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Hausmanowa-Petrusewicz, Irena (1917-2015), 1954, Zespoły neurologiczne w chorobach gośćcowych
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INSTYTUT ARCHEOLOGII I ETNOLOGII POLSKIEJ AKADEMII NAUK
INSTYTUT BADAŃ LITERACKICH POLSKIEJ AKADEMII NAUK
INSTYTUT BADAWCZY LEŚNICTWA
INSTYTUT BIOLOGII DOŚWIADCZALNEJ IM. MARCELEGO NENCKIEGO POLSKIEJ AKADEMII NAUK
INSTYTUT BIOLOGII SSAKÓW POLSKIEJ AKADEMII NAUK
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INSTYTUT CHEMII ORGANICZNEJ PAN
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INSTYTUT HISTORII im. TADEUSZA MANTEUFFLA POLSKIEJ AKADEMII NAUK
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INSTYTUT MATEMATYCZNY PAN
INSTYTUT MEDYCYNY DOŚWIADCZALNEJ I KLINICZNEJ IM.MIROSŁAWA MOSSAKOWSKIEGO POLSKIEJ AKADEMII NAUK
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SIEĆ BADAWCZA ŁUKASIEWICZ - INSTYTUT TECHNOLOGII MATERIAŁÓW ELEKTRONICZNYCH
MUZEUM I INSTYTUT ZOOLOGII POLSKIEJ AKADEMII NAUK
INSTYTUT BADAŃ SYSTEMOWYCH PAN
INSTYTUT BOTANIKI IM. WŁADYSŁAWA SZAFERA POLSKIEJ AKADEMII NAUK
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A 30-year-old patient with suspected myopathy was examined. A biopsy of quadriceps sinister wasperformed. Electronmicroscopy analysis revealed normal muscle fibers containing mitochondriacharacterized by light mitochondrial matrix and partly devoid of mitochondrial cristae (Fig. 1).In some mitochondria, there were no cristae and penetration of the cytoplasm were observed. Fewmitochondria contained crystalline inclusions (Fig. 2,3). It suggests mitochondrial myopathy.zenie miopati iFig. zne zmienione strukturalnie mitochondria o jasnej maci
A 31-year-old patient was examined. A biopsy of quadriceps sinister was performed.Electronmicroscopy analysisrevealed normal myofibrils architecture but numerous fat droplets werevisible.
A 31-year-old patient with suspected mitochondrial myopathy was examined. A biopsy of quadriceps sinister was performed.Electronmicroscopy analysis revealed almost unchanged ultrastructure of fibers and normal, located submembranously nuclei. Although myofibers were characterized by preserved sarcomeres structure, significant changes in mitochondria were observed, including swelling and complete loss of mitochondrial cristae. However, the crystalline inclusions in the mitochondria typical for mitochondrial myopathy have not been observed.
A 31-year-old patinet with suspected facioscopulohumeral muscular dystrophy (FHSD) was examined. A biopsy of biceps dexter was performed. In some fibres electronmicroscopy analysis revealed changes in the sarcomeres structure and a local loss of myofibrils. Abnormal, folded nuclei penetrating deep into the cytoplasm with large gap between inner and outer nuclear membrane were observed. Few autophagal srtuctures were seen. The image of specimen suggests nucleopathy. Asseessment of activity of lamin A and ermetrin is advisable.
A 32-year-old patient with suspected myopathy was examined. A quadriceps biopsy was performed. Electron microscopy analysis revealed unchanged muscle fibers structure, however, numerous structures of various diameter, some of them containing glycogen were present (probably mitochondrial remains) (Fig 1,2,3). In some fibers mitochondria were characterized by blurred structure of mitochondrial cristae or were almost completely devoid of cristae. They were swollen and characterized by bright mitochondrial matrix. (Fig 4,5).
