ACE2 activation alleviates sepsis-induced cardiomyopathy by promoting MasR-Sirt1-mediated mitochondrial biogenesis.

Sepsis-induced cardiomyopathy (SIC), caused by a dysregulated host response to infection, is a major contributor to high mortality. Angiotensin-converting enzyme 2 (ACE2), a crucial component of the renin-angiotensin system (RAS), has protective effects against several cardiovascular diseases, such as myocardial infarction and heart failure. However, the role of ACE2 in the pathogenesis of SIC and underlying mechanisms remain unknown. The present study was designed to examine the effects of ACE2 activation or inhibition on SIC in C57BL/6 mice. The ACE2 activator diminazene aceturate (DIZE) and ACE2 inhibitor MLN-4760 were applied for treatment. Myocardial function, inflammatory response, oxidative stress, apoptosis and mitochondrial biogenesis were investigated. Major assays were echocardiography, H&E staining, immunofluorescence staining, DHE staining, TUNEL staining, Western blot, qPCR analysis, ELISA and corresponding kits. We confirmed that ACE2 was markedly downregulated in septic heart tissues. Pharmacological activation of ACE2 by DIZE ameliorated cecal ligation puncture (CLP)-induced mortality, cardiac dysfunction, inflammatory response, oxidative stress and the cardiomyocyte apoptosis by promoting MasR-Sirt1-mediated mitochondrial biogenesis. In contrast, SIC was aggravated via inhibiting MasR-Sirt1-mediated mitochondrial biogenesis by the use of ACE2 inhibitor MLN-4760. Consequently, activation of ACE2 may protect against SIC by promoting MasR-Sirt1-mediated mitochondrial biogenesis.

Action mechanism of the potential biocontrol agent Brevibacillus laterosporus SN19-1 against Xanthomonas oryzae pv. oryzae causing rice bacterial leaf blight.

The causal agent of rice bacterial leaf blight (BLB) is Xanthomonas oryzae pv. oryzae (Xoo), which causes serious damage to rice, leading to yield reduction or even crop failure. Brevibacillus laterosporus SN19-1 is a biocontrol strain obtained by long-term screening in our laboratory, which has a good antagonistic effect on a variety of plant pathogenic bacteria. In this study, we investigated the efficacy and bacterial inhibition of B. laterosporus SN19-1 against BLB to lay the theoretical foundation and research technology for the development of SN19-1 as a biopesticide of BLB. It was found that SN19-1 has the ability to fix nitrogen, detoxify organic phosphorus, and produce cellulase, protease, and siderophores, as well as IAA. In a greenhouse pot experiment, the control efficiency of SN19-1 against BLB was as high as 90.92%. Further investigation of the inhibitory mechanism of SN19-1 on Xoo found that the biofilm formation ability of Xoo was inhibited and the pathogenicity was weakened after the action of SN19-1 sterile supernatant on Xoo. The activities of enzymes related to respiration and the energy metabolism of Xoo were significantly inhibited, while the level of intracellular reactive oxygen species was greatly increased. Scanning electron microscopy observations showed folds on the surface of Xoo. A significant increase in cell membrane permeability and outer membrane permeability and a decrease in cell membrane fluidity resulted in the extravasation of intracellular substances and cell death. The results of this study highlight the role of B. laterosporus SN19-1 against the pathogen of BLB and help elucidate the underlying molecular mechanisms.

Forming a Double-Helix Phase of Single Polymer Chains by the Cooperation between Local Structure and Nonlocal Attraction.

Double-helix structures, such as DNA, are formed in nature to realize many unique functions. Inspired by this, researchers are pursuing strategies to design such structures from polymers. A key question is whether the double helix can be formed from the self-folding of a single polymer chain without specific interactions. Here, using Langevin dynamics simulation and theoretical analysis, we find that a stable double-helix phase can be achieved by the self-folding of single semiflexible polymers as a result of the cooperation between local structure and nonlocal attraction. The critical temperature of double-helix formation approximately follows T^{cri}∼ln(k_{θ}) and T^{cri}∼ln(k_{τ}), where k_{θ} and k_{τ} are the polymer bending and torsion stiffness, respectively. Furthermore, the double helix can exhibit major and minor grooves due to symmetric break for better packing. Our results provide a novel guide to the experimental design of the double helix.

Association of Carotid Plaque and Serum Lipoprotein-Associated Phospholipase A2 (LP-PLA2) with Postoperative Delirium in Geriatric Patients Undergoing Hip Replacement: A Prospective Cohort Study.

