ObjectiveTo investigate the chemical hazards in the production line of lithium batteries, so as to provide a scientific basis for the management of occupational-health risk and to promote the healthy and sustainable development of the lithium battery industry. MethodsAn on-site survey on the process flow of the production of lithium battery was conducted in an enterprise. Volatile organic compounds (VOCs) in the occupational environment were collected by Summa canisters, carbonates and N-methyl pyrrolidone (NMP) were collected using activated carbon tubes, and airborne metals were collected using filter membranes. VOCs, carbonates and NMP were detected by gas chromatography-mass spectrometry (GC-MS), and airborne metal elements in the dust samples were analyzed by inductively coupled plasma mass spectrometry (ICP-MS). ResultsNon-targeted environmental monitoring results indicated that NMP was detected in the negative /positive electrode coating, assembly and drying filling workstations, dimethyl carbonate (DMC) was detected in the assembly, drying and electrolyte injection workstations, and ethyl methyl carbonate (EMC) was detected solely in the electrolyte injection workstation. Semi-quantitative analyses of VOCs identified 136 pollutants, including acrylonitrile and halohydrocarbons. Quantitative targeted environmental monitoring results revealed the highest geometric mean (GM) concentration of EMC (31.450 mg·m^-3) was found in the assembly and drying workstations, diethyl carbonate (DEC) was detected in all workstations. While vinylene carbonate (VC) and ethylene carbonate (EC) were detected only in electrolyte injection, assembly and drying workstations. NMP was detected in all positive electrode coating samples, with a GM concentration of 5.68 mg·m^-3 (concentration range: 4.0‒ 7.4 mg·m^-³). Lithium was exclusively detected in dust samples from the liquid injection workstation (GM: 0.014 μg·m^-³). ConclusionNMP, EMC, DEC, and other chemicals are identified at the key workstations such as the positive electrode coating, electrolyte injection, assembly and drying in the lithium production line. Furthermore, semi-quantitative VOCs analyses identified 136 pollutants, demonstrating a characteristic of multicomponent chemical exposure.

Objective:To develop a deep learning-based segmentation model MT-UNet to automatically segment bone metastases and benign bone lesions in bone scintigraphy with SPECT/CT.Methods:A total of 93 patients (48 males and 45 females, age 28-84 years) who underwent bone SPECT/CT in the Department of Nuclear Medicine, General Hospital of Northern Theater Command from June 2023 to December 2023 were enrolled retrospectively in this study, with a total of 184 bone lesions (94 benign lesions and 90 metastatic tumors). The MT-UNet was employed to segment bone lesions in SPECT, CT and SPECT/CT images respectively. Comparative analysis with 8 segmentation models was performed. The training set and validation set were divided by using 5-fold cross-validation and transfer learning was introduced to further enhance the robustness of the model. An additional cohort of 22 patients (15 males and 7 females, age 37-87 years) who received bone SPECT/CT in the Department of Nuclear Medicine, General Hospital of Northern Theater Command from April 2023 to May 2023 were included, comprising 40 bone lesions (22 benign lesions and 18 metastatic tumors) as the test set of MT-UNet. Segmentation performance of different models was assessed using accuracy, sensitivity, specificity, AUC, intersection over union and Dice similarity coefficient (DSC). Delong test was used to compare the segmentation efficacy among different models in the test set.Results:In the validation set, MT-UNet demonstrated DSC of 0.940, 0.962, and 0.963 for SPECT, CT, and SPECT/CT bone lesion segmentation, respectively, which were outperformed other models. Following transfer learning implementation, the SPECT/CT model′s DSC was improved to 0.984. In the test set, MT-UNet maintained comparable segmentation performance to the validation set, with significant AUC differences among the three models ( Z values: from -15.42 to -9.27, all P<0.01). Compared with conventional image interpretation, MT-UNet-based segmentation reduced physician interpretation time from 164min to 102min. Conclusion:MT-UNet has shown good performance in automatic segmentation of bone metastases and benign bone lesions, and is expected to become an important part of SPECT/CT image intelligent diagnosis system for bone metastases.

