形成性考核是指对学生学习过程的全面测评以及对学习成果和学习目标的阶段性考核,是课程考核的重要组成部分,可以更好地满足个性化学习的要求,有助于学生综合素质的培养和综合能力的提高.形成性考核与终结性考核不同,但又与后者相辅相成.近年来,全国各大院校"以学生为中心"的教学理念和以培养学生能力为目标的素质教育使得形成性考核的方式方法成为研究热点[1-3].云班课作为一个移动教学平台,可集教师的备课、课堂内外的师生互动、对学生的学习答疑和指导、布置及批改作业等环节于云服务平台.教师可以将各种资源如授课课件、视频、音频、图片、参考资料等上传至云班课,方便学生课前预习和课后复习;与课堂教学相配合,教师可在云班课上发布丰富的活动如实习作业、每章测试题、答疑/讨论、案例分析、头脑风暴等,可以有效地调动学生的自主学习热情.与此同时,学生应用云班课的学习过程如观看课件、视频、参考资料,完成作业、测试、答疑/讨论、头脑风暴等,在云班课中都有详细的数据记载,教师还可以根据学生的学习情况给予相应的分值.因此,借助于云班课移动教学平台进行形成性考核具有方便、及时、全面、客观、可信、易量化等优点,受到了教师的青睐[4-6],但在云班课各类活动的权重设计以及折合计算并形成量化的形成性考核方面尚未见报道.

OBJECTIVE:The present study is aimed at investigating the anti-inflammatory, antioxidative, and antiapoptotic effects of methane on lipopolysaccharide- (LPS-) induced acute orchitis and its potential mechanisms.METHODS:Adult male rats were intraperitoneally (i.p.) injected with methane-rich saline (MS, 20 mL/kg) following LPS (5 mg/kg, i.p.). The survival rate was assessed every 12 h until 72 h after LPS induction, and surviving rats were sacrificed for further detection. The wet/dry (W/D) ratio was determined, and testicular damage was histologically assessed. Inflammatory cytokines in the testes and serum, including interleukin-1β (IL-1β), IL-6, IL-10, and tumor necrosis factor-α (TNF-α), were measured using ELISA and RT-qPCR. Oxidative stress was evaluated by the level of superoxide dismutase (SOD) and malondialdehyde (MDA). Testicular apoptosis was detected via TUNEL staining. The expression of prokineticin 2 (PK2)/prokineticin receptor 1 (PKR1) was also analyzed using RT-qPCR, western blotting, and immunohistochemistry.RESULTS:It was found that methane significantly prolonged rat survival, decreased the W/D ratio, alleviated LPS-induced histological changes, and reduced apoptotic cells in the testes. Additionally, methane suppressed and promoted the production of pro- and anti-inflammatory cytokines, respectively. Furthermore, methane significantly increased SOD levels, decreased MDA levels, and decreased testicular expression of PK2 and PKR1. Therefore, methane exerts therapeutic effects on acute orchitis and might be a new and convenient strategy for the treatment of inflammation-related testicular diseases.

目的 本文在简要介绍我校留学生解剖学授课模式的基础上,分别阐述了为上好留学生解剖学系统解剖学辅导课和局部解剖学辅导课所采取的措施与方法,以期提高留学生解剖学的学习效果.

Calcium plays an important role in plant growth, development, and response to environmental stimuli. Copines are conserved plasma membrane-localized calcium-binding proteins which regulate plant immune responses and development. In this study, we found that copine proteins BON2 and BON3, the paralogs of BON1, physically interact with calcium pumps ACA8 and ACA10 in Arabidopsis. Notably, ACA9, the closest homologue of ACA8 and ACA10 functioning in pollen tube growth, interacts with all three copines. This is consistent with the protein–protein interactions between the two protein families, the aca8, aca10, aca8/aca10, bon1/2/3 mutants as well as aca9 mutant exhibited defects on pollen germination and seed production. Taken together, plasma membrane-localized interacting calcium pumps and copines coordinately control pollen tube growth, likely through manipulating calcium efflux.