BACKGROUND The aim of this study was to investigate the relationships among carotid plaque (CP), serum lipoprotein-associated phospholipase (LP-PLA2), and POD in elderly patients. MATERIAL AND METHODS Sixty-two elderly patients undergoing hip replacement with spinal-epidural anesthesia were divided into CP and non-CP groups based on the preoperative presence or absence of carotid atherosclerotic plaques, as assessed by ultrasound. POD was diagnosed by means of the Confusion Assessment Method (CAM). Blood samples were collected (preoperatively, postoperatively, and postoperative day 2) for the assessment of serum LP-PLA2 by enzyme-linked immunosorbent assay. The CP group was further divided into POD and no-POD subgroups based on the occurrence of POD. RESULTS The incidence of POD was higher in the CP group than in the non-CP group (P0.05), it was higher in the CP group than in the non-CP group postoperatively and on postoperative day 2 (P0.05), but was significantly higher in the POD subgroup than in the no-POD subgroup on postoperative day 2 (P<0.05). Furthermore, the LP-PLA2 level on postoperative day 2 was an independent risk factor for POD (odds ratio: 1.03, 95% confidence interval: 1.00-1.07). CONCLUSIONS The preoperative presence of carotid plaque is closely associated with a higher incidence of POD. The potential mechanism may involve the increased expression of LP-PLA2 in the serum, which can lead to plaque destabilization and subsequent inflammatory cascades.

Nicotine-Induced Neuroprotection against Cognitive Dysfunction after Partial Hepatectomy Involves Activation of BDNF/TrkB Signaling Pathway and Inhibition of NF-κB Signaling Pathway in Aged Rats.

Introduction: The main purpose of this study was to investigate the effects and possible mechanisms of nicotine pre-treatment on postoperative cognitive dysfunction (POCD) in aged rats. Methods: Nicotine (0.5 mg/kg) was given i.p. immediately after anesthesia induction. After the Morris water maze test was used to evaluate the rats' spatial learning and memory, serum and hippocampal tissues were harvested 1 and 3 days after intervention. Inflammatory cytokines in the serum were evaluated by Enzyme-linked Immunosorbent Assay (ELISA). Brain-derived neurotrophic factor (BDNF), p-TrkB, neuroinflammation cytokines, NF-κB p65, and cleaved caspase-3 were measured by western blotting; neuronal apoptosis in the hippocampal CA1 region was also evaluated by TUNEL staining. Results: We found that nicotine markedly attenuated the POCD and reduced the elevated levels of inflammatory cytokines in the serum, including IL-1ß and high mobility group box-1 (HMGB1), on postoperative day 1. Additionally, nicotine suppressed the surgery-induced release of IL-1ß, TNF-ɑ, HMGB1, and NF-κB p65 in the hippocampus on postoperative day 1 and day 3. In addition, operated rats displayed lower BDNF and p-TrkB in the hippocampus on postoperative day 1, returning to baseline by postoperative day 3. However, nicotine pre-treatment clearly reversed the surgical stress-induced decrease in both BDNF and p-TrkB expression in the hippocampus. Furthermore, nicotine pre-treatment significantly alleviated the surgery-induced increase in the neuronal apoptosis in the hippocampus on postoperative day 1 and day 3. Conclusions: Our results showed that nicotine-induced neuroprotection against POCD may involve activation of the BDNF/TrkB signaling pathway and inhibition of the NF-κB signaling pathway. Implications: Nicotine has long been considered a potent therapeutic agent for neuroprotection. This study reported the positive effect of nicotine treatment on cognitive dysfunction after partial hepatectomy in aged rats. Furthermore, the underlying mechanism may involve activation of the BDNF/TrkB signaling pathway and inhibition of the NF-κB signaling pathway in the hippocampus.

The Role of AGGF1 in the Classification and Evaluating Prognosis of Adult Septic Patients: An Observational Study.

