Ossifying Fibroma of Non-odontogenic Origin: A Fibro-osseous Lesion in the Craniofacial Skeleton to be (Re-)considered

In the cranio-facial skeleton, a heterogeneous group of well characterized fibro-osseous lesions can be distinguished. Whereas fibrous dysplasia can affect any skeletal bone, ossifying fibroma and cemento-osseous dysplasia exclusively develop in the cranio-facial region, with most subtypes restricted to the tooth bearing areas of the jaws. Herein we present a series of 20 fibro-osseous lesions that developed mostly in the frontal bone and in the mandible, presenting as expansile intramedullary tumors with a unique histologic appearance and an indolent clinical course. We provide evidence that these tumors are distinct from the categories included in the WHO classification and are therefore currently unclassifiable. The definition of cemento-ossifying fibroma as an odontogenic neoplasm developing only in close proximity to teeth should be re-considered and incorporate also extragnathic lesions as shown here.Supplementary InformationThe online version contains supplementary material available at 10.1007/s12105-021-01351-3.     

Seroprevalence of Powassan Virus in New England Deer, 1979–2010

Powassan virus and its subtype, deer tick virus, are closely related tick-borne flaviviruses that circulate in North America. The incidence of human infection by these agents appears to have increased in recent years. To define exposure patterns among white-tailed deer, potentially useful sentinels that are frequently parasitized by ticks, we screened serum samples collected during 1979–2010 in Connecticut, Maine, and Vermont for neutralizing antibody by using a novel recombinant deer tick virus–West Nile virus chimeric virus. Evidence of exposure was detected in all three states. Overall our results demonstrate that seroprevalence is variable in time and space, suggesting that risk of exposure to Powassan virus is similarly variable.     

Cervical muscle response during whiplash: evidence of a lengthening muscle contraction

OBJECTIVE: To assess the potential for cervical muscle injury from a rear-end automobile collision. DESIGN: Experimental design in which human subjects were exposed to low-speed rear-end collisions. The influence of independent variable (gender, speed change, muscle group, and motion phase) on dependent variables (kinematic response, muscle onset and muscle activation level) was examined using repeated-measures analysis of variance. BACKGROUND: Injuries to various tissues of the cervical spine have been proposed, yet little attention has been focused on the cervical muscles as a site of injury. METHODS: 42 subjects (21 males, 20-40 yr) were exposed to collisions of 4 and 8 km/h speed change while measuring kinematic response of the head and torso and electromyography of the sternocleidomastoid and cervical paraspinal muscles. RESULTS: Muscle activation occurred earlier in females and in the 8 km/h speed change. Sternocleidomastoid onset preceded paraspinal onset. Muscle activation level varied significantly with speed change, motion phase and muscle group. Initial rearward retraction of the head relative to the torso resulted in lengthening of the activated sternocleidomastoid, consistent with a contraction-induced muscle injury. CONCLUSIONS: The cervical muscles contract rapidly in response to impact and the potential exists for muscle injury due to lengthening contractions. RELEVANCE: The clinician should recognize the role of cervical retraction in the mechanism of whiplash injury and avoid aggressive motion in that plane during diagnosis and treatment. An understanding of whiplash injury mechanisms should improve patient education and preventative measures.     

