Biochar-based composites for removing chlorinated organic pollutants: Applications, mechanisms, and perspectives.

Chlorinated organic pollutants constitute a significant category of persistent organic pollutants due to their widespread presence in the environment, which is primarily attributed to the expansion of agricultural and industrial activities. These pollutants are characterized by their persistence, potent toxicity, and capability for long-range dispersion, emphasizing the importance of their eradication to mitigate environmental pollution. While conventional methods for removing chlorinated organic pollutants encompass advanced oxidation, catalytic oxidation, and bioremediation, the utilization of biochar has emerged as a prominent green and efficacious method in recent years. Here we review biochar's role in remediating typical chlorinated organics, including polychlorinated biphenyls (PCBs), triclosan (TCS), trichloroethene (TCE), tetrachloroethylene (PCE), organochlorine pesticides (OCPs), and chlorobenzenes (CBs). We focus on the impact of biochar material properties on the adsorption mechanisms of chlorinated organics. This review highlights the use of biochar as a sustainable and eco-friendly method for removing chlorinated organic pollutants, especially when combined with biological or chemical strategies. Biochar facilitates electron transfer efficiency between microorganisms, promoting the growth of dechlorinating bacteria and mitigating the toxicity of chlorinated organics through adsorption. Furthermore, biochar can activate processes such as advanced oxidation or nano zero-valent iron, generating free radicals to decompose chlorinated organic compounds. We observe a broader application of biochar and bioprocesses for treating chlorinated organic pollutants in soil, reducing environmental impacts. Conversely, for water-based pollutants, integrating biochar with chemical methods proved more effective, leading to superior purification results. This review contributes to the theoretical and practical application of biochar for removing environmental chlorinated organic pollutants.

Development of a CT-Based comprehensive model combining clinical, radiomics with deep learning for differentiating pulmonary metastases from noncalcified pulmonary hamartomas, a retrospective cohort study.

BACKGROUND: Clinical differentiation between pulmonary metastases and noncalcified pulmonary hamartomas (NCPH) often presents challenges, leading to potential misdiagnosis. However, the efficacy of a comprehensive model that integrates clinical features, radiomics, and deep learning (CRDL) for differential diagnosis of these two diseases remains uncertain. OBJECTIVE: This study evaluated the diagnostic efficacy of a Clinical Features, Radiomics, and Deep Learning (CRDL) model in differentiating pulmonary metastases from noncalcified pulmonary hamartomas (NCPH). METHODS: We retrospectively analyzed the clinical and imaging data of 256 patients from Hospital A and 85 patients from Hospital B, who were pathologically confirmed pulmonary hamartomas or pulmonary metastases after thoracic surgery. Employing Python 3.7 software suites, we extracted radiomic features and deep learning attributes from patient datasets. The cohort was divided into training set, internal validation set, and external validation set. The diagnostic performance of the constructed models was evaluated using receiver operating characteristic (ROC) curve analysis to determine their effectiveness in differentiating between pulmonary metastases and NCPH. RESULTS: Clinical features such as white blood cell count (WBC), platelet count (PLT), history of cancer, carcinoembryonic antigen (CEA) level, tumor marker status, lesion margin characteristics (smooth or blurred) and maximum diameter were found to have diagnostic value in differentiating between the two diseases. In the domains of radiomics and deep learning. Of the 1,130 radiomics features and 512 deep learning features, 24 and 7, respectively, were selected for model development. The area under the ROC curve (AUC) values for the four groups were 0.980, 0.979, 0.999, and 0.985 in the training set, 0.947, 0.816, 0.934, and 0.952 in the internal validation set, and 0.890, 0.904, 0.923, and 0.938 in the external validation set. This demonstrated that the CRDL model showed the greatest efficacy. CONCLUSIONS: The comprehensive model incorporating clinical features, radiomics, and deep learning shows promise for aiding in the differentiation between pulmonary metastases and hamartomas.

A potential antiviral role for CCR5+CD8+ T cells in children with hepatitis B.

