Retirement of professional soccer players - A systematic review from social sciences perspectives.

Retiring professional athletes face multifaceted changes and potential issues of adjustment, occupational development, and well-being, which raises concerns around the world. The study systematically reviewed the available research investigating professional soccer players' sport retirement from social sciences perspectives. The literature search in electronic databases and a "snowballing" procedure yielded 17 eligible studies investigating > 2,200 retired professional soccer players. The review followed the PRISMA statement. Nine studies focused on an early transition phase to retirement period; four studies investigated later periods of ten years or longer after retirement. Around half of the players reported involuntary retirement, often associated with declining performance and/or injury. Studies suggest issues of adjustment and mental health during early years after retirement, while psychological issues had apparently declined around 1-2 decades after retirement. However, available studies had notable limitations including lack of evidenced representative samples, report of measures' reliability, and control for confounders. Furthermore, while theoretical models emphasise a holistic perspective, quantitative research often took a narrow rather than holistic perspective. In summary, available knowledge is fraught with some uncertainty regarding reliability and representativeness of the population of retired professional soccer players. We offer future directions to advance the development of a theory of sport retirement.

Trabeculectomy offers better intraocular pressure reduction in intrapatient comparison to transscleral cyclophotocoagulation.

PURPOSE: Both trabeculotomy (TE) as well as transscleral endodiode laser cyclophotocoagulation (CPC) are common approaches in glaucoma surgery. The purpose of this study was to perform an intraindividual comparison of these procedures carried out by the same surgeon in the same patient on the same day. METHODS: An observational monocentric retrospective cohort study was conducted. Patients with a bilateral refractory open-angle glaucoma who underwent trabeculectomy in one eye and transscleral endodiode laser cyclophotocoagulation in the fellow eye simultaneously were included and followed up with over the course of 1 year. RESULTS: Eighty-two eyes of 41 patients were included. Seventeen patients (41.5%) were men and 24 (58.5%) women. The mean age was 68.7 ± 9.5 years. The diagnosis comprised 33 (80.5%) patients with a primary open-angle glaucoma, five (12.2%) patients with pseudoexfoliation glaucoma, and three (7.3%) patients with pigment dispersion glaucoma. A reduction in intraocular pressure (IOP) was seen in both after TE (from 26.2 ± 13.2 to 10.6 ± 4.1 mmHg, 52 weeks post-treatment) as well as CPC (from 24.2 ± 9.9 to 15.0 ± 5.4 mmHg, 52 weeks post-treatment). In comparison to each other, TE was significantly more effective in lowering the IOP (10.6 ± 4.1 vs. 13.4 ± 5.0; p = 0.0030, 52 weeks post-treatment) and needed antiglaucomatous medications (0.45 ± 0.80 vs. 1.24 ± 1.13; p = 0.0009, 52 weeks post-treatment). Consistently, the achievement rate of an IOP ≤ 16 mmHg without antiglaucomatous medications was significantly higher in TE-treated eyes (65.8% vs. 31.6%; p = 0.0019). Re-interventions, including 10 secondary TEs, were commonly required in those eyes undergoing CPC, especially in younger patients. CONCLUSIONS: Trabeculectomy was demonstrated to be more effective in reducing IOP in comparison to fellow eyes receiving CPC. In particular, in younger patients, an additional TE in the CPC-treated eyes was necessary. The outcome of those secondary TEs however was comparable to the primarily performed TEs. Our study thus supports the use of CPC as tool to control IOP, especially in the context of bilateral refractive glaucoma.

Effects of chronic oral L-arginine administration on the L-arginine/NO pathway in patients with peripheral arterial occlusive disease or coronary artery disease: L-Arginine prevents renal loss of nitrite, the major NO reservoir.