A 32-year-old patient with suspected myopathy was examined.Muscle fibers with a preserved myofibril structure were seen, however, significant damage of part ofthe mitochondria was observed - they were swollen and devoid of mitochondrial cristae. Droplets offat were present (Fig. 1,2).Biochemical evaluation of carnitine palmitoyltransferase in the muscle tissue was performed and theresult was 1,30 nM/mgB/min. (Norm 6,5-18 nM/mgB/min.).
A 32-year-old patinet with polymyositis was examined. A biopsy of quadriceps sinister was performed. Ultrastructurally unchanged myofibrils were observed. Fat droplets were seen.
A 32-year-old patinet with suspected metabolic myopathy was examined. A biopsy of quadriceps dexter was proformed. Electronmicroscopy analysis reveald ultrastructurally unchanged muscle fibers, normal structure of majority of mitochondria and unchanged, submembranously located nuclei.
A 33-year-old patient with suspected limb-girdle muscular dystrophy was examined. A biopsy of quadriceps sinister was performed. In some muscle fibers many disrupted and swollen mitochondria characterized by light mitochondrial matrix were seen. Majority of them were partially or even totally devoid of mitochondrial cristae.
A 33-year-old patient with suspected MELAS syndrome was examined. A biopsy of quadricepsdexter was performed.Electronmicroscopy analysis revealed well-preserved myofibres without changes in myofibrils andnuclei and few lipofuscin deposits . In some of type-1 fibers damage within mitochondriawere observed. They were characterized by loss of mitochondrial cristae and light matrix.In the extracellular space structures of bacterial morphology were present. They were scatteredbetween the muscle fibres, no penetration into the fibres was observed.
A 33-year-old patient with suspected myopathy was examined. A biopsy of quadriceps sinister was performed. Muscle fibers showed almost unchanged architecture and normal nuclei located under the sarcolemma but abundant lipofuscin deposits were observed. Altered and swollen mitochondria were seen, some of them were partially or even totally devoid of mitochondrial cristae. In some muscle fibers crystalline inclusions in the mitochondria were observed. Biochemical evaluation of carnitine palmitoyltransferase in the muscle tissue was performed and the result was 4,55 nM/mgB/min. (Norm 6,5-18 nM/mgB/min.).
A 34-year-old-patient with suspected Becker dystrophy was examined. A biopsy of quadriceps sinister was performed. Electronmicroscopy analysis revealed muscule fibers of normal diameter and presenved structure of sarcomers. Morphologically unchanged, located sub-membranously nuclei were seen. Part of mitochondria were significantly damaged, swollen and characterized by a loss of mitochondrial cristae. Some fat droplets were seen.
A 34-year-old patient with suspected myopathy was examined. A biopsy of quadriceps dexter was performed. Electronmicroscopy analysis revealed that some muscle fibers were ultrastructurally unchanged and characterized by normal sarcomere and myofibrils structure (Fig. 1,2). Also muscle fibers of smaller diameter, characterized by the presence of multiply cell nuclei were seen (Fig. 3,4,5,6). At the same time mononuclear myotubes-like muscle fibers showing significant disrupture of the contractile apparatus were observed (Fig. 7,8,9,10,11).
A 34-year-old patinet with suspected laminopathy was examined. A biopsy of quadriceps sinister was perfomed. Electromicroscopy analysis showed unchanged muscule architecture but numerous fat droplets located peripherally were seen. Fat droplets of different diameters were visible also within the muscle fibers. In muscle fibers of smaller diameter, fat structures filled most of the fiber. A metabolic defect was suspected. Bochemical examination of carnitine palmitoyltransferase was performed and the results was 1,78 nM/mgB/min. (Norm 6,5-18 08 nM/mgB/min.)
A 35-year-old patient with suspected metabolic defect was examined. A biopsy of quadriceps sinis-ter was performed. Electron microscopy did not reveal significant changes in muscle fibers architecture, but damaged mitochondria partially devoid of mitochondrial cristae were seen. Also quite numerous fat droplets were observed. A microscopic image suggests defect of mitochondrial enzymes. Biochemical examination of car-nitine palmitoyltransferase in the muscle tissue was performed and the result was 0,15 nM/mgB/min (Norm 6,5-18 nM/mgB/min).
