Training artificial neural networks using self-organizing migrating algorithm for skin segmentation.

This study presents an application of the self-organizing migrating algorithm (SOMA) to train artificial neural networks for skin segmentation tasks. We compare the performance of SOMA with popular gradient-based optimization methods such as ADAM and SGDM, as well as with another evolutionary algorithm, differential evolution (DE). Experiments are conducted on the skin dataset, which consists of 245,057 samples with skin and non-skin labels.

Machine learning-enhanced gesture recognition through impedance signal analysis.

Gesture recognition is a crucial aspect in the advancement of virtual reality, healthcare, and human-computer interaction, and requires innovative methodologies to meet the increasing demands for precision. This paper presents a novel approach that combines Impedance Signal Spectrum Analysis (ISSA) with machine learning to improve gesture recognition precision. A diverse dataset that included participants from various demographic backgrounds (five individuals) who were each executing a range of predefined gestures.

Crossmixed convolutional neural network for digital speech recognition.

Digital speech recognition is a challenging problem that requires the ability to learn complex signal characteristics such as frequency, pitch, intensity, timbre, and melody, which traditional methods often face issues in recognizing. This article introduces three solutions based on convolutional neural networks (CNN) to solve the problem: 1D-CNN is designed to learn directly from digital data; 2DS-CNN and 2DM-CNN have a more complex architecture, transferring raw waveform into transformed images using Fourier transform to learn essential features. Experimental results on four large data sets, containing 30,000 samples for each, show that the three proposed models achieve superior performance compared to well-known models such as GoogLeNet and AlexNet, with the best accuracy of 95.

Whole exome sequencing analysis in a couple with three children who died prematurely due to carnitine-acylcarnitine translocase deficiency.

Objective: We investigated a strategy of exome sequencing DNA from the unaffected parents and applied a set of filtering criteria to identify genes where both partners are heterozygous for a potentially pathogenic variant.

Case Report: We report a non-consanguineous couple who had three daughters, all spontaneous preterm birth at 36 weeks gestation and died in the first period after birth, suspected inborn errors of metabolism. Two days after birth, the first daughter presented with difficulty breathing, cyanosis and died; the second died at 33 days old; the third daughter was isolated under special care and was taken to the mother's room, developed the same symptoms and died after 5 days.

Microcephaly primary hereditary (MCPH): Report of novel ASPM variants and prenatal diagnosis in a Vietnamese family.

Objective: MCPH (microcephaly primary hereditary) is a group of autosomal recessive developmental disorders with microcephaly present at birth and intellectual disability. Since a second trimester ultrasound is not able to detect subtypes with minimal prenatal presentations, only prenatal diagnosis by genetic testing can confirm these cases and allow for effective genetic counseling, especially a family with a previously affected child.

Case Report: A 37-year-old women was pregnant for the third time and had two prior children with profound microcephaly and mental retardation.

A case of self-improving collodion ichthyosis in Vietnam.

Autosomal recessive congenital ichthyosis is a heterogeneous group of congenital disorders characterized by aberrant skin cornification and diffuse skin scaling. Some patients with this condition are born encased in a collodion membrane which is later shed, revealing the underlying skin disorder. Self-healing collodion baby (SHCB) is a less common phenotype of this disorder, accounting for about 10% of the patients, in which the membrane peels after several weeks, leaving no underlying skin aberration.

CORRELATION BETWEEN MICRO-CT SECTIONS AND HISTOLOGICAL SECTIONS OF MOUSE SKULL DEFECTS IMPLANTED WITH ENGINEERED CARTILAGE.

One advantage of using cartilage to replace/repair bone is that the implant disappears as bone is formed by endochondral ossification. Previously, we showed that cartilage spheroids, grown in a rotating bioreactor (Synthecon, Inc.) and implanted into a 2 mm skull defect, contributed to healing of the defect.

Local inhibition of Rho signaling by cell-permeable recombinant protein BA-210 prevents secondary damage and promotes functional recovery following acute spinal cord injury.

Spinal cord injury (SCI) leads to robust Rho activation at the lesion site. Here, we demonstrate that BA-210, a cell-permeable fusion protein derived from C3 transferase, formulated in fibrin sealant and delivered topically onto the dura matter, diffuses into the spinal cord and inactivates Rho in a dose-dependent manner. Treatment with BA-210 in rats with thoracic spinal cord contusion increased tissue sparing around the lesion area and led to significant improvement of locomotor function.

Role of aldosterone in angiotensin II-induced cardiac and aortic inflammation, fibrosis, and hypertrophy.

Activation of the renin-angiotensin-aldosterone system is associated with increased extracellular matrix and inflammatory markers in the cardiovascular system. We evaluated the effects of aldosterone antagonism on cardiovascular structure, collagen deposition, and expression of inflammatory markers in 2-week angiotensin (Ang) II-infused rats (120 ng.kg-1.

