Background: Myofibroblasts (MYFs) are generally considered the principal culprits in excessive extracellular matrix deposition and scar formation in the pathogenesis of lung fibrosis. Lipofibroblasts (LIFs), on the other hand, are defined by their lipid-storing capacity and are predominantly found in the alveolar regions of the lung. They have been proposed to play a protective role in lung fibrosis. We previously reported that a LIF to MYF reversible differentiation switch occurred during fibrosis formation and resolution. In this study, we tested whether WI-38 cells, a human embryonic lung fibroblast cell line, could be used to study fibroblast differentiation towards the LIF or MYF phenotype and whether this could be relevant for idiopathic pulmonary fibrosis (IPF). Methods: Using WI-38 cells, Fibroblast (FIB) to MYF differentiation was triggered using TGF-β1 treatment and FIB to LIF differentiation using Metformin treatment. We also analyzed the MYF to LIF and LIF to MYF differentiation by pre-treating the WI-38 cells with TGF-β1 or Metformin respectively. We used IF, qPCR and bulk RNA-Seq to analyze the phenotypic and transcriptomic changes in the cells. We correlated our in vitro transcriptome data from WI-38 cells (obtained via bulk RNA sequencing) with the transcriptomic signature of LIFs and MYFs derived from the IPF cell atlas as well as with our own single-cell transcriptomic data from IPF patients-derived lung fibroblasts (LF-IPF) cultured in vitro. We also carried out alveolosphere assays to evaluate the ability of the proposed LIF and MYF cells to support the growth of alveolar epithelial type 2 cells. Results: WI-38 cells and LF-IPF display similar phenotypical and gene expression responses to TGF-β1 and Metformin treatment. Bulk RNA-Seq analysis of WI-38 cells and LF-IPF treated with TGF-β1, or Metformin indicate similar transcriptomic changes. We also show the partial conservation of the LIF and MYF signature extracted from the Habermann et al. scRNA-seq dataset in WI-38 cells treated with Metformin or TGF-β1, respectively. Alveolosphere assays indicate that LIFs enhance organoid growth, while MYFs inhibit organoid growth. Finally, we provide evidence supporting the MYF to LIF and LIF to MYF reversible switch using WI-38 cells. Conclusions: WI-38 cells represent a versatile and reliable model to study the intricate dynamics of fibroblast differentiation towards the MYF or LIF phenotype associated with lung fibrosis formation and resolution, providing valuable insights to drive future research.

UNASSIGNED: This study aims to investigate whether the concept of doubling time in hydatid cysts differs according to different parameters such as age, sex, and whether the cyst is located in the lung or liver. Background: This study aims to investigate whether the concept of doubling time in hydatid cysts differs according to different parameters such as age, sex, and whether the cyst is located in the lung or liver.
UNASSIGNED: Between January 2012 and August 2023, a total of 138 hydatid cysts were retrospectively analyzed. There were 55 pulmonary (32 males, 23 females; mean age: 25.6±23.8 years; range, 2 to 77 years) and 83 hepatic hydatid cyst patients (32 males, 51 females; mean age: 31.1±22.8 years; range, 3 to 75 years).
UNASSIGNED: The mean doubling times for pulmonary and hepatic hydatid cysts were 73.4±41.8 and 172.6±108.8 days, respectively (p<0.001). When children (≤18 years old) and adult cases were compared for pulmonary hydatid cysts, the mean doubling times were 61.1±17.6 and 87.1±55.3 days, respectively (p=0.119), and for hepatic hydatid cysts, 110.6±48.4 and 215.6±118.3 days, respectively (p<0.001). While comparing male and female cases, the mean doubling time for pulmonary hydatid cysts was 77.6±32.2 and 67.6±52.6 days, respectively (p=0.018), while for hepatic hydatid cysts, it was 192.0±111.7 and 160.4±106.2 days, respectively (p=0.250).
UNASSIGNED: The doubling time seems to be approximately 10 weeks in the lung and approximately 25 weeks in the liver. Hydatid cysts grow faster in children than adults in both the lungs and liver.

