A Bayesian network for estimating hypertension risk due to occupational aluminum exposure.

Background: The correlation between metals and hypertension, such as sodium, zinc, potassium, and magnesium, has been confirmed, while the relationship between aluminum and hypertension is not very clear. This study aimed to evaluate the correlation between plasma aluminum and hypertension in electrolytic aluminum workers by the Bayesian networks (BN). Methods: In 2019, 476 male workers in an aluminum factory were investigated. The plasma aluminum concentration of workers was measured by inductively coupled plasma mass spectrometry. The influencing factors on the prevalence of hypertension were analyzed by the BN. Results: The prevalence of hypertension was 23.9% in 476 male workers. The risk of hypertension from plasma aluminum in the Q2, Q3, and Q4 groups was 5.20 (1.90-14.25), 6.92 (2.51-19.08), and 7.33 (2.69-20.01), respectively, compared with that in the Q1 group. The risk of hypertension from the duration of exposure to aluminum of >10 years was 2.23 (1.09-4.57), compared without aluminum exposure. Area under the curve was 0.80 of plasma aluminum and the duration of exposure to aluminum was based on covariates, indicating that aluminum exposure had important predictive value in the prevalence of hypertension in the occupational population. The results of the study using the BN model showed that if the plasma aluminum of all participants was higher than Q4 (≥47.86 µg/L) and the participants were drinking, smoking, diabetes, central obesity, dyslipidemia, and aged >50 years, the proportion of hypertension was 71.2%. Conclusions: The prevalence of hypertension increased significantly with the increase of plasma aluminum level.

TFEB/LAMP2 contributes to PM0.2-induced autophagy-lysosome dysfunction and alpha-synuclein dysregulation in astrocytes.

Atmospheric particulate matter (PM) exacerbates the risk factor for Alzheimer's and Parkinson's diseases (PD) by promoting the alpha-synuclein (α-syn) pathology in the brain. However, the molecular mechanisms of astrocytes involvement in α-syn pathology underlying the process remain unclear. This study investigated PM with particle size <200 nm (PM0.2) exposure-induced α-syn pathology in ICR mice and primary astrocytes, then assessed the effects of mammalian target of rapamycin inhibitor (PP242) in vitro studies. We observed the α-syn pathology in the brains of exposed mice. Meanwhile, PM0.2-exposed mice also exhibited the activation of glial cell and the inhibition of autophagy. In vitro study, PM0.2 (3, 10 and 30 µg/mL) induced inflammatory response and the disorders of α-syn degradation in primary astrocytes, and lysosomal-associated membrane protein 2 (LAMP2)-mediated autophagy underlies α-syn pathology. The abnormal function of autophagy-lysosome was specifically manifested as the expression of microtubule-associated protein light chain 3 (LC3II), cathepsin B (CTSB) and lysosomal abundance increased first and then decreased, which might both be a compensatory mechanism to toxic α-syn accumulation induced by PM0.2. Moreover, with the transcription factor EB (TFEB) subcellular localization and the increase in LC3II, LAMP2, CTSB, and cathepsin D proteins were identified, leading to the restoration of the degradation of α-syn after the intervention of PP242. Our results identified that PM0.2 exposure could promote the α-syn pathological dysregulation in astrocytes, providing mechanistic insights into how PM0.2 increases the risk of developing PD and highlighting TFEB/LAMP2 as a promising therapeutic target for antagonizing PM0.2 toxicity.

Effects of perineal massage at different stages on perineal and postpartum pelvic floor function in primiparous women: a systematic review and meta-analysis.

