Miracle-dz/UniFAR-FTUs huggingface dataset:
Pediatric Traumatic Brain Injury: Characteristic Features, Diagnosis, and Management

Traumatic brain injury (TBI) is the leading cause of death and disability in children. Pediatric TBI is associated with several distinctive characteristics that differ from adults and are attributable to age-related anatomical and physiological differences, pattern of injuries based on the physical ability of the child, and difficulty in neurological evaluation in children. Evidence suggests that children exhibit a specific pathological response to TBI with distinct accompanying neurological symptoms, and considerable efforts have been made to elucidate their pathophysiology. In addition, recent technical advances in diagnostic imaging of pediatric TBI has facilitated accurate diagnosis, appropriate treatment, prevention of complications, and helped predict long-term outcomes. Here a review of recent studies relevant to important issues in pediatric TBI is presented, and recent specific topics are also discussed. This review provides important updates on the pathophysiology, diagnosis, and age-appropriate acute management of pediatric TBI.
Gut microbiota induce IGF-1 and promote bone formation and growth

Significance New interventions are needed to improve bone health and reduce the risk for osteoporosis and fracture. Dysbiosis is increasingly linked to metabolic abnormalities, although the effect of the microbiota on skeletal health is poorly understood. Previous studies suggest microbiota are detrimental to bone by increasing resorption. In this report, we show that the gut resident microbiota promote bone formation, as well as resorption, with long-term exposure to microbiota resulting in net skeletal growth. Microbiota induce the hormone insulin-like growth factor 1 (IGF-1), which promotes bone growth and remodeling. Short-chain fatty acids (SCFAs), produced when microbiota ferment fiber, also induce IGF-1, suggesting a mechanism by which microbiota affect bone health. Manipulating the microbiome or its metabolites may afford opportunities to optimize bone health and growth. Appreciation of the role of the gut microbiome in regulating vertebrate metabolism has exploded recently. However, the effects of gut microbiota on skeletal growth and homeostasis have only recently begun to be explored. Here, we report that colonization of sexually mature germ-free (GF) mice with conventional specific pathogen-free (SPF) gut microbiota increases both bone formation and resorption, with the net effect of colonization varying with the duration of colonization. Although colonization of adult mice acutely reduces bone mass, in long-term colonized mice, an increase in bone formation and growth plate activity predominates, resulting in equalization of bone mass and increased longitudinal and radial bone growth. Serum levels of insulin-like growth factor 1 (IGF-1), a hormone with known actions on skeletal growth, are substantially increased in response to microbial colonization, with significant increases in liver and adipose tissue IGF-1 production. Antibiotic treatment of conventional mice, in contrast, decreases serum IGF-1 and inhibits bone formation. Supplementation of antibiotic-treated mice with short-chain fatty acids (SCFAs), products of microbial metabolism, restores IGF-1 and bone mass to levels seen in nonantibiotic-treated mice. Thus, SCFA production may be one mechanism by which microbiota increase serum IGF-1. Our study demonstrates that gut microbiota provide a net anabolic stimulus to the skeleton, which is likely mediated by IGF-1. Manipulation of the microbiome or its metabolites may afford opportunities to optimize bone health and growth.
Age and copper intake do not affect copper absorption, measured with the use of 65Cu as a tracer, in young infants.

BACKGROUND Copper homeostasis involves a high degree of regulation in which changes in absorption and biliary excretion are the main mechanisms. Whether neonates and small infants can make these changes efficiently is unknown. OBJECTIVE We evaluated the effect of age and copper intake on copper absorption in infants during the first 3 mo of life. DESIGN Thirty-nine healthy infants (19 infants aged 1 mo and 20 infants aged 3 mo) were selected. One-half of the subjects were randomly assigned to receive oral supplementation of 80 mg Cu (as copper sulfate). kg body wt(-1). d(-1) for 15 d. At the end of the trial, copper absorption was measured by using orally administered (65)Cu as a tracer and fecal monitoring of recovered (65)Cu. RESULTS Mean (+/- SD) copper absorption at 1 mo of age was 83.6 +/- 5.8% and 74.8 +/- 9.1% for the unsupplemented and supplemented infants, respectively. The corresponding figures at 3 mo of age were 77.6 +/- 15.2% and 77.7 +/- 11.3%. A two-way analysis of variance showed that age, copper supplementation, and the interaction between age and copper supplementation did not have a significant effect on copper absorption. There was an inverse correlation between total fecal copper and the percentage of (65)Cu absorption (r = -0.50, P < 0.003). CONCLUSION Copper absorption in young infants is high but does not respond to copper intake within the range tested.
Regulation of fiber size, oxidative potential, and capillarization in human muscle by resistance exercise.

