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Background: One factor that may negatively impact male reproductive health is the illegal use of testosterone and anabolic-androgenic steroids. This study aimed to evaluate the prevalence of testosterone use in recreational athletes, as well as factors associated with its use, and to determine the profile of a person using testosterone. Methods: A cross-sectional analysis of data from an anonymous, online questionnaire of men recruited from gyms, randomly selected in Wrocław, Poland, has been performed. The minimal sample size was evaluated with the univariate logistic regression model. The association between testosterone use and other factors was also evaluated with the univariate logistic regression model. Results: A total of 35% of respondents used testosterone. The main purposes of testosterone use were the improvement of training effects and the improvement of body shape. The respondents most likely to use testosterone and other anabolic-androgenic steroids were men aged 26-35, whose earnings were at the level of the middle class or higher, who were married, had children, had training experience of at least 6 months, exercised at least once a week, took part in weightlifting competitions, were managers in a corporation or enterprise, or were self-employed. Most of the people using testosterone had self-treated side effects. Conclusions: The profile of the person most likely to use testosterone corresponds to the characteristics of men in optimal socio-demographic conditions for reproduction. These results indicate that this is a significant social problem that may impact male reproductive health.

In this review article, we describe the unrecognized roles of glutamate and glutamate receptors in malignant glioma biology. The neurotransmitter glutamate released from malignant glioma cells in the extracellular matrix is responsible for seizure induction and at higher concentration neuronal cell death. This neuronal cell death will create vacated place for tumor growth. Glutamate also stimulates the growth and the migration of glial tumor cells by means of the activation of glutamate receptors on glioma cells in a paracrine and autocrine manner. The multitude of effects of glutamate in glioma biology supports the rationale for pharmacological targeting of glutamate receptors and transporters in the adjuvant treatment of malignant gliomas in neurology and neuro-oncology. Using the website www.clinicaltrials.gov/ as a reference - a service developed by the National Library of Medicine for the National Health Institute in USA - we have evoked the few clinical trials completed and currently ongoing with therapies targeting the glutamate receptors.

Microscopic indocyanine green videoangiography (mICG-VA) has gained wide acceptance during intracranial aneurysm surgery by lowering rates of incomplete clipping and occlusion of surrounding vessels. However, mICG-VA images are limited to the microscopic view and some deeper areas, including the aneurysm sac/neck posterior side, cannot be efficiently assessed as they are hidden by the aneurysm, clips, or surrounding structures. Contrarily, endoscopes allow a wider area of visualization, but neurosurgical endoscopes to date only provided visual data. We describe the first application of endoscope ICG-integrated technology (eICG) applied in an initial case of anterior communicating artery aneurysm clipping. This new technique provided also relevant information regarding aneurysm occlusion and patency of parent and branching vessels and small perforating arteries. eICG-VA provided additional information compared to mICG-VA by magnifying areas of interest and improving the ability to view less accessible regions, especially posterior to the aneurysm clip. Obtaining eICG sequences required currently the microscope to be moved away from the operating field. eICG-VA was only recorded under infrared illumination which prevented tissue handling, but white-infrared light views could be interchanged instantaneously. Further development of angled endoscopes integrating the ICG technology and dedicated filters blocking the microscopic light could improve visualization capacities even further. In conclusion, as a result of its ability to reveal structures around corners, the eICG-VA technology could be beneficial when used in combination with mICG-VA to visualize and confirm vessel patency in areas that were previously hidden from the microscope.

