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Summary: Background: Augmentation mammoplasty with subpectoral prosthesis implantation is a frequent performed procedure in plastic surgery for reconstructive and aesthetic purposes. Although prosthesis implantation in a pocket under the major pectoralis muscle has been related to volumetric and functional alterations, there is not much information about the associated short- and long-term histological changes. Therefore, the aim of our study was to describe the acute and chronic histological muscle alterations associated with subpectoral prosthesis implantation. Materials and Method: We collected samples from patients with breast tissue expander (1 year after implantation) and from patients without implantation as a control group. The samples were processed for assessing their histological, histochemical and immunohistochemical properties. Results: In the control group, no relevant histological findings were identified. Additionally, in the patients with expander, we observed mild augmentation of the internalised nuclei, normal morphology, significant muscle atrophy and fibrosis, whereas in the patients with prosthesis considerable augmentation of internalised nuclei, significant muscle atrophy, fibrosis and alteration of normal muscle morphology were observed. Conclusion: Prosthesis implantation induces histological changes in the periprosthetic striated muscle. Chronic fibrosis and inflammation play key roles in this process, which should be characterised in more detail from the histological and molecular biological perspective.

Background: In volumetric muscle loss (VML) injuries, spontaneous muscle regeneration capacity is limited. The implantation of autologous adipose tissue in the affected area is an option to treat these lesions; however, the effectiveness of this therapy alone is insufficient for a complete recovery of the damaged muscle. This study examined the influence of treadmill exercise on the rehabilitation of VML injuries reconstructed with autologous adipose tissue, as a strategy to counteract the limitations of spontaneous regeneration observed in these injuries., Methods: Forty adult male Wistar rats were divided into eight groups of five individuals each: normal control (NC), regenerative control (RC), VML control (VML), VML injury reconstructed with fresh autologous adipose tissue (FAT), exercise-rehabilitated control (RNC), exercise-rehabilitated regenerative control (RRC), exercise-rehabilitated VML injury (RVML), and exercise-rehabilitated VML injury reconstructed with fresh autologous adipose tissue (RFAT). Histological and histochemical staining techniques were used for the analysis of structural features and histomorphometric parameters of the tibialis anterior muscle. Grip strength tests were conducted to assess muscle force., Results: Exercise rehabilitation decreased the proportion of disoriented fibers in RFAT vs. FAT group. The percentage of fibrosis was significantly higher in FAT and RFAT groups versus NC and RNC groups but did not vary significantly between FAT and RFAT groups. Overall, muscle grip strength and fiber size increased significantly in the exercise-rehabilitated groups compared to control groups., Conclusions: To conclude, rehabilitation with physical exercise tended to normalize the process of muscle repair in a model of VML injury reconstructed with fresh autologous adipose tissue, but it did not reduce the intense fibrosis associated with these injuries.

Background: Augmentation mammoplasty with subpectoral prosthesis implantation is a frequent performed procedure in plastic surgery for reconstructive and aesthetic purposes. Although prosthesis implantation in a pocket under the major pectoralis muscle has been related to volumetric and functional alterations, there is not much information about the associated short- and long-term histological changes. Therefore, the aim of our study was to describe the acute and chronic histological muscle alterations associated with subpectoral prosthesis implantation., Materials and Method: We collected samples from patients with breast tissue expander (<6 months after implantation) and prosthesis (>1 year after implantation) and from patients without implantation as a control group. The samples were processed for assessing their histological, histochemical and immunohistochemical properties., Results: In the control group, no relevant histological findings were identified. Additionally, in the patients with expander, we observed mild augmentation of the internalised nuclei, normal morphology, significant muscle atrophy and fibrosis, whereas in the patients with prosthesis considerable augmentation of internalised nuclei, significant muscle atrophy, fibrosis and alteration of normal muscle morphology were observed., Conclusion: Prosthesis implantation induces histological changes in the periprosthetic striated muscle. Chronic fibrosis and inflammation play key roles in this process, which should be characterised in more detail from the histological and molecular biological perspective., Competing Interests: The authors declare that there is no conflict of interest., (© 2024 The Authors.)

