BACKGROUND & AIMS: PURPOSE OF REVIEW:Bortezomib-based combinations are being investigated in relapsed or refractory multiple myeloma with the aim of improving outcomes. This review presents recent data from clinical trials of these combinations and discusses their implications. RECENT FINDINGS:Preclinical findings indicating additive or synergistic activity of bortezomib plus conventional and novel agents for multiple myeloma appear to be supported by clinical studies of bortezomib-based combinations. Bortezomib combined with a broad set of active agents results in enhanced response rates, including high complete response rates. Encouraging responses to bortezomib and its combinations are also seen in elderly patients, patients with adverse prognostic factors such as refractory disease and increased beta2-microglobulin, patients with cytogenetic abnormalities such as chromosome 13 deletion, advanced bone disease, extramedullary involvement, and patients with renal impairment, including patients with renal failure requiring dialysis. Toxicities are predictable and manageable and comparable to those seen with bortezomib monotherapy. SUMMARY:Bortezomib-based combinations show promising activity in relapsed or refractory multiple myeloma, including reversal of chemoresistance to previously used agents. As high complete and overall response rates translate into longer survival, bortezomib-based combinations appear likely to have a significant impact on the multiple myeloma treatment algorithm and on the course of the disease itself.

背景与目标：

BACKGROUND & AIMS: OBJECTIVE:Accumulating findings suggest that in acute myeloid leukemia (AML) patients, proinflammatory cytokines and growth factors play important roles in the proliferation and survival of AML cells in an autocrine and paracrine manner, leading to deterioration of AML. JTE-607 is a multiple cytokine inhibitor that potently suppresses production of proinflammatory cytokines. In the present study, we investigated the potency of JTE-607 as an antileukemic agent by exploiting a SCID mouse acute leukemia model. METHODS:SCID mice injected with anti-asialo-GM1 antibody were exposed to sublethal total-body irradiation at a dose of 3 Gy and then inoculated intravenously with AML cells. JTE-607 was administered using osmotic minipumps. The effects of JTE-607 on mouse survival time, human interleukin (IL)-8 levels in mouse plasma, and proportion of human CD45(+) cells in the bone marrow were studied. RESULTS:The survival time of the mice was strictly dependent on the number of U-937 cells proliferating in vivo. Administration of JTE-607 during the initial 7 days significantly prolonged survival of the mice, suggesting killing activity of JTE-607 against AML cells in vivo. Delayed administration of JTE-607 also prolonged the survival of mice bearing established leukemia with an effect comparable to the maximum tolerable dose of cytarabine. Flow cytometer analysis of bone marrow cells revealed decreased number of human CD45(+) cells. Human IL-8 level was also reduced by JTE-607. CONCLUSION:Our results indicate that JTE-607 has potential to be a new class of antileukemic drug that exerts inhibitory activities against both the proliferation and proinflammatory cytokine production of AML cells.

背景与目标：

BACKGROUND & AIMS: OBJECTIVE:In this article we focus on the role that chemokines and chemokine receptors play in the pathogenesis of multiple myeloma and the associated bone destructive process, and consider their utility as novel therapeutic targets for treating this devastating disease. METHODS:Current research on the role that chemokine and chemokine receptors play in the pathogenesis of myeloma is reviewed. RESULTS:The chemokines, MIP-1alpha, MCP-1, IL-8, and SDF-1, and their receptors play important roles in homing of MM cells, tumor growth, and bone destruction in myeloma. They are attractive therapeutic targets for treating myeloma patients. CONCLUSION:Addition of chemokine antagonists to current treatment regimens for myeloma should result in better therapeutic responses because of the loss of both the protective effect of the marrow microenvironment on the MM cells and the induction of osteoclast activity.

