Real-time screening tool for identifying post-traumatic stress disorder in facial trauma patients in a UK maxillofacial trauma clinic

Post-traumatic stress disorder (PTSD) is a distressing consequence of a traumatic event associated with an increased suicide risk and reduced quality of life. Surgeons often have low confidence in identifying psychological problems. The prevalence of PTSD following facial trauma ranges from 23% to 41%. This highlights the importance of identifying and managing at-risk patients to optimize both mental and physical recovery. IMPARTS (Integrating Mental and Physical healthcare: Research, Training and Services) provides electronic screening tools to guide the non-mental health clinician in the ‘real-time’ identification, documentation, and management of potential mental health problems. The bespoke IMPARTS facial trauma screening tool was piloted in a UK oral and maxillofacial surgery trauma clinic from July 2015 to November 2017. A total of 199 patients completed screening, with 48 (24%) screening positive for possible PTSD. Further analysis of these 48 patients revealed that four (8%) had PTSD symptoms alone; three (6%) also screened positive for depression, 17 (35%) for co-existing symptoms of anxiety, and 24 (50%) for PTSD, anxiety, and depression. IMPARTS was found to be a highly effective tool aiding the non-mental health clinician to screen for PTSD and initiate prompt management. The data captured informs planning of the psychological support service.     

锌转运体3、TSQ及Zinquin三种荧光染色对癫痫小鼠海马苔藓纤维出芽的研究

目的研究锌转运体3、TSQ及Zinquin荧光染色在癫痫小鼠海马苔藓纤维出芽的染色情况。方法小鼠腹腔注射匹罗卡品建立小鼠癫痫模型,应用锌转运体3、TSQ及Zinquin三种荧光染色技术对造模后15d,30d,60d的模型小鼠苔藓纤维出芽进行标记染色。结果在造模后15d,三种荧光染色开始出现在小鼠海马的颗粒细胞层。造模后30d,三种荧光染色出现在海马内分子层。而在造模后60d,海马内分子层芽生的苔藓纤维的荧光染色进一步加强。结论锌转运体3、TSQ及Zinquin三种荧光染色可以做为苔藓纤维出芽的标记方法。     

Capture of extracellular zinc ions by astrocytes

Synaptic zinc ions released during synaptic transmission interact with pre- and postsynaptic neuroreceptors, thus modulating neurotransmission. It is likely that they have to be efficiently cleared from the extracellular milieu to assure subsequent synaptic events. Both neurons and glia are assumed to participate in this clearance by mechanisms that are not fully understood. In this study, electron microscopic zinc cytochemistry has shown zinc-electrondense particles associated with hippocampal astrocytic membranes frequently found accumulated in stacked lamellae. In cultured astrocytes, the use of zinc fluorochromes and endocytic markers allowed the simultaneous imaging of the capture of extracellular zinc simultaneously to plasma membrane markers; this endocytic process was inhibited by high sucrose concentrations. Finally, electron microscopy of zinc-loaded and fluorochrome photoconverted cells demonstrated some early events of extracellular zinc capture as well as its late accumulation in lysosome-like organelles.     

大鼠长期热证造模的舌扫描电镜观察

目的 :观察大鼠长期热证造模的活体舌象 ,舌组织病理和舌扫描电镜变化。方法 :成年Wistar大鼠按体重配对随机分为对照组和热证组 ,热证组以热性药物造模。另取幼年大鼠为幼年组。结果 :热证组动物舌质偏红 ,舌面苍老 ;舌固有层乳头密度增加 ,基底层细胞核分裂相频数增加 ,颗粒层细胞嗜碱性颗粒粗大 ,丝状乳头软角质减少 ,角化上皮剥脱明显 ,丝状乳头颗粒层细胞核空泡变明显 ;菌状乳头密度增大 ;幼年组动物与对照组比较 ,舌的病理改变也以上皮增殖加快、代谢旺盛为其主要特征。结论 :上述改变显示热证组动物有火热亢盛、代谢加快为主的病理 ,并与其全身性变化一致。     

