全口义齿修复后造成松软牙槽嵴和／或牙槽嵴粘膜增生的原因初探

目的:研究松软牙槽嵴和/或牙槽嵴粘膜增生形成的原因,探讨预防和治疗措施。方法:对180例戴用全口义齿一年以上的患者进行临床调查研究。研究内容包括缺牙原因,义齿戴用的时间,牙槽嵴粘膜情况,松软牙槽嵴和/或牙槽嵴粘膜增生发生的部位,人工牙的类型等。结果:①180例全口义齿病例中,有松软牙槽嵴者20例,占22％,男:女=6:4,其中下牙槽嵴占60％,上牙槽嵴占,20％,上下牙槽嵴均有者占20％。患牙槽嵴粘膜增生者共8例,占4.4％,最多发生在下舌侧,其次为下唇沟。同时患有松软牙槽嵴和牙槽嵴粘膜增生的有4例,占患牙槽嵴粘膜增生病例的一半。②在患松软牙槽嵴的病例中,人工牙为塑料牙和瓷牙各占50％。缺牙原因为牙周病者共12例,占60％,龋病2例,占10％,龋病-牙周病者8例,占30％。③在患松软牙槽嵴的病例中,下颌牙槽嵴条件均为差,上颌牙槽嵴条件均为中或差。在患增生的粘膜组织的病例中,75％病例义齿固位为中或差,25％义齿固位为较好。结论:发病原因与患者缺牙原因,牙槽嵴部位,牙槽嵴条件,人工牙类型等有关。因此可以认为,牙槽嵴粘膜松软是戴用全口义齿后出现的不可忽视的问题,而牙槽嵴粘膜松软和/或增生的粘膜组织是相辅相成的。所以一副全口义齿不是一劳永逸的,使用一定的时间后需要更换,特别对牙槽嵴条件较差的患者     

Lipidomic characterization and localization of phospholipids in the human lung

Lipids play a central role in lung physiology and pathology; however, a comprehensive lipidomic characterization of human pulmonary cells relevant to disease has not been performed. The cells involved in lung host defense, including alveolar macrophages (AMs), bronchial epithelial cells (BECs), and alveolar type II cells (ATIIs), were isolated from human subjects and lipidomic analysis by LC-MS and LC-MS/MS was performed. Additionally, pieces of lung tissue from the same donors were analyzed by MALDI imaging MS in order to determine lipid localization in the tissue. The unique distribution of phospholipids in ATIIs, BECs, and AMs from human subjects was accomplished by subjecting the large number of identified phospholipid molecular species to univariant statistical analysis. Specific MALDI images were generated based on the univariant statistical analysis data to reveal the location of specific cell types within the human lung slice. While the complex composition and function of the lipidome in various disease states is currently poorly understood, this method could be useful for the characterization of lipid alterations in pulmonary disease and may aid in a better understanding of disease pathogenesis.     

不同海拔地区健康成人的肺泡气测定与质量通气

对世居和长期移居在不同海拔高度(10、2260、3680、4280米)的健康成人共359名进行了静息F_AO_2、F_ACO_2测定和动脉血气分析。结果表明,从F_ACO_2导出的P_ACO_2数值与血气分析P_aCO_2测值非常接近,说明所用肺泡气取样方法是可靠的。所获资料表明,F_AO_2、P_AO_2、P_ACO_2和(A-a)Do_2均随海拔升高而下降,独有F_ACO_2因海拔升高而增大。平原人和高原人的F_ACO_2数值间有显著差异(P<0.05～0.001)。 在恒定的co_2情况下,F_ACO_2和_A(STPD)互为倒数关系,所以F_ACO_2可以作为观察_A改变的可靠指标。F_ACO_2愈高,则质量通气愈低、气体交换效率愈高。高原人质量通气低于平原人是慢性低氧条件下通气改变的特征,是他们在长期低氧影响下,获得了更为有效适应的结果。     

肺泡II型上皮细胞转分化

哺乳动物肺泡上皮细胞主要由肺泡II型上皮细胞(AECII)和肺泡I型上皮细胞(AECI)组成。在肺发育和肺损伤修复过程中,AECII可转分化为AECI,体外原代培养的AECII有这种转分化的特性。现对AECII转分化的标志、影响及调控因素及其在肺损伤中的作用进行综述。     

Extracellular signal-regulated kinase (ERK) participates in the hypercapnia-induced Na,K-ATPase downregulation

Hypercapnia has been shown to impair alveolar fluid reabsorption (AFR) by decreasing Na,K-ATPase activity. Extracellular signal-regulated kinase pathway (ERK) is activated under conditions of cellular stress and has been known to regulate the Na,K-ATPase. Here, we show that hypercapnia leads to ERK activation in a time-dependent manner in alveolar epithelial cells (AEC). Inhibition of ERK by U0126 or siRNA prevented both the hypercapnia-induced Na,K-ATPase endocytosis and impairment of AFR. Moreover, ERK inhibition prevented AMPK activation, a known modulator of hypercapnia-induced Na,K-ATPase endocytosis. Accordingly, these data suggest that hypercapnia-induced Na,K-ATPase endocytosis is dependent on ERK activation in AEC and that ERK plays an important role in hypercapnia-induced impairment of AFR in rat lungs.     

