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O6-methylguanine DNA methyltransferase (MGMT) is a crucial determinant of temozolomide (TMZ) sensitivity in patients with glioblastoma (GBM). The therapeutic potential of small interfering RNA (siRNA) targeting MGMT to enhance TMZ sensitivity has been hampered by serum nuclease degradation, off-target effects, poor accumulation at tumor sites, and low circulation in blood stream. In this study, we developed a framework nucleic acid-based nanoparticles (FNN), which is constructed from a six-helix DNA bundle, to encapsulate and protect siMGMT for improving TMZ sensitivity in GBM treatment. For better blood-brain barrier (BBB) penetration and GBM targeting, we conjugated Angiopep-2 (ANG) targeting modules to each end of the FNN. Nucleolin (NCL)-responsive locks were engineered along the sides of the six-helix DNA bundle, which safeguard siMGMT before tumor entry. Upon interaction with tumor-overexpressed NCL, these locks unlock, exposing siMGMT, this allows for effective suppression of MGMT, resulting in a significant improvement of TMZ therapeutic efficacy in GBM. This innovative strategy has the potential to transform the current treatment landscape for GBM.
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Antineoplásicos Alquilantes , Barrera Hematoencefálica , Neoplasias Encefálicas , Glioblastoma , Nanopartículas , Temozolomida , Glioblastoma/tratamiento farmacológico , Glioblastoma/patología , Temozolomida/farmacología , Temozolomida/administración & dosificación , Temozolomida/uso terapéutico , Humanos , Neoplasias Encefálicas/tratamiento farmacológico , Neoplasias Encefálicas/patología , Neoplasias Encefálicas/genética , Antineoplásicos Alquilantes/farmacología , Antineoplásicos Alquilantes/uso terapéutico , Nanopartículas/química , Animales , Barrera Hematoencefálica/metabolismo , Barrera Hematoencefálica/efectos de los fármacos , Resistencia a Antineoplásicos/efectos de los fármacos , Línea Celular Tumoral , Proteínas de Unión al ARN/metabolismo , Enzimas Reparadoras del ADN/metabolismo , Enzimas Reparadoras del ADN/genética , Metilasas de Modificación del ADN/metabolismo , Nucleolina , Fosfoproteínas/metabolismo , Proteínas Supresoras de Tumor/metabolismo , Proteínas Supresoras de Tumor/genética , ARN Interferente Pequeño/administración & dosificación , Ácidos Nucleicos , PéptidosRESUMEN
Background: Remimazolam is a novel ultra-short-acting benzodiazepine sedative that has the potential to be an alternative for procedural sedation due to its rapid sedation and recovery, no accumulation effect, stable hemodynamics, minimal respiratory depression, anterograde amnesia effect, and specific antagonist. Here, we aimed to compare the safety and efficacy of remimazolam with dexmedetomidine for awake tracheal intubation by flexible bronchoscopy (ATI-FB). Methods: Ninety patients scheduled for ATI-FB were randomly divided into three groups, each consisting of 30 cases: dexmedetomidine 0.6 µg/kg + sufentanil (group DS), remimazolam 0.073 mg/kg + sufentanil (group R1S), or remimazolam 0.093 mg/kg + sufentanil (group R2S). The primary outcome was the success rate of sedation. Secondary outcomes were MOAA/S scores, hemodynamic and respiratory parameters, intubation conditions, intubation time, tracheal intubation amnesia, and adverse events. Results: The success rates of sedation in groups R2S and DS were higher than that in group R1S (93.3%, 86.7%, respectively, vs 58.6%; P = 0.002), and intubation conditions were better than those in group R1S (P < 0.05). Group R2S had shorter intubation times than groups R1S and DS (P = 0.003), and a higher incidence of tracheal intubation amnesia than group DS (P = 0.006). No patient in the three groups developed hypoxemia or hypotension, and there were no significant differences in oligopnea, PetCO2, or bradycardia (P > 0.05). Conclusion: In conclusion, both DS and R2S had higher success rates of sedation, better intubation conditions, and minor respiratory depression, but R2S, with its shorter intubation time, higher incidence of anterograde amnesia, and ability to be antagonized by specific antagonists, may be a good alternative sedation regimen for patients undergoing ATI-FB.