In this study, we investigated the effect of transcranial magnetic stimulation (TMS) on the ultrastructure of muscle fibers and satellite cells in rats with experimental autoimmune encephalomyelitis (EAE). EAE-induced animals were treated with TMS (60 Hz at 0.7 mT) for 2 hours in the morning, once a day, 5 days a week, for 3 weeks, starting on day 15 post-immunization. The rats were sacrificed on day 36 post-immunization, and the soleus muscles were evaluated by light microscopy and transmission electron microscopy. Findings were compared with a non-treated EAE group. Electron microscopy analysis showed the presence of degenerated mitochondria, autophagic vacuoles, and altered myofibrils in non-treated EAE group. This correlates with the presence of acid phosphatase activity in muscle fibers and core-targetoid lesions with desmin immunohistochemistry. Most myonuclei in the EAE group showed apoptotic features. In contrast, EAE induced-TMS treated animals had less ultrastructural changes in the mitochondria and the myofibrils, together with less frequent apoptotic nuclear features. Peripheral desmin+ protrusions, as a marker of active satellite cells, were significantly increased in TMS-treated group. This correlates ultrastructurally with the presence of active features in satellite cells in the TMS group. In conclusion, the attenuation of ultrastructural alterations in muscle fibers and activation response of satellite cells caused by EAE indicated that skeletal muscle had a regenerative response to TMS.

Skeletal muscle is affected in experimental autoimmune encephalomyelitis (EAE), which is a model of multiple sclerosis that produces changes including muscle atrophy; histological features of neurogenic involvement, and increased oxidative stress. In this study, we aimed to evaluate the therapeutic effects of transcranial magnetic stimulation (TMS) on the involvement of rat skeletal muscle and to compare them with those produced by natalizumab (NTZ). EAE was induced by injecting myelin oligodendrocyte glycoprotein (MOG) into Dark Agouti rats. Both treatments, NTZ and TMS, were implemented from day 15 to day 35. Clinical severity was studied, and after sacrifice, the soleus and extensor digitorum longus muscles were extracted for subsequent histological and biochemical analysis. The treatment with TMS and NTZ had a beneficial effect on muscle involvement in the EAE model. There was a clinical improvement in functional motor deficits, atrophy was attenuated, neurogenic muscle lesions were reduced, and the level of oxidative stress biomarkers was lower in both treatment groups. Compared to NTZ, the best response was obtained with TMS for all the parameters analyzed. The myoprotective effect of TMS was higher than that of NTZ. Thus, the use of TMS may be an effective strategy to reduce muscle involvement in multiple sclerosis.

Different types of scaffolds are used to reconstruct muscle volume loss injuries. In this experimental study, we correlated ultrasound observations with histological findings in a muscle volume loss injury reconstructed with autologous adipose tissue. The outcome is compared with decellularized and porous matrix implants. Autologous adipose tissue, decellularized matrix, and a porous collagen matrix were implanted in volumetric muscle loss (VML) injuries generated on the anterior tibial muscles of Wistar rats. Sixty days after implantation, ultrasound findings were compared with histological and histomorphometric analysis. The muscles with an autologous adipose tissue implant exhibited an ultrasound pattern that was quite similar to that of the regenerative control muscles. From a histological point of view, the defects had been occupied by newly formed muscle tissue with certain structural abnormalities that would explain the differences between the ultrasound patterns of the normal control muscles and the regenerated ones. While the decellularized muscle matrix implant resulted in fibrosis and an inflammatory response, the porous collagen matrix implant was replaced by regenerative muscle fibers with neurogenic atrophy and fibrosis. In both cases, the ultrasound images reflected echogenic, echotextural, and vascular changes compatible with the histological findings of failed muscle regeneration. The ultrasound analysis confirmed the histological findings observed in the VML injuries reconstructed by autologous adipose tissue implantation. Ultrasound can be a useful tool for evaluating the structure of muscles reconstructed through tissue engineering.