Objective:To evaluate the relationship between the mechanism of mild hypothermia-induced reduction of neuronal apoptosis during cerebral ischemia-reperfusion (I/R) and calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2)/adenosine monophosphate-activated protein kinase (AMPK) signaling pathway in rats.Methods:Forty SPF male Sprague-Dawley rats, aged 6-8 weeks, weighing 200-250 g, were divided into 5 groups ( n=8 each) using a random number table method: sham operation group (Sham group), cerebral I/R group (IR group), hypothermia + cerebral I/R group (HIR group), hypothermia + cerebral ischemia-reperfusion + solvent group (HIR-DMSO group) and hypothermia + ischemia-reperfusion + CaMKK2 inhibitor STO-609 group (HIR-STO609 group). A global cerebral I/R injury model was established using the four-vessel occlusion method. In HIR group, HIR-DMSO group, and HIR-STO609 group, an ice blanket was used to reduce the body temperature immediately after cerebral ischemia, bringing the core body temperature down to 32.5-33.5 ℃, and rewarming was carried out 4 h later. One hour before developing the model, STO-609 solution 4 μl was injected into the lateral ventricle in HIR-STO609 group, and the equal volume of dimethyl sulfoxide solution was given instead in HIR-DMSO group. At the end of reperfusion, the modified neurological severity score (mNSS) was performed. Then the rats were sacrificed under deep anesthesia, and the hippocampal tissues were taken to observe the pathological results of the hippocampal tissues (using HE staining and Nissl staining) and to determine the apoptosis rate of neurons (by TUNEL method) and expression of B-cell lymphoma 2(Bcl-2), Bcl-2-associated X (Bax), CaMKK2, phosphorylated AMPK (p-AMPK) and AMPK (by Western blot). Results:Compared with Sham group, the mNSS and apoptosis rate of neurons in the hippocampal tissues were significantly increased, the expression of Bax was up-regulated, the expression of Bcl-2, CaMKK2 and p-AMPK was down-regulated, and the ratio of p-AMPK/AMPK was decreased in IR group ( P<0.05). Compared with IR group, the mNSS and apoptosis rate of neurons in the hippocampal tissues were significantly decreased, the expression of Bax was down-regulated, the expression of Bcl-2, CaMKK2 and p-AMPK was up-regulated, and the ratio of p-AMPK/AMPK was increased in HIR group ( P<0.05). Compared with HIR group, the mNSS and apoptosis rate of neurons in the hippocampal tissues were significantly increased, the expression of Bax was up-regulated, the expression of Bcl-2, CaMKK2 and p-AMPK was down-regulated, the ratio of p-AMPK/AMPK was decreased ( P<0.05), and no significant change was found in the aforementioned parameters in HIR-DMSO group ( P>0.05). Conclusions:Mild hypothermia can inhibit neuronal apoptosis by up-regulating the CaMKK2/AMPK signaling pathway, thus reducing cerebral I/R injury in rats.

