Biocompatibility of mineral trioxide aggregate flow and biodentine.

AIM: To evaluate the influence of powder-to-gel ratio (0.19 g powder to 50 µL of gel, thick MTA Flow, and 0.06 g powder to 50 µL of gel, fluid MTA Flow) on biocompatibility of MTA Flow (Ultradent Products Inc., South Jordan, UT, USA, lot: 2015122901) and compare it with Biodentine (Septodont Inc., Saint-Maur-des-Fossés, France, lot: B18542A). METHODOLOGY: The materials were manipulated and inserted into polyethylene tubes for implantation in twenty rats. After 7, 15, 30 and 60 days, the specimens were removed and embedded in paraffin. Haematoxylin and eosin sections were used to count the number of inflammatory cells (IC) and fibroblasts mm-2 (Fb). In the Masson's trichrome-stained sections, the fibrous capsule thickness was measured; picrosirius red-stained sections were used for birefringent collagen quantification. The data were submitted to two-way ANOVA and Tukey test (P ≤ 0.05). RESULTS: A significantly lower number of IC and consequently higher number of Fb were observed in the capsules adjacent to thick MTA Flow at all periods, in comparison with other materials (P ≤ 0.05). At 60 days, the quantity of birefringent collagen was significantly greater in the tissue in contact with thick MTA Flow, when compared with fluid MTA Flow and Biodentine. CONCLUSIONS: Although thick MTA Flow induced a less intense inflammatory response, all evaluated materials are biocompatible because they allowed regression of this process after 60 days.

Tratamento de displasia coxofemoral com uso de medicamento homeopático / Treatment of hip dysplasia with the use of homeopathic medicament

Os quadros de displasia coxofemoral são cada vez mais comuns nos animais de companhia, acometem principalmente raças de grande porte como Rottweiler, Pastor alemão, Lavrador, etc., mas já existem relatos nos cães de pequeno porte como os Lhasa Apso e em gatos de grande porte como os da raça Main Coon, que têm predisposição a desenvolver essa doença. Os animais acometidos apresentam dor e dificultade ou incapacidade total de locomoção. A ocorrência é maior em animais jovens e tem caráter hereditário. As opções de tratamento incluem cirurgias, tratamentos regeneradores articulares e o uso de analgésicos, todos com o objetivo de minorar a dor do animal. Há também a opção de tratamento com o uso de medicamentos homeopáticos. Este trabalho apresenta a eficãcia dos medicamentos homeopáticos, em dois casos clínicoes de displasia coxofemoral tratados com complexo homeopático Displasia.

Tratamento de displasia coxofemoral com uso de medicamento homeopático / Treatment of hip dysplasia with the use of homeopathic medicament

Os quadros de displasia coxofemoral são cada vez mais comuns nos animais de companhia, acometem principalmente raças de grande porte como Rottweiler, Pastor alemão, Lavrador, etc., mas já existem relatos nos cães de pequeno porte como os Lhasa Apso e em gatos de grande porte como os da raça Main Coon, que têm predisposição a desenvolver essa doença. Os animais acometidos apresentam dor e dificultade ou incapacidade total de locomoção. A ocorrência é maior em animais jovens e tem caráter hereditário. As opções de tratamento incluem cirurgias, tratamentos regeneradores articulares e o uso de analgésicos, todos com o objetivo de minorar a dor do animal. Há também a opção de tratamento com o uso de medicamentos homeopáticos. Este trabalho apresenta a eficãcia dos medicamentos homeopáticos, em dois casos clínicoes de displasia coxofemoral tratados com complexo homeopático Displasia®.(AU)

Region-specific expression and hormonal regulation of the first exon variants of rat prolactin receptor mRNA in rat brain and anterior pituitary gland.

