Mode Of Degeneration Research Articles

Arabidopsis BECLIN1-induced autophagy mediates reprogramming in tapetal programmed cell death by altering the gross cellular homeostasis

In flowering plants, the tapetum degeneration in post-meiotic anther occurs through developmental programmed cell death (dPCD), which is one of the most critical and sensitive steps for the proper development of male gametophytes and fertility. Yet the pathways of dPCD, its regulation, and its interaction with autophagy remain elusive. Here, we report that high-level expression of Arabidopsis autophagy-related gene BECLIN1 (BECN1 or AtATG6) in the tobacco tapetum prior to their dPCD resulted in developmental defects. BECN1 induces severe autophagy and multiple cytoplasm-to-vacuole pathways, which alters tapetal cell reactive oxygen species (ROS)-homeostasis that represses the tapetal dPCD. The transcriptome analysis reveals that BECN1- expression caused major changes in the pathway, resulting in altered cellular homeostasis in the tapetal cell. Moreover, BECN1-mediated autophagy reprograms the execution of tapetal PCD by altering the expression of the key developmental PCD marker genes: SCPL48, CEP1, DMP4, BFN1, MC9, EXI1, and Bcl-2 member BAG5, and BAG6. This study demonstrates that BECN1-mediated autophagy is inhibitory to the dPCD of the tapetum, but the severity of autophagy leads to autophagic death in the later stages. The delayed and altered mode of tapetal degeneration resulted in male sterility.

Five-year outcomes of transcatheter mitral valve implantation and redo surgery for mitral prosthesis degeneration.

Transcatheter mitral valve replacement (TMVR) has emerged as a feasible alternative to redo surgical mitral valve replacement (SMVR) in patients with degenerated mitral prostheses, with limited comparative data. We compared mid-term outcomes in patients with degenerated mitral valve prostheses treated with TMVR or redo SMVR. The primary endpoint was survival at 5 years of follow-up. From 2014 to 2020, 215 patients presented with degenerated mitral valve prostheses. Of whom 86 (40%) were treated with TMVR (75[87%] valve-in-valve and 11[13%] valve-in-ring), while 129 patients (60%) underwent SMVR. The TMVR cohort was older (p < 0.0001), more symptomatic (p = 0.0003) and had more chronic lung disease (p = 0.02), worse renal function (p = 0.02) and higher right ventricular systolic pressures (p < 0.0001). Thirty-day mortality was lower with TMVR versus SMVR (2.4% vs. 10.2%, OR4.69 [95% CI 1.25-30.5], p = 0.04) with probability of mortality at 1, 2, and 5 years being 14.7% versus 17.5%, 24.5% versus 20.7%, and 49.9% versus 34.0%, respectively. Mode of prosthesis degeneration, baseline hemodynamics, and valve selection did not appreciably impact outcomes. TMVR for degenerated mitral prostheses is associated with better early survival compared to SMVR despite a greater burden of comorbidities. In contrast, 5 year survival rates appear more favorable with SMVR, which may reflect the lower baseline risk of this population. Clinical, hemodynamic, and echocardiographic follow-up support the mid-term durability of TMVR for degenerated mitral prostheses. Further dedicated studies, however, are required to optimize outcomes in this challenging patient cohort and to navigate the choice of approach for each individual patient.

Mitoautophagy: A Unique Self-Destructive Path Mitochondria of Upper Motor Neurons With TDP-43 Pathology Take, Very Early in ALS.

