Multicellular ecotypes shape progression of lung adenocarcinoma from ground-glass opacity toward advanced stages.

Lung adenocarcinoma is a type of cancer that exhibits a wide range of clinical radiological manifestations, from ground-glass opacity (GGO) to pure solid nodules, which vary greatly in terms of their biological characteristics. Our current understanding of this heterogeneity is limited. To address this gap, we analyze 58 lung adenocarcinoma patients via machine learning, single-cell RNA sequencing (scRNA-seq), and whole-exome sequencing, and we identify six lung multicellular ecotypes (LMEs) correlating with distinct radiological patterns and cancer cell states. Notably, GGO-associated neoantigens in early-stage cancers are recognized by CD8+ T cells, indicating an immune-active environment, while solid nodules feature an immune-suppressive LME with exhausted CD8+ T cells, driven by specific stromal cells such as CTHCR1+ fibroblasts. This study also highlights EGFR(L858R) neoantigens in GGO samples, suggesting potential CD8+ T cell activation. Our findings offer valuable insights into lung adenocarcinoma heterogeneity, suggesting avenues for targeted therapies in early-stage disease.

Intentional wedge resection versus segmentectomy for ≤2 cm Ground-Glass-Opacity-Dominant Non-Small cell lung cancer: a Real-World study using inverse probability of treatment weighting.

BACKGROUND: Whether wedge resection is oncological suitable for ground glass opacity (GGO)-dominant non-small cell lung cancer (NSCLC) ≤2 cm is still debatable. The aim of this study is to investigate the short-term and long-term outcomes of intentional wedge resection and segmentectomy for those patients. MATERIALS AND METHODS: This was a real-world study from one of the largest thoracic surgery centers in XX. Patients who underwent intentional wedge resection or segmentectomy for ≤2 cm CTR(consolidation-to-tumor)≤0.5 NSCLC were consecutively included between December 2009 and December 2018. Data were prospectively collected and retrospectively reviewed. Inverse probability of treatment weighting (IPTW) was used to balance baseline characteristics. Long-term outcomes, including overall survival (OS), recurrence-free survival (RFS) and lung cancer-specific survival (LCSS), were analyzed using Cox proportional model. RESULTS: A total of 1209 patients were included (497 in the wedge resection group, 712 in the segmentectomy group). Compared to segmentectomy, wedge resection had a significantly lower rate of complications (3.8% vs. 7.7%, P=0.008), a shorter operating time (65min vs. 114min, P<0.001), and a shorter postoperative stay (3d vs. 4d, P<0.001). The median follow-up was 70.1 months. The multivariate Cox model indicated that wedge resection had survival outcomes that were similar to segmentectomy in terms of 5-year OS (98.8% vs. 99.6%, HR=1.98, 95%CI: 0.59-6.68, P=0.270), 5-year RFS (98.8% vs. 99.5%, HR=1.88, 95%CI: 0.56-6.31, P=0.307) and 5-year LCSS (99.9% vs. 99.6%, HR=1.76, 95%CI: 0.24-13.15, P=0.581). CONCLUSION: Intentional wedge resection is an appropriate choice for ≤2 cm GGO-dominant NSCLC.

Tet methylcytosine dioxygenase 2 (TET2) deficiency elicits EGFR-TKI (tyrosine kinase inhibitors) resistance in non-small cell lung cancer.

Despite epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKI) have shown remarkable efficacy in patients with EGFR-mutant non-small cell lung cancer (NSCLC), acquired resistance inevitably develops, limiting clinical efficacy. We found that TET2 was poly-ubiquitinated by E3 ligase CUL7FBXW11 and degraded in EGFR-TKI resistant NSCLC cells. Genetic perturbation of TET2 rendered parental cells more tolerant to TKI treatment. TET2 was stabilized by MEK1 phosphorylation at Ser 1107, while MEK1 inactivation promoted its proteasome degradation by enhancing the recruitment of CUL7FBXW11. Loss of TET2 resulted in the upregulation of TNF/NF-κB signaling that confers the EGFR-TKI resistance. Genetic or pharmacological inhibition of NF-κB attenuate the TKI resistance both in vitro and in vivo. Our findings exemplified how a cell growth controlling kinase MEK1 leveraged the epigenetic homeostasis by regulating TET2, and demonstrated an alternative path of non-mutational acquired EGFR-TKI resistance modulated by TET2 deficiency. Therefore, combined strategy exploiting EGFR-TKI and inhibitors of TET2/NF-κB axis holds therapeutic potential for treating NSCLC patients who suffered from this resistance.

