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Biomedical subjects

M Del Fabbro

Publications and source records attributed to M Del Fabbro.

At least 19 recordsLinked to original sources

Relation between serum creatinine and body mass index in elite athletes of different sport disciplines.

OBJECTIVES: To document the relation between serum creatinine concentration and body mass index in elite athletes from five different sports, and to study potential differences among athletes performing different sports with different features and requirements. METHODS: Before the start of the competitive season, serum creatinine was measured in 151 elite athletes from five different sports: rugby (n = 44), soccer (n = 27), alpine skiing (n = 34), sailing (n = 22), cycling (n = 24). Pearson's correlation analysis was used to evaluate the relation between serum creatinine and body mass index (BMI). Analysis of variance and unpaired Student's t test were used to compare creatinine concentration and BMI in different sport disciplines. RESULTS: In the whole group of athletes, a positive correlation between serum creatinine and BMI was found (r = 0.48, p<0.001). Significant differences in creatinine concentration and BMI were found between athletes competing in different sports: their mean (SD) values were respectively 1.31 (0.12) mg/dl and 28.83 (2.41) for rugby players, 1.27 mg/dl (0.10) and 23.10 (1.01) for soccer players, 1.15 (0.11) mg/dl and 25.8 (1.50) for skiers, 1.08 (0.11) mg/dl and 26.93 (2.36) for sailors, and 0.91 (0.07)mg/dl and 21.33 (1.21) for cyclists. CONCLUSIONS: There is a correlation between creatinine concentration and BMI in elite athletes competing in different sports characterised by different kinds of training, competitive season, and involvement of aerobic and anaerobic metabolism. Interpretation of creatinine concentrations in male athletes should consider professional status as well as the specific sport performed. All athletes should be monitored with consecutive creatinine assessments, using as the baseline the concentration determined before the start of training and the competitive season, but taking into consideration the specific sport performed and the BMI until equations that include creatinine and factors that affect its concentration are used.

Adolescent↗

Haematological parameters in elite rugby players during a competitive season.

We assessed haematological parameters and possible modifications in elite rugby players throughout a competitive season for increasing the knowledge of physiological characteristics of these sportsmen. Blood samples were collected from the members of the Italian National rugby team at four consecutive training camps during a whole competitive season. Forty-four athletes were recruited for the first camp, 36 for the second, 30 for the third and 32 for the fourth. Due to turnover of the subjects during the season only 13 athletes could be examined at all four camps, and another six in the first three camps. Therefore, we selected the data of these 19 athletes. Iron and transferrin saturation were stable, whilst ferritin increased at the end of the season. The modifications of the soluble transferrin receptor (sTFR) were linked to those of haematocrit: sTFR increased after training and during the competition period when haemoglobin and haematocrit decreased, and decreased at the end of the season. Haemoglobin and haematocrit showed slightly higher levels during the first part of the season and decreased in the second half, when physical demand was high, as demonstrated by biochemical additional tests. Leucocytes and platelets were stable throughout the season. Haematological and iron metabolism parameters in the elite rugby players examined during a whole season fall within physiological range of values. The variability of the parameters during the season is related to training and competition workload. Reticulocytes and sTFR are the most sensitive parameters for studying the iron metabolism of the athletes.

Analysis of Variance↗

Endoscopic periradicular surgery: a prospective clinical study.

We did apicectomies of 30 teeth with periradicular lesions in 23 patients, using a 3 mm endoscope. Two patients failed to attend for postoperative assessment and of the remaining 21 patients who had 28 teeth treated the operation was judged after 1 year to be a success in 26 (93%).

Adult↗

Effect of root-end resection and root-end filling on apical leakage in the presence of core-carrier root canal obturation.

