Галерея 3311733

Галерея 3311733

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Serengeti National Park tourists watch as a lion eats their vehicle's TIRE

Terrifying: Tourists watched in fear as lions in the Serengeti National Park spent an hour attacking their vehicle
Attack: One of the lions could be seen gnawing at the wheels of the truck, destroying one of its tires
Hunting: The animals 'wreaked havoc' destroying the wheels and attempting to crack the enforced glass windows
The dramatic images were captured by safari tour guide Emmanuel Bayo, from Arusha, Tanzania earlier this month
Fear: The tour guide said that the lions may have attacked the truck because they 'hadn't had a kill for a while'

By Julian Robinson for MailOnline

11:11 10 Nov 2015, updated 18:24 10 Nov 2015

This is the moment terrified tourists watched a lion eating the tires of their vehicle while they were on a safari drive in Tanzania.
Pictures taken in the Serengeti National Park show hungry lions gnawing at the wheels of the truck during an hour-long attack.
Holidaymakers can be seen cowering inside as the animals 'wreaked havoc' destroying the tires and attempting to crack the enforced-glass windows.
The dramatic images were captured by safari tour guide Emmanuel Bayo, from Arusha, Tanzania earlier this month.
He said: 'It was quite scary really - the lions are very hungry in the park and hadn't had a kill for a while.
'The truck was driving past with people inside and the lions smelt the humans.
'Then they were trying to get inside for about an hour and wreaked havoc.
'They destroyed the wheels and tried to smash the windows - even though we have enforced glass which stops this. It would have been a disaster if we hadn't.
'It was scary but exhilarating - I think everyone should come on safari with me to have these experiences.'
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Pediatr Transplant. Author manuscript; available in PMC 2013 Nov 1.
1 Department of Neurology, Lahey Clinic Medical Center, 41 Mall Road, Burlington, MA, 01805 and Department of Neurology, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115. gro.yehal@oh.t.neerod , (Ph) 781-744-8844; (F) 781-744-5581
2 Division of Nephrology, Children’s Hospital Boston, Hunnewell 3, 300 Longwood Avenue, Boston, MA 02115. ude.dravrah.snerdlihc@gidor.ycnan , (Ph) 617-355-6129; (F) 617-730-0569
3 Department of Surgery, Children’s Hospital Boston, Fegan 3, 300 Longwood Avenue, Boston, MA 02115. ude.dravrah.snerdlihc@mik.gnueh , (Ph) 617-355-8544; (F) 617-730-0475
4 Department of Pathology, Children’s Hospital Boston, Bader 1, 300 Longwood Avenue, Boston, MA 02115. ude.dravrah.snerdlihc@vodil.trah (Ph) 617-355-7435; (F) 617-730-0207
5 Department of Orthopaedic Surgery, Children’s Hospital Boston, 300 Longwood Avenue, Boston, MA 02115. ude.dravrah.snerdlihc@oripahs.cirederf , (Ph) 617-355-6753; (F) 617-730-0236
6 Division of Child Neurology, Weill Cornell Medical College, 525 East 68 th Street, New York, NY 10065. ude.llenroc.dem@1009rrp , (Ph) 212-746-1279; (F) 212-746-4001
7 Department of Neurology, Children’s Hospital Boston, 300 Longwood Avenue, Boston, MA 02115. ude.dravrah.snerdlihc@gnak.retep , (Ph) 617-355-8235; (F) 617-730-0279
Corresponding author: Peter B. Kang, MD, Department of Neurology, Children’s Hospital Boston, 300 Longwood Avenue, Boston, MA 02115, Ph: 617-355-8235, Fax: 617-730-0279, ude.dravrah.snerdlihc@gnak.retep
The publisher's final edited version of this article is available at Pediatr Transplant
Keywords: Renal transplantation, renal failure, uremia, neuropathy
1. Krishnan AV, Kiernan MC. Uremic Neuropathy: Clinical Features and new pathophysiological insights. Muscle and Nerve. 2007; 35 :273–290. [ PubMed ] [ Google Scholar ]
2. Hurkx W, Hulstijn-Dirkmaat I, Pasman J, Rotteveel J, Visco Y, Schroder C. Evoked Potentials in children with chronic renal failure, treated conservatively or by continuous ambulatory peritoneal dialysis. Pediatr Nephrol. 1995; 9 :325–328. [ PubMed ] [ Google Scholar ]
3. Asbury AK. Uremic Polyneuropathy. In: Dyck PJ, Thomas PK, editors. Peripheral Neuropathy. 3rd edition. Philadelphia: WB Saunders; 1993. pp. 1251–1257. [ Google Scholar ]
4. Scribner BH. Discussion. Trans Am Soc. Artif Intern Organs. 1965; 11 :29. [ Google Scholar ]
5. Nielsen VK. The peripheral nerve function in chronic renal failure. VII. Longitudinal course during terminal renal failure and regular dialysis. Acta Med Scan. 1974; 195 :155–162. [ PubMed ] [ Google Scholar ]
