Retinal ischemia/reperfusion (I/R) injury is a major cause of vision loss, characterized by retinal edema and progressive retinal ganglion cell (RGC) death. Aquaporin-4 (AQP4), a water channel abundantly expressed in glial cells, plays a pivotal role in edema formation by regulating water homeostasis. Geranylgeranylacetone (GGA), a clinically approved anti-ulcer drug, functions as a potent and non-toxic inducer of heat shock protein 70 (HSP70) and has recently been implicated in the regulation of aquaporin trafficking. In parallel, the sorting nexin 27 (SNX27)-retromer complex is a key mediator of endosomal sorting and recycling of membrane proteins back to the plasma membrane, thereby maintaining their functional activity. In this study, we demonstrate that retinal I/R injury triggers altered subcellular localization of AQP4, with enhanced internalization compared with sham retinas. Concomitantly, SNX27-retromer expression was significantly upregulated at both mRNA and protein levels, and biochemical as well as imaging assays confirmed its interaction with AQP4. In a pre-ischemia dosing paradigm (prophylactic), GGA markedly attenuated retinal edema and RGC loss, and promoted the interaction between HSP70 and the SNX27-retromer complex. Importantly, GGA treatment reduced SNX27-retromer expression, thereby limiting AQP4 recycling to the plasma membrane and favoring its lysosome-associated trafficking. These effects were largely reversed by quercetin, a pharmacological inhibitor of HSP70, highlighting an HSP70-dependent mechanism. Together, our findings identify a previously unrecognized role of HSP70 in regulating SNX27-retromer-mediated AQP4 trafficking. By disrupting AQP4 recycling, GGA alleviates early retinal edema following I/R injury, providing mechanistic rationale for future therapeutic development.

Bilirubin encephalopathy (BE) is a neurological disorder caused by the accumulation of unconjugated bilirubin (UCB) in the brain of newborns, resulting in various degrees of neuronal impairment. BE is characterized by cytotoxic edema and neuronal apoptosis. Aquaporin-4 (AQP4), a water channel abundantly expressed in the central nervous system, plays a critical role in maintaining water homeostasis. Dysregulation of AQP4 expression or trafficking is closely associated with brain edema, suggesting that modulation of AQP4 may offer a potential therapeutic approach for BE. Previous studies have indicated that melatonin (MT) possesses neuroprotective and therapeutic potential against BE; however, its precise mechanisms remain unclear. In this study, we optimized rat BE model to investigate the therapeutic effects of melatonin on AQP4 expression, trafficking, and apoptosis in parietal cortical neurons. Furthermore, we explored the molecular mechanisms underlying melatonin’s neuroprotective actions, including the regulation mechanism of AQP4 expression, brain edema formation, and apoptosis induced by UCB accumulation. The results indicate that in the BE model, pathological injury of parietal cortex was significantly aggravated and AQP4’s expression peaked at 24 h after BE modeling. MT activated PI3K/AKT signaling pathway in rat parietal cortex to downregulate AQP4 expression, apoptosis related proteins, and decreased SNX27’s expression to promote the internalization of AQP4, reducing bilirubin induced cytotoxic edema and cortical apoptosis. This data suggest that MT has a neuroprotective role in BE, by potentially delaying its progression.

BACKGROUND:Aquaporin-8 (AQP8) is involved in impacting glioma proliferation and can effect tumour growth by regulating Intracellular reactive oxygen species (ROS) signalling levels. In addition to transporting H2O2, AQP8 has been shown to affect ROS signaling, but evidence is lacking in gliomas. In this study, we aimed to investigate how AQP8 affects ROS signaling in gliomas.MATERIALS AND METHODS:We constructed A172 and U251 cell lines with AQP8 knockdown and AQP8 rescue by CRISPR/Cas9 technology and overexpression of lentiviral vectors. We used CCK-8 and flow cytometry to test cell proliferation and cycle, immunofluorescence and Mito-Tracker CMXRos to observe the distribution of AQP8 expression in glioma cells, Amplex and DHE to study mitochondria release of H2O2, mitochondrial membrane potential (MMP) and NAD+/NADH ratio to assess mitochondrial function and protein blotting to detect p53 and p21 expression.RESULT:We found that AQP8 co-localised with mitochondria and that knockdown of AQP8 inhibited the release of H2O2 from mitochondria and led to increased levels of ROS in mitochondria, thereby impairing mitochondrial function. We also discovered that AQP8 knockdown resulted in suppression of cell proliferation and was blocked at the G0/G1 phase with increased expression of mitochondrial ROS signalling-related p53/p21.CONCLUSIONS:This finding provides further evidence for mechanistic studies of AQP8 as a prospective target for the treatment of gliomas.