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Amnesia Anterógrada , Dexmedetomidina , Insuficiencia Respiratoria , Humanos , Amnesia/inducido químicamente , Amnesia Anterógrada/inducido químicamente , Benzodiazepinas , Broncoscopía/efectos adversos , Dexmedetomidina/efectos adversos , Hipnóticos y Sedantes/efectos adversos , Intubación Intratraqueal/efectos adversos , Insuficiencia Respiratoria/inducido químicamente , Sufentanilo , Vigilia , Método Doble CiegoRESUMEN
Moyamoya disease (MMD) is a rare condition that affects the blood vessels of the central nervous system. This cerebrovascular disease is characterized by progressive narrowing and blockage of the internal carotid, middle cerebral, and anterior cerebral arteries, which results in the formation of a compensatory fragile vascular network. Currently, digital subtraction angiography (DSA) is considered the gold standard in diagnosing MMD. However, this diagnostic technique is invasive and may not be suitable for all patients. Hence, non-invasive imaging methods such as computed tomography angiography (CTA) and magnetic resonance angiography (MRA) are often used. However, these methods may have less reliable diagnostic results. Therefore, High-Resolution Magnetic Resonance Vessel Wall Imaging (HR-VWI) has emerged as the most accurate method for observing and analyzing arterial wall structure. It enhances the resolution of arterial walls and enables quantitative and qualitative analysis of plaque, facilitating the identification of atherosclerotic lesions, vascular entrapment, myofibrillar dysplasia, moyamoya vasculopathy, and other related conditions. Consequently, HR-VWI provides a new and more reliable evaluation criterion for diagnosing vascular lesions in patients with Moyamoya disease.
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Temozolomide (TMZ) resistance remains the major obstacle in the treatment of glioblastoma (GBM). Lactylation is a novel post-translational modification that is involved in various tumors. However, whether lactylation plays a role in GBM TMZ resistance remains unclear. Here it is found that histone H3K9 lactylation (H3K9la) confers TMZ resistance in GBM via LUC7L2-mediated intron 7 retention of MLH1. Mechanistically, lactylation is upregulated in recurrent GBM tissues and TMZ-resistant cells, and is mainly concentrated in histone H3K9. Combined multi-omics analysis, including CUT&Tag, SLAM-seq, and RNA-seq, reveals that H3K9 lactylation is significantly enriched in the LUC7L2 promoter and activates LUC7L2 transcription to promote its expression. LUC7L2 mediates intron 7 retention of MLH1 to reduce MLH1 expression, and thereby inhibit mismatch repair (MMR), ultimately leading to GBM TMZ resistance. Of note, it is identified that a clinical anti-epileptic drug, stiripentol, which can cross the blood-brain barrier and inhibit lactate dehydrogenase A/B (LDHA/B) activity, acts as a lactylation inhibitor and renders GBM cells more sensitive to TMZ in vitro and in vivo. These findings not only shed light on the mechanism of lactylation in GBM TMZ resistance but also provide a potential combined therapeutic strategy for clinical GBM treatment.
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Resistencia a Antineoplásicos , Glioblastoma , Histonas , Intrones , Homólogo 1 de la Proteína MutL , Temozolomida , Animales , Humanos , Ratones , Antineoplásicos Alquilantes/farmacología , Antineoplásicos Alquilantes/uso terapéutico , Neoplasias Encefálicas/genética , Neoplasias Encefálicas/tratamiento farmacológico , Neoplasias Encefálicas/metabolismo , Línea Celular Tumoral , Modelos Animales de Enfermedad , Resistencia a Antineoplásicos/genética , Resistencia a Antineoplásicos/efectos de los fármacos , Glioblastoma/genética , Glioblastoma/tratamiento farmacológico , Glioblastoma/metabolismo , Histonas/metabolismo , Histonas/genética , Intrones/genética , Ratones Desnudos , Homólogo 1 de la Proteína MutL/genética , Homólogo 1 de la Proteína MutL/metabolismo , Temozolomida/farmacología , FemeninoRESUMEN
Mitochondria are dynamic organelles responsible for cellular energy production. In addition to regulating energy homeostasis, mitochondria are responsible for calcium homeostasis, clearance of damaged organelles, signaling, and cell survival in the context of injury and pathology. In stroke, the mechanisms underlying brain injury secondary to intracerebral hemorrhage are complex and involve cellular hypoxia, oxidative stress, inflammatory responses, and apoptosis. Recent studies have shown that mitochondrial damage and autophagy are essential for neuronal metabolism and functional recovery after intracerebral hemorrhage, and are closely related to inflammatory responses, oxidative stress, apoptosis, and other pathological processes. Because hypoxia and inflammatory responses can cause secondary damage after intracerebral hemorrhage, the restoration of mitochondrial function and timely clearance of damaged mitochondria have neuroprotective effects. Based on studies on mitochondrial autophagy (mitophagy), cellular inflammation, apoptosis, ferroptosis, the BNIP3 autophagy gene, pharmacological and other regulatory approaches, and normobaric oxygen (NBO) therapy, this article further explores the neuroprotective role of mitophagy after intracerebral hemorrhage.