Recent studies have revealed the occurrence of five first exon variants of the rat prolactin receptor mRNA, suggesting that multiple promoters direct prolactin receptor transcription in response to different regulatory factors. In the present study, regional expression of these first exon variants, as well as two prolactin receptor subtypes generated by alternative splicing, was examined in the brains and anterior pituitary glands of female rats. Expression of the long-form was detected in the choroid plexus, hypothalamus, hippocampus, cerebral cortex and anterior pituitary gland, whereas the short form was detected only in the choroid plexus. E1-3 mRNA, a first exon variant, was detected in the choroid plexus, hypothalamus, and anterior pituitary gland, whereas E1-4 was detected only in the choroid plexus. Other variants were not detectable by the polymerase chain reaction protocol employed in this study. Ovariectomy increased the short form in the choroid plexus and the E1-3 expression in the choroid plexus and pituitary gland, but changes in the long-form and E1-4 expression were minimal. Replacement of oestrogens and prolactin suggest that oestrogens down-regulate E1-3 expression in the choroid plexus and pituitary gland, and that the negative effect of oestrogen is mediated by prolactin in the pituitary gland. The present results revealed the region-specific promoter usage in prolactin receptor mRNA transcription, as well as the involvement of oestrogens in the regulation of E1-3 mRNA expression in the brain and pituitary gland.

Possible participation of outer mitochondrial membrane cytonchrome B5 in steroidogenesis in zona glomerulosa of rat adrenal cortex.

Outer mitochondrial membrane cytochrome b5 (OMb) originally found in rat liver is an isoform of cytochrome b5 (b5) of the endoplasmic reticulum. In contrast to accumulated data on the physiological roles of b5, functions of OMb have not been well characterized except for its involvement in regeneration of ascorbic acid [i.e., in a semidehydroascorbate reductase (SDAR) system]. By using highly specific antibodies against rat OMb, we found immunohistochemically that OMb in the rat adrenal gland was most abundant in the zona glomerulosa (zG) among the three cortical zones, and the expression level was enhanced on angiotensin II-stimulation. SDAR activity was found in zG and inhibited by anti-OMb antibody. Moreover, the increase in plasma aldosterone concentration under Na+ -deficiency was suppressed by limited ascorbic acid (Asc) availability in rat mutants unable to synthesize Asc, while plasma corticosterone concentration was not affected. These data suggest that OMb, present abundantly in zG, participates in aldosterone formation in zG of rat under angiotensin II-stimulation through regeneration of Asc.

Abdominal aortic aneurysm with left-sided inferior vena cava. Report of a case.

The combination of abdominal aortic aneurysms and congenital anomalies of the inferior vena cava and its tributaries, such as double inferior vena cava, left-sided inferior vena cava, circumaortic renal collar, and retroaortic renal vein, are very rare but of clinical importance to vascular surgeons since these conditions can increase the difficulty of aneurysm resection as well as the risk of venous injury and subsequent excessive bleeding. This report describes a case of an abdominal aortic aneurysm with a left-sided inferior vena cava, and reviews of the incidence, diagnosis, and treatment of these conditions.

[Recurrent right atrial myxoma five years after removal of left atrial myxoma; report of a case].

A 41-year-old man had undergone resection of a left atrial myxoma 5 years previously. Echocardiography revealed a new mass in the right atrium. Because of had increased in size gradually, removal of the right atrial mass involving full-thickness resection of the fossa ovalis was performed. Cardiac myxoma has the potential for heterotopic recurrence.

Measles virus infection in the placenta of monozygotic twins.

We report a case of monozygotic twins whose mother was infected with measles at 19 weeks' gestation. One of the twins died in utero at 32 weeks' gestation. The placenta of the stillbirth showed massive fibrin deposition, and some residual trophoblasts contained many inclusion bodies positive for measles virus antigen. Fetal organs and cells other than a few splenic lymphocytes showed no evidence of measles virus infection. The placenta of the surviving infant showed focal intervillous fibrin deposits, and only a few syncytiotrophoblasts were positive for measles virus antigen. At present, 7 months after the delivery, the surviving infant has not developed any sign of measles virus infection. Postpartum course of the mother has been uneventful, although high titers of serum anti-measles virus IgM persisted for 6 months after delivery. This case is informative in the following respects: the villous trophoblasts had diagnostic inclusion bodies and ultrastructural evidence of measles virus infection, the degree of viral involvement within the monochorionic placenta was uneven, both of the twins were virtually free from measles virus infection despite the marked involvement of the placenta, and measles virus infection had persisted in the monochorionic placenta for approximately 13 weeks.

