Caries increment in Bosnian women associated with caries risk factors according to the Cariogram during pregnancy. A four-year longitudinal study.

AIM: The aim of this study was to determine dental caries increment in women after four years associated with caries risk factors according to the Cariogram during pregnancy. MATERIALS: Study design: The study population consisted of 96 pregnant women between 20 and 42 years of age at the start of the study. After four years, 80 women (83.33% recall rate) were re-examined by the baseline examiner using the same procedure employed at baseline. Caries prevalence was registered according to the WHO criteria and presented by the Decayed Missing and Filled Teeth (DMFT) index. Saliva tests were carried out according to instructions of the manufacturer. Nine factors/variables were entered into the Cariogram to obtain an individual caries risk profile. The chance of avoiding caries was scored into the five Cariogram risk categories. CONCLUSION: The results suggest that the dental caries increment in women after four years is significantly associated with caries risk factors according to the Cariogram during pregnancy.

Expression and intracellular localization of ACA and TRA-1-81 in smooth muscle cell tumors.

We studied the expression and intracellular localization of ACA and TRA-1-81 in smooth muscle cell tumors. The study was performed on tissue specimens obtained during surgery from patients with uterine leiomyoma and leiomyosarcoma (mean age 34 and 51 years, respectively). ACA was present in leiomyoma, leiomyosarcoma, and control myometrium. Intracellular expression of ACA varied in different types of tumors and was minimum in normal myometrium and maximum in leiomyosarcoma. Membrane localization of the protein is typical of common and cellular leiomyoma, while in the growth zones of mitotically active leiomyoma and leiomyosarcoma the reaction product was primarily located in tumor cell cytoplasm. TRA was detected in some leiomyosarcoma cells. Thus, ACA dysregulation was revealed in the growth zones of leiomyomas and in leiomyosarcomas, which manifested in enhanced expression of this protein and its detachment from the plasma membrane, which leads ACA translocation into the cytoplasm and nucleus of tumor cells and potentiates their proliferative activity.

A novel human glycoprotein ACA is an upstream regulator of human hematopoiesis.

A central issue in stem cell biology is a better understanding of the molecular mechanisms that regulate self-renewal of human hematopoietic stem cells (HSCs). Control of the specific function of HSCs like self-renewal and differentiation might be regulated by a common set of critical genes. However, the regulation among these genes is yet to be elucidated. Here, we show that activation by a novel human GPI-linked glycoprotein ACA at the surface of human peripheral blood progenitor cells induces via PI3K/Akt/mTor/PTEN upregulation of WNT, Notch1, Bmi-1 and HoxB4 genes thus, promoting self-renewal and generation of primitive HSCs. ACA-generated self-renewing cells retained their lympho-myeloid repopulating potential in NOD/SCID mouse xeno-transplantation model with long term functional capacity. We conclude that ACA is an essential regulator of the genes involved in maintaining hematopoiesis and its use in clinical praxis could overcome many of the barriers present so far in transplantation medicine.

Activation by ACA induces pluripotency in human blood progenitor cells.

Reprogramming of human somatic cells by transcription factors to pluripotent state holds great promise for regenerative medicine. However, low efficiencies of current reprogramming methods, immunogenicity and lack of understanding regarding the molecular mechanisms responsible for their generation, limits their utilization and raises questions regarding safety for therapeutic application. Here we report that ACA signaling via PI3K/Akt/mTor induces sustained de-differentiation of human blood progenitor cells leading to generation of ACA pluripotent stem cells. Blood-derived pluripotent stem cells differentiate in vitro into cell types of all three germ layers, exhibiting neuronal, liver, or endothelial characteristics. Our results reveal insight into the molecular events regulating cellular reprogramming and also indicate that pluripotency might be controlled in vivo through binding of a natural ligand(s) to ACA receptor enabling reprogramming through defined pathway(s) and providing a safe and efficient method for generation of pluripotent stem cells which could be a breakthrough in human therapeutics.