A 37-year-old patient was examined. A biopsy of quadriceps sinister was performed.Muscle fibers with preserved myofibril architecture, characterized by the presence of numerouslarge vacuoles, probably derived from the sarcoplasmic reticulum were seen. Fibers characterized by focal loss of myofibrils and the presence of autophagal structures were observed. In some myofibers abnormal myofibrils and Z-line streaming were seen.Microscopic analysis revealed nonspecific structural changes with features of fiber structure primary damage.
A 37-year-old patient with suspected metabolic myopathy was examined. A biopsy of biceps sinister was performed.Electronmicroscopy analysis revealed no ultrastructural changes in the structure of the muscle fibers contractile apparatus. Cell nucleus located in the center of the fiber, not sub-membranou. Numerous lipid droplets located in the interfibrillar spaces as well as sub-membranous were observed. Sarcomer architecture were unchanged.The observed changes suggests that an assessment of carnitine and palmitylotransferase is necessary
A 37-year-old patient with suspected myopathy was examined. A biopsy of quadriceps dexter was performed.Electronmicroscopy analysis revealed in the majority of the specimen ultrastructurally unchanged muscle fibers of normal myofibrils structure. In some muscle fibers the contractile apparatus is focally altered and sarcomers structure was changed. Also damage to nuclear envelope and ultrastructural abnormalities within nuclei were observed within some cells were observed.
A 37-year-old patient with suspected myopathy was examined. A biopsy of quadriceps dexter was performed.Electronmicroscopy analysis revealed in the majority of the specimen ultrastructurally unchanged muscle fibers of normal myofibrils structure. In some muscle fibers the contractile apparatus is focally altered and sarcomers structure was changed.Also damage to nuclear envelope and ultrastructural abnormalities within nuclei were observed within some cells were observed.
A 38-year-old patient with suspected muscular dystrophy was examined. A biopsy of biceps sinister was performed. Electronmicroscopy analysis revealed some fibers of correct diameter and preserved myofibrils structure. Also fibers with normal located under the sarcolemma nuclei but with visible alterations in the miofibrils architecture were seen.In some fibers, multiply centrally located nuclei were visible, and between the fibers abundant connective tissue was present.Numerous muscle fibers of myotube-like morphology, characterized by small diameter and centrally located nuclei, usually single or in number of two were observed. They showed abnormal sarcomeres structure and loss of A line.Intramuscular nerves characterized by the presence of a 2-3-layer myelin sheath resembling the "onion bulb" structure were observe.Microscopic image of the biopsy suggests congenital fiber-type disproportion (CFTS) associated with defect of actin or tropomyosin.
A 38-year-old patient with suspected myopathy was examined. A biopsy of quadriceps sinister was performed.Myofibres with unchanged structure of myofibrils, sarkomers and normal sub membranous nuclei(Fig. 1).In some of type 1 muscle fibres destroyed mitochondria, characterized by light mitochondria matrixand lack of cristae were observed.In the biopsy there were no changes characteristic for congenital fiber type disproportion, observedin case of patient's son (Case 14/11).
A 38-year-old patient with suspicion of chronic neurogenic injury was examined. A biopsy ofbiceps dexter was performed.Electron microscopy analysis revealed atrophied muscle fibers characterized by accumulationof cell nuclei. Irregular arrangement of myofibrils were observed in many fibers.Numerous fat droplets were seen.
A 39-year-old patient was examined. A biceps biopsy was performed.Electronmicroscopy analysis revealed fibers characterized by disruption of the contractile apparatusand with A line loss in the sarcomeric system.Mononuclear fibers of small diameter, showing the features of immaturity, perhaps in the course ofregeneration, also show changes in the structure of sarcomers. Swollen mitochondria partly devoidof mitochondrial cristae were observed.Single "vacuoles", probably originating from distended sarcoplasmic reticulum channels were seen.