牙周病摄片数字化分析用于临床诊断的探讨

本文探讨了牙周病摄片数字化分析,即纹理分析技术,应用于牙周病诊断的可能性。数字化分析能提供牙槽骨图象的细部特征特征描述和定量表达的形式,将为牙周病提供一种新的诊断方法。     

Induction of interleukin 8 (IL-8) production by Pseudomonas nitrite reductase in human alveolar macrophages and epithelial cells.

Interleukin-8 (IL-8) participates in the generation of dense neutrophil accumulations in bronchopulmonary infections caused by Pseudomonas aeruginosa (P. aeruginosa). We have recently reported that nitrite reductase, a bifunctional enzyme located in the periplasmic space of P. aeruginosa, induces IL-8 generation in bronchial epithelial cells (K. Oishi et al. Infect. Immun. 65: 2648-2655, 1997). We examined whether or not Pseudomonas nitrite reductase (PNR) could also stimulate human alveolar macrophages (AM) and pulmonary type II epithelial-like cells (A549) to induce IL-8 production and mRNA expression as well as the production of TNF alpha and IL-1beta. We demonstrated a time- and dose-dependent IL-8 protein synthesis and IL-8 mRNA expression, but no TNF alpha or IL-1beta production, by A549 cells in response to PNR. New protein translation was not required for PNR-mediated IL-8 mRNA expression in the same cells. Furthermore, simultaneous stimulation of PNR with serial doses of TNF alpha or IL-1beta resulted in additive IL-8 production in A549 cells. In adherent AM, PNR enhanced IL-8 protein synthesis and IL-8 mRNA expression in a time-dependent fashion. PNR similarly induced a time-dependent production of TNF alpha and IL-1beta by human adherent AM. Neutralization of TNF alpha or IL-1beta did not influence the levels of IL-8 production in adherent AM culture. We also evaluated whether the culture supernatants of the A549 cells or AM stimulated with PNR could similarly mediate neutrophil migration in vitro. When anti-human IL-8 immunoglobulin G was used for neutralizing neutrophil chemotactic factor (NCF) activities in the culture supernatants of these cells stimulated with 5 microg/ml of PNR, the mean percent reduction of NCF activities were 49-59% in A549 cells and 24-34% in AM. Our present data support that PNR directly stimulates AM and pulmonary epithelial cells to produce IL-8. PNR also mediates neutrophil migration, in part, through IL-8 production from AM and pulmonary epithelial cells. These data suggest the contribution of PNR to the pathogenesis of bronchopulmonary infections due to P. aeruginosa.     

In vitro assessment of environmental toxicology using alveolar cells astarget

Biphasic culture of alveolar cells (alveolar macrophages and type II cells) has been widely developed and permits a precise evaluation of the toxic effects of air pollutants. Clearly, in vitro exposure of alveolar cells to high concentrations of oxidant gases is responsible for a loss of cell viability. In contrast, when exposed to realistic concentrations of gases (NO₂, O₃), cell viability is not altered and various proinflammatory mediators are released. This in vitro model has proved to be sensitive at levels of gas exposure of ambient air quality standards and appears a sensitive biological indicator of air pollutant cell toxicity.Abbreviations AM alveolar macrophages     

From growth factor dependence to growth factor responsiveness: The genesis of an alveolar macrophage cell line