AimsTransplantation of a tissue engineered cardiac pacemaker (TECP) may represent a novel therapy for cardiac sinus node dysfunction. We previously reported that cardiac progenitor cells (CPCs) derived from embryonic heart tubes could differentiate into cardiac pacemaking cells after endothelin-1 treatment. We aimed to examine the feasibility of TECP fabricated from CPCs-derived pacemaking cells and vascularization of TECP fabricated from CPCs-derived pacemaking cells and endothelial progenitor cells (EPCs) in vitro and in vivo implantation.Main methodsTECP created using CPCs-derived pacemaking cells and vTECP created by mixing CPCs and EPCs in vitro were implanted into rat hearts. Sinus node damaged was induced by formaldehyde insult.Key resultsSpontaneous beating tissues, namely TECP, were obtained after seeding CPCs-derived pacemaking cells into Matrigel. ECG and epicardial multielectrode array (MEA) measurements confirmed implanted TECP have electrical activity. TECP implantation promoted individual survival in sinus node damage models (15/22 animals lived versus 0/17 control). vTECP fabricated by mixing the both EPCs and CPCs-derived pacemaking cells with Matrigel in equal proportions optimally formed pre-vascularization in vitro. The implantation of vTECP enhanced electrical activity in vivo, which may correlate with increased vascularization. PI3K-Akt-VEGF/VEGFR signaling was involved with vascular ingrowth in vTECP.SignificanceOur data supports the therapeutic potential of TECP fabricated with the CPCs-derived pacemaking cells for sinus node dysfunction. Vascularization by the addition of EPCs is an important factor to sustain viability of the TECP in vivo.

Interleukin-1β-induced disruption to endothelial stability and vascular permeability in a human in vitro model is shown to be independent of downstream nuclear factor-κB activation, relying instead on a MYD88–ARNO–ARF6 signalling cascade; inhibiting proteins involved in this pathway is shown to improve outcomes in animal models of inflammatory disease. Cytokines, the circulating proteins that activate the immune system, also disrupt cell–cell junctions and can trigger tissue oedema and destruction. Using an in vitro human endothelial cell model, this study shows that the disruptive effects of one such cytokine, interleukin-1 β, are NF-κB independent. Instead they depend on a novel non-canonical pathway involving intracellular GTPases that regulate cadherin trafficking and cell–cell interactions. Targeting of this signalling cascade in an animal model of arthritis prevents cytokine-mediated disruption of endothelial cell barriers and limits tissue damage. The innate immune response is essential for combating infectious disease. Macrophages and other cells respond to infection by releasing cytokines, such as interleukin-1β (IL-1β), which in turn activate a well-described, myeloid-differentiation factor 88 (MYD88)-mediated, nuclear factor-κB (NF-κB)-dependent transcriptional pathway that results in inflammatory-cell activation and recruitment1,2,3,4. Endothelial cells, which usually serve as a barrier to the movement of inflammatory cells out of the blood and into tissue, are also critical mediators of the inflammatory response5,6. Paradoxically, the cytokines vital to a successful immune defence also have disruptive effects on endothelial cell–cell interactions and can trigger degradation of barrier function and dissociation of tissue architecture7,8,9. The mechanism of this barrier dissolution and its relationship to the canonical NF-κB pathway remain poorly defined. Here we show that the direct, immediate and disruptive effects of IL-1β on endothelial stability in a human in vitro cell model are NF-κB independent and are instead the result of signalling through the small GTPase ADP-ribosylation factor 6 (ARF6) and its activator ARF nucleotide binding site opener (ARNO; also known as CYTH2). Moreover, we show that ARNO binds directly to the adaptor protein MYD88, and thus propose MYD88–ARNO–ARF6 as a proximal IL-1β signalling pathway distinct from that mediated by NF-κB. Finally, we show that SecinH3, an inhibitor of ARF guanine nucleotide-exchange factors such as ARNO, enhances vascular stability and significantly improves outcomes in animal models of inflammatory arthritis and acute inflammation.

The mechanisms governing the development of cardiac pacemaking and conduction system are not well understood. In order to provide evidence for the derivation of pacemaking cells and the signal that induce and maintain the cells in the developing heart, Nkx2.5(+) cardiac progenitor cells (CPCs) were isolated from embryonic heart tubes of rats. Endothelin-1 was subsequently added to the CPCs to induce differentiation of them towards cardiac pacemaking cells. After the treatment, Nkx2.5(+) CPCs displayed spontaneous beating and spontaneously electrical activity as what we have previously described. Furthermore, RT-PCR and immunofluorescence staining demonstrated that Tbx3 expression was increased and Nkx2.5 expression was decreased in the induced cells 4 days after ET-1 treatment. And the significantly increased expression of Hcn4 and connexin-45 were detected in the induced cells 10 days after the treatment. In addition, Nkx2.5(+) CPCs were transfected with pGCsi-Tbx3 4 days after ET-1 treatment in an attempt to determine the transcription regulatory factor governing the differentiation of the cells into cardiac pacemaking cells. The results showed that silencing of Tbx3 decreased the pacemaking activity and led to down-regulation of pacemaker genes in the induced cells. These results confirmed that Nkx2.5(+) CPCs differentiated into cardiac pacemaking cells after being treated with ET-1 and suggested that an ET-1-Tbx3 molecular pathway govern/mediate this process. In conclusion, our study support the notion that pacemaking cells originate from Nkx2.5(+) CPCs present in embryonic heart tubes and endothelin-1 might be involved in diversification of cardiomyogenic progenitors toward the cells.

