SLC7A11-associated ferroptosis in acute injury diseases: mechanisms and strategies.

Ferroptosis is a kind of iron-dependent renewal programmed death. Its main mechanism is to catalyze the unsaturated fatty acids highly expressed on the cell membrane under the effect of divalent iron, to produce lipid peroxidation, thus inducing cell death. SLC7A11 is a known iron death-related factor. It has been proved that iron death is involved in the occurrence and development of acute diseases, but the specific mechanism is unknown. The purpose of this review is to highlight the regulatory properties of SLC7A11 and gain a deeper understanding of its role in ferroptosis-related acute injury diseases. This is a narrative review. PubMed was used as the main source to randomly implement literature search strategy to index Scopus articles. No specific terms are used. Studies have shown that SLC7A11 may affect the sensitivity of cells to iron ptosis by regulating it at the transcriptional or post-transcriptional level, which is related to the pathology of many acute injury diseases, such as acute lung injury (ALI), acute kidney injury (AKI), acute liver injury, myocardial ischemia-reperfusion injury, and acute cerebral hemorrhage. In order to clarify this point, more and more researchers turn their attention to the study of the specific mechanism between SLC7A11 and ferroptosis-related acute injury diseases. In summary, this review summarized some specific mechanisms by which ferroptosis could be controlled by SLC7A11 and clarified the underlying mechanisms of a series of diseases caused by SLC7A11-associated ferroptosis. It also provided more scientific justification for the clinical application of targeting ferroptosis in preventing and treating various diseases.

Visualizing dopamine released from living cells using a nanoplasmonic probe.

We report the development of an ultrasensitive nanoplasmonic probe for discriminative detection and imaging of dopamine released from living cells. The sensing mechanism is based on the dopamine-induced seeded-growth of Au nanoparticles (Au NPs) that leads to the shift of the plasmon band. This platform allows for the detection of dopamine with a detection limit down to 0.25 pM within 1 min. This nanoplasmonic assay is further applied to visualize the release of dopamine from living rat pheochromocytoma (PC12) cells under ATP-stimulation with dark-field microscopy (DFM). The DFM results together with real time fluorescence imaging of PC12 cells stained with the Fluo calcium indicator, suggested that ATP stimulated-release of dopamine is concomitant with the Ca(2+) influx, and the influx of Ca(2+) is through ATP-activated channels instead of the voltage-gated Ca(2+) channel (VGC).

Unexpected recurrent seizures following repeated spinal injections of tetracaine--a case report.

A 36-year-old male patient was scheduled to undergo ureteroscopic lithotomy because of left ureteral stone under spinal anesthesia. After receiving a renewed spinal anesthesia with 8 mg tetracaine to compensate for the first attempt (with 10 mg tetracaine), which proved to be a failure, he was soon seized with episodic seizure attacks. Central nervous system toxicity of the local anesthetic might be the cause of the seizure. We brought forward this case for discussion for warning that the possibility of systemic toxicity of local anesthetic might exist despite a seemingly undisputable spinal anesthesia.

Pneumocephalus and respiratory depression after accidental dural puncture during epidural analgesia--a case report.

A case of pneumocephalus and respiratory depression after dural puncture during lumbar epidural analgesia is reported. The loss of resistance to air technique was employed to identify the epidural space. Severe respiratory depression and stuporous consciousness developed one hour after a bolus of 2 mg morphine was given epidurally at the end of operation. With computerized tomographic brain scanning and continuous observation of clinical course, the neurologic symptoms were thought to be a mixed complication of pneumocephalus and possible intrathecal morphine overdose. We suggest that in order to avoid iatrogenic pneumocephalus by inadvertent dural puncture in the attempt to identify the epidural space the use of the loss of resistance to normal saline technique or the hanging-drop technique is more reliable than the loss of resistance to air technique. A small test dose prior to a full dose is given and should not be omitted to further confirm the proper placement of the epidural catheter during epidural analgesia.

Priming reversal of profound atracurium blockade by edrophonium and neostigmine.

Accelerated reversal of moderate neuromuscular blockade has been reported to be effective by giving anticholinesterase in divided doses (priming reversal). To evaluate its effectiveness in profound blockade, forty ASA physical status I or II patients were studied. After receiving 0.5mg/kg of atracurium during N2O-O2-halothane anesthesia, they were reversed at 5% spontaneous recovery of first twitch height (T1) measured by train-of-four (TOF) stimulation. Edrophonium 1mg/kg was administered intravenously either in a single bolus dose (Group I, n = 10) or in an initial priming dose of 0.2mg/kg followed one minute later by 0.8mg/kg (Group II, n = 10). Neostigmine 0.05mg/kg was administered in a single bolus dose (Group III, n = 10) or in divided priming dose of 0.01 mg/kg followed one minute later by 0.04mg/kg (Group IV, n = 10). The recovery time from the first injection of the reversal agents until the TOF ratio reached 75% was significantly longer (p < 0.05) in Group III (681.5 +/- 77.5 sec) compared to Groups I, II, and IV (451.3 +/- 72.3 sec, 470.6 +/- 39.8 sec, and 448.1 +/- 42.5 sec, respectively; no statistical difference among these three groups). It is concluded that priming reversal by neostigmine, but not edrophonium, produced a significantly faster recovery of profound atracurium blockade. Using the priming method, neostigmine may reach a similar recovery time as edrophonium in profound blockade under equipotent doses.

Fate of fossil fuel carbon dioxide and the global carbon budget.

The fate of fossil fuel carbon dioxide released into the atmosphere depends on the exchange rates of carbon between the atmosphere and three major carbon reservoirs, namely, the oceans, shallow-water sediments, and the terrestrial biosphere. Various assumptions and models used to estimate the global carbon budget for the last 20 years are reviewed and evaluated. Several versions of recent atmosphere-ocean models appear to give reliable and mutually consistent estimates for carbon dioxide uptake by the oceans. On the other hand, there is no compelling evidence which establishes that the terrestrial biomass has decreased at a rate comparable to that of fossil fuel combustion over the last two decades, as has been recently claimed.

Atmospheric carbon dioxide: its role in maintaining phytoplankton standing crops.

The rate of invasion of carbon dioxide into an artificially eutrophic Canadian Shield lake with insufficient internal sources of carbon was determined by two methods: measuring the carbon : nitrogen : phosphorus ratios of seston after weekly additions of nitrogen and phosphorus, and measuring the loss of radon-222 tracer from the epilimnion. Both methods gave an invasion rate of about 0.2 gram of carbon per square meter per day. The results demonstrate that invasion of atmospheric carbon dioxide may be sufficient to permit eutrophication of any body of water receiving an adequate supply of phosphorus and nitrogen.