Summary A rat pulmonary alveolar macrophage (PAM) cell line (NR8383) was initiated in culture in the presence of a gerbil lung cell conditioned medium (GLCM), and has been propagated continuously for over 36 mo. When examined at different times throughout this in vitro period, NR8383 exhibited characteristics typical of macrophages: (a) Zymosan ingestion was seen in 90 to 98% of the cells examined; (b)Pseudomonas aeruginosa phagocytosis in 50 to 80%; (c) Nonspecific esterase activity in >95%. During the first 6 mo., the PAM replicated with doubling times approximating 15 to 20 d. Throughout this period, GLCM dependence was evident. After 27 wk in vitro, NR8383 replication increased markeldy, and within 2 wk, the doubling time was less than 48h. NR8383 was readily monitored by [³H]thymidine (TdR) blastogenesis assay. In the presence of GLCM uptake of [³H]TdR was fivefold greater than in control cultures. Adherence and growth kinetics were effectively controlled by modulation of GLCM or serum content in culture medium. It was demonstrated that PAM growth factor(s) is ubiquitous, not species-specific, and under certain conditions, may be derived from “endogenous” sources of persisting non-PAM populations within the parent, uncloned line NR8383. Cloned progeny remain devoid of non-PAM “feeder” cells, but retain macrophage properties, including interleukin-1 secretion, Fc receptors, and H₂O₂ production. This work was supported in part by grants #A119811 and #HL25378, Project 1B, from the National Institutes of Health, Bethesda, MD.     

Assessment of the risk of perforation of the mandibular canal by implant drill using density and thickness parameters

Gerodontology 2009; doi: 10.1111/j.1741‐2358.2009.00362.x
Assessment of the risk of perforation of the mandibular canal by implant drill using density and thickness parameters Objective: The objective of this study was to investigate whether the resistance of the bone surrounding the mandibular canal had sufficient density and thickness to avoid perforation by drills when preparing the bed of the implant. Background: Damage to the inferior alveolar nerve (IAN) is more common than expected. This injury may lead to serious complications ranging from mild paresthesia to total anaesthesia of the lower jaw. Materials and methods: The CT images of 99 patients, whose ages ranged between 20 and 79 years, and who applied for an implant application to the posterior aspect of the mandible were included in this study. Results: The overall average bone thickness in the premolar and molar regions was 0.8717 ± 0.1818 and 0.8556 ± 0.1756 mm, respectively, whereas the bone density in the premolar and molar regions was 649.18 ± 241.42 and 584.44 ± 222.73 Hounsfield Units (HU), respectively (p < 0.001). Conclusion: It was determined that the average density and thickness of the bone that surrounds the mandibular canal was not sufficient to resist the implant drill. It can be concluded that the risk of injury to the IAN may be minimised by accurately determining the bone mass on the canal prior to the implant procedure, and avoiding excessive force when approaching the canal.     

The evaluation of liquid-based ''Cyto-SEDTM'' cytology of bronchioalveolar lavage specimens in the diagnosis of pulmonary neoplasia against conventional direct smears

Historically, bronchioalveolar lavage (BAL) samples have been prepared by a direct smear (DS) technique. Recent advances in liquid-based cytology have led to a revolution in cytological specimen preparation. Cyto-SED system (CS) is a manual liquid-based cytology system, designed for small-scale use. A total of 137 samples from patients with radiographically detectable lesions underwent BAL procedures at Papworth Hospital NHS Trust over a 4-month period. After preparation for diagnostic purposes with the DS method, the remaining sample was prepared using the CS system. The slides produced were allocated a blind study number and screened by three independent screeners. The cellular morphology was well preserved and comparable between both techniques. Of the 137 patients, 38% were confirmed as malignant by cytology or histology; 71% of these malignant diagnosis were confirmed by the DS technique and 91% confirmed by the CS. The results demonstrate that the CS is a viable alternative to the DS technique. The cytological detail is clearly defined without a loss of three-dimensional information, thus aiding the differential diagnosis of malignancy. Cyto-SED cytology system yields a higher diagnostic accuracy than the conventional direct smear technique without compromising on cytological detail.     

Iatrogenic molar borings in 18th and early 19th century Native American dentitions

Six iatrogenic dental borings were identified in four individuals of a Native American skeletal collection from an 18th and early 19th century Middle Columbia River burial site. The borings, all in maxillary first molars with severe dental attrition and secondary dentin, demonstrate striated walls and associated periapical alveolar lesions. An ethnographic review of the subsistence pattern during the burial period indicates a diet that is consistent in dental attrition with other riverine fisher-hunter-gathers. Histological changes of dental pulp tissue during the process of attrition may result in dental necrosis. Access into the pulp chamber is a technique used to drain necrotic fluid. A common Euro-American therapeutic dental practice of the 18th and 19th centuries for diseases of the pulp was dental extraction. Multiple dental borings indicate that the practice of molar drilling into the pulp chamber was an effective and independent technique used by the Wishram and Wasco people.     

Clonal isolation of differentiated rat lung cells

Summary A number of diploid clones have been isolated from an enzymatic dispersion of normal rat lung. Four of these clones are epithelial in morphology, the remainder fibroblastic. On the basis of electron microscopic observations, two of the epithelial clones appear to have originated from type II alveolar pneumonocytes. Supported by funds from the W. Alton Jones Foundation and the American Lung Association.     

