Temporal Bone Trauma: Typical CT and MRI Appearances and Important Points for Evaluation.

Temporal bone trauma is frequently encountered in the emergency department. Technologic advances have enabled timely acquisition of thin-section images and multiplanar reconstructions such that temporal bone anatomy can be evaluated in great detail, with excellent delineation of fractures. The temporal bone is composed of a myriad of tiny structures, including many fissures and canals, that must be distinguished from true fractures. In addition, injury to important structures may result in serious complications such as hearing loss, dizziness, imbalance, perilymphatic fistula, cerebrospinal fluid leakage, facial nerve paralysis, and vascular injury. Structures that should be examined include the tympanic cavity and tegmen, the ossicular chain, the bony labyrinth, the facial canal, the internal carotid artery, the jugular foramen and venous sinuses, and the intracranial contents. Radiologists should be familiar with the anatomy of the temporal bone and be able to describe any pathologic findings and make suggestions to referring clinicians to guide management and determine the prognosis. The authors describe the typical CT and MRI appearances of temporal bone trauma, entities that mimic this injury and thus must be differentiated, and compulsory points for evaluating clinically relevant associated complications. Instruction is provided for acquiring the diagnostic skills necessary to report suggested injury status, complications, and likely sequelae to clinicians.©RSNA, 2020.

Effect of 50 Hz electric field in diacylglycerol acyltransferase mRNA expression level and plasma concentration of triacylglycerol, free fatty acid, phospholipid and total cholesterol.

BACKGROUND: The effects of exposure to a 50 Hz electric field (EF) on plasma level of triacylglycerol, free fatty acids, total cholesterol and phospholipid and mRNA expression level of diacylglycerol acyltransferase (DGAT) 1 and 2 in liver and intestines from C57BL/6 J mice were studied. METHODS: The test was based on comparison between mice post treated with 50 Hz EF of 45 kV/m intensity for 30 min per day for 11 days or without EF. DGATs mRNA expression was analyzed by real-time quantitative polymerase chain reaction. RESULTS: There was no difference in the gene expression level of DGAT1 in liver and intestines. The DGAT2 gene expression level in liver derived from mice treated with EF was significantly lower than those in the control (P < 0.001). Both plasma total cholesterol (P < 0.01) and phospholipid (P < 0.05) in the group exposed to EF were lower than those in the control, but there was no difference in triacylglycerol or free fatty acid levels. CONCLUSION: Exposure to 50 Hz EF decrease the plasma levels of total cholesterol and phospholipids, and downregulated DGAT2 mRNA expression in liver. The mechanisms for the effects of EF on lipid metabolism are not well understand yet, but altered DGAT2 activity may be involved.

Expression of erythropoietic cytokines in α-tocopherol transfer protein knockout mice with murine malaria infection.

Malaria infection leads to anemia in humans which generally occurs during the chronic phase of the infection. The role that erythropoietic molecules play for anemia during malaria at low parasitemia levels is still controversial due to the lack of suitable animal models which might mimic this condition. In this regard, α-tocopherol transfer protein knockout mice, with undetectable levels of vitamin E in circulation, were possibly used as a model to investigate the role that erythropoietic molecules such as erythropoietin (EPO), erythropoietin receptor (EPOR), and macrophage migration inhibitory factor (MIF) play on the outcome of anemia during uncomplicated malaria infection at low parasitemias. The results indicate that the degree of parasitemia unlikely plays any important effect on mRNA expression of EPO and EPOR in different organs. Moreover, even though EPO and EPOR productions are impaired in the kidney and bone marrow, respectively, other organs such as the liver and spleen intend to compensate production of these cytokines to prevent anemia in the infected animals.

Alpha-tocopherol transfer protein disruption confers resistance to malarial infection in mice.