A prospective clinical study on inhaled nitric oxide therapy for neonates in Japan.

BACKGROUND: This is the first report about a prospective clinical investigation to study the efficacy and safety of nitric oxide (NO) inhalation in infants with persistent pulmonary hypertension of the newborn (PPHN) in Japan. METHODS: Patients in the present study had to meet the following entry criteria: (i) they had to be younger than 7 days of age; (ii) they had to have evidence of PPHN as defined by echocardiograph; (iii) they had to have severe systemic hypoxemia under mechanical ventilation at 100% oxygen supplementation; and (iv) they had to have a failure to respond to conventional therapies. Patients were excluded from this trial if they had any of the following: hypoplastic lung, structural cardiac lesions or severe multiple anomalies. RESULTS: Nitric oxide inhalation therapy was performed in 68 infants who had severe PPHN at 18 hospitals between May 1995 and May 1997. At birth, 21 of 68 infants (31%) weighed less than 1,500 g and 39 infants weighed more than 2,500 g. The diagnoses associated with PPHN were as follows: 27 infants had meconium aspiration syndrome, 15 infants had dry lung syndrome, nine infants had congenital diaphragmatic hernia, six infants had respiratory distress syndrome, three infants had pneumonia and eight infants had other diagnoses. The mean oxygenation index (OI) before NO inhalation therapy in 68 infants was 43.2; 55 infants (81%) had good responses. CONCLUSIONS: These results may be valuable for further randomized controlled and double-blind trials in Japan to evaluate whether NO inhalation therapy is more effective than conventional therapy in infants with severe PPHN.

Blockade of the extracellular signal-regulated kinase pathway induces marked G1 cell cycle arrest and apoptosis in tumor cells in which the pathway is constitutively activated: up-regulation of p27(Kip1).

Constitutive activation of the ERK pathway is associated with the neoplastic phenotype of a relatively large number of human tumor cells. Blockade of the ERK pathway by treatment with PD98059, a specific inhibitor of mitogen-activated protein (MAP) kinase/ERK kinase (MEK), completely suppressed the growth of tumor cells in which the pathway is constitutively activated (RPMI-SE and HT1080 cells). Consistent with its prominent antiproliferative effect, PD98059 induced a remarkable G(1) cell cycle arrest, followed by a modest apoptotic response, in these tumor cells. Selective up-regulation of p27(Kip1) was observed after PD98059 treatment of RPMI-SE and HT1080 cells. Overexpression in RPMI-SE cells of either a kinase-negative form of MEK1 or wild-type MAP kinase phosphatase-3 also induced up-regulation of p27(Kip1). The up-regulation of p27(Kip1) correlated with increased association of p27(Kip1) with cyclin E-cyclin-dependent kinase (CDK) 2 complexes, a concomitant inhibition of cyclin E-CDK2 kinase activity, and a consequent decrease in the phosphorylation state of retinoblastoma protein, which would culminate in the marked G(1) cell cycle arrest observed in these tumor cells. These results suggest that the complete growth suppression that follows specific blockade of the ERK pathway in tumor cells in which the pathway is constitutively activated is mediated by up-regulation of p27(Kip1).

Terminal warm blood cardioplegia improves the recovery of myocardial electrical activity. A retrospective and comparative study.

