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Thread: WHAT'S GOING ON IN SPAIN?

  1. #1

    WHAT'S GOING ON IN SPAIN?

    HI, DOES ANYONE KNOWS WHAT IS BEEN DONE IN SPAIN , I MEAN RESEARCH , I LIVE HERE AND I WOULD LIKE TO FIND OUT WHERE TO LOOK AND WHAT CAN I EXPECT TO FIND. THANKS A LOT

  2. #2
    Run a search for "Almudena" and you'll find many articles

  3. #3
    Here are some selected abstracts of published spinal cord injury studies from Spain:


    • Cervero F (1995). Visceral pain: mechanisms of peripheral and central sensitization. Ann Med. 27 (2): 235-9. Summary: This paper describes the responses of peripheral and central visceral nociceptive systems to acute injury and discusses these observations in relation to the concept of 'pre-emptive analgesia'. Visceral nociceptors are known to respond to injury but are also known to become sensitized to non-noxious stimuli during the inflammatory process that follows intense noxious stimulation. The afferent barrages triggered in visceral nociceptors by the acute injury and the enhanced responses evoked in sensitized nociceptors during the repair process can, in turn, increase the excitability of central nociceptive systems. The maintenance of central hypersensitivity is, however, dependant on the continuing presence of afferent volleys from sensitized nociceptors because the central changes cannot be sustained in the absence of a peripheral drive. Therefore it is proposed that the concept of 'pre-emptive analgesia', as such, has no neurophysiological basis. Any analgesic procedure aimed at reducing postoperative pain must not only prevent the arrival in the CNS of the initial afferent barrage evoked in nociceptive endings but also reduce or eliminate the persistent discharges of sensitized nociceptors during the inflammatory repair process that are critically important for the maintenance of the central pain state. <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&li st_uids=7632420> Department of Physiology and Pharmacology, University of Alcala de Henares, Madrid, Spain.

    • Cuevas P and Carceller F (2001). Therapeutic implications of fibroblast growth factors in traumatic spinal cord injury. Neurol Res. 23 (2-3): 207-9. Summary: Neurological damage after acute traumatic spinal cord injury (SCI) results from both the primary mechanical injury as well as the subsequent activation of cell death cascades mediating delayed tissue damage. Since secondary injury following traumatic SCI is a tightly regulated process in which several neurotrophic factors seem to be implicated, administration of these proteins has a clinical interest. Fibroblast growth factor may be one of the agents to be used for the treatment of traumatic SCI. <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&li st_uids=11320601> Servicio de Histologia, Departamento de Investigacion, Hospital Ramon y Cajal, E-28034, Madrid, Spain. pedro.cuevas@hrc.es

    • Esclarin De Ruz A, Garcia Leoni E and Herruzo Cabrera R (2000). Epidemiology and risk factors for urinary tract infection in patients with spinal cord injury. J Urol. 164 (4): 1285-9. Summary: PURPOSE: To our knowledge risk factors for urinary tract infection associated with various drainage methods in patients with spinal cord injury have never been evaluated overall in the acute period. We identified the incidence and risk factors associated with urinary tract infection in spinal cord injured patients. MATERIALS AND METHODS: We prospectively followed 128 patients at our spinal cord injury reference hospital for 38 months and obtained certain data, including demographic characteristics, associated factors, methods of urinary drainage, bladder type, urological complications and predisposing factors of each infection episode. Logistic regression modeling was done to analyze variables and identify risk factors that predicted urinary tract infection. RESULTS: Of 128 patients 100 (78%) were male with a mean age plus or minus standard deviation of 32 +/- 14.52 years. All patients had a nonfatal condition by McCabe and Jackson guidelines, and 47% presented with associated factors. The incidence of urinary tract infection was expressed as number episodes per 100 patients daily or person-days. The overall incidence of urinary tract infection was 0.68, while for male indwelling, clean intermittent, condom and female suprapubic catheterization, and normal voiding the rate was 2.72, 0.41, 0.36, 0. 34 and 0.06, respectively. The risk factors associated with urinary tract infection were invasive procedures without antibiotic prophylaxis, cervical injury and chronic catheterization (odds ratio 2.62, 3 and 4, respectively). Risk factors associated with repeat infection were a functional independence measure score of less than 74 and vesicoureteral reflux (odds ratio 10 and 23, respectively). CONCLUSIONS: Spinal cord injured patients with complete dependence and vesicoureteral reflux are at highest risk for urinary tract infection. <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&li st_uids=10992382> Departments of Physical Medicine and Rehabilitation, and Medicine, Hospital Nacional de Paraplejicos, Toledo and Department of Preventive Medicine, Universidad Autonoma de Madrid, Madrid, Spain.