BACKGROUND: Perineal massage, as a preventive intervention, has been shown to reduce the risk of perineal injuries and may have a positive impact on pelvic floor function in the early postpartum period. However, there is still debate concerning the best period to apply perineal massage, which is either antenatal or in the second stage of labor, as well as its safety and effectiveness. Meta-analysis was used to evaluate the effect of implementing perineal massage in antenatal versus the second stage of labor on the prevention of perineal injuries during labor and early postpartum pelvic floor function in primiparous women. METHODS: We searched nine different electronic databases from inception to April 16, 2024. The randomized controlled trials (RCTs) we included assessed the effects of antenatal and second-stage labor perineal massage in primiparous women. All data were analyzed with Revman 5.3, Stata Statistical Software, and Risk of Bias 2 was used to assess the risk of bias. Subgroup analyses were performed based on the different periods of perineal massage. The primary outcomes were the incidence of perineal integrity and perineal injury. Secondary outcomes were perineal pain, duration of the second stage of labor, postpartum hemorrhage, urinary incontinence, fecal incontinence, and flatus incontinence. RESULTS: This review comprised a total of 10 studies that covered 1057 primigravid women. The results of the analysis showed that perineal massage during the second stage of labor reduced the perineal pain of primigravid women in the immediate postpartum period compared to the antenatal period, with a statistical value of (MD = -2.29, 95% CI [-2.53, -2.05], P < 0.001). Additionally, only the antenatal stage reported that perineal massage reduced fecal incontinence (P = 0.04) and flatus incontinence (P = 0.01) in primiparous women at three months postpartum, but had no significant effect on urinary incontinence in primiparous women at three months postpartum (P = 0.80). CONCLUSIONS: Reducing perineal injuries in primiparous women can be achieved by providing perineal massage both antenatally and during the second stage of labor. Pelvic floor function is improved in the postnatal phase by perineal massage during the antenatal stage. TRIAL REGISTRATION: CRD42023415996 (PROSPERO).

Poricoic acid A promotes angiogenesis and myocardial regeneration by inducing autophagy in myocardial infarction.

Myocardial infarction (MI) is a kind of cardiovascular diseases with high morbidity and mortality. Poricoic acid A (PAA) is the main active substance in Poria cocos, which has been discovered to exhibit an ameliorative role in the progression of many diseases. However, no report has been focused on the regulatory effects of PAA on MI progression. In this study, at first, oxygen glucose deprivation (OGD) treatment was performed in human cardiac microvascular endothelial cells (HCMECs) to mimic MI cell model. Our findings demonstrated that cell proliferation was reduced post OGD treatment, but which was reversed by PAA treatment. Moreover, PAA suppressed cell apoptosis in OGD-triggered HCMEC cells. Next, it revealed that PAA induced autophagy in OGD-treated HCMEC cells through enhancing LC3-II/LC3-I level and reducing P62 level. In addition, PAA strengthened the angiogenesis ability and migration ability in OGD-induced HCMEC cells. Lastly, it was uncovered that PAA modulated the AMPK/mTOR signaling pathway through affecting the p-mTOR/mTOR and p-AMPK/AMPK levels. In conclusion, PAA can promote angiogenesis and myocardial regeneration after MI by inducing autophagy through modulating the AMPK/mTOR pathway. This work suggested that PAA may be a potential and useful drug for MI treatment.

Reversible acute heart failure induced by thyrotoxic cardiomyopathy: A case report.

RATIONALE: Thyrotoxic cardiomyopathy is a rare but severe complication of thyrotoxicosis, leading to episodes of acute heart failure. This case report highlights a rare presentation of thyrotoxic cardiomyopathy with low-output heart failure, emphasizing the importance of early diagnosis and comprehensive management. The report aims to increase awareness among clinicians about the potential reversibility of this condition and the effective strategies for managing such complex cases. PATIENT CONCERNS: This patient presented with dyspnea and chest constriction, without any antecedent predisposing factors. Subsequently, the patient abruptly manifested symptoms indicative of acute heart failure during outpatient consultation. Electrocardiography revealed rapid atrial fibrillation with type A preexcitation syndrome, whereas cardiac ultrasonography demonstrated global cardiac enlargement with a diminished ejection fraction (EF). DIAGNOSES: After a comprehensive evaluation, the patient was diagnosed with thyrotoxic cardiomyopathy, acute heart failure, and atrial fibrillation with preexcitation syndrome. INTERVENTIONS: Immediate interventions comprised diuretic administration, oxygen therapy, and antiarrhythmic agents, addressing acute heart failure concomitant with preexcitation syndrome. Following a fortnight of comprehensive therapeutic measures, the patient was discharged with a prescription for oral medications, notably methimazole. OUTCOMES: Following the intervention, the patient showed significant improvement with the resolution of heart failure symptoms and dyspnea, restoration of sinus rhythm, improved left ventricular ejection fraction (LVEF improved from 36% to 45%), and normalization of thyroid function. These outcomes underscore the efficacy of the intervention strategy and offer a hopeful prognosis for similar cases. LESSONS: Thyrotoxicosis may cause cardiomyopathy in patients with heart failure that manifests as dilated cardiac chambers. Clinicians should carefully screen patients for this reversible condition. Diagnosis requires a comprehensive assessment of various tests, and the therapeutic goal is to restore normal thyroid function.

