Search Results (1,092)

Background: Carotid plaque composition is central to stroke risk, but some aspects of plaque characterization are derived from ex vivo imaging, while clinical decision-making relies on in vivo ultrasound (US) and computed tomography (CT). High correlation of clinical in vivo and ex vivo imaging is necessary when including ex vivo plaque features in artificial intelligence (AI) models, but the extent of this correlation between CT and US remains poorly understood. Methods: Patients undergoing carotid endarterectomy (n = 188) were enrolled. Preoperative carotid US (n = 182) and CT (n = 156) were performed. Plaque specimens from 187 patients were imaged on ex vivo CT and US. Quantitative metrics included plaque volumes, relative calcified/non-calcified volumes, HU and grayscale distributions, Agatston and calcification scores, and heterogeneity indices (coefficient of variation). Qualitative US parameters (echogenicity, juxtaluminal echolucency, discrete white areas) were visually graded. Correlation between in vivo and ex vivo imaging was assessed, and agreement was quantified for parameters with the highest correlation with Bland–Altman analysis. Results: CT of patients and ex vivo CT showed moderate to strong correlation for total, calcified, and non-calcified plaque volumes and whole-plaque mean HU (r = 0.55–0.79; CCC = 0.43–0.74). Agatston and calcification scores correlated strongly (r = 0.78–0.80; CCC = 0.63–0.76). In contrast, most non-calcified and heterogeneity metrics showed negligible-to-weak correlation. Correlations between in vivo and ex vivo US were substantially weaker (maximum correlation: 75th grayscale percentile r = 0.35). In vivo CT overestimated calcified volume (bias: 8.7%) and in vivo US underestimated the 75th grayscale quantile (bias: −25.5 grayscale). Conclusions: Quantitative CT metrics—particularly relative calcified plaque volume and calcium scores—translate reasonably well from ex vivo to in vivo imaging and represent robust candidates for radiomics and AI-based stroke risk models, even ex vivo. Ultrasound parameters show limited translational validity, underscoring the need for volumetric clinical US and discouraging the inclusion of ex vivo ultrasound features for machine learning applications. Full article

Background and Objectives: Obesity, heart failure (HF), and atherosclerosis have common pathways, including chronic inflammation, immune cells activation, and metabolic disturbances. These pathways often coexist and overlap, increasing cardiometabolic risk. Growth differentiation factor 15 (GDF-15) is an emerging cytokine linked to inflammation, oxidative stress, and metabolic dysregulation, which are common pathways between heart failure, obesity and atherosclerosis. Beyond its established prognostic value in cardiovascular diseases (CVD) and HF, recent evidence suggests that GDF-15 may also reflect subclinical atherosclerosis, potentially improving early risk stratification in obese and HF populations. The aim of this review is to synthesize current evidence on the association between GDF-15 and markers of subclinical atherosclerosis, and to evaluate whether GDF-15 may serve as an integrative biomarker reflecting shared cardiometabolic pathways. Materials and Methods: We conducted a systematic review following PRISMA recommendations registered by CRD420251267457 number on PROSPERO. PubMed, Embase, Scopus, and Web of Science were searched for human studies evaluating the correlation between markers of subclinical atherosclerosis and GDF-15 concentration. We excluded the studies not published in English, not involving human participants, and not meeting the inclusion criteria. We assessed the risk of bias using the Joanna Briggs Institute appraisal tool. Due to the heterogeneity of studies, a narrative synthesis was performed. Result: The review included 18 studies, which evaluated the association between GDF-15 and subclinical atherosclerosis markers, such as intima media thickness, coronary artery calcium score, ankle-brachial index, and atherosclerotic plaques. Studies included patients with metabolic disorders, chronic inflammatory diseases, HIV cohorts, and general population samples. Most of the studies reported that GDF-15 levels were associated with greater atherosclerotic burden; however, results were frequently influenced by confounders. Methodological limitations, such as limited or highly specified samples, cross-sectional designs, variability in atherosclerotic-imaging technique, and inconsistent adjustment for confounders, restrict generalization of the results. Conclusions: Current evidence supports GDF-15 as a biomarker integrating inflammatory and metabolic stress signals, indirectly linking obesity, HF and subclinical atherosclerosis. While current data supports its prognostic relevance, further studies are needed to confirm its clinical utility in routine assessment and preventive cardiovascular care. Full article

