Altered Membrane Research Articles

Isobavachalcone enhances sensitivity of colistin-resistant Klebsiella pneumoniae: In vitro and in vivo proof-of-concept studies

ObjectiveAntibiotic resistance poses a considerable worldwide concern, particularly in clinical environments where drug-resistant Gram-negative bacteria like Klebsiella pneumoniae (K. pneumoniae) present a major challenge. The objective of this research was to investigate the mechanisms by which isobavachalcone (IBC) restores the sensitivity of K. pneumoniae to colistin in vitro and to validate the synergistic therapeutic effect in vivo. ResultsThe results indicate that the combined administration of colistin and IBC exhibits a potent antibacterial effect both in vitro and in vivo. The in vitro concurrent administration of colistin and IBC resulted in increased membrane permeability, compromised cell integrity, diminished membrane fluidity, and disrupted membrane homeostasis. Additionally, this combination reduced biofilm production, inhibited the synthesis of the autoinducer factor, altered membrane potential, and affected levels of reactive oxygen species and adenosine triphosphate synthesis, ultimately leading to bacterial death. In vivo experiments on Galleria mellonella and mice demonstrated that the co-administration of colistin and IBC increased the survival rate and significantly reduced pathological damage compared to colistin alone. ConclusionThese results suggested that IBC effectively restores the sensitivity of colistin by inducing physical disruption of bacterial membranes and oxidative stress. The combination therapy of colistin and IBC presents a viable and safe strategy to combat drug-resistant K. pneumoniae-associated infections.

Design and fabrication of high-performance ultrafiltration membranes for low-temperature conditions

The influence of cold weather conditions on ultrafiltration (UF) membrane performance is noteworthy. Investigating alterations in UF membrane fouling behavior under low-temperature conditions and developing strategies to enhance their performance holds significant importance for advancing membrane separation technology in cold regions. We initiate an exploration into how low-temperature conditions impact the permeation and separation capabilities of unmodified PES UF membranes, concurrently scrutinizing the associated influencing mechanisms. Employing molecular design, we strategically incorporate hydrophilic carboxyl-functionalized groups into the molecular structure of poly (aryl ether sulfone) materials. This method facilitates the development of a series of PAES-modified UF membranes (LTM-x%), exhibiting exceptional performance in low-temperature conditions, grounded in the principles of the hydration layer theory. In a low-temperature condition (5±1 °C), the BSA solution flux and SA solution flux of the LTM-80 membrane surpass the pristine PES membrane flux by 187.38 % and 171.82 %, respectively. Notably, compared to the solution flux at room temperature (22±1 °C), the LTM-80 membrane shows only a slight decrease in the 5±1 °C temperature (flux decline rates of 18.52 % for BSA solution and 15.12 % for SA solution), in contrast to the pronounced decline observed in the pristine PES membrane (49.24 % for BSA and 47.67 % for SA). This investigation unveils an effective and viable strategy for designing and developing high-performance UF membranes suitable for cold regions.

Effects of cardanol-based phospholipid analogs on Trichomonas vaginalis

Trichomonas vaginalis is a protist parasite of the urogenital tract, responsible for human trichomoniasis, an infection sexually transmitted that affects approximately 156 million people worldwide. This pathology is more evident in females and can cause miscarriages, premature births, and infertility. The disease can also lead to a greater predisposition to HIV infection and cervical and prostate cancer. Metronidazole (MTZ) is a drug that treats human trichomoniasis. The data from studies involving human subjects are limited regarding MTZ use during pregnancy. In addition to the toxicity of the treatment, some isolates have become resistant to MTZ. Therefore, searching for new compounds active for treating trichomoniasis becomes necessary. In the present study, we report results obtained using new phospholipid analogs. Two cardanol-based compounds designated LDT117 and LDT134 were active against T. vaginalis with an IC50 of 4.58 and 10.24 μM, respectively. These compounds were not toxic to epithelial cells in culture. Scanning electron microscopy observations revealed a rounding of the cells, a shortening of the flagella, and protrusions on the surface of drug-treated cells. Transmission electron microscopy of treated cells revealed alterations in the plasma membrane with formations of blebs, protrusions, depressions, and vacuoles with myelin figures and vacuolization in the cytoplasm after incubation. Furthermore, after treatments with the compounds LDT117 and LDT134, the parasites presented a positive reaction for TUNEL, indicating death by a mechanism like apoptosis. Given the results obtained, further in vivo studies using animal experimental models are necessary to validate that these compounds are effective for treating human trichomoniasis.

