Outcomes and rate of return to play in elite athletes following arthroscopic surgery of the hip.

BACKGROUND: The tremendous physical demands of elite performance increase the risk of elite athletes sustaining various orthopaedic injuries. Hip pain is common in high-level athletes representing up to 6% of all athletic injuries. Expedient diagnosis and effective treatment are paramount for their future sporting careers and to prevent subsequent joint degeneration. PURPOSE: This systematic review aimed to evaluate the outcome and the rate of return to play (RTP) following arthroscopic procedures in the hip (osteoplasty, chondroplasty, labral repair and/or debridement, capsulotomy, capsulorrhaphy or any soft tissue procedure) in elite athletes. Elite athletes were defined as those who represented their country in international contests or were competing professionally for the purpose of this study. METHODS: A computer-based systematic search, following the PRISMA Guidelines, was performed on CENTRAL, PUBMED, EMBASE, SCOPUS, EBSCO, Google Scholar and Web of Science from inception until January 1, 2020, identifying studies that looked at return to sports post-hip arthroscopy in elite athletes. Weighted means were calculated for the RTP rate and duration and for patient-reported outcome measures (PROMs). RESULTS: After eligibility screening, 22 articles were included with a total of 999 male and seven female patients, 1146 hips and a mean age of 28.4 ± 3.2 years. The mean follow-up period was 35.8 ± 13.4 months and 15.9 ± 9.6% of athletes had undergone bilateral procedures. Overall, 93.9% (95% CI: 90.5, 96.6, P < 0.0001) of patients demonstrated RTP after 6.8 ± 2.1 months post-surgery and all PROMs improved post-operatively. During follow-up, 9.6% (95% CI: 5.2, 15.2, P = 0.025) patients needed further intervention. CONCLUSION: A high percentage of elite athletes return to the same level of competition after hip arthroscopy, with a low rate of further interventions. Hip arthroscopy appears to be an efficacious treatment for hip and/or groin pain, caused by pathologies such as FAI or labral tears, in elite athletes in the shorter term. Long term outcomes need further evaluation.

Keeping children safe: a model for predicting families at risk for recurrent childhood injuries.

OBJECTIVE: Existing research on recurrent unintentional injury (UI) focuses on the individual child rather than family risks. This study developed a statistical model for identifying families at highest risk, for potential use in targeting public health interventions. STUDY DESIGN: A retrospective birth cohort study of hospital and emergency room (ER) medical records of children born in Ziv hospital between 2005 and 2012, attending ER for UI between 2005 and 2015, was conducted. METHODS: Using national IDs, we assigned children to mothers and created the family entity. Data were divided into two time periods. Negative binomial regression was used to examine predictive factors in the first period for recurrent child UI in the second period. Sensitivity analyses were conducted to examine the model's robustness. RESULTS: Eight predictive factors for child injury (P < 0.05) were found: male gender, the number of UI visits, the number of illness visits, age 36-59 months, birth weight <1500 g, maternal ER visits, siblings' UI visits, and the number of younger siblings. Some predictive factors are documented in the literature; others are novel. Five were significant in all sensitivity analyses. CONCLUSIONS: These factors can assist in predicting risk for a child's repeat UI and family's cumulative UI risk. The model may offer a valuable and novel approach to targeting interventions for families at highest risk.

Anti-phosphorylated histone H2AThr120: a universal microscopic marker for centromeric chromatin of mono- and holocentric plant species.

Based on the analysis of 20 different monocot and eudicot species, we propose that the centromeric distribution of the phosphorylated histone H2AThr120 is evolutionary highly conserved across species with mono- and holocentric chromosomes. Therefore, antibodies recognizing the phosphorylated threonine 120 of the histone H2A can serve as a universal marker for the cytological detection of centromeres of mono- and holokinetic plant species. In addition, super resolution microscopy of signals specific to the centromere-specific histone H3 variant CENH3 and to H2AThr120ph revealed that these histone variants are incorporated into different nucleosomes, which form distinct, partly intermingled chromatin domains. This specific arrangement of both histone variants suggests different centromeric functions during the cell cycle.

