Thrombin activatable fibrinolysis inhibitor activity, thrombin-antithrombin complex and D-dimer levels in preterm neonates with early respiratory distress syndrome

Intraalveolar fibrin deposition found in neonates with respiratory distress syndrome (RDS) is explained by the activation of the coagulation system and inefficient fibrinolysis. However, thrombin activatable fibrinolysis inhibitor activity (TAFIa), an inhibitor of fibrinolysis, and the ratio of D-dimer to thrombin-antithrombin complex (D-dimer/TAT), an index of fibrinolytic activity, have not been reported previously in neonatal RDS. Aim of this study is to evaluate the influence of plasma TAFIa levels on the fibrinolytic state in neonatal RDS. The RDS group (Group 1) consisted of 29 neonates, and 18 neonates served as the control group (Group 2). Plasma TAFIa levels and D-dimer/TAT ratios were evaluated in all neonates in the first 6 hr of life. Neonates in the RDS group were further divided into two subgroups; Group 1a consisted of 12 neonates with evidence of mild asphyxia (Apgar score at 5 min <7 and cord pH <7.26), and Group 1b consisted of 17 nonasphyxiated neonates. No significant difference was found in TAFIa levels and D-dimer/TAT ratios between Groups 1 and 2 [214% (56.2-361%) and 124.3 (4.4-3,921) in Group 1 and 201% (60.3-381%) and 147 (5.9-1,426) in Group 2]. There were negative correlations between cord pH and TAFIa levels in both groups. Increased TAFIa levels and decreased D-dimer/TAT ratios and platelet counts were detected in mildly asphyxiated neonates when compared with nonasphyxiated ones. TAFIa is not responsible for the hypofibrinolytic state reported in RDS. However, asphyxia influences TAFIa levels and increased TAFIa levels depress fibrinolysis.     

The spectrum of diseases causing fever of unknown origin in Turkey: a multicenter study.

OBJECTIVE: The purpose of this trial was to determine the spectrum of diseases with fever of unknown origin (FUO) in Turkey. METHODS: A prospective multicenter study of 154 patients with FUO in twelve Turkish tertiary-care hospitals was conducted. RESULTS: The mean age of the patients was 42+/-17 years (range 17-75). Fifty-three (34.4%) had infectious diseases (ID), 47 (30.5%) had non-infectious inflammatory diseases (NIID), 22 (14.3%) had malignant diseases (MD), and eight (5.2%) had miscellaneous diseases (Mi). In 24 (15.6%) of the cases, the reason for high fever could not be determined despite intensive efforts. The most common ID etiologies were tuberculosis (13.6%) and cytomegalovirus (CMV) infection (3.2%). Adult Still's disease was the most common NIID (13.6%) and hematological malignancy was the most common MD (7.8%). In patients with NIID, the mean duration of reaching a definite diagnosis (37+/-23 days) was significantly longer compared to the patients with ID (25+/-12 days) (p=0.007). In patients with MD, the mean duration of fever (51+/-35 days) was longer compared to patients with ID (37+/-38 days) (p=0.052). CONCLUSIONS: Although infection remains the most common cause of FUO, with the highest percentage for tuberculosis, non-infectious etiologies seem to have increased when compared with previous studies.     

Mood and metabolic consequences of sleep deprivation as a potential endophenotype’ in bipolar disorder

It has been commonly recognized that circadian rhythm and sleep/wake cycle are causally involved in bipolar disorder. There has been a paucity of systematic research considering the relations between sleep and mood states in bipolar disorder. The current study examines the possible influences of sleep deprivation on mood states and endocrine functions among first-degree relatives of patients with bipolar disorder and healthy controls. Blood samples were taken at two time points in the consecutive mornings at predeprivation and postdeprivation periods. Participants simultaneously completed the Profiles of Mood States at two time points after giving blood samples. Plasma T3 and TSH levels increased after total sleep deprivation in both groups. Sleep deprivation induced TSH levels were reversely associated with depression–dejection among healthy controls. A paradoxical effect was detected for only the first-degree relatives of the patients that changes in plasma cortisol levels negatively linked to depression–dejection and anger–hostility scores after total sleep deprivation. Plasma DHEA levels became correlated with vigor-activity scores after sleep deprivation among first-degree relatives of bipolar patients. On the contrary, significant associations of depression–dejection, anger–hostility, and confusion–bewilderment with the baseline plasma DHEA levels became statistically trivial in the postdeprivation period. Findings suggested that first-degree relatives of patients with bipolar disorder had completely distinct characteristics with respect to sleep deprivation induced responses in terms of associations between endocrine functions and mood states as compared to individuals whose relatives had no psychiatric problems. Considering the relationships between endocrine functions and mood states among relatives of the patients, it appears like sleep deprivation changes the receptor sensitivity which probably plays a pivotal role on mood outcomes among the first-degree relatives of patients with bipolar disorder.     