Despite saturation of nitric oxide (NO) synthase (NOS) by its substrate L-arginine (Arg), oral and intravenous supplementation of Arg may enhance NO synthesis, a phenomenon known as "The L-arginine paradox". Yet, Arg is not only a source of NO, but is also a source for guanidine-methylated (N (G)) arginine derivatives which are all inhibitors of NOS activity. Therefore, Arg supplementation may not always result in enhanced NO synthesis. Concomitant synthesis of N (G)-monomethyl arginine (MMA), N (G),N (G)-dimethylarginine (asymmetric dimethylarginine, ADMA) and N (G),N (G´)-dimethylarginine (symmetric dimethylarginine, SDMA) from supplemented Arg may outweigh and even outbalance the positive effects of Arg on NO. Another possible, yet little investigated effect of Arg supplementation may be alteration of renal function, notably the influence on the excretion of nitrite in the urine. Nitrite is the autoxidation product of NO and the major reservoir of NO in the circulation. Nitrite and Arg are reabsorbed in the proximal tubule of the nephron and this reabsorption is coupled, at least in part, to the renal carbonic anhydrase (CA) activity. In the present placebo-controlled studies, we investigated the effect of chronic oral Arg supplementation of 10 g/day for 3 or 6 months in patients suffering from peripheral arterial occlusive disease (PAOD) or coronary artery disease (CAD) on the urinary excretion of nitrite relative to nitrate. We determined the urinary nitrate-to-nitrite molar ratio (UNOxR), which is a measure of nitrite-dependent renal CA activity before and after oral intake of Arg or placebo by the patients. The UNOxR was also determined in 6 children who underwent the Arg test, i.e., intravenous infusion of Arg (0.5 g Arg/kg bodyweight) for 30 min. Arg was well tolerated by the patients of the three studies. Oral Arg supplementation increased Arg (plasma and urine) and ADMA (urine) concentrations. No appreciable changes were seen in NO (in PAOD and CAD) and prostacyclin and thromboxane synthesis (in PAOD). In the PAOD study, UNOxR did not change in the Arginine group (480 ± 51 vs 486 ± 50), but fell in the Placebo group (422 ± 67 vs 332 ± 42, P = 0.025). In the CAD study, UNOxR did not change significantly in the Arginine group (518 ± 77 at start vs 422 ± 40 after 3 months vs 399 ± 66 after 6 months), but fell in the Placebo group (524 ± 69 vs 302 ± 36 vs 285 ± 31; P = 0.025 for 0 vs 3 months). Infusion of Arg tended to decrease the UNOxR in the children (317 ± 41 vs 208 ± 16, P = 0.06). We propose that oral long-term Arg supplementation prevents loss of NO bioactivity by saving nitrite. The optimum Arg dose needs to be elaborated and is likely to be less than 10 g per day in adults. Orally and intravenously administered arginine was well tolerated by the elderly patients and young children, respectively.

Long-term surgical outcomes of two different Ahmed Valve implantation techniques in refractory glaucoma: Scleral flap vs scleral tunnel.

PURPOSE: To compare the outcomes and complications of the partial-thickness scleral flap technique to the long scleral tunnel technique in patients who underwent mitomycin C (MMC)-augmented Ahmed glaucoma valve (AGV) implantation. PATIENTS AND METHODS: In this retrospective study, we reviewed 139 eyes of 137 patients with refractory glaucoma who underwent AGV-Model FP7 implantation. The eyes were divided into the scleral flap group (n = 74) and the scleral tunnel group (n = 65). RESULTS: The mean follow-up was 57.91 ± 18.18 months for the flap and 61.18 ± 15.13 months for the tunnel group (p = 0.2499). The postoperative intraocular pressure (IOP) at 1 to 6 years was significantly lower than the baseline IOP in each group (p < 0.001). The average number of postoperative glaucoma medications decreased in the tunnel group (p = 0.0001) and in the flap group (p = 0.6194) compared to baseline. No statistically significant differences in postoperative visual acuity (p = 0.6396) and cumulative success (p = 0.054) were noted between the two groups. Conjunctival erosion or tube migration only occurred in the flap group. Significantly more reoperations were performed in the flap than in the tunnel group (p = 0.048). CONCLUSIONS: Both MMC-augmented AGV tube implantation methods lowered IOP. The flap technique was associated with higher rates of postoperative serious complications and more reoperations than the tunnel technique. Previous glaucoma surgery and the technique used to implant the surgical tube proved to be significant risk factors for conjunctival erosion.