背景与目标：

BACKGROUND & AIMS: :cAMP signaling pathways play crucial roles in photoreceptor cells and other retinal cell types. Previous studies demonstrated a circadian rhythm of cAMP level in chick photoreceptor cell cultures that drives the rhythm of activity of the melatonin synthesizing enzyme arylalkylamine N-acetyltransferase and the rhythm of affinity of the cyclic nucleotide-gated channel for cGMP. Here, we report that the photoreceptor circadian clock generates a rhythm in Ca(2+)/calmodulin-stimulated adenylyl cyclase activity, which accounts for the temporal changes in the cAMP levels in the photoreceptors. The circadian rhythm of cAMP in photoreceptor cell cultures is abolished by treatment with the l-type Ca(2+) channel antagonist nitrendipine, while the Ca(2+) channel agonist, Bay K 8644, increased cAMP levels with continued circadian rhythmicity in constant darkness. These results indicate that the circadian rhythm of cAMP is dependent, in part, on Ca(2+) influx. Photoreceptor cell cultures exhibit a circadian rhythm in Ca(2+)/calmodulin-stimulated adenylyl cyclase enzyme activity with high levels at night and low levels during the day, correlating with the temporal changes of cAMP in these cells. Transcripts encoding two of the Ca(2+)/calmodulin-stimulated adenylyl cyclases, type 1 and type 8 (Adcy1 and Adcy8), displayed significant daily rhythms of mRNA expression under a light-dark cycle, but only the Adcy1 transcript rhythm persisted in constant darkness. Similar rhythms of Adcy1 mRNA level and Ca(2+)/calmodulin-stimulated adenylyl cyclase activity were observed in retinas of 2-week-old chickens. These results indicate that a circadian clock controls the expression of Adcy1 mRNA and Ca(2+)/calmodulin-stimulated adenylyl cyclase activity; and calcium influx into these cells gates the circadian rhythm of cAMP, a key component in the regulation of photoreceptor function.

背景与目标： : cAMP信号通路在感光细胞和其他视网膜细胞类型中起着至关重要的作用。先前的研究表明，雏鸡感光细胞培养物中cAMP水平的昼夜节律驱动褪黑激素合成酶芳基烷基胺N-乙酰基转移酶的活性节律和环状核苷酸门控通道对cGMP的亲和力节律。在这里，我们报告了感光体昼夜节律时钟在Ca(2)/钙调蛋白刺激的腺苷酸环化酶活性中产生节律，这说明了感光体中cAMP水平的时间变化。通过用l型Ca(2) 通道拮抗剂尼群地平处理，消除了感光细胞培养物中cAMP的昼夜节律，而Ca(2) 通道激动剂Bay K 8644在持续的黑暗中增加了cAMP水平，并持续了昼夜节律。这些结果表明，cAMP的昼夜节律部分取决于Ca(2) 的流入。感光细胞培养物在Ca(2)/钙调蛋白刺激的腺苷酸环化酶活性中表现出昼夜节律，夜间水平高，白天水平低，与这些细胞中cAMP的时间变化相关。编码两个Ca(2)/钙调蛋白刺激的腺苷酸环化酶 (1型和8型) (Adcy1和Adcy8) 的转录本在明暗循环下显示出明显的每日mRNA表达节律，但只有Adcy1转录本节律持续持续黑暗。在2周龄鸡的视网膜中观察到Adcy1 mRNA水平和Ca(2)/钙调蛋白刺激的腺苷酸环化酶活性的相似节律。这些结果表明，生物钟控制Adcy1 mRNA的表达和Ca(2)/钙调蛋白刺激的腺苷酸环化酶活性; 钙流入这些细胞中，激活了cAMP的昼夜节律，cAMP是调节感光细胞功能的关键组成部分。

BACKGROUND & AIMS: Environmental sensing in bacteria often involves the concerted action of sensor kinases and response regulators. Degenerate oligonucleotide primers were designed on the basis of amino acid similarity in the response regulators of these two-component systems. The primers were used in PCR to specifically amplify an internal DNA segment corresponding to the receiver module domain from genes encoding response regulators. Amplification products of the expected size were obtained from 12 different Gram-positive and Gram-negative bacteria. Sequence analysis revealed that 22 DNA fragments, which clearly originated from response regulator genes, were amplified from Escherichia coli, Agrobacterium tumefaciens, Bacillus subtilis and Lactobacillus bulgaricus. In each of these four species the receiver module of putative response regulator genes, which do not seem to be related to any of the already characterized genes, was identified. This simple and powerful method is therefore particularly useful for discovering new signal transduction systems which cannot be revealed by usual genetic studies.