    • Fenollosa P, Pallares J, Cervera J, Pelegrin F, Inigo V, Giner M and Forner V (1993). Chronic pain in the spinal cord injured: statistical approach and pharmacological treatment. Paraplegia. 31 (11): 722-9. Summary: We include in this article the results of a postal inquiry into chronic pain in SCI patients in Valencia (Spain), and our experience with their management. A mailed questionnaire including lesion and chronic pain data was sent to all of the 380 SCI patients who live in the region of Valencia. We received 202 answers, with 145 questionnaires being accurately answered and these were analysed for this study. The results show that chronic pain (that is, lasting more than 6 months) is very common (65.5%). The most frequent type was deafferentation pain (phantom pain), described as burning or a painful numbness. Since 1988 we have been treating a sample of 33 patients suffering from resistant pain according to the following therapies: 1 amitriptyline + clonazepam+NSAID (nonsteroidal antiinflammatory drugs); 2 amitriptyline + clonazepam + 5-OH-tryptophane + TENS (transcutaneous electrical nerve stimulation); 3 amitriptyline + clonazepam + SCS (spinal cord stimulation); 4 morphine, by continuous intrathecal infusion. After almost 4 years using these therapies we can affirm that the results regarding analgesia reached 80% in all cases, and that morphine used by intrathecal route is very safe and useful in selected patients. <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&li st_uids=7507585> Department of Aneasthesiology, University Hospital, La Fe, Valencia, Spain.

    • Nieto-Sampedro M (1999). Neurite outgrowth inhibitors in gliotic tissue. Adv Exp Med Biol. 468: 207-24. Summary: Gliotic tissue is the major obstacle to axon regeneration after CNS injury. We designed tissue culture assays to search for molecules responsible for neurite outgrowth inhibition in gliotic tissue. All the inhibitory activity in injured brain tissue was located in a plasma membrane heparan-sulphate and condroitin-sulphate type-proteoglycan of apparent molecular weight 200 kDalton. The proteoglycan core protein (apparent MW 48,000 kD) was biologically inactive, whereas the glycosamine-glycan (GAG) chains accounted for the inhibitory activity. Because of its cell location and mode of induction, the inhibitor was called injured membrane proteoglycan, IMP. IMP prevented neurite outgrowth initiation when attached to the culture substrate and caused growth cone collapse when added in solution to neurons with already growing neurites. We concluded that IMP was responsible for preventing injured CNS fibre regeneration. Double-staining immunohistochemistry of normal and gliotic tissue with anti-IMP monoclonal antibodies together with glial and neuronal markers, permitted the unequivocal definition of inhibitor presenting cells by confocal microscopy. IMP-immunostaining in normal CNS was observed exclusively on neurons. However, after a lesion, immunostaining occurred primarily on intensely GFAP-positive reactive astrocytes, but not on OX-42 positive microglia. The availability of antibodies permitted rapid affinity-purification of the neurite inhibitor and comparison with similar molecules possibly expressed during development. IMP itself or a highly related form, was expressed in embryonic brain, reaching maximal expression around postnatal day 3 and decreasing strongly in normal adult tissue. Perinatal rat brain proteoglycans inhibited neurite outgrowth similarly, though not identically, to IMP. Our data suggest that perinatal membrane and injured membrane proteoglycans may differ in GAG composition. IMP-like immunoreactivity was also found in developing brain, predominantly in neurons in normal brain, associating after a lesion with reactive astrocytes. Thes results suggest that injury evokes re-expression of IMP previously expressed during CNS development. One of the monoclonal antibodies to IMP blocked inhibitory activity, restoring neurite outgrowth in vitro. We are currently preparing Fab fragments to test the possibility that the antibody may block inhibition of central sprout growth in vivo. The combined use of blocking antibody fragments to neurite outgrowth inhibitors and transplants of growth-promoting glia, may help in the repair brain and spinal cord lesions. <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&li st_uids=10635031> Neural Plasticity Group, Cajal Institute, Madrid, Spain. mns@cajal.csic.es

