Prediction of Loss of Muscle Mass in Sarcopenia Using Ultrasonic Diaphragm Excursion
Background: The diagnosis of sarcopenia is based on the mass and function of appendicular skeletal muscle. It is not clear whether diaphragm excursion is related to muscle mass loss. We try to fill the gap by measuring ultrasonic diaphragm excursion during quiet breathing (Dq) and forced deep breathing (Df) and test whether they could predict the muscle mass loss in sarcopenia.
Methods: The subjects are recruited from the elderly patients diagnosed with pulmonary nodules in community physical examination. According to the definition, the subjects were divided into group A (who did not meet the diagnostic criteria for muscle mass loss in sarcopenia) and group B (who met the criteria). Participants were assessed for ultrasonic diaphragm excursion, pulmonary function, and cardiopulmonary exercise testing. Logistic regression was used to assess the correlation between right diaphragm excursion and skeletal muscle mass, and receiver-operating characteristic curve (ROC) was applied to determine the best threshold.
Results: We recruited 64 elderly participants: 52 in group A (39 males) and 12 in group B (8 males). The Df in group A were higher than in group B (6.02 (5.44-6.60) vs. 4.31 (3.53-5.09) cm, P=0.008). The difference also exists in FVC, FEV1.0, PEF, Pimax, WRmax, and VO2max, but neither in Dq. Logical regression showed that Df was negatively related to muscle mass (B = -0.525, OR = 0.591 (0.378-0.926), P=0.022), even after adjusted age. Based on ROC, a cutoff value of 5.27 cm (AUC = 0.7783, P=0.0028) was selected, and Df ≤ 5.27 cm indicates the increase in odds https://biodas.org/ of existing muscle mass loss.
Conclusion: Ultrasonic diaphragm excursion in forced deep breath is helpful for predicting muscle mass loss in sarcopenia.
Application and Validation of the Tricuspid Annular Plane Systolic Excursion/Systolic Pulmonary Artery Pressure Ratio in Patients with Ischemic and Non-Ischemic Cardiomyopathy
The main aim of this study was to assess the prognostic utility of TAPSE/PASP as an echocardiographic parameter of maladaptive RV remodeling in cardiomyopathy patients using cardiac magnetic resonance (CMR) imaging. Furthermore, we sought to compare TAPSE/PASP to TAPSE. The association of the echocardiographic parameters TAPSE/PASP and TAPSE with CMR parameters of RV and LV remodeling was evaluated in 111 patients with ischemic and non-ischemic cardiomyopathy and cut-off values for maladaptive RV remodeling were defined.
In a second step, the prognostic value of TAPSE/PASP and its cut-off value were analyzed regarding mortality in a validation cohort consisting of 221 patients with ischemic and non-ischemic cardiomyopathy. A low TAPSE/PASP (<0.38 mm/mmHg) and TAPSE (<16 mm) were associated with a lower RVEF and a long-axis RV global longitudinal strain (GLS) as well as higher RVESVI, RVEDVI and NT-proBNP.
A low TAPSE/PASP, but not TAPSE, was associated with a lower LVEF and long-axis LV GLS, and a higher LVESVI, LVEDVI and T1 relaxation time at the interventricular septum and the RV insertion points. Furthermore, in the validation cohort, low TAPSE/PASP was associated with a higher mortality and TAPSE/PASP was an independent predictor of mortality. TAPSE/PASP is a predictor of maladaptive RV and LV remodeling associated with poor outcomes in cardiomyopathy patients.
Preoperative Computed Tomography Angiography Reveals Leaflet-Specific Calcification and Excursion Patterns in Aortic Stenosis
Background: Computed tomography-based evaluation of aortic stenosis (AS) by calcium scoring does not consider interleaflet differences in leaflet characteristics. Here, we sought to examine the functional implications of these differences.
Methods: We retrospectively reviewed the computed tomography angiograms of 200 male patients with degenerative calcific AS undergoing transcatheter aortic valve replacement and 20 male patients with normal aortic valves. We compared the computed tomography angiography (CTA)-derived aortic valve leaflet calcification load (AVLCCTA), appearance, and systolic leaflet excursion (LEsys) of individual leaflets. We performed computer simulations of normal valves to investigate how interleaflet differences in LEsys affect aortic valve area. We used linear regression to identify predictors of leaflet-specific calcification in patients with AS.
