X线及MRI对聚丙烯酰胺凝胶隆胸后乳腺病变诊断价值的评价与比较

目的对聚丙烯酰胺凝胶(PAG)注射式隆胸术后,出现并发症或合并乳腺其他病变的X线与MRI的诊断价值进行评估。方法回顾性分析26例PAG隆胸术后钼靶X线与MRI的影像表现。结果钼靶X线及MRI能显示充填物位置、形态,合并乳腺病变4例,X线全部漏诊,MRI能检出病灶。结论钼靶X线是PAG隆胸术后普查、随访的首选方法,但出现并发症或者合并乳腺病变时,MRI具有无法比拟的优越性,在临床诊断与治疗中发挥了重要作用。     

The nuclei of origin of brain stem enkephalin and substance P projections to the rodent nucleus raphe magnus

The sites of origin of brain stem enkephalin and substance P projections to the rodent nucleus raphe magnus were studied utilizing the combined horseradish peroxidase retrograde transport-peroxidase-antiperoxidase immunohistochemical technique. Several brain stem areas were found to contain both enkephalin- and substance P-like immunoreactive double labeled neurons following injection of horseradish peroxidase into the raphe magnus. Nuclei providing both enkephalin and substance P inputs to the raphe magnus include the nucleus reticularis paragigantocellularis, the nucleus cuneiformis, the nucleus solitarius and the trigeminal subdivision of the lateral reticular nucleus. Enkephalin projections to the raphe magnus were also found to originate from the dorsal parabrachial nucleus, the nucleus reticularis gigantocellularis pars α and from an area which corresponds to the A5 group of Dahlström &; Fuxe. Additional neurons containing substance P-like immunoreactivity and horseradish peroxidase reaction product were identified in the superior central raphe nucleus and the nucleus pontis oralis. The midbrain periaqueductal gray contributes very few enkephalin and substance P fibers to the raphe magnus.The nucleus raphe magnus is a key structure in the intrinsic analgesia system and it has also been implicated in other diverse and non-nonciceptive functions. The present study identifies several brain stem sites which provide enkephalin and substance P input to this raphe nucleus. Several of these nuclei have been implicated in central analgesic mechanisms or in non-nociceptive autonomic functions. The present investigation raises the possibility that these brain stem regions may modulate neuronal activity in the raphe magnus via enkephalin or substance P projections and thus influence the involvement of the raphe magnus in both opiate related mechanisms of pain control and non-nociceptive functions.     

A dopamine D1 receptor agonist improved learning and memory in morphine-treated rats

ABSTRACT

Objective: The objective of this article is to study the role of the dopamine (DA) D1 receptor in the midbrain periaqueductal grey (PAG) on learning and memory in morphine-addicted rats.

Methods: DA D1 receptor agonist SKF81297 and D1 receptor antagonist SCH SCH23390 were administrated into the PAG, respectively, and the learning and memory behavioral changes of morphine addicted rats were detected by water maze. Western blot and immunohistochemistry were used to detect glutamate decarboxylase 67 (GAD67) and tyrosine receptor kinase B (TrkB) in PAG.

Results: D1 receptor agonist shortened the latency to platform and increased the number of platform crossings, indicating improved learning and memory ability of morphine addict rat. D1 receptor agonist increased GAD67 expression and decreased TrkB in PAG.

Conclusion: (1) The PAG is involved in the learning and memory changes of the addicted rats; (2) the activation of DA D1 receptor will increase the GAD67, reduce the damage to peripheral neurons, and improve the learning and memory of the addicted rats; and (3) D1 receptor agonists further reduced TrkB expression in morphine-addicted rats, whereas TrkB levels deviated from changes in rat behavior.     

Too hard to control: compromised pain anticipation and modulation in mild traumatic brain injury

Mild traumatic brain injury (MTBI) is a vulnerability factor for the development of pain-related conditions above and beyond those related to comorbid traumatic and emotional symptoms. We acquired functional magnetic resonance imaging (fMRI) on a validated pain anticipation task and tested the hypotheses that individuals with a reported history of MTBI, compared with healthy comparison subjects, would show increased brain response to pain anticipation and ineffective pain modulation after controlling for psychiatric symptoms. Eighteen male subjects with a reported history of blast-related MTBI related to combat, and eighteen healthy male subjects with no reported history of MTBI (healthy controls) underwent fMRI during an event-related experimental pain paradigm with cued high or low intensity painful heat stimuli. No subjects in either group met diagnostic criteria for current mood or anxiety disorder. We found that relative to healthy comparison subjects, after controlling for traumatic and depressive symptoms, participants with a reported history of MTBI showed significantly stronger activations within midbrain periaqueductual grey (PAG), right dorsolateral prefrontal cortex and cuneus during pain anticipation. Furthermore, we found that brain injury was a significant moderator of the relationship between anticipatory PAG activation and reported subjective pain. Our results suggest that a potentially disrupted neurocognitive anticipatory network may result from damage to the endogenous pain modulatory system and underlie difficulties with regulatory pain processing following MTBI. In other words, our findings are consistent with a notion that brain injury makes it more difficult to control acute pain. Understanding these mechanisms of dysfunctional acute pain processing following MTBI may help shed light on the underlying causes of increased vulnerability for the development of pain-related conditions in this population.     

Non-targeted metabolomic biomarkers and metabotypes of type 2 diabetes: A cross-sectional study of PREDIMED trial participants

Aim

To characterize the urinary metabolomic fingerprint and multi-metabolite signature associated with type 2 diabetes (T2D), and to classify the population into metabotypes related to T2D.