    • Perez-Castrillon JL, Olmos JM, Gomez JJ, Barrallo A, Riancho JA, Perera L, Valero C, Amado JA and Gonzalez-Macias J (2000). Expression of opioid receptors in osteoblast-like MG-63 cells, and effects of different opioid agonists on alkaline phosphatase and osteocalcin secretion by these cells. Neuroendocrinology. 72 (3): 187-94. Summary: We have previously shown that several stressful situations associated with tissue injury determine a decrease in serum osteocalcin concentration. Since reduced osteocalcin production is a marker of decreased osteoblastic activity, this finding could be related to the pathogenesis of osteoporosis secondary to some diseases. Endogenous opioids are involved in stress response. Proenkephalin-derived peptides have been shown to inhibit alkaline phosphatase activity, another marker of bone formation, in the murine cell line ROS-17/2.8. On the other hand, serum osteocalcin has been reported as being low in heroin abusers. We have therefore thought it of interest to study the presence of opioid receptors in the human osteoblast-like cell line MG-63, and to evaluate the effects of different opioid agonists on the secretion of alkaline phosphatase and osteocalcin by these cells. The presence of opioid receptors was studied by means of RT-PCR and immunohistochemistry. RT-PCR studies suggested the presence of specific mRNA for the three types of receptors, and immunohistochemistry clearly showed their occurrence. Osteocalcin synthesis was significantly inhibited by high concentrations of the mu agonists morphine and (D-Ala(2), N-MePhe(4),Gly(5)-ol)-enkephalin although no changes were seen with the delta agonist (D-Ala(2),D-leu(5))-enkephalin. Morphine-induced osteocalcin inhibition was abolished when osteoblastic cells were incubated simultaneously with naloxone, whereas it was potentiated when cells were preincubated with naloxone. None of the opioid agonists modified the secretion of alkaline phosphatase. In conclusion, human osteoblast-like cells MG-63 express the three types of opioid receptors. Endogenous opioids may be involved in the reduction of osteocalcin observed in stressful situations associated with tissue injury. <http://www.online.karger.com/library...d=NEN.nen72187
    http://www.ncbi.nlm.nih.gov/entrez/q...uids=11025413> Departamento de Medicina Interna, Hospital Marques de Valdecilla, Universidad de Cantabria, Santander, Spain.

    • Ramon-Cueto A (2000). Olfactory ensheathing glia transplantation into the injured spinal cord. Prog Brain Res. 128: 265-72. Summary: <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&li st_uids=11105686> Institute of Biomedicine, Spanish Council for Scientific Research (CSIC), Valencia, Spain. aramon@ibv.csic.es