Retinal ischemia-reperfusion (I/R) injury is a common pathophysiological stress state connected to various diseases, including acute glaucoma, retinal vascular obstruction, and diabetic retinopathy. Recent studies have suggested that geranylgeranylacetone (GGA) could increase heat shock protein70 (HSP70) level and reduce retinal ganglion cells (RGCs) apoptosis in a rat retinal I/R model. However, the underlying mechanism remains unclear. Moreover, the injury caused by retinal I/R includes not only apoptosis but also autophagy and gliosis, and the effects of GGA on autophagy and gliosis have not been reported. Our study established a retinal I/R model by anterior chamber perfusion pressuring to 110 mmHg for 60 min, followed by 4 h of reperfusion. The levels of HSP70, apoptosis-related proteins, GFAP, LC3-II, and PI3K/AKT/mTOR signaling proteins were determined by western blotting and qPCR after treatment with GGA, HSP70 inhibitor quercetin (Q), PI3K in-hibitor LY294002, and mTOR inhibitor rapamycin. Apoptosis was evaluated by TUNEL staining, meanwhile, HSP70 and LC3 were detected by immunofluorescence. Our results demonstrated that GGA-induced HSP70 expression significantly reduced gliosis, autophagosome accumulation, and apoptosis in retinal I/R injury, indicating that GGA exerted protective effects on retinal I/R injury. Moreover, the protective effects of GGA mechanistically relied on the activation of PI3K/AKT/mTOR signaling. In conclusion, GGA-induced HSP70 overexpression has protective effects on retinal I/R injury by activating PI3K/AKT/mTOR signaling.

BACKGROUND:Endoplasmic reticulum (ER) stress and oxidative stress are the major pathologies encountered after intracerebral hemorrhage (ICH). Inositol-requiring enzyme-1 alpha (IRE1α) is the most evolutionarily conserved ER stress sensor, which plays a role in monitoring and responding to the accumulation of unfolded/misfolded proteins in the ER lumen. Recent studies have shown that ER stress is profoundly related to oxidative stress in physiological or pathological conditions. The purpose of this study was to investigate the role of IRE1α in oxidative stress and the potential mechanism.METHODS:A mouse model of ICH was established by autologous blood injection. The IRE1α phosphokinase inhibitor KIRA6 was administrated intranasally at 1 h after ICH, antagomiR-25 and agomiR-25 were injected intraventricularly at 24 h before ICH. Western blot analysis, RT-qPCR, immunofluorescence staining, hematoma volume, neurobehavioral tests, dihydroethidium (DHE) staining, H2O2 content, brain water content, body weight, Hematoxylin and Eosin (HE) staining, Nissl staining, Morris Water Maze (MWM) and Elevated Plus Maze (EPM) were performed.RESULTS:Endogenous phosphorylated IRE1α (p-IRE1α), miR-25-3p, and Nox4 were increased in the ICH model. Administration of KIRA6 downregulated miR-25-3p expression, upregulated Nox4 expression, promoted the level of oxidative stress, increased hematoma volume, exacerbated brain edema and neurological deficits, reduced body weight, aggravated spatial learning and memory deficits, and increased anxiety levels. Then antagomiR-25 further upregulated the expression of Nox4, promoted the level of oxidative stress, increased hematoma volume, exacerbated brain edema and neurological deficits, whereas agomiR-25 reversed the effects promoted by KIRA6.CONCLUSION:The IRE1α phosphokinase activity is involved in the oxidative stress response through miR-25/Nox4 pathway in the mouse ICH brain.