A new hypothesis about hematopoietic Pbx-interaction protein (HPIP): Can it be a key factor in neurodegeneration in the post-menopausal period?

Neuronal degeneration in the post-menopausal term leads to cognitive symptoms such as anxiety, difficulty in concentrating, overreacting to minor upsets, quickly becoming irritated and forgetfulness in approximately 70–80% of all women around the world. These symptoms, which result from microtubule damage in the axon extensions of hippocampal neurons in during menopause, greatly reduce individuals’ life quality. Thus, an investigation of the estrogen receptor-signaling pathway–microtubule dynamic triangle and the possible links between them is important when it comes to explaining the possible mechanism of neurodegeneration. Hematopoietic Pbx-interaction protein (HPIP), a microtubule-binding protein, is a novel scaffolding protein. The detection of this protein on neurons represents the most important step in our hypothesis. The importance of the hypothesis is that it might provide important clues about the possible role of HPIP and its mechanism through in vivo and in vitro studies of estrogen receptors–microtubules and the HPIP triangle in terms of neuronal degeneration in the post-menopausal period.     

Comparison of conventional radiography and MDCT in suspected scaphoid fractures

AIM: To determine the diagnostic accuracy and radiation dose of conventional radiography and multidetector computed tomography(MDCT) in suspected scaphoid fractures.METHODS: One hundred twenty-four consecutive patients were enrolled in our study who had suffered from a wrist trauma and showed typical clinical symptoms suspicious of an acute scaphoid fracture. All patients had initially undergone conventional radiography. Subsequent MDCT was performed within 10 d because of persisting clinical symptoms. Using the MDCT data as the reference standard, a fourfold table was used to classify the test results. The effective dose and impaired energy were assessed in order to compare the radiation burden of the two techniques. The Wilcoxon test was performed to compare the two diagnostic modalities.RESULTS: Conventional radiography showed 34 acute fractures of the scaphoid in 124 patients(42.2%). Subsequent MDCT revealed a total of 42 scaphoid fractures. The sensitivity of conventional radiography for scaphoid fracture detection was 42.8% and its specificity was 80% resulting in an overall accuracy of 59.6%. Conventional radiography was significantly inferior to MDCT(P < 0.01) concerning scaphoidfracture detection. The mean effective dose of MDCT was 0.1 m Sv compared to 0.002 m Sv of conventional radiography.CONCLUSION: Conventional radiography is insufficient for accurate scaphoid fracture detection. Regarding the almost negligible effective dose, MDCT should serve as the first imaging modality in wrist trauma.     

Topical N-Acetylcysteine Improves Wound Healing Comparable to Dexpanthenol: An Experimental Study

In this study, we aimed to compare the effects of dexpanthenol and N-acetylcysteine on wound healing. The wound healing process is a multifaceted sequence of activities associated with tissue restoration process. A number of investigations and clinical studies have been performed to determine new approaches for the improvement of wound healing. A total of 30 rats were divided into 3 equal groups. A linear 2-cm incision was made in the rats'' skin. No treatment was administered in the first (control) group. Dexpanthenol cream was administered to the rats in the second group and 3% N-acetylcysteine cream was administered to the rats in the third group. The wound areas of all of the rats were measured on certain days. On the 21st day, all wounds were excised and histologically evaluated. The epithelialization and granulation rates between the groups were revealed to be similar in microscopic evaluations. Although the fibrosis was remarkable in the control group as compared with the other groups, it was similar in N-acetylcysteine and dexpanthenol groups. Angiogenesis rate was remarkable in the N-acetylcysteine group compared with the others. In multiple-comparison analysis, Dexpanthenol and N-acetylcysteine groups had similar results in terms of wound healing rates (P < 0.05), which were both higher than in the control group (P > 0.05). The efficacy of N-acetylcysteine in wound healing is comparable to dexpanthenol, and both substances can be used to improve wound healing.Key words: N-acetylcysteine, Dexpanthenol, Wound healingWound healing is a multifaceted sequence of activities associated with the tissue restoration process.¹ This activity takes place in 4 main steps: inflammation, proliferation, matrix deposition, and remodeling.^2,3 Moreover, there are many factors that might have harmful effects on the wound healing process. In this regard, there have been numerous analyses and clinical studies aiming to find new methods for the improvement of wound healing processes.⁴Dexpanthenol is the biologically-active alcohol of pantothenic acid, which leads to an elevation in the amount of coenzyme A in the cell. Dexpanthenol is extensively used in topical form, since it can easily penetrate the skin even at large local concentrations. When used in formulations, dexpanthenol is most effective for the stimulation of epithelialization, granulation, and the mitigation of itching.⁵N-acetylcysteine (NAC) is a prodrug that supplies bioavailable cysteine for glutathione replenishment and prevents oxidative damage as well as inflammation. It also leads to glutathione (GSH) formation in the body. Besides fostering angiogenesis, it is used to scavenge free radicals. NAC has a number of functions in the stages of repair process, including cell proliferation, migration, and scratch wound healing. Moreover, NAC has also been reported to promote wound healing in diabetic rats.⁶In this study, we aimed to compare the effects of dexpanthenol, a molecule that is widely used to improve wound healing, and NAC, a molecule that reduces oxidative stress and inflammation, on wound healing.     