While dysfunctional exhausted CD8+ T cells hamper viral control when children acquire hepatitis B virus (HBV) infection, it's crucial to recognize that CD8+ T cells have diverse phenotypes and functions. This study explored a subset of CD8+ T cells expressing C-C chemokine receptor type 5 (CCR5) in children with HBV infection. Thirty-six patients in the immune tolerant group, 33 patients in the immune active group, 55 patients in the combined response group, and 22 healthy control children were enrolled. The frequency, functional molecules, and effector functions of the CCR5+CD8+ T cell population in different groups were evaluated. The frequency of CCR5+CD8+ T cells correlated positively with the frequency of CCR5+CD4+ T cells and patient age, and it correlated negatively with alanine aminotransferase, aspartate transaminase, HBV DNA, hepatitis B surface antigen, and lactic dehydrogenase levels. CCR5+CD8+ T cells had higher levels of inhibitory and activated receptors and produced higher levels of IFN-γ, IL-2, and TNF-α than CCR5-CD8+ T cells. CCR5+CD8+ T cells were partially exhausted but possessed a stronger antiviral activity than CCR5-CD8+ T cells. The identification of this subset increases our understanding of CD8+ T cell functions and serves as a potential immunotherapeutic target for children with HBV infection.

Synthesis and proton-conductive behaviour of two MOFs with covalently bonded imidazoles in the channels.

Immobilization of imidazole molecules as proton carriers into MOFs to facilitate proton conduction is a general strategy for developing high proton conductive materials. Herein, we designed two imidazole substituted phthalic acid ligands and constructed two novel MOFs, {[Zr6(OH)16(H3L1)4]Cl8·20H2O}n [Zr-MOF; H3L1 = 2-(1H-imidazol-4-yl) methylaminoterephthalic acid] and {Gd(HCOO)(H2L2)2}n [Gd-MOF; H3L2 = 5-(1H-imidazol-4-yl)methylaminoisophthalic acid] and fully studied their porous nature, stability and water-assisted proton conduction. The resulting Zr-MOF exhibits a high proton conductivity of 1.82 × 10-2 S cm-1 at 98% RH and 80 °C, while Gd-MOF has a proton conductivity of 3.01 × 10-3 S cm-1 at 98% RH and 60 °C.

A Case of Organizing Pneumonia Resembling Lung Cancer.

BACKGROUND: Organizing pneumonia (OP) is a pathologic diagnosis with clinical and imaging manifestations that often resemble other diseases, such as infections and cancers, which can lead to delays in diagnosis and inappropriate management of the underlying disease. In this article, we present a case of organized pneumonia that resembles lung cancer. METHODS: We report a case of initial suspicion of pulmonary malignancy, treated with anti-inflammatory medication and then reviewed with CT suggesting no improvement, and finally confirmed to be OP by pathological biopsy taken via transbronchoscopy. A joint literature analysis was performed to raise clinicians' awareness of the diagnosis and treatment of OP. RESULTS: Initially, because of the atypical auxiliary findings, we thought that the disease turned out to be a lung tumor, which was eventually confirmed as OP by pathological diagnosis. CONCLUSIONS: The diagnosis and treatment of OP requires a combination of clinical information and radiological expertise, as well as biopsy to obtain histopathological evidence. That is, clinical-imaging-pathological tripartite cooperation and comprehensive analysis.

Artificial Intelligence-Guided Gut-Microenvironment-Triggered Imaging Sensor Reveals Potential Indicators of Parkinson's Disease.

The gut-brain axis has recently emerged as a crucial link in the development and progression of Parkinson's disease (PD). Dysregulation of the gut microbiota has been implicated in the pathogenesis of this disease, sparking growing interest in the quest for non-invasive biomarkers derived from the gut for early PD diagnosis. Herein, an artificial intelligence-guided gut-microenvironment-triggered imaging sensor (Eu-MOF@Au-Aptmer) to achieve non-invasive, accurate screening for various stages of PD is presented. The sensor works by analyzing α-Syn in the gut using deep learning algorithms. By monitoring changes in α-Syn, the sensor can predict the onset of PD with high accuracy. This work has the potential to revolutionize the diagnosis and treatment of PD by allowing for early intervention and personalized treatment plans. Moreover, it exemplifies the promising prospects of integrating artificial intelligence (AI) and advanced sensors in the monitoring and prediction of a broad spectrum of diseases and health conditions.