[Tetramethylpyrazine regulates angiogenesis of endothelial cells in cerebral ischemic stroke injury via SIRT1/VEGFA signaling pathway].

This study aims to investigate whether tetramethylpyrazine(TMP) can stimulate angiogenesis in cerebral microvascular endothelial cells and alleviate cerebral ischemic stroke(CIS) and to explore the underlying mechanisms. In the animal study, adult Sprague-Dawley rats(n=15) were assigned into sham surgery(sham), middle cerebral artery occlusion/reperfusion(MCAO/R), and MCAO/R+TMP(intraperitoneal injection of 20 mg·kg~(-1)) groups. The neurological function was evaluated by the Z-Longa method. The cerebral infarction volume was detected by TTC staining. Enzyme-linked immunosorbent assay(ELISA) was employed to detect the expression of vascular endothelial growth factor(VEGF), angiopoietin(Ang), and platelet-derived growth factor(PDGF). Immunofluorescence staining was employed to detect Ki67 and the expression of vascular endothelial growth factor A(VEGFA) and slient information regulator 1(SIRT1). Western blot was employed to determine the expression levels of VEGFA, SIRT1, angiopoietin-2(Ang-2), and platelet-derived growth factor B(PDGFB). In the cell study, mouse brain-derived endothelial cells(Bend.3) were cultured, and the optimal concentration of TMP was determined. Then, VEGF, Ang, and PDGF were detected by ELISA after the addition of cabozantinib. Western blot was employed to measure the expression of VEGFA, Ang-2, and PDGFB. Immunofluorescence staining was used to detect CD31, CD34, and Ki67, and the proliferation, migration, and tube formation ability of Bend.3 cells were observed in vitro. Western blot and immunofluorescence staining were performed to measure the expression of SIRT1 and VEGFA after addition of the SIRT1-specific inhibitor selisistat(EX-527). The results showed that compared with the sham group, the MCAO/R group had severe neurological function damage, increased infarction volume, up-regulated expression of VEGF, VEGFA, Ang, Ang-2, PDGF, and PDGFB, and down-regulated expression of Ki67 and SIRT1(P<0.01). Compared with the MCAO/R group, the MCAO/R+TMP group presented alleviated neurological function damage, reduced infarction volume, and activated expression of VEGF, VEGFA, Ang, Ang-2, PDGF, PDGFB, Ki67, and SIRT1(P<0.01). The cell experiments showed that compared with the normal group, Bend.3 cells were activated by oxygen glucose deprivation/reoxygenation(OGD/R) treatment(P<0.05, P<0.01). Compared with the OGD/R group, the OGD/R+TMP group upregulated the expression levels of VEGF, VEGFA, Ang, Ang-2, PDGF, PDGFB, SIRT1, Ki67, CD31, and CD34, enhanced the angiogenic ability of Bend.3 cells without being inhibited by BMS or EX-527(P<0.05, P<0.01, P<0.001). The results suggest that TMP can activate the SIRT1/VEGFA signaling pathway to stimulate angiogenesis and alleviate CIS injury.

Passive smoking and risk of gestational diabetes mellitus: A systematic review and meta-analysis.

INTRODUCTION: Pregestational smoking increases the risk of gestational diabetes mellitus (GDM) and is a common health problem during pregnancy, with its incidence on the rise worldwide, especially in China. This study is a meta-analysis of passive smoking as a risk factor associated with GDM. METHODS: Two independent reviewers searched passive smoking and the risk of GDM in PubMed, Medline, Web of Knowledge, Science Direct, China National Knowledge Internet (CNKI) and Wanfang databases (up to May 2023). The authors extracted the study data independently and used the Newcastle-Ottawa scale (NOS) to evaluate the quality of the included articles. A meta-analysis was conducted using a random effects model depending on the size of the heterogeneity. Begg's and Egger's tests were performed to assess publication bias. RESULTS: The overall relative risk for GDM caused by passive smoking was 1.47 (95% CI: 1.31-1.64), with moderate heterogeneity between studies (I2=41.7%, p=0.079). Subgroup and sensitivity analyses were stable, and no evidence of publication bias was found. CONCLUSIONS: Passive smoking is a risk factor for GDM, even in those who are not active smokers. To eliminate the effects of other confounding factors, larger prospective cohort studies are required to clarify the relationship between passive smoking and the occurrence of GDM.

Non-coding RNAs are key players and promising therapeutic targets in atherosclerosis.