High glucose-induced proliferation of vascular smooth muscle cells (VSMCs) plays an important role in the development of diabetic vascular diseases. However, molecular mediators responding for the proliferation of VSMCs remain to be determined. In this study, VSMCs were isolated from the rat thoracic aorta, and two cell models with Irf-1 knockdown and overexpression were established by transfecting cells with pGCsi-FU-Irf-1 and pGC-FU-Irf-1, respectively. Subsequently, high glucose was added to cells to induce proliferation. Proliferation assays were performed to see whether Irf-1 was involved in high glucose-induced proliferation of VSMCs. In addition, the expression of Irf-1 was detected in VSMCs stimulated with high glucose and the thoracic aorta of diabetic rats to confirm the relationship between Irf-1 expression and the proliferation of hyperglycemia-dependent VSMCs. The results showed that Irf-1 expression was significantly higher in the thoracic aorta of diabetic rats and VSMCs stimulated with high glucose than that in nondiabetic rats and untreated cells. Overexpression of Irf-1 accelerated the proliferation of VSMCs, and down-regulation of Irf-1 expression significantly depressed the proliferative ability of VSMCs under high-glucose conditions, indicating that Irf-1 was a positive regulator for high glucose-induced proliferation of VSMCs. It could be presumed that Irf-1 is associated with the accelerated proliferation of VSMCs in diabetic vascular diseases and may prove to be a potential target gene for disease treatment.

Objective: To investigate the mechanism underlying ciliary neurotrophic factor (CNTF) involved in dedifferentiation of glial cells in injured optic nerves. Methods: Sixty-five adult male SD rats were randomly divided into 3 groups: normal control group, optic nerve injured group and CNTF treat group. Optic nerves were harvested at the 7th or the 14th day after surgery and detected by gene chip, real-time PCR, HE staining and immunohistochemistry. Results Comparison with those of injury group, there were 608 genes expression up-regulated and 417 ones down-regulated in the CNTF treated group at the 7th day after operation, including genes related to chromatin configuration, transcription regulation, neural stem cells, neural differentiation and development, proliferation, apoptosis, ion channel, receptor, signal transduction and so on. Result of real-time PCR for selected genes was consistent with that of gene chip, supporting the validity of gene chip data. We also found that cells revealed by HE staining and immunoreactivity of Nestin, myelin basic protein (MBP) , Erk1/2, and glial fibrillary acidic protein (GFAP) were increased in the distal optic nerves, but immunoreactivity of neurofilament (NF) was increased in the proximal optic nerves in the CNTF treated group compared with the optic nerve injured group. Conclusion: CNTF induces dedifferentiation of glia cells in the injured optic nerves and promotes regeneration of injured optic nerves through regulating the expression of related genes and proteins.

Objective: To study the effect of pre-degenerated common peroneal nerve on apoptosis and proliferation in injured rat optic nerve. Methods: One hundred and fifteen adult male rats were divided into normal, injured and transplantation group. Cell number, apoptosis/proliferation, proliferating cell nuclear antigen (PCNA) expression and apoptosis/proliferation related gene expression in rat optic nerves were examined respectively using HE staining, flow cytometry, Western blotting, gene chips and real-time PCR. Results: Cells in the optic nerve of the injury group increased compared with that in the normal group, but was lower than that in the transplantation group. Compared with the normal group, apoptotic cells increased and proliferated cells decreased in the injury group; Compared with the injury group, apoptotic cells decreased and proliferated cells increased in the transplantation group. Compared with the normal group, PCNA expression was down-regulated in the injury group, but PCNA expression was up-regulated in the transplantation group than that in the injury group. Compared with normal group, thirty seven apoptosis and proliferation related genes expressed differentially in the injury group; Compared with the injury group, three genes expressed differentially in the transplantation group. Conclusion: The cellular apoptosis increases and the cellular proliferation decreases in the distal part of the optic nerve after the optic nerve injury. Autograft transplantation of the common peroneal nerve could reduce the cellular apoptosis and promote the cellular proliferation. In addition, some corresponding gene expressions changed.