Calpain-1 weakens the nuclear envelope and promotes the release of neutrophil extracellular traps

The inducers of neutrophil extracellular trap (NET) formation are heterogeneous and consequently, there is no specific pathway or signature molecule indispensable for NET formation. But certain events such as histone modification, chromatin decondensation, nuclear envelope breakdown, and NET release are ubiquitous. During NET formation, neutrophils drastically rearrange their cytoplasmic, granular and nuclear content. Yet, the exact mechanism for decoding each step during NET formation still remains elusive. Here, we investigated the mechanism of nuclear envelope breakdown during NET formation. Immunofluorescence microscopic evaluation revealed a gradual disintegration of outer nuclear membrane protein nesprin-1 and alterations in nuclear morphology during NET formation. MALDI-TOF analysis of NETs that had been generated by various inducers detected the accumulation of nesprin-1 fragments. This suggests that nesprin-1 degradation occurs before NET release. In the presence of a calpain-1, inhibitor nesprin-1 degradation was decreased in calcium driven NET formation. Microscopic evaluation confirmed that the disintegration of the lamin B receptor (LBR) and the collapse of the actin cytoskeleton occurs in early and later phases of NET release, respectively. We conclude that the calpain-1 degrades nesprin-1, orchestrates the weakening of the nuclear membrane, contributes to LBR disintegration, and promoting DNA release and finally, NETs formation.

Effect of the insecticide clothianidin on the photosynthetic electron transport chain in pea.

Clothianidin (CL) is a neonicotinoid insecticide widely used in crop protection against insect pests. However, its effects on photosynthesis remain largely unknown. Here, by investigating the influence of CL at the concentrations of 22 and 110 μg/L on the primary processes of photosynthesis, membrane fluidity and structural changes of pea chloroplasts, we located several primary binding sites of this pesticide. Similar dynamics were observed for both concentrations. However, statistically significant differences were only found at 110 μg/L for all methods used. The light saturated rate of linear electron flow decreased mainly due to the disturbance of electron flow on the acceptor side of photosystem II (PSII) associated with the appearance of QB-nonreducing centers and empty QB binding sites of PSII. The functioning of the donor side of PSII, the activity of photosystem I (PSI) and the maximum quantum yield of PSII photochemistry (Fv/Fm) were not found to be significantly altered. Increased membrane fluidity and structural alterations of the thylakoid membrane led to a decrease in the development of the proton gradient ΔрН and membrane energization processes.

Amoebicidal activity of essential oils and essential oil-based microemulsions of Aloysia citrodora Ortega ex Pers., Cymbopogon winterianus Jowitt ex Bor, and Ocimum gratissimum L. against Acanthamoeba polyphaga trophozoites.

Evaluate the in vitro efficacy of the essential oils derived from Aloysia citrodora (Verbenaceae), Cymbopogon winterianus (Poaceae), and Ocimum gratissimum (Lamiaceae) against Acanthamoeba polyphaga trophozoites. Additionally, microemulsions formulated with these essential oils, along with their major components, were analyzed. The prepared microemulsions were characterized using polarized light microscopy and rheological techniques. The amoebicidal activity was determined by measuring the inhibitory concentration (IC50). Flow cytometry was employed to detect membrane damage and alterations in trophozoites size. The results revealed transparent and thermodynamically stable microemulsions. The essential oil from O. gratissimum exhibited a lower IC50, with values of 280.66 and 47.28µg ml-1 after 24 and 48 h, respectively. When microemulsions containing essential oils were tested, the IC50 values exhibited a reduction of over 80% after 24 h. Particularly, eugenol, a constituent of the O. gratissimum essential oil, displayed higher amoebicidal activity. The essential oils also caused damage to the cell membrane, resulting in the subsequent death of the trophozoites. The EOs of A. citrodora, C. winterianus, and O. gratissimum and their microemulsions showed antiparasitic effect against A. polyphaga trophozoites, representing promising alternatives for the treatment of diseases caused by this protozoan.