Purpose: Previous experiments in rats have indicated that there are histological changes in skeletal muscle in drowning deaths; these changes include muscle fibers that contain ragged red fibers (RRF). The purpose of this study was to examine whether these changes also occur in humans., Methods: Histologic and histochemical examinations of three muscles (diaphragm, pectoralis, and psoas) were performed on 24 cadavers with three different causes of death: 8 drowning, 8 hanging, and 8 sudden cardiac disease. Muscle samples were stained with hematoxylin-eosin, MGT, nicotinamide adenine dinucleotide-tetrazolium reductase, succinate dehydrogenase, ATPase, and acid phosphatase via standard staining procedures., Results: There were statistically significant differences in the detection of RRFs in these cohorts. Additionally, several other cytoarchitectural changes (whorled and core-like fibers) were observed in the diaphragm in the drowning cohort and to a lesser extent in the hangings. These structural abnormalities were not observed in the sudden cardiac disease deaths, thus suggesting a common mechanism for the production of these muscular changes that is not shared in the cardiac death group. The mechanism is most likely intense hypoxia and mechanical trauma of the respiratory muscles in the setting of active blood circulation with intense muscle contraction., Conclusions: Our results confirmed that there are histological changes in the diaphragm in drownings and, to a lesser extent, in hangings.

The purpose of this study was to determine the histological characteristics of a skeletal muscle reconstructed by means of the implantation of autologous adipose tissue following an experimentally-induced volumetric muscle loss. A cylindrical piece in the belly of the rat anterior tibial muscle was removed. In the hole, inguinal subcutaneous adipose tissue of the same rat was grafted. Animals were sacrificed 7, 14, 21, 28 and 60 days posttransplantation. Histological, histochemical, immunohistochemical and morphometric techniques were used. At all times analyzed, the regenerative muscle fibers formed from the edges of the muscle tissue showed histological, histochemical and immunohistochemical differences in comparison with the control group. These differences are related to delays in the maturation process and are related to problems in reinnervation and disorientation of muscle fibers. The stains for MyoD and desmin showed that some myoblasts and myotubes seem to derive from the transplanted adipose tissue. After 60 days, the transplant area was 20% occupied by fibrosis and by 80% skeletal muscle. However, the neo-muscle was chaotically organized showing muscle fiber disorientation and centronucleated fibers with irregular shape and size. Our results support the hypothesis that, at least from a morphological point of view, autologous adipose tissue transplantation favors reconstruction following a volumetric loss of skeletal muscle by combining the inherent regenerative response of the organ itself and the myogenic differentiation of the stem cells present in the adipose tissue. However, in our study, the formed neo-muscle exhibited histological differences in comparison with the normal skeletal muscle.

Purpose: The objective of the present study was to determine whether a denervated muscle extract (DmEx) could stimulate satellite cell response in denervated muscle., Methods: Wistar rats were divided into 4 groups: normal rats, normal rats treated with DmEx, denervated rats, and denervated rats treated with DmEx. The soleus muscles were examined using immunohistochemical techniques for proliferating cell nuclear antigen, desmin, and myogenic differentiation antigen (MyoD), and electron microscopy was used for analysis of the satellite cells., Results: The results indicate that while denervation causes activation of satellite cells, DmEx also induces myogenic differentiation of cells localized in the interstitial space and the formation of new muscle fibers. Although DmEx had a similar effect in nature on innervated and denervated muscles, this response was of greater magnitude in denervated vs . intact muscles., Conclusion: Our study shows that treatment of denervated rats with DmEx potentiates the myogenic response in atrophic denervated muscles.

This study was conducted to determine the effects of extracts obtained from both normal and denervated muscles on different muscle types. Wistar rats were used and were divided into a control group and four experimental groups. Each experimental group was treated intraperitoneally during 10 consecutive days with a different extract. These extracts were obtained from normal soleus muscle, denervated soleus, normal extensor digitorum longus, and denervated extensor digitorum longus. Following treatment, the soleus and extensor digitorum longus muscles were obtained for study under optic and transmission electron microscope; morphometric parameters and myogenic responses were also analyzed. The results demonstrated that the treatment with normal soleus muscle and denervated soleus muscle extracts provoked hypertrophy and increased myogenic activity. In contrast, treatment with extracts from the normal and denervated EDL had a different effect depending on the muscle analyzed. In the soleus muscle it provoked hypertrophy of type I fibers and increased myogenic activity, while in the extensor digitorum longus atrophy of the type II fibers was observed without changes in myogenic activity. This suggests that the muscular responses of atrophy and hypertrophy may depend on different factors related to the muscle type which could be related to innervation.