Effect of captopril on serum lipid levels and cardiac mitochondrial oxygen consumption in experimentally-induced hypercholesterolemia in rabbits.

Angiotensin converting enzyme inhibitors are widely used in therapy of cardiovascular diseases. However, the consensus on effects of these inhibitors in control of myocardial oxygen consumption during the process of experimental hypercholesterolemia and under the condition of endothelial dysfunction has not been reached. Here we examined effects of captopril, an angiotensin converting enzyme inhibitor, on serum lipid levels and oxygen consumption rate in mitochondria isolated from heart of rabbits treated by hypercholesterolemic diet. During the twelve-week period, the Chinchilla male rabbits were daily treated by saline (controls); 1 % cholesterol diet; 5 mg/kg/day captopril or 1 % cholesterol + 5 mg/kg/day captopril. Total- and high-density lipoprotein cholesterol and triglyceride in serum were measured spectrophotometrically. The left ventricle mitochondrial fraction was isolated and myocardial oxygen consumption was measured by Biological Oxygen Monitor. Mitochondria isolated from hearts of rabbits exposed to hypercholesterolemic diet showed significantly reduced respiration rates (state 3 and state 4) with altering adenosine diphosphate/oxygen ratio, whereas the respiratory control ratio was not affected when compared to controls. Mitochondria from cholesterol/captopril-treated animals showed significantly reduced respiration rates without altering adenosine diphosphate/oxygen ratio index or respiratory control ratio. Although captopril did not exert the favorable effect on serum lipid levels in cholesterol-treated animals, it restored the mitochondrial oxygen consumption. Further studies should be performed to define the underlying physiological and/or pathophysiological mechanisms and clinical implications.

[Development of new intracranial saccular aneurysms].

Newly formed aneurysms developing from a cerebral vessel which had appeared to be normal in a previous angiographic study are very rare. Four cases of angiographically documented newly developed saccular aneurysms are described in this report. In all four patients, the new aneurysms were symptomatic, causing subarachnoid hemorrhage (SAH). Repeat angiography, performed after the second SAH, revealed new aneurysms that were not demonstrated on initial angiograms after the first SAH. They were clipped with good postoperative course. Our observations and literature data suggest that some patients with SAH need further neuroradiological followup. The presence of the risk factors and age of the patient should be taken into consideration.

[Cerebral vasospasm after subarachnoid hemorrhage].

Cerebral vasospasm causes permanent neurolological deficit or death occurance in 13% of clinical cases. Peak frequency is from 8-10th day after SAH. The purpose of this study is factor analysis that may have influence on vasospasm development , as well as predictor determination. The study is prospective and analysis 192 patients treated in Institute of Neurosurgery, Clinical Centre of Serbia, Belgrade. The majority of patients were admitted in hospital in first four days after SAH, and 184 had GCS over 7. Univariate methods of factor analysis were used, and for significance of predictors influence testing multivariante regression analysis was used. Vasospasm occurred in 22,40% of all cases. No relationships have been found between sex, age, previous hypertension, timing of surgery, appearance of hydrocephalus and intracerebral hematoma, hypertermia or mean arterial blood pressure, with occurrence of cerebral vasospasm. Factors with significantly associated with the occurance of vasospasm were: hearth disease, hypernatriemia, Hct, clinical grade on admission as well as preoperative clinical grade and Fisher CT scan grade. In the first four days after SAH, Fisher scan grade, preoperative clinical grade and Hct, appeared as predictors. After four days, clinical grade on admission and hypernatiemia, showed as poredictors.

[New trends in neuromonitoring patients with with aneurysmal subarachnoid haemorrhage].