Metformin normalizes mitochondrial function to delay astrocyte senescence in a mouse model of Parkinson's disease through Mfn2-cGAS signaling.

BACKGROUND: Senescent astrocytes play crucial roles in age-associated neurodegenerative diseases, including Parkinson's disease (PD). Metformin, a drug widely used for treating diabetes, exerts longevity effects and neuroprotective activities. However, its effect on astrocyte senescence in PD remains to be defined. METHODS: Long culture-induced replicative senescence model and 1-methyl-4-phenylpyridinium/α-synuclein aggregate-induced premature senescence model, and a mouse model of PD were used to investigate the effect of metformin on astrocyte senescence in vivo and in vitro. Immunofluorescence staining and flow cytometric analyses were performed to evaluate the mitochondrial function. We stereotactically injected AAV carrying GFAP-promoter-cGAS-shRNA to mouse substantia nigra pars compacta regions to specifically reduce astrocytic cGAS expression to clarify the potential molecular mechanism by which metformin inhibited the astrocyte senescence in PD. RESULTS: We showed that metformin inhibited the astrocyte senescence in vitro and in PD mice. Mechanistically, metformin normalized mitochondrial function to reduce mitochondrial DNA release through mitofusin 2 (Mfn2), leading to inactivation of cGAS-STING, which delayed astrocyte senescence and prevented neurodegeneration. Mfn2 overexpression in astrocytes reversed the inhibitory role of metformin in cGAS-STING activation and astrocyte senescence. More importantly, metformin ameliorated dopamine neuron injury and behavioral deficits in mice by reducing the accumulation of senescent astrocytes via inhibition of astrocytic cGAS activation. Deletion of astrocytic cGAS abolished the suppressive effects of metformin on astrocyte senescence and neurodegeneration. CONCLUSIONS: This work reveals that metformin delays astrocyte senescence via inhibiting astrocytic Mfn2-cGAS activation and suggest that metformin is a promising therapeutic agent for age-associated neurodegenerative diseases.

Recent progresses in analytical method development for 210Pb in environmental and biological samples.

As a decay product of uranium series, 210Pb spreads widely in the nature and imposes strong radiological and chemical toxicity. It is vital to establish reliable and efficient radioanalytical methods for 210Pb determination to support environment and food radioactivity monitoring programs. This article critically reviews analytical methods developed for determining 210Pb in environmental and biological samples, especially new development in recent years. Techniques applied throughout different analytical steps including sample pretreatment, separation, purification, and detection are summarized and their pros and cons are discussed to provide a holistic overview for 210Pb environmental and biological assay.

Growth hormone promotes myelin repair after chronic hypoxia via triggering pericyte-dependent angiogenesis.

White matter injury (WMI) causes oligodendrocyte precursor cell (OPC) differentiation arrest and functional deficits, with no effective therapies to date. Here, we report increased expression of growth hormone (GH) in the hypoxic neonatal mouse brain, a model of WMI. GH treatment during or post hypoxic exposure rescues hypoxia-induced hypomyelination and promotes functional recovery in adolescent mice. Single-cell sequencing reveals that Ghr mRNA expression is highly enriched in vascular cells. Cell-lineage labeling and tracing identify the GHR-expressing vascular cells as a subpopulation of pericytes. These cells display tip-cell-like morphology with kinetic polarized filopodia revealed by two-photon live imaging and seemingly direct blood vessel branching and bridging. Gain-of-function and loss-of-function experiments indicate that GHR signaling in pericytes is sufficient to modulate angiogenesis in neonatal brains, which enhances OPC differentiation and myelination indirectly. These findings demonstrate that targeting GHR and/or downstream effectors may represent a promising therapeutic strategy for WMI.