Octreotide prevents the early increase in renal insulin-like growth factor binding protein 1 in streptozotocin diabetic rats.

The early renal growth in streptozotocin (STZ)-induced diabetic rats is preceded by a transient rise in renal tissue insulin-like growth factor (IGF)-I concentration. Administration of the long-acting somatostatin analog octreotide to STZ diabetic rats inhibits the early increase in kidney IGF-I and the increase in kidney size without affecting metabolic control. We studied the effects of octreotide treatment on the intrarenal IGF axis at 2 and at 7 days after the induction of STZ diabetes. Two days after induction of diabetes, kidney IGF-I was increased from 850 +/- 43 ng/g tissue in controls to 1,648 +/- 165 ng/g tissue (P < 0.001) in diabetic animals. The diabetes-associated increase in renal IGF-I 48 h after STZ injection was totally prevented by octreotide (IGF = 780 +/- 57 ng/g tissue). However, 7 days after the induction of diabetes, kidney IGF-I was similar to that of control and was not affected by octreotide. No difference in serum IGF-I was observed between controls and diabetic rats after 2 days of diabetes; however, octreotide treatment resulted in a significant decrease of serum IGF-I after 2 days when compared with control rats (P < 0.05). Renal IGF-I mRNA was significantly decreased to the same extent in both diabetic groups 2 and 7 days after the induction of diabetes, while renal IGF-I receptor (IGF-IR) mRNA was unchanged in rats from either group. Two days after induction of diabetes, renal insulin-like growth factor binding protein (IGFBP)-1 mRNA and 30-kDa IGFBPs (containing IGFBP-1) increased by 186 and 192%, respectively, in untreated diabetic animals compared with controls. Octreotide treatment prevented the diabetes-associated rise in renal IGFBP-1 mRNA and protein. However, 7 days after the induction of diabetes, renal IGFBP-1 mRNA and protein were similarly increased in both octreotide-treated or untreated diabetic rats. Renal IGFBP-3 gene expression and protein and IGFPB-5 mRNA remained unchanged after 2 and 7 days of diabetes when treated or untreated with octreotide. We conclude that the well-known inhibitory effect of octreotide on the early increase in renal IGF-I concentration and renal size in diabetes may be mediated through a direct effect on renal IGFBP-1 levels.

The effect of low dose octreotide administration on renal function and on gene expression of IGF-I axis components in experimental diabetes mellitus.

The present study was undertaken to assess the chronic effects of low dose octreotide (Oc) administration in rats with experimental diabetes mellitus (DM). Metabolic and clearance studies were performed in control normal rats, in rats with streptozotocin-induced DM of 1 week duration and in similar DM rats treated with Oc, 10-20 microg/day. Gene expression of IGF-I, IGF-I receptor (IGF-I R) and IGF-binding protein-1 (IGFBP-1) was examined in renal tissue from normal DM animals and DM animals treated with Oc 10, 20 and 100 microg/day. Seven days of Oc administration, 10 microg/day, in rats with experimental DM, was associated with enhanced hyperglycemia, increased glomerular filtration rate and urinary sodium excretion as compared with untreated DM animals. After a higher Oc dose, 20 microg/day, however, there were no significant changes in renal function and in glycemic control. Significant increases in kidney weight and kidney weight/body weight ratio were seen in DM rats as compared with control intact animals. These changes were not affected by Oc therapy in various doses. Induction of DM was associated with a marked increase in renal IGFBP-1 mRNA expression. There were no significant changes in the expression of IGF-I or IGF-I R mRNA. Oc therapy in a low or high dose did not affect gene expression of IGF-I, IGF-I R or IGFBP-1. Thus, the response to chronic low dose Oc administration of DM rats may vary from enhanced hyperglycemia and hyperfiltration to a lack of change in renal function or in glycemic control. Low dose Oc therapy was not associated with significant variations in renal mass or in the gene expression of IGF-I axis components. These findings are at variance with previously published studies which show a suppressive effect of Oc on renal function and growth in experimental diabetes. This apparent discrepancy may be related to the duration of treatment or to a biphasic physiological effect of Oc when used in different doses.

