure, showing more exposure to cardiovascular risk factors. Conclusions: The risk of combined CVD and stroke was not increased in MHO subjects. The new metabolic health criterion is superior to the traditional criterion and can effectively identify individuals with obesity with a lower risk of combined CVD. Blood pressure levels may be responsible for the inconsistent risk of combined CVD in MHO subjects diagnosed with both criteria.

Copper-catalysed difluorocarbene transfer enables modular synthesis.

The use of metal catalysts to produce and control the reactivity of carbenes has long offered a powerful approach to organic synthesis; however, difluorocarbene transfer catalysed by metal is an outlier and remains a substantial challenge. In that context, copper difluorocarbene chemistry has been elusive so far. Here we report the design, synthesis, characterization and reactivity of isolable copper(I) difluorocarbene complexes, which enable the development of a copper-catalysed difluorocarbene transfer reaction. The method offers a strategy for the modular synthesis of organofluorine compounds from simple and readily available components. This strategy facilitates a modular difluoroalkylation by coupling difluorocarbene with two inexpensive feedstocks, silyl enol ethers and allyl/propargyl bromides, in a one-pot reaction via copper catalysis, providing a diversity of difluoromethylene-containing products without laborious multistep synthesis. The approach enables access to various fluorinated skeletons of medicinal interest. Mechanistic and computational studies consistently reveal a mechanism involving nucleophilic addition to an electrophilic copper(I) difluorocarbene.

Reductive Catalytic Difluorocarbene Transfer via Palladium Catalysis.

A palladium-catalyzed reductive difluorocarbene transfer reaction that tames difluorocarbene to couple with two electrophiles has been developed, representing a new mode of difluorocarbene transfer reaction. The approach uses low-cost and bulk industrial chemical chlorodifluoromethane (ClCF2 H) as the difluorocarbene precursor. It produces a variety of difluoromethylated (hetero)arenes from widely available aryl halides/triflates and proton sources, featuring high functional group tolerance and synthetic convenience without preparing organometallic reagents. Experimental mechanistic studies reveal that an unexpected Pd0/II catalytic cycle is involved in this reductive reaction, wherein the oxidative addition of palladium(0) difluorocarbene ([Pd0 (Ln )]=CF2 ) with aryl electrophile to generate the key intermediate aryldifluoromethylpalladium [ArCF2 Pd(Ln )X], followed by reaction with hydroquinone, is responsible for the reductive difluorocarbene transfer.

Down-regulation of WWP2 aggravates Type 2 diabetes mellitus-induced vascular endothelial injury through modulating ubiquitination and degradation of DDX3X.

BACKGROUND: Endothelial injury caused by Type 2 diabetes mellitus (T2DM) is considered as a mainstay in the pathophysiology of diabetic vascular complications (DVCs). However, the molecular mechanism of T2DM-induced endothelial injury remains largely unknown. Here, we found that endothelial WW domain-containing E3 ubiquitin protein ligase 2 (WWP2) act as a novel regulator for T2DM-induced vascular endothelial injury through modulating ubiquitination and degradation of DEAD-box helicase 3 X-linked (DDX3X). METHODS: Single-cell transcriptome analysis was used to evaluate WWP2 expression in vascular endothelial cells of T2DM patients and healthy controls. Endothelial-specific Wwp2 knockout mice were used to investigate the effect of WWP2 on T2DM-induced vascular endothelial injury. In vitro loss- and gain-of-function studies were performed to assess the function of WWP2 on cell proliferation and apoptosis of human umbilical vein endothelial cells. The substrate protein of WWP2 was verified using mass spectrometry, coimmunoprecipitation assays and immunofluorescence assays. The mechanism of WWP2 regulation on substrate protein was investigated by pulse-chase assay and ubiquitination assay. RESULTS: The expression of WWP2 was significantly down-regulated in vascular endothelial cells during T2DM. Endothelial-specific Wwp2 knockout in mice significantly aggravated T2DM-induced vascular endothelial injury and vascular remodeling after endothelial injury. Our in vitro experiments showed that WWP2 protected against endothelial injury by promoting cell proliferation and inhibiting apoptosis in ECs. Mechanically, we found that WWP2 is down-regulated in high glucose and palmitic acid (HG/PA)-induced ECs due to c-Jun N-terminal kinase (JNK) activation, and uncovered that WWP2 suppresses HG/PA-induced endothelial injury by catalyzing K63-linked polyubiquitination of DDX3X and targeting it for proteasomal degradation. CONCLUSION: Our studies revealed the key role of endothelial WWP2 and the fundamental importance of the JNK-WWP2-DDX3X regulatory axis in T2DM-induced vascular endothelial injury, suggesting that WWP2 may serve as a new therapeutic target for DVCs.

UHRF1-induced connexin26 methylation is involved in hearing damage triggered by intermittent hypoxia in neonatal rats.

Ubiquitin-like with plant homeodomain and ring finger domains 1 (UHRF1) promotes the maintenance of established patterns of DNA methylation in mammalian cells. Extensive methylation of connexin26 (COX26) during hearing impairment has been demonstrated. The present study aims to determine whether UHRF1 can induce the methylation of COX26 in cochlea damaged by intermittent hypoxia (IH). After the establishment of the cochlear injury model through IH treatment or isolation of the cochlea containing Corti's organ, pathological changes were observed via HE staining. Expressions of COX26 and UHRF1 were detected by quantitative reverse-transcription polymerase chain reaction and Western blot. The effect of COX26 methylation levels was analyzed by methylation-specific PCR (MSP). Phalloidin/immunofluorescence staining was used to observe structural changes. The binding relationship between UHRF1 and COX26 was verified by chromatin immunoprecipitation. IH caused cochlear damage, accompanied by increased methylation of COX26 and expression of UHRF1 in the cochlea of neonatal rats. CoCl2 treatment caused the loss of cochlear hair cells, downregulation and hypermethylation of COX26, abnormal upregulation of UHRF1, and disordered expressions of apoptosis-related proteins. UHRF1 in cochlear hair cells binds to COX26, and its knockdown upregulated COX26 level. Overexpressed COX26 partially alleviated the CoCl2-caused cell damage. UHRF1 induces COX26 methylation and aggravates the cochlear damage caused by IH.