BACKGROUND: Various factors impact the severity of malaria, including the nutritional status of the host. Vitamin E, an intra and extracellular anti-oxidant, is one such nutrient whose absence was shown previously to negatively affect Plasmodium development. However, mechanisms of this Plasmodium inhibition, in addition to means by which to exploit this finding as a therapeutic strategy, remain unclear. METHODS: alpha-TTP knockout mice were infected with Plasmodium berghei NK65 or Plasmodium yoelii XL-17, parasitaemia, survival rate were monitored. In one part of the experiments mice were fed with a supplemented diet of vitamin E and then infected. In addition, parasite DNA damage was monitored by means of comet assay and 8-OHdG test. Moreover, infected mice were treated with chloroquine and parasitaemia and survival rate were monitored. RESULTS: Inhibition of alpha-tocopherol transfer protein (alpha-TTP), a determinant of vitamin E concentration in circulation, confers resistance to malarial infection as a result of oxidative damage to the parasites. Furthermore, in combination with the anti-malarial drug chloroquine results were even more dramatic. CONCLUSION: Considering that these knockout mice lack observable negative impacts typical of vitamin E deficiency, these results suggest that inhibition of alpha-TTP activity in the liver may be a useful strategy in the prevention and treatment of malaria infection. Moreover, a combined strategy of alpha-TTP inhibition and chloroquine treatment might be effective against drug resistant parasites.

Effects of a synthetic N-terminal fragment of stanniocalcin on the metabolism of mammalian bone in vitro.

A synthetic peptide corresponding to the N-terminal amino acid residues of stanniocalcin (STC1-20) and including a region that is known to be an active site in teleosts was prepared and tested for its effects on the metabolism of mammalian bone in vitro. STC1-20 (10(-10)-10(-12) M) inhibited increases in the number of tartrate-resistant acid phosphatase-positive, multinucleated cells promoted by an N-terminal fragment of human parathyroid hormone (hPTH1-34) in cultures of murine hemopoietic cells. STC1-20 also slightly decreased the rate of loss of radioactivity from calvariae of fetal rats that had been prelabeled with 45Ca, both with and without stimulation by hPTH1-34. The accumulation of cAMP induced by hPTH1-34 in ROS 17/2.8-5 cells was suppressed by STC1-20 (10(-10)-10(-12) M). Treatment with STC1-20 (10(-11)-10(-13) M) caused increases of the rate of incorporation of [3H]proline into the collagenase-digestible protein of calvariae in newborn mice. From these results, it appears that STC1-20 has diverse effects on the metabolism of mammalian bone, causing a biphasic response. Such effects have not been observed with intact stanniocalcin or with materials from the corpuscles of Stannius and they are also different from the effects of hPTH1-34.

Evidence for stanniocalcin gene expression in mammalian bone.

Stanniocalcin (STC) acts as a regulator of calcium and phosphate homeostasis in an endocrine manner in bony fish. Recently, complementary DNAs encoding human and mouse STC have been characterized, and the messenger RNA (mRNA) expression was identified in various tissues, such as kidney, small intestine, prostate, thyroid, and ovary. Because previous studies concerning the effects of fish STC on mammalian bone have been discussed, there is a good possibility that mammalian STC is a local factor in bone. Here, we demonstrated STC mRNA expression in neonatal mouse calvaria, the primary cultured mouse osteoblast-rich fractions, and human and mouse osteoblastic cell lines. We also mapped the cellular distribution of the STC mRNA in femur and calvaria in developing mice. Several transcripts with a major 4-kb band were detected in all samples. The cellular distribution of the mRNA expression corresponded closely to osteoblasts in both femur and calvaria. Significant labeling of the STC mRNA was also identified in chondrocytes but not in osteoclasts and other bone marrow elements. These results are the first evidence that hormone may be actually expressed in osteoblasts and chondrocytes, and they strongly implicate the involvement of local STC in both endochondral and membrane bone as an autocrine/paracrine factor.

In situ hybridization analysis of stanniocalcin mRNA expressing cells in the mouse kidney.