6. Caccia MR, Mangili A, Mecca G, Ubiali E, Zanoni P. Effects of hemodialytic treatment on uremic neuropathy. A clinical and electrophysiologic follow-up study. J Neurol. 1977; 217 :123–131. [ PubMed ] [ Google Scholar ]
7. Tenckhoff H, Boen FS, Jebsen RH, Spiegler JH. Polyneuropathy in chronic renal insufficiency. JAMA. 1965; 192 :91. [ PubMed ] [ Google Scholar ]
8. Hupperts RMM, Leuissen KML, Van Hooff JP, Lodder J. Recovery of uremic neuropathy after renal transplant. Clin Neurol Neurosurg. 1990:87–89. 92-1. [ PubMed ] [ Google Scholar ]
9. Bolton CF. Electrophysiological changes in uremic neuropathy after successful renal transplantation. Neurology. 1976; 26 :152–161. [ PubMed ] [ Google Scholar ]
10. El-Hussieni AA, Abu-Hegazy M, El-Tantawi Ael-H, Sobh MA, Ghoneim-MA Neurophysiologic changes in live related kidney transplant children and adolescents. Pediatr Transplantation. 2005; 9 :579–583. [ PubMed ] [ Google Scholar ]
11. Bolton CF, Baltzan MA, Baltzan RB. Effects of renal transplantation in uremic neuropathy: A clinical and electrophysiologic study. N Engl J Med. 1971; 284 :1170–1175. [ PubMed ] [ Google Scholar ]
12. Appenzeller O, Kornfield MA, Macgee J. Neuropathy in chronic renal disease. Arch Neurol. 1971; 24 :449–461. [ PubMed ] [ Google Scholar ]
13. Dyck PJ, Johnson WJ, Lambert EH, O’brien PC. Segmental demyelination secondary to axonal degeneration in uremic neuropathy. Mayo Clin Proc. 1971; 46 :400. [ PubMed ] [ Google Scholar ]
14. Said G, Boudier L, Selva J, Zingraff J, Drueke T. Different patterns of uremic polyneuropathy: Clinicopathologic study. Neurology. 1983; 33 :567–574. [ PubMed ] [ Google Scholar ]
1. Krishnan AV, Kiernan MC. Uremic Neuropathy: Clinical Features and new pathophysiological insights. Muscle and Nerve. 2007; 35 :273–290. [ PubMed ] [ Google Scholar ] [ Ref list ]
2. Hurkx W, Hulstijn-Dirkmaat I, Pasman J, Rotteveel J, Visco Y, Schroder C. Evoked Potentials in children with chronic renal failure, treated conservatively or by continuous ambulatory peritoneal dialysis. Pediatr Nephrol. 1995; 9 :325–328. [ PubMed ] [ Google Scholar ] [ Ref list ]
3. Asbury AK. Uremic Polyneuropathy. In: Dyck PJ, Thomas PK, editors. Peripheral Neuropathy. 3rd edition. Philadelphia: WB Saunders; 1993. pp. 1251–1257. [ Google Scholar ] [ Ref list ]
4. Scribner BH. Discussion. Trans Am Soc. Artif Intern Organs. 1965; 11 :29. [ Google Scholar ] [ Ref list ]
5. Nielsen VK. The peripheral nerve function in chronic renal failure. VII. Longitudinal course during terminal renal failure and regular dialysis. Acta Med Scan. 1974; 195 :155–162. [ PubMed ] [ Google Scholar ] [ Ref list ]
6. Caccia MR, Mangili A, Mecca G, Ubiali E, Zanoni P. Effects of hemodialytic treatment on uremic neuropathy. A clinical and electrophysiologic follow-up study. J Neurol. 1977; 217 :123–131. [ PubMed ] [ Google Scholar ] [ Ref list ]
7. Tenckhoff H, Boen FS, Jebsen RH, Spiegler JH. Polyneuropathy in chronic renal insufficiency. JAMA. 1965; 192 :91. [ PubMed ] [ Google Scholar ] [ Ref list ]
8. Hupperts RMM, Leuissen KML, Van Hooff JP, Lodder J. Recovery of uremic neuropathy after renal transplant. Clin Neurol Neurosurg. 1990:87–89. 92-1. [ PubMed ] [ Google Scholar ] [ Ref list ]
9. Bolton CF. Electrophysiological changes in uremic neuropathy after successful renal transplantation. Neurology. 1976; 26 :152–161. [ PubMed ] [ Google Scholar ] [ Ref list ]
10. El-Hussieni AA, Abu-Hegazy M, El-Tantawi Ael-H, Sobh MA, Ghoneim-MA Neurophysiologic changes in live related kidney transplant children and adolescents. Pediatr Transplantation. 2005; 9 :579–583. [ PubMed ] [ Google Scholar ] [ Ref list ]
11. Bolton CF, Baltzan MA, Baltzan RB. Effects of renal transplantation in uremic neuropathy: A clinical and electrophysiologic study. N Engl J Med. 1971; 284 :1170–1175. [ PubMed ] [ Google Scholar ] [ Ref list ]
12. Appenzeller O, Kornfield MA, Macgee J. Neuropathy in chronic renal disease. Arch Neurol. 1971; 24 :449–461. [ PubMed ] [ Google Scholar ] [ Ref list ]
13. Dyck PJ, Johnson WJ, Lambert EH, O’brien PC. Segmental demyelination secondary to axonal degeneration in uremic neuropathy. Mayo Clin Proc. 1971; 46 :400. [ PubMed ] [ Google Scholar ] [ Ref list ]
14. Said G, Boudier L, Selva J, Zingraff J, Drueke T. Different patterns of uremic polyneuropathy: Clinicopathologic study. Neurology. 1983; 33 :567–574. [ PubMed ] [ Google Scholar ] [ Ref list ]

