Estabilização zigomática e retalho de avanço facial lateral em canino filhote / Zygomatic stabilization and lateral facial advancement flap in a puppy dog

O trauma é frequentemente relatado na rotina clínica de pequenos animais, podendo gerar fraturas de componentes ósseos e lesões de tecidos moles adjacentes. No presente trabalho, objetivou-se relatar o caso de um canino, macho, sem raça definida, de sete meses de idade, vítima de trauma craniomaxilofacial decorrente de mordedura, diagnosticado com fratura e deslocamento de osso zigomático, além de importante laceração de pele. O tratamento estabelecido baseou-se no debridamento da ferida, estabilização cirúrgica de arco zigomático com fios de Nylon e na sutura dos ferimentos de pele causados. Em um segundo tempo cirúrgico, foi realizada enucleação e recobrimento do defeito na órbita com malha cirúrgica de polipropileno, além de remoção de tecido exuberante e confecção de retalho subdérmico de avanço facial lateral para recobrimento do defeito cutâneo. A complicação evidenciada na primeira intervenção cirúrgica foi a deiscência das suturas de pele, enquanto no segundo tempo cirúrgico, não houve sinais de complicações. No pós-operatório, o paciente apresentou evolução clínica satisfatória, recebendo alta médica 21 dias após o segundo procedimento cirúrgico realizado. Tendo em vista a adequada evolução clínica, bem como os reduzidos efeitos colaterais, sugere-se que a conduta clínica e técnicas cirúrgicas adotadas para tratamento do paciente em questão foram efetivas.

Trauma is frequently reported in the small animal clinics, and can lead to fractures of cranial bone components and injuries to the adjacent soft tissues. In the present study, the objective was to report the case of a seven-month-old male mongrel dog, that had a craniomaxillofacial trauma resulting from a bite, characterized by zygomatic bone fracture and displacement, in addition to a major skin laceration. The stablished treatment was based on wound debridement, surgical stabilization of the zygomatic arch with nylon threads and in the suturing of skin wounds. In a second surgical procedure, enucleation was performed and a surgical polypropylene mesh was applied to cover the orbital defect, exuberant tissue was removed and a subdermal advancement flap was used to cover the skin defect. The complication observed in the first surgical intervention was dehiscence of the skin sutures, while in the second surgical procedure, there were no signs of complications. Postoperatively, the patient had a satisfactory clinical recovery, being discharged 21 days after the second surgical procedure. Considering the adequate clinical evolution and the reduced complications, it issuggestedthat the clinical conduct and surgical techniques adopted for the treatment of the patient in question were effective.

Effects of protein restriction during gestation and lactation on cell proliferation in the hippocampus and subventricular zone: functional implications. Protein restriction alters hippocampal/SVZ cell proliferation.

There is no consensus about the effects of protein restriction on neurogenesis and behavior. Here, for the first time, we evaluated the effects of protein restriction during gestation and lactation, on the two major neurogenic regions of the adult brain, the subgranular zone (SGZ) of the hippocampal dentate gyrus and the subventricular zone (SVZ), simultaneously. We also assessed different types of behavior relevant to each region. After mating, pregnant Wistar rats were divided into a control group (CG) that received a normal diet (20% protein); and a protein-restriction group (PRG) that received a low-protein diet (8% protein). After birth, the same diets were provided to the mother and pups until weaning, when some rats were analyzed and others received a normal-protein diet until adulthood. Different sets of rats were used for cellular and behavioral studies in juvenile or adult age. Brains were processed for immunohistochemistry anti-BrdU, anti-Ki67, or anti-pHisH3. Juvenile and adult rats from distinct litters also underwent several behavioral tests. Our data show that early protein restriction results in a reduction of hippocampal progenitors and deficits in object recognition during adult life. Moreover, longer periods of immobility in the tail suspension and in the forced swimming tests revealed that PRG rats show a depressive behavior at 21 days of age (P21) and in adulthood. Furthermore, we suggest that despite the reduced number/proliferation of neural stem cells (B and/or E cells) in SVZ there is a compensatory mechanism in which the progenitors (types C and A cells) proliferate in a higher rate, without affecting olfactory ability in adulthood.

Neuroprotective effects and magnetic resonance imaging of mesenchymal stem cells labeled with SPION in a rat model of Huntington's disease.