Distribution of histochemically reactive zinc in the forebrain of the rat

The major cytoarchitectonic regions of the rat brain that stain with the Timm-Danscher metal stain were tested with the flourescent probe for zinc, 6-methoxy 8-para toluene sulfonamide quinoline (TSQ). Throughout most of the striatum, cerebral cortex and limbic system, the diffuse, even neuropil staining produced by the Timm-Danscher method was mirrored by comparable fluorescence in TSQ-stained sections. Blockade of the TSQ fluorescence by prior treatment with sulphide indicated that the Timm Danscher and the TSQ procedures both labeled the same pool of endogenous metal, which is inferred to be the zinc that is in axonal boutons. It is concluded that the Timm Danscher staining generally indicates zinc-containing axonal boutons. The distribution of the zinc-containing axonal boutons throughout the forebrain is described.     

Routes of zinc entry in mouse cortical neurons: role in zinc-induced neurotoxicity

Exposure of central neurons to Zn2+ triggers neuronal death. The routes of Zn2+ entry were investigated in living cortical neurons from the mouse using the specific Zn2+ fluorescent dye N-(6-methoxy-8-quinolyl)-p-toluene sulphonamide (TSQ), which preferentially detects membrane-bound Zn2+. Exposure of cortical neurons to increasing concentrations of Zn2+ (1-100 microM) induced a progressive increase in the fluorescence of TSQ. This fluorescence signal was not attenuated by the permeation of plasma membrane with digitonin. Accordingly, the major part of TSQ fluorescence (two-thirds) was associated to the particulate fraction of cortical neurons exposed to Zn2+. These results suggest that Zn2+ detected with TSQ in neurons is mainly bound to membranes. TSQ fluorescence measured in neurons exposed to 3 microM Zn2+ was enhanced by Na+-pyrithione, a Zn2+ ionophore, alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), N-methyl-D-aspartate (NMDA) or KCl-induced depolarization. However, in the absence of any treatment, TSQ labelling of neurons exposed to 3 microM Zn2+ was only decreased by NMDA receptor antagonists, whereas it remained unaltered in the presence of antagonists of AMPA receptors or L-type voltage-gated Ca2+ channels. Zn2+ entry through NMDA receptors did not contribute to Zn2+-induced neuronal death, as it was prevented by antagonists of NMDA receptors only when they were added after the Zn2+ exposure. Finally, Zn2+ induced a delayed accumulation of extracellular glutamate which might be responsible for the delayed NMDA receptor activation that leads to neuronal death.     

Evidence that synaptically-released zinc contributes to neuronal injury after traumatic brain injury

Prior evidence indicates that synaptically-released zinc enters postsynaptic neurons in toxic excess during ischemia and seizures. In addition, prevention of this zinc translocation has been shown to be neuroprotective in both ischemia and seizures. Here we show evidence that the same translocation of zinc from presynaptic boutons into postsynaptic neurons occurs after mechanical injury to the brain. Specifically, using a rat model of traumatic brain injury, we show that trauma is associated with (i) loss of zinc from presynaptic boutons (ii) appearance of zinc in injured neurons, and (iii) neuroprotection by intraventricular administration of a zinc chelator just prior to brain impact. The possible use of zinc chelators for neuroprotection after head trauma is considered.     

