The mitochondrial calcium uniporter of pulmonary type 2 cells determines severity of acute lung injury.

Acute Lung Injury (ALI) due to inhaled pathogens causes high mortality. Underlying mechanisms are inadequately understood. Here, by optical imaging of live mouse lungs we show that a key mechanism is the viability of cytosolic Ca buffering by the mitochondrial Ca uniporter (MCU) in the lung's surfactant-secreting, alveolar type 2 cells (AT2).

The Mitochondrial Calcium Uniporter of Pulmonary Type 2 Cells Determines Severity of ARDS.

Acute lung immunity to inhaled pathogens elicits defensive pneumonitis that may convert to the Acute Respiratory Distress Syndrome (ARDS), causing high mortality. Mechanisms underlying the conversion are not understood, but are of intense interest because of the ARDS-induced mortality in the ongoing Covid-19 pandemic. Here, by optical imaging of live lungs we show that key to the lethality is the functional status of mitochondrial Ca2+ buffering across the mitochondrial Ca2+ uniporter (MCU) in the alveolar type 2 cells (AT2), which protect alveolar stability.

Dual-port distal gastrectomy for the early gastric cancer.

Background: Although recent trends in laparoscopic procedures have been toward minimizing the number of incisions, four or five ports are normally required to complete laparoscopic gastrectomy because of the complexity of this procedure. Multi-channel ports, such as the SILS port (Covidien, JAPAN), are now available and are crucial for performing single-incision laparoscopic surgery (SILS) or reduced port surgery (RPS). We carried out reduced port distal gastrectomy (RPDG) using a dual-port method with a SILS port.

F-actin scaffold stabilizes lamellar bodies during surfactant secretion.

Alveolar type 2 (AT2) cells secrete surfactant that forms a protective layer on the lung's alveolar epithelium. Vesicles called lamellar bodies (LBs) store surfactant. Failure of surfactant secretion, which causes severe lung disease, relates to the manner in which LBs undergo exocytosis during the secretion.

Acid contact in the rodent pulmonary alveolus causes proinflammatory signaling by membrane pore formation.

Although gastric acid aspiration causes rapid lung inflammation and acute lung injury, the initiating mechanisms are not known. To determine alveolar epithelial responses to acid, we viewed live alveoli of the isolated lung by fluorescence microscopy, then we microinjected the alveoli with HCl at pH of 1.5.

Connexin 43 mediates spread of Ca2+-dependent proinflammatory responses in lung capillaries.

Acute lung injury (ALI), which is associated with a mortality of 30-40%, is attributable to inflammation that develops rapidly across the lung's vast vascular surface, involving an entire lung or even both lungs. No specific mechanism explains this extensive inflammatory spread, probably because of the lack of approaches for detecting signal conduction in lung capillaries. Here, we addressed this question by applying the photolytic uncaging approach to induce focal increases in Ca2+ levels in targeted endothelial cells of alveolar capillaries.

[A case of spindle cell type hepatocellular carcinoma responding to hepatic intra-arterial infusion chemotherapy].

We report herein a case of spindle cell type hepatocellular carcinoma responding to hepatic intra-arterial infusion chemotherapy. A 50-year-old woman was hospitalized for right epigastralgia. A computed tomography scan demonstrated cloudy liver tumor with a diameter of 12 cm in S5 and S8.