Enzymatic Debridement in Necrotizing Pancreatitis

Multiple organ failure and pancreatic necrosis are the factors that determine prognosis in acute pancreatitis attacks. We investigated the effects of collagenase on the debridement of experimental pancreatic necrosis. The study covered 4 groups; each group had 10 rats. Group I was the necrotizing pancreatitis group. Group II was the collagenase group with pancreatic loge by isotonic irrigation following necrotizing pancreatitis. Group III was the collagenase group with pancreatic loge following necrotizing pancreatitis. Group IV was the intraperitoneal collagenase group following necrotizing pancreatitis. The progress of the groups was compared hematologically and histopathologically. There was no difference among the groups regarding the levels of leukocyte, hemogram, and urea. The differences in AST levels between Group I and II; and differences in glucose, calcium, LDH, AST, and amylase between Group II and III; between Group II and IV; between Group I and III; and between Group I and IV were statistically significant (P < 0.05). There were statistically significant differences between Group II and III, and Group II and IV regarding edema, acinar necrosis, inflammatory cell infiltration, hemorrhage, and fat necrosis (P < 0.05). In conclusion, the collagenase preparation used in this experimental pancreatitis model was found to be effective in the debridement of pancreatic necrosis.Key words: Acute pancreatitis, Necrose, Collagenase, DebridementAcute pancreatitis (AP) is a nonbacterial inflammatory disease of the pancreas that can range from interstitial edema to pancreatic necrosis in its severest form. In about 20% of AP attacks necrosis can develop in the pancreas while the disease limits itself and regresses in a couple of days in many patients (80%).¹The definitions that are still widely in effect today regarding the classification of acute pancreatitis were determined in 1992 at the Atlanta Conference.² The conference aimed at achieving a common classification for AP and its complications. Within severe acute pancreatitis, of which necrotizing pancreatitis is a part, organ failure and local complications can be seen (necrosis, pseudocyst, and abscess). Multiple organ failure and pancreatic necrosis are the factors that determine the prognosis. Half of the mortalities are observed within a period of 1 or 2 weeks. Necrotizing pancreatitis makes up for the 10–20% of AP cases. Severe pancreatitis has a high mortality rate and functional diseases like diabetes are seen in one-third to one-fifth of the recovered patients.³While the mortality rates are about 10% in the presence of sterile pancreatic necrosis, they go up over 30% in the existence of infected necrosis.¹ Regarding acute necrotizing pancreatitis, there is still no consensus on surgical indications and the time of surgical intervention, the surgical method to be used, and which patients need conservative treatment and which ones need surgical treatment. The goal in the surgical treatment of acute necrotizing pancreatitis is to isolate the necrotic tissue that might cause sepsis and multiple organ failure and to reduce the risk of mortality. The timing of necrosectomy as well as the way in which necrosectomy is performed is significant in necrotizing pancreatitis. The issue of the possibility that necrosectomy can be performed through minimally-invasive interventions instead of open surgery is still being discussed.³We planned to investigate the activity of collagenase clostridiopeptidase A (EC 3.424.3), which has never been attempted before in the debridement of experimental pancreatic necrosis (but which has been used for enzymatic debridement), and the enzyme preparation containing the accompanying proteases (Sterile Novuxol^®, Abbott, Uetersen, Germany). We aimed to evaluate the response of the disease to treatment through laboratory and histopathologic data, by using the enzyme preparation to treat necrotizing pancreatitis.