Objective To investigate the mechanism that bFGF promotes the regeneration of injured optic nerve and induces dedifferentiation of glial cells in it. Methods Fifty-five adult male SD rats were randomly divided into 3 groups as normal control group, injury group and bFGF group. At day 7 post operation, optic nerves from injury group and bFGF group were detected by gene chip and real-time PCR. At day 7, 14 post operation, optic nerves were harvested and detected by HE staining and immunohistochemistry. Results Compared with the injury group, there were 645 genes expression up-regulated and 458 genes down-regulated including genes related neural stem cell or precursor cell neural development, proliferation, apoptosis, chromatin configuration, transcription regulation, signal transduction, neural growth and so on in the bFGF group. There were bigger nuclei, more cells, more immunoreactivity of nestin, extracellular signal-regulated kinase(Erk1/2), glial fibrillary acidic protein(GFAP), and myelin basic protein(MBP) in the distal optic nerves and more immunoreactivity of neurofilament(NF) in the proximal optic nerves in the bFGF group than that in the injury group.Conclusion bFGF could promote the proliferation of neuroglia cells, dedifferentiation of neural glias and improve the microenvironment to favour the regeneration of injured optic nerve.

Objective To construct rat amniotic epithelial cells (AECs) modified with human basic fibroblast growth factor (bFGF) gene that combined with nerve growth factor (NGF) secreting peptide utilizing lentivirus vector, by which bFGF could be stably synthesized and secreted. Methods Amniotic epithelial cells were collected from the term rats by trypsin-treating process, and subcultured AECs were identified by immunocytochemistry and RT-PCR methods. Lentiviral vector with human bFGF gene was constructed, and lentivirus packaging was performed after DNA sequencing. Afterwards, AECs were infected with viral supernatant, then selected with blasticidin. Furthermore, the selected cells were detected for bFGF expression and secretion by immunocytochemistry, RT-PCR and ELISA methods. Thereafter, growth activity of AECs chimaera was investigated, and the biological functions of secreted bFGF was evaluated by culturing PC12 cells with conditioned medium of AECs chimaera. Results Immunocytochemical staining and RT-PCR showed that the rat AECs expressed epithelial-specific markers CK-19, neural cell markers nestin and GFAP, as well as pluripotent cells markers SSEA-4, Oct-4, Nanog, Sox2 and vimentin. The AECs chimaera sustainable expressing bFGF were obtained after infection and screening processes. Immunocytochemistry staining and RT-PCR showed that most of the AECs chimaera expressed bFGF, compared with the non-expression before transfection. ELISA results implicated that AECs chimaera were able to secrete bFGF peptide. AECs chimaera survived in the screening procedure grew much faster compared with common AECs. The conditional culture medium of AECs chimaera could stimulate PC12 cells growth and neurites development, as compared with AECs group. Conclusion bFGF gene could be transferred into rat AECs successfully by lentiviral vector, and the AECs chimaera could express and secret bFGF afterwards, indicating robust growth activity and significant neurotrophic activity.

Objective To investigate the effect of cultured hair follicle neural stem cells(HFNSCs) on dedifferentiation of macroglial cells in injured optic nerve of rats. Methods Follicle bulge cells isolated from vibrissa pad of male SD rats weighing about 90g were cultured in DMEM/F12 without serum or containing 15% FBS, identified as HFNSCs by immunofluorescence cytochemistry and PCR.The cells were stably transfected with rAAV2-EGFP.Adult male SD rats were randomly divided into 3 groups as normal control group,injury group and transplantation group in which HFNSCs were transplanted into injured optic nerves.At 7 days,14 days and 30 days after EGFP-HFNSCs transplantation,optic nerves were observed under fluorescence microscope.At 7 days post operation,optic nerves from injury group and transplantation group were detected by gene chip of Affymetrix and real-time PCR.At 7 days,14 days post operation,optic nerves were harvested and detected by HE staining and immunohistochemistry. Results Bulge cell in primary culture were labeled by neural progenitor cell markers,however the cells induced by 15% FBS expressed some makers of mature neural cells.EGFP-HFNSCs could survive and migrate in the injured optic nerve 30 days after transplantation. With the injury group,there were 240 differentially expressed genes including genes related stem cell,apoptosis,proliferation,transcription,differentiation and development, cell adhesion,signal transduction and so on in the transplantation group.The result of real time PCR was consistent with that of gene chip.There were more cells,more immunoreactivity of Nestin,MBP,Erk1/2,and less immunoreactivity of GFAP in the distal optic nerves and more immunoreactivity of NF in the proximal optic nerves in the transplantation group than that in the injured group.Conclusion HFNSCs regulate some genes expression of glial cells in the injured optic nerve to promote macroglial cells dedifferentiation and nerve regeneration.

