Accurate measurement of the minimum distance between bony structures of the humeral head and the acromion or coracoid helps advance a better understanding of the shoulder anatomical features. Our goal was to precisely determine the minimum acromiohumeral distance (AHD), coracohumeral distance (CHD), and glenohumeral distance (GHD) in a sample of the Chinese population as an in vivo anatomical analysis. We retrospectively included 146 patients who underwent supine computed tomography (CT) examination of the shoulder joint. The minimum AHD, CHD, and GHD values were quantitatively measured using three-dimensional (3D) CT reconstruction techniques. The correlation between minimum AHD, CHD, and GHD value and age with different sexes was evaluated using Pearson Correlation Coefficient. The mean value of minimum AHD in males was greater than that in females (male 7.62 ± 0.98 mm versus female 7.27 ± 0.86 mm, p = 0.046). The CHD among different sexes differed significantly (male 10.75 ± 2.40 mm versus female 8.76 ± 1.38 mm, p < 0.001). However, we found no statistical differences in GHD with different sexes (male 2.00 ± 0.31 mm versus female 1.96 ± 0.36 mm, p > 0.05). In terms of age correlation, a negative curve correlation existed between age and AHD among the different sexes (male R2 = 0.124, p = 0.030, female R2 = 0.112, p = 0.005). A negative linear correlation was found in CHD among the different sexes (male R2 = 0.164, p < 0.001, female R2 = 0.122, p = 0.005). There were no differences between age and minimum GHD in both sexes. The 3D CT reconstruction model can accurately measure the minimum AHD, CHD, and GHD value in vivo and is worthy of further investigation for standard clinical anatomical assessment. Aging may correlate with AHD and CHD narrowing for both sexes.
Ferroptosis has emerged as a deliberate type of programmed cell death that manifests marked importance ubiquitously in health and diseases. However, after a decade of research, the mechanisms of ferroptosis execution remain unclear. Here we identify chloride ions (Cl-) as essential determinants of ferroptosis. Water homeostasis manipulated by extracellular solute concentration disrupts ferroptotic cell death. Hyperosmotic stress attenuates ferroptosis and endues cells with high lipid peroxidation. Analyses of a fluorescent chloride probe show that Cl- fluxes into the cytoplasm during ferroptosis, substantiating a role for Cl- to drive water flow. Depletion of extracellular chloride ions ([Cl-]o) from culture media congruously confers resistance to ferroptosis. The [Cl-]o-depleted ferroptotic cells fall into two populations: cells with low lipid peroxidation; cells with high lipid peroxidation but not cell swelling or cell rupture. Contrarily, solitary [Cl-]o overload is sufficient to elicit ferroptosis without canonical ferroptosis inducers. Further experiments show that ferroptotic cells depolarize and [Cl-]o is positively correlated with this process. Membrane depolarization upregulates the level of lipid peroxidation, suggesting that membrane potential may be a universal mechanism governing ferroptosis. Together, our findings reveal that ferroptosis is determined by chloride ions.
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