Pulmonary blastoma is successfully treated with immunotherapy and targeted therapy.

Pulmonary blastomas (PB) are an extremely rare type of lung cancer. Currently, no standard treatment exists for PB. Immunotherapy with checkpoint inhibitors and anti-angiogenesis treatments has been an effective method for lung cancer; however, studies on PB treatment are lacking. Herein, we present a case report of successful conversion therapy with immunotherapy and targeted therapy for PB. After receiving treatment with a PD-1 inhibitor (penpulimab) and a multi-target tyrosine kinase inhibitor (anlotinib) treatment, the patient showed an impressive response and underwent a successful operation. We also summarized and reviewed literature reports on PubMed from January 1, 2000, to December 31, 2022, using the keyword "pulmonary blastoma", discussing the efficacy and specifics of chemotherapy and radiotherapy. Immunotherapy, in combination with targeted therapy, should be considered a potential therapeutic strategy for PB.

Perioperative outcomes of uniportal versus three-port video-assisted thoracoscopic surgery in lung cancer patients aged ≥ 75 years old: a cohort study.

BACKGROUND: Increasing attention has been raised on the surgical option for lung cancer patients aged ≥75 years, however, few studies have focused on whether uniportal video-assisted thoracoscopic surgery (VATS) is safe and feasible for these patients. This study aimed to evaluate short-term results of uniportal versus three-port VATS for the treatment of lung cancer patients aged ≥75 years. METHODS: We retrospectively evaluated 582 lung cancer patients (≥75 years) who underwent uniportal or three-port VATS from August 2007 to August 2021 based on the Western China Lung Cancer Database. The baseline and perioperative outcomes between uniportal and three-port VATS were compared in the whole cohort (WC) and the patients undergoing lobectomy (lobectomy cohort, LC) respectively. Propensity score matching (PSM) was used to minimize confounding bias between the uniportal and three-port cohorts in WC and LC. RESULTS: Intraoperative blood loss was significantly less in the uniportal than three-port LC (50 mL vs. 83 mL, P = 0.007) before PSM and relatively less in the uniportal than three-port LC (50 mL vs. 83 mL, P = 0.05) after PSM. Significantly more lymph nodes harvested (13 vs. 9, P = 0.007) were found in the uniportal than three-port LC after PSM. In addition, in WC and LC, there were no significant differences between uniportal and three-port cohorts in terms of operation time, the rate of conversion to thoracotomy during surgery, nodal treatments (dissection or sampling or not), the overall number of lymph node stations dissected, postoperative complications, volume and duration of postoperative thoracic drainage, hospital stay after operation and hospitalization expenses before and after PSM (P > 0.05). CONCLUSIONS: There were no significant differences in short-term outcomes between uniportal and three-port VATS for lung cancer patients (≥75 years), except relatively less intraoperative blood loss (P < 0.05 before PSM and P = 0.05 after PSM) and significantly more lymph nodes harvested (P < 0.05 after PSM) were found in uniportal LC. It is reasonable to indicate that uniportal VATS is a safe, feasible and effective operation procedure for lung cancer patients aged ≥75 years.

Correction: Pu et al. Exosome miRNA Expression in Umbilical Cord Blood of High-Parity Sows Regulates Their Reproductive Potential. Animals 2022, 12, 2456.

In the original publication [...].

Endothelial H2S-AMPK dysfunction upregulates the angiocrine factor PAI-1 and contributes to lung fibrosis.