Platelet-activating factor in vasoobliteration of oxygen-induced retinopathy

PURPOSE: To test whether platelet-activating factor (PAF) directly causes retinovascular endothelial cell (EC) death. METHODS: Retinovascular density was calculated in rat pups exposed to 80% O(2) from postnatal days (P)6 to P14 (to produce oxygen-induced retinopathy [OIR]), using the adenosine diphosphatase (ADPase) technique, in animals treated with distinct PAF receptor blockers (PCA-4248, BN52021, or THG315). PAF levels were then measured in the retinas. Viability of ECs from piglets and humans in response to C-PAF (a stable PAF analogue) was determined by the reduction of the tetrazolium salt 3-(4,5-dimethyl thiazol-2yl)-2,5-diphenyl tetrazolium bromide (MTT) by viable cells, incorporation of propidium iodide (PI), TUNEL assay, and release of lactate dehydrogenase. Release of thromboxane (TX) was measured in the cell media. RESULTS: PAF levels in retina were markedly increased by exposure of isolated rat retinas to H(2)O(2) (1 micro M) and of rat pups placed in 80% O(2). Exposure to 80% O(2) induced retinal vasoobliteration, which was equally significantly inhibited ( approximately 60%) by all PAF receptor blockers tested. C-PAF increased incorporation of PI by isolated rat retinal microvasculature. Also, C-PAF caused time- and concentration-dependent death of cultured retinal ECs, which was prevented by the PAF receptor antagonist CV-3988. This effect of C-PAF was selective on retinal and neurovascular ECs, but not on other ECs. DNA fragmentation (TUNEL) was hardly detected, and inhibition of apoptosis-related processes by nicotinamide, cyclosporin A, and Z-DEVD-FMK and Z-VAD-FMK (caspase inhibitors) barely protected against death in EC, whereas C-PAF increased release of lactate dehydrogenase, implying that necrosis is the nature of EC death. Finally, C-PAF-induced cell death was preceded by an increase in TXB(2) levels and was prevented by TXA(2) synthase inhibition (with CGS12970). CONCLUSIONS: The data suggest PAF plays a major role in vasoobliteration in OIR by triggering death of neuroretinal microvascular ECs. The cell death seems to be mediated at least in part by TXA(2). These effects of PAF may participate in ischemic retinopathies such as diabetes and retinopathy of prematurity.     

Kinetics of DNA adduct formation and removal in mouse hepatocytes following in vivo exposure to 5,9-dimethyldibenzo[c,g]carbazole

5,9-Dimethyldibenzo[c,g]carbazole (DMDBC), a potent mouse hepatocarcinogen, has been shown to induce a non-linear increase in mutant frequency in the liver of the transgenic MutaMouse. To gain insight into the mechanisms underlying the mutagenicity of DMDBC in vivo, DNA damage formation and removal were monitored in mouse hepatocytes over 4-144 h after a single skin application of 10 or 90 mg/kg DMDBC. DNA adducts were measured by (32)P-post-labeling. DNA repair was assessed by: (i) the unscheduled DNA synthesis (UDS) assay, which measures [(3)H]thymidine incorporation into hepatocyte DNA undergoing excision repair; (ii) the Comet assay, which detects DNA strand breaks transiently produced between the incision and rejoining steps of the excision repair process. A plateau of approximately 400 DNA adducts/10(8) nucleotides was reached 24 h after treatment with 10 mg/kg and remained unchanged until 144 h. UDS activity was significantly induced at 15 and 24 h, while no DNA strand breaks were observed at any sampling time. These results suggest that DNA repair mechanisms were efficiently induced and the formation of a high degree of DNA damage was avoided at this dose level. Following exposure to 90 mg/kg DMDBC, the number of DNA adducts increased sharply to a maximum at 24 h ( approximately 8000/10(8) nucleotides) and then declined to approximately 500/10(8) nucleotides at 144 h. UDS activity was markedly induced from 15 to 72 h. Low levels of DNA strand breaks were observed at 24 and 48 h. The formation of large numbers of DNA adducts and the emergence of DNA strand breaks despite a strong initial induction of UDS activity suggested that DNA repair mechanisms were saturated at this dose level. This phenomenon could partly account for the non-linear induction of gene mutations previously reported in the liver of the transgenic MutaMouse.     

香蕉果肉饮料的研究

研究了香蕉带果肉饮料加工工艺。为保持香蕉的天然色、香、味，探讨了香蕉果肉褐变的控制和果肉在汁中的稳定性，得出的最佳加工工艺条件为：热烫温度１００℃，热烫时间４ｍｉｎ，果泥含量２０％，糖度１３．５°ＢＸ，酸含量为０．１５％，ｐＨ４．０±０．１，添加０．０５％黄原胶和０．０２％魔芋精粉，经过２次磨胶，排气，１００℃杀菌１５ｍｉｎ。     

Hospital volume differences and five-year survival from breast cancer.

OBJECTIVES: The purpose of this study was to determine the effect of hospital volume on long-term survival for women with breast cancer. METHODS: Survival analysis and proportional-hazard modeling were used to assess 5-year survival and risk of death, adjusting for clinical and sociodemographic variables. RESULTS: At 5 years, patients from very low-volume hospitals had a 60% greater risk of all-cause mortality than patients from high-volume hospitals. CONCLUSIONS: Hospital volume of breast cancer surgical cases has a strong positive effect on 5-year survival. Research is needed to identify whether processes of care, especially postsurgical adjuvant treatments, contribute to survival differences.