AIM: To evaluate the apical seal of canals filled with a core-carrier obturator following root-end resection with and without a root-end filling. METHODOLOGY: Thirty single-rooted human teeth with single canals were used. Root canal treatment was performed and canals filled with a core-carrier obturation technique. The teeth were then randomly assigned to three groups (n = 10). In the first group root canal filling only was performed. After orthograde filling, the teeth of the second group were resected apically, perpendicular to the major axis of the root. In the third group after apical resection, a root-end cavity was prepared using ultrasonic diamond retrotips and the cavities filled with Super-EBA cement. During a period of 3 h and with a headspace pressure of 0.12 atm, methylene-blue solution was forced through a tube that was connected to the apical end of each tooth specimen. The coronal end of the tooth was connected to a capillary tube containing an air bubble. Leakage was evaluated by observing the distal displacement of the air bubble. The roots were then sectioned along their long axis. Using a stereomicroscope, linear dye infiltration at the dentine-cement interface was determined. Kruskal-Wallis and Mann-Whitney tests were used to compare the three groups. RESULTS: Linear dye infiltration was significantly greater in root canals filled with the core-carrier obturators and resected apically (0.9 +/- 0.9 mm) when compared with those that had root-end fillings (0.2 +/- 0.4 mm). Air bubble displacement was not observed. CONCLUSION: Root-end filling improves the sealing of roots with core-carrier obturation following root-end resection.

Adolescent↗

Steady-state pleural fluid flow and pressure and the effects of lung buoyancy.

Both theoretical and experimental studies of pleural fluid dynamics and lung buoyancy during steady-state, apneic conditions are presented. The theory shows that steady-state, top-to-bottom pleural-liquid flow creates a pressure distribution that opposes lung buoyancy. These two forces may balance, permitting dynamic lung floating, but when they do not, pleural-pleural contact is required. The animal experiments examine pleural-liquid pressure distributions in response to simulated reduced gravity, achieved by lung inflation with perfluorocarbon liquid as compared to air. The resulting decrease in lung buoyancy modifies the force balance in the pleural fluid, which is reflected in its vertical pressure gradient. The data and model show that the decrease in buoyancy with perfluorocarbon inflation causes the vertical pressure gradient to approach hydrostatic. In the microgravity analogue, the pleural pressures would be toward a more uniform distribution, consistent with ventilation studies during space flight. The pleural liquid turnover predicted by the model is computed and found to be comparable to experimental values from the literature. The model provides the flow field, which can be used to develop a full transport theory for molecular and cellular constituents that are found in pleural fluid.

Animals↗

Pulmonary interstitial pressure and tissue matrix structure in acute hypoxia.

Pulmonary interstitial pressure was measured via micropuncture in anesthetized rabbits in normoxia and after breathing 12% O(2). In normoxia [arterial PO(2) = 88 +/- 2 (SD) mmHg], pulmonary arterial pressure and pulmonary interstitial pressure were 16 +/- 8 and -9.6 +/- 2 cmH(2)O, respectively. After 6 h of hypoxia (arterial PO(2) = 39 +/- 16 mm Hg), the corresponding values were 30+/-8 and 3.5+/-2.5 cm H(2)O (P<0.05). Pulmonary interstitial proteoglycan extractability, evaluated by hexuronate assay after 0.4 M guanidinium hydrochloride extraction, was 12.3, 32.4, and 60.6 microg/g wet tissue in normoxia and after 3 and 6 h of hypoxia, respectively, indicating a weakening of the noncovalent bonds linking proteoglycans to other extracellular matrix components. Gel filtration chromatography showed an increased fragmentation of chondroitin sulfate- and heparan sulfate-proteoglycans during hypoxic exposure, accounting for a loss of extracellular matrix native architecture and basement membrane structure. Gelatin zymography demonstrated increased amounts of the proteolytically activated form of gelatinase B (matrix metalloproteinase-9) after hypoxic exposure, providing evidence that the activation of proteinases may play a role in hypoxia-induced lung injury.

Animals↗

Pulmonary microvascular and perivascular interstitial geometry during development of mild hydraulic edema.

To study pulmonary arteriolar vasomotion in control conditions and in the transition to hydraulic edema, changes in subpleural pulmonary arteriolar diameter and perivascular interstitial volume were evaluated in anesthetized spontaneously breathing rabbits. Images of subpleural pulmonary microvessels were recorded in control conditions and for up to 180 min during a 0.5 ml x kg(-1) x min(-1) intravenous saline infusion through an intact parietal pleural window. Images were digitized and analyzed with a semiautomatic procedure to determine vessel diameter and perivascular interstitial thickness from which interstitial fluid volume was derived. In control vessels, the diameter of approximately 30-, approximately 50-, and approximately 80-microm arterioles and the perivascular interstitial thickness were fairly stable. During infusion, the diameter increased maximally by 20% in approximately 30 microm vessels, was unchanged in approximately 50 microm vessels, and decreased by 25% in approximately 80-microm arterioles; the perivascular interstitial volume increased by 54% only around 30-microm microvessels. In papaverine-treated rabbits, all arterioles dilated and a larger increase in perivascular interstitial thickness was observed. The data suggest that the opposite vasomotor behavior of 30- and 80-microm arterioles during development of mild edema may represent a local specific response of the pulmonary microcirculation to reduce capillary pressure in the face of an increased transendothelial fluid filtration, thus counteracting progression toward severe edema.