Purpose: Angiogenic factor with G patch and FHA domains 1 (AGGF1) is a crucial angiogenic factor that is involved in a variety of diseases and in the regulation of inflammatory responses. However, its role in sepsis is poorly understood. We have investigated the role of AGGF1 in the classification and prognostic evaluation of adult septic patients in a clinical context. Patients and Methods: A total of 126 septic patients who visited the Emergency Department of Beijing Chao-Yang Hospital and 76 non-sepsis patients visiting the Physical Examination Center of Beijing Chao-Yang Hospital were enrolled. AGGF1 levels in plasma were detected by enzyme-linked immunosorbent assay. Spearman correlation analysis was used to determine correlations between plasma AGGF1 and Sequential Organ Failure Assessment (SOFA) score, Acute Pathology and Chronic Health Evaluation II (APACHE II) score, procalcitonin and lactate. We evaluated the classification significance of AGGF1 in sepsis using receiver operating characteristic (ROC) curves. We also assessed the predictive significance of AGGF1 for 28-day mortality in sepsis using ROC curves and Kaplan-Meier analyses. Results: Plasma AGGF1 levels were higher in sepsis patients than in non-sepsis patients (P < 0.001). Among sepsis patients, plasma AGGF1 levels were higher in non-survivors than in survivors (P < 0.001). Increased plasma AGGF1 levels were positively correlated with SOFA score, APACHE II score, procalcitonin and lactate. Plasma AGGF1 levels could distinguish sepsis patients from non-sepsis patients (area under the curve [AUC] = 0.777). AGGF1 had a higher predictive value than SOFA score, APACHE II score, lactate, procalcitonin, and white blood cell count for 28-day mortality in patients with sepsis (AUC = 0.876). Furthermore, Kaplan-Meier analysis indicated that lower plasma AGGF1 levels were associated with lower 28-day mortality compared with higher plasma AGGF1 levels (log rank P < 0.001). Conclusion: AGGF1 is useful for the classification and evaluating prognosis of adult septic patients.

ACE2 Expressed on Myeloid Cells Alleviates Sepsis-Induced Acute Liver Injury via the Ang-(1-7)-Mas Receptor Axis.

Sepsis-induced acute liver injury (ALI) is common in intensive care units. Angiotensin-converting enzyme 2 (ACE2) plays a vital role in hepatic fibrosis and steatosis; however, its role in sepsis-induced ALI remains unclear. This study found that hepatic ACE2 expression in cecal ligation and puncture (CLP)-treated mice significantly decreased 24 h after CLP. ACE2-transgenic (TG) mice exhibited a significant improvement in CLP-induced ALI, accompanied by the inhibition of hepatocyte apoptosis, oxidative stress, and inflammation, while ACE2-knockout mice demonstrated an opposite trend. During sepsis-induced ALI, ACE2-TG could also elevate the Ang-(1-7) and Mas receptor (MasR) levels in liver tissues. Interestingly, the MasR inhibitor A779 abrogated the favorable effects of ACE2 on CLP-induced ALI. In a bone marrow transplantation experiment, the ACE2-TG transplantation group showed significantly improved inflammation and liver dysfunction, less hepatocyte apoptosis, and reduced oxidative stress after CLP compared with the wild-type transplantation group. In contrast, the ACE2-knockout group showed poor inflammatory response and liver dysfunction, significantly more hepatocyte apoptosis, and elevated oxidative stress than the wild-type transplantation group after CLP. ACE2 protects against sepsis-induced ALI by inhibiting hepatocyte apoptosis, oxidative stress, and inflammation via the Ang-(1-7)-Mas receptor axis. Thus, targeting ACE2 may be a promising novel strategy for preventing and treating sepsis-induced ALI.

ACE2 Rescues Sepsis-Associated Encephalopathy by Reducing Inflammation, Oxidative Stress, and Neuronal Apoptosis via the Nrf2/Sestrin2 Signaling Pathway.

Neuroinflammation and oxidative stress contribute to the progression of sepsis-associated encephalopathy (SAE). Angiotensin-converting enzyme 2 (ACE2) is considered to be a neuroprotective factor due to its anti-inflammatory and antioxidant properties. However, the role of ACE2 on myeloid cells in regulating SAE and the underlying mechanism warrants further exploration. SAE was induced in ACE2 transgenic (TG), knockout (KO), and bone marrow (BM) chimeric mice by cecal ligation and puncture (CLP). The expression levels of apoptosis-, oxidation- and neuroinflammation-associated mediators and morphological changes were monitored by quantitative real-time PCR analyses and histological examinations in the cortex of septic mice. The contents of angiotensin (Ang) II and Ang-(1-7) along with the activity of ACE2 were examined with commercial kits. The expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and Sestrin2 was detected by immunoblotting analysis. Our results indicated that the expression of cortical ACE2 was significantly reduced in the early phase of CLP-induced sepsis. Moreover, ACE2 overexpression in TG mice conferred neuroprotection against sepsis, as evidenced by alleviated neuronal apoptosis, oxidative stress, and proinflammatory M1-like microglial polarization, accompanied by upregulation of the Ang-(1-7), Nrf2, and Sestrin2 protein levels. Conversely, ACE2 deficiency in KO mice exacerbated SAE. The neuroprotective effects of ACE2 were further confirmed in wild-type mice transplanted with ACE2-TG and KO BM cells. Therefore, our data suggest that myeloid ACE2 exerts a protective role in the pathogenesis of SAE, potentially by activating Ang-(1-7)-Nrf2/sestrin2 signaling pathway, and highlight that upregulating ACE2 expression and activity may represent a promising approach for the treatment of SAE in patients with sepsis.

