空气喷磨对预防性树脂充填微渗漏的影响

目的 :体外评价空气喷磨、酸蚀和两者结合对预防性树脂充填微渗漏的影响。方法 :对照组 (I,n =12 )对人离体磨牙常规预防性树脂充填。其余组分别用 5 0 μ(Ⅱ,Ⅲ)和 27μ(Ⅳ ,Ⅴ)氧化铝喷磨 ,其中两组 (Ⅳ ,Ⅴ)酸蚀 30s。每组一半牙齿进行热循环处理 (5～ 5 5℃ ,2500周 )后 ,用亚甲基蓝溶液着色。结果 :不论结合酸蚀与否 ,用 5 0 μ氧化铝喷磨 ,均与对照组不存在显著性差异 (p >0.05)。但喷磨后酸蚀比单纯喷磨能显著地减少微渗漏 (p<0.05)。 5 0 μ较 27μ氧化铝微粒显著地减少微渗漏(p <0.05)。结论 :空气喷磨结合酸蚀能显著地减少预防性树脂充填的微渗漏。     

Mesolimbic neuropeptide W coordinates stress responses under novel environments

Neuropeptide B (NPB) and neuropeptide W (NPW) are endogenous neuropeptide ligands for the G protein-coupled receptors NPBWR1 and NPBWR2. Here we report that the majority of NPW neurons in the mesolimbic region possess tyrosine hydroxylase immunoreactivity, indicating that a small subset of dopaminergic neurons coexpress NPW. These NPW-containing neurons densely and exclusively innervate two limbic system nuclei in adult mouse brain: the lateral bed nucleus of the stria terminalis and the lateral part of the central amygdala nucleus (CeAL). In the CeAL of wild-type mice, restraint stress resulted in an inhibition of cellular activity, but this stress-induced inhibition was attenuated in the CeAL neurons of NPW^−/− mice. Moreover, the response of NPW^−/− mice to either formalin-induced pain stimuli or a live rat (i.e., a potential predator) was abnormal only when they were placed in a novel environment: The mice failed to show the normal species-specific self-protective and aversive reactions. In contrast, the behavior of NPW^−/− mice in a habituated environment was indistinguishable from that of wild-type mice. These results indicate that the NPW/NPBWR1 system could play a critical role in the gating of stressful stimuli during exposure to novel environments.Limbic structures, including the amygdala and bed nucleus of the stria terminalis (BST), where different modalities of environmental stimuli can converge and interact, are critical for the response to stress (1). The basolateral amygdala (BLA) receives sensory information from the thalamus and cortex and transfers that information to the central amygdala (CeA), an output center for the amygdaloid complex. Subsequently, the CeA relays this information through axonal projections to nuclei in diverse areas, such as the hypothalamus, brainstem, and pons (2, 3). These circuits are essential for mediating fear and anxiety, especially for fear conditioning using auditory or visual conditioned stimuli (4, 5). Indeed, in a recent report, optogenetic manipulation of the BLA–CeA pathway was found to modulate the expression of anxiety in the mouse (6).The lateral BST (BSTL) and CeA (CeAL) are two major components of the central extended amygdala, a continuum of telencephalic structures of the forebrain (7, 8). Both the BSTL and CeAL contain numerous GABAergic as well as peptidergic neurons, such as those producing enkephalin, corticotropin-releasing factor, and somatostatin (9–13); these GABAergic neurons form dense local inhibitory circuits within these nuclei. The GABAergic microcircuit in the CeAL is thought to play pivotal roles in mediating fear and anxiety, as recently dissected at the cellular level by studies that combined optogenetics and electrophysiology (14–17). A subpopulation of GABAergic neurons in the CeAL, which is inhibited by a conditioned stimulus (CS), is differentiated by the expression PKCδ (14). These PKCδ⁺ GABAergic neurons were shown to provide feed-forward disinhibition on output neurons in the medial CeA (CeAM), resulting in a conditioned freezing response following exposure to a CS (14, 15). However, PKCδ⁻ GABAergic neurons, which coexpress somatostatin and make reciprocal inhibitory synapses with PKCδ⁺ GABAergic neurons, do not send any significant intra-amygdaloid inhibitory projections to the CeAM. Instead, they send long-range projections to innervate the periaqueductal gray (PAG) and the paraventricular nucleus of the thalamus, i.e., extra-amygdala areas implicated in defensive behavior, and thus contribute to fear conditioning independent of the CeAM (16, 17).The G protein-coupled receptors (GPCRs) neuropeptides B and W receptors 1 and 2 (NPBWR1 and NPBWR2) (originally termed “GPR7” and “GPR8”) were identified as closely related orphan GPCRs by a degenerative PCR screen using primers based on sequences from opioid receptors (18). Although humans and other primates express both NPBWR1 and NPBWR2, no functional NPBWR2 ortholog has been demonstrated in rodents (19). A role for NPBWR1 has been characterized by the phenotypical analysis of NPBWR1-null mice, which demonstrate late-onset obesity with a hyperphagic phenotype (20). These mice also show abnormal social interaction and an aberrant autonomic response to physical stress (21). Recently, an SNP of the human NPBWR1 gene has been shown to influence the evaluation of facial expressions (22). We and other groups have isolated neuropeptide B (NPB) and neuropeptide W (NPW) as cognate endogenous ligands for NPBWR1 and NPBWR2 (23–26). NPB and NPW are encoded by two separate genes and together with NPBWR1 (and NPBWR2 in primates) constitute a neuropeptide receptor system (27). NPB consists of 29 amino acids with a unique brominated N-terminal tryptophan moiety (23, 25), whereas NPW, as the mature peptide, exists in two forms: NPW [1–23] and NPW [1–30]. NPW23 and NPW30 bind and activate NPBWR1 and NPBWR2 with similar nanomolar affinities (24, 27).In a previous report, we described the distribution of NPBWR1, NPB, and NPW mRNA in mouse brain by in situ hybridization (23). In contrast to the relatively widespread distributions of NPBWR1 and NPB mRNA, the neurons expressing NPW mRNA are localized primarily in specific midbrain regions, including the PAG, the ventral tegmental area (VTA), the Edinger–Westphal nucleus, and the dorsal part of the dorsal raphe nucleus (23, 28). This characteristic expression pattern implies a potential role for NPW in the regulation of limbic function. In this regard, we also observed a diffuse expression of NPW mRNA in the CA3 region of adult mouse hippocampus (29). In this study we investigated the potential physiological functions of NPW using histochemical studies and phenotypical analyses of NPW-null mice (Fig. S1), with a particular focus on their behavioral characteristics under environmental stress.Open in a separate windowFig. S1.Targeted disruption of the murine NPW gene. (A) Strategy for the targeted disruption of the NPW gene. The mouse genomic DNA map, targeting vector, and targeted locus map are shown. Restriction enzymes: B, BamHI; Bs, BssHII; HIII, HindIII; RI, EcoRI; Sm, SmaI; Xb, XbaI. (B) Genomic Southern blot analysis of the targeted ES cell DNA using ³²P-labeled 5′ and 3′ outer probes. Extracted ES cell DNA was digested with EcoRI for the 5′ probe and with BamHI for the 3′ probe. (C) PCR genotyping of mouse tail DNA by using two sets of primer pairs that detect the NPW genomic locus and PGK neo, respectively. (D) In situ hybridization of NPW in the PAG of adult mouse brain using a ³⁵S-labeled probe specific for NPW exon 1, which contains the NPW mature peptide-coding sequence.     