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Objective: The role of MMP-2 in patients with ICH is controversial and the impact of plasma MMP-2 level on clinical outcome is still unclear. Materials and methods: In this study, the peripheral venous blood was acquired from 93 patients with ICH and 88 healthy controls within 24 h of hospitalization and at enrollment. We retrospectively investigated plasma MMP-2 levels of patients and healthy controls. The edema volume, the NIHSS score, the GCS score, and mRS were used to assess and quantify neurological deficit following ICH. Logistic regression analysis was configured to determine the independent relation of plasma MMP-2 levels with clinical outcomes. In addition, the plasma MMP-14 levels and complement C4 level were tested to explore the relationship with plasma MMP-2 level. Results: There was a significant reduction of plasma MMP-2 levels in ICH patients than that in healthy controls (38.02 ± 1.71 vs. 54.03 ± 2.15, p < 0.0001), and MMP-2 is negatively correlated with the edema volume (r = -0.2187, p < 0.05), NIHSS score (r = -0.2194, p < 0.05), blood leucocyte count (r = -0.2549, p = 0.012), and complement C4 level (r = -0.2723, p = 0.005). There is positive correlation between MMP-2 level and GCS score (r = 0.2451, p = 0.01) and MMP-14 level (r = 0.7013, p = 0.005). The multivariate analysis revealed that reduced plasma MMP-2 level is associated with elevated edema volume (OR = 0.2604, 95% CI [0.07 to 0.84], p = 0.02). Conclusion: The plasma MMP-2 level in patients with ICH is significantly lower than that of healthy controls, and plasma MMP-2 level may be a prognostic factor. Plasma MMP-2 levels are correlated with the clinical outcomes of patients and negatively correlated with blood leucocyte count and complement C4 level in patients with ICH.
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Vascular dementia (VaD) is the second most prevalent type of dementia after Alzheimer's disease and is caused by impaired nerve cell function resulting from cerebrovascular disease and vascular risk factors. Chronic cerebral hypoperfusion (CCH) is a common pathological and physiological state that may result from cerebral ischemia and hypoxia, causing widespread diffuse lesions in the brain parenchyma which leads to progressive nerve damage. Transferrin (TF) and transferrin receptor 1 (TfR1), two proteins involved in iron uptake, were upregulated by CCH, whereas ferroprotein (FPN), a protein involved in iron efflux, was downregulated. This process may involve various mechanisms including tau and iron regulatory proteins (IRP). CCH can also exacerbate lipid peroxidation caused by an iron imbalance by inhibiting glutathione peroxidase 4 (Gpx4) synthesis and some Gpx4 independent pathways through cystine/glutamate transporters (system Xc-), ultimately leading to ferroptosis in nerve cells and accelerating the progression of VaD.
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Isquemia Encefálica , Demencia Vascular , Ferroptosis , Humanos , Demencia Vascular/metabolismo , Isquemia Encefálica/metabolismo , Encéfalo/metabolismo , Hierro/metabolismoRESUMEN
Chronic cerebral ischemia (CCI), a condition that can result in headaches, dizziness, cognitive decline, and stroke, is caused by a sustained decrease in cerebral blood flow. Statistics show that 70% of patients with CCI are aged > 80 years and approximately 30% are 45-50 years. The incidence of CCI tends to be lower, and treatment for CCI is urgent. Studies have confirmed that CCI can activate the corresponding mechanisms that lead to mitochondrial dysfunction, which, in turn, can induce mitophagy to maintain mitochondrial homeostasis. Simultaneously, mitochondrial dysfunction can aggravate the insufficient energy supply to cells and various diseases caused by CCI. Regulation of mitophagy has become a promising therapeutic target for the treatment of CCI. This article reviews the latest progress in the important role of mitophagy in CCI and discusses the induction pathways of mitophagy in CCI, including ATP synthesis disorder, oxidative stress injury, induction of reactive oxygen species, and Ca2+ homeostasis disorder, as well as the role of drugs in CCI by regulating mitophagy.