This review addresses the challenges of obtaining high-quality quantitative data in the optical imaging of membrane voltage and calcium dynamics. The paper provides a comprehensive overview and systematization of recent studies that analyze factors limiting signal fidelity and propose strategies to enhance data quality. The primary sources of signal degradation in biological optical imaging, with an emphasis on membrane voltage and calcium imaging, are systematically explored across four major indicator classes: voltage-sensitive dyes (VSDs), genetically encoded voltage indicators (GEVIs), calcium-sensitive dyes (CSDs), and genetically encoded calcium indicators (GECIs). Common mechanisms that compromise data quality are classified into three main categories: fundamental photon shot noise, device-related errors, and sample-related measurement errors. For each class of limitation, its physical or biological origin and characteristic manifestations are described, which are followed by an analysis of available mitigation strategies, including hardware optimization, choice of sensors, sample preparation and experimental design, post-processing and computational correction methods. Full article

Purpose: Hyperparathyroidism (HPT) is a condition marked by excessive secretion of parathyroid hormone (PTH), leading to disturbances in calcium, phosphate, and vitamin D metabolism. HPT is classified into primary (pHPT), secondary (sHPT), and tertiary (tHPT) types, which can cause systemic complications. Parathyroidectomy (PTX) remains the cornerstone treatment for pHPT and refractory cases of sHPT and tHPT. Methods: A retrospective review was conducted on 10 pediatric patients who underwent PTX for HPT at our clinic between 2016 and 2024. Demographic data, preoperative imaging, laboratory findings, surgical details, pathology reports, and postoperative outcomes were analyzed. Patients were categorized as having either pHPT (n = 6) or renal HPT (r-HPT; n = 4), which included one case of sHPT and three cases of tHPT. Results: The mean age of pHPT and r-HPT patients was 15 and 13 years, respectively. While 50% of pHPT patients were female, all r-HPT patients were female. Preoperative imaging localized parathyroid lesions using ultrasonography in all cases, but Sestamibi scintigraphy had a lower detection rate (66.7%). Minimally invasive parathyroidectomy was performed in single-gland pHPT cases, while bilateral neck exploration was used for multiglandular pHPT and all r-HPT cases. No intraoperative complications were observed. Postoperatively, all patients demonstrated normalized calcium, phosphate, and PTH levels with significant symptomatic improvement. Hungry bone syndrome developed in one r-HPT patient and was managed successfully. No recurrences were noted during an average follow-up of 39 months. Conclusions: PTX is a safe and effective treatment for pediatric HPT, providing excellent biochemical and clinical outcomes. Multidisciplinary collaboration is crucial in managing pediatric cases, particularly those with complex renal HPT. Full article

The activation of TRPV1 and TRPA1 by UVA light is a complex process involving channel modulation by reactive oxygen species (ROS). The present study describes staurosporine and midostaurin, two protein kinase inhibitors, as photosensitizers that can modulate the activity of TRPV1 and TRPA1 in a UVA light-dependent manner. Patch-clamp and calcium imaging were used to investigate effects of staurosporine and midostaurin on recombinant human (h) TRPV1 and TRPA1 in HEK 293T cells and on native mouse dorsal root ganglion (DRG) cells. Staurosporine applied alone did not induce channel activation, but co-application with UVA light activated both TRPV1 and TRPA1. Staurosporine with UVA light also potentiated TRPV1-mediated membrane currents induced by heat and protons. Midostaurin induced the UVA light-independent activation and sensitization of TRPV1 and TRPA1, and this effect was strongly potentiated by UVA light. Effects induced by both staurosporine and midostaurin were reversed by the reducing agent dithiothreitol (DTT). Midostaurin induced a calcium influx in TRPA1-expressing DRG neurons. Our results show that staurosporine and midostaurin modulate the activity of TRPV1 and TRPA1 channels in the presence of UVA light. These photosensitizing properties can be relevant when staurosporine is used for in vitro experiments, and they may account for the phototoxic side effects of midostaurin. Full article