Stanniocalcin (STC) is a glycoprotein hormone first identified in bony fish in which it regulates calcium and phosphate homeostasis. A mammalian homologue has recently been isolated and STC mRNA is expressed in many tissues including kidney. Mammalian STC appears to inhibit renal phosphate reabsorption in rats, and its immunoreactive cells were detected in specific segments of the renal tubules in humans and rats. We used in situ hybridization with a digoxigenin-labelled cRNA for STC to characterize the intrarenal distribution of STC mRNA in mice. The labelling was detected in most of the cells in nephron tubules and glomerular mesangial cells, suggesting that STC is synthesized in the nephron system and acts in an autocrine/paracrine fashion.

Dexamethasone regulates the actions of endogenous insulin-like growth factor-II during myogenic differentiation.

The effect of dexamethasone (DEX) on the action of endogenous insulin-like growth factor (IGF)-II during myogenic differentiation was investigated by culturing C2C12 mouse myogenic cells in serum-free medium. DEX treatment maintained a high level of creatine kinase (CK) activity, and caused an increase in the number of nuclei per cell, hypertrophy and IGF-II mRNA accumulation in the cells. These effects were abrogated by the glucocorticoid receptor antagonist RU-38486. An anti-IGF-II monoclonal antibody neutralized DEX-dependent CK activity. Thus, we conclude that DEX increases the level of IGF-II mRNA in C2C12 cells, and that DEX may assist myogenic differentiation via, at least in part, its promotive action on IGF-II gene expression.

Autonomous control of expression of genes for insulin-like growth factors during the proliferation and differentiation of C2C12 mouse myoblasts in serum-free culture.

The proliferation and differentiation of skeletal muscle cells in culture are usually controlled by serum components, and the differentiation can be induced by a reduction in the serum concentration. Insulin-like growth factors (IGFs) play a critical role in stimulating myoblast differentiation, and the expression of their genes is controlled by serum factors. We have found that C2C12 myoblasts are capable of proliferation and differentiation even in serum-free medium that does not contain peptide mitogens. During these processes in serum-free medium, the accumulation of mRNAs for IGFs in the cells was observed; and their levels increased with concomitant increases in creatine kinase activity and myotube formation and a decrease in DNA synthesis. Thus, the present results suggest that proliferation and differentiation of C2C12 cells are autonomously controlled and that the increase in the expression of the IGFs may be independent of exogenous components.

Effects of 17 beta-oestradiol and 5 alpha-dihydrotestosterone on the expression of the muscle and heart types of lactate dehydrogenase isozymes in the masseter muscle of developing mice.

17 beta-oestradiol (E2) and/or 5 alpha-dihydrotestosterone (5 alpha-DHT) had no effect on the expression of isozymes of lactate dehydrogenase (LDH) in the masseter muscle of intact male mice. However, treatment with E2 restored the level of the muscle (M) type of LDH isozyme, which had been reduced by testectomy, to that found in intact male mice treated with vehicle only. Moreover, 5 alpha-DHT alone was more effective than E2 in increasing the relative level of this isozyme in testectomized mice. 5 alpha-DHT had a more significant effect on the increase in the relative level of the M-type LDH isozyme when combined with E2. These results suggest that androgens promote, in the presence of oestrogens, the postnatal changes in the characteristics of the masseter muscle of developing male animals.

Restoration of disturbed tooth eruption in osteopetrotic (op/op) mice by injection of macrophage colony-stimulating factor.

Osteopetrotic (op/op) mice show severe osteosclerosis caused by an inherited deficiency of osteoclast and resultant failure of tooth eruption, which can be cured by the injection of macrophage colony-stimulating factor (M-CSF). The present study revealed that consecutive injections of M-CSF in these mutant mice brought about a recovery of bone resorption resulting in the resumption of growth of tooth root and periodontal ligament. Bone resorption at the inner surface of bony crypts was noted on the 5th day after the start of M-CSF injections. This activity was reduced with the progress of root and periodontal ligament formation, being confined to the basal and crestal portion of bony crypts by the 15th day of the experiment. Second molars emerged into the oral cavity on the 15th day, but no eruption of first molars was observed until the 20th day. Throughout the experiment, first molars exhibited appreciable root deformity, which was less severe in second molars. Delayed eruption of first molars was thought to be related to the severity of the disturbance of root formation.