Blockage of S100A8/A9 ameliorates septic nephropathy in mice.

Septic acute kidney injury (AKI) is the commonest cause of complication of sepsis in intensive care units, but its pathophysiology remains unclear. Calprotectin (S100A8/A9), which is a damage-associated molecular patterns (DAMPs) molecule, exerts a critical role in modulating leukocyte recruitment and inflammatory response during various diseases. However, role of S100A8/A9 in septic AKI is largely unknown. In this research, Septic AKI was triggered by cecal ligation and puncture (CLP) operation in wild-type mice, which treated with or without an S100A9 inhibitor, Paquinimod (Paq, 10 mg/kg) that prevents S100A8/A9 to bind to Toll-like receptor 4 (TLR4). Renal function, pathological changes, cell death, and oxidative stress were evaluated. Our research indicated that the mRNA and protein expression of S100A9 are time-dependently elevated in the kidney following CLP. Moreover, the administration of Paq for 24 h significantly improved CLP-induced renal dysfunction and pathological alterations compared with vehicle treatment in mice. These beneficial effects were associated with the inhibition of CLP-triggered renal tubular epithelial cell apoptosis, inflammation, superoxide production, and mitochondrial dynamic imbalance. What's more, we further confirmed the above findings by cell co-culture experiments. Our study demonstrates that S100A9 is a prominent protein to lead to septic AKI, and the selective inhibition of S100A9 could represent a new therapeutic approach which can treat septic AKI.

Prediction of short-term mortality in elderly patients with sepsis using immunoglobulin G2: An observational study.

Background: Sepsis is a global healthcare issue and continues to cause high mortality especially in elderly patients. The humoral immune system plays an important role in protecting from microbial contamination. The goal of this study is to investigate the immune status and prognostic evaluation of elderly patients with sepsis. Methods: A single-center, prospective observational study has been conducted, with the endpoint being the 28-day mortality. Patients 65 years and older who met the diagnostic criteria of Sepsis-3 in the Emergency Department of Beijing Chao-Yang Hospital were divided into survivors and non-survivors groups. Levels of immunoglobulin (Ig) A, IgG, IgM and their subclasses as well as clinical indicators were collected upon enrollment, and the results were statistically analyzed. Results: This study finally enrolled 106 elderly patients, including 68 survivors and 38 non-survivors. Compared with survivors, IgG2 level and IgG4 level were lower in non-survivors ( P < 0.05 ). IgG2 could be regarded as an independent predictor of the 28-day mortality in elderly septic patients. IgG2 had a higher predictive value than other immunoglobulins, lactate, procalcitonin, SOFA score and APACHE II score for mortality in elderly septic patients, and the ratio of IgG2 to IgG had a slightly larger area under the ROC curve compared to IgG2 only (AUC: 0.776 v.s. 0.741). Conclusion: IgG subclasses play important roles in the prognosis of elderly septic patients, with IgG2 being the main component. IgG2 was found to outperform other immunoglobulins, lactate, procalcitonin, SOFA score and APACHE II score in terms of predicting the mortality. A complete immunological evaluation is helpful to guide the prognosis and treatment of patients with age-related infection.

Impact of propofol versus sevoflurane on the incidence of postoperative delirium in elderly patients after spine surgery: study protocol of a randomized controlled trial.