    • Ramon-Cueto A, Cordero MI, Santos-Benito FF and Avila J (2000). Functional recovery of paraplegic rats and motor axon regeneration in their spinal cords by olfactory ensheathing glia. Neuron. 25 (2): 425-35. Summary: Axonal regeneration in the lesioned mammalian central nervous system is abortive, and this causes permanent disabilities in individuals with spinal cord injuries. In adult rats, olfactory ensheathing glia (OEG) transplants successfully led to functional and structural recovery after complete spinal cord transection. From 3 to 7 months post surgery, all OEG-transplanted animals recovered locomotor functions and sensorimotor reflexes. They presented voluntary hindlimb movements, they supported their body weight, and their hindlimbs responded to light skin contact and proprioceptive stimuli. In addition, relevant motor axons (corticospinal, raphespinal, and coeruleospinal) regenerated for long distances within caudal cord stumps. Therefore, OEG transplantation provides a useful repair strategy in adult mammals with traumatic spinal cord injuries. Our results with these cells could lead to new therapies for the treatment of spinal cord lesions in humans. <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&li st_uids=10719896> Centro de Biologia Molecular Severo Ochoa (CSIC-UAM), Facultad de Ciencias, Universidad Autonoma de Madrid, Cantoblanco, Spain. aramon@ibv.csic.es

    • Taylor JS, Muneton-Gomez VC, Eguia-Recuero R and Nieto-Sampedro M (2001). Transplants of olfactory bulb ensheathing cells promote functional repair of multiple dorsal rhizotomy. Prog Brain Res. 132: 641-54. Summary: <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&li st_uids=11545026> Instituto Cajal de Neurobiologia, CSIC, Avenida del Doctor Arce, 37, Madrid 28002, Spain.

    • Terre R, Valles M and Vidal J (2000). Post-traumatic syringomyelia following complete neurological recovery. Spinal Cord. 38 (9): 567-70. Summary: OBJECTIVE: To describe the later neurologic deterioration secondary to the appearance of a post-traumatic syringomyelic cavity, in a patient who, in the initial phase, had an incomplete spinal cord lesion (ASIA C), which improved to ASIA E. METHODS: A 52-year-old male patient who, at the age of 19 (1965), suffered a spinal cord injury. He presented with a fracture of the sixth and seventh cervical neurological segment at the time of the lesion, evolving to ASIA E. Nine years after the traumatism, he began to feel pain accompanied by a sensory and motor deficit. RESULTS: With the aid of myelography and MRI, the existence of a syringomyelic cavity was detected, which extended from the fourth to the seventh cervical segments. The patient was operated on, on various occasions, placing a syringo-subarachnoid shunt. The neurological status of the patient continued to deteriorate and, at present, he has a complete lesion below the fourth neurological cervical segment with a partially preserved sensitive area up to T1. CONCLUSION: The development of the syringomyelic cavity could be one of the causes of later neurologic deterioration in patients with traumatic spinal cord injury with neurological recovery 'ad integrum' in the initial phase of spinal cord injury. <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&li st_uids=11035481> Institut Guttmann, Hospital de Neurorehabilitacio, Institut Universitari UAB, Barcelona, Spain.

    • Ugarriza LF, Cabezudo JM, Porras LF and Rodriguez-Sanchez JA (2001). Cord compression secondary to cervical disc herniation associated with calcification of the ligamentum flavum: case report. Neurosurgery. 48 (3): 673-6. Summary: OBJECTIVE AND IMPORTANCE: Calcification of the ligamentum flavum is a rare disease that occurs almost exclusively in elderly Japanese people. We report the case of a young Caucasian woman who presented with a C5-C6 disc herniation associated with a cervical calcified ligamentum flavum. CLINICAL PRESENTATION: The patient presented with a cord compression syndrome of 76 hours' evolution. At exploration, a Brown-Sequard syndrome at the C6 level was found. Magnetic resonance imaging and computed tomography led to a correct diagnosis and planning for decompression. INTERVENTION: We operated on the patient through a combined anterior and posterior approach. After the patient underwent anterior discectomy with intersomatic arthrodesis, we performed posterior decompression. During the operation, we observed that the dura mater could not be separated from the ligamentum, so an en bloc excision of both structures was performed. Microscopic examination indicated that the excised ligamentum had calcification, and total integration of the dura mater into the structure of the ligamentum was demonstrated. To our knowledge, this circumstance has never been described before. A posterior C3-C7 arthrodesis was performed to prevent postoperative kyphosis. Recovery was successful, with total recovery from neurological deficits 4 months later. CONCLUSION: Calcification of the ligamentum flavum is a progressive disease that starts early in life and becomes symptomatic later in life when spinal stenosis occurs. Magnetic resonance imaging and computed tomography provide adequate diagnosis and allow proper surgical planning for decompression. The presence of hyperintense areas within the spinal cord parenchyma, in the absence of a traumatic antecedent, does not preclude a complete recovery. <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&li st_uids=11270560> Servicio de Neurocirurgia, Hospital Universitario Infanta Cristina, Carretera de Portugal s/n, Badajoz, Spain. med007486@nacom.es

