Comparison of Neutralizing Antibody Response Kinetics in Patients with Hand, Foot, and Mouth Disease Caused by Coxsackievirus A16 or Enterovirus A71: A Longitudinal Cohort Study of Chinese Children, 2017-2019.

Hand, foot, and mouth disease (HFMD), which is mainly caused by coxsackievirus A16 (CVA16) or enterovirus A71 (EV-A71), poses a serious threat to children's health. However, the long-term dynamics of the neutralizing Ab (NAb) response and ideal paired-serum sampling time for serological diagnosis of CVA16-infected HFMD patients were unclear. In this study, 336 CVA16 and 253 EV-A71 PCR-positive HFMD inpatients were enrolled and provided 452 and 495 sera, respectively, for NAb detection. Random-intercept modeling with B-spline was conducted to characterize NAb response kinetics. The NAb titer of CVA16 infection patients was estimated to increase from negative (2.1, 95% confidence interval [CI]: 1.4-3.3) on the day of onset to a peak of 304.8 (95% CI: 233.4-398.3) on day 21 and then remained >64 until 26 mo after onset. However, the NAb response level of EV-A71-infected HFMD patients was much higher than that of CVA16-infected HFMD patients throughout. The geometric mean titer was significantly higher in severe EV-A71-infected patients than in mild patients, with a 2.0-fold (95% CI: 1.4-3.2) increase. When a 4-fold rise in titer was used as the criterion for serological diagnosis of CVA16 and EV-A71 infection, acute-phase serum needs to be collected at 0-5 d, and the corresponding convalescent serum should be respectively collected at 17.4 (95% CI: 9.6-27.4) and 24.4 d (95% CI: 15.3-38.3) after onset, respectively. In conclusion, both CVA16 and EV-A71 infection induce a persistent humoral immune response but have different NAb response levels and paired-serum sampling times for serological diagnosis. Clinical severity can affect the anti-EV-A71 NAb response.

Influence of the COVID-19 pandemic on the vitamin D status of children: A cross-sectional study.

Coronavirus disease 2019 (COVID-19), as well as its prevention and control measures, seriously affected people's livehood, which may have affected the body's level of vitamin D (VD). This study aimed to investigate the effect of the COVID-19 pandemic on the VD status of children in Zhengzhou, China. In this study, we included 12 272 children in 2019 (before the COVID-19 pandemic) and 16 495 children in 2020 (during the COVID-19 pandemic) to examine the changes in VD levels and deficiency rates among children before and during the COVID-19 pandemic. Total VD levels in 2020 were significantly higher than those in 2019 (26.56 [18.15, 41.40] vs. 25.98 [17.92, 40.09] ng/ml, p < 0.001). Further analysis revealed that during the COVID-19 pandemic control period in 2020, the VD levels in February, March, and April were lower than those in the same months of 2019, while the VD deficiency rates were significantly higher. Additionally, our data revealed that VD levels decreased significantly with age. Among children older than 6 years, the VD deficiency rate exceeded 50%. These results indicate that we should pay close attention to VD supplementation during the COVID-19 pandemic control period and in children older than 6 years of age.

Lymphocyte-to-C-Reactive Protein Ratio as an Early Sepsis Biomarker for Neonates with Suspected Sepsis.

Background: Neonatal sepsis is an extremely dangerous and fatal disease among neonates, and its timely diagnosis is critical to treatment. This research is aimed at evaluating the clinical significance of the lymphocyte-to-C-reactive protein ratio (LCR) as an early sepsis indicator in neonates with suspected sepsis. Methods: Between January 2016 and December 2021, 1269 neonates suspected of developing sepsis were included in this research. Among them, sepsis was diagnosed in 819 neonates, with 448 severe cases, as per the International Pediatric Sepsis Consensus. Data related to clinical and laboratory tests were obtained via electronic medical records. LCR was calculated as total lymphocyte (109 cells/L)/C-reactive protein (mg/L). Multivariate logistic regression analysis was employed to evaluate the effectiveness of LCR as an independent indicator for determining sepsis in susceptible sepsis neonates. Receiver operating characteristic (ROC) curve analysis was conducted for investigating the diagnostic significance of LCR in sepsis. When suitable, the statistical tool SPSS 24.0 was used for statistical analyses. Results: LCR decreased significantly in the control, mild, and severe sepsis groups. Further analyses exhibited that there was a substantially greater incidence of sepsis in neonates in the low-LCR group (LCR ≤ 3.94) as opposed to the higher LCR group (LCR > 3.94) (77.6% vs. 51.4%, p < 0.001). Correlation analysis indicated a substantial negative association of LCR with procalcitonin (r = -0.519, p < 0.001) and hospital stay duration (r = -0.258, p < 0.001). Multiple logistic regression analysis depicted LCR as an independent indicator for identifying sepsis and severe cases of this disease. ROC curve analysis indicated the optimal cutoff value of LCR in identifying sepsis to be 2.10, with 88% sensitivity and 55% specificity. Conclusions: LCR has proven to be a potentially strong biomarker capable of identifying sepsis in a timely manner in neonates suspected to have the disease.

