Ultrastructural changes in pneumocyte type II cells following traumatic brain injury in rats.

OBJECTIVE: We aimed to demonstrate the time-dependent ultrastructural changes in pneumocyte type II cells following brain injury, and to propose an electron microscopic scoring model for the damage. METHODS: Forty Wistar-Albino female rats weighing 170-200 g were used. The rats were allocated into five groups. The first group was the control and the second was the craniotomy without trauma. The others were trauma groups. Weight-drop method was used for achieving head trauma. Samples were obtained from the right and left pulmonary lobes at 2-, 8-, and 24-h intervals after transcardiac perfusion. An electron microscopic scoring model was used to reveal the changes. RESULTS: There were no ultrastructural pathological findings pointing to lung injury in any rat of the control groups. There was intense intracellular oedema in type II pneumocyte and interstitial oedema in the adjacent tissue in trauma groups. Oedema in mitochondria and dilatation in both smooth endoplasmic reticulum and Golgi apparatus was more evident in the 8- and 24-h trauma groups. The chromatin dispersion was disintegrated in the nucleus in all trauma groups. Scores of all trauma groups were significantly different from the controls (P<0.05). All trauma groups were different from each other at significant levels (P<0.05 for each trauma groups). CONCLUSIONS: The data suggested that ultrastructural damage is obvious at 2 h and deteriorates with time. The electron microscopic scoring model worked well in depicting the traumatic changes, which were supported by lipid peroxidation. Further experiments are needed to determine the exact outcome after brain death model.     

Ameloblastic carcinoma arising from anterior skull base.

Ameloblastic carcinoma (AC) is an aggressive malignant epithelial odontogenic tumor. It may appear de novo or originate from a pre-existing ameloblastoma or odontogenic cyst. To our knowledge, an AC that originates from the anterior skull base has not been reported before in the English literature. We report a case of an AC that originated from the anterior skull base and invaded the dura of the anterior fossa and discuss its clinical course and treatment.     

Systemic lupus erythematosus and thrombotic thrombocytopenic purpura: a case report.

BACKGROUND: Thrombotic thrombocytopenic purpura (TTP) is a multisystem disorder characterised by platelet aggregation causing microvascular occlusion. Early diagnosis and utilization of plasmapheresis can provide an improvement in prognosis. CASE REPORT: A 17 year old male with classical findings of TTP was later diagnosed as systemic lupus erythematosus (SLE). Plasmapheresis resulted in the significant amelioration of the course. CONCLUSION: The coexistence of TTP and SLE may facilitate a better understanding of in the pathophysiology of TTP. These association may provide the role of autoimmunity in TTP. SLE should be considered in the differential diagnosis of patients with TTP because of therapeutic implications.     

Somatostatin infusion withdrawal in the diagnosis of childhood growth hormone deficiency

OBJECTIVE: An evaluation of growth hormone (GH) testing for GH deficiency (GHD) in childhood is confounded by the lack of a world-wide consensus on the definition of GHD. Although a single GH test remains the most powerful biochemical tool in the evaluation of a child with growth failure, the test remains far from ideal. Withdrawal of somatostatin (SS) infusion is followed by a rebound rise of GH thought to be mediated by endogenous GH-releasing hormone (GHRH) function. This study was designed to compare the GH response to 90 min SS infusion in children with normal GH secretion versus children with GH deficiency. METHODS: Ten children with GHD and 10 healthy controls (NC) have been evaluated for GH response to somatostatin infusion withdrawal (SSIW) and compared with response of two provocative tests, glucagon plus propranolol test and L-Dopa test. All children received constant infusion of somatostatin for 90 min (3 microg/kg per h, Stilamin, Serono, Aubonne, Switzerland). In order to determine GH, blood samples were obtained 90 min before the SS infusion and 0, 15, 30, 45, 60, 75, and 90 min after the cessation of infusion. RESULTS: Growth hormone peak levels with SSIW were significantly lower in GH deficient children than in healthy children (2.5 +/- 1.2 ng/dL, vs 21.9 +/- 5.3 ng/dL, respectively, P < 0.01). No adverse effects were observed during or after somatostatin infusion. CONCLUSION: In the present study, SSIW elicited a significant GH rise in healthy children but not in children with GH deficiency. Although further controlled studies using more data are necessary to expand these findings, the results suggested that children with GH deficiency can be reliably discriminated from healthy children by SSIW.     