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The prognosis of glioblastoma (GBM) patients is poor, and temozolomide (TMZ) resistance has become an important obstacle to its treatment effect. A growing number of researches have revealed the special characteristics of iron metabolism in GBM chemosensitivity. Iron regulatory protein 1 (IRP1) is an important protein for maintaining intracellular iron homeostasis. IRP1 has been indicated to have additional vital roles beyond its conventional metabolic activity, but the underlying mechanisms and biological consequences remain elusive. Here, we unprecedentedly demonstrated that amplifying IRP1 signals can reverse TMZ resistance and suppress tumor growth in vivo via inhibiting NFKB2 in the noncanonical NF-κB signaling pathway. In addition, we identified that NFKB2 affected TMZ sensitivity of GBM by modulating the expression of LCN2 and FPN1. Taken together, this study established a role for the IRP1/NFKB2 pathway in regulating LCN2/FPN1 signaling axis among the progression of TMZ resistance, suggesting a potential innovative GBM therapeutic strategy.
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Objective: The incidence of intraoperative hypothermia remains high in pediatric patients during anesthesia and surgery even though core body temperature monitoring and warming systems have been greatly improved in recent years. We analyzed the risk factors and outcomes of intraoperative hypothermia in neonates and infants undergoing general anesthesia and surgery. Methods: The data on the incidence of intraoperative hypothermia, other clinical characteristics, and outcomes from electronic records of 1,091 patients (501 neonates and 590 infants between 28 days and 1 year old), who received general anesthesia and surgery, were harvested and analyzed. Intraoperative hypothermia was defined as a core temperature below 36°C during surgery. Results: The incidence of intraoperative hypothermia in neonates was 82.83%, which was extremely higher than in infants (38.31%, p < 0.001)-the same as the lowest body temperature (35.05 ± 0.69°C vs. 35.40 ± 0.68°C, p < 0.001) and the hypothermia duration (86.6 ± 44.5â min vs. 75.0 ± 52.4â min, p < 0.001). Intraoperative hypothermia was associated with prolonged PACU, ICU, hospital stay, postoperative bleeding, and transfusion in either age group. Intraoperative hypothermia in infants was also related to prolonged postoperative extubation time and surgical site infection. After univariate and multivariate analyses, the age (OR = 0.902, p < 0.001), weight (OR = 0.480, p = 0.013), prematurity (OR = 2.793, p = 0.036), surgery time of more than 60â min (OR = 3.743, p < 0.001), prewarming (OR = 0.081, p < 0.001), received >20â mL/kg fluid (OR = 2.938, p = 0.004), and emergency surgery (OR = 2.142, p = 0.019) were associated with hypothermia in neonates. Similar to neonates, age (OR = 0.991, p < 0.001), weight (OR = 0.783, p = 0.019), surgery time >60â min (OR = 2.140, p = 0.017), pre-warming (OR = 0.017, p < 0.001), and receive >20â mL/kg fluid (OR = 3.074, p = 0.001) were relevant factors to intraoperative hypothermia in infants along with the ASA grade (OR = 4.135, p < 0.001). Conclusion: The incidence of intraoperative hypothermia was still high, especially in neonates, with a few detrimental complications. Neonates and infants each have their different risk factors associated with intraoperative hypothermia, but younger age, lower weight, longer surgery time, received more fluid, and no prewarming management were the common risk factors.
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Non-traumatic intraparenchymal brain hemorrhage is referred to as intracerebral hemorrhage (ICH). Although ICH is associated with a high rate of disability and case fatality, active intervention can significantly lower the rate of severe disability. Studies have shown that the speed of hematoma clearance after ICH determines the patient's prognosis. Following ICH, depending on the hematoma volume and mass effect, either surgical- or medication-only conservative treatment is chosen. The goal of promoting endogenous hematoma absorption is more relevant because surgery is only appropriate for a small percentage of patients, and open surgery can cause additional trauma to patients. The primary method of removing hematoma after ICH in the future will involve understanding how to produce and manage macrophage/microglial endogenous phagocytic hematomas. Therefore, it is necessary to elucidate the regulatory mechanisms and key targets for clinical purposes.