Increased collagen deposition and diastolic dysfunction but preserved myocardial hypertrophy after pressure overload in mice lacking PKCepsilon.

Overexpression and activation of protein kinase C-epsilon (PKCepsilon) results in myocardial hypertrophy. However, these observations do not establish that PKCepsilon is required for the development of myocardial hypertrophy. Thus, we subjected PKCepsilon-knockout (KO) mice to a hypertrophic stimulus by transverse aortic constriction (TAC). KO mice show normal cardiac morphology and function. TAC caused similar cardiac hypertrophy in KO and wild-type (WT) mice. However, KO mice developed more interstitial fibrosis and showed enhanced expression of collagen Ialpha1 and collagen III after TAC associated with diastolic dysfunction, as assessed by tissue Doppler echocardiography (Ea/Aa after TAC: WT 2.1+/-0.3 versus KO 1.0+/-0.2; P<0.05). To explore underlying mechanisms, we analyzed the left ventricular (LV) expression pattern of additional PKC isoforms (ie, PKCalpha, PKCbeta, and PKCdelta). After TAC, expression and activation of PKCdelta protein was increased in KO LVs. Moreover, KO LVs displayed enhanced activation of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK), whereas p42/p44-MAPK activation was attenuated. Under stretch, cultured KO fibroblasts showed a 2-fold increased collagen Ialpha1 (col Ialpha1) expression, which was prevented by PKCdelta inhibitor rottlerin or by p38 MAPK inhibitor SB 203580. In conclusion, PKCepsilon is not required for the development of a pressure overload-induced myocardial hypertrophy. Lack of PKCepsilon results in upregulation of PKCdelta and promotes activation of p38 MAPK and JNK, which appears to compensate for cardiac hypertrophy, but in turn, is associated with increased collagen deposition and impaired diastolic function.

Sekundo's Applanator: 5 Years of Experience With Transconjunctival Suturing.

Sekundo's Applanator is a new surgical instrument used mainly in transconjunctival scleral flap suturing in cases of postoperative hypotony after trabeculectomy. In contrast to Hoskins lens, it offers better visualization of the border of the scleral flap with good intraoperative stabilization of the globe; thus, it increases the effectiveness and decreases the time of the surgical procedure. Sekundo's Applanator was also found to be useful in reducing the size of an oversized bleb after trabeculectomy and in the closure of leaking sutureless sclerotomies after vitrectomies. In this report, we present and discuss the properties, uses, and advantages of this new instrument to the ophthalmic community.

Increased open probability of single cardiac L-type calcium channels in patients with chronic atrial fibrillation. role of phosphatase 2A.

BACKGROUND: The L-type calcium channel (LCC) plays a crucial role in the electrical remodeling of atrial fibrillation (AF). AF is associated with reduction of L-type calcium current density, due to a transcriptional downregulation of the pore forming alpha(1c)-subunit of LCC. However, it is unclear, whether this current reduction is related to a decrease in channel number or to alterations in channel function. Hence, we performed a single LCC analysis to assess channel gating and function in human AF. METHODS AND RESULTS: We used the cell-attached patch-clamp technique in isolated atrial human cardiomyocytes of 25 patients with sinus rhythm (SR) and 15 patients with chronic AF. Protein expression of the pore-forming alpha(1c)-subunit of LCC was reduced by 40% in AF. Single channel peak average current was 1.7-fold higher in AF than in SR, due to a 3.1-fold higher open probability of LCC. Since phosphatase 2A (PP2A) is known to preferentially reduce LCC open probability via channel dephosphorylation, we assessed whether PP2A expression or activity is reduced in AF. Okadaic acid, an inhibitor of phosphatases, increased channel open probability in SR, but not in AF. However, Western blot analysis of atrial homogenates of the same patient population revealed unchanged expression of PP2A. CONCLUSIONS: Human AF is characterized by increased single LCC activity, due to an increase of channel open probability. The blunted effect of PP2A on LCC as shown by single channel analysis may be related to a reduction of cytosolic PP2A activity or impaired local interaction between PP2A and LCC in AF.

Single L-type Ca(2+) channel regulation by cGMP-dependent protein kinase type I in adult cardiomyocytes from PKG I transgenic mice.