    • Verdu E, Garcia-Alias G, Fores J, Gudino-Cabrera G, Muneton VC, Nieto-Sampedro M and Navarro X (2001). Effects of ensheathing cells transplanted into photochemically damaged spinal cord. Neuroreport. 12 (11): 2303-9. Summary: Transplantation of olfactory ensheathing cells (OECs) into photochemically damaged rat spinal cord diminished astrocyte reactivity and parenchyma cavitation. The photochemical lesion performed at T12--L1 resulted in severe damage to the spinal cord, so that during the first 15 days postoperation all rats dragged their hindlimbs and did not respond to pinprick. The maximal area and volume of the cystic cavities were lower in transplanted than in non-transplanted rats, not significantly at the T12--L1 lesion site, but significantly at T9--T10 and L4--L6 cord levels. The density of astrocytes in the grey matter was similar at T12--L1 and L4--L6 in non-transplanted and trans- planted rats, but lower in the latter at T9--T10 level. However, in non-transplanted rats all astrocytes showed a hypertrophied appearance, with long and robust processes heavily GFAP-positive, and overexpression of proteoglycan inhibitor of neuritogenesis, whereas in transplanted rats only a few astrocytes showed hypertrophy and the majority had short, thin processes. These results indicate that OECs transplanted into damaged adult rat spinal cord exert a neuroprotective role by reducing astrocytic gliosis and cystic cavitation. <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&li st_uids=11496100> Neuroplasticity and Regeneration Group, Department of Cell Biology, Physiology and Immunology, Universitat Autonoma de Barcelona, Edif. M., E-08193 Bellaterra, Spain.

    • Zurita M, Vaquero J and Oya S (2000). Grafting of neural tissue in chronically injured spinal cord: influence of the donor tissue on regenerative activity. Surg Neurol. 54 (2): 117-25. Summary: BACKGROUND: To determine the influence of different nervous tissue grafts on the regenerative activity of chronically injured spinal cord, an experimental study examining the expression of the proliferating cell nuclear antigen (PCNA) in chronically injured spinal cord subjected to neural grafting was performed.METHODS: Three months after induced spinal cord injury, paraplegic Wistar rats were subjected to grafting of neural tissue. Grafts consisted of fetal brain cortex, fetal spinal cord, crushed adult peripheral nerve tissue, or fetal brain cortex combined with crushed adult peripheral nerve tissue. Four months later, the spinal cord was removed and the grafted zone was studied by means of immunohistochemical demonstration of PCNA.RESULTS: Different patterns of PCNA expression were recorded in the different experimental groups. PCNA-immunostained cells in injured spinal cord tissue, mainly ependymal cells and astrocytes, increased when co-transplantation of fetal brain cortex and crushed adult peripheral nerve tissue was used, in comparison to other neural donor tissues. In the grafted tissue, proliferative activity was greater when fetal brain cortex, alone or with peripheral nerve, was used, in comparison to the use of fetal spinal cord or adult peripheral nerve tissue. Nevertheless, the number of PCNA-positive cells does not seem to be influenced by the presence of peripheral nerve tissue in the donor tissue. CONCLUSIONS: Our present findings suggest the effectiveness of co-transplantation of peripheral nerve tissue and fetal brain tissue in attempts at spinal cord reconstruction after injury. <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&li st_uids=11077093> Neuroscience Research Unit of the Mapfre-Medicine Foundation, Puerta de Hierro Clinic, Autonomous University, Madrid, Spain.