为深化院校医学教育改革,重庆医科大学对临床医学专业五年制本科学生全面实施以器官系统为中心的临床医学整合课程教学模式.随着各年级学生不同器官系统整合课程的同时开展,实验室和授课教师出现周期性、暂时性紧缺现象,实验室存在尸体堆积、福尔马林超标等问题,学生反映学习困难等情况.文章就将数字化解剖操作实验教学平台配合重庆医科大学教学模式改革的实施,从平台构建和特点、应用体会和思考等两方面进行探讨,探索解剖教学新模式,以期进一步满足21世纪医学教育对复合性人才、高素质人才培养的要求.

The degranulation of mast cells accounts for the development of neuroinflammation following intracerebral hemorrhage (ICH). Inhibition of IRE1α, a sensor signaling protein related to endoplasmic reticulum stress, has been shown to exert anti-inflammatory effects in several neurological diseases. The objective of this study was to investigate the effects of IRE1α inhibition on mast cells degranulation in an ICH mouse model and to explore the contribution of miR-125/Lyn pathway in IRE1α-mediated mast cells degranulation. Male mice were subjected to ICH by intraparenchymal injection of autologous blood. STF083010, an inhibitor of IRE1α, was administered intranasally at 1 h after ICH induction. AntimiR-125 was delivered by intracerebroventricular (i.c.v.) injection prior to ICH induction to elucidate the possible mechanisms. Western blot analysis, immunofluorescence staining, neurological test, hematoma volume, brain water content, toluidine blue staining and reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR) were performed. Endogenous phosphorylated IRE1α (p-IRE1α), tryptase, interleukin-17A (IL-17A), tumor necrosis factor α (TNF-α) and tryptase mRNA were increased in time dependent manner while miR-125b-2-3p was decreased after ICH. Inhibition of IRE1α, with STF083010, remarkably reduced brain water content, improved neurological function, decreased hematoma volume, upregulated the expression of miR-125b-2-3p, decreased the number of mast cells, and downregulated the protein expression of Lyn kinase, XBP1s (spliced X-box binding protein-1), tryptase, IL-17A and TNF-α. The downregulation of Lyn kinase, tryptase, IL-17A, TNF-α, and decreased mast cells number were reversed by antimiR-125. The present findings demonstrate that IRE1α inhibition attenuates mast cells degranulation and neuroinflammation, at least partially, through IRE1α/miR-125/Lyn signaling pathway after ICH.

目的:研究幼年胆红素脑病(BE)模型大鼠海马中水通道蛋白4(AQP4)的表达变化,并且探究其与海马细胞凋亡及认知功能障碍的关系.方法:采用7 d龄SD幼年大鼠经小脑延髓池注射未结合胆红素(UCB)建立BE模型,根据UCB作用时间的不同将其分为12 h、24 h、48 h、72 h和7 d组.采用HE和Nissl染色观察各组海马病理变化;应用TUNEL染色法检测海马细胞凋亡;应用Western Blot检测海马AQP4、LAMP1、caspase-3和胶质纤维酸性蛋白(GFAP)的表达变化;应用免疫荧光染色检测海马AQP4、LAMP1和GFAP的表达变化及AQP4+/GFAP+细胞数量的变化.结果:HE及Nissl染色显示,随着UCB作用时间的延长,海马神经细胞间隙不断变大,空泡逐渐增多,Nissl小体数量减少.TUNEL染色法显示海马凋亡细胞数量在UCB作用24 h组最多(P＜0.05).Western Blot结果显示,随着UCB作用时间的延长,海马细胞中caspase-3和LAMP1均上升至24 h达峰值(P＜0.05).免疫荧光结果显示,AQP4和GFAP均增加至48 h表达最高(P＜0.05),AQP4+/GFAP+细胞数量在48 h组达最多(P＜0.05).结论:UCB的神经毒性作用可导致海马细胞凋亡增加至24 h达峰值,继发星型胶质细胞代偿性增生,并伴随AQP4的表达增加至48 h达峰值,以上变化可能与BE的认知功能障碍具有密切联系.