OBJECTIVE: The effect of terminal warm blood cardioplegia was analyzed in 191 patients undergoing either coronary artery bypass grafting (CABG) or prosthetic heart valve replacement between Jan. 1990 and Dec. 1995. METHODS: Patients were subdivided into 3 historical cohorts based on the method of myocardial protection: Group A (n = 106), multidose cold crystalloid glucose-potassium cardioplegia, alone; Group B (n = 37), cold crystalloid glucose-potassium cardioplegia plus terminal warm blood cardioplegia, Group C (n = 48), cardioplegia induction with cold crystalloid glucose-potassium cardioplegia, maintenance with multidose cold blood cardioplegia, and terminal warm blood cardioplegia. RESULTS: Of patients undergoing CABG, 5.6% of group A, 70.4% of group B, and 86.7% of group C spontaneously resumed sinus rhythm after aortic declamping, as did 9.1% of group A, 60.0% of group B, and 55.6% of group C of patients undergoing prosthetic heart valve replacement. The incidence of spontaneous recovery was significantly better in groups B and C than in group A (p < 0.05). Over 90% of patients without terminal warm blood cardioplegia developed ventricular fibrillation or tachycardia requiring electrical cardioversion (p < 0.05). Postoperatively, patients without terminal warm blood cardioplegia required temporary epicardial pacing more frequently than those with terminal warm blood cardioplegia (p < 0.05). In patients undergoing prosthetic heart valve replacement, groups B and C, the incidence of postoperative atrial fibrillation was significantly lower than in group A. CONCLUSION: Terminal warm blood cardioplegia thus promoted better postoperative electrophysiological cardiac recovery.

Specific activation of the p38 mitogen-activated protein kinase signaling pathway and induction of neurite outgrowth in PC12 cells by bone morphogenetic protein-2.

Bone morphogenetic protein (BMP)-2 has the capacity to induce the neuronal differentiation of PC12 cells. Unlike nerve growth factor, however, BMP-2 failed to induce the activation of the 41-/43-kDa mitogen-activated protein (MAP) kinase pathway in these cells. In contrast, BMP-2 characteristically induced the sustained activation of the p38 MAP kinase pathway. Pretreatment of PC12 cells with SB203580 inhibited the BMP-2-induced neurite outgrowth formation in a dose-dependent manner; this inhibition coincided well with the ability of SB203580 to inihibit the BMP-2-induced activation of the p38 MAP kinase pathway. Overexpression in PC12 cells of wild-type MAP kinase kinase (MKK)-6 enhanced the BMP-2-induced activation of p38 MAP kinase, whose activation correlated well with the ability of these cells to induce neurite outgrowth in response to BMP-2. Transient expression of kinase-negative forms of MKK3/6 inhibited the formation of neurite outgrowth in response to BMP-2. Furthermore, expression of constitutively active forms of MKK3/6 induced neurite outgrowth without BMP-2 stimulation, and SB203580 inhibited this induction. These results clearly indicate that activation of the p38 MAP kinase pathway is necessary for BMP-2-induced neuronal differentiation of PC12 cells. Our results also suggest that activation of the p38 MAP kinase pathway alone can induce the neuronal differentiation of PC12 cells.

Constitutive activation of the 41-/43-kDa mitogen-activated protein kinase signaling pathway in human tumors.

The 41-kDa and 43-kDa mitogen-activated protein (MAP) kinases play a pivotal role in the mitogenic signal transduction pathway and are essential components of the MAP kinase cascade, which includes MAP kinase kinase (MEK) and Raf-1. As aberrant activation of signal transducing molecules such as Ras and Raf-1 has been linked with cancer, we examined whether constitutive activation of the 41-/43-kDa MAP kinases is associated with the neoplastic phenotype of 138 tumor cell lines and 102 primary tumors derived from various human organs. Constitutive activation of the MAP kinases was observed in 50 tumor cell lines (36.2%) in a rather tissue-specific manner: cell lines derived from pancreas, colon, lung, ovary and kidney showed especially high frequencies with a high degree of MAP kinase activation, while those derived from brain, esophagus, stomach, liver and of hematopoietic origin showed low frequencies with a limited degree of MAP kinase activation. We also detected constitutive activation of the 41-/43-kDa MAP kinases in a relatively large number of primary human tumors derived from kidney, colon and lung tissues but not from liver tissue. Many tumor cells, in which point mutations of ras genes were detected, showed constitutive activation of MAP kinases, however, there were also many exceptions to this observation. In contrast, the activation of the 41-/43-kDa MAP kinases was accompanied by the activation of Raf-1 in the majority of tumor cells and was completely associated with the activation of MEK and p90rsk in all the tumor cells examined. These results suggest that the constitutive activation of 41-/43-kDa MAP kinases in tumor cells is not due to the disorder of MAP kinases themselves, but is due to the disorder of Raf-1, Ras, or some other signaling molecules upstream of Ras.