Animals↗

Fluid dynamics of gingival tissues in transition from physiological condition to inflammation.

BACKGROUND: An increase in gingival sulcular fluid filtration is a common clinical sign of early gingivitis. The aim of this study was to describe the fluid dynamics of the gingival interstitial tissues at the level of the sulcus in the transition towards inflammation. METHODS: In 13 anesthetized rabbits, a silk ligature was placed around incisors close to the gingival margin, in order to prevent mechanical cleaning of plaque deposition. After 2 to 7 days, animals were anesthetized and interstitial fluid pressure measured using glass micropipettes connected to a servonull pressure system at the level of the free and attached gingiva. RESULTS: Interstitial pressure was 3.8 +/- 2.9 cmH2O, significantly higher than the normal physiological value (about -1 cmH2O). Colloid osmotic pressure of interstitial fluid samples collected using the wick technique was measured using an osmometer whose membrane had a molecular cut-off of 30 kD and averaged 12.8 +/- 2.8 cmH2O (unchanged relative to control). Mean gingival sulcular fluid flow, measured by placing a PE tube (0.5 mm OD, 0.28 mm ID) in the sulcus, was 0.16 +/- 0.12 microl/h; the mean colloid osmotic pressure was 13.6 +/- 6.6 cmH2O, corresponding to a protein concentration of approximately 2.8 g/dl. Proteins of gingival fluid may leak from inflamed gingival interstitium or derive from bacteria of dental plaque. Histological analysis of gingival biopsies showed neutrophilic polymorphonuclear leukocyte infiltrates in both the dermis and epidermis layer. CONCLUSIONS: Based on hydraulic and colloid osmotic data, the Starling pressure gradient favored filtration from gingival interstitium to the sulcular space, a condition opposite to that observed in healthy gingiva where fluid filtration is absent.

Animals↗

Immediate loading of Osseotite implants: a case report and histologic analysis after 4 months of occlusal loading.

A growing number of clinical reports show that early and immediate loading of endosseous implants may lead to predictable osseointegration; however, these studies provide mostly short- to mid-term results based only on clinical mobility and radiographic observation. Other methods are needed to detect the possible presence of a thin fibrous interposition of tissue that could increase in the course of time and lead to clinical mobility A histologic evaluation was performed on two immediately loaded Osseotite implants retrieved after 4 months of function from one patient. He had received a total of 12 implants in the mandible, of which six were immediately loaded and six were left to heal in a submerged way Clinical and histologic osseointegration was consistently achieved for both of the retrieved immediately loaded implants. Osteogenesis and bone remodeling on the Osseotite surface were not impeded by immediate loading as shown by histomorphometric evaluation, which revealed high levels of bone-to-implant contact ranging from 78% to 85%. This immediate loading protocol involving bilateral splinting of six Osseotite implants in the mandible proved to be successful after 4 months of loading. Further long-term clinical and histologic studies are needed before introducing this immediate loading protocol as a routine procedure in implant therapy.

Bone Remodeling↗

[Neutrophil physiology: role and mechanism of action in the immune response at gingival level].

Polymorphonuclear neutrophil granulocytes (PMN) are considered the most important cells of the host immune response against bacterial challenge. The functional mechanism of PMN consists of different steps: tethering, rolling, primary adhesion to the vascular wall, firm adhesion to the activated endothelium in the inflamed region, trans-migration across endothelium, chemotaxis, contact with the bacterium and phagocytosis and, finally, killing of the micro-organism by releasing hydrolytic enzymes and/or by production of toxic substances such as free radicals. Each of these steps is controlled by interactions between cells and many components of the immune system or inflammatory mediators. These interactions generate specific signals, important for cell regulation. Recent technological advances in molecular biology and immunobiology allowed to disclose the precise role of various molecules involved in the immune response, that regulate PMN function; conversely, more factors have been identified, whose role is still unknown. In the process of adhesion, for example, many classes of molecules are involved (selectins, integrins, ICAMs). The interaction of these molecules (es.: selectin) with their ligands (non completely discovered) is characteristic of specific stages, but may also regulate the successive steps (integrin activation). In periodontal infections, PMNs of gingival tissue migrate towards bacteria of dental plaque along a chemotactic gradient of specific factors (ICAM-1, IL-8) produced by cells of the junctional epithelium. Such gradient is essential to drive PMNs through molecular traffic. Among the mechanisms used by PMNs to kill bacteria, the importance of nitric oxide (NO) production has been recently pointed out.