Dysfunction of the vascular angiocrine system is critically involved in regenerative defects and fibrosis of injured organs. Previous studies have identified various angiocrine factors and found that risk factors such as aging and metabolic disorders can disturb the vascular angiocrine system in fibrotic organs. One existing key gap is what sense the fibrotic risk to modulate the vascular angiocrine system in organ fibrosis. Here, using human and mouse data, we discovered that the metabolic pathway hydrogen sulfide (H2S)-AMP-activated protein kinase (AMPK) is a sensor of fibrotic stress and serves as a key mechanism upregulating the angiocrine factor plasminogen activator inhibitor-1 (PAI-1) in endothelial cells to participate in lung fibrosis. Activation of the metabolic sensor AMPK was inhibited in endothelial cells of fibrotic lungs, and AMPK inactivation was correlated with enriched fibrotic signature and reduced lung functions in humans. The inactivation of endothelial AMPK accelerated lung fibrosis in mice, while the activation of endothelial AMPK with metformin alleviated lung fibrosis. In fibrotic lungs, endothelial AMPK inactivation led to YAP activation and overexpression of the angiocrine factor PAI-1, which was positively correlated with the fibrotic signature in human fibrotic lungs and inhibition of PAI-1 with Tiplaxtinin mitigated lung fibrosis. Further study identified that the deficiency of the antioxidative gas metabolite H2S accounted for the inactivation of AMPK and activation of YAP-PAI-1 signaling in endothelial cells of fibrotic lungs. H2S deficiency was involved in human lung fibrosis and H2S supplement reversed mouse lung fibrosis in an endothelial AMPK-dependent manner. These findings provide new insight into the mechanism underlying the deregulation of the vascular angiocrine system in fibrotic organs.

Differential response of Hg-methylating and MeHg-demethylating microbiomes to dissolved organic matter components in eutrophic lake water.

Methylmercury (MeHg) production in aquatic ecosystems is a global concern because of its neurotoxic effect. Dissolved organic matter (DOM) plays a crucial role in biogeochemical cycling of Hg. However, owing to its complex composition, the effects of DOM on net MeHg production have not been fully understood. Here, the Hg isotope tracer technique combined with different DOM treatments was employed to explore the influences of DOM with divergent compositions on Hg methylation/demethylation and its microbial mechanisms in eutrophic lake waters. Our results showed that algae-derived DOM treatments enhanced MeHg concentrations by 1.42-1.53 times compared with terrestrial-derived DOM. Algae-derived DOM had largely increased the methylation rate constants by approximately 1-2 orders of magnitude compared to terrestrial-derived DOM, but its effects on demethylation rate constants were less pronounced, resulting in the enhancement of net MeHg formation. The abundance of hgcA and merB genes suggested that Hg-methylating and MeHg-demethylating microbiomes responded differently to DOM treatments. Specific DOM components (e.g., aromatic proteins and soluble microbial byproducts) were positively correlated with both methylation rate constants and the abundance of Hg-methylating microbiomes. Our results highlight that the DOM composition influences the Hg methylation and MeHg demethylation differently and should be incorporated into future Hg risk assessments in aquatic ecosystems.

Wildland Fires Worsened Population Exposure to PM2.5 Pollution in the Contiguous United States.

As wildland fires become more frequent and intense, fire smoke has significantly worsened the ambient air quality, posing greater health risks. To better understand the impact of wildfire smoke on air quality, we developed a modeling system to estimate daily PM2.5 concentrations attributed to both fire smoke and nonsmoke sources across the contiguous U.S. We found that wildfire smoke has the most significant impact on air quality in the West Coast, followed by the Southeastern U.S. Between 2007 and 2018, fire smoke contributed over 25% of daily PM2.5 concentrations at ∼40% of all regulatory air monitors in the EPA's air quality system (AQS) for more than one month per year. People residing outside the vicinity of an EPA AQS monitor (defined by a 5 km radius) were subject to 36% more smoke impact days compared with those residing nearby. Lowering the national ambient air quality standard (NAAQS) for annual mean PM2.5 concentrations to between 9 and 10 µg/m3 would result in approximately 35-49% of the AQS monitors falling in nonattainment areas, taking into account the impact of fire smoke. If fire smoke contribution is excluded, this percentage would be reduced by 6 and 9%, demonstrating the significant negative impact of wildland fires on air quality.