To examine the hypothesis that increases in fiber cross-sectional area mediated by high-resistance training (HRT) would result in a decrease in fiber capillarization and oxidative potential, regardless of fiber type, we studied six untrained males (maximum oxygen consumption, 45.6 ± 2.3 ml ⋅ kg-1 ⋅ min-1; mean ± SE) participating in a 12-wk program designed to produce a progressive hypertrophy of the quadriceps muscle. The training sessions, which were conducted 3 times/wk, consisted of three sets of three exercises, each performed for 6-8 repetitions maximum (RM). Measurements of fiber-type distribution obtained from tissue extracted from the vastus lateralis at 0, 4, 7, and 12 wk indicated reductions ( P < 0.05) in type IIB fibers (15.1 ± 2.1% vs. 7.2 ± 1.3%) by 4 wk in the absence of changes in the other fiber types (types I, IIA, and IIAB). Training culminated in a 17% increase ( P < 0.05) in cross-sectional area by 12 wk with initial increases observed at 4 wk. The increase was independent of fiber type-specific changes. The number of capillaries in contact with each fiber type increased by 12 wk, whereas capillary contacts-to-fiber area ratios remained unchanged. In a defined cross-sectional field, HRT also increased the capillaries per fiber at 12 wk. Training failed to alter cellular oxidative potential, as measured by succinic dehydrogenase (SDH) activity, regardless of fiber type and training duration. It is concluded that modest hypertrophy induced by HRT does not compromise cellular tissue capillarization and oxidative potential regardless of fiber type.
Novel Neuromuscular Electrical Stimulation System for Treatment of Dysphagia after Brain Injury

The purpose of this study was to compare the effects of a novel neuromuscular electrical stimulation (NMES) to the effects of conventional treatment in patients with dysphagia after brain injury. In total, 26 patients were non-randomly divided into an experimental group (n = 12) and a control group (n = 14). The experimental group received NMES intervention followed by conventional treatment, including thermal-tactile stimulation with intensive repetition of a dry-swallow task. The control group received conventional treatment without NMES. NMES at a fixed pulse duration of 50 μs and a frequency of 50 Hz was delivered over the skin areas above the motor point of the target muscles, i.e., the bilateral geniohyoid, mylohyoid/anterior belly of the digastric, and thyrohyoid muscles, using a high-voltage pulsed-current device. The two groups received 40-min treatments once a day, 5 days per week, for 8 weeks. Outcome, assessed before and 8 weeks after treatment, was evaluated with regard to the videofluoroscopic dysphagia scale (VDS), the anterior and superior displacement of the hyoid bone and larynx, and the functional oral intake scale. Both groups exhibited improvement, but the experimental group exhibited more significant improvement in the displacement of the hyoid bone and larynx, VDS-total score, and VDS-pharyngeal score than the control group did. The results suggest that NMES combined with conventional treatment is superior to conventional treatment alone in patients with dysphagia following treatment for brain injury. Further investigations are necessary to examine the effects of NMES in patients with more varied types of diseases.
Consumption of fat-free fluid milk after resistance exercise promotes greater lean mass accretion than does consumption of soy or carbohydrate in young, novice, male weightlifters.