We describe a percutaneous or minimally invasive approach to apply an augmentation of pedicle fenestrated screws by injection of the PMMA bone cement through the implant and determine the safety and efficiency of this technique in a clinical series of 15 elderly osteoporotic patients. Clinical outcome and the function were assessed using respectively the Visual Analogue Scale (VAS) score and the Oswestry Disability Index (ODI). Peri- and post-operative complications were monitored during a minimum of 2 years of follow-up. Radiographic follow-up was based on plain fluoroscopic control at 3, 6 and 12 months and every year. In this approach, four steps were considered with care: optimal positioning of the screws, correct alignment of the screw heads, waiting time before the injection of cement, fluoroscopic control of the cement injection. Using these precautions, only 2 minor complications occurred. VAS scores and ODI questionnaires showed a statistically significant improvement up to 13.3 months postoperatively. No radiological complications were observed. Based on this experience, PMMA augmentation technique through the novel fenestrated screws provided an effective and long lasting fixation in osteoporotic patients. Applying this procedure through percutaneous or minimally invasive approach under fluoroscopic control seems to be safe.

The need to pursue long-term follow-up in patients treated for a ruptured aneurysm remains debated. New aneurysms development is a crucial element to consider but remains scarcely analyzed especially after a mean follow-up longer than 10 years. Our study was designed to provide rates of newly developed aneurysms in patients who have undergone prior clipping who were not followed with serial imaging. Patients were included if they were (1) treated more than 10 years ago by clipping of a ruptured aneurysm, (2) independent at time of discharge, (3) presently younger than 65 years, and if (4) they agreed to undergo a late digital subtraction angiography (DSA) control or to transmit results of a recent one performed elsewhere. Twenty patients were included with a mean delay between aneurysm treatment and late DSA of 18.0 years (10-26.5 years). Out of these patients, six (30%) harbored new aneurysms. Of these six individuals, four (66.6%) presented multiple aneurysms with a total of 15 newly discovered aneurysms. Aneurysm sizes ranged from 1 to 10 mm. One patient suffered from a de novo aneurysm rupture. Multiple aneurysms at the time of the first hemorrhage were a risk factor in developing de novo aneurysm (p=0.0175). In conclusion, based on a 30% rate of new aneurysm formation in patients clipped more than a decade ago, close screening on a very long-term perspective is encouraged. This study suggests aneurysm formation to be a continuous process.

Glioblastoma (GBM) is the most frequent malignant glioma. Treatment of GBM patients is multimodal with maximum surgical resection, followed by concurrent radiation and chemotherapy with the alkylating drug temozolomide (TMZ). The present study aims to identify genes implicated in the acquired resistance of two human GBM cells of astrocytic origin, T98G and U373, to TMZ. Resistance to TMZ was induced by culturing these cells in vitro for months with incremental TMZ concentrations up to 1 mM. Only partial resistance to TMZ has been achieved and was demonstrated in vivo in immunocompromised mice bearing orthotopic U373 and T98G xenografts. Our data show that long-term treatment of human astroglioma cells with TMZ induces increased expression of facilitative glucose transporter/solute carrier GLUT/SLC2A family members, mainly GLUT-3, and of the AKR1C family of proteins. The latter proteins are phase 1 drug-metabolizing enzymes involved in the maintenance of steroid homeostasis, prostaglandin metabolism, and metabolic activation of polycyclic aromatic hydrocarbons. GLUT-3 has been previously suggested to exert roles in GBM neovascularization processes, and TMZ was found to exert antiangiogenic effects in experimental gliomas. AKR1C1 was previously shown to be associated with oncogenic potential, with proproliferative effects similar to AKR1C3 in the latter case. Both AKR1C1 and AKR1C2 proteins are involved in cancer pro-proliferative cell chemoresistance. Selective targeting of GLUT-3 in GBM and/or AKR1C proteins (by means of jasmonates, for example) could thus delay the acquisition of resistance to TMZ of astroglioma cells in the context of prolonged treatment with this drug.