医学相关类专业是指除临床医学外的医学检验技术、医学影像技术、口腔技术、护理、预防医学、临床药学等众多专业,是我国高等医药院校教育的重要组成部分,涵盖面广,且招生人数众多.而医学相关类专业解剖学课程设置没有一个全国性的指导意见,各地院校在教学内容、教材选用上"百花齐放".

(AQP4) regulates retinal water homeostasis and participates in retinal oedema pathophys-iology. p-dystroglycan (p-DG) is responsible for AQP4 polarization and can be cleaved by matrix metalloproteinase-9 (MMP9). Retinal oedema induced by ischemia-reperfusion (I/R) injury is an early complica-tion. Bumetanide (BU) has potential efficacy against cytotoxic oedema. Our study investigated the effects of p -DG cleavage on AQP4 and the roles of BU in a rat retinal I/R injury model. The model was induced by applying 110 mm Hg intraocular pressure to the anterior eye chamber. BU and U0126 (a selective ERK inhibitor) were intraperitoneally administered 15 and 30 min, respectively, before I/R induction. Rhodamine isothiocyanate extravasation detection, quantitative real-time PCR, transmission electron microscopy, hematoxylin-eosin stain-ing, immunofluorescence staining, western blotting, and TUNEL staining were performed. AQP4 lost its polariza-tion in the retinal perivascular domain as a result of p-DG cleavage. BU rescued AQP4 depolarization, suppressed AQP4 protein expression, attenuated retinal cytotoxic oedema, and downregulated p-DG and AQP4 mRNA expres-sion. BU suppressed glial responses and mitochondria-mediated apoptotic protein expression, including that of Caspase-3 and Cyto C, raised the Bcl-2/Bax ratio, and lowered the number of apoptotic cells in the retina. Both BU and U0126 downregulated p-ERK and MMP9 expression. Thus, BU treatment suppressed p-DG cleavage, recov-ered AQP4 polarization partially via inhibiting ERK/MMP9 signaling pathway, and possess potential neuroprotec-tive efficacy in the rat retinal ischemia-reperfusion injury model.(c) 2022 IBRO. Published by Elsevier Ltd. All rights reserved.

笔者在解剖1具男尸过程中,发现其两侧椎动脉起始处走行均异常,且与交感神经节关系密切.现为积累解剖学资料,报道如下. 10％甲醛固定的男尸1具,年龄约60岁,身高约162 cm,解剖出颈部各层次,充分暴露及修洁颈部的血管、神经,观察拍照,并测量血管外径及长度.本例标本左、右两侧椎动脉均起自锁骨下动脉,呈"S"形上行.

Dentin matrix protein 1 (DMP1) is an extracellular matrix phosphoprotein that is known to facilitate mineralization of collagen in bone and promote osteoblast/odontoblast differentiation. Blood-brain barrier (BBB) disruption is the major pathogenesis in secondary brain injury after intracerebral hemorrhage (ICH). This study aimed to investigate the expression pattern of DMP1 in the mouse brain and explore the role of DMP1 in BBB disruption and brain injury in a mouse model of ICH. Mice were subjected to autologous blood injection-induced ICH. Immunofluorescence staining, western blot analysis, neurobehavioral tests, brain water content measurements, Evans blue permeability assay, and transmission electron microscopy were performed. Small interfering RNA targeting DMP1 (DMP1 siRNA) was administered at 72 h prior to ICH. Results showed that DMP1 is expressed extensively in the mouse brain, and is upregulated in the ICH model. Administration of DMP1 siRNA effectively ameliorated BBB disruption, attenuated brain edema, and improved neurological function after ICH. Moreover, the expression of zonula occludens-1 (ZO-1) and occludin were upregulated, and matrix metalloproteinase-9 (MMP-9) was downregulated in the ICH model. DMP1 siRNA administration reversed the expression of ZO-1, occludin, and MMP-9. These results demonstrated that DMP1 upregulation plays an essential role in inducing BBB disruption and brain injury after ICH. The inhibition of DMP1 could be a potential therapeutic strategy for ICH treatment.