背景与目标： 细菌中的环境传感通常涉及传感器激酶和响应调节剂的协同作用。简并寡核苷酸引物是根据这些两组分系统的响应调节剂中的氨基酸相似性设计的。引物用于PCR，以从编码反应调节剂的基因中特异性扩增与接收器模块结构域相对应的内部DNA片段。从12种不同的革兰氏阳性和革兰氏阴性细菌中获得了预期大小的扩增产物。序列分析表明，从大肠杆菌，根癌农杆菌，枯草芽孢杆菌和保加利亚乳杆菌中扩增出22个明显源自响应调节基因的DNA片段。在这四个物种中的每一个物种中，都鉴定了假定的反应调节基因的接收器模块，该模块似乎与任何已经表征的基因无关。因此，这种简单而强大的方法对于发现通常的遗传研究无法揭示的新信号转导系统特别有用。

BACKGROUND & AIMS: :A new optical method is proposed to investigate the reflectance of structurally coloured objects, such as Morpho butterfly wing scales and cholesteric liquid crystals. Using a reflected-light microscope and a digital single-lens reflex (DSLR) camera, we have successfully measured the two-dimensional reflection pattern of individual wing scales of Morpho butterflies. We demonstrate that this method enables us to measure the bidirectional reflectance distribution function (BRDF). The scattering image observed in the back focal plane of the objective is projected onto the camera sensor by inserting a Bertrand lens in the optical path of the microscope. With monochromatic light illumination, we quantify the angle-dependent reflectance spectra from the wing scales of Morpho rhetenor by retrieving the raw signal from the digital camera sensor. We also demonstrate that the polarization-dependent reflection of individual wing scales is readily observed using this method, using the individual wing scales of Morpho cypris. In an effort to show the generality of the method, we used a chiral nematic fluid to illustrate the angle-dependent reflectance as seen by this method.

背景与目标： : 提出了一种新的光学方法来研究结构上色的物体的反射率，例如Morpho蝴蝶翅鳞和胆甾型液晶。使用反射光显微镜和数字单镜头反射 (DSLR) 相机，我们成功地测量了Morpho蝴蝶单个翅膀鳞片的二维反射模式。我们证明了该方法使我们能够测量双向反射率分布函数 (BRDF)。通过在显微镜的光路中插入Bertrand透镜，将在物镜的后焦平面中观察到的散射图像投影到相机传感器上。使用单色光照明，我们通过从数码相机传感器检索原始信号，从Morpho rhetenor的机翼尺度量化与角度相关的反射光谱。我们还证明，使用这种方法，使用Morpho cypis的单个机翼尺度，很容易观察到单个机翼尺度的偏振相关反射。为了显示该方法的通用性，我们使用了手性向列流体来说明该方法所看到的与角度有关的反射率。

BACKGROUND & AIMS: :Alkenylboronic acids have shown important biological activities that contribute to neuroprotection. We have determined their influence on the β-amyloid (βA) aggregation process, β-secretase and acethylcholinesterase activities on cell-free systems, on the redox and lipid peroxidation status, and on the vulnerability to apoptotic death in an APPswe neuroblastoma cell line, before and after hydrogen peroxide treatment. We have discovered that 2-arylvinylboronic acids and some of their esters possess a set of properties which makes them highly useful as neuroprotective agents affecting multiple biological targets involved in AD. These properties are not paralleled by the related 2-arylboronic acids.

背景与目标： : 烯基硼酸显示出重要的生物活性，有助于神经保护。我们已经确定了它们对 β-淀粉样蛋白 (β a) 聚集过程，β-分泌酶和乙胆碱酯酶在无细胞系统上的活性，对氧化还原和脂质过氧化状态以及对APPswe神经母细胞瘤细胞凋亡死亡的脆弱性的影响过氧化氢治疗之前和之后。我们发现2-芳基乙烯基硼酸及其某些酯具有一系列特性，这使它们作为影响AD中涉及的多个生物靶标的神经保护剂非常有用。这些性质与相关的2-芳基硼酸不平行。

BACKGROUND & AIMS: OBJECTIVES:Monochorionic (MC) twins are at increased risk of early fetal loss secondary to vascular complications such as twin-twin transfusion syndrome (TTTS). This study compared the early perinatal loss rates between MC and dichorionic (DC) twins in an era of invasive treatment for TTTS. METHODS:This was a retrospective study of all twin pregnancies of known chorionicity from a large regional cohort of nine hospitals over a 10-year period. Ultrasound data were matched to hospital delivery records and to a mandatory national register of pregnancy losses. Prospective risk of pregnancy loss from 14 to 24 weeks' gestation was calculated and the survival trend of MC and DC twins was analyzed using Kaplan-Meier survival analysis. RESULTS:The analysis included 3117 twin pregnancies (605 MC and 2512 DC). The total risk of early pregnancy loss (miscarriage and neonatal death) before 24 weeks was significantly higher in MC twins (60.3 per 1000 fetuses) than in DC twins (6.6 per 1000 fetuses), with a relative risk of 9.18 (95% CI, 6.0-13.9). Survival analysis showed a significant difference in overall and early mortality between MC and DC twins (log-rank test, P < 0.0001), while no difference was noted after 24 weeks' gestation (log-rank test, P = 0.08). CONCLUSIONS:Early pregnancy loss is significantly more common in MC than in DC twins, but no difference in the prospective risk of mortality between MC and DC twins is evident after 24 weeks' gestation. The observed early mortality rate has almost halved in comparison with previous studies in the published literature. Early detection and prompt treatment of complications in MC twins are likely to have contributed to this improvement in outcome.