Background: The endovascular treatment of intracranial aneurysms can be hampered by the tortuosity of extracranial vessels. Percutaneous or surgical vessel puncture can resolve the problem of inaccessibility., Objective: We describe rerouting of a kinked vertebral artery (VA) to restore transfemoral endovascular access to an aneurysm., Case Report: A 63-year-old woman presented with progressive hemiparesis. Magnetic resonance imaging demonstrated a left fusiform vertebrobasilar aneurysm with mass effect on the brainstem. The patient was found to have a dominant left VA on angiography with a severe kink in its V1 segment. Tight loops of this segment prevented catheter progression past V1 during endovascular treatment., Intervention: The left VA was rerouted from its subclavian origin to the C5 transverse foramen through a combined lateral and supraclavicular approach. Release of the VA off the C6 transverse process and C6 and C7 cranial nerve roots permitted unfolding of the VA. The excess length of the VA, initially present between the subclavian artery and the C6 transverse process, was spread over a longer distance. The tight angles present preoperatively were converted into a harmonious curvature. The rerouted VA was attached to surrounding soft tissue to maintain its position. The patient's postoperative course was uneventful. Endovascular treatment of the aneurysm was performed 15 days later., Conclusion: The VA rerouting technique can be used successfully in patients in whom tight loops in the VA prevent endovascular access to intracranial vessels.

The treatment of glioblastomas requires a multidisciplinary approach because despite the progresses in surgical and iconographic managements associated with research knowledge this disease presently remains incurable and progresses during the 6 months after its diagnose. Current recommendations are that patients with glioblastoma should undergo maximum surgical resection followed by concurrent radiation and chemotherapy with the alkylating drug temozolomide, followed subsequently by additional adjuvant temozolomide for a period of up to 6 months. Temozolomide mechanism of action is complex and we have recently evidenced a temozolomide-associated anti-angiogenic activity in vitro and in vivo on preclinical human glioblastoma models. We describe in the current review the temozolomide-associated antiangiogenic activity. We also describe here the major signaling pathways that can be constitutively activated in migrating glioma cells, and which render these cells resistant to proapoptotic insults such as conventional chemotherapies. In light of this resistance, we therefore describe the targeted therapies and local drug delivery systems which could be used to complement conventional treatments. We have reviewed more than 400 ongoing clinical trials with respect to these new targeted therapy approaches alone or in combination for glioblastoma therapy and we also emphasize the importance of vaccinotherapy. We conclude our review with a therapeutic model that could be used in the light of the present knowledge.

Stroke is a leading cause of morbidity and mortality in the US, with secondary damage following the initial insult contributing significantly to overall poor outcome. Prior investigations have shown that the metabolism of certain polyamines such as spermine, spermidine, and putrescine are elevated in ischemic parenchyma, resulting in an increase in their metabolite concentration. Polyamine metabolites tend to be cytotoxic, leading to neuronal injury in the penumbra following stroke and expansion of the area of infarcted tissue. Although the precise mechanism is unclear, the presence of reactive aldehydes produced through polyamine metabolism, such as 3-aminopropanal and acrolein, have been shown to correlate with the incidence of cerebral vasospasm, disruption of oxidative metabolism and mitochondrial functioning, and disturbance of cellular calcium ion channels. Regulation of the polyamine metabolic pathway, therefore, may have the potential to limit injury following cerebral ischemia. To this end, we review this pathway in detail with an emphasis on clinical applicability.

Object: Despite efforts to elucidate both the molecular mechanism and the clinical predictors of vasospasm after aneurysmal subarachnoid hemorrhage (ASAH), its pathogenesis remains unclear. Monocyte chemoattractant protein-1 (MCP-1) is a chemokine that has been firmly implicated in the pathophysiology of vasospasm and in neural tissue injury following focal ischemia in both animal models and human studies. The authors hypothesized that MCP-1 would be found in increased concentrations in the blood and cerebrospinal fluid (CSF) of patients with ASAH and would correlate with both outcome and the occurrence of vasospasm., Methods: Seventy-seven patients who presented with ASAH were prospectively enrolled in this study between July 2001 and May 2002. Using an enzyme-linked immunosorbent assay, MCP-1 levels were measured in serum daily and in CSF when available. The mean serum and CSF MCP-1 concentrations were calculated for each patient throughout the entire hospital stay. Neurological outcome was evaluated at discharge or 14 days posthemorrhage using the modified Rankin Scale. Vasospasm was evaluated on angiography., Results: The serum MCP-1 concentrations correlated with negative outcome such that a 10% increase in concentration predicted a 25% increase in the probability of a poor outcome, whereas the serum MCP-1 levels did not correlate with vasospasm. Concentrations of MCP-1 in the CSF, however, proved to be significantly higher in patients with angiographically demonstrated vasospasm., Conclusions: These findings suggest a role for MCP-1 in neurological injury and imply that it may act as a biomarker of poor outcome in the serum and of vasospasm in the CSF.