Cations, Divalent↗

[Congenital neutrophil defects and periodontal diseases].

An alteration of the immune system function is one of the main factors involved in the development of periodontal disease. Polymorpho-nuclear neutrophil leukocytes (PMN) play a crucial role in the cell-mediated immune response against bacterial challenge. The mechanism of neutralization of pathogen microorganisms by PMNs involves many different steps: adhesion to capillary endothelium in the inflamed region, trans-endothelial migration, chemotaxis, phagocytosis and, ultimately, bacterial killing by oxidative and non-oxidative mechanisms. A defect in one of these steps leads to altered neutrophil function and, consequently, to a higher host susceptibility to periodontal tissue infection. The main intrinsic neutrophil diseases such as neutropenia, leukocyte adhesion deficiency (LAD-1), Chediak-Higashi syndrome, Papillon-Lefèvre syndrome, chronic granulomatous disease (CGD), are often related to severe and early-onset forms of periodontitis, as described by many evidences in the literature. Therefore PMN dysfunctions, both intrinsic and extrinsic, represent an important risk factor for periodontal disease. Studies on the basic molecular mechanisms of such dysfunctions, also in terms of genetic polymorphisms, recently allowed to identify some specific markers related to a higher susceptibility to the development of disease. Many researches have yet to be performed aiming to gain insight on the dynamics of PMN activation and interaction with other cells, in order to improve and modulate neutrophil function and to develop specific approaches for care and prevention of periodontal diseases.

Humans↗

Subatmospheric pressure in the rabbit pleural lymphatic network.

1. Hydraulic pressure in intercostal and diaphragmatic lymphatic vessels was measured through the micropuncture technique in 23 anaesthetised paralysed rabbits. Pleural lymphatic vessels with diameters ranging from 55 to 950 microm were observed under stereomicroscope view about 3-4 h after intrapleural injection of 20 % fluorescent dextrans. 2. Lymphatic pressure oscillated from a minimum (Pmin) to a maximum (Pmax) value, reflecting oscillations in phase with cardiac activity (cardiogenic oscillations) and lymphatic myogenic activity. With intact pleural space, Pmin in submesothelial diaphragmatic lymphatic vessels of the lateral apposition zone was -9.1 +/- 4.2 mmHg, more subatmospheric than the simultaneously recorded pleural liquid pressure amounting to -3.9 +/- 1.2 mmHg. In extrapleural intercostal lymphatic vessels Pmin averaged -1.3 +/- 2. 7 mmHg. 3. Cardiogenic pressure oscillations (Pmax - Pmin), were observed in all recordings; their mean amplitude was about 5 mmHg and was not dependent upon frequency of cardiac contraction, nor lymphatic vessel diameter, nor the Pmin value. 4. Intrinsic contractions of lymphatic vessel walls caused spontaneous pressure waves of about 7 mmHg in amplitude at a rate of 8 cycles min-1. 5. These results demonstrated the ability of pleural lymphatic vessels to generate pressure oscillations driving fluid from the subatmospheric pleural space into the lymphatic network.

Animals↗

Fluid dynamics of gingival tissues.