In this paper, we constructed a novel acellular nerve xenograft (ANX) seeded with neurons and Schwann cells to bridge long-distance gaps in rat sciatic nerves. The neurons and Schwann cells were induced from Sprague Dawley (SD) rat hair follicle neural crest stem cells with sonic hedgehog/retinoic acid and neuregulin 1, respectively. Fifty male SD rats were randomly divided into two groups (n = 25): ANX + cells group and ANX group. A 4-cm-long sciatic nerve defect was created on the right hind limb and bridged with cell-seeded ANX in ANX + cells group or ANX alone in ANX group. We found that the implanted neurons and Schwann cells could survive by 4 weeks and as far as 52 weeks posttransplantation. In implanted grafts, chemical synaptic structures were also found under transmission electron microscope and confirmed with immunostaining of synapsin 1, a synaptic marker. The number of regenerated axons in ANX + cells group was higher than that in ANX group (P < 0.01). This novel implantation of neurons and Schwann cells via acellular nerve graft may provide an alternative way for repairing peripheral nerve defect.

In order to study the changes and regulation of neural precursor cells in the injured optic nerve of rat,an optic nerve injury model and an autogeneic common peroneal nerve transplantation model were made.Animals were divided into 3 groups:normal,injury and transplantation groups.Neural precursor cells from the optic nerve were cultured in vitro.Morphology and number of the neurospheres formed by neural precursor cells of optic nerve in different groups were measured under a phase contrast microscope.Cells were identified by immunofluorescent cytochemical staining.The results showed that less and smaller neurospheres were found in normal group.Most of the cells were nestin-,GFAP-or GC-immunoreactivity in the neurosphere.The total number of neurospheres somewhat increased after optic nerve injury,but the big neurospheres and the nestin-,GFAP-or GC-positive cells decreased obviously.The number of different kinds of neurospheres increased largely after common peroneal nerve transplantation,the nestin-,GFAP-or GC-positive cells obviously increased too.All results suggest that there are less neural precursor cells with weak proliferation in adult rat optic nerve.Neural precursor cells are also injured after the optic nerve injury and its proliferation is depressed.Nerve autograft may protect the neural precursor cells and facilitate its proliferation.

Objective To investigate the dedifferentiation of neuroglial cells and its induction after optic nerve injury. Methods Adult male SD rats were randomly divided into 4 groups the normal control group,the injury group,the transplantation group and the microcrush and transplantation group.Optic nerves were harvested at days 3,7,14 and 28 after the operation.HE staining was used to count the number of neuroglial cells.Immunohistochemistry,Western blotting and in situ hybridization histochemistry were employed together with computerized image analysis to evaluate the expressions of Nestin,GFAP,MBP,NF,BDNF,Nogo-A and Nogo-A mRNA.Immunofluorescence double staining was used to detect the co-expression of Nestin and GFAP or Nestin and MBP. Results The number of cells only increased at day 7 after the nerve injury, the expressions of Nestin,MBP,Nogo-A and Nogo-A mRNA were up-regulated,the expressions of GFAP,NF and BDNF were down-regulated,and some Nestin-GFAP positive cells and a few of Nestin-MBP positive cells were detected in the injury group.Compared with the injury group,the number of cells was increased sometime after the nerve injury;the expressions of Nestin,GFAP,BDNF and NF were up-regulated,the expressions of MBP,Nogo-A and Nogo-A mRNA were down-regulated,and the number of Nestin-GFAP positive cells increased in the transplantation group and the microcrush and transplantation group.Conclusion After optic nerve injury,some astrocytes undergo dedifferentiation while the macroglial cells display a gene expression pattern that is unfavorable for nerve regeneration.Pre-degenerated peripheral nerves could enhance the dedifferentiation of astrocytes and induce the gene expression pattern of macroglial cells that is favorable for nerve regeneration.