Bone mineral density in familial Mediterranean fever

The aim of this study was to evaluate the bone mineral density (BMD) in familial Mediterranean fever (FMF) and to search the effects of genetic factors, family history of FMF and types of clinical attacks on BMD. Forty-four attack-free patients with FMF and 36 healthy voluntary subjects were included in the study. BMD measurements of lumbar spine and left proximal femur were performed by dual energy X-ray absorptiometry (DEXA). There was no statistically significant difference between patient and control groups regarding median values of lumbar BMD (P?=?0.06), lumbar T (P?=?0.08) and Z (P?=?0.12) scores, femoral neck BMD (P?=?0.13), femoral T (P?=?0.22) and Z (P?=?0.16) scores and total femur BMD (P?=?0.14), T (P?=?0.19) and Z (P?=?0.27) scores. Patients with negative FMF family history had significantly lower femoral neck BMD (P?=?0.018), femoral neck T (P?=?0.009) and Z (P?=?0.01) scores and total femur BMD (P?=?0.033) than patients with positive FMF family history. There was no significant difference among the groups regarding mutation characteristic and types of attacks in lumbar BMD, T and Z scores, femoral neck BMD, T and Z scores and total femur BMD, T and Z scores (P?>?0.05). We found that the bone loss of patients with FMF is not different from that of the controls. The increased bone loss in the patients with negative family history for FMF should be further investigated with larger patient groups taking into consideration of the risk factors related to family history for osteoporosis.     

Effectiveness of Palosuran in Bleomycin-Induced Experimental Scleroderma

Systemic sclerosis (SSc) is a disease characterized by skin and internal organ involvement. There is progressive accumulation of extracellular matrix components in the skin and involved organs. Tissue fibrosis is the prominent reason for mortality, and still, there is no satisfactory treatment. The aim of this study was to evaluate the effects of urotensin-II (U-II) antagonist palosuran in an animal model of scleroderma. We also planned to measure U-II, endothelin-1 (ET-1), and transforming growth factor-β1 (TGF-β1) levels, as well as the association of these levels with dermal thickness. Twenty-four male mice were included in this study and they were divided into three groups—group 1: control group, group 2: fibrosis group, and group 3: fibrosis + palosuran treatment group. Fibrosis + palosuran treatment in group 3 reduced ET-1, U-II, and TGF-β1 levels. In total, the diminished values were statistically significant in the ET-1 and TGF-β1 levels (p?<?0.05). Dermal thickness was higher in the fibrosis group, when compared with the other groups. There was no significant relationship between dermal thickness and ET-1, U-II, or TGF-β1 levels (p?>?0.05). It is believed that U-II is an important mediator in SSc, and its antagonism with palosuran could be a new treatment choice in SSc.     

Urotensin Inhibition with Palosuran Could Be a Promising Alternative in Pulmonary Arterial Hypertension

Pulmonary arterial hypertension (PAH) is a progressive and a life-threatening disease with its high morbidity and mortality ratios. On searching for new shining targets in pathogenesis, we noticed, in our previous studies, urotensin-II (UII) in systemic sclerosis with potent angiogenic and pro-fibrotic features. Owing to the mimicking properties of UII with endothelin-1 (ET1), we attempted to investigate the effect of palosuran in a PAH rat model. Thirty rats were randomly divided into three groups, with each group comprising 10 rats: group 1 (control group) received the vehicle subcutaneously, instead of monocrotaline (MCT) and vehicle; group 2 (MCT group) received subcutaneous MCT and vehicle; and group 3 (MCT + palosuran group) received subcutaneous MCT and palosuran. Serum UII, ET1, transforming growth factor-β1 (TGF-β1) levels, pulmonary arteriolar pathology of different diameter vessels, and cardiac indices were evaluated. The ET1, TGF-β1, and UII levels were significantly diminished in the treatment group, similar to the controls (p?<?0.001). Right ventricular hypertrophy index and mean pulmonary arterial pressure scores were also significantly reduced in the treatment group (p?=?0.001). Finally, in the 50–125-μm diameter arterioles, in contrast to Groups 3 and 1, there was a statistically significant thickness (p?<?0.01) in the arteriolar walls of rats in Group 2. The treatment effect on arteries of more than 125-μm diameters was found to be valuable but not significant. Owing to its healing effect on hemodynamic, histological, and biochemical parameters of MCT-induced PAH, palosuran as an antagonist of UII might be an optional treatment alternative for PAH.     