BACKGROUND Acute consumption of fat-free fluid milk after resistance exercise promotes a greater positive protein balance than does soy protein. OBJECTIVE We aimed to determine the long-term consequences of milk or soy protein or equivalent energy consumption on training-induced lean mass accretion. DESIGN We recruited 56 healthy young men who trained 5 d/wk for 12 wk on a rotating split-body resistance exercise program in a parallel 3-group longitudinal design. Subjects were randomly assigned to consume drinks immediately and again 1 h after exercise: fat-free milk (Milk; n = 18); fat-free soy protein (Soy; n = 19) that was isoenergetic, isonitrogenous, and macronutrient ratio matched to Milk; or maltodextrin that was isoenergetic with Milk and Soy (control group; n = 19). RESULTS Muscle fiber size, maximal strength, and body composition by dual-energy X-ray absorptiometry (DXA) were measured before and after training. No between-group differences were seen in strength. Type II muscle fiber area increased in all groups with training, but with greater increases in the Milk group than in both the Soy and control groups (P < 0.05). Type I muscle fiber area increased after training only in the Milk and Soy groups, with the increase in the Milk group being greater than that in the control group (P < 0.05). DXA-measured fat- and bone-free mass increased in all groups, with a greater increase in the Milk group than in both the Soy and control groups (P < 0.05). CONCLUSION We conclude that chronic postexercise consumption of milk promotes greater hypertrophy during the early stages of resistance training in novice weightlifters when compared with isoenergetic soy or carbohydrate consumption.
Influence of prior Na+ pump activity on pump and Na+/Ca2+exchange currents in mouse ventricular myocytes.

We examined the dependence of peak Na+ pump and Na+/Ca2+exchanger currents on prior Na+pump inhibition induced by exposure to zero extracellular K+ in voltage-clamped adult murine ventricular myocytes. Abrupt activation of the Na+ pump by reexposure of myocytes to extracellular K+ with a rapid solution switcher resulted in the development of a transient peak current at ∼500 ms, followed by a decline over 1-2 min to a steady-state level. The magnitudes of both the peak Na+ pump current ( I p) and the peak outward Na+/Ca2+exchange current, activated by rapidly reducing extracellular Na+ to zero with the solution switcher, were dependent on previous Na+ pump activity. [Na+] gradients (Na+-binding benzofuran isophthalate fluorescence) between the patch pipette and the bulk cytosol were relatively small and could not account for the large differences between peak and steady-state I p and reverse Na+/Ca2+exchanger currents. Our results are consistent with the presence of a subsarcolemmal Na+ concentration gradient, which is similar for the Na+ pump and the Na+/Ca2+exchanger. These findings also support the hypothesis that the Na+ pump and the Na+/Ca2+exchanger are colocalized in the sarcolemma.
Energy expenditure in obese women before and during weight loss, after refeeding, and in the weight-relapse period.

In 10 moderately obese women, 24-h energy expenditure (24EE) was measured in a respiration chamber under four conditions: 1) before weight loss (body weight = 77.9 kg), 2) during weight loss (63.9 kg), 3) after realimentation (62.5 kg), and 4) 6-15 mo after the study diet with ad libitum diet (67.7 kg). The 14 +/- 8 kg (mean +/- SD) weight loss produced a decrease in 24EE of 1498 +/- 1138 kJ/d (P < 0.001), ie, a decrease of weight of 107 kJ.kg body wt-1.d-1. The subsequent 24EE (conditions 3 and 4) remained lower than the value before weight loss. A significant correlation was found between changes before and after weight regain in basal respiratory quotient (RQ) and the spontaneous rate of body-weight gain after cessation of the period of low energy intake (r = 0.89, P < 0.01); this suggests that the value of the postabsorptive RQ may be a predictor of relapse of weight gain. After discontinuation of the low energy diet, an elevated postabsorptive RQ shows that the endogenous lipid oxidation is low, a condition favoring weight gain.
Modelling and Predicting Backstroke Start Performance Using Non-Linear and Linear Models

Abstract Our aim was to compare non-linear and linear mathematical model responses for backstroke start performance prediction. Ten swimmers randomly completed eight 15 m backstroke starts with feet over the wedge, four with hands on the highest horizontal and four on the vertical handgrip. Swimmers were videotaped using a dual media camera set-up, with the starts being performed over an instrumented block with four force plates. Artificial neural networks were applied to predict 5 m start time using kinematic and kinetic variables and to determine the accuracy of the mean absolute percentage error. Artificial neural networks predicted start time more robustly than the linear model with respect to changing training to the validation dataset for the vertical handgrip (3.95 ± 1.67 vs. 5.92 ± 3.27%). Artificial neural networks obtained a smaller mean absolute percentage error than the linear model in the horizontal (0.43 ± 0.19 vs. 0.98 ± 0.19%) and vertical handgrip (0.45 ± 0.19 vs. 1.38 ± 0.30%) using all input data. The best artificial neural network validation revealed a smaller mean absolute error than the linear model for the horizontal (0.007 vs. 0.04 s) and vertical handgrip (0.01 vs. 0.03 s). Artificial neural networks should be used for backstroke 5 m start time prediction due to the quite small differences among the elite level performances.
Endothelium removal induces iNOS in rat aorta in organ culture, leading to tissue damage.