Background/Objectives: Amlodipine, a widely prescribed calcium channel blocker, has been associated with gingival enlargement, yet the mechanisms underlying this adverse effect remain unclear. The present study aimed to explore molecular and histopathological factors potentially contributing to gingival changes in patients receiving amlodipine therapy, with a particular focus on molecules implicated in extracellular matrix turnover and tissue remodeling. Methods: The study included three groups of participants: patients with amlodipine-induced gingival enlargement, patients with gingival enlargement of inflammatory origin, and amlodipine-treated patients without gingival overgrowth. Gingival tissue samples were analyzed using hematoxylin-eosin staining to assess inflammatory changes and general tissue architecture, and Picrosirius Red staining to visualize collagen fibers. Relative gene expression of alpha-smooth muscle actin (α-SMA), IL-13, MMP-1, and procollagen was determined by real-time PCR, while collagen content was quantified using ImageJ software. Results: Histopathological evaluation revealed a less pronounced inflammatory response in amlodipine-related gingival enlargement compared to those who did not use amlodipine. The highest expression of α-SMA was detected in patients who did not receive amlodipine, whereas IL-13 and procollagen expression were markedly elevated in the amlodipine-induced group compared to others. MMP-1 expression was significantly lower in amlodipine-treated patients relative to those who did not use amlodipine, suggesting impaired collagen degradation. These findings, together with our previous results indicating enhanced expression of profibrotic mediators, suggest that altered extracellular matrix metabolism is potentially dominant in this condition. Conclusions: Amlodipine-induced gingival enlargement appears to involve a multifactorial process characterized by a prominent fibrotic component, reduced matrix degradation, and secondary inflammation. Full article

Background/Objectives: Pediatric osteoporosis is a multifactorial condition characterized by impaired bone mineralization and increased fracture risk, particularly vertebral compression fractures. This study aims to evaluate the diverse etiology, diagnostic challenges, and treatment options for pediatric osteoporosis in a cohort of affected children. Methods: We reviewed eleven pediatric patients (aged 5–16 years) diagnosed with vertebral fractures and osteoporosis, who were hospitalized between 2020 and 2024 at the Department of Endocrinology and Metabolic Diseases at PMMH-RI in Lodz. Clinical evaluation included medical history, physical examination, biochemical markers of bone metabolism, and imaging techniques such as dual-energy X-ray absorptiometry (DXA) to determine underlying causes of bone fragility. Results: The cohort presented a broad etiological spectrum, including seven patients with genetic disorders (e.g., mutations in COL1A1, LRP5, SGMS2, and ALPL genes) and secondary osteoporosis due to chronic diseases requiring prolonged glucocorticoid therapy (two patients with Duchenne muscular dystrophy (DMD), one patient with Crohn’s disease) or endocrinological disorders (one patient with Cushing disease). Vertebral fractures were confirmed in all patients, with back pain as the predominant symptom. Low bone mass (BMD Z-score < −2.0) was observed in eight individuals; in others, clinical signs of skeletal fragility were present despite Z-scores above this threshold. Mild biochemical abnormalities included hypercalciuria (3/11 cases) and vitamin D deficiency (6/11 cases). Height adjustment improved BMD interpretation in short-stature patients. Most children received bisphosphonate therapy, supplemented with calcium and vitamin D. In two patients, bisphosphonates were not used due to lack of parental consent or underlying conditions in which such treatment is not recommended. Conclusions: Pediatric osteoporosis requires a multidisciplinary diagnostic and therapeutic approach, integrating clinical, biochemical, and genetic factors. It is a heterogeneous and often underrecognized condition, with vertebral fractures frequently serving as its earliest sign—even in the absence of overt symptoms or low bone mass. This underscores the need for clinical vigilance, as significant skeletal fragility may occur despite normal BMD values. Importantly, pediatric osteoporosis may also impact the attainment of peak bone mass and ultimately affect final adult height. Early diagnosis through thorough assessment, including height-adjusted DXA, and a multidisciplinary approach are essential to ensure timely management and prevent long-term complications. Full article