Gingival hydraulic interstitial pressure was measured with glass micropipettes in 18 anesthetized rabbits at the level of the free gingiva, attached gingiva and oral mucosa facing the incisors and molar teeth. Samples of gingival interstitial tissue fluid were also collected by inserting nylon wicks in the subepithelial layer of the oral mucosa. Colloid osmotic pressure of interstitial fluid samples was measured with an osmometer whose membrane had a molecular cutoff of 30 kD. Hydraulic interstitial pressure from the free gingiva, at an average distance of 300 microns from sulcular space, was -1.3 +/- 0.9 (SD) cmH2O. Mean colloid osmotic pressure of gingival tissues interstitial fluid was 13.1 cmH2O, corresponding to a protein concentration of 2.8 g/dl. The thickness of the sulcular epithelium and of the oral gingival epithelium (data from 2 rabbits) were approximately 100 microns; the minimal distance of microvessels from the surface of the sulcular epithelium was approximately 150 microns. Based on hydraulic and colloid osmotic data, the Starling balance of pressures causes fluid filtration from gingival capillaries to gingival interstitium; however, across the sulcular epithelium, the pressure gradient sustains fluid absorption from the sulcus into the gingival interstitium. Plasma proteins may leak from microvessels into gingival interstitium, down convective bulk flow and via a concentration dependent diffusive component. At sulcular level, proteins may leak into the sulcus down a concentration gradient. Thus, at sulcular level a peculiar condition occurs in that there is an absorption gradient for water but a filtration gradient for plasma proteins.

Absorption↗

An improved technique for studying pleural fluid pressure and composition in rabbits.

Knowledge of pleural liquid pressure (Pliq) and composition is crucial for studies concerning intrapleural fluid dynamics, and pleural fluid turnover. We measured Pliq at intercostal and costal levels in anaesthetized spontaneously breathing rabbits using a minimally invasive method that assures a long-lasting hydraulic continuity between the pleural liquid and the recording system. Polyethylene tubes were glued either to the exposed endothoracic fascia or inserted into a rib to provide a scaled connection to the recording system. After inducing a pneumothorax with nitrous oxide (N2O) via an intrapleural cannula, a hole (approximately 0.7 mm2) was pierced in the parietal pleura through the tube lumen. The tubes were then connected to pressure transducers and the whole system was filled with heparinized saline to the level of the parietal pleura; finally the pneumo-thorax was removed after N2O washout and Pliq recordings were performed. A different kind of tube was used to obtain microsamples of pleural fluid (2.5-3 microliters) during spontaneous breathing; colloid osmotic pressure of the microsamples (pi liq) was measured with an osmometer, and averaged 9.3 +/- 1.5 cm H2o (n = 70 samples). When pooled and plotted against lung height end-expiratory intercostal and costal Pliq data scattered along a single regression line with a slope of -0.83 and -0.90 cm H2O cm(-1) in supine and prone animals, respectively. End-inspiratory costal Pliq was significantly more subatmospheric than intercostal in the ventral region of the chest (P < 0.05), and less subatmospheric in the dorsal region, regardless of posture. The techniques presented here could be helpful in gaining a greater insight into the physiology and pathophysiology of the pleural space in terms of pleural fluid dynamics and turnover.

Animals↗

A semiautomatic procedure for edge detection of in vivo pulmonary microvessels and interstitial space.

OBJECTIVE: To develop an algorithm to detect the edges between lung tissue, perivascular interstitium, and microvessel using digital processing of in vivo microscopic images of lung surface. METHODS: A numerical technique was developed to identify three different regions (namely, pulmonary microvessel, perivascular interstitium, and lung tissue) based on their corresponding gray level distributions. We present a theoretical demonstration of the method and a semiautomatic procedure that, once the edges are detected, determines microvascular diameters and perivascular interstitium thickness. RESULTS: Microvessel diameters and perivascular interstitium thickness were calculated for precapillary arteriolar branching (40 to 140 microns) and saved in an ASCII file. CONCLUSIONS: We proved that the maximum value of the moving variance is useful to detect the edge between two adjacent regions whose gray level distributions satisfy the condition: magnitude of sigma Y2 - sigma X2 < or = (mu X - mu Y)2, where mu X, mu Y, sigma X2, sigma Y2 are the statistical moments of the two regions X and Y. Moreover, when the regions have similar means, the above conditions is not met, but the edge between them can be detected by the maximum of the moving variance error.

Algorithms↗

Estimation of in vivo pulmonary microvascular and interstitial geometry using digital image analysis.