背景与目标：

BACKGROUND & AIMS: OBJECTIVE:Echocardiography is used for the detection of cardiac sarcoid involvement in patients with non-cardiac sarcoidosis. Little information is available regarding temporal changes in left ventricular ejection fraction (LVEF) and left ventricular end-diastolic dimension (LVDd) in non-cardiac sarcoidosis patients. METHODS AND RESULTS:Fifty-four sarcoidosis patients who received periodic follow-up with echocardiography at our institute were enrolled in this study. At the time of initial ultrasonography, 13 patients were diagnosed with cardiac sarcoid involvement. All of the remaining 41 patients with extra-cardiac sarcoidosis only had a LVEF of >50%. During the median follow-up period of 39 months, two (4.9%) of the non-cardiac sarcoidosis patients were diagnosed with cardiac sarcoid involvement; one patient showed a progressive decline in the LVEF over a short period of time. It was also found that two of 41 non-cardiac sarcoidosis patients showed declines in the LVEF of >10% per year; however, they were not diagnosed with cardiac sarcoidosis during the follow-up period. CONCLUSION:Rapid deterioration of left ventricular function may increase the suspicion of sarcoid involvement of the heart in non-cardiac sarcoidosis patients; however, we must be aware that a certain subfraction of patients may not demonstrate significant abnormalities in LVEF or LVDd on periodic echocardiographic follow-up.

背景与目标：

BACKGROUND & AIMS: BACKGROUND:Interleukin-17 (IL-17), which is secreted by Th17 cells, is a proinflammatory cytokine that is implicated in the pathogenesis of multiple sclerosis (MS) and plays a role in nonresponse of MS patients to interferon-β (IFN-β) therapy. OBJECTIVES:The purpose of this study was to establish a correlation between nonresponders (NR) and IL-17A serum titers and binding antibodies (BAbs) to IFN-β, as well as to find a correlation between IL-17A serum levels and other features of MS patients. METHODS:Our prospective study included 72 inactive relapsing-remitting multiple sclerosis (RRMS) patients that had been treated for at least 18 months with IFN-β and 15 healthy subjects. We determined the serum levels of IL-17A and of BAbs. IL-17A levels were considered elevated (IL-17A+) if the recorded value was greater than 1.6 pg/ml. RESULTS:Twenty-seven patients (37.5%) were NR and had a significantly higher serum IL-17A level compared to the responders group. Nineteen patients (26.4%) were IL-17A+ and had had a significantly higher number of relapses in the previous year and a higher Expanded Disability Status Score. The majority of IL-17A+ patients were NR and had a shorter MS duration. CONCLUSIONS:RRMS patients with high serum IL-17A levels do not respond well to IFN-β therapy and have shorter MS duration compared to patients with low IL-17A levels. This response is not influenced by the presence of BAbs.

背景与目标：

BACKGROUND & AIMS: :Molecular dynamics simulations in explicit water were carried out for two stacks, each composed of six 10-strand antiparallel β-sheets for two peptides corresponding to the diverging turn of two homologous Abl-SH3 domains. The first system, referred to as 10×6×MK contained the DLSFMKGE sequence from the Drosophila, while the second one, referred to as 10×6×KK, contained the human DLSFKKGE sequence. It was found that the 10×6×MK β-sheet stack is stable, but the 10×6×KK β-sheet stack is not. The stability of the 10×6×MK β-sheet stack results from the hydrophobic interactions of the methionine and phenylalanine residues and the leucine residues of the neighboring sheets. The Met, Phe, and Leu hydrophobic units make a hydrophobic core for the stack of β-sheets. During the MD run, the Met, Phe, and Leu residues of the neighboring β-sheets acted as a conformational switch moving the β-sheets so that the Phe residue interacted with the Met residue from the neighboring β-sheet. Replacement of Met by Lys destroys the hydrophobic core, which is the stability factor of the β-sheet stack. For the 10×6×KK system, individual β-sheets were preserved during simulations, but the interactions between the β-sheets were lost. The calculations of a six β-sheet stack confirm the conclusion drawn from our earlier studies of single β-sheet systems that the β-sheets must form stacks to be stabilized. These results suggest that the two conserved basic residues at the diverging turn of SH3 domains could act as gatekeepers to avoid aggregation.