Background/Objectives: Cardiotoxicity remains a leading cause of drug withdrawal. Conventional preclinical models, such as two-dimensional (2D) cell cultures and animal studies, often fail to accurately predict human cardiac responses. While 2D cultures lack the complex architecture and dynamic functionality of native myocardium, interspecies differences limit the translational relevance of animal models. The objective of this study was to develop a human-relevant, in vitro platform that enables predictive and functional assessment of drug-induced cardiotoxicity. Methods: Here, we present a high-throughput in vitro platform for cardiotoxicity screening using three-dimensional (3D) cardiac tissues derived from human induced pluripotent stem cells (hiPSCs) within a thermoresponsive extracellular matrix-derived hydrogel. The hydrogel enables homogeneous encapsulation, differentiation in 3D, and long-term assembly into a functional cardiac tissue. Maturation was validated by immunostaining for cardiac-specific markers, and calcium imaging was employed to monitor electrical signal propagation. Contractile performance, defined by beat rate and contraction amplitude, was quantified using video-based motion analysis. The platform was applied to evaluate the dose-dependent effects of various cardioactive compounds, including β-adrenergic agonists ((-) epinephrine and dopamine), a cardiotoxic chemotherapeutic (doxorubicin), a sinus node inhibitor (ivabradine), a calcium channel blocker (verapamil), and a β-adrenergic antagonist (metoprolol). Results: The engineered cardiac tissues exhibited functional maturation and stable contractile behavior. Drug testing demonstrated compound-specific, dose-dependent functional responses. For each compound, the system faithfully reproduced the expected physiological responses. Conclusions: This human-relevant, scalable platform enables sensitive, multiparametric functional assessment of cardiac tissues, offering a cost-effective and predictive tool for preclinical drug safety testing. By bridging the gap between in vitro assays and human physiology, it holds promise to enhance translational accuracy while reducing reliance on animal models. Full article

A thorough understanding of the dispersion characteristics of graphene oxide (GO), its micro-pore enhancement mechanisms, and correlations with mechanical properties are crucial for advancing high-strength, durable green concrete. Introducing recycled concrete powder (RCP) can weaken the interfacial transition zone (ITZ) and inhibit hydration reactions, degrading the pore structure and affecting mechanical strength and durability. However, traditional methods struggle to accurately characterize and quantitatively analyze GO-modified pore structures due to their nanoscale size, microstructural diversity, and characterization technique limitations. To address these challenges, this study integrates deep learning-based backscattered electron image analysis with deep Taylor decomposition feature extraction. This innovative method systematically analyzes pore characteristic evolution and the correlation between porosity and mechanical strength. The results indicate that GO promotes Calcium Silicate Hydrate gel growth, refines pores, and reduces pore connectivity, decreasing the maximum pore size by 33.4–45.2%. Using a Convolutional Neural Network architecture, BSE images are efficiently processed and analyzed, achieving an average recognition accuracy of 94.3–96.9%. The optimized degree of GO coating on enhanced regions reaches 30.2%. Fitting porosity with mechanical strength and chloride ion permeability coefficients reveals that enhanced regions exhibit the highest correlation with mechanical strength and durability in regenerated cementitious materials, with R² values ranging from 0.79 to 0.99. The deep learning-assisted pore structure characterization method demonstrates high accuracy and efficiency, providing a critical theoretical basis and data support for performance optimization and engineering applications of recycled cementitious materials. This research expands the application of deep learning in building materials and offers new insights into the relationship between the microstructural and macroscopic properties of recycled cementitious materials. Full article

Tooth extraction induces changes in both hard and soft tissues, which may compromise implant placement. Leukocyte- and platelet-rich fibrin (L-PRF) is used to promote tissue healing, either alone or in combination with other grafting materials. Objective: This study aimed to compare post-extraction socket healing using L-PRF alone or combined with a biphasic calcium phosphate graft (HA/β-TCP) after eight weeks. Materials and Methods: 15 patients, both sexes, mean age 56.7 ± 8.2 years, requiring alveolar ridge preservation after single-rooted tooth extraction for subsequent implant placement, were included. Sockets were randomly assigned to four groups: control with blood clot only (CTR), autogenous bone graft (AB), L-PRF membrane (LPRF), and L-PRF combined with HA/β-TCP (LPRFHA). The protocol consisted of tooth extraction and immediate graft placement, followed by bone biopsy at 8 weeks for histomorphometric analysis and implant installation. New Bone Formation (NBF) was quantified from ten photomicrographs per sample using ImageJ software (version 1.54, 5 February 2025). One-way ANOVA with Bonferroni post hoc tests was applied, with statistical significance set at p ≤ 0.05. Results: A significant difference in NBF (%) was observed between the control and LPRFHA groups (p = 0.014), with greater bone formation in the control group (62.4 ± 18.6%) compared with LPRFHA (55.8 ± 17.2%; p = 0.012). No significant differences were found among AB, LPRF, and LPRFHA groups. LPRF and AB showed comparable bone formation (60.2 ± 17.5% and 60.1 ± 20.0%, respectively). Conclusions: L-PRF, either alone or combined with HA/β-TCP, can be used for alveolar ridge preservation in maxillary sockets. L-PRF, alone or with synthetic HA/β-TCP graft, effectively preserves the anterior maxillary ridge for early loading at eight weeks. All treatments achieved bone formation for implant placement, with the blood clot alone showing superior results. Full article