Neurointensive care of patients with subarachnoid haemorrhage is based on the theory that clinical outcome is the consequence of the primary haemorrhage and a number of secondary insults in the acute post haemorrhage period. Several neuromonitoring techniques have been introduced or accomplished into clinical practice in the last decade with the purpose of monitoring different but related aspects of brain physiology, such as cerebral blood flow (CBF), pressure within the cranial cavity, metabolism, and oxygenation. The aim of these techniques is to obtain information that can improve knowledge on brain pathophysiology, and especially to detect secondary insults which may cause permanent neurological damage if undetected and untreated in "real time", at the time when they can still be managed. These techniques include intracranial pressure (ICP) measurements, jugular venous oxygen saturation, near-infrared spectroscopy, brain tissue monitoring, and transcranial Doppler. The available devices are limited because they measure a part of complex process indirectly. Expense, technical difficulties, invasiveness, limited spatial or temporal resolution and the lack of sensitivity add to the limitation of any individual monitor. These problems have been partially addressed by the combination of several monitors known as multimodality monitoring. In this review, we describe the most common neuromonitoring methods in patients with subarachnoidal hemorrhage that can assess nervous system function, cerebral haemodynamics and cerebral oxygenation.

[Difference between values of gas analysis of arteries and internal jugular vein in patients with cerebral infarction].

INTRODUCTION: Cerebral infarction is more and more frequently present by massive participation and high percentage of mortality even in young population. It is notified as very hard, vitally endangered disease. OBJECTIVE: To prove whether there is a difference in the gas analyses of the arterial and cerebral venous blood between the patients with the cerebral infarction of the left and right hemisphere and why it is significant for the treatment of those patients. MATERIAL AND METHODS: Sixty-five (65) patients of both sexes who were diagnosed by CT as: cerebral infarction, cerebral multiinfarctions and cerebral haemorrhagic infarctions were investigated. Under the same conditions their radial artery and left and right internal jugular vein were tapped--on the fourth, eighth and tenth day of their disease. Gas analysis, calculation of oxygen content and statistical comparison of testing results were performed from the samples of arterial and venous blood. RESULTS: By continuous monitoring of gas analysis parameters of arterial and cerebral venous blood from internal jugular vein, we can follow up the phases of disease, the velocity of changes of gas analysis parameters and adequacy of brain circulation and to correct therapy adequately for the purpose of preventing basic disease complications and to estimate the results of treatment. CONCLUSION: There is a significant difference between the results of gas analysis of arteries and the internal jugular vein, in patients with infarctions of the left and right hemisphere of the brain.

Myocardial oxygen consumption regulation in isolated mouse heart: assessment by intracoronary administration of exogenous nitric oxide.

In our previous work we have shown that in mouse heart basal level of endothelial produced nitrite, as a marker of nitric oxide (NO) formation, was 9.7 nmol l(-1). Bradykinin (10 microl l(-1)) induced a 5-fold rise in nitrite release, the coronary venous effluent concentration being 58 nmol l(-1), but there was no effect on myocardial oxygen consumption (MVO2). The aim of this study was to assess the levels of authentic nitric oxide solution, exogenously applied, on myocardial oxygen consumption. Isolated mouse hearts (n=36) were paced (500 imp./min) and perfused at constant flow (16.0 +/- 0.3 ml g(-1) min(-1)). When coronary vasculature resistance was carefully controlled by adenosine (1 micromol l(-1)), authentic nitric oxide solution, in a concentration less than 5 micromol l(-1) did not alter myocardial oxygen consumption. Only concentrations of nitric oxide higher than 5 micromol l(-1) induced reduction in myocardial oxygen consumption. Thus in the saline perfused mouse heart, with carefully controlled vasodilatation, modulating myocardial nitric oxide levels using an arterial application of authentic nitric oxide, concentrations higher than 5 micromol l(-1) of nitric oxide were required to induce a decrease in myocardial oxygen consumption.

[Massive hemorrhage and mechanisms of coagulopathy in trauma].