Palladium-catalyzed highly selective gem-difluoroallylation of propargyl sulfonates with gem-difluoroallylboron.

A palladium-catalyzed gem-difluoroallylation of propargyl sulfonates with gem-difluoroallylboron has been developed. The reaction features synthetic simplicity and high functional group tolerance, affording 3,3-difluoro-skipped 1,5-enynes with high efficiency and regioselectivity. In particular, the resulting products can serve as versatile synthons for diversified transformations, having potential applications in medicinal chemistry.

Comparisons of lymphocytes profiles and inflammatory cytokines levels in blood of patients with differed severity of infection by human adenovirus type 7.

BACKGROUND: Human adenovirus (HAdV) infection outbreak causes community-acquired pneumonia. Cellular immune dysfunction and hypercytokinemia play important roles in the pathogenesis of adenovirus respiratory infection. Some soluble factors in peripheral blood can assist in judging the virus-induced disease severity. The expression levels of inflammatory cytokines differ among patients with different disease severity. However, whether and how HAdV-7 infection influences the composition of blood immune cells and serum cytokine levels in patients at different disease stages, as well as the diagnosis values of these parameters, have rarely been intensively studied. We aimed to investigate lymphocytes profiles and cytokines levels in blood of patients at different disease stages upon human adenovirus type 7 (HAdV-7) infections, and explored the diagnosis values of the investigated parameters. METHODS: Patients from two outbreaks of HAdV-7 in military of China were categorized into upper respiratory infection (URI) group, common pneumonia (CP) group and severe pneumonia (SP) group according to disease severity. Peripheral blood samples were subjected to routine laboratory tests, while flow cytometry and ELISA were used to measure the lymphocyte subsets and cytokines in blood, respectively. The receiver operating characteristic (ROC) curves were performed to examine the diagnostic of these blood parameters. RESULTS: Signs of imbalanced lymphocytes composition and hypercytokinemia were observed in HAdV-7-infected patients. The percentages of CD3+ T cells and NK cells were significantly decreased along with the aggravation of the disease, particularly for NK cells and CD4+ T cells. The neutrophil to lymphocyte ratio (NLR) increased significantly in patients with more severe disease. In addition, the levels of serum CXCL10, IL-2 and TNF-α were positively correlated with disease severity, while reduced levels of IFN-γ and IL-10 were found in SP patients. Furthermore, analysis of ROC showed that multiple parameters including the percentage of blood CD3+ cells and serum CXCL10 level could predict the progression of HAdV-7 infection. CONCLUSION: Imbalance of immune state with hypercytokinemia occurred during HAdV-7 infection. The percentages of blood immune cells such as CD3+ T cells and the levels of serum cytokines such as CXCL10 showed potential diagnosis values in HAdV-7 infection.

Optimal Channel Training Design for Secure Short-Packet Communications.

Physical layer security is a promising technique to ensure the confidentiality of short-packet communications, since no additional channel uses are needed. Motivated by the fact of finite coding blocklength in short-packet communications, we attempt to investigate the problem of how many the channel uses utilized for channel training should be allocated to perform secure communications. Based on the finite blocklength information theory, we derive a closed-form expression to approximate the average achievable secrecy throughput. To gain more insights, we also present the asymptotic average secrecy throughput under two special cases, i.e., high signal-to-noise ratio (SNR) and infinite blocklength. Moreover, we determine the optimal channel training length to maximize the average secrecy throughput under the reliability constraint and given blocklength. Numerical results are provided to validate the analysis and demonstrate that the performance gain achieved by the optimal channel training length is remarkable, relative to other benchmark schemes.

Analysis of Serum Inflammatory Markers in Infants Under 6 Months of Age with Non-Syndromic Moderate and Severe Hearing Loss Associated with GJB2 Gene Mutations.

BACKGROUND The GJB2 gene is reported to be the main hereditary factor responsible for non-syndromic hearing impairment in infants. Several kinds of hearing loss have been linked to elevated inflammatory markers. This study aimed to evaluate serum levels of IL-2, IL-4, IL-6, IL-10, IL-17, alpha-TNF, and γ-IFN and the severity of hearing loss. MATERIAL AND METHODS Ninety newborns were divided into 3 groups: severe hearing impairment (31 infants), moderate hearing impairment (30 infants), and normal hearing (29 infants). Hearing screening was performed using otoacoustic emissions test. Mutations of the GJB2 gene were detected with Sanger sequencing. The patients had DNFB1 mutation. Seven blood inflammatory markers were tested using Cytometric Bead Array. We performed the t test to examine differences in expression of 7 inflammatory markers between sexes in the groups. The correlation between indicators within groups was studied using the Pearson correlation test. Correlation of different indicators among groups was studied using the Spearman correlation test. RESULTS When compared among the 3 groups (severe, moderate hearing impairment, and normal hearing group), we found that IL-10 had a positive correlation with the severity of GJB2-associated hearing loss, which was statistically significant (P<0.05). CONCLUSIONS This research aimed to assess the relationship of 7 serum inflammatory markers with GJB2-associated hearing loss in infants. Inflammatory marker IL-10 had a positive correlation with the severity of GJB2-associated infant hearing loss, and it might have the potential to become a future therapeutic target.