Transient receptor potential vanilloid 2 (TRPV2) is a non-selective cation channel involved in diverse physiological and pathological processes. Tranilast has frequently been described and used as a rather specific inhibitor of TRPV2. However, the molecular basis of this inhibition was never been studied in detail. Here, we investigated whether tranilast indeed directly inhibits TRPV2. Rat TRPV2 was expressed in human embryonic kidney (HEK293) cells, and channel function was assessed using whole-cell electrophysiology and calcium imaging in response to established agonists. In parallel, we conducted phagocytosis assays in rat basophilic leukemia (RBL) cells, including a CRISPR/Cas9-generated TRPV2-knockout cell line. Tranilast up to 1 mM did not inhibit TRPV2-mediated currents or calcium influx induced by any agonist. However, when co-applied with the oxidant chloramine T, tranilast diminished oxidation-induced activation of TRPV2. This effect may indicate a general interference of tranilast with redox signaling. Accordingly, tranilast also reduced chloramine T-induced activation of TRPA1 as well as the development of non-inactivating currents of voltage-gated Na⁺ channels. Furthermore, tranilast decreased phagocytic activity in both wildtype and TRPV2-knockout RBL cells. However, the reduction was less pronounced in TRPV2-knockout cells. These findings demonstrate that tranilast does not directly inhibit TRPV2. Instead, tranilast seems to indirectly suppress channel activation by reducing reactive oxygen species (ROS). This refined understanding of how tranilast modulates TRPV2 has important implications for the interpretation of prior and future pharmacological studies targeting TRPV2. Full article

The leading cause of post-surgical hospital readmission is the emergence of hospital-acquired infections (HAIs), where surgical site infections (SSIs) constitute a substantial negative impact on patient outcome and contribute annual direct costs estimated to range from $28.4 billion to $45 billion in the U.S. To address the need for novel antimicrobial coating strategies, previous research has demonstrated that certain microbes can degrade poly(aspartic acid) (PAA)-based coatings, suggesting potential limitations of single-compound approaches that must be considered when designing antimicrobial surfaces. In this proof-of-concept study, we investigated whether ordered sequential coatings combining thermally synthesized PAA (tPAA) and oleic acid (OleA) might produce enhanced antimicrobial effects compared to individual compounds. Despite concerns regarding PAA biodegradability, the benefits of using PAA include low cytotoxicity and an ability to chelate metals such as calcium and facilitate bone mineralization and growth post-surgery. Using simple yet effective methods of surface coating applications which utilize tPAA and OleA, we investigated the potential of these ordered coatings to attenuate planktonic and sessile (biofilm) growth and development in Pseudomonas aeruginosa and Escherichia coli in vitro. Application of these ordered coatings resulted in up to 62% reduction in bacterial carrying capacity for P. aeruginosa and up to 43% reduction in biofilm mass relative to untreated controls. Further, confocal imaging via immunohistochemical labeling revealed methods for evaluating the impact of treatments targeting biofilm development through extracellular DNA quantification. Additionally, these coatings show dose-dependent cytotoxic effects against 3T3 mouse fibroblast cells. These preliminary findings, along with results derived from cytotoxicity assessment and physicochemical characterization via dynamic light scattering, suggest that ordered tPAA-OleA coating systems warrant further investigation as potential antimicrobial strategies, though additional validation, including testing against diverse clinical isolates, mechanistic studies, and in vivo evaluation, would be required before clinical application. Full article