P62/SQSTM1 mediates the autophagy-lysosome degradation of CDK2 protein undergoing PI3Kα/AKT T308 inhibition.

CDK2 forms a complex with cyclin A and cyclin E to promote the progress of cell cycle, but when cyclin A and cyclin E are dissociated from the complex and degraded by the ubiquitin proteasome pathway, the fate of the inactive CDK2 is unclear. In this study, we found that the inactive CDK2 protein was degraded by autophagy-lysosome pathway. In the classic model of G0/G1 phase arrest induced by serum starvation, we found that the mRNA level in CDK2 did not change but the protein level decreased. Subsequently, using PI3K and AKT inhibitors and gene knockout methods, it was found that CDK2 degradation was mediated by the inhibition of PI3Kα/AKTT308. In addition, P62/SQSTM1 was found to bind to the inactivated CDK2 protein to help it enter autophagy-lysosome degradation in a CTSB-dependent manner. Taken together, these results confirm that the PI3Kα/AKTT308 inhibition leads to degradation of CDK2 protein in the autophagy-lysosome pathway. These data reveal a new molecular mechanism of CDK2 protein degradation and provide a new strategy and method for regulating CDK2 protein.

Comparative Genomic Analysis of Streptococcus pneumoniae Strains: Penicillin Non-susceptible Multi-drug-Resistant Serotype 19A Isolates.

Streptococcus pneumoniae can cause several diseases including otitis media, sinusitis, pneumonia, sepsis and meningitis. The introduction of pneumococcal vaccines has changed the molecular epidemiological and antibiotic resistance profiles of related diseases. Analysis of molecular patterns and genome sequences of clinical strains may facilitate the identification of novel drug resistance mechanism. Three multidrug resistance 19A isolates were verified, serotyped and the complete genomes were sequenced combining the Pacific Biosciences and the Illumina Miseq platform. Genomic annotation revealed that similar central networks were found in the clinical isolates, and Mauve alignments indicated high similarity between different strains. The pan-genome analysis showed the shared and unique cluster in the strains. Mobile elements were predicted in the isolates including prophages and CRISPER systems, which may participate in the virulence and antibiotic resistance of the strains. The presence of 31 virulence factor genes was predicted from other pathogens for PRSP 19339 and 19343, while 30 for PRSP 19087. Meanwhile, 33 genes antibiotic resistance genes were predicted including antibiotic resistance genes, antibiotic-target genes and antibiotic biosynthesis genes. Further analysis of the antibiotic resistance genes revealed new mutations in the isolates. By comparative genomic analysis, we contributed to the understanding of resistance mechanism of the clinical isolates with other serotype strains, which could facilitate the concrete drug resistance mechanism study.

Systematic Evaluation of Mycobacterium tuberculosis Proteins for Antigenic Properties Identifies Rv1485 and Rv1705c as Potential Protective Subunit Vaccine Candidates.

The lack of efficacious vaccines against Mycobacterium tuberculosis (MTB) infection is a limiting factor in the prevention and control of tuberculosis (TB), the leading cause of death from an infectious agent. Improvement or replacement of the BCG vaccine with one that reliably protects all age groups is urgent. Concerns exist that antigens currently being evaluated are too homogeneous. To identify new protective antigens, we screened 1,781 proteins from a high-throughput proteome-wide protein purification study for antigenic activity. Forty-nine antigens (34 previously unreported) induced antigen-specific gamma interferon (IFN-γ) release from peripheral blood mononuclear cells (PBMCs) derived from 4,452 TB and suspected TB patients and 167 healthy donors. Three (Rv1485, Rv1705c, and Rv1802) of the 20 antigens evaluated in a BALB/c mouse challenge model showed protective efficacy, reducing lung CFU counts by 66.2%, 75.8%, and 60%, respectively. Evaluation of IgG2a/IgG1 ratios and cytokine release indicated that Rv1485 and Rv1705c induce a protective Th1 immune response. Epitope analysis of PE/PPE protein Rv1705c, the strongest candidate, identified a dominant epitope in its extreme N-terminal domain accounting for 90% of its immune response. Systematic preclinical assessment of antigens Rv1485 and Rv1705c is warranted.