OBJECTIVE: To determine microvascular diameter and perivascular interstitium thickness at the lung surface in the in situ, in vivo lung. METHODS: Microscopic images of the lung surface collected through a "pleural window" by a videocamera were digitized with a monochrome frame grabber (512 x 512 pixels, 8 bits per pixels) to be computer analyzed by image processing techniques. RESULTS: We found that the maxima in the distribution of the standard deviations of gray levels in adjacent neighbors 7 x 7 pixels wide identify the edges between the microvessel lumen and the surrounding perivascular interstitium. Furthermore, the maxima in the distribution of the standard deviation of the standard deviations of gray levels identify the edges between the perivascular interstitium and the lung tissue. CONCLUSIONS: This technique can be applied to microvessels ranging in diameter from 30 microns to 200 microns and perivascular interstitial thickness of the order of 10-150 microns. Our approach allows for the definition of microvascular geometry even for noisy images and represents an improvement compared to other edge detection methods. The proposed analytical procedure may provide a useful tool to study lung fluid balance and microvascular reactivity in the in situ lung in the normal state and in response to a variety of functional conditions.

Animals↗

Pulmonary interstitial pressure in anesthetized paralyzed newborn rabbits.

In anesthetized paralyzed term newborn rabbits at various postgestational ages (from birth up to 16 days), we measured by micropuncture technique the hydraulic pressure of the pulmonary interstitium (Pip), the extrapleural parietal interstitium, and the pleural liquid. Birth data refer to cesarian-delivered nonbreathing rabbits. Pip increased from 0.5 +/- 2 to 6 +/- 0.7 cmH2O from birth up to 2 h and then decreased, becoming subatmospheric at 5 h and attaining -6 +/- 1.6 cmH2O at 16 days. Over the same period of time, pressure in the extrapleural parietal interstitium and the pleural liquid remained fairly constant at an average value of approximately -1.5 and -2 cmH2O, respectively. The wet-to-dry weight ratio of the lungs decreased from 7.8 +/- 0.4 to 4.9 +/- 0.1 at 16 days. Plasma protein concentration was 4.2 +/- 0.4 g/dl at birth, decreased to 3.2 +/- 0.5 g/dl at 1 h from delivery, and increased back to 4 +/- 0.6 g/dl at 16 days. Pleural liquid protein concentration was 3 +/- 0.1 g/dl at birth and decreased to 1.2 +/- 0.2 g/dl at 16 days. In the first hours of postnatal life, the marked increase in Pip appears to be a key factor in favoring fluid clearance from pulmonary interstitium into the pulmonary capillaries and the pleural space. This factor vanishes after approximately 6 h because of the marked decrease in Pip.

Animals↗

Pulmonary interstitial pressure in intact in situ lung: transition to interstitial edema.

In anesthetized rabbits (n = 25) subject to slow intravenous saline loading (0.4 ml.min-1.kg-1) for 3 h, we measured pulmonary interstitial pressure (Pip) in intact in situ lungs with glass micropipettes inserted directly into the lung parenchyma via a "pleural window." Measurements were done in apneic animals at the end-expiratory volume with O2 delivered in the trachea. Pip was -10 +/- 1.5 (SD) cmH2O in control and increased to 0.6 +/- 3.8 and 5.7 +/- 3.3 cmH2O at 66 and 180 min, respectively. The wet-to-dry weight ratio (W/D) of the lung was 5.04 +/- 0.2 in the control group and 5.34 +/- 0.7 at 180 min (+6%); the corresponding W/D for intercostal muscles were 3.25 +/- 0.03 and 4.19 +/- 0.5 (+28%). Pulmonary interstitial compliance was 0.47 ml.mmHg-1.100 g wet wt-1. Pulmonary arterial and left atrial pressures were 18.4 +/- 2 and 3 +/- 1 cmH2O in control and increased to 19.5 +/- 2.9 and 4.6 +/- 1.7 cmH2O at 180 min, respectively. Aortic flow (cardiac output) increased from 103 +/- 35 to 131 +/- 26 ml/min; pulmonary resistance fell from 0.17 +/- 0.06 to 0.14 +/- 0.05 cmH2O.min.ml-1 (-18%), suggesting that the increase in Pip did not limit blood flow. The pulmonary capillary-to-interstitium filtration pressure gradient decreased sharply from a control value of 10 cmH2O to 0 cmH2O within 60 min because of the increase in Pip and remained unchanged for < or = 180 min. Data suggest that the pulmonary interstitial matrix can withstand fluid pressures above atmospheric, preventing the development of pulmonary alveolar flooding.

Air Pressure↗