Cardiovascular disease (CVD) is the primary cause of death in humans. Atherosclerosis (AS) is the most common CVD and a major cause of many CVD-related fatalities. AS has numerous risk factors and complex pathogenesis, and while it has long been a research focus, most mechanisms underlying its progression remain unknown. Noncoding RNAs (ncRNAs) represent an important focus in epigenetics studies and are critical biological regulators that form a complex network of gene regulation. Abnormal ncRNA expression disrupts the normal function of tissues or cells, leading to disease development. A large body of evidence suggests that ncRNAs are involved in all stages of atherosclerosis, from initiation to progression, and that some are significantly differentially expressed during AS development, suggesting that they may be powerful markers for screening AS or potential treatment targets. Here, we review the role of ncRNAs in AS development and recent developments in the use of ncRNAs for AS-targeted therapy, providing evidence for ncRNAs as diagnostic markers and therapeutic targets.

Hydroxyfasudil regulates immune balance and suppresses inflammatory responses in the treatment of experimental autoimmune encephalomyelitis.

Multiple sclerosis (MS) is a central nervous system (CNS) disease with complicated etiology. Multifocal demyelination and invasion of inflammatory cells are its primary pathological features. Fasudil has been confirmed to improve experimental autoimmune encephalomyelitis (EAE), an animal model of MS. However, Fasudil is accompanied by several shortcomings in the clinical practice. Hydroxyfasudil is a metabolite of Fasudil in the body with better pharmaceutical properties. Therefore, we attempted to study the influence of Hydroxyfasudil upon EAE mice. The results demonstrated that Hydroxyfasudil relieved the symptoms of EAE and the associated pathological damage, reduced the adhesion molecules and chemokines, decreased the invasion of peripheral immune cells. Simultaneously, Hydroxyfasudil modified the rebalance of peripheral T cells. Moreover, Hydroxyfasudil shifted the M1 phenotype to M2 polarization, inhibited inflammatory signaling cascades as well as inflammatory factors, and promoted anti-inflammatory factors in the CNS. In the end, mice in the Hydroxyfasudil group expressed more tight junction proteins, indirectly indicating that the blood-brain barrier (BBB) was protected. Our results indicate that Hydroxyfasudil may be a prospective treatment for MS.

Association of urinary metal levels with metabolic syndrome in coal workers.

Studies have indicated that metal exposure is associated with an increased risk of metabolic syndrome (MetS). However, it is unclear whether overexposure to heavy metals occurs in miners and is associated with MetS risk remains unclear. In a cross-sectional study, analysis for metal exposure levels of 3428 participants from three types of workplaces was conducted. Relationships between metals in urine and MetS were characterized using a multivariate binary logistic regression model and restricted cubic spline analysis. The association between urinary metals and workplaces with respect to MetS was studied via mediation analysis and multiplicative interaction analysis. And a sensitivity analysis was performed to assess the robustness of the association between MetS and urinary metals in participants without obesity (n = 2811). Zn, Cu, Fe, Co, and Ni were found to be associated with MetS in the single-metal models, whereas only Zn and Cu showed considerable associations in the multimetal model. The odds ratios (95% CI) for MetS in the highest quartiles were 2.089 (1.611, 2.707) for urinary Zn and 1.394 (1.084, 1.794) for urinary Cu (both false discovery rate for both was < 0.05). Urinary Zn and Cu were positively associated with hypertriglyceridemia. In addition, higher Zn exposure was confirmed in underground workers than ground workers and office workers, and there was a significant association between urinary metal exposure and workplace, which together influenced the occurrence of MetS. These results provided scientific evidence for the relationship between Zn, Cu, workplaces, and MetS in coal workers and indicated that it is critical to reduce occupational metal exposure, especially in underground workers.

Quercetin relieves coronary atherosclerosis via regulating fibroblast growth factor 2.