Poly(ADP-Ribose) Polymerase Activity and Coronary Artery Disease in Type 2 Diabetes Mellitus: An Observational and Bidirectional Mendelian Randomization Study.

OBJECTIVE: Experimental evidence suggests a close link between PARP (poly[ADP-ribose] polymerase) activation and diabetic endothelial dysfunction. Here, we tested whether PARP activity in circulating leukocytes was associated with coronary artery disease (CAD) among patients with type 2 diabetes mellitus (T2DM). Approach and Results: We performed observational and bidirectional Mendelian randomization studies of 3149 Chinese individuals with T2DM who underwent coronary angiography, with leukocyte PARP activity, 16 tag single-nucleotide polymorphisms in PARP1 and PARP2, and 17 CAD risk single-nucleotide polymorphisms analyzed. Of 3149 participants, 1180 who further received percutaneous coronary intervention were prospectively followed for 1 year to track major adverse cardiovascular and cerebrovascular events. Overall, greater PARP activity was cross-sectionally associated with an odds ratio of 1.23 for obstructive CAD, and prospectively with a hazard ratio of 1.34 for 1-year major adverse cardiovascular and cerebrovascular events after percutaneous coronary intervention (both P<0.001). Using a genetic score of 5 screened single-nucleotide polymorphisms in PARP1 and PARP2 as the instrumental variable, genetically predicted elevation in PARP activity showed a causal association with obstructive CAD (odds ratio=1.35, P<0.001). In contrast, the genetic risk of CAD had no significant effect on PARP activity. Ex vivo and in vitro cultures of human monocytes showed that rs747657, as the lead single-nucleotide polymorphism strongly associated with PARP activity, caused the differential binding of transcription factor GATA2 (GATA-binding protein 2) to an intronic regulatory region in PARP1, thus modulating PARP1 expression and PARP activity. CONCLUSIONS: Greater PARP activity may have causal roles in the development of obstructive CAD among patients with diabetes mellitus.

Identification of a compound heterozygote in LYST gene: a case report on Chediak-Higashi syndrome.

BACKGROUND: Chediak-Higashi Syndrome (CHS) is a rare autosomal recessive disease caused by loss of function of the lysosomal trafficking regulator protein. The causative gene LYST/CHS1 was cloned and identified in 1996, which showed significant homology to other species such as bovine and mouse. To date, 74 pathogenic or likely pathogenic mutations had been reported. CASE PRESENTATION: Here we describe a compound heterozygote in LYST gene, which was identified in a 4-year-old female patient. The patient showed skin hypopigmentation, sensitivity to light, mild splenomegaly and reduction of platelets in clinical examination. Giant intracytoplasmic inclusions were observed in the bone marrow examination, suggesting the diagnosis of CHS. Amplicon sequencing was performed to detect pathogenic mutation in LYST gene. The result was confirmed by two-generation pedigree analysis base on sanger sequencing. CONCLUSION: A compound heterozygote in LYST gene, consisting of a missense mutation c.5719A > G and an intron mutation c.4863-4G > A, was identified from the patient by using amplicon sequencing. The missense mutation is reported for the first time. Two-generation pedigree analysis showed these two mutations were inherited from the patient's parents, respectively. Our result demonstrated that amplicon sequencing has great potential for accelerating and improving the diagnosis of rare genetic diseases.

MicroRNA-92b acts as an oncogene by targeting PTEN/AKT in NSCLC.