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The risk factors, outcomes, and typical patterns of intraoperative hypothermia were studied in neonates to better guide the application of insulation measures in the operating room. This retrospective study enrolled 401 neonates undergoing surgery under general anaesthesia with tracheal intubation, including abdominal surgery, thoracic surgery, brain surgery, and others. The study collected basic characteristics, such as age, sex, weight, birth weight, gestational week, primary diagnosis and American Society of Anaesthesiologists (ASA) grade. Perioperative data included preoperative body temperature, length of hospital stay, length of intensive care unit (ICU) stay, intubation time, postoperative bleeding, postoperative pneumonia, postoperative death, and total cost of hospitalization. Intraoperative data included surgical procedures, anaesthesia duration, operation duration, blood transfusion, fluid or albumin infusion, and application of vasoactive drugs. The incidence of intraoperative hypothermia (< 36 °C) was 81.05%. Compared to normothermic patients, gestational week (OR 0.717; 95% CI 0.577-0.890; P = 0.003), preoperative temperature (OR 0.228; 95% CI 0.091-0.571; P = 0.002), duration of anaesthesia (OR 1.052; 95% CI 1.027-1.077; P < 0.001), and type of surgery (OR 2.725; 95% CI 1.292-5.747; P = 0.008) were associated with the risk of intraoperative hypothermia. Patients with hypothermia had longer length of ICU stay (P = 0.001), longer length of hospital stay (P < 0.001), and higher hospital costs (P < 0.001). But there were no association between clinical outcomes and intraoperative hypothermia in the multivariable regression adjusted analysis. The lowest point of intraoperative body temperature was approximately 1 h 30 min. Then, the body temperature of patients successively entered a short plateau phase and a period of slow ascent. The greatest decrease in body temperatures occurred in preterm babies and neonates with preoperative hypothermia. The lowest core temperatures that occurred in neonates with preoperative hypothermia was lower than 35 °C. This study shows that there is a high incidence of intraoperative hypothermia in the neonate population. The intraoperative body temperature of neonates dropped to the lowest point in 1-1.5 h. The greatest decrease in core temperatures occurred in preterm babies and neonates with lower preoperative temperature.
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Hipotermia , Recién Nacido , Humanos , Hipotermia/diagnóstico , Estudios Retrospectivos , Temperatura Corporal , Factores de Riesgo , Anestesia General/efectos adversosRESUMEN
Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive decline, accompanied by amyloid-ß (Aß) overload and hyperphosphorylated tau accumulation in the brain. Synaptic dysfunction, an important pathological hallmark in AD, is recognized as the main cause of the cognitive impairments. Accumulating evidence suggests that synaptic dysfunction could be an early pathological event in AD. Pathological tau, which is detached from axonal microtubules and mislocalized into pre- and postsynaptic neuronal compartments, is suggested to induce synaptic dysfunction in several ways, including reducing mobility and release of presynaptic vesicles, decreasing glutamatergic receptors, impairing the maturation of dendritic spines at postsynaptic terminals, disrupting mitochondrial transport and function in synapses, and promoting the phagocytosis of synapses by microglia. Here, we review the current understanding of how pathological tau mediates synaptic dysfunction and contributes to cognitive decline in AD. We propose that elucidating the mechanism by which pathological tau impairs synaptic function is essential for exploring novel therapeutic strategies for AD.
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Enfermedad de Alzheimer , Enfermedades Neurodegenerativas , Enfermedad de Alzheimer/patología , Péptidos beta-Amiloides , Humanos , Sinapsis/patología , Proteínas tauRESUMEN
Background: Intraoperative hypothermia (core temperature <36.0°C) is common during the perioperative period and can result in adverse consequences, especially in children. We aimed to determine the incidence of intraoperative hypothermia and its risk factors in pediatric patients during burn surgery. Methods: In the present study we enrolled 197 pediatric patients with burn injury undergoing surgical debridement and skin grafting. Factors, such as total burn surface area (TBSA), were collected and analyzed to identify the potential risk factors for intraoperative hypothermia. Results: The incidence of intraoperative hypothermia among all patients was 17.8%. Compared with patients with normothermia, children with hypothermia were associated with larger TBSA (25% vs 15%, p<0.001) and with less intraoperative active warming (34.28% vs 54.93%, p<0.05). In addition, compared with patients with moderate-degree burn, patients with severe and extremely severe burn were associated with much higher risk of intraoperative hypothermia [severe: odds ratio (OR)=3.805, 95% confidence interval (CI)=1.396-10.368, p=0.009; extremely severe: OR=6.933, 95% CI=2.604-18.462, p<0.001]. TBSA was the only independent risk factor that emerged as being strongly associated with intraoperative hypothermia (OR=1.068, p=0.001) and could be used to predict the occurrence of hypothermia when combined with other factors. TBSA for predicting intraoperative hypothermia by receiver operating characteristic (ROC) curve analysis showed a good predictive ability with an area under the ROC curve of 0.758. Conclusion: TBSA is an important risk factor for intraoperative hypothermia in pediatric patients with burn.