    • Zurita M, Vaquero J, Oya S and Montilla J (2001). Functional recovery in chronic paraplegic rats after co-grafts of fetal brain and adult peripheral nerve tissue. Surg Neurol. 55 (5): 249-54; discussion 254-5. Summary: BACKGROUND: In recent years, experimental studies have sought some type of functional improvement in traumatic paraplegia by transplanting neural tissue into the injured spinal cord. The aim of this work is to study the possibility of functional recovery in chronic paraplegic rats after co-transplantation of fetal cerebral tissue and adult peripheral nerve tissue. METHODS: Seventy adult female Wistar rats were subjected to spinal cord injury at the T6-T8 level, causing complete paraplegia. Three months later, in 50 rats (grafted group) the injured spinal cord tissue received a graft of fetal brain cortex associated with crushed adult peripheral nerve. All the animals (grafted and control groups) were subjected to daily rehabilitation procedures from the first week after the injury, and evaluated weekly for motor and sensory recovery. Statistical analysis of different behavioral data between control and grafted animals was performed using the Kruskal-Wallis ANOVA and the nonparametric Wilcoxon test. RESULTS: Between 8 and 12 months after transplantation, progressive signs of functional recovery were observed in the grafted animals, associated with an increase in muscle mass in the lower extremities, findings that were significantly different from those in nongrafted animals (p < 0.05). At this time, donor cerebral tissue is integrated into previously injured spinal cord and results in formation of bundles of nerve fibers that emerge from the area of the transplant and surround the spinal cord beneath the lesion. CONCLUSIONS: Delayed co-transplantation of fetal cerebral tissue and peripheral nerve tissue can be used to achieve anatomical remodeling and long-term functional recovery in rats rendered paraplegic as result of severe spinal cord injury. These findings support the possibility of functional recovery after chronic traumatic paraplegia. <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&li st_uids=11516457> Neuroscience Research Unit of the Mapfre-Medicine Foundation, Puerta de Hierro Clinic, Autonomous University, Madrid, Spain.

    • Zurita M, Vaquero J and Zurita I (2001). Presence and significance of CD-95 (Fas/APO1) expression after spinal cord injury. J Neurosurg. 94 (2 Suppl): 257-64. Summary: OBJECT: A glycoprotein, CD95 (Fas/APO1) is widely considered to be implicated in the development of apoptosis in a number of tissues. Based on the hypothesis that apoptosis is related to cell death after spinal cord injury (SCI), the authors studied the presence and distribution of CD95 (Fas/APO1)-positive cells in injured spinal cord tissue for the purpose of determining the significance of this protein during the early phases of SCI. METHODS: The presence and distribution of cells showing positive immunostaining for CD95 (Fas/APO1) were studied 1, 4, 8, 24, 48, and 72 hours and 1, 2, and 4 weeks after induction of experimental SCI in rats. Studies were conducted using a monoclonal antibody to the CD95 (Fas/APO1) protein. Positivity for CD95 (Fas/APO1) was observed in apoptotic cells, mainly in the gray matter, 1 hour after trauma, and the number of immunostained cells increased for the first 8 hours, at which time the protein was expressed in both gray and white matter. From 24 to 72 hours postinjury, the number of immunostained cells decreased in the gray matter, but increased in the white matter. From then on, there were fewer CD95 (Fas/APO1)-positive cells, but some cells in the white matter still exhibited positive immunostaining 1 and 2 weeks after injury. At 4 weeks, there remained no CD95 (Fas/APO1)-positive cells in injured spinal cord. CONCLUSIONS: These findings indicate that CD95 (Fas/APO1) is expressed after SCI, suggesting a role for this protein in the development of apoptosis after trauma and the possibility of a new therapeutic approach to SCI based on blocking the CD95 (Fas/APO1) system. <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&li st_uids=11302628> Neuroscience Research Unit of the Mapfre-Medicine Foundation, Neurosurgical Service, Puerta de Hierro Clinic, Autonomous University, Madrid, Spain.

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