Objective:To evaluate the relationship between the mechanism of mild hypothermia-induced reduction of neuronal apoptosis during cerebral ischemia-reperfusion (I/R) and calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2)/adenosine monophosphate-activated protein kinase (AMPK) signaling pathway in rats.Methods:Forty SPF male Sprague-Dawley rats, aged 6-8 weeks, weighing 200-250 g, were divided into 5 groups ( n=8 each) using a random number table method: sham operation group (Sham group), cerebral I/R group (IR group), hypothermia + cerebral I/R group (HIR group), hypothermia + cerebral ischemia-reperfusion + solvent group (HIR-DMSO group) and hypothermia + ischemia-reperfusion + CaMKK2 inhibitor STO-609 group (HIR-STO609 group). A global cerebral I/R injury model was established using the four-vessel occlusion method. In HIR group, HIR-DMSO group, and HIR-STO609 group, an ice blanket was used to reduce the body temperature immediately after cerebral ischemia, bringing the core body temperature down to 32.5-33.5 ℃, and rewarming was carried out 4 h later. One hour before developing the model, STO-609 solution 4 μl was injected into the lateral ventricle in HIR-STO609 group, and the equal volume of dimethyl sulfoxide solution was given instead in HIR-DMSO group. At the end of reperfusion, the modified neurological severity score (mNSS) was performed. Then the rats were sacrificed under deep anesthesia, and the hippocampal tissues were taken to observe the pathological results of the hippocampal tissues (using HE staining and Nissl staining) and to determine the apoptosis rate of neurons (by TUNEL method) and expression of B-cell lymphoma 2(Bcl-2), Bcl-2-associated X (Bax), CaMKK2, phosphorylated AMPK (p-AMPK) and AMPK (by Western blot). Results:Compared with Sham group, the mNSS and apoptosis rate of neurons in the hippocampal tissues were significantly increased, the expression of Bax was up-regulated, the expression of Bcl-2, CaMKK2 and p-AMPK was down-regulated, and the ratio of p-AMPK/AMPK was decreased in IR group ( P<0.05). Compared with IR group, the mNSS and apoptosis rate of neurons in the hippocampal tissues were significantly decreased, the expression of Bax was down-regulated, the expression of Bcl-2, CaMKK2 and p-AMPK was up-regulated, and the ratio of p-AMPK/AMPK was increased in HIR group ( P<0.05). Compared with HIR group, the mNSS and apoptosis rate of neurons in the hippocampal tissues were significantly increased, the expression of Bax was up-regulated, the expression of Bcl-2, CaMKK2 and p-AMPK was down-regulated, the ratio of p-AMPK/AMPK was decreased ( P<0.05), and no significant change was found in the aforementioned parameters in HIR-DMSO group ( P>0.05). Conclusions:Mild hypothermia can inhibit neuronal apoptosis by up-regulating the CaMKK2/AMPK signaling pathway, thus reducing cerebral I/R injury in rats.

Objective:To develop a deep learning-based segmentation model MT-UNet to automatically segment bone metastases and benign bone lesions in bone scintigraphy with SPECT/CT.Methods:A total of 93 patients (48 males and 45 females, age 28-84 years) who underwent bone SPECT/CT in the Department of Nuclear Medicine, General Hospital of Northern Theater Command from June 2023 to December 2023 were enrolled retrospectively in this study, with a total of 184 bone lesions (94 benign lesions and 90 metastatic tumors). The MT-UNet was employed to segment bone lesions in SPECT, CT and SPECT/CT images respectively. Comparative analysis with 8 segmentation models was performed. The training set and validation set were divided by using 5-fold cross-validation and transfer learning was introduced to further enhance the robustness of the model. An additional cohort of 22 patients (15 males and 7 females, age 37-87 years) who received bone SPECT/CT in the Department of Nuclear Medicine, General Hospital of Northern Theater Command from April 2023 to May 2023 were included, comprising 40 bone lesions (22 benign lesions and 18 metastatic tumors) as the test set of MT-UNet. Segmentation performance of different models was assessed using accuracy, sensitivity, specificity, AUC, intersection over union and Dice similarity coefficient (DSC). Delong test was used to compare the segmentation efficacy among different models in the test set.Results:In the validation set, MT-UNet demonstrated DSC of 0.940, 0.962, and 0.963 for SPECT, CT, and SPECT/CT bone lesion segmentation, respectively, which were outperformed other models. Following transfer learning implementation, the SPECT/CT model′s DSC was improved to 0.984. In the test set, MT-UNet maintained comparable segmentation performance to the validation set, with significant AUC differences among the three models ( Z values: from -15.42 to -9.27, all P<0.01). Compared with conventional image interpretation, MT-UNet-based segmentation reduced physician interpretation time from 164min to 102min. Conclusion:MT-UNet has shown good performance in automatic segmentation of bone metastases and benign bone lesions, and is expected to become an important part of SPECT/CT image intelligent diagnosis system for bone metastases.