Atrophy or hypertrophy in chronic renal ischemia: role of the IGF-I system.

To examine the role of insulin-like growth factor-1 (IGF-1) in renal atrophy of rats with two-kidney, one-clip (2K1C), in which the clipped kidney atrophies, and in the one-kidney, one-clip (IK1C) model of renovascular hypertension, in which it hypertrophies, we studied levels of IGF-I, mRNA, and protein in 2K1C, IK1C, and unilateral nephrectomy (NPX) in rats by solution-hybridization RNase protection, and radioimmunoassay, respectively, both cross-reactively and longitudinally at 3, 10, and 30 days after clipping. Three days after clipping, there were no differences in blood pressure or kidney size; however, 10 and 30 days postoperation, the clipped kidney shrank in the 2K1C model. The nonclipped 2K1C and the clipped lK1C and unilateral nephrectomy kidneys increased in weight (P < .05. At day 3 the IGF-I levels were lower (557 +/- 54, 335 +/- 61 ng/g in control and clipped 2K1C, P < .05, v 1,074 +/- 186, 1,109 +/- 54, and 1,154 +/- 200 ng/g kidney, nonclipped 2K1C, 1K1C, and NPX, respectively). At 30 days the IGF-I levels were 300 +/- 24 ng/g in control (P < .05) v clipped 2K1C, 160 +/- 19, 218 +/- 20 ng/g in nonclipped 2K1C and 406 +/- 33 and 470 +/- 34 ng/g in 1K1C and NPX, respectively (P < .05) v control and clipped 2K1C. Kidney mRNA was increased in the clipped 2K1C. In conclusion, the kidney that had higher IGF-I levels early in nonclipped 2K1C, 1K1C, and nephrectomy hypertrophied, and the kidney (clipped 2K1C) that failed to increase IGF-I atrophied. IGF-I levels are dissociated from the local mRNA message.

Insulin-like growth factor-I (IGF-I) and IGF-I receptor gene expression in the kidney of the chronically hypoinsulinemic rat and hyperinsulinemic rat.

Acute streptozotocin (STZ)-induced diabetes in rats causes a transient increase in insulin-like growth factor-I (IGF-I) in the kidney, followed by a rapid renal hypertrophy and constant renal hyperperfusion. However, renal IGF-I levels return to normal within 4 days. Thus, hyperperfusion, which is independent of renal hypertrophy of the chronically diabetic kidney, is not explained by increased renal IGF-I. We studied IGF-I and IGF-I receptor gene expression in the kidney of rats with long-standing STZ-induced diabetes. IGF-I mRNA level in the chronically diabetic kidney was approximately 50% of that in control rats, whereas IGF-I receptor mRNA was increased approximately threefold. Ten days' treatment with insulin 65 days after induction of diabetes resulted in a glucose-dependent decrease in IGF-I receptor mRNA. Chronic hyperinsulinemia with near normoglycemia did not change gene expression of either IGF-I or IGF-I receptor. The studies suggest that glucose levels per se, independent of insulin levels, play an important role in the regulation of IGF-I receptor gene expression in the chronically diabetic kidney. Furthermore, kidney hyperperfusion in chronic diabetes is coupled with the increase in IGF-I receptor mRNA, despite normal kidney IGF-I levels.

Gene expression of insulin-like growth factor-I, its receptor and binding proteins in retina under hypoxic conditions.