背景与目标： : 在显式水中对两个堆栈进行了分子动力学模拟，每个堆栈由两个肽的六个10链反平行 β-折叠组成，对应于两个同源Abl-SH3域的发散转向。第一个系统 (称为10 × 6 × mk) 包含果蝇的DLSFMKGE序列，而第二个系统 (称为10 × 6 × kk) 包含人类DLSFKKGE序列。发现10 × 6 × mk β-折叠堆叠是稳定的，而10 × 6 × kk β-折叠堆叠则不稳定。10 × 6 × mk β-薄片堆叠的稳定性是由蛋氨酸和苯丙氨酸残基与相邻薄片的亮氨酸残基的疏水相互作用引起的。Met，Phe和Leu疏水单元为 β-折叠堆叠形成疏水核心。在MD运行期间，相邻 β-sheet的Met，Phe和Leu残基充当构象开关，移动 β-sheet，以使Phe残基与相邻 β-sheet的Met残基相互作用。用Lys代替Met会破坏疏水核，这是 β-折叠堆叠的稳定性因子。对于10 × 6 × kk系统，在模拟过程中保留了单个 β-折叠，但是 β-折叠之间的相互作用丢失了。六个 β-sheet堆栈的计算证实了我们先前对单个 β-sheet系统的研究得出的结论，即 β-sheet必须形成堆栈才能稳定。这些结果表明，在SH3结构域发散的转弯处的两个保守的碱性残基可以充当网守以避免聚集。

BACKGROUND & AIMS: :Over an 8 year period, 170 patients with multiple sclerosis (MS) and 134 healthy controls were assessed at monthly intervals in order to ascertain environmental factors which might be important in producing exacerbation or progression of the illness, and to compare the frequency of common viral infections in the two groups. During cumulative periods designated "at risk" (2 weeks before the onset of infection until 5 weeks afterwards) annual exacerbation rates were almost 3-fold greater than those during periods not at risk. Approximately 9% of infections were temporally related to exacerbations, whereas 27% of exacerbations were related to infections. Frequency of common infections was approximately 20-50% less in MS patients than controls; it was progressively less in those with greater disability. Even in minimally disabled patients with similar potential for infectious contacts, the infection rate was significantly less than in controls, suggesting that MS patients could have superior immune defences against common viruses.

背景与目标： : 在8年的时间里，每月对170名多发性硬化症 (MS) 患者和134名健康对照者进行评估，以确定可能对疾病恶化或进展很重要的环境因素，并比较两组中常见病毒感染的频率。在指定为 “处于危险中” 的累积期间 (感染发作前2周至之后5周)，年恶化率几乎是无危险期间的3倍。大约9% 的感染在时间上与恶化有关，而27% 的恶化与感染有关。MS患者的常见感染频率比对照组低约20-50%; 残疾程度较高的患者逐渐减少。即使在具有类似感染接触潜力的最小残疾患者中，感染率也明显低于对照组，这表明MS患者可以对普通病毒具有出色的免疫防御能力。

BACKGROUND & AIMS: Mees' lines, or transverse striate leukonychia, are classically associated with arsenic poisoning, but have been described in other cases of acute or chronic illness. Their pathogenesis is thought to be a disruption of nail plate keratinization secondary to systemic stress. Mees' lines are observed in a patient with helminthic and amebic infections and no history of arsenic exposure. This case demonstrates another clinical setting in which Mees' lines can appear, providing further evidence that Mees' lines may chronicle systemic disease.