A diagnosis of drowning is a challenge in legal medicine as there is generally a lack of pathognomonic findings indicative of drowning. This article investigates whether the skeletal muscle undergoes structural changes during death by drowning. Eighteen Wistar rats were divided into 3 equal groups according to the cause of death: drowning, exsanguination, and cervical dislocation. Immediately after death, samples of the masseter, sternohyoid, diaphragm, anterior tibial, soleus, and extensor digitorum longus muscles were obtained and examined by light and electron microscopy.In the drowning group, all muscles except the masseter displayed scattered evidence of fiber degeneration, and modified Gomori trichrome staining revealed structural changes in the form of abnormal clumps of red material and ragged red fibers. Under the electron microscope, there was myofibrillar disruption and large masses of abnormal mitochondria. In the exsanguination group, modified Gomori trichrome staining disclosed structural changes and mitochondrial abnormalities were apparent under light microscopy; however, there was no evidence of degeneration. No alterations were observed in the cervical dislocation group.As far as we know, this is the first time that these histological findings are described in death by drowning and are consistent with rhabdomyolysis and intense anoxia of skeletal muscle.

A diagnosis of drowning is a challenge in legal medicine, as there is generally a lack of pathognomonic findings indicative of drowning. Diatom analysis has been considered very supportive for a diagnosis of drowning, although the test is still controversial for some investigators. We assessed diatoms association with drowning in the peripheral tissues of drowned rats and the effects of the drowning medium on the diatom yield. A modified acid digestion method was optimised for diatom recovery in water and rat tissues. Eighteen adult Wistar rats were employed for the study, subdivided into six groups of three rats. Groups 1, 3 and 5 were drowned in seawater, lake water, or river water respectively, while groups 2, 4 and 6 were controls (immersed after death in seawater, lake water or river water respectively). Water samples were taken from the sea, lake and river in Málaga and Córdoba (Spain) for the purposes of diatomological mapping and drowning of the rats. Diatoms were successfully recovered from all water samples and matched with tissues of the drowned rats. There were significant differences in diatom numbers between control and test samples for all the tissues studied, as well as within test samples. Histological investigations conducted on lung samples obtained from drowned rats provided complementary and valuable information. This study demonstrates the feasibility of the diatom test as a reliable method for the diagnosis of drowning, especially if adequate precautions are taken to avoid contamination, and if interpretation of the analysis is performed in light of other complementary investigations., (© The Author(s) 2014.)

Introduction: Skeletal muscle is a target organ in multiple sclerosis, a chronic debilitating disease of the central nervous system caused by demyelination and axonal deterioration. Since the experimental autoimmune encephalomyelitis model reproduces the relapsing-remitting course found in most multiple sclerosis patients, this model was used to compare the histological features of skeletal muscle at onset with those observed at the start of the second relapse., Material and Methods: Histological, histochemical and ultrastructural changes, as well as biochemical oxidative damage and antioxidant-system markers, were examined in the soleus and extensor digitorum longus muscles of Dark Agouti rats in which experimental autoimmune encephalomyelitis had been induced by active immunization using myelin oligodendrocyte glycoprotein., Results: Histological examination at disease onset revealed ragged-red fibers and ultrastructural evidence of mitochondrial degeneration. At the second relapse, neurogenic changes included a wide range of cytoarchitectural lesions, skeletal muscle atrophy and the appearance of intermediate fibers; however, differences were observed between soleus and extensor digitorum longus lesions. Biochemical tests disclosed an increase in oxidative stress markers at onset, which was more pronounced at the second relapse., Conclusions: Microscopic findings suggest that two patterns can be distinguished at disease onset: an initial phase characterized by muscle mitochondrial alterations, and a second phase dominated by a histological muscle pattern of clearly neurogenic origin., (Copyright © 2015 Elsevier GmbH. All rights reserved.)

There is evidence to suggest that the neuroprotective effect of exposure of extremely low-frequency electromagnetic fields (ELF-EMF) may be due, at least in part, to the effect of these fields on neurotrophic factors levels and cell survival, leading to an improvement in behavior. This study was undertaken to investigate the neuroprotective effects of ELFEF in a rat model of 3-nitropropionic acid (3NP)-induced Huntington's disease. Behavior patterns were evaluated, and changes in neurotrophic factor, cell damage, and oxidative stress biomarker levels were monitored in Wistar rats. Rats were given 3NP over four consecutive days (20 mg/kg body weight), whereas ELFEF (60 Hz and 0.7 mT) was applied over 21 days, starting after the last injection of 3NP. Rats treated with 3NP exhibited significantly different behavior in the open field test (OFT) and the forced swim test (FST), and displayed significant differences in neurotrophic factor levels and oxidative stress biomarkers levels, together with a neuronal damage and diminished neuronal density, with respect neuronal controls. ELFEF improved neurological scores, enhanced neurotrophic factor levels, and reduced both oxidative damage and neuronal loss in 3NP-treated rats. ELFEF alleviates 3NP-induced brain injury and prevents loss of neurons in rat striatum, thus showing considerable potential as a therapeutic tool., (Copyright © 2012 IBRO. Published by Elsevier Ltd. All rights reserved.)