Bone marrow mesenchymal stem cells (MSC) have been tested and proven effective in some neurodegenerative diseases, but their tracking after transplantation may be challenging. Our group has previously demonstrated the feasibility and biosafety of rat MSC labeling with iron oxide superparamagnetic nanoparticles (SPION). In this study, we investigated the therapeutic potential of SPION-labeled MSC in a rat model of Huntington's disease, a genetic degenerative disease with characteristic deletion of striatal GABAergic neurons. MSC labeled with SPION were injected into the striatum 1h after quinolinic acid injection. FJ-C analysis demonstrated that MSC transplantation significantly decreased the number of degenerating neurons in the damaged striatum 7 days after lesion. In this period, MSC transplantation enhanced the striatal expression of FGF-2 but did not affect subventricular zone proliferation, as demonstrated by Ki67 proliferation assay. In addition, MSC transplantation significantly reduced the ventriculomegaly in the lesioned brain. MRI and histological techniques detected the presence of the SPION-labeled cells at the lesion site. SPION-labeled MSC produced magnetic resonance imaging (MRI) signals that were visible for at least 60 days after transplantation. Our data highlight the potential of adult MSC to reduce brain damage under neurodegenerative diseases and indicate the use of nanoparticles in cell tracking, supporting their potential as valuable tools for cell therapy.

Nicotinic acetylcholine receptor activation reduces skeletal muscle inflammation of mdx mice.

Mdx mice develop an inflammatory myopathy characterized at different ages by myonecrosis with scattered inflammatory infiltrates followed by muscular regeneration and later persistent fibrosis. This work aimed to verify the putative anti-inflammatory role of nicotinic acetylcholine receptor (nAChR) in the mdx muscular lesion. Mitigation of myonecrosis and decreased TNFα production were accompanied by increased numbers of F4/80 macrophages expressing nAChRα7. In vivo treatment with nicotine attenuated muscular inflammation characterized by reduced metalloprotease MMP-9 activity, TNFα and NFkB content and increased muscular regeneration. Our data indicate that nAChR activation influences local inflammatory responses in the muscular lesion of mdx mice.

Therapeutic window for treatment of cortical ischemia with bone marrow-derived cells in rats.

The beneficial effect of treatment with bone marrow mononuclear cells (BMMCs) was evaluated in different therapeutic windows in a rat model of focal ischemia induced by thermocoagulation of the blood vessels in the left motor, somestesic, and sensorimotor cortices. We also compared the therapeutic benefits between BMMCs and bone marrow-derived mesenchymal stem cells (MSCs). BMMCs and MSCs were obtained from donor rats and injected into the jugular vein after ischemia. BMMCs-treated animals received approximately 3x10(7) cells at post-ischemic days (PIDs) 1, 7, 14, or 30. MSCs-treated animals received approximately 3x10(6) cells at PIDs 1 and 30. Control animals received only the vehicle. The animals were then evaluated for functional sensorimotor recovery weekly with behavioral tests (cylinder test and adhesive test). Significant recovery of sensorimotor function was only observed in the cylinder test in animals treated with BMMCs at PIDs 1 and 7. Similar effects were also observed in the animals treated with MSCs 1 day after ischemia, but not in animals treated with MSCs 30 days after ischemia. Significant decrease in glial scarring did not seem to be a mechanism of action of BMMCs, since treatment with BMMCs did not change the level of expression of GFAP, indicating no significant change in the astrocytic scar in the periphery of the ischemic lesion. These results suggest that BMMCs might be an efficient treatment protocol for stroke only in the acute/subacute phase of the disease, and its efficiency in inducing functional recovery is similar to that of MSCs.

Lack of association between PSA-NCAM expression and migration in the rostral migratory stream of a Huntington's disease transgenic mouse model.

Huntington's disease is a neurodegenerative autosomal disorder characterized by selective loss of striatal and cortical neurons. The mammalian brain subventricular zone contains a population of neural precursors involved in postnatal neurogenesis. These newly generated cells migrate from the subventricular zone along the rostral migratory stream and differentiate into mature olfactory bulb neurons throughout adulthood. The establishment of this pathway depends upon a variety of molecules, including polysialylated neural cell adhesion molecule (PSA-NCAM). We used a murine model of Huntington's disease, the R6/2 transgenic mouse, and in vivo bromodeoxyuridine administration to label cells undergoing proliferation and to follow their migration along the rostral migratory stream. Bromodeoxyuridine labeling did not show any significant increase in proliferation of progenitor cells in symptomatic R6/2 mice, but migration of neuroblasts along the rostral migratory stream was significantly diminished. The decrease in neuroblast migration was not due to an alteration in the expression of PSA-NCAM along the rostral migratory stream since immunohistochemical analysis showed no significant differences between R6/2 and wild type mice. In addition, we used Fluoro-Jade C to evaluate apoptosis and demonstrated that the number of apoptotic cells in the rostral migratory stream is similar in affected and wild type animals, suggesting that cell death is not responsible for the differences observed in neuroblast migration. We conclude that in R6/2 mice, progenitor cells have an impaired migration in their route to the olfactory bulb, with accumulation of cells in the caudal rostral migratory stream that does not result from changes in PSA-NCAM expression and/or cell death.