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Prenatal hypoxic-ischemic insult (HI) may lead to a variety of neurological consequences that may persist throughout adulthood. In the most severe cases, HI is known to increase pain sensitivity which profoundly impacts quality of life. Periaqueductal gray matter (PAG) is a relevant region of the descending pain pathway and its function may be modulated by a complex network that includes nitrergic neurons and glial response, among other factors. Astrocytes, central players in pain modulation, are known to respond to HI by inducing hyperplasia, hypertrophy and increasing the number of their processes and the staining of glial fibrillary acidic protein (GFAP). In this work we investigated the effects of prenatal HI on touch and pain sensitivity, besides the distribution of the neuronal isoform of Nitric Oxide Synthase (nNOS) and GFAP in the PAG of young and adult male rats. At 18 days of gestation, rats had their uterine arteries clamped for 45 min (HI group). SHAM-operated animals were also generated (SHAM group). At post-natal day 30 (P30) or 90 (P90), the offspring was submitted to the behavioral tests of Von Frey and formalin or histological processing to perform immunohistochemistry for nNOS and GFAP. Although there was no significant difference between the groups concerning touch sensitivity, we observed an increase in pain sensitivity in HI P30 and HI P90. The number of nNOS + cells was reduced in HI adult animals in dlPAG and vlPAG. GFAP immunostaining was increased in HI P90 in dlPAG and dmPAG. Our results demonstrated for the first time an increase in pain sensitivity as a consequence of prenatal HI in an animal model. It reinforces the relevance of this model to mimic the effects of prenatal HI, as hyperalgesia., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Introduction: Decubitus ulcers of the sacral region are common conditions in bedridden patients. Deep lesions (Stages III and IV) often require surgical treatment for closure. Flaps of the region are the first choice for treatment. We present our experience in the treatment of these lesions and compare two different approaches: local fasciocutaneous flap and gluteus maximus myocutaneous flap with V-Y advancement., Method: From March 2009 to May 2014, 32 patients underwent closure of sacral pressure ulcers by flaps, 17 of them with rotational local fasciocutaneous flaps and 15 with myocutaneous flaps of the gluteus maximus muscle with V-Y advancement. Evolution regarding complications and rate of success after two months was compared between the groups., Results: Out of the 32 operated patients we obtained resolution of lesions after two months in 23 (71.8%), 10 patients in the fasciocutaneous flap group (58.8%) and 13 cases in the myocutaneous flap group (86.6%). The most common complication was partial dehiscence of sutures in 12 patients (37.5%), 8 patients in the fasciocutaneous flap group (47%) and 4 patients in the myocutaneous flap group (26.6%). The group of patients reconstructed with local fasciocutaneous flaps presented 3 cases with seroma, one with hematoma and 6 with partial cutaneous necrosis; these patients also required more drainage time., Conclusions: Both the local rotational fasciocutaneous flap and the myocutaneous flap of the gluteus maximus muscle in V-Y flap can be used in the surgical treatment of sacral ulcers. In our experience, a reduced success rate and more complications were found in the local fasciocutaneous reconstructive method., (© 2017 The Author(s).)

Background: Sleep restriction alters pain perception in animals and humans, and many studies have indicated that paradoxical sleep deprivation (PSD) promotes hyperalgesia. The hyperalgesia observed after mechanical nociceptive stimulus is reversed through nitric oxide synthase (NOS) inhibition. Both nitric oxide (NO) and the dorsolateral periaqueductal gray matter (dlPAG) area of the brainstem are involved in hyperalgesia. Thus, in this work, we investigated the pain-related behavior response after mechanical noxious stimuli (electronic von Frey test), and the activity of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), an indicator of NOS activity, within the dlPAG of paradoxical sleep-deprived rats. We also evaluated the effects of pre-treatment with L-NAME on these parameters., Results: These data revealed that PSD reduced the hindpaw withdrawal threshold (-47%, p < 0.0001) confirming the hyperalgesic effect of this condition. In addition, there were more NADPH-d positive cells in dlPAG after PSD than in control rats (+ 59%, p < 0.0001). L-NAME treatment prevented the reduction in the hindpaw withdrawal threshold (+ 93%, p < 0.0001) and the increase in the NADPH-d positive cells number in the dlPAG of PSD-treated rats (-36%, p < 0.0001)., Conclusion: These data suggest that the hyperalgesic response to mechanical noxious stimuli in paradoxical sleep-deprived rats is associated with increased NOS activity in the dlPAG, which presumably influences the descending antinociceptive pathway.