Hypoxia is the main stimulus for neovascularization in the retina. Insulin-like growth factor-I (IGF-I) is thought to be one of the mediators of this process. Severe persistent hypoxia, as occurs in central retinal artery occlusion, is associated with less retinal neovascularization than relative hypoxia. To study the influence of different types of hypoxia on the IGF system, we used a model of neonatal rat retina that responds with neovascularization to a relative hypoxic stimulus produced by alternating oxygen concentrations in the respired air. We studied the influence of 24-hour hypoxia (10% oxygen), 48-hour hyperoxia (75% oxygen), and relative hypoxia (shifting from 48 hours in 75% oxygen to 24 hours in room air) on the gene expression of IGF-I, IGF-I receptor (IGF-IR), and IGF binding protein-1 (IGFBP-1), IGFBP-2, and IGFBP-3 in retina using a solution hybridization RNase protection assay. Hypoxia induced a significant increase in retinal IGF-IR (178%), IGFBP-2 (227%), and IGFBP-3 (317%) mRNA; however, retinal IGF-I mRNA was reduced, as well as serum growth hormone (GH). Relative hypoxia caused a similar but less pronounced trend in the gene expression of IGF-IR and the binding proteins, whereas retinal IGF-I mRNA was unchanged and serum GH was elevated. Both hypoxia and relative hypoxia may cause IGF system stimulation in the retina through upregulation of IGF-IR and IGFBPs. This stimulation may result in neovascularization. However, during hypoxia, low levels of tissue oxygenation and reduced local production of IGF-I may impede the neovascularization process.

Odor stimuli modulate retinal excitability in fish.

Recording electroretinograms (ERGs) of fish prior to olfactory stimulation and after application of odor substances to the nostrils revealed a modulatory effect by chemoreceptive afferents on retinal responsiveness. The b-wave amplitude was increased in animals previously stimulated with dissolved food extracts. It is suggested that this phenomenon is related to well known behavioral effects of chemoreceptive stimulation on visually guided postural control mechanisms. The result for the first time suggests a behaviorally significant function of efferent optic nerve fibers.

Sequence periodicity in complete genomes of archaea suggests positive supercoiling.

The topological state of genomic DNA is of importance for its replication, recombination and transcription. The wrapping of the DNA around nucleosomes is associated with sequence periodicities (Trifonov and Sussman, Proc. Natl. Acad. Sci. USA, 77, pp. 3816-20). Recently, also the negative supercoiling of eubacterial DNA was related to 11 base pair (bp) periodicity (Herzel et al. Physica A, 249, pp. 449-59). Archaeal plasmids and a virus-like particle from Sulfolobus are positively supercoiled, but the superhelical conformation of archaeal genomic DNA is still uncertain. The problem of superhelicity can now be addressed via a comparative statistical analysis of the available complete genomes. For this purpose one has to look for periodicities which are in phase with the helical repeat of 10-11 bp. Similar periodicities are induced, however, by the amphipatic character of alpha-helices of encoded proteins (Zhurkin, Nucl. Acids Res., 9, pp. 1963-71). We show that these protein-induced periodicities are extended over a few periods only. The periods of additional long-ranging oscillations deviate significantly from the value for free DNA. A period of 11 bp in Eubacteria reflects negative supercoiling, whereas the significantly different period of thermophilic Archaea close to 10 bp suggests positive supercoiling of archaeal genomes.

Optimization of road networks using evolutionary strategies

A road network usually has to fulfill two requirements: (i) it should as far as possible provide direct connections between nodes to avoid large detours; and (ii) the costs for road construction and maintenance, which are assumed proportional to the total length of the roads, should be low. The optimal solution is a compromise between these contradictory demands, which in our model can be weighted by a parameter. The road optimization problem belongs to the class of frustrated optimization problems. In this paper, a special class of evolutionary strategies, such as the Boltzmann and Darwin and mixed strategies, are applied to find differently optimized solutions (graphs of varying density) for the road network, depending on the degree of frustration. We show that the optimization process occurs on two different time scales. In the asymptotic limit, a fixed relation between the mean connection distance (detour) and the total length (costs) of the network exists that defines a range of possible compromises. Furthermore, we investigate the density of states, which describes the number of solutions with a certain fitness value in the stationary regime. We find that the network problem belongs to a class of optimization problems in which more effort in optimization certainly yields better solutions. An analytical approximation for the relation between effort and improvement is derived.