背景与目标： Mees线或横纹白斑病通常与砷中毒有关，但在其他急性或慢性疾病病例中也有描述。它们的发病机理被认为是继发于全身压力的指甲板角质化的破坏。在患有蠕虫和阿米巴感染且没有砷暴露史的患者中观察到mees的行。该病例展示了另一种可能出现Mees' 线的临床环境，提供了进一步的证据表明Mees' 线可能会记录全身性疾病。

BACKGROUND & AIMS: :Stem cells have been widely assumed to be capable of replacing lost or damaged cells in a number of diseases, including Parkinson's disease (PD), in which neurons of the substantia nigra (SN) die and fail to provide the neurotransmitter, dopamine (DA), to the striatum. We report that undifferentiated human neural stem cells (hNSCs) implanted into 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated Parkinsonian primates survived, migrated, and had a functional impact as assessed quantitatively by behavioral improvement in this DA-deficit model, in which Parkinsonian signs directly correlate to reduced DA levels. A small number of hNSC progeny differentiated into tyrosine hydroxylase (TH) and/or dopamine transporter (DAT) immunopositive cells, suggesting that the microenvironment within and around the lesioned adult host SN still permits development of a DA phenotype by responsive progenitor cells. A much larger number of hNSC-derived cells that did not express neuronal or DA markers was found arrayed along the persisting nigrostriatal path, juxtaposed with host cells. These hNSCs, which express DA-protective factors, were therefore well positioned to influence host TH+ cells and mediate other homeostatic adjustments, as reflected in a return to baseline endogenous neuronal number-to-size ratios, preservation of extant host nigrostriatal circuitry, and a normalizing effect on alpha-synuclein aggregation. We propose that multiple modes of reciprocal interaction between exogenous hNSCs and the pathological host milieu underlie the functional improvement observed in this model of PD.

背景与目标： : 人们普遍认为干细胞能够替代许多疾病中丢失或受损的细胞，包括帕金森氏病 (PD)，其中黑质 (SN) 的神经元死亡，无法向纹状体提供神经递质多巴胺 (DA)。我们报告了植入1-甲基-4-苯基-1,4，2,3-四氢吡啶处理的帕金森氏灵长类动物中的未分化人类神经干细胞 (hNSCs) 存活，迁移并通过行为改善定量评估具有功能影响在这个DA-缺陷模型中，其中帕金森氏征与DA水平降低直接相关。少数hNSC后代分化为酪氨酸羟化酶 (TH) 和/或多巴胺转运蛋白 (DAT) 免疫阳性细胞，这表明受损的成年宿主SN内部和周围的微环境仍允许通过反应性祖细胞发展DA表型。发现大量不表达神经元或DA标记的hNSC衍生细胞沿持续的黑质纹状体路径排列，与宿主细胞并列。因此，这些表达DA保护因子的hNSCs可以很好地影响宿主TH细胞并介导其他稳态调节，这反映在恢复到基线内源性神经元数量与大小之比，保留现存的宿主黑质纹状体回路以及对 α-突触核蛋白聚集的正常化作用。我们建议外源性hNSCs与病理性宿主环境之间相互作用的多种模式是该PD模型中观察到的功能改善的基础。

BACKGROUND & AIMS: :Mesial temporal lobe epilepsy (mTLE) is a neurological condition characterized by the occurrence of spontaneous recurrent seizures originating from mesial structures involving the hippocampus within the temporal lobe. This condition is often associated with pathological features in the hippocampus such as neuronal cell loss, widening of the granule cell layer, astrogliosis and mossy fibre spouting. At present, the mechanisms underlying these pathological features are unclear. However, recent advances in adult neurogenesis studies in mTLE animals and patients suggest that newly generated neurons may contribute to the pathogenesis of ongoing epileptogenesis. This article will review the recent animal and human studies on adult neurogenesis in mTLE and discuss how these results suggests that adult endogenous neurogenesis may not always be reparative in the mTLE and may be targeted in new therapeutic strategies for mTLE.

背景与目标： : 颞叶内侧癫痫 (mTLE) 是一种神经系统疾病，其特征是发生自发性复发性癫痫发作，起源于颞叶内海马的内侧结构。这种情况通常与海马的病理特征有关，例如神经元细胞丢失，颗粒细胞层变宽，星形胶质细胞增生和苔藓状纤维喷出。目前，这些病理特征的机制尚不清楚。然而，在mTLE动物和患者中进行的成人神经发生研究的最新进展表明，新生的神经元可能有助于正在进行的癫痫发生的发病机理。本文将回顾最近有关mTLE中成人神经发生的动物和人类研究，并讨论这些结果如何表明成人内源性神经发生可能并不总是在mTLE中修复，并且可能在mTLE的新治疗策略中靶向。