Results: In patients with AS, the noncoronary cusp (NCC) carried the greatest AVLCCTA (365.9 [237.3-595.4] Agatston unit), compared to the left coronary cusp (LCC, 278.5 [169.2-478.8] Agatston unit) and the right coronary cusp (RCC, 240.6 [137.3-439.0] Agatston unit; both P<0.001). However, LCC conferred the least LEsys (42.8º [38.8º-49.0º]) compared to NCC (44.8º [41.1º-49.78º], P=0.001) and RCC (47.7º [42.0º-52.3º], P<0.001) and was more often characterized as predominantly thickened (23.5%) compared to NCC (12.5%) and RCC (16.5%). Computer simulations of normal valves revealed greater reductions in aortic valve area following closures of NCC (-32.2 [-38.4 to -25.8]%) and RCC (-35.7 [-40.2 to -32.9]%) than LCC (-24.5 [-28.5 to -18.3]%; both P<0.001). By linear regression, the AVLCCTA of NCC and RCC, but not LCC, predicted LEsys (both P<0.001) in patients with AS. Both ostial occlusion and ostial height of the right coronary artery predicted AVLCCTA, RCC (P=0.005 and P=0.001).
Conclusions: In male patients, the AVLCCTA of NCC and RCC contribute more to AS than that of LCC. LCC’s propensity for noncalcific leaflet thickening and worse LEsys, however, should not be underestimated when using calcium scores to assess AS severity.
Keywords: aortic valve stenosis; calcium; computed tomography angiography; computer simulation; transcatheter aortic valve replacement.
Polysomnographic Plethysmography Excursions are Reduced in Obese Elderly Men
Sleep apnea is a widespread disorder and is defined by the complete or partial cessation of breathing. Obstructive sleep apnea (OSA) is caused by an obstruction in the upper airway while central sleep apnea (CSA) is characterized by a diminished or absent respiratory effort. It is crucial to differentiate between these respiratory subtypes as they require radically different treatments.
Currently, diagnostic polysomnography (PSG) is used to determine respiratory thoracic and abdominal movement patterns using plethysmography belt signals, to distinguish between OSA and CSA. There is significant manual technician interrater variability between these classifications, especially in the evaluation of CSA. We hypothesize that an increased body mass index (BMI) will cause decreased belt signal excursions that increase false scorings of CSA.
The hypothesis was investigated by calculating the envelope as a continuous signal of belt signals in 2833 subjects from the MrOS Sleep Study and extracting a mean value of each of the envelopes for each subject. Using linear regression, we found that an increased BMI was associated with lower excursions during REM sleep (-0.013 [mV] thoracic and -0.018 [mV] abdominal, per BMI) and non-REM (-0.014 [mV] thoracic and -0.012 [mV] abdominal, per BMI). We conclude that increased BMI leads to lower excursions in the belt signals during event-free sleep, and that OSA and CSA events are harder to distinguish in subjects with high BMI. This has a major implication for the correct identification of CSA/OSA and its treatment.
TRAC Antibody |
|||
| 1-CSB-PA024144LA01HU | Cusabio |
|
|
TRAC Polyclonal Antibody |
|||
| A55102 | EpiGentek | 100 µg | 570.55 EUR |
TRAC Antibody, HRP conjugated |
|||
| 1-CSB-PA024144LB01HU | Cusabio |
|
|
TRAC Antibody, FITC conjugated |
|||
| 1-CSB-PA024144LC01HU | Cusabio |
|
|
TRAC Antibody, Biotin conjugated |
|||
| 1-CSB-PA024144LD01HU | Cusabio |
|
|
TRAC-1 Polyclonal Antibody |
|||
| ES6685-100ul | ELK Biotech | 100ul | 279 EUR |
TRAC-1 Polyclonal Antibody |
|||
| ES6685-50ul | ELK Biotech | 50ul | 207 EUR |
TRAC-1 Polyclonal Antibody |
|||
| ABP55686-003ml | Abbkine | 0.03ml | 158 EUR |
TRAC-1 Polyclonal Antibody |
|||
| ABP55686-01ml | Abbkine | 0.1ml | 289 EUR |
TRAC-1 Polyclonal Antibody |
|||
| ABP55686-02ml | Abbkine | 0.2ml | 414 EUR |
Anti-TRAC-1 antibody |
|||
| STJ96080 | St John's Laboratory | 200 µl | 197 EUR |
Anti-TCR alpha/TRAC Antibody |
|||
| A05315 | BosterBio | 100ug/vial | 334 EUR |
TRAC Polyclonal Antibody, Biotin Conjugated |
|||
| A55099 | EpiGentek | 100 µg | 570.55 EUR |
TRAC Polyclonal Antibody, FITC Conjugated |
|||
| A55100 | EpiGentek | 100 µg | 570.55 EUR |
TRAC Polyclonal Antibody, HRP Conjugated |
|||
| A55101 | EpiGentek | 100 µg | 570.55 EUR |
Anti-TRAC-1 / RNF125 antibody |
|||
| STJ70554 | St John's Laboratory | 100 µg | 359 EUR |
TRAC ORF Vector (Human) (pORF) |
|||
| ORF034213 | ABM | 1.0 ug DNA | Ask for price |
T Cell Receptor Alpha (TRAC) Antibody |
|||
| abx415683-01mg | Abbexa | 0.1 mg | 592 EUR |
T Cell Receptor Alpha (TRAC) Antibody |
|||
| abx415684-50ug | Abbexa | 50 ug | 537 EUR |