Lung Type(肺型)到底是什麼？
Lung Type 肺型 - The whole bone Madelung type (as opposed to the distal type) and a distal radial notch were independent, significant predictors for the presence of the ligament. [1] The potential for biofuel development for the Nyamplung type is 10,130 hectares, with an area of 5,477 hectares in critical lands. [2] 0% for brain or lung type, 5. [3] Pleural and abdominal effusions were more common in chest, lung type and abdominal paragliasis, and serous effusion disappeared with the effect of deworming. [4]全骨Madelung型（與遠端型相反）和遠端橈切跡是韌帶存在的獨立重要預測因素。 [1] Nyampung 類型的生物燃料開發潛力為 10,130 公頃，關鍵土地面積為 5,477 公頃。 [2] 腦型或肺型為 0%，5。 [3] 胸腹腔積液多見於胸型、肺型和腹型膠質瘤，隨著驅蟲效果，漿液性積液消失。 [4]
Human Lung Type
Methods Human lung type II epithelial cells (A549) were transfected with NRP1 over-expression lentiviral vector and NRP1 inhibition vector to construct two cell models of NRP1high-A549 and NRP1low-A549. [1] The present study aimed to explore the role of endoplasmic reticulum calcium (ER Ca2+) in the apoptosis of human lung type II alveolar epithelial A549 cells induced by paraquat (PQ) in vitro. [2]方法 用NRP1過表達慢病毒載體和NRP1抑制載體轉染人肺II型上皮細胞（A549），構建NRP1high-A549和NRP1low-A549兩種細胞模型。 [1] 本研究旨在探討內質網鈣（ER Ca2+）在百草枯（PQ）誘導的人肺Ⅱ型肺泡上皮A549細胞凋亡中的作用。 [2]
lung type ius 肺型 Ius
Severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), the responsible agent for the coronavirus disease 2019 (Covid-19), has its entry point through interaction with angiotensin converting enzyme 2 (ACE2) receptors, highly expressed in lung type II alveolar cells and other tissues, like heart, pancreas, brain, and vascular endothelium. [1] Our study of lung type II pneumocyte cells (A549) demonstrated that ORF7, an open reading frame (ORF) in the genome of SARS-CoV-2, induced the production of CCL2, a chemokine that promotes the chemotaxis of monocytes, and decreased the expression of IL-8, a chemokine that recruits neutrophils. [2] SARS-CoV-2 infection of host cells is driven by binding of the SARS-CoV-2 spike-(S)-protein to lung type II pneumocytes, followed by virus replication. [3] Rat lung Type II epithelial cells (L2) and human club-like epithelial cells (H441) were also exposed to Br2 (100 ppm for 10 min). [4] Furthermore, bioinformatics revealed that a subset of lung type II cell genes were differentially regulated in the lungs of COVID-19 patients. [5] Our study of lung type II pneumocyte cells (A549) demonstrated that ORF7, an open reading frame (ORF) in the genome of SARS-CoV-2, induced the production of CCL2, a chemokine that promotes the chemotaxis of monocytes, and decreased the expression of IL-8, a chemokine that recruits neutrophils. [6] Results: We screened 1,584 high-confidence immune system proteins in ACE2 and TMPRSS2 co-expressing cells, finding 25 potential therapeutic targets significantly overexpressed in nasal goblet secretory cells, lung type II pneumocytes, and ileal absorptive enterocytes of patients with several immunopathologies. [7] In 2016, we reported a child with bilateral lung cysts and left lung type II pleuropulmonary blastoma (PPB), classic phenotypes of DICER1 syndrome; we identified a DICER1 hotspot mutation c. [8] Transcription factor profiling in microarray datasets revealed that several members of AP1, ATF, NF-kB, and C/EBP families involved in diverse responses were expressed in mouse lung type II cells. [9] Methods Human lung type II epithelial cells (A549) were transfected with NRP1 over-expression lentiviral vector and NRP1 inhibition vector to construct two cell models of NRP1high-A549 and NRP1low-A549. [10] We also found paclitaxel could attenuate TLR 4-NF-κB/p65 activation both in lung tissues of septic mice and LPS-stimulated lung type II epithelial cell line A549. [11] The present study aimed to explore the role of endoplasmic reticulum calcium (ER Ca2+) in the apoptosis of human lung type II alveolar epithelial A549 cells induced by paraquat (PQ) in vitro. [12] We have previously shown that endoplasmic reticulum stress (ER stress) represses the PTEN inducible kinase 1 (PINK1) in lung type II alveolar epithelial cells (AECII) reducing mitophagy and increasing the susceptibility to lung fibrosis. [13]嚴重急性呼吸綜合徵冠狀病毒 2 (SARS-CoV-2) 是 2019 年冠狀病毒病 (Covid-19) 的病原體，它的切入點是與在肺型中高表達的血管緊張素轉換酶 2 (ACE2) 受體相互作用II 肺泡細胞和其他組織，如心臟、胰腺、腦和血管內皮。 [1] 我們對肺 II 型肺細胞 (A549) 的研究表明，SARS-CoV-2 基因組中的一個開放閱讀框 (ORF) ORF7 誘導了 CCL2 的產生，CCL2 是一種促進單核細胞趨化性的趨化因子，並降低了IL-8 是一種招募中性粒細胞的趨化因子。 [2] 宿主細胞的 SARS-CoV-2 感染是由 SARS-CoV-2 刺突-(S)-蛋白與肺 II 型肺細胞結合，然後是病毒複製驅動的。 [3] 大鼠肺 II 型上皮細胞 (L2) 和人類棒狀上皮細胞 (H441) 也暴露於 Br2（100 ppm，10 分鐘）。 [4] 此外，生物信息學顯示，肺 II 型細胞基因的一個子集在 COVID-19 患者的肺中受到差異調節。 [5] 我們對肺 II 型肺細胞 (A549) 的研究表明，SARS-CoV-2 基因組中的一個開放閱讀框 (ORF) ORF7 誘導了 CCL2 的產生，CCL2 是一種促進單核細胞趨化性的趨化因子，並降低了IL-8 是一種招募中性粒細胞的趨化因子。 [6] 結果：我們篩選了 ACE2 和 TMPRSS2 共表達細胞中的 1,584 種高置信度免疫系統蛋白，發現 25 個潛在治療靶點在多種免疫病理學患者的鼻杯狀分泌細胞、肺 II 型肺細胞和迴腸吸收性腸細胞中顯著過表達。 [7] 2016 年，我們報導了一名患有雙側肺囊腫和左肺 II 型胸膜肺母細胞瘤 (PPB) 的兒童，這是 DICER1 綜合徵的經典表型；我們發現了一個 DICER1 熱點突變 c。 [8] 微陣列數據集中的轉錄因子分析表明，參與多種反應的 AP1、ATF、NF-kB 和 C/EBP 家族的幾個成員在小鼠肺 II 型細胞中表達。 [9] 方法 用NRP1過表達慢病毒載體和NRP1抑制載體轉染人肺II型上皮細胞（A549），構建NRP1high-A549和NRP1low-A549兩種細胞模型。 [10] 我們還發現紫杉醇可以減弱膿毒症小鼠肺組織和 LPS 刺激的肺 II 型上皮細胞系 A549 中的 TLR 4-NF-κB/p65 活化。 [11] 本研究旨在探討內質網鈣（ER Ca2+）在百草枯（PQ）誘導的人肺Ⅱ型肺泡上皮A549細胞凋亡中的作用。 [12] 我們之前已經表明，內質網應激（ER 應激）抑制肺 II 型肺泡上皮細胞（AECII）中的 PTEN 誘導激酶 1（PINK1），從而減少線粒體自噬並增加對肺纖維化的易感性。 [13]
lung type 2 肺型 2
Pathophysiological abnormalities and percentages of lung type 2 innate lymphoid cells (ILC2s) and Th9 cells were measured. [1] hUC-MSC treatment attenuated lung type 2 (Th2 and type 2 innate lymphoid cell) inflammation in both models. [2] Lung type 2 innate lymphoid cells express cysteinyl leukotriene re‐ ceptor 1, which regulates TH2 cytokine production. [3] In addition, A/J mice had significantly more lung type 2 innate lymphoid cells (ILC2s) cells than C57BL/6J mice. [4]測量了肺 2 型先天淋巴細胞 (ILC2s) 和 Th9 細胞的病理生理異常和百分比。 [1] hUC-MSC 治療減輕了兩種模型中的 2 型肺（Th2 和 2 型先天性淋巴細胞）炎症。 [2] 肺 2 型先天性淋巴細胞表達半胱氨酰白三烯受體 1，它調節 TH2 細胞因子的產生。 [3] 此外，A/J 小鼠的肺 2 型先天淋巴細胞 (ILC2s) 細胞明顯多於 C57BL/6J 小鼠。 [4]
lung type i
PMab-225 specifically detected aPDPN-overexpressed Chinese hamster ovary (CHO)-K1 (CHO/aPDPN) cells using flow cytometry and western blotting, and strongly stained alpaca tissues such as lung type I alveolar cells by immunohistochemistry. [1] Further, PMab-225 strongly stained lung type I alveolar cells, colon lymphatic endothelial cells, and kidney podocytes via immunohistochemistry. [2] Furthermore, PMab-235 strongly detected lung type I alveolar cells, renal podocytes, and lymphatic endothelial cells of colon by immunohistochemistry. [3] Podoplanin (PDPN), also known as T1alpha, has been used as a lung type I alveolar cell marker in the pathophysiological condition. [4]PMab-225 使用流式細胞術和蛋白質印跡特異性檢測 aPDPN 過表達的中國倉鼠卵巢 (CHO)-K1 (CHO/aPDPN) 細胞，並通過免疫組織化學對羊駝組織如肺 I 型肺泡細胞進行強染色。 [1] 此外，PMab-225 通過免疫組織化學對肺 I 型肺泡細胞、結腸淋巴管內皮細胞和腎足細胞進行強染色。 [2] 此外，PMab-235 通過免疫組織化學強烈檢測到肺 I 型肺泡細胞、腎足細胞和結腸淋巴管內皮細胞。 [3] Podoplanin (PDPN)，也稱為 T1alpha，已被用作病理生理條件下的肺 I 型肺泡細胞標誌物。 [4]
lung type 1
Pancreatic acinar-, β-, and δ cells, but rarely α cells, were tdTomato-positive, as were renal arteriolar smooth muscle cells; endothelial cells of the liver, portal vein, and endocardium; aortal tunica media; and lung type 1 and type 2 pneumocytes. [1] We conducted a systematic review to evaluate the available evidence on the effect of outdoor air pollutants on the lung type 1 (ILC1) and type 2 ILCs (ILC2) subsets. [2]胰腺腺泡細胞、β 細胞和 δ 細胞，但很少有 α 細胞，是 tdTomato 陽性的，腎小動脈平滑肌細胞也是如此；肝臟、門靜脈和心內膜的內皮細胞；主動脈中膜；和肺 1 型和 2 型肺細胞。 [1] 我們進行了系統評價，以評估室外空氣污染物對肺 1 型 (ILC1) 和 2 型 ILC (ILC2) 亞群影響的現有證據。 [2]