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Ocean-derived dimethyl sulfide (DMS) is widely concerning because of its hypothesized influence on global climate change. This study aims to explore the distribution characteristics and influencing factors of DMS and partial pressure of carbon dioxide (pCO2) in the Northwest Pacific Ocean, as well as the potential relationship between DMS and pCO2. A high-resolution, underway, shipboard measurement device was used to determine the DMS and pCO2 of the surface seawater and atmosphere in the Northwest Pacific and its marginal seas during November 2019. The result show that atmospheric and surface seawater DMS concentrations ranged from 3 to 125 pptv and 0.63 to 2.28 nmol L-1, respectively, with mean values of 46 ± 19 pptv and 1.08 ± 0.34 nmol L-1. The average sea surface pCO2 was 371 ± 16 μatm (range from 332 to 401 μatm). The trends in the surface seawater DMS in different current systems were primarily associated with phytoplankton abundance and composition. Biological activity and physical processes such as cooling jointly influenced the sea surface pCO2. A cold eddy along the transect in the Northwest Pacific Ocean increased DMS at the sea surface by 10% and CO2 uptake by 3%. We found a significant negative correlation between DMS and pCO2 in the Northwest Pacific Ocean at the 0.1° resolution [DMS]seawater = -0.0161[pCO2]seawater + 7.046 (R2 = 0.569, P < 0.01). The DMS and pCO2 sea-air fluxes were estimated to range from 0.04 to 25.3 μmol m-2·d-1 and from -27.0 to 4.22 mmol m-2·d-1 throughout the survey area. The Northwest Pacific Ocean, especially the Oyashio Current, is an important sink of CO2 and a source of DMS.

Massive pulmonary embolism (MPE) is a high-risk medical emergency. Seizure as the clinical presentation of MPE is extremely rare, and to our knowledge, there have been no reports on successful percutaneous, catheter-based treatment of MPE presenting with new-onset seizures and cardiac arrest. In this report, we discuss the case of a 64-year-old woman who presented with an episode of seizure that lasted 5 h. Seizure occurred four times within 12 h after arrival at the hospital, and in the end, she sustained a cardiac arrest. The patient had no past history of seizure or cardiopulmonary disease. Bilateral MPE was detected by a computed tomography pulmonary angiogram, and she was successfully treated with percutaneous, catheter-directed anticoagulant therapy. Pulmonary embolism-related seizures are more difficult to diagnose and have higher mortality rates than seizures. MPE should be suspected in patients presenting with new-onset seizures and hemodynamic instability.

Although diabetic cognitive impairment is one of the most common complications of type 2 diabetes mellitus (T2DM), optimized therapeutic strategies are not available yet. Astragalosides IV (AS-IV) is a traditional Chinese medicine possessing diverse pharmacological properties including anti-inflammatory and antioxidant effects. However, the effects of AS-IV on diabetes-related cognitive impairment and its precise mechanisms remain largely unknown. T2DM mice, induced by a high-fat diet (HFD) and an intraperitoneal injection of low-dose streptozotocin (STZ) were administrated with AS-IV every other day for eight consecutive weeks. Learning and memory abilities were assessed subsequently using the Ymaze test and the anxious behavior was evaluated using an open field test. Then, the morphology and number of neurons and microglia were observed by HE staining or immunohistochemistry. Oxidative stress biomarkers and pro-inflammatory cytokines were determined using relevant kits. In addition, the expression levels of Nrf2, Keap1, HO-1, and NQO1 were determined by Western blot analyses. The results indicated that AS-IV administration significantly improved neuronal damage and cognitive deficit in T2DM mice. Meanwhile, oxidative stress and neuroinflammation were also ameliorated in T2DM mice, which might be attributed to the regulation of Nrf2/Keap1/HO-1/NQO1 pathway in T2DM mice. Taken together, these data suggested that AS-IV ameliorates cognitive impairment in T2DM mice by attenuating oxidative stress and neuroinflammation, possibly through modulating the Nrf2/Keap1/HO1/NQO1 pathway.

BackgroundElderlies and tinnitus patients often find it challenging to process acoustic signals in noisy environments. The sensitivity to temporal fine structure (TFS), the transient storage capacity for TFS, and the ultra-high frequency (UHF) thresholds are all associated with aging-related damage, evidenced by speech-in-noise perception deficits. In the present study, we aimed to investigate the relationships among TFS sensitivity, transient storage capacity, and UHF thresholds in tinnitus patients and normal adults of different ages.MethodsIn the present study, 38 tinnitus patients (age ranging from 21 to 65) and 23 non-tinnitus adults (age ranging from 22 to 56) were enrolled, and some of their auditory indicators were examined, including the TFS-adaptive frequency (TFS-AF), break in interaural correlation (BIAC) delay threshold, and UHF thresholds.ResultsWe found no significant difference in TFS-AF thresholds and BIAC delay thresholds between the tinnitus group and normal group, while their relationships with age were more evident in the tinnitus group. Moreover, these two tests were only significantly correlated in the tinnitus group. UHF thresholds were significantly correlated with TFS-AF thresholds only in the tinnitus group, suggesting that the UHF hearing was positively associated with the TFS sensitivity.ConclusionThese findings indicated that the influencing factors, such as tinnitus and UHF thresholds, should be fully considered when examining age-related hearing decline, because the combination of tinnitus and poor UHF hearing might play a role in affecting hearing ability, such as TFS sensitivity.

Chondrocyte dysfunction is a key mechanism underlying osteoarthritis. Metformin has shown protective effects in many diseases. The present study aimed to investigate the effects of metformin on autophagy and apoptosis in the process of osteoarthritis. A mouse osteoarthritis model was set up by surgically destabilizing medial meniscus in the knee. Intraarticular injection of metformin or vehicle was applied in the right knee for eight weeks. Mouse articular chondrocytes were isolated and passaged for in vitro experiments. Small interfering RNA (siRNA) transfection was used to silence target genes. Western blotting, immunohistochemistry, transmission electron microscopy were used. After eight weeks, metformin restored surgery-induced upregulation of MMP13 and downregulation of type II collagen in the joint cartilage. In cultured primary murine chondrocytes, IL-1β aggravated apoptosis and catabolic response in a dose-dependent manner. In the presence of IL-1β, metformin increased phosphorylated levels of AMPKα and upregulated SIRT1 protein expression, leading to an increase in autophagy as well as a decrease in catabolism and apoptosis. Inactivating AMPKα or inhibiting SIRT1 prevented the augmented autophagy in the presence of metformin. Silencing AMPKα2, but not AMPKα1, reduced SIRT1 expression and downregulated autophagy in cultured chondrocytes. Metformin protects against IL-1β-induced extracellular matrix (ECM) degradation in cultured chondrocytes and in mouse osteoarthritis model through activating AMPKα/SIRT1 signaling. Metformin shed light on the treatment of osteoarthritis.