Introduction: In this study we correlated ultrasound findings with histological changes taking place during experimentally induced degeneration-regeneration in rat skeletal muscle., Methods: Gastrocnemius muscles were injected with mepivacaine, and the progress of the muscle injury was monitored by ultrasound from day 1 to day 20. Muscles were extracted on the same days for histological examination., Results: The degenerative phase was characterized by increased echogenicity in the injured area; thereafter, echogenicity gradually diminished during the regenerative phase, attaining normal levels by 20 days postinjection. By this stage, histological examination revealed that regeneration was complete. The heteroechoic texture observed from day 4 to day 10 appeared to reflect the coexistence of degenerative and regenerative processes., Conclusions: The results suggest that the degenerative and regenerative phases of muscle injury may be distinguished sonographically through differences in echogenicity and echotexture and, using Doppler ultrasound, differences in the degree of vascularization., (Copyright © 2012 Wiley Periodicals, Inc.)

Purpose: Removal of the meniscus leads to progressive degenerative arthritis of the knee on a long-term basis; therefore, meniscal allograft transplantation has been proposed as an alternative to meniscectomy. Preservation methods are required to build up operational stocks and to provide living grafts of a practical size at the right time for patients. Methods for meniscus preservation have been published, and relevant literature confirms that using standard cryopreservation, the chondrocyte survival in situ is inadequate and extremely variable and the cryoinjury mechanisms are not completely established. The aim of the present study is to further investigate possible cellular injury caused by cryopreservation by analysing apoptosis and ultrastructural damage to menisci., Methods: Seven human menisci that were cryopreserved by standard method were used. All tissue samples were processed simultaneously for routine light microscopy, scanning and transmission electron microscopy as well as apoptosis assessment by the use of ISOL method., Results: With respect to cellularity, significant differences (P < 0.05) between the fresh (14.6 ± 3.5) (mean ± SD) and cryopreserved menisci (9.2 ± 2.8) (mean ± SD) were observed. Apoptosis using ISOL method was observed in fibrochondrocytes of fresh and cryopreserved menisci. The quantitative analysis revealed significant differences (P < 0.05) between fresh meniscus samples, where the apoptotic index was 0.8 ± 2.3% (mean ± SD), and cryopreserved meniscus samples, where this index was 50 ± 18.1% (mean ± SD)., Conclusion: The results suggest that apoptosis occurs during meniscus cryopreservation. The major findings of this study are cellular damage in meniscus cryopreservation suggesting apoptosis-mediated cell loss. The findings reported herein encourage to further investigations in preservation procedures to enhance maximum long-term clinical survival.

We studied the effects of transcranial magnetic stimulation (TMS, 60 Hz and 0.7 mT for 4 h/day for 14 days) on oxidative and cell damage caused by olfactory bulbectomy (OBX) in Wistar rats. The levels of lipid peroxidation products and caspase-3 were enhanced by OBX, whereas it prompted a reduction in reduced glutathione (GSH) content and antioxidative enzymes activities. The treatment with TMS reverted towards normality the biomarkers indicative of oxidative stress and apoptosis. In conclusion, our data show that TMS induced a protection against cell and oxidative damage induced by OBX, as well as they support the hypothesis that oxidative stress may play an important role in depression.