Mitochondrial dysfunction is one of the converging paths for many neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), and TDP-43 pathology is the most common proteinopathy detected in ALS and ALS/Frontotemporal lobar degeneration (ALS/FTLD). We recently identified mitochondrial problems in corticospinal motor neurons (CSMN) and in Betz cells of patients with TDP-43 pathology. However, the timing and the extent of mitochondrial defects, and their mode of degeneration have not been revealed. Because it is important to reveal when problems first begin to emerge and whether they are shared or unique, we investigated the health and integrity of mitochondria in CSMN of prpTDP-43A315T, PFN1G118V, and hSOD1G93A mice at P15 (post-natal day 15)—a very early age in mice without any sign of cellular degeneration.Utilization of immuno-coupled electron microscopy for a detailed surveillance of mitochondria in CSMN and other non-CSMN cells revealed presence of a novel self-destructive path of mitochondrial degeneration, which we named mitoautophagy. Mitoauthopgy is different from mitophagy, as it does not require autophagosome-mediated degradation. In contrast, in this novel path, mitochondria can clear themselves independently. We find that even at this early age, all diseased CSMN begin to display mitochondrial defects, whereas mitochondria in non-CSMN cells are healthy. Our findings not only reveal mitoautophagy as a novel path of mitochondrial clearance that occurs prior to neuronal vulnerability, but it also highlights that it is present mainly in the upper motor neurons of prpTDP-43A315T and PFN1G118V mice, which mimic many aspects of the disease in patients with TDP-43 pathology.

LGMD AUTOSOMAL RESSESSIVE AND DOMINANT: P.99Limb-girdle muscular dystrophy 2Z in a Bulgarian family

Mutations in POGLUT1 (protein O‐glucosyltransferase 1), an enzyme involved in Notch posttranslational modification and function have been recently identified as causing a new type of limb-girdle muscular dystrophy, known as LGMD2Z. The clinical features of the identified patients encompassed variable clinical onset from 1st to 5th decade, muscle weakness predominantly in the proximal lower limbs, followed by upper limb involvement and wheelchair confinement. We report a Bulgarian family with three affected sisters, homozygous for R98W mutation in POGLUT1. They underwent neurological examination, electromyography, measurement of creatine kinase, ventilatory assessment, electrocardiography, echocardiography and muscle muscle magnetic resonance imaging (MRI). The initial complaints in two of them were noticed at the age of 24-25 years, while in the third- at the age of 44 years. The leading symptoms at onset were muscle weakness in the proximal leg muscles with difficulties in climbing stairs and getting up from squatting position. The involvement of the upper limbs was noticed between 6 and 23 years after the lower limb weakness. CK was within normal range in all three affected. The cardiac function seamed spared, mild restrictive respiratory involvement was observed in only one of the sisters. MRI of the legs revealed early fatty replacement of internal regions of thigh muscles and sparing of the external areas. In conclusion POGLUT1 mutations are associated with late onset AR LGMD with specific MRI pattern of inside-to-outside mode of fatty degeneration in the lower limbs.

Influence of osteoclasts and osteoprotegerin on the mode of calcific degeneration of aortic valves.

Calcific aortic valve disease is associated with inflammation and calcification, thus the osteoprotegerin (OPG), receptor activator of nuclear factor κB (RANK) and its ligand (RANKL) system involved in osteoclastogenesis and inflammation may play a significant role in valve degeneration. The aim of this study was to assess whether circulating OPG, sRANKL, and other bone metabolism markers can predict the presence of osteoclasts in stenotic valves and to evaluate their impact on the mode of degeneration. The study involved 60 patients with aortic stenosis who underwent valve replacement surgery and subsequently were divided into 2 groups: osteoclastic (n = 12) and nonosteoclastic (n = 48), according to the presence or absence of intravalvular osteoclasts. Before the surgery, we measured serum levels of OPG, sRANKL, osteocalcin, osteopontin, tumor necrosis factor α (TNF-α), interleukin (IL) 1β, and IL-6. Immunohistochemistry and morphometry were used to determine the extent of valve calcification, lipid accumulation, neovascularization, and the number and phenotype of macrophages. Compared with the nonosteoclastic group, patients with intravalvular osteoclasts had lower levels of OPG (P = 0.0006) and TNF-α (P = 0.02) and less frequently had diabetes (P = 0.04). Their valves showed higher incidence of ossification (P = 0.002), higher total (P = 0.008) and M2 macrophage counts (P = 0.0002), increased neovascularization (P = 0.003), and lower accumulation of lipids (P = 0.04). They also showed a negative correlation between valve calcification and age (r = -0.79, P = 0.002), which was not observed in patients without osteoclasts. In a multivariate analysis, low circulating OPG levels and the absence of diabetes were predictors of intravalvular osteoclastic differentiation. The presence of osteoclasts in stenotic valves associated with low circulating OPG levels and an enhanced proportion of M2 macrophages can represent a variant of calcific aortic valve disease with a specifically regulated calcification process.