After endothelial damage in vivo, there is an induction of nitric oxide synthase (NOS) in the underlying smooth muscle cells. We hypothesized that intrinsic factors could induce NOS independently of blood elements. This was tested using an in vitro organ culture technique. Rat aortas with endothelium removed before 24-h organ culture (ERB) failed to constrict to phenylephrine after culture, whereas with endothelium removal after culture there was a normal constrictor response. Constrictor activity in ERB aortas was restored by the concomitant treatment with either the protein synthesis inhibitor cycloheximide (1 μM) or the NOS inhibitorl- N 5-(1-iminoethyl)ornithine hydrochloride (l-NIO, 100 μM). The ERB aortas also had an elevated NOS activity and induced NOS (iNOS) immunoreactivity. The constrictor response to phenylephrine in ERB aortas was only partially restored by acute application ofl-NIO subsequent to the 24-h organ culture, which suggests that other effects during culture contributed to the diminished tissue response. When ERB aortas were treated with reduced glutathione (GSH, 3 mM for 24 h), acute application of l-NIO then fully restored the constrictor effect. This suggests that peroxynitrite produced during culture may in part be responsible for loss of constrictor effects, and this was substantiated by the presence of nitrated tyrosine residues in aortic proteins and also widespread DNA damage, which was prevented by bothl-NIO and GSH. Thus some of the immediate (24-h) effects of endothelium removal involve intrinsic mechanisms resulting in iNOS synthesis, which leads to both nitric oxide and peroxynitrite generation, with resultant tissue damage and loss of contractile function.
Long-chain n-6 polyunsaturated fatty acids in breast milk decrease the risk of HIV transmission through breastfeeding.

BACKGROUND Breastfeeding accounts for a sizable proportion of infant HIV infections. Some fatty acids (FAs) are potent immunomodulators with virucidal activity, and their primary source in breastfed children is breast milk. OBJECTIVES The aims of the study were to examine whether the percentage weight concentration of FAs in breast milk was associated with the risk of mother-to-child transmission (MTCT) of HIV by breastfeeding and with shedding of cell-free virus (CFV) or cell-associated virus (CAV) in breast milk. DESIGN We conducted a case-control study nested within a cohort of HIV-infected Tanzanian women and children. We matched 59 incident breastfeeding MTCT cases to 59 nontransmitting controls based on the child's age at sample collection. We quantified FAs, CFV, and CAV in a breast milk sample collected before the infant's first positive HIV test. RESULTS After adjustment for indicators of maternal HIV disease stage, the risk of MTCT was inversely related to 11c,14c-eicosadienoic acid [odds ratio (OR) for quartile 4 compared with quartile 1: 0.21; P for trend = 0.04], arachidonic acid (OR: 0.21; P for trend = 0.03), and dihomo-gamma-linolenic acid (OR: 0.24; P for trend = 0.03); the latter 2 were also linearly, inversely related to virus shedding in breast milk. Lauric acid and pentadecanoic acid were associated with increased MTCT, whereas trans FAs were related to higher CAV and CFV. CONCLUSION Increasing concentrations of long-chain n-6 polyunsaturated FAs in breast milk might reduce the risk of MTCT.
Sequential and rapid activation of select caspases during apoptosis of normal intestinal epithelial cells.