The role of gastroesophageal reflux disease in the middle ear pathology formation

The extraesophageal reflux effect investigation on the middle ear structures in adults is of considerable interest. The gastroesophageal reflux disease associated otitis media formation mechanism is closely related to such concepts as nasopharyngeal reflux and laryngopharyngeal reflux. It has been established that the pathophysiological mechanism originates in the nasopharynx and further spread to the middle ear structures. The tympanic cavity mucous membrane under the gastric enzymes influence is prone to remodeling, which results in the various chronic inflammation types gradual formation. The study purpose was to analyze medical literature from 1990 to 2024, aimed at studying the middle ear cavity inflammation causes and mechanisms formed by the gastric contents influence. As materials and methods, this article uses publications in such scientific databases as PubMed, eLIBRARY, Science Direct, Research Gate. The analyzed scientific materials provide insight into the relationship between the tympanic cavity inflammation formation and extraesophageal manifestations of GERD, as well as the potential negative H. Pylori impact on the middle ear structures. Conclusions. A detailed understanding of the middle ear cavity inflammation formation by pathophysiological mechanisms of the extraesophageal reflux influence, consisted of various gastrointestinal tract components had been obtained. The potential H. Pylori role in the tympanic cavity mucous membrane alteration remains controversial. This is due to the large number of scientific publications conflicting results in this research field. Major scientific studies confirm that gastroesophageal reflux disease acts as a risk factor for the different types middle ear cavity inflammation formation

Long-Term Use of Metformin and Vitamin B12 Deficiency in Diabetes.

This extensive review delves into the complex relationship between prolonged use of metformin and the possible emergence of vitamin B12 deficiency (VB12D) in diabetic patients. Metformin, a pivotal element in diabetes management, is constantly linked with decreased absorption of vitamin B12, prompting concerns about the enduring consequences of this interaction. The review systematically amalgamates current evidence, elucidating the prevalence, mechanisms, and clinical ramifications of VB12D induced by consistent consumption of metformin. Exploring the different pathways through which metformin might disrupt the absorption of Vitamin B12, the review encompasses interference with the calcium-dependent membrane activity and alterations of the microbiota present in the gut. A meticulous analysis of experimental studies and human trials is undertaken, accentuating the prevalence of variable VB12D among individuals on long-duration treatment of metformin across diverse populations and age groups. Clinical indications of cobalamin deficiency, spanning haematological abnormalities to neurological complications, are systematically examined. Furthermore, the review delves into the potential implications of cobalamin deficiency associated with metformin on diabetes-related complications and overall patient health. This review offers a comprehensive overview of the intricate interplay between the use of metformin and deficiency of vitamin B12 in diabetic patients, emphasizing the importance that lies in routine monitoring, early detection, and personalized interventions to optimize the long-period safety and efficiency of metformin in the treatment of diabetes. It also proposes future research directions to refine clinical guidelines and enhance the understanding regarding the correlation between diabetes, metformin, and vitamin B12.

Regulation of cholesterol biosynthesis by CTCF and H3K27 methylation is critical for cell migration

CTCF is a key factor in three-dimensional chromatin folding and transcriptional control that was found to affect cancer cell migration by a mechanism that is still poorly understood. To identify this mechanism, we used mouse melanoma cells with a partial loss of function (pLoF) of CTCF. We found that CTCF pLoF inhibits cell migration rate while leading to an increase in the expression of multiple enzymes in the cholesterol biosynthesis pathway along with an elevation in the cellular cholesterol level. In agreement with the cholesterol change we detected altered membrane dynamics in CTCF pLoF cells as measured by reduced formation of migrasomes, extracellular vesicles formed at the rear side of migrating cells. Inhibition of cholesterol synthesis in CTCF pLoF cells restored the cellular migration rate and migrasome formation, suggesting that CTCF supports cell migration by suppressing cholesterol synthesis. Detailed analysis of the promoter of Hmgcs1, an early enzyme in the cholesterol synthesis pathway, revealed that CTCF prevents formation of a loop between that promoter and another promoter 200 kb away. CTCF also supports PRC2 recruitment to the promoter and deposition of H3K27me3. H3K27me3 at the promoter of Hmgcs1 prevents SREBP2 binding and activation of transcription. By this mechanism, CTCF fine-tunes cholesterol levels to support cell migration. Notably, genome wide association studies suggest a link between CTCF and cholesterol-associated diseases, thus CTCF emerges as a new regulator of cholesterol biosynthesis.

The respiratory profile of tafazzin-deficient cells is robust against lipid supplementation-induced alterations of mitochondrial membranes

The respiratory profile of tafazzin-deficient cells is robust against lipid supplementation-induced alterations of mitochondrial membranes

Endocannabinoid regulation of inward rectifier potassium (Kir) channels.