The purpose of this study was to analyze the health-related quality of life (HRQL) of patients with cervical dystonia (CD) and the impact of botulinum toxin A (BTX-A) therapy in these patients. The authors recruited 101 patients with CD, all previously treated with BTX-A. Both before and 4 weeks after injection of BTX-A the patients were assessed using the Toronto Western Spasmodic Torticollis Rating Scale (TWSTRS), a Visual Analogue Scale for pain (VAS: 0-100%), the Short Form 36 health survey questionnaire (SF-36), and the Montgomery-Asberg Depression Rating Scale (MADRS). A control group of 84 healthy volunteers was also evaluated. The patients? baseline SF-36 scores were worse in all the domains when compared with those of the controls. Depression was found in 47.5% of the patients. Improvements were noticed 4 weeks after the single BTX-A injections in all the SF-36 domains, and in the VAS, TWSTRS and MADRS scores. The TWSTRS results did not correlate with any of the SF-36 subscores. Stepwise backward regression analysis revealed depression as the main predictor of poor HRQL, as well as female sex, poor financial situation, and living alone. On contrary, longer treatment with BTX-A was associated with better scores. Cervical dystonia has a marked impact on HRQL and treatment with BTX-A injections has a beneficial effect, seen both in objective and in subjective measures. Depression in CD patients is a main predictor of worse HRQL.

We present a case of a 21-year-old female with a giant cavernoma (5 cm x 3.1 cm x 3.6 cm) located in the left temporal region. Giant cavernomas are very rarely diagnosed. In our research we wanted to focus on the occurrence of these vascular malformations and diagnostic problems related to this matter.

Background: Necrotizing enterocolitis (NEC) presents with well-recognized signs of intestinal inflammation such as bilious vomiting, bloody stool, abdominal distension, and tenderness. The authors observed otherwise unexplained changes in the respiratory status requiring increased respiratory support during the 24 hours before direct evidence of the intestinal disorder in patients with severe NEC., Methods: To study this observation the authors collected data on 10 consecutive patients in whom NEC required an operation., Results: Eight of these patients were recovering from respiratory distress syndrome (RDS). During the 24 hours before any direct sign of intestinal dysfunction seven of these eight had a respiratory prodrome needing increased respiratory support. Two patients required intubation and mechanical ventilation. Five needed increased supplemental oxygen. This prodrome included decreased oxygenation in seven, increased respiratory rate in five, and increased PCO2 in five, preceded by hypocarbia in three., Conclusions: These changes in the respiratory condition revisit the concept of high output respiratory failure. This term was introduced to describe the respiratory failure in adult patients who suffer acute intestinal illness. Increased metabolic demand from the intestinal illness was thought to stress the ability of the patient to delivery oxygen and remove carbon dioxide. The ability of the respiratory system to meet the increased demands is limited by the intestinal dysfunction itself (abdominal pain and distension). In our patients recovering from RDS the pulmonary reserve is inherently limited. Because they are carefully monitored, it is easy to retrieve evidence of respiratory changes that precede the direct signs of intestinal disease. In the earliest stages of intestinal illness before the direct signs of intestinal dysfunction, these patients often manifest unexplained signs of respiratory compensation and decompensation and require increased respiratory support. Regardless of the pathophysiology, these alterations in respiratory status represent an early warning sign of NEC.