We evaluated the effects of nicotine on cell and oxidative damage caused by olfactory bulbectomy (OBX). The rats were divided into seven groups as follows: i) control; ii) vehicle (6% ethanol); iii) treated with nicotine; iv) sham operated; v) olfactory bulbectomy (OBX); vi) OBX+vehicle; and vii) OBX+Nic. The OBX was performed using the trepanation of frontal bone. The olfactory bulbs were cut and removed without damage to the frontal cortex. Two weeks after surgery nicotine was administered chronically once daily for 14 days, intraperitoneally (i.p.) in doses of 1.5 mg/kg, two weeks after surgery. OBX caused an increase in lipid peroxidation products and caspase-3 but prompted a reduction in reduced glutathione (GSH) content and antioxidative enzyme activity. All these changes were reverted by treatment of nicotine (14 days). In conclusions: i) OBX induces oxidative stress and cell death by apoptosis; and ii) nicotine presents antidepressant and antioxidant effect. All these findings suggest that nicotine would be a therapeutic tool for depression, although more studies are needed in this area to define the appropriate treatment regime., (Copyright (c) 2009 Elsevier B.V. All rights reserved.)

In this study we analyzed the effects of melatonin (Mel, 1 mg/kg ip) on behavioral changes as well as cell and oxidative damage prompted by bilaterally olfactory bulbectomy. Olfactory bulbectomy caused an increase in lipid peroxidation products and caspase-3, whereas it prompted a decrease of reduced glutathione (GSH) content and antioxidative enzymes activities. Additionally, olfactory bulbectomy induced behavioral changes characterized by the enhancement of immobility time in the forced swim test and hyperactivity in the open field test. All these changes were normalized by treatment of Mel (14 days). Our data show that Mel has a beneficial neuropsychiatric action against oxidative stress, cell damage and behavior alterations.

We investigated the effect of magnetic field stimulation (MS) on oxidative damage and skeletal muscle injury prompted by mepivacaine injection in the anterior tibial muscle of Wistar rats. The effects of mepivacaine and MS on oxidative stress were evaluated by lipid peroxidation, GSH levels and catalase activity. Muscle regeneration was analyzed by haematoxylin-eosin stained, NADH-TR histochemical reaction, desmin immunostaining as well as by morphometric parameters such as fibers density and fiber area were evaluated. Our data revealed that mepivacaine induced oxidative stress, that MS prevents the harmful effects induced by mepivacaine and that it facilitates the regeneration process of skeletal muscle. In conclusion, the results show the ability of MS to modify skeletal muscle response to mepivacaine.

The present study evaluated 17beta-estradiol (17betaE(2)) (2.5 mg/kg sc) effects on bilateral OBX-induced behavioral changes and oxidative stress. OBX in male Wistar rats produced an increase in lipid peroxidation products and a decline in reduced glutathione (GSH) content and glutathione peroxidase (GSH-Px) activity, together with an increase in caspase-3 activity. Additionally, OBX triggered changes of behavior such as an enhancement of immobility time in the forced swim test and hyperactivity in the open field test. These changes were reversed by treatment with 17betaE(2) (14 days). Our results reveled that 17betaE(2) has a protective effect against oxidative stress, cell damage and behavioral changes induced by OBX, and present antidepressant and antianxiety properties.

This paper evaluates the effects of testosterone (0.5 mg/kg subcutaneously (s.c.) for 8 days) on oxidative stress and cell damage induced by 3-nitropropionic acid (20 mg/kg intraperitoneally (i.p.) for 4 days) in ovariectomized rats. Gonadectomy triggered oxidative damage and cell loss, evaluated by the detection of caspase-3, whereas 3-nitropropionic acid increased the levels of oxidative stress induced by ovariectomy and prompted cell damage characterized by enhanced levels of lactate dehydrogenase. These changes were blocked by testosterone administration. Our results support the following conclusions: i) ovariectomy triggers oxidative and cell damage via caspase-3 in the striatum; ii) 3-nitropropionic acid exacerbates oxidative stress induced by ovariectomy and leads to cell damage characterized by increased levels of lactate dehydrogenase; iii) testosterone administration decreases oxidative stress and cell damage. Additionally, these data support the hypothesis that testosterone might play an important role in the onset and development of neurodegenerative diseases.

An investigation was conducted on the effect of transcranial magnetic field stimulation (TMS) on the free radical production and neuronal cell loss produced by 3-nitropropionic acid in rats. The effects of 3-nitropropionic acid were evaluated by examining the following changes in: the quantity of hydroperoxides and total radical-trapping antioxidant potential (TRAP), lipid peroxidation products, protein carbonyl groups, reduced glutathione (GSH) content, glutathione peroxidase (GSH-Px), catalase and succinate dehydrogenase (SDH) activities; total nitrite and cell death [morphological changes, quantification of neuronal loss and lactate dehydrogenase (LDH) levels]. Our results reveal that 3-nitropropionic acid induces oxidative and nitrosative stress in the striatum, prompts cell loss and also shows that TMS prevents the harmful effects induced by the acid. In conclusion, the results show the ability of TMS to modify neuronal response to 3-nitropropionic acid.