The inward rectifier potassium channel Kir2.1 (KCNJ2) is an important regulator of resting membrane potential in both excitable and non-excitable cells. The functions of Kir2.1 channels are dependent on their lipid environment, including the availability of PI(4,5)P2, secondary anionic lipids, cholesterol and long-chain fatty acids acyl coenzyme A (LC-CoA). Endocannabinoids are a class of lipids that are naturally expressed in a variety of cells, including cardiac, neuronal, and immune cells. While these lipids are identified as ligands for cannabinoid receptors there is a growing body of evidence that they can directly regulate the function of numerous ion channels independently of CBRs. Here we examine the effects of a panel of endocannabinoids on Kir2.1 function and demonstrate that a subset of endocannabinoids can alter Kir2.1 conductance to varying degrees independently of CBRs. Using computational and Surface plasmon resonance analysis, endocannabinoid regulation of Kir2.1 channels appears to be the result of altered membrane properties, rather than through direct protein-lipid interactions. Furthermore, differences in endocannabinoid effects on Kir4.1 and Kir7.1 channels, indicating that endocannabinoid regulation is not conserved among Kir family members. These findings may have broader implications on the function of cardiac, neuronal and/or immune cells.

Transient Adaptation of Toxoplasma gondii to Exposure by Thiosemicarbazone Drugs That Target Ribosomal Proteins Is Associated with the Upregulated Expression of Tachyzoite Transmembrane Proteins and Transporters.

Thiosemicarbazones and their metal complexes have been studied for their biological activities against bacteria, cancer cells and protozoa. Short-term in vitro treatment with one gold (III) complex (C3) and its salicyl-thiosemicarbazone ligand (C4) selectively inhibited proliferation of T. gondii. Transmission Electron Microscopy (TEM) detected transient structural alterations in the parasitophorous vacuole membrane and the tachyzoite cytoplasm, but the mitochondrial membrane potential appeared unaffected by these compounds. Proteins potentially interacting with C3 and C4 were identified using differential affinity chromatography coupled with mass spectrometry (DAC-MS). Moreover, long-term in vitro treatment was performed to investigate parasitostatic or parasiticidal activity of the compounds. DAC-MS identified 50 ribosomal proteins binding both compounds, and continuous drug treatments for up to 6 days caused the loss of efficacy. Parasite tolerance to both compounds was, however, rapidly lost in their absence and regained shortly after re-exposure. Proteome analyses of six T. gondii ME49 clones adapted to C3 and C4 compared to the non-adapted wildtype revealed overexpression of ribosomal proteins, of two transmembrane proteins involved in exocytosis and of an alpha/beta hydrolase fold domain-containing protein. Results suggest that C3 and C4 may interfere with protein biosynthesis and that adaptation may be associated with the upregulated expression of tachyzoite transmembrane proteins and transporters, suggesting that the in vitro drug tolerance in T. gondii might be due to reversible, non-drug specific stress-responses mediated by phenotypic plasticity.

Amyloid-β Pathology Is the Common Nominator Proteinopathy of the Primate Brain Aging.

Senile plaques, mainly diffuse, and cerebral amyloid-β (Aβ) angiopathy are prevalent in the aging brain of non-human primates, from lemurs to non-human Hominidae. Aβ but not hyper-phosphorylated tau (HPtau) pathology is the common nominator proteinopathy of non-human primate brain aging. The abundance of Aβ in the aging primate brain is well tolerated, and the impact on cognitive functions is usually limited to particular tasks. In contrast, human brain aging is characterized by the early appearance of HPtau pathology, mainly forming neurofibrillary tangles, dystrophic neurites of neuritic plaques, and neuropil threads, preceding Aβ deposits by several decades and by its severity progressing from selected nuclei of the brain stem, entorhinal cortex, and hippocampus to the limbic system, neocortex, and other brain regions. Neurofibrillary tangles correlate with cognitive impairment and dementia in advanced cases. Aβ pathology is linked in humans to altered membrane protein and lipid composition, particularly involving lipid rafts. Although similar membrane alterations are unknown in non-human primates, membrane senescence is postulated to cause the activated β-amyloidogenic pathway, and Aβ pathology is the prevailing signature of non-human and human primate brain aging.