BACKGROUND: Postoperative delirium in elderly patients is a common and costly complication after surgery. Propofol and sevoflurane are commonly used anesthetics during general anesthesia, and the sedative and anti-inflammatory mechanisms of the two medications are different. The aim of this trial is to compare the impact of propofol with sevoflurane on the incidence of postoperative delirium in elderly patients after spine surgery. METHODS: A single-center randomized controlled trial will be performed at First Affiliated Hospital of Shandong First Medical University, China. A total of 298 participants will be enrolled in the study and randomized to propofol infusion or sevoflurane inhalation groups. The primary outcome is the incidence of delirium within 7 days after surgery. Secondary outcomes include the day of postoperative delirium onset, duration (time from first to last delirium-positive day), and total delirium-positive days among patients who developed delirium; tracheal intubation time in PACU; the length of stay in PACU; the rate of postoperative shivering; the rate of postoperative nausea and vomiting; the rate of emergence agitation; pain severity; QoR40 at the first day after surgery; the length of stay in hospital after surgery; and the incidence of non-delirium complications within 30 days after surgery. DISCUSSION: The primary objective of this study is to compare the impact of propofol and sevoflurane on the incidence of postoperative delirium for elderly patients undergoing spine surgery. The results may help inform strategies to the optimal selection of maintenance drugs for general anesthesia in elderly patients undergoing spine surgery. TRIAL REGISTRATION: ClinicalTrials.gov NCT05158998 . Registered on 14 December 2021.

Aldehyde Dehydrogenase 2 Protects Against Lipopolysaccharide-Induced Myocardial Injury by Suppressing Mitophagy.

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Sepsis-induced circulatory and cardiac dysfunction is associated with high mortality rates. Mitophagy, a specific form of autophagy, is excessively activated in lipopolysaccharide-induced myocardial injury. The present study investigated whether aldehyde dehydrogenase 2 (ALDH2) regulates mitophagy in sepsis-induced myocardial dysfunction. After lipopolysaccharide administration, cardiac dysfunction, inflammatory cell infiltration, biochemical indicators of myocardial cell injury, and cardiomyocyte apoptosis were ameliorated in mice by ALDH2 activation or overexpression. In contrast, cardiac dysfunction and cardiomyocyte apoptosis were exacerbated in mice followed ALDH2 inhibition. Moreover, ALDH2 activation or overexpression regulated mitophagy by suppressing the expression of phosphatase and tensin homolog-induced putative kinase 1 (PINK1)/Parkin, by preventing the accumulation of 4-hydroxy-trans-nonenal. Conversely, ALDH2 inhibition promoted the expression of LC3B by increasing 4-hydroxy-trans-2-nonenal accumulation. Consequently, ALDH2 may protect the heart from lipopolysaccharide-induced injury by suppressing PINK1/Parkin-dependent mitophagy.

A pH-/thermo-responsive hydrogel formed from N,N'-dibenzoyl-l-cystine: properties, self-assembly structure and release behavior of SA.

In this study, we report a pH-/thermo-responsive hydrogel formed by N,N'-dibenzoyl-l-cystine (DBC). It is difficult to dissolve DBC in water even on heating, and it exhibits no gelation ability. Interestingly, DBC is readily soluble in NaOH solution at room temperature and the self-assembled hydrogels are obtained by adjusting the basic DBC aqueous solution with HCl to achieve a given pH value (<3.5). When NaOH is added to the hydrogel (pH > 9.4), it becomes a sol again. This small-molecule hydrogel is characterized by scanning electron microscopy, Fourier transform infrared spectroscopy, rheological measurement and differential scanning calorimetry. The results indicate that the DBC hydrogel exhibits excellent mechanical properties, thermo-reversibility, and pH-responsive properties. Fortunately, the single crystal of DBC is obtained by volatilizing its acid aqueous solution. It crystallizes in the monoclinic space group P21 (Z = 2) with lattice parameters a = 10.8180 (11) Å, b = 9.0405 (9) Å, c = 10.9871 (11) Å and ß = 90.798 (3)°. By comparing the X-ray diffraction result of the DBC single crystal with that of its xerogel, the self-assembled structure of DBC in hydrogel has been ascertained. The gelators are self-assembled via strong intermolecular hydrogen bonds linking neighboring amide and carboxyl groups, π-π stacking interactions for aromatic rings, and hydrogen bonds between water molecules. In addition, the release behavior of salicylic acid (SA) molecules from the DBC gel is also investigated taking into account the DBC concentration, phosphate buffer solution (PBS) pH and SA concentration. When the concentrations of DBC and SA are 3.0 g L-1 and 200 mg L-1, respectively, the release ratio in PBS (pH = 4.0) reaches 58.02%. The diffusion-controlled mechanism is in accordance with Fickian diffusion control within the given time range.