A 39-year-old patient with suspected metabolic myopathy was examined. A biopsy of quadriceps sinister was performed. Electron microscopy analysis revealed the presence ultrastructurally unchanged muscle fibers (Fig 1). Capillaries with features of endothelial necrosis were seen. (Figure 2). Large droplets of fat and vacuolar structures were present under the sarcolemma of some muscle cells (Fig. 3,4).
A 39-year-old patient with suspected metabolic myopathy was examined. A biopsy of quadricepssinister was performed.Electronmicroscopy analysis did not revealed significant changes in myofibres and nuclei structure,but numerous fat droplets within the muscle fibers were observed.A defect of mitochondrial enzymes was suspected. Biochemical examination of carnitinepalmitoyltransferase is advisable.
A 39-year-old patient with suspected mitochondrial myopathy was examined.Unchanged muscle fibers and normal, submembrane located nucleus were visible . In some fibers we observed mitochodria of small diameter, electron dense mitochondrial matrix and blurred mitochondrial cristae.In some myofibers, the sarcomer structure was preserved, but mitochondria were swollen, characterized by light mitochondrial matrix and partially or completely devoid of mitochondrial cristae. In some myofibers except disrupted mitochondria we observed damages in contractile apparatus.
A 4-year-old patient was examined. A biceps sinister biopsy was performed.Muscle fibers showing signs of damage, necrosis, serious rupture of the contractile apparatus, char-acterised by presence of completely destroyed mitochondria and numerous vacuoles were seen.Electron microscopy analysis revealed also abnormalities in the structure of cell nuclei. Abundant connective tissue was observed.
A 4-year-old patient with congenital miopathy was examined. A biceps sinister biopsy was performed.Electronmicroscopy analysis revealed damaged, swollen mitochondria characterized by lightmitochondrial matrix and significant loss of mitochondrial cristae. Cell nuclei in some muscle fiberswere located centrally. Numerous fat droplets were visible.Carnitine level in the muscle tissue within the normal range (34,65 nM/mgB; norm 17-48nM/mgB)
A 4-year-old patient with suspicion of spinal muscular atrophy was examined. A quadriceps biopsy was performed. Electronmicroscopy analysis of the biopsy revealed single fibers of the diameter characteristic for age and unchanged structure. Small diameter fibers with the features of the myotube with centrally located, single nuclei predominate. A massive accumulation of connective and adipose tissue between the fibers was observed.Microscopic image of the biopsy suggests the arrest of fiber development in the early stage of myogenesis
A 40-year-old patient with congenital myopathy was examined. A biceps sinister biopsy wasperformed.Electronmicroscopy analysis revealed presence of normal diameter muscle fibers. They werecharacterized by preserved myofibrils and sub-membranous located cell nuclei but damage to nuclearenvelope and ultrastructural abnormalities within nuclei were observed. In some fibres focal ruptureof contractile apparatus was observed.Also fibers of small diameter characterized by decay of contractile apparatus were seen.The accumulation of a large amount of autophagal structures was observed. In some fibres almostthe entire muscle fiber was filled by autophagal structures.
A 40-year-old patient with muscle pain in the lower extremities was examined. A biceps biopsy was performed. Electronmicroscopy analysis revealed normal myofibrils structure. Although, quite numerous fat droplets were visible and we observed mitochondria swelling (Fig. 1,2,3).A defect of mitochondrial enzymes was suspected. Biochemical evaluation of carnitine palmitoyltransferase in the muscle tissue is advisable.
A 40-year-old patient with suspected facio-scapulo-humeral dystrophy (FSHD) was examined. Abiceps biopsy was performed.On the cross-section of some normal diameter fibres, myofibrillles arranged circumferentially andforming “ring binden” structures were observed.Atrophied fibres characterized by accumulation of nuclei were seen.Some mononuclear muscle fibers of small diameter with myotube-like morphology showingsignificant disrupture of the contractile apparatus were observed.Some of neuromuscular junctions were characterized by poor postsynaptic apparatus.Nerve fibres with the characteristics of “onion bulb” were seen.