Brain of miyoshi myopathy/dysferlinopathy patients presents with structural and metabolic anomalies

Miyoshi myopathy/dysferlinopathy (MMD) is a rare muscle disease caused by DYSF gene mutations. Apart from skeletal muscles, DYSF is also expressed in the brain. However, the impact of MMD-causing DYSF variants on brain structure and function remains unexplored. To investigate this, we utilized magnetic resonance (MR) modalities (MR volumetry and 31P MR spectroscopy) in a family with seven children, four of whom have the illness. The MMD siblings showed distinct differences from healthy controls: (1) a significant (p < 0.001) right-sided volume asymmetry (+ 232 mm3) of the inferior lateral ventricles; and (2) a significant (p < 0.001) decrease in [Mg2+], along with a modified energy metabolism profile and altered membrane turnover in the hippocampus and motor and premotor cortices. The patients' [Mg2+], energy metabolism, and membrane turnover measures returned to those of healthy relatives after a month of 400 mg/day magnesium supplementation. This work is the first to describe anatomical and functional abnormalities characteristic of neurodegeneration in the MMD brain. Therefore, we call for further examination of brain functions in larger cohorts of MMD patients and testing of magnesium supplementation, which has proven to be an effective corrective approach in our study.

Quantifying Membrane Alterations with Tailored Fluorescent Dyes: A Rapid Antibiotic Resistance Profiling Methodology.

Accurate detection of bacterial antibiotic sensitivity is crucial for theranostics and the containment of antibiotic-resistant infections. However, the intricate task of detecting and quantifying the antibiotic-induced changes in the bacterial cytoplasmic membrane, and their correlation with other metabolic pathways leading to antibiotic resistance, poses significant challenges. Using a novel class of 4-aminophthalimide (4AP)-based fluorescent dyes with precisely tailored alkyl chains, namely 4AP-C9 and 4AP-C13, we quantify stress-mediated alterations in E. coli membranes. Leveraging the unique depth-dependent positioning and environment-sensitive fluorescence properties of these dyes, we detect antibiotic-induced membrane damage through single-cell imaging and monitoring the fluorescence peak maxima difference ratio (PMDR) of the dyes within the bacterial membrane, complemented by other methods. The correlation between the ROS-induced cytoplasmic membrane damage and the PMDR of dyes quantifies sensitivity against bactericidal antibiotics, which correlates to antibiotic-induced lipid peroxidation. Significantly, our findings largely extend to clinical isolates of E. coli and other ESKAPE pathogens like K. pneumoniae and Enterobacter subspecies. Our data reveal that 4AP-Cn probes can potentially act as precise scales to detect antibiotic-induced membrane damage ("thinning") occurring at a subnanometer scale through the quantification of dyes' PMDR, making them promising membrane dyes for rapid detection of bacterial antibiotic resistance, distinguishing sensitive and resistant infections with high specificity in a clinical setup.

Safety of low-intensity extracorporeal shock wave therapy in prostate disorders: in vitro and in vivo evidence.

Recent evidence suggests that low-intensity extracorporeal shock wave therapy (Li-ESWT) is a promising treatment for chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS); however, its safety in pelvic organs, particularly prostate tissues and cells, remains unclear. The current study evaluates the risks of prostate cell damage or oncogenesis following the administration of Li-ESWT for prostatitis. To this end, a robust in vitro model (Cell Counting Kit-8 [CCK-8] assay, clone formation assay, cell scratch assay, lactate dehydrogenase [LDH] release assay, flow cytometry, and immunoblotting assay) was designed to examine the effects of Li-ESWT on cell proliferation, clonogenicity, migration, membrane integrity, and DNA damage. Exome sequencing of Li-ESWT-treated cells was performed to determine the risk of carcinogenesis. Furthermore, an in vivo rat model ( n = 20) was employed to assess the effects of Li-ESWT on cancer biomarkers (carcinoembryonic antigen [CEA], Ki67, proliferating cell nuclear antigen [PCNA], and gamma-H2A histone family member X, phosphorylation of the H2AX Ser-139 [ γ -H2AX]) in prostate tissue. Based on our findings, Li-ESWT promotes cellular growth and motility without inducing significant cell membrane or DNA damage or alterations. Genetic analyses did not demonstrate an increase in mutations, and no damage to prostate tissue or upregulation of cancer biomarkers was detected in vivo. This comprehensive in vitro and in vivo assessment confirms the safety of Li-ESWT in managing prostate disorders.

Naringenin Against Cadmium Toxicity in Fibroblast Cells: An Integrated Network Pharmacology and In Vitro Metabolomics Approach.

