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Wen Kong

Publications and source records attributed to Wen Kong.

4 recordsLinked to original sources

Conditional Diffusion Model-Based Method for Annotation of Antibiotic Resistance Gene Properties.

The crisis of bacterial antibiotic resistance, which has led to a decline in the effectiveness of antibiotics originally used to combat bacterial infections, has emerged as an urgent challenge for public health. Antibiotic resistance genes (ARGs) are one of the key reasons for bacteria to develop resistance to antibiotics. Therefore, accurately identifying and annotating the critical properties of ARGs is of great importance for addressing the antibiotic resistance emergency. Although existing deep learning models demonstrate remarkable effectiveness in extracting local features from sequence data, they still face limitations in the capacity to further gain the enriched latent representations within the data. To address the critical challenge of extracting higher-quality representations from ARGs sequence data, we propose a novel ARGs properties annotation method based on the conditional diffusion model which is used to learn latent representations through domain-specific knowledge injection. Specifically, during the conditional information integration phase, we systematically incorporate ARGs' domain knowledge to guide the diffusion process in generating high-quality latent representations. To overcome information redundancy caused by direct concatenation of conditional information and intermediate features, we design a cross-attention mechanism that enables feature fusion between heterogeneous information sources, thereby enhancing further the quality of obtained representations. Experimental results on widely used data sets demonstrate the framework's effectiveness in achieving superior prediction performance compared to existing methods.

Anti-Bacterial Agents↗

The effect of the mtDNA4834 deletion on hearing.

Mutations in mitochondrial DNA (mtDNA) are associated with diverse pathological states in humans, notably sensorineural deafness. In humans, mtDNA4977 deletion, known as common deletion, is thought to play a critical role in presbyacusis. A similar mtDNA deletion occurs in the naturally aging rats is mtDNA4834 deletion. Today, it is still obscure about the effect of common mtDNA deletion on the presbyacusis and hearing loss. We establish a model of rat associated with mtDNA4834 deletion in inner ear by d-galactose. It was found that the malondialdehyde (MDA) increased with superoxide dismutase (SOD) decreasing in the inner ear of the rat treated with d-galactose than of the control. However, there was no significant difference in elevation of ABR threshold between the rat with mtDNA4834 deletion induced by d-galactose and control. After aminoglycoside antibiotic injected, the hearing threshold of the rats carrying mtDNA4834 deletion increased significantly compared with the rats without mtDNA4834 deletion. The results show that resembled accelerated aging in the inner ear of the rat could be induced by injecting d-galactose. Moreover, those suggest that mtDNA4834 deletion can not directly induce the hearing loss, but acting as a predisposing factor which can greatly enhance the sensitivity of the inner ear to the aminoglycoside antibiotic.

Aging↗

Effect of methylation-associated silencing of the death-associated protein kinase gene on nasopharyngeal carcinoma.

Death-associated protein kinase (DAPK) is a Ca/calmodulin-regulated serine/threonine kinase and a positive mediator of apoptosis. Loss of expression of the DAPK gene by aberrant promoter methylation may play an important role in cancer development and progression. The aim of this study was to investigate the frequency of gene promoter methylation of DAPK in nasopharyngeal carcinoma (NPC) and the effect of 5-Aza-2'-deoxycytidine (5-Aza-CdR), a demethylating agent, on CNE cells, a human nasopharyngeal carcinoma cell line, and on xenografts of CNE cells. Methylation-specific PCR and RT-PCR were used to determine the promoter methylation status and mRNA expression of the DAPK gene in NPC. Furthermore, CNE cells were treated in vitro and in vivo with 5-Aza-CdR to explore the effect of demethylating agents on DAPK mRNA expression and tumor growth. Hypermethylation of the DAPK gene promoter was found in 35 (76.1%) of 46 NPC samples. There was no significant difference in the promoter hypermethylation rate among samples from patients with different TNM stages. No promoter hypermethylation of the DAPK gene was found in all six chronic inflammatory nasopharyngeal tissue specimens. DAPK mRNA expression was not detected in NPC tumor specimens with promoter hypermethylation. However, DAPK mRNA expression was observed in unmethylated NPC tumors and in the chronic inflammatory nasopharyngeal tissue specimens. Promoter hypermethylation of the DAPK gene was found and no DAPK mRNA expression was detected in CNE cells. DAPK mRNA expression in CNE cells and xenografts could be restored by treatment with 5-Aza-CdR. The CNE cell xenografts of nude mice treated with 5-Aza-CdR were obviously smaller in tumor volume than those of nude mice treated with PBS. These results demonstrate that loss of DAPK expression could be associated with promoter region methylation in NPC. 5-Aza-CdR may slow the growth of CNE cells in vitro and in vivo by reactivating the DAPK gene silenced by de novo methylation.

Adult↗

[Establishment of model with inner ear mimetic aging and mtDNA 4834 bp deletion in rats].

OBJECTIVE: To explore the establishment of the mimetic aging effect in the inner ear of the rat. METHOD: Twenty-four Wistar rats were randomly divided into two groups: group A (D-galactose group, n = 14), which were treated with hypodermic 5% D-galactose (150 mg x kg(-1) x d(-1)) for 8 weeks and then with intraperitoneal saline for 10 days, and group B (control group, n = 10), which were given saline only. Auditory brainstem response(ABR) was used to detect the hearing threshold of rats, and colorimetry was used to analyze the activity of the glutathione peroxidase (GSH-PX). The inner ear tissue was harvested and mitochondrial DNA was amplified to identify the 4 834 bp deletion mutation by nested primer polymerase chain reaction (nested PCR) technique. RESULT: The incidence of mitochondrial DNA 4 834 bp deletion of group A was 100% (28/28), while the deletion of group B was 0. The activity of the GSH-PX in group A (59.07 +/- 8.70 U) was lower than that in group B (142.10 +/- 7.02 U). The difference between group A and group B was significant (t-test, P < 0.01). Variation in ABR threshold of (5.36 +/- 3.08) dB peSPL was observed in group A, and (6.50 +/- 3.37) dB peSPL in group B. The difference in shift of ABR threshold between group A and group B was not significant (P > 0.05). CONCLUSION: The mimetic aging effect in the inner ear of the rat can be induced by D-galactose, and this rat model presents high incidence of mtDNA4834 deletion. But no hearing loss was found in this model.

Aging, Premature↗