This study aims to investigate the role of quercetin in coronary atherosclerosis and explore its possible mechanisms. Hematoxylin-eosin (H&E), immunohistochemical (IHC), and aniline blue staining were used to analyze the pathological changes in the cross-section of the aorta. Traditional Chinese Medicine Systems Pharmacology Database (TCMSP), Swiss Target Prediction, and PubChem were utilized to predict and screen the bioactive ingredients of traditional Chinese medicine (Huanglian, Yuxingcao, and Jinyinhua) for coronary atherosclerosis. Inflammatory factors and vascular protection parameters were quantitatively detected using ELISA and western blot. The proliferation and migration of vascular smooth muscle cells (VSMC) were evaluated using the Cell Counting Kit-8 (CCK-8), 5-ethynyl-2-deoxyuridine (EdU), and wound healing assays. The targets of quercetin were predicted using DisGeNET, Matascape, SWISSMODEL, cellular thermal shift assay (CETSA), and fluorescence titrimetric methods. Based on our findings, quercetin was identified as the active component of Huanglian, Yuxingcao, and Jinyinhua that exerted a positive effect on coronary atherosclerosis. In vivo and in vitro data demonstrated that quercetin improved the pathological changes in model mice and inhibited the proliferation, migration, and inflammatory response of VSMC cells. Specifically, we found that fibroblast growth factor 2 (FGF2) is a direct target of quercetin, and overexpression of FGF2 attenuated the anti-atherosclerosis function of quercetin. Overall, our study confirms the functional role of the quercetin-FGF2 axis in the progression of coronary atherosclerosis, providing a potential target for its treatment.

Hypermethylation of the Promoter of miR-338-5p Mediates Aberrant Expression of ETS-1 and Is Correlated With Disease Severity Of Astrocytoma Patients.

The pro-oncogene ETS-1 (E26 transformation-specific sequence 1) is a key regulator of the proliferation and invasion of cancer cells. The present work examined the correlation of the aberrant expression of ETS-1 with histological or clinical classification of astrocytoma: grade I (pilocytic astrocytoma), grade II (diffuse astrocytoma), grade III (anaplastic astrocytoma), and grade IV (glioblastoma multiforme). MicroRNA, miR-338-5p, was predicted by an online tool (miRDB) to potentially target the 3' untranslated region of ETS-1; this was confirmed by multi-assays, including western blot experiments or the point mutation of the targeting sites of miR-338-5p in ETS-1's 3'untralation region (3'UTR). The expression of miR-338-5p was negatively associated with that of ETS-1 in astrocytoma, and deficiency of miR-338-5p would mediate aberrant expression of ETS-1 in astrocytoma. Mechanistically, hypermethylation of miR-338-5p by DNA methyltransferase 1 (DNMT1) resulted in repression of miR-338-5p expression and the aberrant expression of ETS-1. Knockdown or deactivation of DNMT1 decreased the methylation rate of the miR-338-5p promoter, increased the expression of miR-338-5p, and repressed the expression of ETS-1 in astrocytoma cell lines U251 and U87. These results indicate that hypermethylation of the miR-338-5p promoter by DNMT1 mediates the aberrant expression of ETS-1 related to disease severity of patients with astrocytoma.

Wood dust exposure and risks of nasopharyngeal carcinoma: a meta-analysis.

BACKGROUND: Wood dust has been confirmed as one kind of human carcinogen. However, there are inconsistent study results of exploring the relationship of exposure to wood dust and occurrence of nasopharyngeal cancer (NPC). For a greater clarification, the authors systemically reviewed the relevant published articles on the relationship of exposure to wood dust and occurrence of NPC. And meta-analysis was conducted. METHODS: The databases of PubMed, U.S. National Library of Medicine (MEDLINE), Embase and Science Direct were searched for the relevant publications. And Newcastle-Ottawa scale was employed for judging the quality of articles. Random-effect model was utilized for meta-analysis. RESULTS: Among a total of 583 retrieved items, 10 case-control studies and 1 cohort study were selected. The ratio of maximal/minimal exposure concentration of wood dust yielded a pooled odd ratio (OR) of 2.18 (95% CI = 1.62-2.93, P = 0.063) with a moderate heterogeneity (I2: 43.0%; P = 0.001). And subgroup analysis was performed for such factors as exposure status, exposure population and geographic region. No publishing bias was noted. Exposing to a high concentration of wood dust was positively proportional to occurring risk of NPC. CONCLUSION: It hints at the contributing effect of wood dust upon NPC. For eliminating the effects of other confounding factors, larger prospective cohort studies are required for further elucidating the relationship of exposure to wood dust and occurrence of NPC.

[Role of ubiquitin ligase Ring2 in DNA damage induced by benzo[a]pyrene].