Cadmium, a heavy metal, disrupts cellular homeostasis and is highly toxic, with no effective treatments currently available against its toxicity. According to studies, phytochemicals provide a promising strategy for mitigating cadmium toxicity. Naringenin (NG), a potent antioxidant found primarily in citrus fruits, showed protective properties against cadmium toxicity in rats. Nonetheless, the precise mechanism of cadmium cytotoxicity in fibroblasts remains unknown. This study evaluated NG against cadmium (CdCl2) toxicity utilizing network pharmacology and in silico molecular docking, and was further validated experimentally in rat fibroblast F111 cells. Using network pharmacology, 25 possible targets, including the top 10 targets of NG against cadmium, were identified. Molecular docking of interleukin 6 (IL6), the top potential target with NG, showed robust binding with an inhibition constant (Ki) of 58.76 μM, supporting its potential therapeutic potential. Pathway enrichment analysis suggested that "response to reactive oxygen species" and "negative regulation of small molecules metabolic process" were the topmost pathways targeted by NG against cadmium. In vitro analysis showed that NG (10 μM) attenuated CdCl2-induced oxidative stress by reducing altered intracellular ROS, mitochondrial mass, and membrane potential. Also, NG reversed CdCl2-mediated nuclear damage, G2/M phase arrest, and apoptosis. GC/MS-based metabolomics of F111 cells revealed CdCl2 reduced cholesterol levels, which led to alterations in primary bile acid, steroid and steroid hormone biosynthesis pathways, whereas, NG restored these alterations. In summary, combined in silico and in vitro analysis suggested that NG protected cells from CdCl2 toxicity by mitigating oxidative stress and metabolic pathway alterations, providing a comprehensive understanding of its protective mechanisms against cadmium-induced toxicity.

Lipid lysination by MprF contributes to hemolytic pigment retention in group B Streptococcus

Group B Streptococcus (GBS) is the leading cause of neonatal sepsis and meningitis. A major virulence factor is a pigmented beta-haemolytic/cyto-lysin (β-h/c) toxin with an ornithine rhamnolipid structure. We initially observed that absence of MprF enzyme altered pigmentation and haemolytic activity in GBS. Next, we showed that MprF-dependent lipid lysination contributes to the retention of the ornithine rhamnolipid within GBS membrane. Furthermore, cationic lipidation by MprF altered membrane properties contributing to resistance to the cyclic lipopeptide daptomycin and to acidic pH. This study highlights the importance of cationic lipids in cell envelope homeostasis and in modulating β-h/c activity.

Application of Principal Component Analysis for the Elucidation of Operational Features for Pervaporation Desalination Performance of PVA-Based TFC Membrane

Principal Component Analysis (PCA) serves as a valuable tool for analyzing membrane processes, offering insights into complex datasets, identifying crucial factors influencing membrane performance, aiding in design and optimization, and facilitating monitoring and fault diagnosis. In this study, PCA is applied to understand operational features affecting pervaporation desalination performance of PVA-based TFC membranes. PCA-biplot representation reveals that the first two principal components (PCs) accounted for 62.34% of the total variance, with normalized permeation with selective layer thickness (Pnorm), water permeation flux (P), and operational temperature (T) contributing significantly to PC1, while salt rejection dominates PC2. Membrane clustering indicates distinct influences, with membranes grouped based on correlation with operational factors. Excluding outliers increases total variance to 74.15%, showing altered membrane arrangements. Interestingly, the adopted strategy showed a high discrepancy between P and Pnorm, indicating the relevance of comparing between PVA membranes with specific layers and those with none. PCA results showed that Pnorm is more important than P in operational features, highlighting its significance in both research and practical applications. Our findings show that even know P remains a key performance property; Pnorm is critical for developing high-performance, efficient, and economically viable pervaporation desalination membranes. Subsequent PCA for membranes without specific layers (M1 to M6) and with specific layers (M7 to M11) highlights higher total variance and influence of variables, aiding in understanding membranes’ behavior and suitability under different conditions. Overall, PCA effectively delineates performance characteristics and potential applications of PVA-based TFC membranes. This study would confirm the applicability of the PCA approach in monitoring the operational efficiency of pervaporation desalination via these membranes.

Alectinib-induced Non-immune Hemolytic Anemia due to Erythrocyte Membrane Alterations: A Retrospective Evaluation

Alectinib-induced Non-immune Hemolytic Anemia due to Erythrocyte Membrane Alterations: A Retrospective Evaluation