MicroRNAs can act as tumour suppressors or oncogenes by regulating cellular differentiation, proliferation and apoptosis, and the dysregulation of miRNA is involved in the occurrence and development of NSCLC. Here, we provided evidence that miR-92b as an oncogene in NSCLC by targeting PTEN/AKT. We found that miR-92b was up-regulated in human NSCLC tissues and cell lines. MiR-92b knockdown suppressed the NSCLC cells proliferation and migration in both in vivo and in vitro models. Conversely, miR-92b overexpression induced an aggressive phenotype. Moreover, miR-92b-mediated regulation of NSCLC cell proliferation and migration depended on binding to PTEN mRNA, which then led to the degradation of PTEN and activation of the downstream AKT signalling pathway. Overall, this study revealed the oncogenic roles of miR-92b in NSCLC by targeting PTEN/AKT, and provided novel insights for future treatments of NSCLC patients. SIGNIFICANCE OF THE STUDY: MiR-92b was up-regulated in human NSCLC tissues and cell lines. Our study demonstrated that miR-92b as an oncogene in NSCLC by targeting PTEN/AKT in both in vivo and in vitro models and provided novel insights for future treatments of NSCLC patients.

The Role of Matrix Metalloproteinase-9 in Atherosclerotic Plaque Instability.

Matrix metalloproteinase-9 (MMP-9) belongs to the MMP family and has been widely investigated. Excessive MMP-9 expression can enhance extracellular matrix degradation and promote plaque instability. Studies have demonstrated that MMP-9 levels are higher in vulnerable plaques than in stable plaques. Additionally, several human studies have demonstrated that MMP-9 may be a predictor of atherosclerotic plaque instability and a risk factor for future adverse cardiovascular and cerebrovascular events. MMP-9 deficiency or blocking MMP-9 expression can inhibit plaque inflammation and prevent atherosclerotic plaque instability. All of these results suggest that MMP-9 may be a useful predictive biomarker for vulnerable atherosclerotic plaques, as well as a therapeutic target for preventing atherosclerotic plaque instability. In this review, we describe the structure, function, and regulation of MMP-9. We also discuss the role of MMP-9 in predicting and preventing atherosclerotic plaque instability.

Neutrophil Extracellular Traps: Signaling Properties and Disease Relevance.

Neutrophil extracellular traps (NETs) are characterized as extracellular DNA fibers comprised of histone and cytoplasmic granule proteins. NETs were first described as a form of innate response against pathogen invasion, which can capture pathogens, degrade bacterial toxic factors, and kill bacteria. Additionally, NETs also provide a scaffold for protein and cell binding. Protein binding to NETs further activate the coagulation system which participates in thrombosis. In addition, NETs also can damage the tissues due to the proteins they carry. Many studies have suggested that the excessive formation of NETs may contribute to a range of diseases, including thrombosis, atherosclerosis, autoimmune diseases, and sepsis. In this review, we describe the structure and components of NETs, models of NET formation, and detection methods. We also discuss the molecular mechanism of NET formation and their disease relevance. Modulation of NET formation may provide a new route for the prevention and treatment of releated human diseases.

Age-Related Differences in the Association between Plasma High-Sensitivity C-Reactive Protein and Noncalcified or Mixed Coronary Atherosclerotic Plaques.

BACKGROUND: Previous studies have demonstrated that plasma high-sensitivity C-reactive protein (hsCRP) was the predictor for unstable coronary plaque. Patients with noncalcified plaque (NCP) or mixed plaque (MP) have a higher risk of poor outcomes. However, the association between hsCRP and the presence of NCP or MP (NCP/MP) in old adults remains unclear, and if present, whether there exist differences between young and old adults remain unknown. Thus, the aim of this study was to investigate the role of hsCRP in predicting the presence of NCP/MP and evaluate whether age has any impact on this association. METHODS: A total of 951 subjects were included in this study. Complete clinical and laboratory data were collected. According to the characteristics of the most stenotic plaque, we divided them into 2 groups: calcified plaque (CP) and NCP/MP. Subjects with no plaque were classified as the control group (CR). Subjects with age ≥ 60 years were defined as older adults, and those with age < 60 years were classified as nonelderly people. RESULTS: Patients with NCP/MP had significantly higher hsCRP level compared with subjects with CR or CP in older adults but not in nonelderly people. The proportion of NCP/MP was significantly increased from 27.0% in the hsCRP < 1.25 mg/L group to 42.7% in the hsCRP > 2.70 mg/L group in older adults. Multiple logistic regression analysis showed that hsCRP was an independent risk factor for the presence of NCP/MP (odds ratio (OR) = 1.093, 95% CI 1.032-1.157, P = 0.001) only in older adults. CONCLUSIONS: hsCRP is independently associated with the presence of NCP/MP in older adults but not in nonelderly people. These results suggest the potential significance of hsCRP-lowering regimens in older adults with NCP/MP.