Outcome prediction using the Mortality in Emergency Department Sepsis score combined with procalcitonin for influenza patients.

BACKGROUND: Severe influenza is often associated with bacterial coinfection and can trigger sepsis, which increases the severity, complexity and mortality of the disease. To determine an effective method for predicting 28-day mortality of emergency department (ED) patients with influenza, we investigated the Mortality in Emergency Department Sepsis (MEDS) score, procalcitonin (PCT) and other relevant biomarkers. METHODS: We conducted a retrospective, observational, monocentric study, and the endpoint was 28-day mortality. Independent predictors were identified and a new combination predictive model was created both by logistic regression, and the model was evaluated by a receiver operating characteristic (ROC) curve. RESULTS: A total of 364 consecutive ED admitted patients with influenza were enrolled and 45 patients died within 28 days. For predicting 28-day mortality, the MEDS score and PCT were independent predictors with adjusted odds ratio of 1.318 (95% CI 1.206-1.439) and 1.038 (95% CI 1.010-1.065), and with AUCs of 0.817 (95% CI 0.756-0.878) and 0.793 (95% CI 0.725-0.861), respectively. The new combination of the MEDS score with PCT significantly improved the efficacy for predicting 28-day mortality with an AUC of 0.857 (95% CI 0.809-0.905), and was superior to the SOFA score with an AUC of 0.837 (95% CI 0.779-0.894). CONCLUSION: The MEDS score and PCT, especially when combined, perform well for predicting mortality of ED admitted patients with influenza.

[Effects of Organic Carbon Content on the Residue and Migration of Polycyclic Aromatic Hydrocarbons in Soil Profiles].

The effects of total organic carbon content (TOC) on the migration of polycyclic aromatic hydrocarbons (PAHs) in the soil were investigated. This study analyzed the vertical properties of the concentrations and distributions of PAHs and TOC at various soil profiles from functionally different environmental regions including nature reserves, ploughs, orchards, farmlands, metropolitan areas, and industrial parks. The vertical migration properties of PAHs in soils were examined by conducting leaching experiments in soil columns. The concentrations of PAHs varied from region to region and showed strong, positive correlations with TOC in the same region. Furthermore, based on the leaching experiments, the transport abilities of PAHs were significantly influenced by TOC, although they could all be transported to the deep layers by TOC in soil columns. The downward migration of PAHs decreased with the increase in TOC and vice versa. The properties of the composition and structure of PAHs also had an obvious influence on their residues and migration in soil profiles at the same TOC conditions. In addition, the transport of PAHs was related to the amount of leaching water, the leaching time, and the additional PAHs.

Distribution and sources of oxygenated non-hydrocarbons in topsoil of Beijing, China.

The oxygenated non-hydrocarbon compounds are widely distributed in soil. To investigate the distribution and origin of these compounds in topsoil of Beijing, their contents and compositions were measured in topsoil from 62 sites in Beijing. The research results showed that oxygenated non-hydrocarbons were composed primarily of C6∼C28 n-fatty acids, C12∼C28 n-fatty alcohols, n-fatty acid methyl esters, phthalates, sterols, and dehydroabietic acid in the topsoil of Beijing. The contents and compositions of these compounds varied with the sampling site. The concentrations of n-fatty acids and phthalate esters were the highest at all sites, followed by sterols, n-fatty acid methyl esters, fatty alcohols, and dehydroabietic acid in order. The n-fatty acids had a main peak of C16, followed by C18. An odd or even carbon number predominance was not observed in the low-molecular-weight n-fatty acids, indicating a fossil fuel or organic matter source. However, some high-molecular-weight n-fatty acids with an even carbon predominance may derive from a biomass. The n-fatty alcohols showed a main peak of C22 and were predominated by an even carbon number, suggesting plant, microbial, or other natural origins. Phthalates, including diethyl phthalate (DEP), diisobutyl phthalate (DIBP), dibutyl phthalate (DBP), diethylhexyl phthalate (DEHP), and dimethylphthalate (DMP), were detected. The content of phthalate esters was higher in the samples collected from dense human activity areas. The concentrations of DBP, DEHP, and DIBP were relatively high, indicating an anthropogenic source. The sterols (predominantly ß-sitosterol) originated from biological sources, especially plants. The n-fatty acid methyl esters and dehydroabietic acid in topsoil showed apparent even carbon predominance with the former mainly derived from microorganisms or plants and the latter from cork combustion products.