Intraoperative management for patients during orthotopic lung transplantation may be performed without mechanical circulatory support, with veno-arterial extracorporeal membrane oxygenation (VA-ECMO), or cardiopulmonary bypass (CPB). For certain patients, an intraoperative conversion from VA-ECMO to CPB may be indicated. If a VA-ECMO patient requires CPB conversion, the previous model at our institution used two separate machines and was overall inefficient. The primary aim of this project was to develop a CPB pack modification to create a circuit that easily converts from VA-ECMO to CPB if indicated. The secondary aim was to create new supportive protocols and a comprehensive education and training curriculum for our large perfusion department to enhance patient safety. The new circuit was carefully designed and evaluated to minimize changes to the current CPB circuit while allowing for the safest configuration of VA-ECMO. A new protocol was designed with multi-disciplinary collaboration. A comprehensive education and training curriculum, as well as an objective competency assessment tool, were created. The circuit was subjectively evaluated by perfusionists and outscored our previous model in the areas of ease of setup, use, and CPB conversion. It received positive feedback from cardiothoracic surgeons and anesthesiologists as well. Lastly, it provided a financial benefit to our institution.

BACKGROUND: Heparin is an essential drug used as an anticoagulant. Access to raw material suitable for heparin extraction is critical for creating a viable business opportunity. In Saudi Arabia, large amounts of raw material with potential for heparin extraction are wasted.
OBJECTIVE: To extract heparin and low-molecular-weight heparin (LMWH) from the camel lung, and measure its potency and activity.
METHODS: Heparin preparation included three steps: extraction, electrophoretic identification, and activity measurement. Fresh lung tissue (100 g) was minced and homogenized in a blender. Crude heparin extracts were prepared using Charles\'s or Volpi\'s method with slight modifications. Heparin was purified by electrophoresis using high-purity agarose gels in barium acetate buffer. The heparin activity of purified samples was assayed spectrophotometrically using commercial heparin kits.
RESULTS: Charles\'s and Volpi\'s extraction methods were simple and easy to establish. The yield was 90 mg crude heparin per 100 g of camel lung tissue following Volpi\'s extraction protocol, whereas Charles\'s method did not yield any heparin. The separation of heparin and LMWH by gel electrophoresis resulted in sharp and clear product bands using material prepared according to Volpi\'s method. The heparin preparation had an anti-factor Xa activity of 37 IU/mg, indicating weak potency.
CONCLUSIONS: Preparation of active heparin from camel lung tissue is a technology applicable in manufacturing. Further method development is needed to increase heparin purity and potency.

The aloe vera plant has become increasingly popular in recent years. This study aimed to research the effect of aloe vera to prevent renal and lung tissue damage in an experimental ischemia-reperfusion (I/R) injury model. The study included 21 male Wistar Albino rats, which were categorized into control group, n = 7 (no procedures), Sham group n = 7 (I/R); and aloe vera therapy group, n = 7 (aloe vera and I/R). Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and malondialdehyde (MDA) were evaluated from lung and kidney tissues for biochemical investigations. As histopathological, hematoxylin and eosin and anti-iNOS were also examined. In biochemical investigations, SOD, CAT, and GPx levels of the Sham group were found to be lower compared with the other groups (P < 0.05). The aloe vera therapy group was not statistically different from control groups but significantly different compared with the Sham group. In the same way, the MDA levels of kidney and lung tissues were statistically significant in the aloe vera therapy group, compared to the Sham group. In the Sham group, the peribronchial and perialveolar edema were observed in lung parenchyma. Also, excess interstitial hemorrhage, leukocyte infiltration, and alveolar wall thickening were identified in ischemic groups. The histopathological changes were much lighter than in the aloe vera therapy group. In renal tissues, excess epithelial cell deterioration, tubular desqumination, and glomerular atrophy were observed in the Sham group. The histopathological changes were markedly reduced in the aloe vera therapy  group. In the kidney and lung tissue, the level of iNOS activity in the Sham group was significantly higher than in the control and aloe vera therapy group. This study indicated that aloe vera is protective against oxidative damage formed by I/R in distant organs like the lungs and kidneys.