Phagocytosis induction of chemiluminescence and chemoattractant increased superoxide anion release from activated human alveolar macrophages in asthma

Human alveolar macrophages (AM) were demonstrated to generate reactive toxic derivatives of oxygen in many pulmonary disorders. These cells are involved in local inflammation which characterizes bronchial asthma. In the present work, we studied the ability of stimulated macrophages from healthy volunteers, and asthmatic patients to generate oxygen species in vitro. AM obtained by bronchoalveolar lavage were purified by adherence. The production of oxygen species was measured by luminol-enhanced chemiluminescence (CL) after challenge with opsonized zymosan. The maximal values were significantly (p < 0.03 and p < 0.01) higher in AM from asthmatics than in AM from healthy subjects. A significant correlation (p < 0.01) was observed between maximal value of CL and the severity of asthma as assessed by the clinical score. But, no difference was observed between AM from asthmatics in a stable state and healthy subjects. On the other hand, assays for superoxide anion generation emphasized the activation state of these macrophages stimulated by formyl-peptides.     

胶原膜与羟基磷灰石应用于牙周牙髓联合病变的探讨

目的：初步探索胶原膜与羟基磷灰石在治疗牙周牙髓联合病变中牙槽骨缺损的作用。方法：患牙进行根管治疗,调颌及牙周翻瓣术。其中２１例患牙的牙周骨缺损区植入胶原膜和羟基磷灰石;２０例以传统血充盈法关闭骨腔。二组患牙于治疗后１、３、６、１２、２４个月分别进行随访;结果：提示应用胶原膜和羟基磷灰石组的疗效明显优于对照组,并有统计学上差异。结论：胶原膜加羟基磷灰石治疗牙周牙髓联合病变的方法值得提倡。     

KGF‐2 targets alveolar epithelia and capillary endothelia to reduce high altitude pulmonary oedema in rats

High altitude pulmonary oedema (HAPE) severely affects non‐acclimatized individuals and is characterized by alveolar flooding with protein‐ rich oedema as a consequence of blood‐gas barrier disruption. Limited choice for prophylactic treatment warrants effective therapy against HAPE. Keratinocyte growth factor‐2 (KGF‐2) has shown efficiency in preventing alveolar epithelial cell DNA damages in vitro. In the current study, the effects of KGF‐2 intratracheal instillation on mortality, lung liquid balance and lung histology were evaluated in our previously developed rat model of HAPE. We found that pre‐treatment with KGF‐2 (5 mg/kg) significantly decreased mortality, improved oxygenation and reduced lung wet‐to‐dry weight ratio by preventing alveolar‐capillary barrier disruption demonstrated by histological examination and increasing alveolar fluid clearance up to 150%. In addition, KGF‐2 significantly inhibited decrease of transendothelial permeability after exposure to hypoxia, accompanied by a 10‐fold increase of Akt activity and inhibited apoptosis in human pulmonary microvascular endothelial cells, demonstrating attenuated endothelial apoptosis might contribute to reduction of endothelial permeability. These results showed the efficacy of KGF‐2 on inhibition of endothelial cell apoptosis, preservation of alveolar‐capillary barrier integrity and promotion of pulmonary oedema absorption in HAPE. Thus, KGF‐2 may represent a potential drug candidate for the prevention of HAPE.     

Plasminogen activator production in a rat model of Pneumocystis carinii pneumonia

Several studies have indicated that the serine protease urokinase-plasminogen-activator (uPA) is an important factor in host defense against pulmonary pathogens. To gain a better insight into the role of uPA in Pneumocystis carinii (P. carinii) pneumonia (PCP), we evaluated PA production in alveolar macrophages (AMs) obtained from rats with steroid-induced PCP. Treatment with cortisone acetate favored PCP in 91% of rats. In the bronchoalveolar lavage (BAL) samples of immunosuppressed rats both with and without PCP, we observed a decrease in uPA activity as well as a decrease in cell number. Urokinase-PA production by AMs was reduced in rats treated with cortisone alone. However, an increase in cell-associated uPA was observed in rats with PCP. This increase appears to be produced in response to P carinii infection. In fact, when AMs obtained from untreated healthy or immunosuppressed uninfected rats were challenged with P carinii, a significant increase in PA activity in cell lysates was observed, though a lower response was obtained in cortisone-treated animals. Our results suggest that healthy AMs respond to the presence of P carinii with an increase in uPA production and that this response in immunodepressed rat-AMs is partially impaired.