Trauma is disease of the young, mainly affecting people between 15-40 years of age. Uncontrolled massive bleeding is the leading cause of early in-hospital mortality, within 48h of admission, and the second leading cause of prehospital death in victims of both military and civilian trauma, accounting for 40-45% of the total fatalities. Coagulopathy develops early after injury and is present in 25-36% of trauma victims upon admission to the emergency department. Coagulopathy correlates to the severity of trauma and is associated with an increased risk of mortality. The aim of this paper is to explain pathophysiology of developing coagulopathy in trauma. The coagulopathy in the trauma patient is complex and multifactorial. It includes: dilutional coagulopathy, hypothermia, acidosis, hyperfibrinolysis, anemia and consumption coagulopathy. When the patient develops the so called "lethal triad" of hypothermia, acidosis and coagulopathy, surgical restoration of vascular integrity may be insufficient to achieve a deffinitive control of blood loss and non-mechanical bleeding from small vessels, usually terminated by spontaneous coagulation, becomes a life-threatening condition.

[Determination of beta-endorphin plasma concentrations in surgical patients with acute abdominal pain]. / Odredjivanje plazma koncentracija opiodnog peptida beta-endorfina kod hirurskih bolesnika sa abdominalnim bolom.

Abdominal pain and surgery, frequently associated with this kind of pain, modify plasma levels of stress-hormones and iniciates the response of endogenous analgetic system. The aim of this study was to determine serum concentration of beta-endorphine in patients with acute abdominal pain (n=12), which were surgically treated. Serum concentration of beta-endorphin was measured on five data points: before, during and after surgery. During abdominal surgery serum concentration of beta-endorphin was increased by 7% compared to preoperative period; in postoperative period the concentration continued to rise and remained increased within next hours. The maximal levels of beta-endorphine were not observed during, and immediately after surgery. Postoperatively, between 6 and 8 p.m. on the day of surgery, maximal level of beta-endorphin was noted, which was even ten times higher than to preoperative value. Plasma level of beta-endorphin fell to the baseline values 24 hours after surgery. In conclusion, abdominal surgery induces a postponed (delayed) increase in serum beta-endorphine levels, which are associated with modulation of preoperative, intraoperative and postoperative pain perception.

[Intrahepatic B3 cholangiojejunostomy in the palliative surgery of high unresectable malignant biliary obstruction]. / Intrahepaticna B3 holangiojejunostomija u palijativnom hirurskom tretmanu visokih neresektabilnih malignih bilijarnih opstrukcija.

Palliating the effects of biliary obstruction is a major goal of therapy in patients with unresectable cancer at the hepatic duct confluence. We reviewed our expirience with intrahepatic holangioenteric bypass to the segmental bile duct B3 as a palliative therapy in patients with unresectable malignant diseases involving the ductal confluence or the common hepatic duct. Since March 2001, we have performed intrahepatic segmental bile duct B3 cholangiojejunostomy by Roux-en-Y fashion utilizing a round ligament approach in 13 patients with malignant obstructive jaundice due to unresectable hilar holangiocarcinoma (8 cases) and gallbladder cancer (5 cases). Mean hospital stay was 123 days and mean blood loss was 25060 mL. Postoperative complications occurred in 3 patients (23%), but there was no surgical complications such as postoperative bleeding, bile leakage or abscess formation. 30-day mortality was 7.7% (1 patient). Late complications (37.5%) were observed in 3 of the 8 patients who survived for more than 5 months after the surgery. Median survival after B3 cholangiojejunostomy was 9 months (range, 10 days-22 months). Median survival time was significantly greater in patients with hilar cholangio-carcinoma (11.8 months; range: 2-22 months) compared with those with gallbladder cancer (4.6 months; range: 10 days-11.5 months) (P-0.032 log rank test; P-0.049 Tarone-Ware test). Intrahepatic B3 cholangiojejunostomy when combined with careful patient selection, can provide useful palliation from jaundice, pruritus and cholangitis with acceptable mortality and morbidity rates.