2-D ultrasound shear wave elastography (SWE) could be considered as a new noninvasive tool for monitoring fetal lung development based on evaluation of mechanical properties during pregnancy. Interesting results are available concerning the use of SWE on developing organs, especially on premature infants and animal models. The main objective in this study is to evaluate the feasibility of 2-D SWE in human fetal lungs between 24 and 34 weeks of gestation (WG). The secondary objective is to modellise fetal lung-to-liver elastography ratio (LLE ratio) and to assess variations between normal lung and lung surfactant-enriched after a corticosteroids course indicated for a threatened preterm labour (TPL).
A prospective case-control study will be performed between 24 and 34 WG. Fetal lungs and liver will be explored by SWE into two groups: fetuses of women with an uncomplicated pregnancy (control group) and fetuses of women with a TPL requiring administration of corticosteroids (cases group). LLE ratio will be defined as the value of the lung elasticity divided by the value of the liver elasticity.Primary judgement criterion is the value of elasticity modulus expressed in kilopascal. Lungs and liver will be explored through three measurements to define the most reproducible regions with the lowest intra- and inter-observer variability. Feasibility will be evaluated by assessing the number of examinations performed and the number of examinations with interpretable results. Intra- and inter-observer reproducibility will be evaluated by means of the intra-class correlation coefficient.
Approval of the study protocol was obtained from the human ethical research committee (Comité de Protection des Personnes EST II, process number 15/494) and the French National Agency for Medicines and Health Products Safety (process number 2015-A01575-44). All participants will sign a statement of informed consent.
NCT02870608; Recruiting.

Glycogen synthase kinase-3β (GSK-3β) plays an important role in the regulation of apoptosis. To investigate its involvement in acquired cadmium (Cd) resistance, Cd-resistant cells (RH460) were established from H460 lung carcinoma cells. Cd resistance led to interruption of apoptosis and autophagy, as determined by an apoptotic sub-G1 population, procaspase-3 clevage, and LC3-II induction. Cd-induced autophagy preceded apoptosis as determined by 3-methyladenine or zVAD and time-course experiments after Cd treatment. Despite β-catenin accumulation, phospho(p)-Ser/Tyr GSK-3α/β increased in the nucleus until 12h after treatment and then p-Ser partly translocated to the cytoplasm. The GSK-3 inhibitor lithium augmented Cd-induced p-Ser GSK-3α/β, which accumulated in the nucleus and cytoplasm, and increased autophagy. SB216763 inhibited p-Ser/p-Tyr GSK-3α/β and subsequent autophagy. GSK-3β knockdown decreased Cd-induced autophagy. Cd exposure to RH460 cells overexpressed with pcDNA-GSK-3β-HA strongly phosphorylated Ser(9)/Tyr(216) residues and decreased LC3-II. Constitutively active pcDNA-GSK-3β(S9A)-HA overexpression phosphorylated Tyr(216) and decreased LC3-II, suggesting that p-Tyr inhibits autophagy. PI3K inhibitors decreased Cd-induced p-Ser GSK-3αβ and LC3-II, whereas a Ser/Thr phosphatase inhibitor, okadaic acid, hyperphosphorylated Ser residues, which accumulated in the nucleus and cytosol, and enhanced LC3-II. The general tyrosine kinase inhibitor genistein suppressed Cd-induced p-Tyr/p-Ser GSK-3α/β and LC3-II. Mouse lung tissues respond to long-term Cd exposure increased p-Tyr, downregulated LC3-II, and accumulated full-length Bax and procaspase-3. Taken together, this study shows that acquired Cd resistance is regulated by GSK-3β phosphorylation state, but not activation state, and intracellular localization of p-Ser GSK-3 regulates Cd-induced autophagy and apoptosis.