Effect of ligamenta flava hypertrophy on lumbar disc herniation with contralateral symptoms and signs: a clinical and morphometric study

Introduction: The purpose of this study was to determine whether ligamentum flavum hypertrophy among disc herniated patients causes contralateral pain symptoms For this reason we measured the thickness of the ligament in disc herniated patients with ipsilateral or contralateral symptoms

Anatomic Origin and Molecular Genetics in Neuroblastoma

Neuroblastoma is considered as the most common extracranial solid tumor occurring during childhood, but takes place rarely after the age of 10 years. The tumors are considered as embryonal tumors that result from the fetal or early postnatal life development and are formed from neural crest-derived cells, and their origination is from the early nerve cells which are called as neuroblasts of sympathetic nervous system. Being heterogeneous in their biological, genetic, and morphological characteristics, tumors which are distinct from other solid tumors due to their biological heterogeneity result in the clinical pattern changes from spontaneous regression to a highly aggressive metastatic disease. Neuroblastoma tumorigenesis is regulated by Myc oncogene, leading to aggressive tumor subset. Many epigenetic factors play crucial role in the disease induction and development, while regulatory effect and outcome result in epigenetic patterns distinguishing neuroectoderm, neural crest, and more mature neural states. Neuroblastoma patients’ clinical management is based on prognostic categories subtracted from studies correlating outcome and clinico-biological variables. Neuroblastoma anatomic boundaries include primarily autonomic nervous system besides other rare locations. Neuroblastoma molecular pathogenesis classifies the tumor according to the different clinical behaviors that are important for the improvement of the patients outcome and overall survival according to the different therapy modalities applied

Correction: The effect of activated protein C on experimental acute necrotizing pancreatitis

PubMe

The effect of activated protein C on experimental acute necrotizing pancreatitis

INTRODUCTION: Acute pancreatitis is a local inflammatory process that leads to a systemic inflammatory response in the majority of cases. Bacterial contamination has been estimated to occur in 30–40% of patients with necrotizing pancreatitis. Development of pancreatic necrosis depends mainly on the degree of inflammation and on the microvascular circulation of the pancreatic tissue. Activated protein C (APC) is known to inhibit coagulation and inflammation, and to promote fibrinolysis in patients with severe sepsis. We investigated the effects of APC on histopathology, bacterial translocation, and systemic inflammation in experimental acute necrotizing pancreatitis. MATERIALS AND METHOD: Forty-five male Sprague-Dawley rats were studied. Rats were randomly allocated to three groups. Acute pancreatitis was induced in group II (positive control; n = 15) and group III (treatment; n = 15) rats by retrograde injection of taurocholate into the common biliopancreatic duct. Group I rats (sham; n = 15) received an injection of normal saline into the common biliopancreatic duct to mimic a pressure effect. Group III rats were treated with intravenous APC 6 hours after induction of pancreatitis. Pancreatic tissue and blood samples were obtained from all animals for histopathological examination and assessment of amylase, tumor necrosis factor-α, and IL-6 levels in serum. Bacterial translocation to pancreas and mesenteric lymph nodes was measured. RESULTS: Acute pancreatitis developed in all groups apart from group I (sham), as indicated by microscopic parenchymal necrosis, fat necrosis and abundant turbid peritoneal fluid. Histopathological pancreatitis scores in the APC-treated group were lower than in positive controls (10.31 ± 0.47 versus 14.00 ± 0.52; P < 0.001). Bacterial translocation to mesenteric lymph nodes and to pancreas in the APC-treated group was significantly decreased compared with controls (P < 0.02 and P < 0.007, respectively). Serum amylase, tumor necrosis factor--α, and IL-6 levels were also significantly decreased in comparison with positive controls (P < 0.001, P < 0.04 and P < 0.001, respectively). CONCLUSION: APC improved the severity of pancreatic tissue histology, superinfection rates and serum markers of inflammation during the course of acute necrotizing pancreatitis

Anatomical, Biological, and Surgical Features of Basal Ganglia

Basal ganglia refers to the deep gray matter masses on the deeply telencephalon and encompasses a group of nuclei and it influence the information in the extrapyramidal system. In human they are related with numerous significant functions controlled by the nervous system. Gross anatomically, it is comprised of different parts as the dorsal striatum that are consisted of the caudate nucleus and putamen and ventral striatum which includes the nucleus accumbens, olfactory tubercle, globus pallidus, substantia nigra, and subthalamic nucleus. Nucleus accumbens, is also associated with reward circuits and has two parts; the nucleus accumbens core and the nucleus accumbens shell. Neurological diseases are characterized through the obvious pathology of the basal ganglia, and there are important findings explaining striatal neurodegeneration on human brain. Some of these diseases are induced by bacterial and/or viral infections. Surgical interference can be one alternative for neuronal disease treatment like Parkinson’s Disease or Thiamine Responsive Basal Ganglia Disease or Wilson’s Disease, respectively in addition to the vascular or tumor surgery within this area. Extensive knowledge on the morphological basis of diseases of the basal ganglia along with motor, behavioral and cognitive symptoms can contribute significantly to the optimization of the diagnosis and later patient’s treatment

Ursodeoxycholic acid treatment improves hepatocyte ultrastructure in rat liver fibrosis

AIM: To examine the ultrastructural changes after ursodeoxycholic acid (UDCA) treatment in hepatocytes from experimentally induced fibrotic livers