WP1130 reveals USP24 as a novel target in T-cell acute lymphoblastic leukemia.

BACKGROUND: T-cell acute lymphoblastic leukemia (T-ALL) is a lymphoid malignancy caused by the oncogenic transformation of immature T-cell progenitors with poor outcomes. WP1130 has shown potent activity against a variety of cancer but whether WP1130 has anti-T-ALL activity is not clear. USP24, one target of WP1130, is one of the largest deubiquitinases and its detailed mechanism is poorly understood. The aim of this study was to explore whether WP1130 could suppress T-ALL and the role of USP24 in T-ALL. METHODS: Molecular docking and cellular thermal shift assay were performed to determine whether and how WP1130 directly interact with USP24. Mitochondrial transmembrane potential assay was measured via Rhodamine 123 staining. USP24 was reactivated using the deactivated CRISPR-associated protein 9 (dCas9)-synergistic activation mediator (SAM) system. The in vivo results were examined by tumor xenografts in NOD-SCID mice. All statistical analyses were performed with the SPSS software package. RESULTS: WP1130 treatment decreased the viability and induces apoptosis of T-ALL cells both in vitro and in vivo. Furthermore, we demonstrated that knockdown of USP24 but not USP9X could significantly induce growth inhibition and apoptosis of T-ALL cells. Oncomine database showed that USP24 expression was upregulated in T-ALL samples and Kaplan-Meier results indicated that the USP24 was negatively but USP9X was positively associated with survival in T-ALL patients. Additionally, we proposed that WP1130 directly interacts with the activity site pocket of USP24 in T-ALL cells, which leads to the decrease of its substrates Mcl-1. Mechanistically, WP1130 induces apoptosis by accelerating the collapse of mitochondrial transmembrane potential via USP24-Mcl-1 axis. CONCLUSIONS: Altogether, using WP1130 as a chemical probe, we demonstrate that USP24 but not USP9X is a novel target in T-ALL cells. Moreover, we uncovered that WP1130 induces apoptosis by accelerating the collapse of mitochondrial transmembrane potential via USP24-Mcl-1 axis. These results provide that USP24-Mcl-1 axis may represent a novel strategy in the treatment of T-ALL and WP1130 is a promising lead compound for developing anti-T-ALL drugs.

Vertical distribution of aerosol optical properties based on aircraft measurements over the Loess Plateau in China.

Vertical distributions of aerosol optical properties based on aircraft measurements over the Loess Plateau were measured for the first time during a summertime aircraft campaign, 2013 in Shanxi, China. Data from four flights were analyzed. The vertical distributions of aerosol optical properties including aerosol scattering coefficients (σsc), absorption coefficients (σab), Angström exponent (α), single scattering albedo (ω), backscattering ratio (ßsc), aerosol mass scattering proficiency (Qsc) and aerosol surface scattering proficiency (Qsc(')) were obtained. The mean statistical values of σsc were 77.45 Mm(-1) (at 450 nm), 50.72 Mm(-1) (at 550n m), and 32.02 Mm(-1) (at 700 nm). The mean value of σab was 7.62 Mm(-1) (at 550 nm). The mean values of α, ßsc and ω were 1.93, 0.15, and 0.91, respectively. Aerosol concentration decreased with altitude. Most effective diameters (ED) of aerosols were less than 0.8 µm. The vertical profiles of σsc,, α, ßsc, Qsc and Qsc(') showed that the aerosol scattering properties at lower levels contributed the most to the total aerosol radiative forcing. Both α and ßsc had relatively large values, suggesting that most aerosols in the observational region were small particles. The mean values of σsc, α, ßsc, Qsc, Qsc('), σab and ω at different height ranges showed that most of the parameters decreased with altitude. The forty-eight hour backward trajectories of air masses during the observation days indicated that the majority of aerosols in the lower level contributed the most to the total aerosol loading, and most of these particles originated from local or regional pollution emissions.

[A novel splicing mutation in COL1A1 gene caused type I osteogenesis imperfecta in a Chinese family].