Bilirubin encephalopathy (BE) is a neurological syndrome in newborns, mainly caused by neuronal injury due to excessive oxidative stress produced by unconjugated bilirubin (UCB). Neuroglobin (NGB) can protect the brain by removing oxidative stress species, but its expression and significance in BE are not clear. To address this question, the neonatal BE model was established by injecting UCB into the cerebellomedullary cistern of 7-day-old SD rats. Rats were divided into a sham and BE 6 hr group, BE 12 hr group, BE 24 hr group, and BE 7 d group according to UCB action times. Hematoxylin/eosin and Nissl staining, and electron microscopy were employed to observe the pathological and ultrastructural changes of nerve cells in each group. Immunofluorescence staining was used to detect NGB expression sites and cell types. Western blotting and quantitative PCR served to detect NGB expression and test the mitochondrial apoptosis signal pathway. The results confirm that UCB can lead to pathological damage and ultrastructural changes in rats' temporal cortex, increasing the expression of apoptosis-related proteins Bax, Bcl-2, Cyt c, Caspase-3, and neuronal NGB. UCB promotes NGB expression with an increase in action time and reach a peak at 12 hr. In summary, brain damage induced by UCB will cause an increase in NGB expression, the increasing NGB can inhibit neuron apoptosis in early BE phases. Therefore, promoting the expression of endogenous NGB, to act as a neuroprotective agent may be a potential treatment strategy for BE.

本研究通过电针刺激介导胆红素脑病(bilirubin encephalopathy,BE)模型鼠大脑颞叶皮质神经珠蛋白(neuroglobin,NGB)及PI3K/AKT通路、凋亡通路相关蛋白质的表达变化,以明确电针(electroacupuncture,EA)对于胆红素脑病的治疗作用,并探讨神经珠蛋白在该过程中的作用机制.将39只7日龄SD乳鼠分为假手术(Sham)组、BE模型组、电针治疗(BE+EA)组.经小脑延髓池注射胆红素溶液(10 μg胆红素/g体重)制备BE模型,假手术组注射等量生理盐水作为对照,BE+EA组选取百会穴与曲池穴以频率2/15 Hz的疏密波,于造模前12h、造模完成时及造模后12 h进行3次电针干预,每次15 min.使用HE、尼氏(Nissl)染色及透射电镜检测各组鼠脑颞叶皮质的病理变化及神经元超微结构的改变,结果显示电针处理可减轻BE乳鼠脑颞叶皮质神经元的损伤及增加尼氏体的数量,透射电镜则证实电针处理可改善神经元线粒体的水肿程度.应用免疫荧光染色法检测各组鼠脑颞叶皮质NGB的表达部位及其表达的细胞种类,结果显示NGB主要表达于颞叶皮质神经元中.进一步通过免疫印迹法检测各组鼠脑颞叶皮质中NGB蛋白及PI3K/AKT通路、线粒体凋亡信号通路相关蛋白质的表达,结果显示电针处理可增加NGB、PI3K p110α和pAKT Ser473的表达(分别为P＜ 0.05、0.05和0.01),上调凋亡相关蛋白Bcl-2/Bax比值(P＜0.001),进而抑制切割胱天蛋白酶3的激活(P＜0.05).通过TUNEL染色法检测各组凋亡细胞的数量,结果证实电针处理使凋亡细胞的数量减少(BE模型组186.00±13.86 vs BE+EA组78.67±11.85,P＜0.01).该研究初步证实,电针刺激可促进胆红素脑病鼠脑颞叶皮质中神经珠蛋白的表达,并进一步激活PI3K/AKT通路,而发挥其神经细胞保护功能,抑制凋亡反应的发生,电针可能成为胆红素脑病治疗潜在的方法.