Paradoxical sleep deprivation (PSD) increases pain sensitivity and reduces morphine antinociception. Because dopaminergic neurons in the periaqueductal gray matter (PAG) participate in pain modulation and opioid-induced antinociception, we evaluated the effects of PSD on thermal pain sensitivity, morphine- and L-DOPA-induced antinociception and dopaminergic functionality in the PAG by assessing tyrosine hydroxylase (TH) immunoreactivity. Rats that were subjected to 96h of PSD received vehicle, morphine (2.5, 5 or 10mg/kg), L-DOPA (50 or 100mg/kg) or L-DOPA (50mg/kg)+morphine (2.5 and 5mg/kg) and were tested with a 46°C hot plate 1h after. The paw withdrawal latency responses to the hot plate were decreased in PSD rats and were modified by the highest dose of morphine, L-DOPA and L-DOPA+morphine. Analgesic effects were observed in control groups for all of the morphine doses as well as 100mg/kg of L-DOPA and L-DOPA (50mg/kg)+morphine (5mg/kg). The number of cell bodies that were immunopositive for TH in the PAG was reduced in PSD rats. In conclusion, increased thermal sensitivity was reversed by L-DOPA and could be caused by a reduction TH levels in the PAG. Our data also suggest a relationship between central dopaminergic networks and opiate-induced analgesia in rats., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Sleep deprivation has been associated with hyperalgesia in humans and in animal models. The tricyclic antidepressant amitriptyline is used as an analgesic drug in patients and in animal models of chronic pain, including that associated with spinal nerve injury. Pain hypersensitivity following paradoxical sleep deprivation (PSD) and that following peripheral nerve injury seem to share common spinal mechanisms. Accordingly, we evaluated the effects of amitriptyline (acutely and chronically administered) on the increased thermal response observed in PSD rats (72 or 96 h). Rats were evaluated for thermal sensitivity using a hot plate (52 degrees C or 46 degrees C) at 1 or 24 h after the last administration of the drug. Following the hot plate test, motor behavior was analyzed in an open field arena for a period of 5 min. Paw withdrawal latency response to temperatures of 46 degrees C and 52 degrees C was significantly lower in PSD and in 24-hour post-PSD rats than in controls and it was not modified by amitriptyline (3, 10 and 30 mg/kg). Analgesic effects and reduced motor behavior were only observed in control groups. Overall, these findings indicate that a period of PSD can influence pain modulatory mechanisms, and that amitriptyline action is insufficient to reduce PSD-enhanced thermal sensitivity.

The acute administration of amantadine (AMA), a dopaminomimetic and NMDA glutamatergic receptor antagonist also used as an anti-Parkinsonian agent, stimulates male rat sexual behaviour. However it remains unclear whether long term AMA supplementation might also provoke a similar increase in male rat sexual conduct. In the present study, male rats were administered AMA (5-50 mg/kg/day) or vehicle daily for 21 days and their sexual response was monitored weekly. Chronic treatment with AMA effectively increased the sexual response of male rats, similarly to what had been observed before with acute amantadine treatment. The main effect of chronic AMA treatment occurs in arousal and in ejaculatory response, whilst the excitatory component was not affected. The 21-day treatment with AMA did not lead to tolerance, suggesting that perhaps AMA could be used in male human patients to prevent sexual inhibition caused by anti-depressant and anti-psychotic agents.