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1 Department of Neurology, Lahey Clinic Medical Center, 41 Mall Road, Burlington, MA, 01805 and Department of Neurology, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115. gro.yehal@oh.t.neerod , (Ph) 781-744-8844; (F) 781-744-5581
2 Division of Nephrology, Children’s Hospital Boston, Hunnewell 3, 300 Longwood Avenue, Boston, MA 02115. ude.dravrah.snerdlihc@gidor.ycnan , (Ph) 617-355-6129; (F) 617-730-0569
3 Department of Surgery, Children’s Hospital Boston, Fegan 3, 300 Longwood Avenue, Boston, MA 02115. ude.dravrah.snerdlihc@mik.gnueh , (Ph) 617-355-8544; (F) 617-730-0475
4 Department of Pathology, Children’s Hospital Boston, Bader 1, 300 Longwood Avenue, Boston, MA 02115. ude.dravrah.snerdlihc@vodil.trah (Ph) 617-355-7435; (F) 617-730-0207
5 Department of Orthopaedic Surgery, Children’s Hospital Boston, 300 Longwood Avenue, Boston, MA 02115. ude.dravrah.snerdlihc@oripahs.cirederf , (Ph) 617-355-6753; (F) 617-730-0236
6 Division of Child Neurology, Weill Cornell Medical College, 525 East 68 th Street, New York, NY 10065. ude.llenroc.dem@1009rrp , (Ph) 212-746-1279; (F) 212-746-4001
7 Department of Neurology, Children’s Hospital Boston, 300 Longwood Avenue, Boston, MA 02115. ude.dravrah.snerdlihc@gnak.retep , (Ph) 617-355-8235; (F) 617-730-0279
Clinical and pathologic studies on adults with uremic neuropathy are numerous, but less is known about this disorder in children and adolescents. We report the clinical, electrophysiologic, and pathologic findings in an adolescent female with uremic neuropathy. Electrophysiologic findings were consistent with a primarily axonal sensorimotor polyneuropathy. Sural nerve biopsy revealed areas of focal depletion in myelin sheaths and loss of axons. Axonal degeneration with secondary myelin changes appears to be the characteristic pathology in this case, one of the youngest to our knowledge for which nerve biopsy data are available. Our patient experienced dramatic recovery after renal transplantation, similar to reports of older patients.
Although uremic neuropathy is a common complication of end stage renal disease, the exact mechanism of uremic neuropathy remains unknown ( 1 ). Pathological studies of adult patients with uremic neuropathy have demonstrated axonal degeneration with secondary demyelination. Existing studies focus on adults with uremic neuropathy; however, studies in younger individuals are limited. We report the clinical, electrophysiologic, and pathologic findings in an adolescent with this disorder who demonstrated dramatic improvement after renal transplant.
A 16-year-old girl with focal segmental glomerulosclerosis presented with progressive weakness of her lower extremities, at first in association with leg cramping. The weakness progressed over three months and she began to have frequent falls. She also developed weakness in her hands and a left facial droop. She denied paresthesias, numbness, dysphagia, dysarthria, or breathing difficulties. She otherwise had no antecedent illnesses or fevers.
Birth history was unremarkable. She presented with nephrotic syndrome associated with normal renal function at age 12 years and was initially treated with prednisone 60 mg daily. After four weeks of therapy, she had no improvement and therefore underwent percutaneous renal biopsy. The pathology was consistent with focal segmental glomerulosclerosis. She was subsequently treated with a 12 week course of oral cyclophosphamide and weaning doses of prednisone but remained resistant to therapy. Further immunosuppressive therapy was discussed but declined. She was provided supportive management and had progressive decline in renal function. Approximately four years after presentation, she reached end-stage renal disease and initiated hemodialysis. Her leg weakness developed at the same time. Medications at presentation were enalapril, losartan, calcitriol, iron polysaccharide, and darbepoetin alpha. She was a high school senior who lived at home with her parents. She had not traveled recently and had no significant family history.