Diverse cellular and molecular modes of axon degeneration.

The elimination of large portions of axons is a widespread event in the developing and diseased nervous system. Subsets of axons are selectively destroyed to help fine-tune neural circuit connectivity during development. Axonal degeneration is also an early feature of nearly all neurodegenerative diseases, occurs after most neural injuries, and is a primary driver of functional impairment in patients. In this review we discuss the diversity of cellular mechanisms by which axons degenerate. Initial molecular characterization highlights some similarities in their execution but also argues that unique genetic programs modulate each mode of degeneration. Defining these pathways rigorously will provide new targets for therapeutic intervention after neural injury or in neurodegenerative disease.

Special Lagrangian curvature

We define the notion of special Lagrangian curvature, showing how it may be interpreted as an alternative higher dimensional generalisation of two dimensional Gaussian curvature. We obtain first a local rigidity result for this curvature when the ambient manifold has negative sectional curvature. We then show how this curvature relates to the canonical special Legendrian structure of spherical subbundles of the tangent bundle of the ambient manifold. This allows us to establish a strong compactness result. In the case where the special Lagrangian angle equals (n − 1)π/2, we obtain compactness modulo a unique mode of degeneration, where a sequence of hypersurfaces wraps ever tighter round a geodesic.

The Temporal Dynamics of Processes Underlying Y Chromosome Degeneration

Y chromosomes originate from ordinary autosomes and degenerate by accumulating deleterious mutations. This accumulation results from a lack of recombination on the Y and is driven by interference among deleterious mutations (Muller's ratchet and background selection) and the fixation of beneficial alleles (genetic hitchhiking). Here I show that the relative importance of these processes is expected to vary over the course of Y chromosome evolution due to changes in the number of active genes. The dominant mode of degeneration on a newly formed gene-rich Y chromosome is expected to be Muller's ratchet and/or background selection due to the large numbers of deleterious mutations arising in active genes. However, the relative importance of these modes of degeneration declines rapidly as active genes are lost. In contrast, the rate of degeneration due to hitchhiking is predicted to be highest on Y chromosomes containing an intermediate number of active genes. The temporal dynamics of these processes imply that a gradual restriction of recombination, as inferred in mammals, will increase the importance of genetic hitchhiking relative to Muller's ratchet and background selection.

Glial cell-mediated spread of retinal degeneration during detachment: A hypothesis based upon studies in rabbits

In human subjects with peripheral retinal detachments, visual deficits are not restricted to the detached retina but are also present in the non-detached tissue. Based upon studies on a rabbit model of rhegmatogenous retinal detachment, we propose a glial cell-mediated mechanism of spread of retinal degeneration into non-detached retinal areas which may also have importance for the understanding of alterations in the human retina. Both detached and attached portions of the rabbit retina display photoreceptor cell degeneration and cystic degeneration of the innermost layers. An inverse mode of photoreceptor cell degeneration in the attached tissue suggests a disturbed support of the photoreceptor cells by Müller cells which show various indications of gliosis (increased expression of intermediate filaments, cell hypertrophy, decreased plasma membrane K + conductance, increased Ca 2+ responsiveness to purinergic stimulation) in both detached and attached tissues. We propose that gliotic alterations of Müller cells contribute to the degeneration of the attached retina, via disturbance of glial homeostasis mechanisms. A down-regulation of the K + conductance of Müller cells may prevent effective retinal K + and water clearance, and may favor photoreceptor cell degeneration and edema development.