Objective:To evaluate the effect of panaxydol on ventilator-induced lung injury(VILI) in mice, and the relationship with Kelch-like ECH-associated protein 1 (Keap1)/nuclear factor E2-related factor 2 (Nrf2) signaling pathway.Methods:Fifty healthy clean-grade male C57BL/6 mice, aged 6-8 weeks, weighing 20-25 g, were divided into 5 groups ( n=10 each) using a random number table method: control group (group C), VILI group, low-dose panaxydol group (L-PX group, 5 mg/kg), medium-dose panaxydol group (M-PX group, 10 mg/kg) and high-dose panaxydol group (H-PX group, 20 mg/kg). The corresponding doses of panaxydol were intraperitoneally injected for 7 consecutive days once a day in L-PX group, M-PX group and H-PX group. The equal volume of normal saline was given instead in C group and VILI group. Only tracheotomy was performed and animals kept spontaneous breathing for 4 h in group C, and the animals were mechanically ventilated (tidal volume 30 ml/kg, respiratory rate 70 breaths/min, inspiratory/expiratory ratio 1∶2, fraction of inspired oxygen 21%) for 4 h in VILI, L-PX, M-PX and H-PX groups. Blood samples from the femoral artery were collected for arterial blood gas analysis at 4 h of ventilation, and PaO 2 was recorded. The mice were then sacrificed under deep anesthesia, and bronchoalveolar lavage fluid (BALF), lung tissues and serum samples were collected. The concentrations of TNF-α and IL-1β in BALF and serum were measured by enzyme-linked immunosorbent assay. The wet/dry lung weight (W/D) ratio was measured, the protein concentrations in BALF were measured by bicinchoninic acid assay, the pathological changes of lung tissues were examined by HE staining, lung injury was scored, and the level of ROS in lung tissues was detected by DCFH-DA fluorescence probe.The expression of Keap1 and Nrf2 in lung tissues was detected by Western blot. Results:Compared with group C, the PaO 2 was significantly decreased, the lung injury score, W/D ratio, protein concentrations in BALF and concentrations of TNF-α and IL-1β in BALF and serum were increased, the expression of Keap1 and Nrf2 was up-regulated, and the fluorescence of ROS was enhanced in the other four groups ( P<0.05). Compared with group VILI, PaO 2 was significantly increased, the lung injury score was decreased, lung W/D ratio, protein concentrations in BALF, and concentrations of TNF-α and IL-1 β in BALF and serum were decreased, and the fluorescence of ROS was weakened in L-PX, M-PX, and H-PX groups, and the expression of Keap1 was down-regulated, the fluorescence of ROS was weakened, and the expression of Nrf2 was up-regulated in M-PX and H-PX groups ( P<0.05). Compared with group L-PX, PaO 2 was significantly increased, the lung injury score, W/D ratio, protein concentrations in BALF and concentrations of TNF-α and IL-1β in BALF were decreased, the expression of Keap1 was down-regulated, and the expression of Nrf2 was up-regulated and the fluorescence of ROS was weakened in M-PX and H-PX groups ( P<0.05). Compared with group M-PX, PaO 2 was significantly increased, the lung injury score, W/D ratio, protein concentrations in BALF and concentrations of TNF-α and IL-1β in BALF were decreased, the expression of Keap1 was down-regulated, the expression of Nrf2 was up-regulated, and the fluorescence of ROS was weakened in H-PX group( P<0.05). Conclusions:Panaxydol can reduce VILI in mice, and the mechanism may be related to activation of the Keap1/Nrf2 signaling pathway and inhibition of oxidative stress.