The aim of present study was to clarify the role of female sex hormones in the development and course of neurodegenerative disease in an experimental model of Huntington's disease induced by 3-nitropropionic acid (NPA) (30 mg/kg intraperitoneally (i.p.)/day for 4 days) in ovariectomized rat. Gonadectomy prompted oxidative stress and cell death evaluated by the detection of caspase-3, whereas 3-nitropropionic acid enhanced the oxidative stress induced by ovariectomy and it triggered cell damage characterized by increases of LDH levels. These changes were prevented by administration of 17 beta-estradiol. Our findings suggested that: (i) ovariectomy induced oxidative stress and apoptosis in the brain; (ii) 3-nitropropionic acid exacerbated oxidative stress induced by ovariectomy and shifting cell to cell death; and (iii) 17 beta-estradiol administration decreased oxidative stress and cell death induced by ovariectomy and 3-nitropropionic acid. These results revealed that sex ovarian hormones play a important role in onset and development of neurodegenerative diseases, as well as neuroprotective effects of 17 beta-estradiol against the changes induced ovariectomy and ovariectomy plus 3-nitropropionic acid.

Light microscopy and electron microscopy were used to study the formation of ring fibers induced experimentally in regenerating muscle subjected to tenotomy-induced tension deficiency. Anterior tibial rat muscles were injured by intramuscular injection of mepivacain, tenotomized at varying stages of the regenerative process, and analyzed 30 days after sectioning the tendon. The combination of regeneration and tenotomy led to the appearance of ring fibers at different developmental stages. Ring fibers were not observed in regenerating control muscles and were scarce in tenotomized controls. Our results showed that the regenerative phase in which tension deficiency was established had a significant influence on the number of developing ring fibers; the number increased when tenotomy was performed during subsarcolemmic myofibrillogenesis in regenerating fibers. As a consequence, one might hypothesize that tension deficiency during muscle fiber repair plays a critical role in ring fiber formation.

A study was made of the myotrophic effects of denervated muscle extracts on normal Wistar rat soleus muscle. Extracts obtained 1 h, 2, 4 and 7 days after sectioning of the sciatic nerve were administered intraperitoneally over five consecutive days. Soleus muscles were routinely processed for morphological and morphometrical analysis using light microscopic techniques. Quantitative differences were observed in the effects of different extracts on total muscle area, fibre cross-sectional area, mean minimum diameter and number of fibres/ area. The greatest myotrophic response was elicited by extracts obtained at 2 and 4 days; differences with respect to controls and extracts obtained at 1 day were significant (P < 0.05) for all parameters studied. Statistically significant differences (P < 0.05) were also recorded for fibre cross-sectional area and mean minimum diameter between the 2- and 4-day groups and the 7-day group. It may thus be concluded that the time elapsing between denervation and extract obtention influences the effect of the extract on normal rat muscle.

In the present study, two histologically-distinct cases of granulomatous lymphadenitis induced by dimethylpolysiloxane (silicone polymer) implants were studied. Four and six years after implant, and following surgery for breast cancer, painful homolateral axillary adenopathies were observed and biopsied. In both cases, histological examination led to a diagnosis of "silicone-induced granulomatous adenitis" requiring removal of implants. Foreign-body granulomas (siliconomas) were observed in surrounding tissue with no apparent rupture of implant capsules; however, visible retraction, hardening and scattered calcifications were noted. The presence of silica was revealed by incineration of a number of biopsied lymph nodes, a technique not hitherto used in the study of this pathology. A review is offered of the literature available.

Qualitative and quantitative analysis of satellite cells in regenerating muscles was performed at 4, 7 and 30 days after necrosis induced by mepivacaine injection. At 4 days, the small regenerating fibers were accompanied by a high number of satellite cells showing signs of activation; at 7 days, the number of satellite cells decreased and two morphological types of these cells were observed; at 30 days, satellite cells were similar in both number and characteristics to those of the control group. These results would indicate that satellite cells may vary both in number and morphological and morphometric features, according to the degree of maturity of the regenerating muscle fiber.