A 40-year-old patient with suspected metabolic myopathy was examined. A biceps sinister biopsy was performed.Muscle fibres of a diameter within a normal range, with preserved myofibril architecture,separatedby a trace amount of connective tissue were seen. Quite numerous droplets of fat, located mainly under sarcolemma were observed.
A 41-year-old patient with suspected metabolic miopathy was examined. A biopsy of quadricepssinister was performed.Majority of muscle fibers showed normal diameter and architecture, unchanged, laying undersarcolemma nuclei were seen.Electron microscopy revealed numerous fat droplets within the muscle fibers.Abnormal mitochondria with crystalline inclusions were observed.A defect of mitochondrial enzymes was suspected. Biochemical evaluation of carnitinepalmitoyltransferase in the muscle tissue was performed and the result was 1,5 nM/mgB/min. (Norm6,5-18 nM/mgB/min.).Microscopic image of the biopsy and reduced carnitine palmitoyltransferase suggest metabolicmyopathy CPT deficiency type.
A 41-year-old patient with suspected structural defect was examined. A biopsy of quadriceps sinister was performed.Atrophic muscle fibers characterized by loss of myofibrils and accumulation of cell nuclei.Ultrastructurally altered mitochondria characterized either by blurred mitochondrial cristae or partially/completely devoid of them. Submembrane focal glycogen accumulation was seen.In some myofibers mitochondria with dark mitochondrial matrix and a blurred structure of mitochondrial cristae were observed. Lysosomes were visible.
A 42-year-old patient with suspected polymyositis was examined. A biceps dexter biopsy was performed. Electron microscopy analysis revealed unchanged muscle fibers and mitochondria structure. Numerous lipid droplets were seen (Fig 1,2). Defect of mitochondrial enzymes was suspected.Biochemical examination of carnitine palmitoyltransferase was performed and the result was 0,37 nM/mgB/min (norm 6,5-18 nM/mgB/min.). Carnitine level in the muscle was 13,79 nM/mgB (norm 17-48 nM/mgB).
A 43-year-old patient was examined. A biceps biopsy was performed. Electronmicroscopy analysis revealed the presence of fat droplets and lipofuscin with in the muscle fibers.We observed focal accumulation of glycogen and presence of myelin-like bodies. A defect of mitochondrial enzymes was suspected.Biochemical assesment of carnitine palmitotransferase is advisable.
A 43-year-old patient was examined. A biopsy of quadriceps dexter was performed.Electronmicroscopy analysis revealed normal ultrastructure of muscle fibers. Unchanged nuclei, mitochondria and a few fat droplets laying submembranous were visible.
A 43-year-old patient with polineuropathy was examined. A biopsy of quadriceps sinister was perfomed. Electronmicroscopy analysis revealed numerous changes in the nuclei structure including loss of the unclear membrane and penetration of the sarcoplasm into the nucleus as well as seperation of the outer and inner nuclear envelopes with the formation of vacuoles adjacent to nuclei. Abundant connective tissue was abserved between the muscule fibers. Ultrastructural image of the biopsy suggests a defect of lamin B receptor.
A 44-year-old patient was examined. A biopsy of biceps sinister was performed. The muscle fibers with preserved myofibril structure and unchanged sarcomeric arrangement were observed. Myocytes were characterized by massive deposition of granulo-filamentous, electron-dense material
A 44-year-old patient with fatique and suspected myopathy was examined. A biopsy of quadriceps sinister was performed. Electronmicroscopy analysis revealed well-preserved myofibres and quite numerous lipid droplets (Fig. 1,2). Ultrastructurally unchanged nucleus laying under sarcolemma was seen but at the same time mitochondrial damage was significant – they were characterized by light mitochondrial matrix and lack of cristae. (Fig. 3).
A 44-year-old patinet with suspected polymyositis was examined. A biopsy of quadriceps was performed. Utrastructurally , a part from the infilltration of inflammatory cells, there were no signs of inclusion body myositis (no inclusions characteristic for this disease were observed).