Wildfire worsens population exposure to PM2.5 pollution in the Continental United States.

As wildfires become more frequent and intense, fire smoke has significantly worsened ambient air quality, posing greater health risks. To better understand the impact of wildfire smoke on air quality, we developed a modeling system to estimate daily PM2.5 concentrations attributed to both fire smoke and non-smoke sources across the Continental U.S. We found that wildfire smoke has the most significant impact on air quality in the West Coast, followed by the Southeastern U.S. Between 2007 and 2018, fire smoke affected daily PM2.5 concentrations at 40% of all regulatory air monitors in EPA's Air Quality System (AQS) for more than one month each year. People residing outside the vicinity of an EPA AQS monitor were subject to 36% more smoke impact days compared to those residing nearby. Lowering the national ambient air quality standard (NAAQS) for annual mean PM2.5 concentrations to between 9 and 10 µg/m3 would result in approximately 29% to 40% of the AQS monitors falling in nonattainment areas without taking into account the contribution from fire smoke. When fire smoke impact is considered, this percentage would rise to 35% to 49%, demonstrating the significant negative impact of wildfires on air quality.

The divergent effects of nitrate and ammonium application on mercury methylation, demethylation, and reduction in flooded paddy slurries.

The production of methylmercury (MeHg) in flooded paddy fields determines its accumulation in rice grains; this, in turn, results in MeHg exposure risks for not only rice-eating humans but also wildlife. Nitrogen (N) fertilizers have been widely applied in rice cultivation fields to supply essential nutrients. However, the effects of N fertilizer addition on mercury (Hg) transformations are not unclear. This limits our understanding of MeHg formation in rice paddy ecosystems. In this study, we spiked three Hg tracers (200HgII, Me198Hg, and 202Hg0) in paddy slurries fertilized with urea, ammonium, and nitrate. The influences of N fertilization on Hg methylation, demethylation, and reduction and the underlying mechanisms were elucidated. The results revealed that dissimilatory nitrate reduction was the dominant process in the incubated paddy slurries. Nitrate addition inhibited HgII reduction, HgII methylation, and MeHg demethylation. Competition between nitrates and other electron acceptors (e.g., HgII, sulfate, or carbon dioxide) under dark conditions was the mechanism underlying nitrate-regulated Hg transformation. Ammonium and urea additions promoted HgII reduction, and anaerobic ammonium oxidation coupled with HgII reduction (Hgammox) was likely the reason. This work highlighted that nitrate addition not only inhibited HgII methylation but also reduced the demethylation of MeHg and therefore may generate more accumulation of MeHg in the incubated paddy slurries. Findings from this study link the biogeochemical cycling of N and Hg and provide crucial knowledge for assessing Hg risks in intermittently flooded wetland ecosystems.

Comparison of uniport versus triport thoracoscopic single or combined basal segmentectomy for stage IA lung cancer.

