Kofoedbeatty4921
Report a series of cases in which patients have concomitant superior semicircular canal dehiscence (SSCD) and a dehiscent tegmen tympani with Dural contact to the malleus head (DCMH).
An analysis of radiologic and audiologic data in 4 patients who presented with SSCD and DCMH at a tertiary care institution. A pertinent literature review was performed.
Four patients (5 ears) had SSCD and DCMH. In 3 patients with unilateral DCMH, the mean maximum air-bone gap was 15 dB in the ear with DCMH compared to 50 dB in the ear without DCMH. Of the 5 ears with DCMH, the mean air conduction threshold at 250 Hz was 17 dB compared to 42 dB in the 3 ears without DCMH.
We report the findings of DCMH in a series of 4 patients with bilateral SSCD. This limited series suggests that ears with SSCD and DCMH have less of an air-bone gap than would be expected, as 1 would expect an additive effect of DCMH and SSCD on the air-bone gap.
We report the findings of DCMH in a series of 4 patients with bilateral SSCD. This limited series suggests that ears with SSCD and DCMH have less of an air-bone gap than would be expected, as 1 would expect an additive effect of DCMH and SSCD on the air-bone gap.We have recently shown that pharmacologic inhibition of PTEN significantly increases cardiac arrest survival in a mouse model, however, this protection required pretreatment 30 min before the arrest. To improve the onset of PTEN inhibition during cardiac arrest treatment, we have designed a TAT fused cell-permeable peptide (TAT-PTEN9c) based on the C-terminal PDZ binding motif of PTEN for rapid tissue delivery and protection. Western blot analysis demonstrated that TAT-PTEN9c peptide significantly enhanced Akt activation in mouse cardiomyocytes in a concentration- and time-dependent manner. Mice were subjected to 8 min asystolic arrest followed by CPR, and 30 mice with successful CPR were then randomly assigned to receive either saline or TAT-PTEN9c treatment. Survival was significantly increased in TAT-PTEN9c-treated mice compared with that of saline control at 4 h after CPR. The treated mice had increased Akt phosphorylation at 30 min resuscitation with significantly decreased sorbitol content in heart or brbitol in critical organs.Despite a decline in popularity over the past several decades, cigarette smoking remains a leading cause of cardiovascular morbidity and mortality. Yet, the effects of cigarette smoking on vascular structure and function are largely unknown. To evaluate changes in the mechanical properties of the aorta that occur with chronic smoking, we exposed female apolipoprotein E-deficient mice to mainstream cigarette smoke daily for 24 wk, with room air as control. By the time of euthanasia, cigarette-exposed mice had lower body mass but experienced larger systolic/diastolic blood pressure when compared with controls. Smoking was associated with significant wall thickening, reduced axial stretch, and circumferential material softening of the aorta. Although this contributed to maintaining intrinsic tissue stiffness at control levels despite larger pressure loads, the structural stiffness became significantly larger. Furthermore, the aorta from cigarette-exposed mice exhibited decreased ability to store elastic energy athe aorta to store elastic energy and by decreasing aortic distensibility. Combined with a more vulnerable atherosclerotic phenotype, these findings reveal the biomechanical mechanisms that support the development of cardiovascular disease due to cigarette smoking.Right ventricular failure (RVF) is a serious adverse event after left ventricular assist device (LVAD) implantation but difficult to be characterized. This study aimed to visualize the dynamic circulatory equilibrium of acute RVF after LVAD implantation using a new four-quadrant diagram constructed by 1) cardiac function with central venous pressure (CVP) and cardiac index (CI) axes, 2) arterial vascular resistance with CI and mean blood pressure (mBP) axes, 3) pressure-diuretic function with mBP and net urinary sodium output (net U-Na) axes, and 4) venous compliance with net U-Na and CVP axes. Twenty LVAD patients were stratified into two groups, group S (≤10 days) and group L (>10 days), according to duration of postoperative inotropic support. The preoperative equilibrium loops were small in both groups. In the early postoperative phase, the loop in group S became dramatically enlarged to the left and upward, indicating increased CVP and CI by LVAD support. In group L, however, augmentation of CI was small new system physiological framework can serve as a useful guide for prompt and optimal management of circulatory malfunction.Cardiovascular disease (CVD) affects one in three adults and remains the leading cause of death in America. Advancing age is a major risk factor for CVD. Recent plateaus in CVD-related mortality rates in high-income countries after decades of decline highlight a critical need to identify novel therapeutic targets and strategies to mitigate and manage the risk of CVD development and progression. Vascular dysfunction, characterized by endothelial dysfunction and large elastic artery stiffening, is independently associated with an increased CVD risk and incidence and is therefore an attractive target for CVD prevention and management. Vascular mitochondria have emerged as an important player in maintaining vascular homeostasis. As such, age- and disease-related impairments in mitochondrial function contribute to vascular dysfunction and consequent increases in CVD risk. This review outlines the role of mitochondria in vascular function and discusses the ramifications of mitochondrial dysfunction on vascular health in the setting of age and