Axonal dystrophy of dorsal root ganglion sensory neurons in a mouse model of Niemann–Pick disease type C

Niemann–Pick disease type C (NP-C) is a progressive and fatal neurological disorder characterized by intracellular accumulation of cholesterol and glycolipid. A Balb/c-npc1 mutant strain is a genetically authentic murine model of NP-C, and homozygous mice show progressive weight loss and tremor or ataxia until death at 12–14 weeks of age. Neuropathologically, this model is known to faithfully reproduce the cardinal histologic features of NP-C including neuronal storage, appearance of swollen axons (spheroids), and neuronal loss, although the cellular mechanisms of neural degeneration are largely unknown. To investigate the mode of neural degeneration of sensory neurons in NP-C, we studied the central processes of dorsal root ganglion (DRG) neurons at the level of the medullary dorsal column nuclei and the spinal dorsal horn with special attention to the ultrastructural changes of presynaptic axon terminals. The appearance of axonal spheroids in the dorsal column nuclei and the loss of axons in the spinal nerve roots were assessed quantitatively. We show that the gracile nuclei develop numerous axonal spheroids after only 3 weeks. At 6 and 9 weeks, dystrophic axons, which were separated from simple axonal spheroids by the ultrastructural presence of distinctive tubulo-vesicular elements, progressively increased in size and number. These neuropathological findings are identical to those of gracile axonal dystrophy (GAD) of the normal aging mouse. Presynaptic elements were exclusively involved in spheroid formation. The cuneate nuclei and the spinal dorsal horn revealed fewer axonal spheroids and only rare dystrophic changes. This was associated with a significant drop in the number of L4–5 dorsal root axons in NP-C mouse at 9 weeks of age compared with controls. These results support the existence of a length-dependent axonopathy in the central processes of DRG neurons and are consistent with the view that altered axonal transport, which is implicated in the pathogenesis of GAD in physiological aging, may be an underlying mechanism in neuronal degeneration in NP-C. Clinically, the premature development of GAD may be responsible for ataxia, one of the early manifestations of this disease.

Exposure of sperm head equatorin after acrosome reaction and its fate after fertilization in mice.

Equatorin is a sperm head equatorial protein, possibly involved in sperm-oocyte fusion (Toshimori et al., Biol Reprod 1998; 59:22-29). In the present work, we have shown that equatorin contained in the posterior acrosome is detectable only after spontaneous or induced acrosome reactions following fixation and permeabilization, but not in intact spermatozoa. The presence of protease inhibitors during sonication or ionophore treatments does not inhibit the exposure of the antigenic epitope. The zona-penetrated spermatozoa lying in the perivitelline space display equatorin, similar to those of the acrosome-reacted ones. After sperm-egg fusion during in vitro fertilization (IVF), the equatorin dissociates from the sperm head equatorial region and remains at the vicinity of the decondensing male pronuclei. During pronuclear apposition stage, it is pushed away from the pronuclei, possibly by the perinuclear microtubules. After first cleavage, equatorin is inherited by one of the proembryonic cells. The residual equatorin disappears after the second cleavage. Microinjected whole spermatozoa or sperm heads into the MII stage oocytes display equatorin similar to those of the perivitelline sperm. After activation, it dissociates from the sperm nuclei in a similar manner as during IVF. The mode of equatorin degeneration during fertilization is similar to those of the sperm tail components or mitochondria, but different from those of the membrane associated proteins.