3-Methyl-4-nitrophenol Exposure Deteriorates Oocyte Maturation by Inducing Spindle Instability and Mitochondrial Dysfunction.

3-methyl-4-nitrophenol (PNMC), a well-known constituent of diesel exhaust particles and degradation products of insecticide fenitrothion, is a widely distributed environmental contaminant. PNMC is toxic to the female reproductive system; however, how it affects meiosis progression in oocytes is unknown. In this study, in vitro maturation of mouse oocytes was applied to investigate the deleterious effects of PNMC. We found that exposure to PNMC significantly compromised oocyte maturation. PNMC disturbed the spindle stability; specifically, it decreased the spindle density and increased the spindle length. The weakened spindle pole location of microtubule-severing enzyme Fignl1 may result in a defective spindle apparatus in PNMC-exposed oocytes. PNMC exposure induced significant mitochondrial dysfunction, including mitochondria distribution, ATP production, mitochondrial membrane potential, and ROS accumulation. The mRNA levels of the mitochondria-related genes were also significantly impaired. Finally, the above-mentioned alterations triggered early apoptosis in the oocytes. In conclusion, PNMC exposure affected oocyte maturation and quality through the regulation of spindle stability and mitochondrial function.

Reusable thiol-modification Lactobacillus plantarum embedded in cellulose nanocrystals composite aerogel for efficient removal of Ochratoxin A in grape juice.

Ochratoxin A (OTA) contamination in grape juice has attracted widespread concern as OTA can lead to kidney disease and cause adverse neurological effects. An effective method to remove OTA is to make use of highly adsorbent materials that are able to remove the toxic contaminant. Recently, inactivated Lactobacillus plantarum-based biosorbents have shown to be an efficient, cost-effective and environmentally friendly bioremediation method in removing toxic pollutants such as OTA. We used five chemical thiol-modification methods to improve the adsorption efficiency of OTA in grape juice. The esterification of Lactobacillus plantarum (L-Es) significantly increased the sulfhydryl contents (-SH) by 251.33 µmol/g and >90% of OTA was removed. However, the inactivated microbial adsorbent was difficult to separate after adsorption and therefore, the prepared L-Es were embedded into the cellulose nanocrystals (L-Es@CNCs). Moreover, L-Es@CNCs significantly increased the adsorption rate of OTA in grape juice samples by 88.28% with negligible effects on juice quality due to the properties of easy re-use and excellent biodegradability. This showcases its potential application for OTA removal in the grape juice industry.

FBXO32-mediated degradation of PTEN promotes lung adenocarcinoma progression.

FBXO32, a member of the F-box protein family, is known to play both oncogenic and tumor-suppressive roles in different cancers. However, the functions and the molecular mechanisms regulated by FBXO32 in lung adenocarcinoma (LUAD) remain unclear. Here, we report that FBXO32 is overexpressed in LUAD compared with normal lung tissues, and high expression of FBXO32 correlates with poor prognosis in LUAD patients. Firstly, we observed with a series of functional experiments that FBXO32 alters the cell cycle and promotes the invasion and metastasis of LUAD cells. We further corroborate our findings using in vivo mouse models of metastasis and confirmed that FBXO32 positively regulates LUAD tumor metastasis. Using a proteomic-based approach combined with computational analyses, we found a positive correlation between FBXO32 and the PI3K/AKT/mTOR pathway, and identified PTEN as a FBXO32 interactor. More important, FBXO32 binds PTEN via its C-terminal substrate binding domain and we also validated PTEN as a bona fide FBXO32 substrate. Finally, we demonstrated that FBXO32 promotes EMT and regulates the cell cycle by targeting PTEN for proteasomal-dependent degradation. In summary, our study highlights the role of FBXO32 in promoting the PI3K/AKT/mTOR pathway via PTEN degradation, thereby fostering lung adenocarcinoma progression.

Analysis of risk factors of preeclampsia in pregnant women with chronic hypertension and its impact on pregnancy outcomes.