OBJECTIVE: To study a family affected with osteogenesis imperfecta for potential mutations in COL1A1 gene. METHODS: Clinical data of an affected family was collected. Potential mutation of the COL1A1 gene was screened using polymerase chain reaction and direct sequencing. Suspected mutation was detected in 20 unaffected relatives and 200 unrelated healthy controls. RESULTS: Analysis of RNA splicing has revealed a c.3208G/A mutation, which created a new splice sites and led to a frameshift mutation. The same mutation was not detected in the unaffected relatives or the 200 healthy controls. CONCLUSION: Mutations of the COL1A1 gene are one of the major causes of osteogenesis imperfecta in Chinese population. Our finding has enriched the mutation spectrum of type I collagen genes.

Clinical characteristics and risk factors for neonatal bloodstream infection due to carbapenem-resistant Enterobacteriaceae: A single-centre Chinese retrospective study.

OBJECTIVES: To analyse the clinical characteristics and risk factors for bloodstream infections (BSIs) caused by carbapenem-resistant Enterobacteriaceae (CRE) in neonates. METHODS: This single-centre, retrospective study included all patients with BSIs admitted to a neonatal intensive care unit between 1 January 2015 and 30 April 2022. The clinical and microbiological data of patients were collected; predictors of 30-day mortality in patients with CRE BSIs were also identified in this study. RESULTS: Among the 224 neonates with Enterobacteriaceae BSIs, 39.29% (88/224) of the patients developed CRE BSIs. The 30-day mortality rate reached up to 21.59% (19/88). The Quick Sequential Organ Failure Assessment score > 2 (odds ratio [OR] and 95% credibility interval [CI]: 3.852 [1.111-13.356], P < 0.05), prior to more than two kinds of antibiotics use (OR and 95% CI: 9.433 [1.562-56.973], P < 0.05), pneumonia (OR and 95% CI: 3.847 [1.133-13.061], P < 0.05), and caesarean section (OR and 95% CI: 2.678 [1.225-5.857], P < 0.05) were independent risk factors associated with CRE BSIs. Moreover, the risk factors for mortality in neonates with CRE BSIs were significantly associated with neonatal Sequential Organ Failure Assessment score > 6 (OR and 95% CI: 16.335 [1.446-184.517], P < 0.05). CONCLUSION: Prior to more than two kinds of antibiotics use, Quick Sequential Organ Failure Assessment score > 2, pneumonia and caesarean section were independent risk factors for CRE BSIs. The Neonatal Sequential Organ Failure Assessment score > 6 was a risk factor for mortality associated with CRE BSIs.

The role of programmed cell death in osteosarcoma: From pathogenesis to therapy.

Osteosarcoma (OS) is a prevalent bone solid malignancy that primarily affects adolescents, particularly boys aged 14-19. This aggressive form of cancer often leads to deadly lung cancer due to its high migration ability. Experimental evidence suggests that programmed cell death (PCD) plays a crucial role in the development of osteosarcoma. Various forms of PCD, including apoptosis, ferroptosis, autophagy, necroptosis, and pyroptosis, contribute significantly to the progression of osteosarcoma. Additionally, different signaling pathways such as STAT3/c-Myc signal pathway, JNK signl pathway, PI3k/AKT/mTOR signal pathway, WNT/ß-catenin signal pathway, and RhoA signal pathway can influence the development of osteosarcoma by regulating PCD in osteosarcoma cell. Therefore, targeting PCD and the associated signaling pathways could offer a promising therapeutic approach for treating osteosarcoma.

Applications of tandem mass spectrometry (MS/MS) in antimicrobial peptides field: Current state and new applications.

Antimicrobial peptides (AMPs) constitute a group of small molecular peptides that exhibit a wide range of antimicrobial activity. These peptides are abundantly present in the innate immune system of various organisms. Given the rise of multidrug-resistant bacteria, microbiological studies have identified AMPs as potential natural antibiotics. In the context of antimicrobial resistance across various human pathogens, AMPs hold considerable promise for clinical applications. However, numerous challenges exist in the detection of AMPs, particularly by immunological and molecular biological methods, especially when studying of newly discovered AMPs in proteomics. This review outlines the current status of AMPs research and the strategies employed in their development, considering resent discoveries and methodologies. Subsequently, we focus on the advanced techniques of mass spectrometry for the quantification of AMPs in diverse samples, and analyzes their application, advantages, and limitations. Additionally, we propose suggestions for the future development of tandem mass spectrometry for the detection of AMPs.