Characterization of spinal motoneuron degeneration following different types of peripheral nerve injury in neonatal and adult mice

Experimental lesions have been used widely to induce motoneuron (MN) degeneration as a model to test the ability of different trophic molecules to prevent lesion-induced alterations. However, the morphological mechanisms of spinal MN death following different types of lesions is not clear at the present time. In this study, we have characterized the morphological characteristics of MN cell death by examining DNA fragmentation and the ultrastructural and light microscopic morphological features of MNs following different types of spinal nerve injury (i.e., axotomy and avulsion) in the developing and adult mouse. In neonatal mice, axotomy induced cell death as well as the atrophy of MNs that survived the injury. DNA fragmentation could be detected by using the terminal deoxynucleotidyl transferase (TUNEL) method during the cell death process following neonatal axotomy, whereas TUNEL labeling was not observed following either neonatal or adult avulsion. However, with the exception of TUNEL labeling, the morphological characteristics of MN death following neonatal axotomy and avulsion were similar, and both resembled most closely the form of programmed cell death termed cytoplasmic or type 3B, which exhibits similarities as well as differences with currently accepted definitions of apoptosis. By contrast, adult avulsion resulted in a type of degeneration that resembled necrosis more closely. However, even there, the morphology was mixed, showing characteristics of both apoptosis and necrosis. These results indicate that the mode of MN degeneration is complex and is related to developmental age and type of lesion.

Peripheral nerve insult induces NMDA receptor-mediated, delayed degeneration in spinal neurons.

Injury of a peripheral nerve gives rise to adaptive functional and structural alterations in spinal neurons. We report that the rearrangement of the spinal circuitry in response to sciatic nerve transection in adult rats involves a delayed mode of degeneration of lumbar spinal cord neurons. Nuclear fragmentation was detected by the TUNEL technique 7 days after sciatic neurectomy but not after 3 or 14 days. Dying cells were preferentially located in the ipsilateral superficial dorsal horn and expressed the neuronal cytoskeletal marker SMI-31. Degeneration was prevented by continuous systemic treatment with the NMDA receptor-antagonist MK-801. These data are supportive that apoptosis is induced in spinal neurons in a transsynaptic manner by an early signal from injured afferent fibres via activation of spinal NMDA receptors.

An anatomic investigation of the elbow joint, with special reference to aging of the articular cartilage

The architecture of the articular surface of the elbow joint and the location of cartilage degeneration with aging was analyzed. The study included 131 elbow joints of 66 cadavers preserved by embalming. The age of subjects at death ranged from 49 to 96 years (mean 79 years). The elbow joint was observed macroscopically and analyzed. The degenerative changes in the radiohumeral joint were always more advanced than those in the humeroulnar joint. The erosion or chondral defect in the capitulum is located in the area 45° anterior to the long axis of the humerus. The anterior part of the erosion in the crest separating the trochlea from the capitulum was roughly 48.5° to the long axis of the humerus. It was similar in position to the erosion found in the capitulum. Based on the degree and area of cartilage degeneration, the changes in the radial head could be divided into four types. The mode of radial head cartilage degeneration correlated well with cartilage degeneration in the radiohumeral articulation and also with osteoarthritis of the elbow joint. Simplistically, one could classify elbow joint osteoarthritis by knowing the extent of radial head degeneration.

A comparative ultrastructural study of endophytic basidiomycetes in the parasitic achlorophyllous hepatic Cryptothallus mirabilis and the closely allied photosynthetic species Aneura pinguis (Metzgeriales)