A study was made of the characteristics of the capillaries surrounding regenerating muscle fibers at three different stages of their development. Mepivacaine was injected in the anterior tibial muscles of Wistar rats in order to obtain muscle and capillary degeneration which was followed by muscle and capillary regeneration. Muscles were examined at 4, 8 and 30 days post-injection. Capillaries were subjected to quantitative and qualitative examination using electron microscopy. Results showed the morphological and morphometrical variations taking place in capillaries as the regenerative fiber matures. Changes were most evident in the capillaries surrounding the most immature fibers. It was concluded that although capillary morphology suggests that the supply of blood to regenerative fibers may be hindered, morphometric data appear to indicate no such obstacle.

This study describes the capillary supply of individual regenerating muscle fiber during three stages of its development. Regeneration was induced by the injection of mepivacaine in the anterior tibial muscle of rats. Muscle fiber capillarization during regeneration was analysed in semithin sections, employing the following parameters: the number of capillaries around a fiber and the number of capillaries per fiber cross-sectional area. The results revealed that during development of regenerating fibers, the fiber cross-sectional area increased, the number of capillaries around each fiber increased and the number of capillaries per fiber cross-sectional area decreased. These data indicated a greater capillary supply of the individual regenerating muscle fiber during its early stage of maturation.

A study was made of Wistar rat soleus muscle following intraperitoneal administration of denervated muscle extract over 1 and 2 days. Light microscopy revealed the appearance on fiber surfaces of basophilic satellite structures whose histochemical behaviour differed from that of the parent fiber. Small fibers showing regenerative characteristics were also detected, mainly in the extrafascicular spaces. At ultrastructural examination, activated satellite cells were visible, and there was evidence of splitting in subsarcolemmal regions of apparently hypertrophic muscle fibers. Interstitial cells were occasionally observed, containing structures like myofilaments. The hypothesis is advanced that denervated muscle extract contains substances able to stimulate new fiber formation in adult skeletal muscle.

The effects of systemic administration of muscle extract on normal muscle were studied. Male Wistar rats received intraperitoneal injections of normal and denervated muscle extract over 5 consecutive days. Soleus muscles were then submitted to histological, histochemical and quantitative-morphometric analysis. The group receiving denervated muscle extract showed considerable muscle fiber hypertrophy, together with the formation of new fibers suggestive of hyperplasia. The systemic administration of denervated muscle extract was shown to have a considerable myotrophic effect on normal muscle, evident in the hypertrophy and hyperplasia of muscle fibers.

Electron microscopic analysis was used to study the ultrastructural changes taking place in rat soleus muscle following intraperitoneal administration of pure heroin. Degenerative changes observed consisted primarily of hypercontracted fibers at different stages of development. Evidence of regeneration was also found. Results show the myotoxic effect of pure heroin on skeletal muscle. The pathogenesis of muscle damage is discussed.

Quantitative methods were used to analyze changes in the capillarization of skeletal muscle during regeneration. The H-E staining technique was used to establish three arbitrary stages of fiber regeneration on the basis of qualitative histological evaluation. ATPase and light microscopic techniques were used to calculate capillary density, the number of capillaries surrounding each fiber, and the fiber area served by each capillary, for each of the three stages established. The results obtained indicated variations in the vascularization of regenerating fibers from one stage of maturity of another: capillarization was greater in the initial stages of regeneration, returning gradually to normal values by the final stages of the process. Interestingly enough the pattern in the capillarization of skeletal muscle during regeneration seems to be similar to that taking place during postnatal muscle development. Both processes appear to be governed by the increase in fiber size.

This report describes the regeneration pattern of anterior tibial muscle of the rat after the inoculation of the snake venom of Bothrops jararacussu. The results show that this regeneration pattern is rather similar to the pattern described in other experimental models. Three days after the injection, three differentiated areas are established: a peripheric one of surviving fibres, a second one called myogenic area, and the last one, more internal, made of necrotic fibres that are phagocytized by macrophages. The surface of the surviving muscle fibres has myoblasts sticking to it and five days after, the myogenic area is occupied by many of them. Both the previous phagocytosis and the myoblasts came from the area of current uninjured fibres. After 30 and 60 days the regeneration is completed and there are only a few marks that show that the regeneration has taken place.