Objective:To reveal the primary mechanism of changing permeability in DENV-2 infected pHDMECs. Methods:pHDMECs was incubated by DENV-2 on the concentration of 103 TCID50 ,and the penetrability of the cell was detected by Transwell at 4,8,12,24,48 h,respectively. Then,the partial sequence of DENV-2 NS1 was analyzed by Real time-PCR,and NS1 protein was detected by immunofluorescence and flow cytometer (FCM). The apoptosis rate of pHDMECs was assayed by FCM. Finally,IL-6 and IL-8 secreted by pHDMECs were analyzed by Real time-PCR and double antibody sandwich ELISA. Results:The relative expression of NS1 gene was elevated but NS1 protein was not detected;the permeability of DENV-2 infected pHDMECs had dramatically increased both at 24,48 h,but the apoptosis rate has little changed even been influenced by DENV-2 at 72 h. However,the relative expression of IL-6/IL-8 mRNA was boosted at 8,24 h[(2. 49±0. 50) and (6. 82±1. 69) fold,respectively,P<0. 05]. In protein level,compared with control(869. 6±50. 70)pg/ml,IL-6 secreted by DENV-2 infected pHDMECs could reach by(1 248. 8±86. 9)pg/ml(P<0. 05),and IL-8 was(1 331. 0±86. 3)pg/ml(P<0. 05) while the control was (967. 6±156. 6)pg/ml. Conclusion:Indeed,pHDMECs can be infected by DENV-2;the increasing permeability of DENV-2 infected pHDMECs may not be caused by the pHDMECs′ apoptosis but the enhancing of pro-inflammatory cytokine IL-6 /IL-8.

Objective To investigate the effects of dengue type 2 virus(DENV-2)on the apopto-sis and autophagy of primary human hepatic sinusoidal endothelial cells(HHSECs)and the expression of ICAM-1 and Beclin-1 at mRNA level and to analyze the possible pathogenic mechanism of DENV-2. Meth-ods Immunohistochemistry(IHC)and flow cytometry analysis(FCM)were performed to identify HHSECs by detecting factor Ⅷ and CD31. The DENV-2 strain was identified by using PCR and HindⅢ. The 50%tissue culture infective dose(TCID50 )of DENV-2 was calculated after infecting C6 / 36 cells with DENV-2. Dynamic changes of DENV-2 NS1 were measured by real-time PCR after infecting HHSECs with DENV-2. CCK-8 was used to dynamically detect the cytotoxicity of DENV-2 to HHSECs. The transcriptional levers of Beclin-1 and ICAM-1 in DENV-2-infected HHSECs were detected by real-time PCR. FCM was performed to analyze the apoptosis of HHSECs and the expression of LC3B and ICAM-1. Results The cells in the exper-imental group were stained brown by DAB and the positive expression rate of CD31 reached 87. 1% . The TICD50 of DENV-2 to C6 / 36 cells was 10-6. 845 / 0. 1 ml. Compared with the uninfected cells,partial se-quences of NS1 gene were expressed in DENV-2-infected HHSECs. DENV-2 suppressed the cell activities of HHSECs. The suppression rates of DENV-2 to HHSECs at 12 h,24 h,36 h and 48 h were respectively (10. 90±1. 24)% ,(16. 40±0. 42)% ,(17. 00±0. 46)% and(29. 60±0. 26)%(P﹤0. 05). The tran-scriptional levels of Beclin-1 and ICAM-1 in HHSECs were significantly increased at the time point of 24 h after DENV-2 infection,the 2-△△Ct values of which were 46. 77±2. 55 and 40. 97±4. 91,respectively. The expression of LC3B and ICAM-1 in DENV-2-infected HHSECs were increased,the peaks of which were reached at 24 h(14. 7% )and 36 h(35. 5% ),respectively. The apoptosis of DENV-2-infected HHSECs was remarkably enhanced at 12 h with an apoptosis rate of 13. 17% . Conclusion HHSECs was susceptible to DENV-2. DENV-2 induced the upregulation of ICAM-1 and the activation of HHSECs. Moreover,autoph-agy and apoptosis of HHSECs could also be induced by DENV-2.