PPAR-gamma inhibits ANG II-induced cell growth via SHIP2 and 4E-BP1.

The present study evaluated the effects of peroxisome proliferator-activated receptor (PPAR)-gamma activators on ANG II-induced signaling pathways and cell growth. Vascular smooth muscle cells (VSMC) derived from rat mesenteric arteries were treated with ANG II, with/without the AT1 receptor blocker valsartan or the AT2 receptor blocker PD-123319, after pretreatment for 24 h with the PPAR-gamma activators 15-deoxy-delta(12,14)-prostaglandin J2 (15d-PGJ2) or rosiglitazone. Both 15d-PGJ2 and rosiglitazone decreased ANG II-induced DNA synthesis.

Long-term effects of the PPAR gamma activator pioglitazone on cardiac inflammation in stroke-prone spontaneously hypertensive rats.

We investigated the long-term effects of the thiazolidinedione PPARgamma activator pioglitazone on cardiac inflammation in stroke-prone spontaneously hypertensive rats (SHRSP), a model of malignant of hypertension. Six-week-old SHRSP were treated with pioglitazone (10 mg/kg per day p.o.

PPAR alpha activator fenofibrate inhibits myocardial inflammation and fibrosis in angiotensin II-infused rats.

Background: Peroxisome proliferator-activated receptor (PPAR)alpha is highly expressed in the heart. PPAR alpha may play a role in cardiac hypertrophy, but effects on cardiac function, inflammation, and fibrosis are unknown. We tested the hypothesis that the PPAR alpha activator fenofibrate prevents myocardial inflammation and fibrosis in angiotensin (Ang) II-infused rats.

SAM68: a downstream target of angiotensin II signaling in vascular smooth muscle cells in genetic hypertension.

We investigated whether phosphatidylinositol 3-kinase (PI3K) and 68-kDa Src associated during mitosis (SAM68) are involved in angiotensin II (ANG II) growth signaling in vascular smooth muscle cells (VSMCs) from spontaneously hypertensive rats (SHR). PI3K activity was assessed by measuring the phosphorylation of the regulatory subunit p85alpha and kinase activity of the catalytic 110-kDa subunit of PI3K. The PI3K-SAM68 interaction was assessed by coimmunoprecipitation, and SAM68 activity was evaluated by poly(U) binding.

Peroxisome proliferator-activated receptors: vascular and cardiac effects in hypertension.

Peroxisome proliferator-activated receptors (PPAR) are nuclear receptors acting as transcription factors on numerous target genes after heterodimerization with the retinoid X receptor. PPAR-alpha and PPAR-gamma may be activated by different agonists, although the endogenous ligands are unknown. Although PPAR-alpha is mainly involved in fatty acid oxidation and expressed in liver, kidney, and skeletal muscle, and PPAR-gamma is mainly involved in fat cell differentiation and insulin sensitivity, both are expressed in smooth muscle cells and myocardium, although PPAR-gamma are scarce in the latter.

Peroxisome proliferator-activated receptor-alpha and receptor-gamma activators prevent cardiac fibrosis in mineralocorticoid-dependent hypertension.

Peroxisome proliferator-activated receptor (PPAR) activation may prevent cardiac hypertrophy and inhibit production of endothelin-1 (ET-1), a hypertrophic agent. The aim of this in vivo study was to investigate the effects of PPAR activators on cardiac remodeling in DOCA-salt rats, a model overexpressing ET-1. Unilaterally nephrectomized 16-week-old Sprague-Dawley rats (Uni-Nx) were randomly divided into 4 groups: control rats, DOCA-salt, DOCA-salt+rosiglitazone (PPAR-gamma activator, 5 mg/kg per day), and DOCA-salt+fenofibrate (PPAR-alpha activator, 100 mg/kg per day).

Effect of peroxisome proliferator-activated receptor-alpha and -gamma activators on vascular remodeling in endothelin-dependent hypertension.

Objective: Peroxisome proliferator-activated receptors (PPARs) may modulate in vitro the vascular production of vasoactive peptides such as endothelin-1 (ET-1). Thus, we investigated in vivo the interaction between PPARs and ET-1 in deoxycorticosterone acetate (DOCA)-salt rats that overexpress vascular ET-1.

Methods And Results: Unilaterally nephrectomized 16-week-old Sprague-Dawley rats (Uni-Nx) were divided into 4 groups (n=6 each): control group, DOCA-salt group, DOCA-salt+PPAR-gamma activator (rosiglitazone, 5 mg x kg(-1) x d(-1)), or DOCA-salt+PPAR-alpha activator (fenofibrate, 100 mg x kg(-1) x d(-1)).

PPARalpha activator effects on Ang II-induced vascular oxidative stress and inflammation.