This ultrastructural study of two closely related liverworts with contrasting modes of nutrition reveals very similar interactions with endophytic dikaryotic basidiomycetes. In both hepatics, collected from a variety of sites, the fungus is confined to specific regions of the gametophyte thallus, and hyphal contact with the substratum is via the rhizoids. The colonization cycle comprises a growth phase when the fungus forms large intracellular coils, host cytoplasm proliferates and the starch content of the plastids decreases, followed by senescence when the hyphae die back and aggregate into large masses. Repeated colonization cycles are frequent. Young hyphae contain abundant glycogen and sometimes amyloid deposits in Cryptothallus. In terms of dolipore substructure, hyphal dimensions, highly characteristic multilayered walls, absence of clamp connections, and the mode of hyphal degeneration, the endophyte in Cryptothallus is virtually identical to that in Aneura from alpine sites but very different from the fungus in Aneura from sand dunes and a chalk pit. It is suggested that Cryptothallus evolved from an Aneura-like ancestor through association with a fungal saprophyte of waterlogged peaty soils. Differences in dolipore morphology in the ectomycorrhizal fungus of Betula roots growing in association with Cryptothallus indicate that these two hosts do not share the same fungus. Remarkable similarities between the fungal associations in Cryptothallus and Aneura and orchidaceous mycorrhizae include the same colonization cycle, absence of polyphosphate granules, and separation of the host plasma membrane from thin-walled, exclusively intracellular hyphae by a prominent interfacial matrix. Key words: basidiomycetes, dolipores, liverworts, mycorrhiza, symbiosis, ultrastructure.

ビタミンB&lt;sub&gt;6&lt;/sub&gt;（ピリドキシン）大量投与ラットの腰部第一次感覚ニューロンの変性過程

The morphologic effects of the toxicity of high doses of pyridoxine hydrochloride (vitamin B6) on the lumbar primary sensory neurons in rats were studied. The test rats were treated with 1,200 mg/kg of pyridoxine hydrochloride by intraperitoneal injection once a day, and were sacrificed by perfusion at periods ranging from one to seven days after the injection, together with the control rats. Initial lesions consisted of eccentricity and crenation of the nucleus and vacuole formation in the cytoplasm of large dorsal root ganglion neurons, 2 days after the injection. These lesions were followed by segregation of the nucleolus, axon reaction-like changes in the cytoplasm and axonal degeneration of both peripheral axons in the sural nerve and central axons in the fasciculus gracilis. The frequency of teased myelinated fibers showing axonal degeneration during tests was significantly greater than in control 3 to 7 days after the injection. No significant difference of such frequency was found between the proximal and distal sural nerve during tests. The number of large myelinated fibers per nerve in the sural nerve, when compared with control, was preferentially decreased during tests. In the fasciculus gracilis, the decrease of the density of myelinated fibers was more pronounced in the third cervical segment than in the fifth thoracic segment. Because both peripheral and central axons were similarly affected and the initial lesions were found in the neuronal cell body, the mode of degeneration of axons in this study was regarded as "neuronopathy". By both light and electron microscopy, accumulation of mitochondria, vesicles, multilamellar and dense bodies were found in the nodal and distal paranodal axons of myelinated fibers in the sixth dorsal root ganglion on the 2nd day after the injection, which preceded the degeneration of both peripheral and central axons. Such accumulation, revealed for the first time in this study, may reflect the presence of a blockade of the axoplasmic transport in the proximal axon and cell body of the lumbar primary sensory neuron and subsequently give rise to the degeneration of both peripheral and central axons of the lumbar primary sensory neuron. The pathologic alterations at the different sites of the lumbar primary sensory neuron revealed in this study should be taken into consideration for the better understanding not only of the pathogenesis of human pyridoxine-induced sensory neuropathy, but also of other human and experimental neuropathies.

A review of recent observations concerning the synaptic organization of the basilar pontine nuclei.

Ultrastructural studies are described that have identified in the basilar pontine nuclei (BPN), the synaptic boutons formed by the corticopontine, cerebellopontine, tectopontine, and dorsal column nuclei-pontine afferent projection systems. In addition, immunocytochemical studies visualized neuronal somata, dendrites, and synaptic boutons that contain immunoreactivity for GABA or the synthesizing enzyme glutamic acid decarboxylase (GAD). Based upon differences in the mode of degeneration and postsynaptic locus of degenerative synaptic boutons in the BPN, it is suggested that two types of cortical neurons and three classes of deep cerebellar nuclear cells project to the BPN. For similar reasons, it appears that two types of neurons in the dorsal column nuclei project to the BPN while only one type of afferent synaptic bouton takes origin from the superior colliculus. Furthermore it appears that the population of BPN neurons projecting to the paramedian lobule receives convergent inputs from the cutaneous periphery and the corresponding region of sensorimotor cortex. Studies employing GAD immunohistochemistry indicate that GABA-ergic neurons and axon terminals are present in the BPN and thus support the suggestion that a local inhibitory interneuron is present within the BPN. Taken together these observations suggest that basilar pontine neurons might play a more active role in the integration of various types of information destined for the cerebellar cortex than has previously been recognized.