Assessments of the associations of thrombus localization with accompanying disorders,risk factors,D-dimer levels,and the red cell distribution width in pulmonary embolism

OBJECTIVE:

Pulmonary embolisms occur as a wide spectrum ranging from clinically asymptomatic thrombi to massive thrombi that lead to cardiogenic shock. The purpose of this study was to determine the associations of thrombus localization with risk factors, accompanying disorders, D-dimer levels and the red blood cell distribution width in patients with pulmonary embolism.

MATERIAL AND METHODS:

In 148 patients diagnosed with pulmonary embolism, the presence and anatomical localization of the thrombus were assessed via computed tomographic pulmonary angiography. The accompanying disorders, risk factors, serum D-dimer levels, and red blood cell distribution width of the patients were retrospectively evaluated. ClinicalTrials.gov: NCT02388841.

RESULTS:

The mean age of the patients was 54±16.0 years, and 48 patients were ≥65 years of age. The most frequent accompanying disorders were chronic obstructive pulmonary disease (22%) and malignancy (10.1%), and the most frequent risk factors were recent operation (14.1%) and immobilization (18.2%). Thrombi were most frequently observed in the right pulmonary artery (37.8%). In 31% of the patients, the thrombus was localized to the main pulmonary arteries. Immobile patients exhibited a higher proportion of thrombi in the main pulmonary arteries than mobile patients. The mean D-dimer level and the mean red blood cell distribution width in the patients with thrombi in the main pulmonary arteries were higher than those in the patients with thrombi in more distal pulmonary arterial branches.

CONCLUSION:

Significant associations of proximally localized thrombi with immobilization, the D-dimer levels, and the red blood cell distribution width were observed.     

Lead Exposure Is Related to Impairment of Aortic Elasticity Parameters

Arterial hypertension is one of the physical complications of chronic lead exposure. Hypertension has effects on aortic elastic properties. The aim of this study was to evaluate the aortic elastic properties in workers occupationally exposed to lead. Forty‐one workers who were exposed to lead and 39 healthy controls were included in the study. All patients underwent transthoracic echocardiography for detecting aortic elastic parameters. There were no differences in baseline characteristics between the lead‐exposure group and controls. Aortic strain (9.4%±4.5% vs 12.4%±4.2%, P=.004) and aortic distensibility (0.45±0.21 cm²/dyn vs 0.55±0.20 cm²/dyn, P=.046) were decreased in patients with lead exposure compared with controls. There was a negative significant weak correlation between aortic strain and (r=−0.294, P=.008) lead levels. There was no significant correlation between aortic distensibility and any other echocardiographic parameters. This study suggests that chronic exposure to lead is related to impairment of aortic elasticity parameters.

Lead contamination (such as that emitted from house paint, gasoline, batteries, and other sources) may cause a wide variety of body organ complications.¹ Despite the still manifested divergences of opinion, it seems that chronic exposure to lead represents a risk for arterial hypertension development. Functional changes within the arterial wall both in smooth muscles and the endothelium might result in arterial hypertension caused by chronic exposure to lead compounds.² Blood pressure (BP) was found to be increased in workers with blood lead concentrations of 7 μg/L on average.³ According to the World Health Organization (2000), the level of 400 μg/L is accepted as safe to avoid possible adverse health effects, but American Conference Governmental and Industrial Hygienists suggest an even lower value of <300 μg/L.Hypertension has effects on the aorta (decreased aortic distensibility and increased aortic stiffness). Aortic strain is a simple and useful parameter of transthoracic echocardiography. Some studies have suggested that aortic elastic parameters can be used as an independent predictor of all‐cause and cardiovascular mortality in hypertensive patients.⁴, ⁵ In previous studies, the relationship between lead exposure and arterial hypertension has been demonstrated, and findings suggest that arterial hypertension and organ complications of arterial hypertension are more frequent in workers with lead exposure. Until now, there have been no data on the effects of lead exposure on aortic stiffness. The aim of this study was to evaluate the effects of lead on aortic elasticity parameters.