Docosahexaenoic acid (DHA), a peroxisome proliferator-activated receptor-alpha (PPARalpha) activator, reduces blood pressure (BP) in some hypertensive models by unclear mechanisms. We tested the hypothesis that DHA would prevent BP elevation and improve vascular dysfunction in angiotensin (Ang) II-infused rats by modulating of NADPH oxidase activity and inflammation in vascular wall. Sprague-Dawley rats received Ang II (120 ng/kg per minute SC) with or without DHA (2.

Impaired myocardial fatty acid oxidation and reduced protein expression of retinoid X receptor-alpha in pacing-induced heart failure.

Background: The nuclear receptors peroxisome proliferator-activated receptor-alpha (PPARalpha) and retinoid X receptor alpha (RXRalpha) stimulate the expression of key enzymes of free fatty acid (FFA) oxidation. We tested the hypothesis that the altered metabolic phenotype of the failing heart involves changes in the protein expression of PPARalpha and RXRalpha.

Methods And Results: Cardiac substrate uptake and oxidation were measured in 8 conscious, chronically instrumented dogs with decompensated pacing-induced heart failure and in 8 normal dogs by infusing 3 isotopically labeled substrates: 3H-oleate, 14C-glucose, and 13C-lactate.

Structure, endothelial function, cell growth, and inflammation in blood vessels of angiotensin II-infused rats: role of peroxisome proliferator-activated receptor-gamma.

Background: Pioglitazone and rosiglitazone, thiazolidinedione peroxisome proliferator-activated receptor-gamma (PPARgamma) activators, reduce blood pressure (BP) in some hypertensive models by unclear mechanisms. We tested the hypothesis that pioglitazone or rosiglitazone would prevent BP elevation and vascular dysfunction in angiotensin (Ang) II-infused rats by direct vascular effects.

Methods And Results: Sprague-Dawley rats received Ang II (120 ng x kg(-1) x min(-1) SC) with or without pioglitazone (10 mg x kg(-1) x d(-1)) or rosiglitazone (5 mg x kg(-1) x d(-1)) for 7 days.

Effect of AT(1) receptor blockade on cardiac apoptosis in angiotensin II-induced hypertension.

Angiotensin II (ANG II) via AT(1) receptors induces apoptosis in cardiomyocytes in vitro. We tested the hypothesis that in vivo AT(1) receptor stimulation is accompanied by cardiac apoptosis and attempted to elucidate the molecular mechanisms involved in the death signaling pathway. Male Sprague-Dawley rats received ANG II (120 ng x kg(-1) x min(-1) sc) for 7 days with or without the AT(1) receptor antagonist losartan (10 mg x kg(-1) x day(-1) orally).

Increased expression of peroxisome proliferator-activated receptor-alpha and -gamma in blood vessels of spontaneously hypertensive rats.

Peroxisome proliferator-activated receptors (PPARs) are a family of ligand-activated transcription factors that include PPAR-alpha, PPAR-gamma, and PPAR-delta. We hypothesized that PPAR expression in blood vessels could be reduced in hypertension to result in increased vascular growth and reduced apoptosis. We investigated the abundance of PPAR-alpha and PPAR-gamma in aorta and mesenteric arteries from young (6-week-old) and adult (16-week-old) spontaneously hypertensive rats (SHR) compared with age-matched control Wistar-Kyoto rats (WKY).

Differential activation of extracellular signal-regulated protein kinase 1/2 and p38 mitogen activated-protein kinase by AT1 receptors in vascular smooth muscle cells from Wistar-Kyoto rats and spontaneously hypertensive rats.

Objectives: The present study investigates effects of angiotensin II on activation of extracellular signal-regulated protein kinase (ERK) 1/2, p38 mitogen activated-protein kinase (p38MAPK) and c-Jun amino terminal kinase (JNK) in vascular smooth muscle cells from spontaneously hypertensive rats (SHR).

Methods: Vascular smooth muscle cells (VSMC) from mesenteric arteries of Wistar-Kyoto (WKY) rats and SHR were studied. Angiotensin II-induced phosphorylation of ERK1/2, JNK and p38MAPK were assessed by Western blot analysis.

Expression of cell cycle proteins in blood vessels of angiotensin II-infused rats: role of AT(1) receptors.

Angiotensin II is an important modulator of cell growth through AT(1) receptors, as demonstrated both in vivo and in vitro. We investigated the role of proteins involved in the cell cycle, including cyclin D1, cyclin-dependent kinase 4 (cdk4), and cyclin-dependent kinase inhibitors p21 and p27 in blood vessels of angiotensin II-infused rats and the effect therein of the AT(1)-receptor antagonist losartan. Male Sprague-Dawley rats were infused for 7 days with angiotensin II (120 ng/kg per minute SC) and/or treated with losartan (10 mg/kg per day orally).