A 46-year-old patient with suspected metabolic myopathy was examined. A biceps sinister biopsywas performed.No ultrastructural changes in muscle fibers structure were observed. Electron microscopyanalysis revealed unchanged intramuscular nerves and normal normal structure of neuromuscular junctions.
A 47-year-old patient with suspected limb-girdle muscular dystrophy was examined. A bicepssinister biopsy was performed.The correct diameter muscle fibers exhibiting ultrastructural changes within the mitochondria wereseen. Mitochondria damaged, swollen, characterized by light matrix and significant loss of mitochondrial cristae or completely devoid of mitochondrial cristae. Fat droplets were observed. Muscle fibers of very small diameter and one centrally located cell nucleus werepresent in the biopsy. Numerous lymphoid cells were visible around the vessel. In the extracellularspace structures of bacterial morphologywere present. No penetration intothe fibres was observed.
A 48-year-old patient was examined. A biopsy of biceps sin. was performed.No significant ultrastructural changes in muscle fibers were observed, myofibrils structure was preserved. Electronmicroscopy analysis revealed the presence of few fat droplets within the muscle fibers and small lipofuscin deposits under sarcolemma.
A 48-year-old patient with suspected myopathy was examined. A biopsy of biceps dexter was perforle umed. Electronmicroscopy analysis revealed normal diameter and ultrastructure of muscle fibers, sarcomere pattern was preserved. Morphologically unchanged nuclei located under the sarcolemma were seen. Numerous fat droplets were observed.
A 48-year-old patient with suspected myopathy was examined. A biopsy of quadriceps sinister wasperformed.Muscle fibers of various diameters: normal, atrophic (characterized by accumulation of nuclei) andhypertrophic fibers were observed in the biopsy. The fibers of the normal diameter revealedunchanged ultrastructure and preserved sarcomeres system. Most of mitochondria were unchanged.Some fat droplets were seen.In some fibers part of mitochondria showed signs of swelling and cristae damage
A 5-month-old patient with suspected myasthenic syndrome was examined. A biopsy of quadricepswas performed. Electronmicroscopy analysis revealed numerous ultrastructural abnormalities ofmuscle fibers with features of immaturity. Local disintegration of myofibrils and swollenmitochondria were observed. Mitochondria were characterized by partial or total lack ofmitochondrial cristae. Massive glycogen depositions were seen (Fig. 1,2). In some part of myocytesloss of myofibrils were visible. Empty areas were filled with homogeneous myofibril-like material(Fig. 3).Multi-shaped nuclei with the characteristic accumulation of heterochromatin and cleavageofthe outer nuclear membrane were observed. Mitochondria were swollen, with blurred cristae andmitochondrial membranes (Fig 4,5,6). Nuclei of irregular shape with clear features of nucleopathy(disrupted nuclear membrane, mitochondria within the nuclei) were seen (Fig 8,9).
A 50-year-old patient with suspected limb-girdle muscular dystrophy was examined. A biopsy of quadriceps sinister was performed. Electronmicroscopy analysis revealed normal ultrastructure of muscle fibers. The sarcomeres were preserved. Normal nuclei located under sarcolemma were observed. Majority of mitochondria were unchanged, in few loss of mitochondrial cristae was seen. Few fat droplets were present..No fibers of smaller diameter were found in the biopsy.
A 50-year-old patient with suspected myopathy or polymyositis. Electronmicroscopy analysis did not reveal significant ultrastructural changes. Normal, located under sarcolemma nuclei were seen and a few lipid droplets were observed. In some mitochondria damage of cristae was visible
A 50-year-old patient with suspected myopathy was examined. A biopsy of quadriceps sinister was performed. Electronmicroscopy analysis revealed the presence of fat droplets within the muscle fibers (Fig. 1,2,3). Altered mitochondria characterized by light mitochondrial matrix and devoid of cristae were observed (Fig.4). A defect of mitochondrial enzymes was suspected. Biochemical examination of carnitine palmitoyltransferase was performed and the result was 6,73 nM/mgB/min. (Norm 6,5-18 nM/mgB/min.)