On her initial physical examinations, she was alert and appeared well. She had paralysis of both upper and lower portions of her left face. A hemodialysis catheter in the right subclavian vein limited assessment of strength in the proximal right arm. In the upper extremities, she had mild distal weakness in bilateral finger intrinsic muscles but normal proximal left arm strength. In the lower extremities, she had no antigravity movement in bilateral distal leg muscles, mild weakness in knee flexion and extension and full strength in bilateral hip flexors. Muscle bulk, tone, and coordination were normal. She had mildly decreased vibration at the toes. Reflexes were absent in all extremities with flexor plantar responses. She could rise from a seated position with minimal support. She was unable to stand independently and she had difficulty lifting her feet off the ground when she walked.
Serum creatinine and blood urea nitrogen were 10.3 mg/dl and 157 mg/dl, respectively (glomerular filtration rate < 10 ml/min/1.73M 2 ). Total carnitine, thyroid stimulating hormone, vitamin B12, human immunodeficiency virus, lyme antibodies, and urine heavy metal screen were unremarkable. Examination of cerebrospinal fluid revealed 0 erythrocytes/mm 3 , 2 leukocytes/mm 3 , glucose 71 mg/dl (normal 60–80 mg/dl), and protein 31 mg/dl (normal 15–45 mg/dl). Magnetic resonance imaging of the thoracic and lumbosacral spine with contrast was normal. Nerve conduction and needle electromyography demonstrated significant axonal loss in the lower extremities.
For her renal failure, she received hemodialysis followed by continuous ambulatory peritoneal dialysis. Because of the facial and upper extremity involvement, chronic inflammatory demyelinating polyradiculoneuropathy was considered as a diagnostic alternative to uremic neuropathy. Plasma exchange was initiated, but then discontinued after one exchange due to patient discomfort. Her bilateral leg weakness continued to worsen. She underwent a course of intravenous immunoglobulin without improvement in symptoms. She began to experience dysesthesias in her feet and pain in the soles of her feet. Walking was limited by the ankle and foot weakness and sensory changes but was considerably improved by the use of well padded foam and semi-pneumatic full length walking braces.
A sural nerve biopsy was performed approximately six months after onset of leg weakness. It demonstrated a paucity of large myelinated fibers, an increase in collagen, and loss of axons ( Figures 1 and and2). 2 ). Twelve months after initiation of dialysis, the patient underwent renal transplantation. She reported a dramatic improvement in strength in the first one to two weeks after surgery, followed by slower improvement over months. Post-operatively, her medications included tacrolimus, mycophenolate mofetil, prednisone, nifedipine, potassium and sodium phosphate, valganciclovir, and sulfamethoxazole with trimethoprim. Five weeks after renal transpla
Китайская модель без трусов Суе Линг
Такие телки в Сальвадоре
Реальный азиатский транс Сара в купальнике и без

Галерея 3311733

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