disease. The adverse vascular consequences of increased mitochondrial-derived reactive oxygen species, impaired mitochondrial quality control, and defective mitochondrial calcium cycling are emphasized, in particular. Current evidence for both lifestyle and pharmaceutical mitochondrial-targeted strategies to improve vascular function is also presented.Extracellular matrix (ECM) exerts a series of biological functions and contributes to almost 30% of the osteogenic process. Periostin is a secreted protein that can alter ECM remodeling in response to vascular injury. read more However, the role of periostin in vascular calcification has yet to be fully investigated. As found in this study, recombinant periostin accelerated the thoracic aortas calcification, increased the expression of glycolysis key enzymes, and disturbed the normal oxidative phosphorylation (OXPHOS) ex vivo, which could be alleviated by the peroxisome proliferation-activated receptor γ (PPARγ) agonist pioglitazone. In vascular smooth muscle cells (VSMCs), periostin promoted VSMC-osteoblastic phenotype transition and calcium deposition and suppressed PPARγ expression. Mechanistically, periostin caused overactivation of glycolysis and mitochondrial dysfunction in VSMCs as assessed by extracellular acidification rate, oxygen consumption rate, and mitochondrial respiratory chain complex activities. Targed arterial calcification and corrected abnormal glycolysis and unbalanced mitochondrial homeostasis. There exists a relationship between periostin and lactate in patients with CAC.Major depressive disorder (MDD) is an independent risk factor for cardiovascular disease (CVD) and its complications; however, causal mechanisms remain unclear. In the present study, we investigate cardiac structural and functional alterations and associated changes in myocardial glycosaminoglycans (GAGs) disaccharide profile in mice that exhibit depression-like behavior. Mice were assigned to the chronic mild stress (CMS) group and nonstress control group (CT). The CMS group was exposed to a series of mild, unpredictable stressors for 7 wk. Mice in the CMS group show a significant decrease in protein expression of hippocampal brain-derived neurotrophic factor (BDNF) and exhibit depression-like behavioral changes, such as learned helplessness and decreased exploration behavior, as compared with the control group. Although cardiac function remained unchanged between the groups, echocardiography analysis showed slightly increased left ventricular wall thickness in the CMS group. Furthermore, the CMS group showsGAGs) of the extracellular matrix, is unexplored. To the best of our knowledge, this is the first study to characterize cardiac proteoglycan/glycosaminoglycan profile in response to depression-like behavioral changes in mice. We observed that chronic mild stress (CMS)-induced depression-like behavior and alterations in glycosaminoglycan profile were associated with structural changes in the heart.
This study sought to investigate complication rates/perioperative metrics after endoscopic carpal tunnel release (eCTR) via wide-awake, local anesthesia, no tourniquet (WALANT) versus sedation or local anesthesia with a tourniquet.
Patients aged 18 years or older who underwent an eCTR between April 28, 2018, and December 31, 2019, by 1 of 2 fellowship-trained surgeons at our single institution were retrospectively reviewed. Patients were divided into 3 groups monitored anesthesia care with tourniquet (MT), local anesthesia with tourniquet (LT), and WALANT.
Inclusion criteria were met by 156 cases; 53 (34%) were performed under MT, 25 (16%) under LT, and 78 (50%) under WALANT. The MT group (46.1 ± 9.7) was statistically younger compared with LT (56.3 ± 14.1,
= .007) and WALANT groups (53.5 ± 15.8,
= .008),
(2, 153) = 6.465,
= .002. Wide-awake, local anesthesia, no tourniquet had decreased procedural times (10 minutes, SD 2) compared with MT (11 minutes, SD 2) and LT (11 minutes, SD 2),
(2, 153) = 5.732,
= .004). Trends favored WALANT over MT and LT for average operating room time (20 minutes, SD 3 vs 32 minutes, SD 6 vs 23 minutes, SD 3, respectively,
(2, 153) = 101.1,
< .001), postanesthesia care unit time (12 minutes, SD 7 vs 112 minutes, SD 26 vs 20 minutes, SD 22, respectively,
(2, 153) =171.1,
< .001), and door-to-door time (137 minutes, SD 21 vs 251 minutes, SD 40 vs 146 minutes, SD 33, respectively,
(2, 153) = 109.3,
< .001). There were no differences in complication rates.
Our data suggest favorable trends for patients undergoing eCTR via WALANT versus MT versus LT.
Our data suggest favorable trends for patients undergoing eCTR via WALANT versus MT versus LT.
To provide higher level evidence on the benefits of a Chinese patent medicine (CPM) (Fufang E'jiao Syrup, FFEJS) for alleviating cancer-related fatigue (CRF), this article describes a protocol for a randomized controlled trial.
We designed a double-blind, placebo-controlled stratified permuted block randomization clinical trial on CRF among 3 types of cancer in China. Participants will be equally allocated to FFEJS group or placebo group according to the randomization sequence and the hospitals they were enrolled at. Each patient will receive 20 ml of either the study formula FFEJS or a placebo formula, 3 times a day for 6 weeks. The follow-up period will be another 4 weeks for safety evaluation. The primary outcome is the difference in improvement of fatigue as measured with the Revised Piper Fatigue Scale-Chinese Version (RPFS-CV). Secondary outcomes include change in fatigue (measured by routine blood panel and hormones in peripheral blood) and QoL (measured by Edmonton symptom assessment scale and Functional Assessment of Cancer Therapy).