A 50-year-old patient with suspected myopathy was examined. A biopsy of quadriceps sinister was performed. Electronmicroscopy analysis revealed unchanged myofibrils structure but quite numerous fat droplets were visible (Fig. 1,2). Mitochondrial ultrastructure was preserved, and sub-membranously located cell nuclei were seen (Fig. 3,4). Normal structure of the neuromuscular junction was observed but some mitochondria were characterized by partial lack of mitochondrial cristae (Fig. 5,6,7,8,9).Defect of mitochondrial enzymes was suspected. Biochemical examination of carnitine palmitoyltransferase in the muscle biopsy was performed and the result was 2,13 nM/mgB/min (norm 6,5-18 nM/mgB/min.).
A 51-year-old patient with suspected metabolic myopathy was examined. A biopsy of quadricepssinister was performed.Muscle fibers with fairly well preserved morphology, however, serious damage within themitochondria was observed. They were characterized by partial or total lack of mitochondrialcristae and a light mitochondrial matrix.. In some fibers rupture of contractileapparatus and numerous fat droplets were seen.
A 51-year-old patient with suspected polymyositis was examined. A biopsy of quadriceps sinisterwas performed.Muscle fibers of varying diameter, showing signs of contractile apparatus damage were visible. Insome of them also breaks in the nuclear envelope were observed.Numerous fat dropletslocated sub-membranous were seen.Muscle fibers characterized by accumulation of cell nuclei were observed.Microscopic image of the biopsy suggests diagnosis of limb-girdle muscular dystrophy.
A 52-year-old patient with suspected Pompe disease was examined. A biopsy of quadricepssinister was performed.Electron microscopy analysis revealed muscle fibers containing numerous vacuoles (Figs. 17). Observed changes indicate type II glycogenosis.Results of other studies:Muscle glycogen 358.83 ug / mg protein / 11-38 ug / mg proteinAcid maltase 2.11 nM / mg protein / 2.2-3.3 nM / mg proteinNeutral maltase 1.76 nM / mg protein / 0.6-1.7 nM / mg protein
A 53-year-old patient with suspected mitochondrial changes was examined. A biopsy of bicepssinister was performed.Electronmicroscopy analysis revealed normal myofibril structure and the presence of numerous lipiddroplets within the muscle fibers. Altered mitochondria characterized by light mitochondrial matrix and lack of cristae were seen, many of them were characterized by crystallineinclusion.Carnitine level in the muscle tissue was 16,22 nM/mgB (Norm 17-48 nM/mgB)
A 54-year-old patient was examined. A biceps sinister biopsy was performed. Electronmicroscopy analysis revealed muscle fibers characterized with preserved miofibrils structure and normal sub-membranously located nuclei. Numerous fat droplets were observed. Ultrastructural image suggests palmitoyltransferase deficiency. Biochemical evaluation of carnitine palmitoyltransferase in the muscle tissue was performed and the result was 0,39 nM/mgB/min. (Norm 6,5-18 nM/mgB/min.).
A 54-year-old patient with suspected inclusion body myositis was examined, A biopsy of biceps sinister was examined. Electron microscopy analysis revealed ultrastructurally altere fibers among fibers with normal structure. Fig.1 Numerous autophagous were observed both in the center of the muscle cells (Figes 2,3) and under the cell membrane (Figes 4,5).
A 54-year-old patient with suspected miopathy was examined. A biopsy of quadriceps sinister wasperformed.Electronmicroscopy analysis did not reveal changesin muscle fibers architecture. Quite numerous fatdroplets were seen. The lipid profile analysis is recommended
A 56-year-old patient with suspected congenital dystrophy and scoliosis was examined. A biopsy ofbiceps dexter was performed. Electronmicroscopy analysis revealed abnormal, swollenmitochondria, characterized by lack of mitochondrial cristae. Local disintegration of myofibrils isobserved (Fig. 1,2). Characteristic crystalline structures are observed in vast majority ofmitochondria (Fig. 3,4,5,6,7,8).
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