Objective To investigate the effect of honokiol on demyelination after compressed spinal cord injury (CSCI) and it's possible mechanism. Design Animal experiment study. Setting Institute of Neuroscience of Chongqing Medical University. Interventions Total of 69 Sprague-Dawley (SD) rats were randomly divided into 3 groups: sham group (n=15), honokiol group (n=27) and vehicle group (n=27). After established CSCI model by a custom-made compressor successfully, the rats of sham group were subjected to the limited laminectomy without compression; the rats of honokiol group were subjected to CSCI surgery and intraperitoneal injection of 20 mg/kg honokiol; the rats of vehicle group were subjected to CSCI surgery and intraperitoneal injection of an equivalent volume of saline. Outcome measures: The locomotor function of each group was assessed using the Basso, Beattie and Bresnahan (BBB) rating scale. The pathological changes of myelinated nerve fibers of spinal cord in 3 groups were detected by osmic acid staining and transmission electron microcopy (TME). Immunofluorescence and Western blot were used to research the experessions of active caspase-3, caspase-12, cytochrome C and myelin basic protein (MBP) respectively. Results In the vehicle group, the rats became paralyzed and spastic after injury, and the myelin sheath became swollen and broken down along with decreased number of myelinated nerve fibers. Western blot analysis manifested that active caspase-3, caspase-12 and cytochrome C began to increase 1 d after injury while the expression of MBP decreased gradually. After intervened with honokiol for 6 days, compared with the vehicle group, the locomotor function and the pathomorphological changes of myelin sheath of the CSCD rats were improved with obviously decreased expression of active caspase-3, caspase-12 and cytochrome C. Conclusions Honokiol may improve locomotor function and protect neural myelin sheat from demyelination via prevention oligodendrocytes (OLs) apoptosis through mediate endoplasmic reticulum (ER)-mitochondria pathway after CSCI.

目的 观察电针百会、肾俞两穴对阿尔茨海默病(AD)模型大鼠学习记忆能力及前额叶皮质(PFC)P35/P25-周期蛋白依赖性激酶5(CDK5)-Tau蛋白磷酸化信号通路的影响,以探讨电针治疗AD的相关机制.方法 雄性成年Sprague-Dawley大鼠随机分为正常对照组、假手术组、模型组和电针组,每组6只.后两组双侧海马注射Aβ25-35,假手术组注射等量生理盐水.造模后次日,电针组电针百会、肾俞,留针15 min,每天1次,共10 d.治疗后,行Morris水迷宫实验,免疫组织化学染色和Western blotting检测各组PFC P35/P25-CDK5-Tau蛋白磷酸化相关蛋白的表达情况.结果 与正常对照组和假手术组比较,模型组的逃避潜伏期和搜索路径均增加(P<0.05),穿越平台次数减少(P<0.05);与模型组比较,电针组逃避潜伏期和搜索路径均缩短(P<0.05),穿越平台次数增加(P<0.05).模型组P35/P25和CDK5阳性表达明显高于正常对照组和假手术组(P<0.01),电针组显著低于模型组(P<0.001).模型组P35/P25、CDK5、Tau[pS199]、Tau[pS202]相对表达量高于正常对照组和假手术组(P<0.05),电针组上述蛋白的表达低于模型组(P<0.05).结论 电针刺激能有效改善AD大鼠的学习记忆和空间探索能力,可能通过影响大鼠PFC的P35/P25-CDK5-Tau蛋白磷酸化信号通路,延缓AD的发生与发展.