OBJECTIVE: To investigate the risk factors and maternal and fetal outcomes of preeclampsia after pregnancy in patients with primary chronic hypertension. METHODS: A total of 500 singleton pregnant women with a history of hypertension who were admitted for delivery at our Hospital from March 2015 to May 2022 were retrospectively collected by random sampling and divided into the non-occurrence group (n = 200) and the occurrence group (n = 300) according to whether they were complicated by preeclampsia. Afterward, the general data and the pregnancy-related data of patients were collected for comparison. RESULTS: The univariate analysis showed significant differences between the non-occurrence group and the occurrence group in terms of the proportion of preeclampsia history (4.00% VS 24.67%, χ2 = 37.383, P < 0.001), duration of hypertension > 3 years (18.00% VS 31.67%, χ2 = 11.592, P < 0.001), systemic therapy (20.50% VS 10.00%, χ2 = 10.859, P < 0.001), gestational age at admission [37.72 (34.10, 38.71) VS 35.01 (31.91, 37.42) weeks, Z = -9.825, P < 0.001]. Meanwhile, the multivariate analysis showed that a history of preeclampsia (OR = 6.796, 95% CI: 3.575 ∼ 10.134, χ2 = 8.234, P < 0.001), duration of hypertension > 3 years (OR = 3.456, 95% CI: 2.157 ∼ 5.161, χ2 = 9.348, P < 0.001), and a lack of systemic antihypertensive treatment (OR = 8.983, 95% CI: 7.735 ∼ 9.933, χ2 = 9.123, P < 0.001) were risk factors for chronic hypertension complicated by preeclampsia during pregnancy. CONCLUSION: A history of preeclampsia, a longer duration of hypertension, and a lack of systematic antihypertensive treatment are risk factors for chronic hypertension complicated by preeclampsia during pregnancy. The occurrence of preeclampsia in pregnant women with chronic hypertension increases the incidence of maternal HELLP syndrome and fetal distress.

Declined flesh quality resulting from niacin deficiency is associated with elevated glycolysis and impaired mitochondrial homeostasis in grass carp (Ctenopharyngodon idella).

Energy metabolism exerts profound impacts on flesh quality. Niacin can be transformed into nicotinamide adenine dinucleotide (NAD), which is indispensable to energy metabolism. To investigate whether niacin deficiency could affect energy metabolism and flesh quality, six diets with graded levels of 0.49, 9.30, 21.30, 33.30, 45.30 and 57.30 mg/kg niacin were fed to grass carp (Ctenopharyngodon idella) for 63 days. The results showed that niacin deficiency declined flesh quality by changing amino acid and fatty acid profiles, decreasing shear force, increasing cooking loss and accelerating pH decline. The accelerated pH decline might be associated with enhanced glycolysis as evident by increased hexokinase (HK), pyruvate kinase (PK) and lactic dehydrogenase (LDH) activities, and mitochondrial dysfunction as evident by destroyed mitochondrial morphology, impaired respiratory chain complex I and antioxidant ability. Based on PWG and cooking loss, the niacin requirements for sub-adult grass carp were 31.95 mg/kg and 29.66 mg/kg diet, respectively.

Aflatoxin B1 inhibited the development of primary myoblasts of grass carp (Ctenopharyngodon idella) by degrading extracellular matrix.