[Mitral valve replacement for three cases of hypertrophic obstructive cardiomyopathy--surgical treatment].

Three patients with obstructive cardiomyopathy underwent surgical treatment. Mitral valve replacement was performed in all three cases and myectomy of hypertrophic septal muscle was performed in one case. The pressure gradients between the left ventricle and the aorta was less than 10 mmHg in all cases after surgery, Clinical symptoms strikingly improved in three cases. An accurate surgical treatment could be achieved by choosing either myotomy-myectomy, mitral valve replacement or both in the setting of individual condition of each patients.

Activation of the 41/43 kDa mitogen-activated protein kinase signaling pathway is required for hepatocyte growth factor-induced cell scattering.

Hepatocyte growth factor (HGF) markedly induced the spreading, dissociation and scattering of Madin-Darby canine kidney epithelial cells (MDCK) and human stomach adenocarcinoma cells (TMK1). Scattering of MDCK and TMK1 cells was induced by 12-O-tetradecanoyl-phorbol-13-acetate (PMA) and epidermal growth factor (EGF), respectively. In all these agent-stimulated cells, rapid activation of Raf-1, MAP kinase/ERK kinase (MEK), 41/43 kDa MAP kinases and p90rsk was commonly observed. In contrast, PMA neither induced the scattering nor activation of all these kinases in TMK1 cells. Pretreatment of MDCK and TMK1 cells with 2-(2-amino-3-methoxyphenyl) choromone (AMPC), a specific inhibitor of MEK, selectively inhibited the HGF-, PMA- and EGF-stimulated activities of MEK, 41/43 kDa MAP kinases and p90rsk in a dose dependent manner. AMPC-pretreatment, however, did not affect HGF-, PMA- or EGF-induced activation of Raf-1, nor HGF-induced activation of phosphatidylinositol 3-kinase in these cells. Importantly, HGF-, PMA- and EGF-induced scattering of MDCK and TMK1 cells was inhibited at doses of AMPC similar to those that gave comparable levels of inhibition of the activities of MEK, 41/43 kDa MAP kinases and p90rsk. These results suggest that activation of the 41/43 kDa MAP kinase signaling pathway is required for the motility response of MDCK and TMK1 cells induced by agents such as HGF, PMA and EGF.

[High-dose methylprednisolone-containing chemotherapy in advanced invasive thymoma--report of three cases].

During the period from May, 1995 to August, 1996, three patients with Stage III or IVa invasive thymoma received chemotherapy consisting of cisplatin, doxorubicin and methylprednisolone (1000 mg on days 1 through 5, and 500 mg on days 6 and 7). The first case, a 55-year-old woman, who underwent extended thymectomy 7 years ago, was found to have a recurrent tumor in the left pleural cavity. The second case, a 38-year-old man, who had first operation 3 years ago, developed recurrent tumor in the right pleural cavity. These two patients were treated with the above regimen as the primary mode of therapy. The third case, a 61-year-old woman, had a thymoma with direct invasion to right upper lobe. The same chemotherapy regimen was employed as the induction chemotherapy. All patients showed a major response to treatment with only a small amount of tumor remaining. The effectiveness of chemotherapy in the treatment of malignant tumors has been recently reported to be at least partly due to induction of apoptosis. Steroids are known to induce apoptosis in normal thymic cells, and thus steroid in chemotherapy regimen against invasive thymoma may enhance the effect of anti-cancer drugs through the induction of apoptosis.