OBJECTIVE: To investigate the role of ubiquitin ligase Ring2 in the DNA damage induced by benzo[a]pyrene (B[a]P). METHODS: The expression of Ring2 in human bronchial epithelial (16HBE) cells was inhibited by small interfering RNA (siRNA) to obtain siRNA-Ring2 16HBE cells. The siRNA-Ring2 16HBE cells, as well as normal 16HBE cells, were exposed to B[a]P (0, 1, 2, 4, 8, 16, and 32 µmol/L) for 24 h; other siRNA-Ring2 16HBE cells and normal 16HBE cells were exposed to B [a]P (16 µmol/L) for 0, 1, 2, 4, 8, 12, and 24 h. The levels of DNA damage were evaluated by alkaline single cell gel electrophoresis assay. RESULTS: After being treated with siRNA for 36 h, the siRNA-Ring2 16HBE cells showed a 72% decrease in Ring2 expression compared with normal 16HBE cells. The analysis of covariance showed that whether to be treated with siRNA and concentration of B[a]P had impacts on Olive tail moment (OTM) (P = 0.032 and P < 0.001); the adjusted mean of OTM was significantly higher in siRNA-Ring2 16HBE cells than in normal 16HBE cells. Whether to be treated with siRNA and B[a]P exposure time had impacts on OTM (P = 0.031 and P < 0.001); the adjusted mean of OTM was significantly higher in siRNA-Ring2 16HBE cells than in normal 16HBE cells. CONCLUSION: The DNA of 16HBE cells with decreased Ring2 expression has increased susceptibility to B[a]P, which may be due to reduced H2A monoubiquitination following decrease in Ring2 expression.

Role of ubiquitin protein ligase Ring2 in DNA damage of human bronchial epithelial cells exposed to benzo[a]pyrene.

Ubiquitylation of histones plays a pivotal role in DNA repair. The ubiquitin ligase Ring2 was recently shown to be the dominant ubiquitin ligase of histone H2A. In a series of experiments using the human bronchial epithelia cells (16HBE) and small interfering RNA (siRNA)-Ring2 cells exposed to benzo(a)pyrene (BaP), we measured dynamic changes in the levels of DNA damage, expressions of ubiquitinated histone H2A, and nucleotide excision repair (NER) subunit xeroderma pigmentosum (XP) groups A, C, and F (XPA, XPC, XPF). We found that in vitro exposure to BaP increased DNA damage in a time- and dose-dependent manner in 16HBE and siRNA-Ring2 cells. The results show that although decrease of Ring2 causes DNA hypersensitivity to BaP, the levels of XPA, XPC, and XPF were not affected. These results indicated that Ring2 may effect the DNA repair through other pathways but not through the expressions of NER protein.

[Clinical significance of protein Z alteration in patients with cardio-cerebral thrombotic diseases].

OBJECTIVE: To study the alteration of protein Z (PZ) in patients with cardio-cerebral thrombotic diseases, its clinical significance and relations with FX. METHODS: PZ and FX:Ag were measured by ELISA, and plasma FX:C by first stage method. In 170 patients with acute ischemic stroke (AIS), 40 acute myocardial infarction (AMI) and 60 healthy adults as contrast, PZ, FX:C and FX:Ag were measured and compared between incipience and recurrence, different ages and genders. RESULTS: In AIS and AMI groups, PZ levels decreased significantly to (940.02 +/- 229.82) microg/L and (1071.44 +/- 180.52) microg/L, respectively \[the contrast group was (2257.97 +/- 479.76) microg/L, P < 0.001\]. But FX:C and FX:Ag raised to (136.73 +/- 34.93)% and (135.54 +/- 54.39)% in AIS group; and to (139.53 +/- 29.18)%, (129.75 +/- 21.91)% in AMI group, respectively, while in the contrast group they were (94.33 +/- 22.00)% and (77.22 +/- 13.19)% (P < 0.001). In the comparative research between the AIS group, AMI group and the contrast group, PZ level was clearly found to negatively relate to the level of FX:C and FX:Ag (P < 0.001). Meanwhile, PZ level, FX:C and FX:Ag in recur-AIS group and recur-AMI group exhibited significant differences (P < 0.05) from those in the primary AIS and AMI groups, suggesting that the decrease of PZ levels reflected the pathological process of the disease. In addition, PZ level gradually decreased with the increase of age (P < 0.05), while FX:C and FX:Ag had no relations with age (P > 0.05). No correlation was found in sex with PZ level, FX:C, FX:Ag (P > 0.05). CONCLUSION: PZ level was significantly decreased in AIS and AMI patients and was negatively related to FX:C and FX:Ag. The mechanism leading to FX increase may partially related with the decreased of PZ. PZ level was different in the primary and recurrent disease and was gradually decreased with the increase of age. Lack of PZ might be a etiological factor of cardio-cerebral thrombotic diseases.