Ismet Gavrankapetanović

Antioxidant capacity in postmortem brain tissues of Parkinson’s and Alzheimer’s diseases

Oxidative stress has been associated with damage and progressive cell death that occurs in neurodegenerative disorders such as Parkinsons disease (PD) and Alzheimers disease (AD). The aim of this study was to investigate the antioxidant capacity in postmortem motor cortex (MC), nucleus caudatus (NC), gyrus temporalis (GT) and substantia nigra (SN) from controls (C) and patients with PD and AD. The initial samples consisted of 68 subjects of PD, AD and C. Brains were matched for age, sex and postmortem time. Brain tissue was homogenized in a phosphate buffer pH 7.3 and separated with two-step centrifugation at 15,000rpm for 30 min and 15,000 rpm for 10 min at 4 degrees C. Antioxidant capacity in the supernatants was measured using the oxygen radical absorbance assay (ORAC). The results showed that in the SN of parkinsonians brain the balance between production of free radicals and the neutralization by a complex antioxidant system is disturbed. No changes in the antioxidant capacity of postmortem MC and NC of parkinsonians brain in comparison with C were found. In the SN of parkinsonians brain, antioxidant capacity seems to be lower in comparison with C (p < 0.05). Antioxidant capacity against peroxyl radical showed that MC of AD patients was lower than in the MC of C (p < 0.005). In NC of AD patients the antioxidant capacity against hydroxyl radical was increased in comparison with C (p < 0.04). No changes in the antioxidant capacity were found in brain tissues of AD in comparison with C, when CuSO4 was used as a free radical generator.

Brain antioxidant capacity in rat models of betacytotoxic-induced experimental sporadic Alzheimer’s disease and diabetes mellitus

It is believed that oxidative stress plays a central role in the pathogenesis of metabolic diseases like diabetes mellitus (DM) and its complications (like peripheral neuropathy) as well as in neurodegenerative disorders like sporadic Alzheimers disease (sAD). Representative experimental models of these diseases are streptozotocin (STZ)-induced diabetic rats and STZ-intracerebroventricularly (STZ-icv) treated rats, in which antioxidant capacity against peroxyl (ORAC(-ROO)*) and hydroxyl (ORAC(-OH)*) free radical was measured in three different brain regions (hippocampus, cerebellum, and brain stem) by means of oxygen radical absorbance capacity (ORAC) assay. In the brain of both STZ-induced diabetic and STZ-icv treated rats decreased antioxidant capacity has been found demonstrating regionally specific distribution. In the diabetic rats these abnormalities were not associated with the development of peripheral diabetic neuropathy. Also, these abnormalities were not prevented by the icv pretreatment of glucose transport inhibitor 5-thio-D-glucose in the STZ-icv treated rats, suggesting different mechanism for STZ-induced central effects from those at the periphery. Similarities in the oxidative stress alterations in the brain of STZ-icv rats and humans with sAD could be useful in the search for new drugs in the treatment of sAD that have antioxidant activity.

Developmental Dysplasia of the Hip in Childhood – Etiology, Diagnostics and Conservative Treatment

Since developmental dysplasia of the hip (DDH) represents one of the most common con‐ genital deformations of the musculoskeletal system and the most common deformation of the hip joint, the aim is to emphasize the importance of early recognition and diagnosis of DDH as well as comprehensive screening among newborns. DDH represents a dynamic process that results in the action of a number of exogenous and endogenous factors, physiological and mechanical, exerted to the mother and to the child during pregnancy and after delivery. Summary of all current knowledge about the origin of this deformity suggests that the most important factors in the development are hard abdominal muscles and uterine muscles, as limiting factors for fetal movement, which prevents its physio‐ logical turn, and reinforces the pelvic presentation of the fetus in uterus. Considering the fact that developmental dysplasia of the hip demands multidisciplinary approach and cooperation among gynecologists, neonatologists, pediatricians, radiologists, and ortho‐ pedic surgeons, the goal of this chapter is to make a consensus about early conservative treatment among clinicians, time of commencement, and its efficacy.

Fat Embolism in Orthopedic Surgery

Every long bone fracture in orthopedic surgery represents a possible scenario for development of embolism complication, especially the fat embolism. There is no scientific explanation why fat embolism occurs and what are the hypotheses for development of fat embolism or the proper way of prevention, but just speculations and possible theories in the evolution of the clinical picture of fat embolism syndrome. Throughout this chapter, the authors will explain the possible theories of development of fat embolism, risk factors, pathology, and pathophysiology during progress of the clinical picture and signs of the fat embolism syndrome and therapy.

Gluteal compartment syndrome caused by traumatic rupture of the superior gluteal artery

Introduction. We report a case of a sixty-year-old man diagnosed with gluteal compartment syndrome caused by traumatic rupture of the superior gluteal artery associated with fracture of the inferior pubic ramus and blunt trauma. Case report. A patient was injured falling from a height of four meters. Signs of compartment syndrome and sciatic nerve compression developed three hours after the injury. The patient went through a computerized tomography (CT) scan procedure with contrast, which showed a hematoma in the gluteal region, but without signs of active bleeding. However, after observation and monitoring of the patient, CT angiography was performed which revealed a rupture of the superior gluteal artery. Fasciotomy and debridement were performed and the patient was diagnosed with gluteal compartment syndrome and rupture of the superior gluteal artery. Surgery resulted in a significant improvement of the patient’s condition. Conclusion. Traumatic gluteal compartment syndrome is a rare condition. Gluteal compartment syndrome should be taken into consideration in each patient with pelvic trauma and hematoma in the gluteal region whose neurological status is affected. Prompt diagnosis and fasciotomy are crucial in the treatment and fasciotomy presents the gold standard in the treatment.

Treatment of Common Cold and Influenza by Administration of Large Doses of Ascorbic Acid

Introduction: Progressive pseudorheumatoid dysplasia (PPD) is an autosomal recessive genetic disorder reported to be caused by gene alterations of the Wnt1-inducible signaling pathway protein 3 corresponding gene (WISP3) located on chromosome position 6q22. Up to date, there is only a handful of WISP3 mutations identified in Europe, whereas most mutations are identified in Asia and Middle East. According to our knowledge, this is the first report of genetic dissection of WISP3 associated with spondyloepiphyseal dysplasia tarda from Bosnia and Herzegovina. Based on clinical examination findings (general manifestations, physical examination, characteristics of their bones on X-ray and laboratory results), an index patient was directed to WISP3 genotyping for confirmation of suspected diagnosis of PPD. Methods: DNA was extracted from peripheral blood leukocytes. All 5 exons and their exon-intron boundaries of the WISP3 gene were amplified by polymerase chain reaction (PCR) and sequenced by Sanger method. Segregation analysis was done to confirm the familial carrier status. Results: A missense mutation (C223G) homozygous T to G transition at c.667 in exon 4 was identified in index patient. This mutation changed codon CAG to TAG and resulted in a subsequent change of the cysteine to glycine codon. Same mutation was observed in both parents in heterozygous form confirming the familial segregation. Conclusion: Due to its nature, the identified mutation C223G in exon 4 in WISP3 gene is the most probably causative for PPD in described patient. Here we describe the PCR based method for genotyping of specific mutation in WISP3 gene. The identification of this mutation might be a valuable addition to a regional databases on rare genetic variant although a functional analysis should be performed to explain its pathological effect.