According to the International Agency for Research on Cancer (IARC), aflatoxin B1 (AFB1) has been recognized as a major contaminant in food and animal feed and which is a common mycotoxin with high toxicity. Previous research has found that AFB1 inhibited zebrafish muscle development. However, the potential mechanism of AFB1 on fish muscle development is unknown, so it is necessary to conduct further investigation. In the present research, the primary myoblast of grass carp was used as a model, we treated myoblasts with AFB1 for 24 h. Our results found that 5 µM AFB1 significantly inhibited cell proliferation and migration (P < 0.05), and 10 µM AFB1 promoted lactate dehydrogenase (LDH) release (P < 0.05). Reactive oxygen species (ROS), protein carbonyl (PC) and malondialdehyde (MDA) levels were increased in 15, 5 and 10 µM AFB1 (P < 0.05), respectively. Catalase (CAT), glutathione peroxidase (GPx) and total superoxide dismutase (T-SOD) activities were decreased in 10, 10 and 15 µM AFB1 (P < 0.05), respectively. Furthermore, 15 µM AFB1 induced oxidative damage by Nrf2 pathway, also induced apoptosis in primary myoblast of grass carp. Meanwhile, 15 µM AFB1 decreased MyoD gene and protein expression (P < 0.05). Importantly, 15 µM AFB1 decreased the protein expression of collagen Ⅰ and fibronectin (P < 0.05), and increased the protein levels of urokinase plasminogen activator (uPA), matrix metalloproteinase 9 (MMP-9), matrix metalloproteinase 2 (MMP-2), and p38 mitogen-activated protein kinase (p38MAPK) (P < 0.05). As a result, our findings suggested that AFB1 damaged the cell morphology, induced oxidative damage and apoptosis, degraded ECM components, in turn inhibiting myoblast development by activating the p38MAPK/urokinase-type plasminogen activator (uPA)/matrix metalloproteinase (MMPs)/extracellular matrix (ECM) signaling pathway.

ALTA: a simple nutritional prognostic score for patients with hepatitis B virus-related acute-on-chronic liver failure.

Background: Malnutrition, despite being a common complication, is often neglected in patients with hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF). The objective of this study was to develop a simplified nutritional prognostic score to accurately predict mortality in HBV-ACLF patients. Methods: In this multicenter retrospective study, clinical data from 530 HBV-ACLF patients were used to create a new prognostic score, which was then validated in two external cohorts (n = 229 and 248). Results: Four independent factors were significantly associated with 28-day mortality in HBV-ACLF patients, forming a novel prognostic score (ALTA score = 0.187 × age-0.849 × lymphocyte count-2.033 × total cholesterol-0.148 × albumin-0.971). Notably, the AUROC of ALTA score for 28/90-day mortality (0.950/0.967) were significantly higher than those of three other ACLF prognostic scores (COSSH-ACLF II, 0.864/0.734; MELD, 0.525/0.488; MELD-Na, 0.546/0.517; all P < 0.001), and three known nutritional scores (CONUT, 0.739/0.861; OPNI, 0.279/0.157; NRS-2002, 0.322/0.286; all P < 0.001). The prediction error rates of ALTA score for 28-day mortality were significantly lower than COSSH-ACLF II (7.3%), MELD (14.4%), MELD-Na (12.7%), CONUT (9.0%), OPNI (30.6%), and NRS2002 (34.1%) scores. Further classifying ALTA score into two strata, the hazard ratios of mortality at 28/90 days were notably increased in the high-risk groups compared to the low-risk group (15.959 and 5.740). These results were then validated in two external cohorts. Conclusion: ALTA, as a simplified nutritional prognostic score for HBV-ACLF, demonstrates superiority over the COSSH-ACLF II and other scores in predicting short-term mortality among HBV-ACLF patients. Therefore, it may be used to guide clinical management, particularly in primary care settings.

Determination and human health risk assessment of TFWT, OBT and carbon-14 in seafood around Qinshan Nuclear Power Plant.

This work aims to evaluate the effects of the operation of Qinshan nuclear Power Plant (QNPP) on tritium (3H) and carbon-14 (14C) levels in seafood and assess the health risks caused by seafood consumption. Five kinds of seafood, including marine fish, prawn, razor clam, crabs, and seaweed, were collected from QNPP and the sea around Hangzhou Bay. The activity concentrations of tissue free water tritium (TFWT), organically bound tritium (OBT) and 14C were determined, respectively, and the annual intake and annual effective dose (AED) were calculated. The results showed that the TFWT, OBT, and 14C activity concentrations of the seafood in the surrounding area of QNPP ranged from 2.00 to 74.75 Bq/L, <1.04 to 19.68 Bq/L and 0.09 to 0.17 Bq/g·C, respectively. The TFWT, OBT, and 14C activity concentrations of the seafood in Hangzhou Bay ranged from 1.36 to 10.55 Bq/L, 1.08 to 6.78 Bq/L and 0.07 to 0.13 Bq/g·C, respectively. The differences were not statistically significant. The total AED from 3H and 14C due to the seafood consumption for the residents in the surrounding of QNPP and Hangzhou Bay were 1.96 × 10-4 and 1.61 × 10-4 mSv/year, respectively. The results showed that the operation of QNPP had no obvious effect on 3H and 14C accumulation in seafood, and the dose burden of population was low.