The aim of this study is to find out changes of gene expression profile in injured optic nerves and the effect of autograft predegenerated nerves on it.SD rats were randomly divided into normal group,injury group and nerve transplantation group.On day 7 post operation,intraorbital optic nerves were harvested for detecting the changes of gene expression profile with Agilent Oligo chips.After that,the gene expression profile was confirmed with real-time quantitative PCR,immunohistochemistry and Western Blot.Compared with the normal group,1 340 genes were up-regulated and 940 genes were down-regulated in the injury group.Some genes associated with dedifferentiation,such as genes expressing in the early stage of nerve development,were up-regulated.There were notably differential expressions for some genes related to transcription,apoptosis,proliferation,growth,differentiation or intracellular signal transduction.gene expression changes mostly benefit optic nerve regeneration;but some changes were remarkably related to inhibition of nerve regeneration.Compared with the injury group,106 genes were up-regulated,and 14 genes were down-regulated in the nerve transplantation group,some of which were related to cell dedifferentiation.After optic nerve injury,about 1/10 genes were differentially expressed,some of which might be related to dedifferentiation.Predegenerated peripheral nerves could partially regulate the gene expressions in the injured optic nerves,and stimulate the dedifferentiation of glial cells which finally promote optic nerve regeneration.

视神经在位置上属周围神经系统,但其发育、结构和功能等均具中枢神经系统特性.由于其独特的位置关系,便于暴露,易于建立视神经损伤动物模型.视神经损伤动物模型已成为人们研究中枢神经系统损伤或疾病的突破口,故探讨视神经损伤后再生,对中枢神经系统疾病的治疗或促进中枢神经系统损伤后功能恢复等有重要意义.视神经损伤后,90%～95%视网膜节细胞(RGC)发生凋亡性死亡,受损神经也出现了一系列形态结构变化,如损伤局部组织变性坏死,释放炎性因子;血管充血,血浆和细胞成分渗出,组织水肿;成纤维细胞和巨噬细胞向伤处迁移;局部神经胶质细胞增生、肥大,星形胶质细胞大量表达胶质纤维酸性蛋白(GFAP),最后形成胶质疤痕;少突胶质细胞中抑制轴突生长的因子,尤其是髓鞘源性的抑制因子表达增加;神经营养因子的运输被阻断或减少.这些变化形成了视神经轴突再生的抑制性微环境.目前研究表明视神经损伤后RGC轴突能够再生[1],且RGC存活率已经可以提高到满足视神经再生的要求,但再生的抑制性微环境往往使再生轴突初始发芽萎缩而导致视神经再生失败.因此,视神经再生微环境的调控越来越成为视神经再生研究的焦点.

To investigate the dedifferentiation of glia cells and the expression of related molecules after optic nerve(ON)injury. The expressions of Nestin,glia fibrillary acidic protein(GFAP),myelin bas- ic protein(MBP),neurofilament protein(NF)and Nogo-A mRNA were observed by immunohistochemistry and in situ hybridization bistochemistry with Biosens Digital Imaging System at 3,7,14 and 28 days after ON tran- section in adult male rats. The expression of nestin was up-regulated and the peak expression appeared at 28th day post-operation.The expression of GFAP was down-regulated initially with the lowest level appearing at the 7tb day after ON injury and then up-regulated gradually.MBP level increased firstly and then decreased.The expression of NF was down-regulated remarkably.Levcl of Nogo-A mRNA presented an ascending trend,especially from the 3rd day to the 7th day. These changes of related molecules expression suggest that the glia cells might be induced to dedifferate into neural progenitor cells or neural stem cells, but these cells are not benefitial for ON regeneration.

Accurate estimates of forest productivity are required for sustainable forest management. Sixty-five jack pine (Pinus banksiana Lamb.) plantations (<50 years of age) were sampled to develop height growth and variable growth intercept (GI) models for jack pine plantations in northern Ontario, Canada. Based on the residual plots and model-fitting statistics, these models can be recommended for estimating site index (SI) of young (<40 years) jack pine plantations. To compare SI of plantations with that of natural stands, we used stem-analysis data from 383 plots of natural jack pine stands (aged 50–157 years) from the same geographic region to develop the GI models for natural stands. Also, polymorphic SI curves were developed for young (<40 years) plantations in northern Ontario. These SI curves were different from those for natural stands. Jack pine plantations had a higher site quality (SI) than did the original natural stands on the similar sites. The SI curves developed from natural stands should not be used to predict growth and yield of jack pine plantations before they are calibrated for jack pine plantations. These GI models will be used to estimate SI for silviculture and forest-management planning.