Background: Single or combined basal segmentectomy (CBS), excluding common basal segmentectomy, is the most difficult of all types of segmentectomies. The purpose of this study was to compare the perioperative outcomes and oncological prognosis between uniport thoracoscopic basal segmentectomy (UTBS) and triport thoracoscopic basal segmentectomy (TTBS). Methods: This study retrospectively collected 300 patients who underwent thoracoscopic single or CBS at the West China Hospital of Sichuan University from April 2015 to May 2022, including 67 and 233 patients in the UTBS and TTBS groups, respectively. Propensity score matching (PSM) was used to reduce confounding bias between the two groups. The primary outcome was recurrence-free survival (RFS). The secondary outcomes were overall survival (OS) and perioperative outcomes. Results: After PSM, the UTBS group (n=64) had significantly less intraoperative blood loss than the TTBS group (n=64) (20 vs. 30 mL, P=0.001). Other perioperative outcomes, including the operation time, number of lymph nodes and lymph node stations harvested, duration of chest tube drainage, postoperative hospital stay, and postoperative complications, were comparable. Subgroup analysis demonstrated that the operative time in the group underwent single basal segmentectomy (SBS) was significantly shorter compared to the group underwent CBS (110 vs. 120 min, P=0.002). There were 5 cases of recurrence in the overall cohort and no recurrence in the matched cohort. No deaths were observed in the overall cohort. Therefore, a survival analysis was conducted only for RFS in the overall cohort. The RFS rate and OS rate of the overall cohort were 98.3% and 100%, respectively. The surgical approach (UTBS vs. TTBS) was not an independent risk factor for RFS (HR: 1.120, 95% CI: 0.342-13.051, P=0.879). Conclusions: UTBS provided similar perioperative outcomes and oncological prognoses compared to TTBS.

Systematic review and meta-analysis of segmentectomy vs. lobectomy for stage IA non-small cell lung cancer.

Background: Whether segmentectomy is appropriate for stage IA non-small cell lung cancer (NSCLC), especially for stage IA NSCLC with a tumor size of 2-3 cm, remains controversial. Thus, we conducted this meta-analysis to compare segmentectomy and lobectomy for stage IA NSCLC with a tumor size of 2-3 cm and IA ≤2 cm NSCLC. Methods: A systematic screening of online databases (PubMed, Embase, Web of Science, and Cochrane Library) was conducted regarding the terms of perioperative outcomes, overall survival (OS), recurrence-free survival (RFS), and disease-free survival (DFS). The inverse-variance and Mantel-Haenszel approaches were used to pool effect sizes for survival outcomes and perioperative outcomes. Results: A total of 10 articles were included in the analysis. The perioperative morbidity [risk ratio (RR): 0.90, P=0.10], mortality (RR: 0.94, P=0.84), intraoperative blood loss [mean difference (MD): 3.07, P=0.86] and operative time (MD: 18.99, P=0.13) were comparable between the segmentectomy and lobectomy groups. The number of lymph nodes harvested was statistically less in segmentectomy than in lobectomy (MD: -5.71, P=0.02). In stage IA patients with a tumor size of 2-3 cm, lobectomy showed superior survival outcomes compared to segmentectomy, with a pooled hazard ratio (HR) of 1.39 (P=0.01) for OS and 1.38 (P=0.06) for RFS or DFS. In stage IA ≤2 cm, lobectomy and segmentectomy had comparable survival outcomes with pooled HRs of 1.18 (P=0.29) for OS and 1.18 (P=0.12) for RFS or DFS. Conclusions: When a patient is in stage IA and the tumor size is less than 2 cm, segmentectomy should be performed. If the tumor size is between 2 and 3 cm, lobectomy is recommended.

Selenium-binding protein 1 inhibits malignant progression and induces apoptosis via distinct mechanisms in non-small cell lung cancer.