Detachment-induced cell death (DICD) is considered to be one of the means by which intestinal epithelial cells (IEC) die of apoptosis as they reach the lumen and are shed. Caspases, a family of cysteine proteases, play a central role in initiating, amplifying, and executing apoptosis; however, the pattern of caspase activation in response to distinct apoptotic stimuli remains unknown. We investigated the kinetics of caspase activation during DICD in freshly isolated human IEC. DNA fragmentation is observed 90 min after detachment and is preceded by the sequential activation of preformed members of the CPP32 family of caspases. Activation of caspase 6 and cleavage of the endogenous caspase substrate poly(ADP-ribose) polymerase (EC 2.4.2.30 ) are detected within 15 min of detachment, 30-45 min before caspase 3 activation. Caspase 1 and caspase 10 are present as proenzymes, yet they remain inactive in response to this trigger of apoptosis. Human IEC are primed to rapidly undergo detachment-induced apoptosis involving the selective and sequential activation of preformed caspases. This study may enhance our understanding of physiological events occurring as IEC are shed. Their rapid apoptotic response to detachment may facilitate the high turnover of cells and ensure homeostasis in the intestinal epithelium.
Dynamic autoregulation in the in vitro perfused hydronephrotic rat kidney.

Renal autoregulation is mediated by tubuloglomerular feedback, operating at 0.03-0.05 Hz, and a faster system, operating at 0.1-0.2 Hz, that has been attributed by exclusion to myogenic vasoconstriction. In this study, we examined dynamic autoregulation in the hydronephrotic rat kidney, which lacks tubuloglomerular feedback but exhibits pressure-induced afferent arteriolar vasoconstriction. Kidneys were harvested under anesthesia from Sprague-Dawley rats and perfused in vitro using defined, colloid-free medium. Renal perfusate flow was assessed during forced pressure fluctuations at mean pressures of 60-140 mmHg. Transfer function analysis revealed passive behavior at 60 mmHg and active, pressure-dependent responses at higher pressures. In all cases, coherence was high (0.89 ± 0.03 between 0.01 and 0.9 Hz). There was a resonance peak in admittance gain at ≈0.3 Hz and an associated broad peak in phase angle. Below this frequency, gain declined progressively. The minimum gain achieved at 0.01-0.05 Hz was pressure sensitive, being 1.08 ± 0.02 at 60 mmHg and 0.71 ± 0.04 at 140 mmHg. These findings are consistent with in vivo results and with model-based predictions of the dynamics of myogenic autoregulation, supporting the postulate that the rapid component of autoregulation reflects operation of a myogenic mechanism.
Regulation of protein synthesis after acute resistance exercise in diabetic rats.

These studies determined whether insulin-like growth factor-I (IGF-I) involvement in exercise-stimulated anabolic processes becomes more evident during hypoinsulinemia. Male Sprague-Dawley rats ( n = 6-12/group) were made diabetic (blood glucose ≅ 300 mg/dl) by partial pancreatectomy (PPX) or remained nondiabetic (glucose ≅ 144 mg/dl). Rats performed acute resistance exercise by repetitive standing on the hindlimbs with weighted backpacks (ex), or they remained sedentary (sed). Resistance exercise caused increases in rates of protein synthesis (nmol Phe incorporated ⋅ g muscle-1 ⋅ h-1, measured for gastrocnemius muscle in vivo 16 h after exercise) for both nondiabetic [sed = 154 ± 6 (SE) vs. ex = 189 ± 7] and diabetic rats (PPXsed = 152 ± 11 vs. PPXex = 202 ± 14, P < 0.05). Arterial plasma insulin concentrations in diabetic rats, ≅180 pM, were less than one-half those found in nondiabetic rats, ≅444 pM, ( P < 0.05). The activity of eukaryotic initiation factor 2B (eIF2B; pmol GDP exchanged/min) was higher ( P < 0.05) in ex rats (sed = 0.028 ± 0.006 vs. ex = 0.053 ± 0.015; PPXsed = 0.033 ± 0.013 vs. PPXex = 0.047 ± 0.009) regardless of diabetic status. Plasma IGF-I concentrations were higher in ex compared with sed diabetic rats ( P < 0.05). In contrast, plasma IGF-I was not different in nondiabetic ex or sed rats. Muscle IGF-I (ng/g wet wt) was similar in ex and sed nondiabetic rats, but in diabetic rats was 2- to 3-fold higher in ex ( P < 0.05) than in sed rats. In conclusion, moderate hypoinsulinemia that is sufficient to alter glucose homeostasis does not inhibit an increase in rates of protein synthesis after acute moderate-intensity resistance exercise. This preserved response may be due to a compensatory increase in muscle IGF-I content and a maintained ability to activate eIF2B.