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The aim of this study was to investigate the protective effect of sulforaphane (SFN) on 1methyl4phenyl pyridine ion (MPP+)induced cytotoxicity and to investigate its possible mechanisms. METHODS: PC12 cell toxicity induced by MPP+ served as a cell model of Parkinson's diseases. The cell culture + experiments were divided into four groups based on the different treatments, namely, vehicle control, SFN, MPP+ and SFN pretreatment plus MPP+. Cell viability and apoptosis were examined by MTT assay and flow cytometry, respectively. Expressions of nuclear factor erythroid 2related factor 2 (Nrf2), heme oxygenase 1 (HO1) and nicotinamide quinone oxidoreductase 1 (NQO1) were detected using western blotting. RESULTS: MPP+ reduced the survival rate of PC12 cells in a dose and timedependent manner. After 24h treatment with 500 µmol/l MPP+, the survival rate of PC12 cells decreased to 58.2±0.03% of that in the control groups. Under the same conditions MPP+ resulted in significant apoptosis of PC12 cells (apoptosis rate: 30.4±0.6%). However, SFN pretreatment significantly attenuated the cell damage induced by MPP+. Furthermore, it was demonstrated that SFN reversed the reduction of Nrf2, HO1 and NQO1 expression induced by MPP+. CONCLUSION: SFN may protect PC12 cells from MPP+induced damage via activating the Nrf2ARE (antioxidant responsive element) pathway.
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Isotiocianatos/farmacología , Factor 2 Relacionado con NF-E2/metabolismo , Estrés Oxidativo/efectos de los fármacos , Células PC12/efectos de los fármacos , Sustancias Protectoras/farmacología , 1-Metil-4-fenilpiridinio/toxicidad , Animales , Elementos de Respuesta Antioxidante , Antioxidantes/farmacología , Antiparkinsonianos/farmacología , Apoptosis/efectos de los fármacos , Supervivencia Celular/efectos de los fármacos , Hemo-Oxigenasa 1/metabolismo , Isotiocianatos/administración & dosificación , NAD(P)H Deshidrogenasa (Quinona)/metabolismo , Enfermedad de Parkinson/tratamiento farmacológico , Ratas , Especies Reactivas de Oxígeno/metabolismo , Transducción de Señal/efectos de los fármacos , Sulfóxidos , Tasa de Supervivencia , Factores de TiempoRESUMEN
OBJECTIVE: To find out the vector ability and function of Nosopsyllus wualis leizhouensis in the transmitting plague. METHODS: In T: 19 degrees C +/- 1 degrees C, RH: 85% +/- 5%, data regarding the vector ability as cluster spreading, single flea spreading, single flea transmitting plague to single animal, formative bacterial embolus and infection fleas life-span through experiments was gathered. RESULTS: The rate of infection on fleas was 94.64%, with 100% transmission rate of colony to spread, and 30% from single flea spreading to single animal. In the experiment of single flea transmission, all of the 388 rattus loseas were bitten by the fleas with bacterial, but only 9 animals were characteristically infected with the transmission potential, vector efficiency, survival potential of embolus, vector index as 0.360, 0.257, 0.868 and 0.223 respectively. The mean survive days of infected flea feed with blood were 17.58 (1 - 58), and the mean survive days of hunger infected flea were 7.25 (1 - 16). Formative bacterial embolus days were 8.80 (2 - 16) and the rate of embolus flea was 78.12%. CONCLUSION: Nosopsyllus wualis leizhouensis could serve as vector and important in the mode of plague transmittion.