Ultrastructure of normal and degenerating glomerular terminals of dorsal root axons in the substantia gelatinosa of the rhesus monkey.

The fine structure of primary sensory terminals within glomerular complexes of lamina II of Rexed (substantia gelatinosa Rolandi) in the spinal cord was investigated in normal adult rhesus monkeys and in monkeys subjected to thoracic or lumbosacral dorsal root transection. Three types of "scalloped" primary sensory terminals were distinguished on the basis of their ultrastructural characteristics, size, and distribution of synaptic vesicle population: (1) dense sinusoid axon (DSA) terminals contain medium-sized (42--46 nm and 58--62 nm) and large (80 nm) clear synaptic vesicles; (2) large dense-core vesicles (LDCV) terminals are equipped with empty synaptic vesicles ranging from 30 to 106 nm, large, (80 nm) and very large, (100 nm) dense-core vesicles; and (3) regular synaptic vesicles (RSV) terminals contain a homogeneous population of 45--50 nm clear synaptic vesicles. Following transection of the dorsal roots, all three types of primary afferents degenerate and become engulfed and phagocytosed by glial cells. However, each type of terminal displays a different mode and tempo of degeneration as seen in monkeys sacrificed 36, 48, and 72 hours following rhizotomy. DSAs follow the osmiophilic degeneration pattern; LDCVs are characterized by a gradual increase in the number of "electron-dense bodies" and, less frequently, by a progressive osmiophilic process; RSVs exhibit signs of a filamentous degeneration, accompanied by clusters of synaptic vesicles. The three types of terminals are distributed in an overlapping but distinct pattern within the posterior horn. Thus DSAs are present in highest numbers in lamina II where they constitute the most frequent terminal type. LDCVs also occur in lamina II in its outer half but are most concentrated in lamina I. RSVs predominate in the deeper layers of the dorsal horn (lamina III) but are also found in the internal half of lamina II. On the basis of these ultrastructural data and a comparison with afferent profiles impregnated according to the Golgi method, it appears that DSAs and LDCVs correspond respectively to superficial and marginal collaterals of small, thin dorsal root fibers whereas RSVs represent terminals of deep collaterals from large, thick dorsal root axons.

The mode of mitochondrial degeneration in gliomas.

Morphologically abnormal mitochondria from human glial tumours are described. For each tumour both the appearances of the mitochondria, and the subsequent mode of degeneration and formation of osmiophilic pigment is characteristic. The significance of these observations is discussed, and it is suggested that the mode of degeneration observed reflects directly a fundamental abnormality in composition compared to normal mitochondria.

Ultrastructural changes and a second mode of flagellar degeneration during ageing of Phytophthora palmivora sporangia.

Ageing of sporangia in Phytophthora palmivora is accompanied by a gradual breakdown of flagella, a transformation of the 'fingerprint' vacuoles, extensive vacuolization of the cytoplasm, accumulation of bundles of microtubules (mastigonemes)contained within cisternae of the rough endoplasmic reticulum, formation of a germination wall lining the inside of the sporangial wall and production of secondary sporangia. The mechanism of flagellar degeneration differs from that observed in directly germinating sporangia. In ageing sporangia and in sporangia induced to germinate directly with germ tubes, there is a close correlation between loss of competence for zoosporogenesis and breakdown of the flagella.