OBJECTIVE: Calcium entry via the L-type Ca(2+) channel (LTCC) is crucial for excitation-contraction (EC) coupling and activation of Ca(2+)-dependent signal transduction pathways in cardiac myocytes. Both nitric oxide (NO), signaling via cGMP, and acetylcholine, signaling via the muscarinic receptor, have been identified as negative regulators of beta-adrenoreceptor-stimulated LTCC activity in cardiac myocytes. METHODS: To examine the potential role of cGMP-dependent protein kinase type I (PKG I) in the inhibitory effects of NO/cGMP and the muscarinic receptor on LTCC activity, we generated transgenic (TG) mice overexpressing PKG I selectively in cardiac myocytes under the control of the alpha-myocin heavy chain promoter. Single LTCC-gating properties were assessed in isolated ventricular myocytes from adult wild-type (WT) and PKG I transgenic (TG) mice. RESULTS: Basal LTCC activity (peak average current, mean open probability, mean availability) was significantly decreased by the nitric oxide donor DEA-NO (0.1 micromol/l) and the cGMP-analog 8-Br-cGMP (1 mmol/l) in TG but not in WT cardiac myocytes. Conversely, muscarinic (carbachol, 1 micromol/l) stimulation had no significant effect on basal LTCC activity in either WT or TG cardiac myocytes. beta-Adrenergic stimulation with isoproterenol (1 micromol/l) increases single LTCC activity in WT and TG cardiac myocytes to the same extent. The inhibitory effects of DEA-NO and 8-Br-cGMP on isoproterenol activation of the LTCC current were significantly enhanced in TG as compared to WT cardiac myocytes. By contrast, carbachol inhibition of isoproterenol-stimulated single LTCC activity was not enhanced in TG cardiac myocytes. CONCLUSION: Transgenic overexpression of PKG I augments NO/cGMP inhibition but not muscarinic inhibition of single LTCC activity, indicating that PKG I is a downstream target for NO/cGMP, but not the muscarinic receptor in adult cardiac myocytes.

Concentration of LAS and boron in the Itter. Comparison of measured data with results obtained by simulation with the GREAT-ER software.

The GREAT-ER software was used to calculate linear alkylbenzene sulphonate [LAS] and boron concentrations in the Itter stream in North Rhine-Westfalia, Germany. The aim was to investigate the predictive strength of this newly developed tool and to compare its results to measured data. Substance-specific input data which were used in this scenario were partly generic (e.g. LAS and sodium perborate tetrahydrate consumption figures for Germany) and partly (site-)specific data (e.g. half-life time for LAS elimination). The comparison with the measured data reveals that the model predictions for LAS and boron are correct at least within a factor of two, only if generic German consumption data is applied. By using refined input data, the accuracy can be increased further.

Induced Chemical Defense in Plants.

Surprising parallels exist between the chemical defense mechanisms of plants and animals. The biosynthesis of defensive substances in plants can be induced by microbial or herbivoral attack. Recent results demonstrate that the chemical defense of plants is mediated by lipid-based signaling systems. Volicitin (1) acts as a chemical signal in a tritrophic interaction of plants and insects. Derivatives of jasmonic acid (2) play a key role in directing the chemical defense response.

The impact of esophagus retraction on early dysphagia after anterior cervical surgery: does a correlation exist?