Background: Crowned dens syndrome (CDS) is characterized by acute neck pain and restricted motion due to calcium pyrophosphate (CPP) crystal deposition around the atlantoaxial joint. Although recognized as sufficient for the diagnosis of CPP deposition disease (CPPD), its prevalence remains uncertain. Given the high prevalence of CPPD in the general population, CDS may be more common than currently appreciated among patients with neck pain undergoing cervical spine imaging. Methods: This retrospective study included patients aged ≥40 years who underwent cervical spine CT for evaluation of neck pain between 2022 and 2024. Of 500 consecutive scans, 195 were eligible after excluding trauma-related, post-operative, and metastatic cases. Results: Periodontoid calcifications were identified in 29.2% of patients (mean age 61.5 ± 11.7 years; 37.4% male). Prevalence increased significantly with age (p < 0.001), reaching nearly 50% in those over 70 years. Linear calcifications were rare before 60 years (1.2%) but present in 24.5% of patients over 70. Calcifications were mentioned in only 3.5% of radiology reports. Conclusions: Periodontoid calcifications are relatively common in patients with neck pain, affecting nearly one-third of individuals over 40 and almost half of those over 70. Their frequent underreporting highlights a critical gap in recognition. Greater awareness and systematic reporting are warranted, as CDS may represent a common, underdiagnosed, and treatable cause of neck pain. Full article

Optic nerve (ON) injury by trauma induces progressive retinal ganglion cell (RGC) death and axonal loss, which leads to irreversible visual impairment and even blindness. Recently, we discovered that cellular senescence is involved in RGC survival regulation post-ON injury, and senolytic (dasatinib and quercetin) treatments can promote RGC survival and electroretinography activity. Here, we aimed to further evaluate the effects of dasatinib and quercetin on RGC dendrites and axons in mice with an ON crush injury. Longitudinal in vivo imaging analysis demonstrated that the RGC dendritic shrinkage was significantly reduced in mice with both individual and combined treatment of dasatinib and quercetin as compared to the vehicle treatment group. Similarly, dasatinib and quercetin treatments significantly promoted axonal regeneration post-ON injury as compared to the vehicle-treated mice. RNA sequencing analysis showed that the differentially expressed genes were enriched in the response to glucocorticoid, calcium ion binding, and cerebral cortex development. Sybr green PCR and immunofluorescence analyses validated that the axonal extension-related gene, meteorin (Metrn), was significantly upregulated in the dasatinib-only and combined dasatinib and quercetin treatments. In summary, this study revealed that dasatinib and quercetin alleviated RGC dendritic shrinkage and promoted axonal regeneration in mice after ON injury, probably mediated through meteorin, suggesting the dendrite repair and axonal regeneration potentials of dasatinib and quercetin for traumatic optic neuropathy treatment. Full article

Metallic implants used in orthopedics, such as titanium alloys, possess excellent mechanical strength but suffer from corrosion and poor bio-integration, often necessitating revision surgeries. Bioactive coatings, particularly hydroxyapatite, can enhance implant osteoconductivity, but high-purity synthetic hydroxyapatite is costly. This study investigates the development and characterization of a low-cost, biocompatible coating using hydroxyapatite derived from an unconventional natural source dromedary bone applied onto a titanium substrate via plasma spraying. Hydroxyapatite powder was synthesized from dromedary femurs through a thermal treatment process at 1000 °C. The resulting powder was then deposited onto a sandblasted titanium dioxide substrate using an atmospheric plasma spray technique. The physicochemical, structural, and morphological properties of both the source powder and the final coating were comprehensively analyzed using Scanning Electron Microscopy, Energy Dispersive X-ray Spectroscopy, X-ray Diffraction, and Fourier-Transform Infrared Spectroscopy. Characterization of the powder confirmed the successful synthesis of pure, crystalline hydroxyapatite, with Fourier-Transform Infrared Spectroscopy analysis verifying the complete removal of organic matter. The plasma-sprayed coating exhibited good adhesion and a homogenous, lamellar microstructure typical of thermal spray processes, with an average thickness of approximately 95 μm. X-ray Diffraction analysis of the coating revealed that while hydroxyapatite remained the primary phase, partial decomposition occurred during spraying, leading to the formation of secondary phases, including tricalcium phosphate and calcium oxide. Scanning Electron Microscopy imaging showed a porous surface composed of fully and partially melted particles, a feature potentially beneficial for bone integration. The findings demonstrate that dromedary bone is a viable and low-cost precursor for producing bioactive hydroxyapatite coatings for orthopedic implants. The plasma spray method successfully creates a well-adhered, porous coating, though process-induced phase changes must be considered for biomedical applications. Full article