Headache induced by a nitric oxide donor (nitroglycerin) responds to sumatriptan. A human model for development of migraine drugs

Experimental "vascular" headache in humans may be used in characterizing new migraine drugs. The effects of sumatriptan on nitroglycerin-(NTG)-induced headache and arterial responses were therefore studied. Following a double-blind randomized crossover design, 10 healthy volunteers received sumatriptan 6 mg s.c. or placebo succeeded by 20 min NTG (0.12 mg/kg/min) infusion. Headache was rated on a 10 points scale. Temporal and radial artery diameters and velocity in the middle cerebral artery (MCA) were measured with ultrasound. Sumatriptan reduced the NTG-induced headache, median score 1.5 versus 4 after placebo ( p <0.01) and decreased temporal and radial artery diameters 75±3 and 86±3% of baseline respectively ( p <0.05), Blood velocity in the MCA was unaffected. The NTG model may prove to be a valuable tool in the development of future migraine drugs. The results suggest that NTG headache in non-migraineurs may share mechanisms with migraine headache.     

A sudden increase in factor VIII inhibitor development in multitransfused hemophilia A patients in The Netherlands. Dutch Hemophilia Study Group

The development of antibodies to factor VIII (inhibitors) in response to clotting-factor concentrates administration in hemophilia is common during the first few years of treatment but rare in multitransfused patients. We have investigated the possible association of a recently introduced factor VIII concentrate (Factor VIII CPS-P) in The Netherlands with the occurrence of inhibitors. To this effect, we conducted two studies. First, we performed a national multicenter study in which clinical information and inhibitor test results were obtained for 447 hemophilia A patients over the period 1988 through 1991. Secondly, for a baseline comparison we estimated the frequency of inhibitor development in a closely followed cohort of 144 patients, from 1984 through 1989. Before the introduction of Factor VIII CPS-P, the incidence of new inhibitors was 4.4/1,000 patient-years in the national study from March 1988 through May 1990, and 3.9/1,000 patient- years in the cohort followed from 1984 through 1989. These figures are similar to the incidence of new inhibitors that was found in a large cohort of patients in the United States followed in the 1970s. In the period that the new concentrate Factor VIII CPS-P was on the market, from June 1990 through November 1991, 11 clinically relevant inhibitors were detected, which yielded an incidence over this interval of 20.1/1,000 patient-years, a 4.5-fold increase compared with the previous interval (C195: 1.4 to 14.3). Nine of these 11 patients had in their lifetime received over 250 infusions with factor VIII preparations. whereas all of the inhibitors detected in the previous time interval, and all of the 24 inhibitor patients described in the US study, had received less than 250 infusions in their lifetime. All patients who developed inhibitors after June 1990 had been exposed to Factor VIII CPS-P, whereas only 75% of the patients who did not develop an inhibitor had been exposed to this product. In a prospective extension of the study, with a second inhibitor measurement after 3 months, we found that one additional inhibitor had developed during 52.5 patient-years of Factor VIII CPS-P use. In conclusion, there has been a sudden increase in the frequency of inhibitor patients, for a large part among multitransfused patients. It seems more than likely that this increase is associated with the introduction of a new factor VIII concentrate in The Netherlands.(ABSTRACT TRUNCATED AT 400 WORDS)     

Operational radiologic image archive on digital optical disks

A digital optical disk archive for storage of computed radiographic, computed tomographic, magnetic resonance, ultrasonographic, and digitized film radiographic images was installed. In the system, digital images enter a minicomputer, are temporarily stored on magnetic disks, and are archived onto write-once read-many optical disks at their full resolution. A pictorial index of minified images is maintained for each patient. After 8 months of operation, 49,400 megabytes of images had been retained on 19 optical disks stored, after January 1987, in a mechanical jukebox-style optical disk library. The success rate for archival capture of images during the initial period was 96.6%. The failures were due to overfilling of the magnetic disk, a problem addressed through the addition of a second magnetic disk unit. There were no medium-related image errors during the early period. Problems resulting from the slow speed of optical disk systems were addressed operationally by initiating recall of a patient's archived images from the optical to the faster magnetic disk as soon as the system received a request to acquire a new image. Also, optical disk retrieval times are expected to improve with technologic development.