STUDY DESIGN: Prospective study of 92 patients who underwent anterior cervical surgery. Intraoperative esophagus retraction and postoperative dysphagia were recorded and evaluated. OBJECTIVE: Early dysphagia after anterior cervical discectomy and fusion is an underestimated side effect. The aim of this study was to investigate whether postoperative swallowing disturbances correlate with the amount of intraoperative retraction of the pharynx/esophagus wall measured during the procedure. SUMMARY OF BACKGROUND DATA: The anterior approach to the cervical spine is a routinely used and, in general, safe procedure. A recent prospective study focused on the underreported side effect of postoperative dysphagia, with an incidence of up to 50% at 1 month and 12.5% at 12 months. The etiology of postoperative dysphagia is not known in detail. METHODS: An online pressure transducer between the retractor and pharynx/esophagus recorded the epi-esophageal pressure in 92 patients. In 31 patients, a transducer was additionally inserted into the pharynx/esophagus in order to measure the endo-esophageal pressure. The patients rated swallowing difficulty during the first postoperative 5 days using a 10-point score. A control group of 32 lumbar surgery patients was also evaluated for swallowing disturbances. RESULTS: Mean epi-esophageal pressure after retractor opening was 76.3 mm Hg, and mean endo-esophageal pressure was 16.3 mm Hg. An adjustment to 75% and 76%, respectively, of the initial value occurred within the first hour. Of patients, 49.3% complained of swallowing disturbances. There was a significant prevalence of the female gender. No correlation between the amount of retraction and postoperative dysphagia was observed. CONCLUSIONS: A correlation between intraoperative pharynx/esophagus retraction and postoperative swallowing disturbances could not be confirmed. The cause of the prevalence of the female gender is unknown. However, the absence of impaired deglutition in the control group suggests that a local phenomenon must be causative of swallowing disturbances following anterior cervical discectomy and fusion.

Intraoperative measurement of pharynx/esophagus retraction during anterior cervical surgery. Part I: pressure.

Temporary dysphagia after anterior cervical discectomy (ACD) is common. However, its mechanism is poorly understood. Pressure induced by retractor blades onto pharynx/esophagus were measured intraoperatively in order to gain more information regarding traumatization of the pharynx/esophagus wall. Thirty-one patients underwent anterior cervical discectomy and fusion (ACDF) for degenerative disc disease. An online pressure transducer was applied to the rear side of the medial retractor blade (epi-esophageal-pressure, epi-P) and a cylindric, inflatable transducer was preoperatively inserted into the pharynx/esophagus under fluoroscopic guidance at the level to be operated on (endo-esophageal-pressure, endo-P). Pressure values were recorded continuously during the operation. Mean arterial pressure (MAP) and endotracheal cuff pressure (ETCP) were recorded additionally. An in vitro model was developed in order to analyze the impact of the retractor blade design onto the epi-esophageal-pressure. Mean epi-P before and following adequate retractor opening for exposure of the disc space was 58.3 and 92.7 mmHg. Thirty, 60 and 90 min later the epi-P decreased to 79, 70 and 66%, respectively. Mean basal endo-P was 9.8 mmHg and increased to 20.6 mmHg after retractor placement. Thirty, 60 and 90 min later the endo-P decreased to 80, 71 and 62%, respectively. The mean MAP was 76 mmHg and the ECTP was adjusted to 25 mmHg during the procedures. In the in vitro model retraction pressure correlated inversely with the contact area between visceral wall and retractor blade. During ACDF the retraction pressure onto the pharyngeal/esophageal wall exceeds MAP and even more the mucosal perfusion pressure of 25 mmHg. Over time the pharynx/esophageal wall adapts to the applied pressure induced by the retractor blade. The contact area between them influences the retraction pressure.

A modified calculation of ankle-brachial pressure index is far more sensitive in the detection of peripheral arterial disease.

BACKGROUND: Ankle-brachial pressure index (ABI) is a simple, inexpensive, and useful tool in the detection of peripheral arterial occlusive disease (PAD). The current guidelines published by the American Heart Association define ABI as the quotient of the higher of the systolic blood pressures (SBPs) of the two ankle arteries of that limb (either the anterior tibial artery or the posterior tibial artery) and the higher of the two brachial SBPs of the upper limbs. We hypothesized that considering the lower of the two ankle arterial SBPs of a side as the numerator and the higher of the brachial SBPs as the denominator would increase its diagnostic yield. METHODS: The former method of eliciting ABI was termed as high ankle pressure (HAP) and the latter low ankle pressure (LAP). ABI was assessed in 216 subjects and calculated according to the HAP and the LAP method. ABI findings were confirmed by arterial duplex ultrasonography. A significant arterial stenosis was assumed if ABI was <0.9. RESULTS: LAP had a sensitivity of 0.89 and a specificity of 0.93. The HAP method had a sensitivity of 0.68 and a specificity of 0.99. McNemar's test to compare the results of both methods demonstrated a two-tailed P < .0001, indicating a highly significant difference between both measurement methods. CONCLUSIONS: LAP is the superior method of calculating ABI to identify PAD. This result is of great interest for epidemiologic studies applying ABI measurements to detect PAD and assessing patients' cardiovascular risk.