BACKGROUND: Selenium is an essential trace element in the human body. In epidemiological and clinical studies, Se supplementation significantly reduced the incidence of lung cancer in individuals with low baseline Se levels. The significant action of selenium is based on the selenium-containing protein as a mediator. Of note, the previous studies reported that the expression of selenium-binding protein 1 (SELENBP1) was obviously decreased in many human cancer tissues including non-small cell lung cancer (NSCLC). However, its roles in the origin and development of NSCLC are still unclear. METHODS: The expression of SELENBP1 was measured by qRT-PCR, Western blotting and IHC in our collected clinical NSCLC tissues and cell lines. Next, the CCK-8, colony formation, wound-haeling, Millicell, Transwell, FCM assay, and in vivo xenograft model were performed to explore the function of SELENBP1 in NSCLC. The molecular mechanisms of SELENBP1 were investigated by Western blotting or IF assay. RESULTS: We further identified that the expression of SELENBP1 was significantly decreased in NSCLC tissues in TCGA database and 45 out of 59 collected clinical NSCLC tissues compared with adjacent nontumor tissues, as well as in four NSCLC cell lines compared with normal lung cells. Particularly, we unexpectedly discovered that SELENBP1 was obviously expressed in alveolar type 2 (AT-II) cells for the first time. Then, a series of in vitro experiments uncovered that overexpression of SELENBP1 inhibited the proliferation, migration, and invasion of NSCLC cells, and induced cell apoptosis. Moreover, overexpression of SELENBP1 also inhibited growth and induced apoptosis of NSCLC cells in vivo. Mechanistically, we demonstrated that overexpression of SELENBP1 inhibited the malignant characteristics of NSCLC cells in part via inactivating the PI3K/AKT/mTOR signal pathway. Meanwhile, we found that overexpression of SELENBP1 inducing the apoptosis of NSCLC cells was associated with the activation of caspase-3 signaling pathway under nonhigh level of oxidative stress, but overexpression of SELENBP1 facilitating the cell apoptosis might be related to its combining with GPX1 and colocalizing in the nucleus under high level of oxidative stress. CONCLUSIONS: Our findings highlighted that SELENBP1 was an important tumor suppressor during the origin and development of NSCLC. It may help to discover novel biomarkers or drug therapy targets for NSCLC.

Metformin attenuates chronic lung allograft dysfunction: evidence in rat models.

BACKGROUND: Chronic lung allograft dysfunction (CLAD) directly causes an abysmal long-term prognosis after lung transplantation (LTx), but effective and safe drugs are not available. Metformin exhibits high therapeutic potential due to its antifibrotic and immunomodulatory effects; however, it is unclear whether metformin exerts a therapeutic effect in CLAD. We sought to investigate the effect of metformin on CLAD based on rat models. METHODS: Allogeneic LTx rats were treated with Cyclosporin A (CsA) in the first week, followed by metformin, CsA, or vehicle treatment. Syngeneic LTx rats received only vehicles. All rats were sacrificed on post-transplant week 4. Pathology of lung graft, spleen, and thymus, extent of lung fibrosis, activity of profibrotic cytokines and signaling pathway, adaptive immunity, and AMPK activity were then studied. RESULTS: Allogeneic recipients without maintenance CsA treatment manifested CLAD pathological characteristics, but these changes were not observed in rats treated with metformin. For the antifibrotic effect, metformin suppressed the fibrosis extent and profibrotic cytokine expression in lung grafts. Regarding immunomodulatory effect, metformin reduced T- and B-cell infiltration in lung grafts, spleen and thymus weights, the T- and B-cell zone areas in the spleen, and the thymic medullary area. In addition, metformin activated AMPK in lung allografts and in α-SMA+ cells and T cells in the lung grafts. CONCLUSIONS: Metformin attenuates CLAD in rat models, which could be attributed to the antifibrotic and immunomodulatory effects. AMPK activation suggests the potential molecular mechanism. Our study provides an experimental rationale for further clinical trials.

Risk-based screening for second primary extrapulmonary malignancies in stage I lung cancer patients: A study based on SEER database.

OBJECTIVES: We conducted this study to identify the risk for second primary malignancy (SPM), especially for second primary extrapulmonary malignancy (SPEM), in resected stage I lung cancer patients. MATERIALS AND METHODS: Resected stage I lung cancer patients were retrospectively enrolled from the SEER database (2008-2017). Standardized incidence ratio (SIR) was used to evaluate the relative risk of SPM of patients as compared to general population. Competing risk model was utilized to identify the risk factors for SPEM of increased risk (rSPEM). A simplified nomogram based on the factors was developed to stratify patients at different risks of rSPEM. RESULTS: A total of 14,495 patients were enrolled, and 1779 (12.27%) patients developed SPM during follow-up, of which 896 (50.37%) were SPEM. Enrolled patients had higher risk of SPM than general population (SIR: 1.92, 95% CI: 1.83 - 2.01). The yearly morbidity of SPM was about 3% - 4% over time. The three most frequent SPEM were prostate cancer, breast cancer, and urinary bladder cancer. The competing-risk multivariable analysis showed that increasing age, male, and white race were independent risk factors for rSPEM. The simplified nomogram showed favorable performance in stratifying patients at different risks of rSPEM (P < 0.001). CONCLUSION: The risk of SPM in stage I lung cancer patients was high. Risk factors for rSPEM were identified and the corresponding simplified nomogram based on the risk factors could discriminate patients at different risks well. The nomogram might help physicians to make more appropriate screening strategy for the SPEM.