A Case of Tuberculosis Misdiagnosed as Sarcoidosis and then Confirmed by NGS Testing.

BACKGROUND: Pulmonary tuberculosis (PTB) is an important infectious disease that threatens the health and life of human beings. In the diagnosis of PTB, imaging plays a dominant role, but due to the increasing drug resistance of Mycobacterium tuberculosis, atypical clinical manifestations, "different images with the same disease" or "different diseases with the same image" in chest imaging, and the low positivity rate of routine sputum bacteriology, which leads to a high rate of misdiagnosis of PTB. We report a case of pulmonary tuberculosis that was misdiagnosed on imaging. We report a case of pulmonary tuberculosis that resembled sarcoidosis on imaging and was negative for antacid staining on sputum smear and alveolar lavage fluid, and was later diagnosed by microbial next-generation sequencing (NGS). The case was initially misdiagnosed as sarcoidosis. METHODS: Alveolar lavage fluid NGS, chest CT, bronchoscopy. RESULTS: Chest CT showed multiple inflammatory lesions in both lungs, multiple nodular foci in both lungs, and multiple enlarged lymph nodes in the mediastinum and hilar region on both sides. Fiberoptic bronchoscopy was performed in the basal segment of the left lower lobe of the lungs to carry out bronchoalveolar lavage, and the lavage fluid was sent to the NGS test and returned the following results: Mycobacterium tuberculosis complex group detected in the number of sequences of 293. Based on the results of the NGS test, the diagnosis of pulmonary tuberculosis could be confirmed. CONCLUSIONS: The diagnosis of pulmonary tuberculosis cannot be easily excluded in patients with "different images with the same disease" or "different diseases with the same image" on chest imaging without the support of sputum positivity. The goal was to improve the alertness of medical personnel to the misdiagnosis of tuberculosis and the application of NGS technology.

[Medium and Long-term Carbon Emission Projections and Emission Reduction Potential Analysis of the Lingang Special Area Based on the LEAP Model].

Based on the existing statistical data of the Lingang Special Area in Shanghai and considering its future socio-economic development， industrial structure， and technological development， a LEAP-Lingang model was developed to analyze the evolution trends of energy demand and carbon emissions under the baseline scenario， low-carbon scenario， and enhanced low-carbon scenario. To enhance the prediction accuracy of the model， the Logistic population growth model was used to predict future population data， and the learning curve model was used to simulate the cost evolution trend of related carbon reduction technologies. In addition， an economic evaluation model for carbon reduction technologies was developed， and the economic costs and emission reduction potential of typical carbon reduction technologies were evaluated by drawing a marginal emission reduction cost curve. The results showed that under the enhanced low-carbon scenario， the renewable energy accounted for 69% of the primary energy consumption， and the electric energy accounted for 91% of the terminal energy demand in 2060. The Lingang Special Area could achieve carbon peak by 2030， and the carbon emissions in 2060 were predicted to decrease by 94% compared to that in the baseline scenario. In terms of contribution to emission reduction， clean energy substitution， industrial structure optimization， and terminal energy efficiency improvement played a key role in reducing carbon emissions near the port. In the medium term （until 2035）， they were predicted to contribute 35.1%， 27.3%， and 16.2% of carbon emissions， respectively， and in the long term （until 2060）， they should contribute 50.6%， 8.75%， and 7.7% of carbon emissions， respectively. Regarding specific carbon reduction technologies， hydrogen power generation； water electrolysis for hydrogen； and carbon capture， utilization， and storage （CCUS） technology were of great significance for achieving net-zero emissions， but the costs of emission reduction were relatively high. The research results can provide ideas and references for the low-carbon and green development of the Lingang Special Area and related areas.