Src family tyrosine kinases inhibit single L-type: Ca2+ channel activity in human atrial myocytes.

OBJECTIVE: Tyrosine kinases (TKs) are important regulators of the L-type Ca(2+) channel (LTCC) current in various cell types. However, there are no data addressing the role of TKs in the control of single LTCC activity in human atrial cardiac myocytes, where changes in LTCC gating properties have been described in a number of disease states. METHODS AND RESULTS: Single LTCC activity was recorded in isolated human atrial myocytes. The broad-spectrum TK inhibitor genistein and the Src family-selective TK inhibitor PP1 significantly enhanced single LTCC ensemble average current, availability, and open probability; the latter was due to significant increases of mean open time and mode 2 gating. Conversely, the tyrosine phosphatase inhibitor bisperoxo-phenanthroline-vanadate inhibited single LTCC activity, indicating that LTCC gating properties in human atrial myocytes are controlled by TKs and tyrosine phosphatases in a reciprocal fashion. The effects of genistein on single LTCC activity were not affected by stimulation (8Br-cAMP) or inhibition (Rp-8-CPT-cAMPS) of protein kinase A (PKA) or by inhibition of serine/threonine phosphatases types I and IIa (okadaic acid), indicating that TKs inhibit LTCC gating in human atrial myocytes independent of PKA and phosphatases types I and IIa. However, inhibition of protein kinase C (PKC) by staurosporine or bisindolylmaleimide reversed the stimulatory effects of genistein on single LTCC gating properties, indicating that PKC is required for the inhibitory effect of TKs on single LTCC activity. CONCLUSION: Src family TKs inhibit single LTCC activity in human atrial myocytes via PKC-dependent, but PKA and phosphatase types I and IIa-independent, molecular pathways.

Inhibition of calcineurin-NFAT hypertrophy signaling by cGMP-dependent protein kinase type I in cardiac myocytes.

Recent investigation has focused on identifying signaling pathways that inhibit cardiac hypertrophy, a major risk factor for cardiovascular morbidity and mortality. In this context, nitric oxide (NO), signaling via cGMP and cGMP-dependent protein kinase type I (PKG I), has been recognized as a negative regulator of cardiac myocyte (CM) hypertrophy. However, the underlying mechanisms are poorly understood. Here, we show that PKG I inhibits CM hypertrophy by targeting the calcineurin-NFAT signaling pathway. Calcineurin, a Ca2+-dependent phosphatase, promotes hypertrophy in part by activating NFAT transcription factors which induce expression of hypertrophic genes, including brain natriuretic peptide (BNP). Activation of PKG I by NO/cGMP in CM suppressed NFAT transcriptional activity, BNP induction, and cell enlargement in response to alpha(1)-adrenoreceptor stimulation but not in response to adenoviral expression of a Ca2+-independent, constitutively active calcineurin mutant, thus demonstrating NO-cGMP-PKG I inhibition of calcineurin-NFAT signaling upstream of calcineurin. PKG I suppressed single L-type Ca2+-channel open probability, [Ca2+]i transient amplitude, and, most importantly, L-type Ca2+-channel current-induced NFAT activation, indicating that PKG I targets Ca2+-dependent steps upstream of calcineurin. Adenoviral expression of PKG I enhanced NO/cGMP inhibitory effects upstream of calcineurin, confirming that PKG I mediates NO/cGMP inhibition of calcineurin-NFAT signaling. In CM overexpressing PKG I, NO/cGMP also suppressed BNP induction and cell enlargement but not NFAT activation elicited by constitutively active calcineurin, which is consistent with additional, NFAT-independent inhibitory effect(s) of PKG I downstream of calcineurin. Inhibition of calcineurin-NFAT signaling by PKG I provides a framework for understanding how NO inhibits cardiac myocyte hypertrophy.