BACKGROUND:Specific highly polarized aquaporin-4 (AQP4) expression is reported to play a crucial role in blood-brain barrier (BBB) integrity and brain water transport balance. The upregulation of polymerase δ-interacting protein 2 (Poldip2) was involved in aggravating BBB disruption following ischemic stroke. This study aimed to investigate whether Poldip2-mediated BBB disruption and cerebral edema formation in mouse bacterial meningitis (BM) model occur via induction of AQP4 polarity loss. METHODS AND RESULTS:Mouse BM model was induced by injecting mice with group B hemolytic streptococci via posterior cistern. Recombinant human Poldip2 (rh-Poldip2) was administered intranasally at 1 hour after BM induction. Small interfering ribonucleic acid (siRNA) targeting Poldip2 was administered by intracerebroventricular (i.c.v) injection at 48 hours before BM induction. A specific inhibitor of matrix metalloproteinases (MMPs), UK383367, was administered intravenously at 0.5 hour before BM induction. Western blotting, immunofluorescence staining, quantitative real-time PCR, neurobehavioral test, brain water content test, Evans blue (EB) permeability assay, transmission electron microscopy (TEM), and gelatin zymography were carried out. The results showed that Poldip2 was upregulated and AQP4 polarity was lost in mouse BM model. Both Poldip2 siRNA and UK383367 improved neurobehavioral outcomes, alleviated brain edema, preserved the integrity of BBB, and relieved the loss of AQP4 polarity in BM model. Rh-Poldip2 upregulated the expression of MMPs and glial fibrillary acidic protein (GFAP) and downregulated the expression of β-dystroglycan (β-DG), zonula occludens-1 (ZO-1), occludin, and claudin-5; whereas Poldip2 siRNA downregulated the expression of MMPs and GFAP, and upregulated β-DG, ZO-1, occludin, and claudin-5. Similarly, UK383367 downregulated the expression of GFAP and upregulated the expression of β-DG, ZO-1, occludin, and claudin-5. CONCLUSION:Poldip2 inhibition alleviated brain edema and preserved the integrity of BBB partially by relieving the loss of AQP4 polarity via MMPs/β-DG pathway.

为了加强基础与临床知识的联系和渗透,以及培养学生的临床胜任力,重庆医科大学进行了器官系统教学模式的改革.此外,学校开展了本科生创新实验课题计划,以培养学生的创新能力和科研思维能力.医学生在参与创新实验课题的过程中,通过查阅文献资料以确定选题、撰写申请书、开展实验及写作论文等不同环节的学习和锻炼,有利于扩大其知识面,增强其自主学习能力、动手能力和团队合作精神等,从而促进其对器官系统课程知识的学习.因此,鼓励学生参加创新实验课题并做好各环节的工作,对于提高器官系统课程的学习效果,培养高素质的创新型医学人才具有重要意义.

It is an important way to improve the teaching quality by carrying out innovative experiments among medical students. In the process of experimental teaching, anatomy teachers expand the anatomy knowledge to basic scientific research techniques, so as to enhance students' confidence in participating in innovative experimental projects. Meanwhile, the teachers combine introduction of the anatomical structures with hot medical research issues, in order to help students to select appropriate innovative experimental topics. What's more, the new media teaching is integrated into the teaching of anatomy, enlightening students to perfect the experimental designs. Finally, in the teaching practice of regional anatomy, students are guided to carry out innovative experiments and write research papers. Abovementioned measures not only improve the teaching quality of anatomy, but also improve the students' scientific research ability, laying a foundation for them to participate in innovative experimental projects.

Alzheimer’s disease (AD) is one of the common neurodegenerative illnesses in aging populations around the world. Recently, psychiatric symptoms are becoming increasingly important in recognizing the manifestations of AD in addition to cognitive impairment. Some studies suggest that the prefrontal cortex (PFC) is closely related to apathy/depression, and a network may exist between the CA1 of hippocampus and PFC. However, whether the injection of Aβ2535 into hippocampi may result in PFC abnormalities in AD model rats is unclear. In this study, it was investigated the changes in the PFCs after the hippocampal injection via the P35/P25 - Cyclin-dependent kinase5 (CDK5) - Tau hyperphosphorylation signaling pathway. Our results demonstrated that rats injected with Aβ25−35 showed decreased learning and memory ability, and increased depression-like behaviors compared with uninjected controls and saline-injected shams. P35/P25, CDK5, Tau[pS199], and Tau[pS202] are significantly elevated in the PFCs and hippocampi after Aβ25−35 was injected into the hippocampi. Furthermore, P35/P25-CDK5 complexes were detected in vivo by immunofluorescence and co-immunoprecipitation. Therefore, the relative expression of proteins associated with the P35/P25-CDK5 pathway showed the same changes in the hippocampi and PFCs after Aβ25−35 injection. These findings demonstrate a potential mechanism for prefrontal-mediated cognitive impairment and the psychiatric symptoms of AD.