A novel homozygous mutation p.E88K in maternal SLC30A2 gene as a cause of transient neonatal zinc deficiency

The SLC30A2 gene encodes zinc transporter ZnT2, which is indispensable for the transport of zinc into the breast milk in the mammary gland. Transient neonatal zinc deficiency (TNZD) is caused by a mutation in the maternal SLC30A2 gene and has a clinical presentation similar to that of acrodermatitis enteropathica (AE). We described the case of a Chinese infant who presented with AE-like lesions 10 days after birth. Sanger sequencing of the AE-causing gene SLC39A4 revealed no mutations in genomic DNA from the infant, excluding the possibility of AE. Detection of the mother's breast milk showed a significantly lower zinc level. Thus, SLC30A2 sequencing was performed on her genomic DNA and a previously unreported homozygous c.262G > A (p.E88K) mutation was disclosed. Functional analysis suggested the novel mutation could lead to a strong disruption of zinc secretion, which indicated a complete loss of function in the ZnT2 protein. We finally diagnosed the infant with TNZD. To the best of our knowledge, this is the first case of TNZD caused by a homozygous mutation in the maternal SLC30A2 gene. Compared to the heterozygous condition, a homozygous mutation seems to result in a more significant decrease in zinc secretion and a more rapid onset of TNZD.     

Residual tinnitus after the medical treatment of sudden deafness

Objectives

Some patients with sudden sensorineural hearing loss (SSNHL) are frustrated by residual tinnitus even after accomplishment of the treatment for SSNHL. In the present prospective study, we examined patients’ backgrounds of sex, laterality and age together with changes in hearing level and the tinnitus score after the onset of SSHNL to determine the prognostic factors of residual tinnitus after the final day of medical treatment for SSNHL.

Methods

Forty-four patients with SSNHL were all treated with systemic administration of steroids for 2 weeks and oral intake of vasoactive drugs and vitamin B12 for 6 months before accomplishment of the treatment for SSNHL. The hearing improvement rate (HIR) was determined by comparing the hearing level before and 6 months after the start of treatment. Tinnitus was subjectively evaluated by the tinnitus scoring questionnaire before, 6 and 24 months after the start of treatment. The score of a five-step evaluation of subjective tinnitus feelings, “loudness”, “duration” and “annoyance”, was recorded.

Results

HIR was significantly correlated with tinnitus score improvement (TSI) in “duration” at 6 months after the start of treatment compared with before treatment. The tinnitus score of all 3 items was significantly improved 6 months after the start of treatment compared with that before treatment but it was not significantly changed between 6 and 24 months after the start of treatment. TSI in “duration” between 6 and 24 months was significantly correlated with the patients’ age and HIR using multiple regression analysis.

Conclusion

According to the tinnitus scoring questionnaire, “duration” is the most reliable item for subjective evaluation of tinnitus accompanied by SSNHL. Generally, subjective feelings for residual tinnitus 6 months after the start of treatment for SSNHL are supposed to be almost the same, even at the 24th post-treatment month. Especially, younger patients with better hearing improvement are predicted to achieve further improvement of tinnitus between 6 and 24 months after the start of treatment.     

氯碘羟喹对小鼠海马苔藓纤维内游离锌离子螯合作用的研究

目的研究金属螯合剂氯碘羟喹（Clioquinol,CQ）对小鼠大脑海马苔藓纤维内游离锌离子的螯合作用。方法3月龄雄性C57BL／6小鼠42只,随机均分为3组：正常对照组,溶剂对照组,CQ组。CQ组和溶剂对照组腹腔注射药物2h后与正常对照组一起断头取脑,制备小鼠海马冰冻切片,应用N-（6-甲氧基-8-喹啉）-P-甲苯磺胺（TSQ）荧光探针技术和金属自显影技术检测各组小鼠大脑海马苔藓纤维游离锌离子的分布和含量。结果CQ处理组小鼠海马苔藓纤维的TSQ荧光强度在CA3区及齿状回均明显低于正常对照组和溶剂对照组（P〈0．01）,而两对照组之间无差别。CQ处理组小鼠大脑金属自显影阳性反应强度在皮层、海马CA3区、齿状回均明显低于正常对照组和溶剂对照组（P〈0．01）,而两对照组之间无差别。结论金属螯合剂CQ对小鼠大脑内游离锌离子有明显的螯合作用,提示CQ可能作为锌离子诱导的神经细胞死亡疾病（如脑缺血和阿尔茨海默病）的潜在治疗药物。