A 7-Tesla MRI study of the periaqueductal gray: resting state and task activation under threat

The periaqueductal gray (PAG) is a region of the midbrain implicated in a variety of behaviors including defensive responses to threat. Despite the wealth of knowledge pertaining to the differential functional roles of the PAG columns in nonhuman and human research, the basic functional connectivity of the PAG at rest has not been well characterized. Therefore, the current study utilized 7-Tesla magnetic resonance imaging (MRI) to characterize PAG functional connectivity at rest and task activation under uncertain threat. A sample of 53 neurologically healthy undergraduate participants (M_age = 22.2, s.d._age = 3.62) underwent structural and resting state functional MRI scans. Supporting previous work, voxel-wise analyses showed that the PAG is functionally connected to emotion regulation and fear networks. The comparison of functional connectivity of PAG columns did not reveal any significant differences. Thirty-five participants from the same sample also completed an uncertain threat task with blocks of three conditions—no shock, predictable shock and unpredictable shock. There were no robust activity differences within the PAG columns or the whole PAG across conditions although there was differential activity at the voxel level in the PAG and in other regions theoretically relevant to uncertain threat. Results of this study elucidate PAG connectivity at rest and activation in response to uncertain threat.     

Hydrogen sulfide is a novel prosecretory neuromodulator in the Guinea-pig and human colon

BACKGROUND & AIMS: Hydrogen sulfide (H(2)S) has been suggested as a novel gasomediator. We explored its unknown neuromodulatory role in human and guinea-pig colon. METHODS: We used immunohistochemistry to detect H(2)S-producing enzymes cystathionine gamma-lyase (CSE) and cystathionine beta-synthase (CBS) in enteric neurons, Ussing chambers to measure mucosal ion secretion, and neuroimaging with voltage- and Ca(++)-sensitive dyes to record H(2)S effects on guinea-pig and human enteric neurons. RESULTS: More than 90% of guinea-pig and human submucous and myenteric neurons were colabeled for CSE and CBS. Myenteric interstitial cells of Cajal were CSE-immunoreactive. The exogenous H(2)S donor NaHS (0.2-2.5 mmol/L) concentration-dependently increased chloride secretion in human and guinea-pig submucosa/mucosa preparations, but not in the colonic epithelial cell line T84. The secretory response was reduced significantly by tetrodotoxin (0.5 micromol/L), capsaicin desensitization (10 micromol/L), and the transient receptor potentials vanilloid receptor 1 antagonist capsazepine (10 micromol/L). The endogenous H(2)S donor L-cysteine also induced secretion that was diminished significantly by capsaicin desensitization, the CBS inhibitor amino-oxyacetic acid, and the CSE inhibitor propargylglycine. NaHS increased spike discharge in 23% of guinea-pig and 36% of human submucous neurons, but had no effect on Ca(++) mobilization in cultured guinea-pig enteric neurons. This excitatory response was reduced significantly by capsaicin desensitization and capsazepine, but not by glibenclamide (10 micromol/L). CONCLUSIONS: The presence of H(2)S-producing enzymes in human and guinea-pig enteric neurons, the excitatory action on enteric neurons, and the prosecretory effects of NaHS suggest H(2)S as a novel gut-signaling molecule. Its action mainly involves transient receptor potentials vanilloid receptor 1 receptors on extrinsic afferent terminals, which in turn activate enteric neurons.     

Ammonia metabolism,the brain and fatigue; revisiting the link

This review addresses the ammonia fatigue theory in light of new evidence from exercise and disease studies and aims to provide a view of the role of ammonia during exercise. Hyperammonemia is a condition common to pathological liver disorders and intense or exhausting exercise. In pathology, hyperammonemia is linked to impairment of normal brain function and the onset of the neurological condition, hepatic encephalopathy. Elevated blood ammonia concentrations arise due to a diminished capacity for removal via the liver and lead to increased exposure of organs, such as the brain, to the toxic effects of ammonia. High levels of brain ammonia can lead to deleterious alterations in astrocyte morphology, cerebral energy metabolism and neurotransmission, which may in turn impact on the functioning of important signalling pathways within the neuron. Such changes are believed to contribute to the disturbances in neuropsychological function, in particular the learning, memory, and motor control deficits observed in animal models of liver disease and also patients with cirrhosis. Hyperammonemia in exercise occurs as a result of an increased production by contracting muscle, through adenosine monophosphate (AMP) deamination (the purine nucleotide cycle) and branched chain amino acid (BCAA) deamination prior to oxidation. Plasma concentrations of ammonia during exercise often achieve or exceed those measured in liver disease patients, resulting in increased cerebral uptake. In this article we propose that exercise-induced hyperammonemia may lead to concomitant disturbances in brain function, potentially through similar mechanisms underpinning pathology, which may impact on performance as fatigue or reduced function, especially during extreme exercise.     

大白鼠中脑导水管周围灰质腹外侧区的传入投射——HRP逆行追踪方法研究

用HRP(horseradish peroxidase)逆行追踪标记技术,研究大白鼠中脑导水管周围灰质(PAG,periaqueductal gray)尾侧半腹外侧区的传入投射。将HRP注入PAG尾侧半的腹外侧区:①在大脑皮层内岛无颗粒层出现中等数量的标记细胞;②基底前脑内的标记细胞较多,主要分布于终纹床核、斜角带核、无名质、杏仁内侧核和腹侧苍白球,外侧隔核和伏核内也出现少量的标记细胞;③下丘脑中大量的标记细胞出现在视前内侧区、视前外侧区和下丘脑外侧区;④底丘脑和背侧丘脑的标记细胞主要分布在未定带和束分核。