Mercury and Sulfur Redox Cycling Affect Methylmercury Levels in Rice Paddy Soils across a Contamination Gradient.

Methylmercury (MeHg) contamination in rice via paddy soils is an emerging global environmental issue. An understanding of mercury (Hg) transformation processes in paddy soils is urgently needed in order to control Hg contamination of human food and related health impacts. Sulfur (S)-regulated Hg transformation is one important process that controls Hg cycling in agricultural fields. In this study, Hg transformation processes, such as methylation, demethylation, oxidation, and reduction, and their responses to S input (sulfate and thiosulfate) in paddy soils with a Hg contamination gradient were elucidated simultaneously using a multi-compound-specific isotope labeling technique (200HgII, Me198Hg, and 202Hg0). In addition to HgII methylation and MeHg demethylation, this study revealed that microbially mediated reduction of HgII, methylation of Hg0, and oxidative demethylation-reduction of MeHg occurred under dark conditions; these processes served to transform Hg between different species (Hg0, HgII, and MeHg) in flooded paddy soils. Rapid redox recycling of Hg species contributed to Hg speciation resetting, which promoted the transformation between Hg0 and MeHg by generating bioavailable HgII for fuel methylation. Sulfur input also likely affected the microbial community structure and functional profile of HgII methylators and, therefore, influenced HgII methylation. The findings of this study contribute to our understanding of Hg transformation processes in paddy soils and provide much-needed knowledge for assessing Hg risks in hydrological fluctuation-regulated ecosystems.

Perioperative and oncological outcomes of uniportal versus three-port thoracoscopic segmentectomy for lung cancer: a propensity score matching analysis.

Background: With an increasing amount of small nodules being detected, segmentectomy has recently received a great deal of attention. We have previously reported the feasibility and safety of uniportal segmentectomy. This study aims to further compare the perioperative and oncological outcomes of uniportal and three-port thoracoscopic segmentectomy in lung cancer patients. Methods: Patients undergoing thoracoscopic segmentectomy for lung cancer from January 2014 to March 2021 were enrolled. Clinical data were collected from the Western China Lung Cancer Database, a prospectively maintained database at the Department of Thoracic Surgery, West China Hospital. Propensity score matching (PSM) was used to reduce the heterogeneity in baseline characteristics. Perioperative outcomes, 1-, 3-, and 5-year overall survival (OS), and progression-free survival (PFS) were compared. Results: Of the 10,063 lung cancer patients who underwent thoracoscopic lung resection, 2,630 patients receiving segmentectomy were selected (uniportal: 400; three-port: 2,230). After matching, similar results were found between the 2 groups (uniportal: 400; three-port: 1,200) regarding the number of lymph nodes harvested, the length of postoperative hospital stays, chest tube drainage volume, and postoperative complication rate. The mean follow-up duration was 27 months. Uniportal regimen showed similar 1- (100% vs. 99.9%, P=0.36), 3- (100% vs. 90.4%, P=0.20), 5-year OS (97.7% vs. 99.4%, P=0.78), as well as PFS, with the three-port regimen. Conclusions: Uniportal video-assisted thoracoscopic segmentectomy is proven to be safe and feasible, and the perioperative outcomes and oncological results were similar between the uniportal and three-port regimens.