The mechanism of control of GAD expression by GABA and excitatory amino acids (EAAs) was studied in chick and rat retina cultures using immunohistochemical and PAGE-immunoblot detection of the enzyme, as well as by measuring enzyme activity. Aggregate cultures were prepared with retina cells obtained from chick embryos at embryonic days 8-9 (E8-E9). Organotypical cultures were also prepared with retinas from E14 chick embryos, post-hatched chicken and P21 rats. GABA (1-20 mM) fully prevented GAD expression in aggregate and organotypical cultures from chick embryo retinas. A substantial, but not complete, reduction of GAD was also observed in organotypical cultures of post-hatched chicken and P21 rats, in which both forms of the enzyme (GAD65 and 67) were affected. The GABA effect was not mimicked by THIP (100 microM), baclofen (100 microM) or CACA (300 microM), agonists of GABAa, b and c receptors, respectively. NNC-711, a potent inhibitor of GABA transporters, reduced by 50% the inhibition of GAD activity promoted by GABA. Aggregates exposed to GABA and treated with glutamate (5 mM) or kainate (100 microM) displayed an intense GAD-like immunoreactivity in many cell bodies, but not in neurite regions. Immunoblot analysis revealed that the increase in GAD-like immunoreactivity by EAA corresponded to a 67-kDa protein. However, GAD activity was not detected. Treatment of aggregates or retina homogenates with SNAP, a NO producing agent (but not its oxidized form), reduced GAD activity by more than 60% indicating that the lack of enzyme activity in GAD-like immunoreactive cells, could be due to NO production by EAA stimulation.

Choline acetyltransferase (ChAT) activity was reduced by more than 85% in cultured retina cells after 16 h treatment with 150 microM kainate (T(1/2) : 3.5 h). Glutamate, AMPA and quisqualate also inhibited the enzyme in equivalent proportion. Cell lesion measured by lactate dehydrogenase (LDH) release, 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide - thiazolyl blue (MTT) reduction and microscopic observation was not detected even after 48 h with kainate. Other retina neurochemical markers were not affected by kainate and full recovery of the enzyme was achieved 9 days after kainate removal. Moreover, hemicolinium-3 sensitive choline uptake and hemicolinium-3 binding sites were maintained intact after kainate treatment. The immunoblot and immunohistochemical analysis of the enzyme revealed that ChAT molecules were maintained in cholinergic neurons. The use of antagonists showed that ionotropic and group 1 metabotropic receptors mediated the effect of glutamate on ChAT inhibition, in a calcium dependent manner. The quisqualate mediated ChAT inhibition and part of the kainate effect (30%) was prevented by 5 mM N(G)-nitro-L-arginine methyl ester (L-NAME). Veratridine (3 microM) also reduced ChAT by a Ca(2+) dependent, but glutamate independent mechanism and was prevented by 1 microM tetrodotoxin.

We report the case of a 47-year-old woman with a large keloid scar on the sternum who was submitted to a simultaneous scar removal with bilateral breast-reduction mammaplasty. Breast reduction was performed to reduce local skin tension and to provide a skin flap for the full reconstruction of the scar-removal site. The association of these surgical procedures stands as a viable alternative for the reconstruction of the sternum region, producing less keloid scarring.

Cutaneous injuries of the inferior third of the leg and dorsum of the foot represent a great challenge for plastic surgeons. The poor vascularization and subsequent poor healing encountered in these regions demand detailed knowledge of the local anatomy to select the best surgical alternative for each patient. In patients in whom local or free muscular flaps are not suitable, the fasciocutaneous flaps seem to be a good alternative. The distal pedicled fasciocutaneous flap of the calf was used to cover skin defects of the leg and foot in 22 patients. In 4 patients the authors designed an island flap to prevent a large defect in the donor area and to decrease the time of hospitalization and recovery of the patient. In a severe defect, the flap was used as a cross-leg flap. The results were satisfactory because the flap provided stable coverage for different defects with few complications. The island flap is a good option for achieving a better aesthetic result and can be used in select patients.

The importance of facial trauma comes from the possibility of leaving serious functional and aesthetic consequences. Since 1990 patients with facial fractures were treated at the Emergency Ward of the Hospital das Clinicas of the Medical Faculty of São Paulo by plastic surgeons. In 24 months, 130 patients with facial fractures were treated there. The main causative factors were motor vehicle accidents (51%) and the main bone fracture was that of mandible (46%). A correlation between the kind of trauma and the kind of fracture is made.

The authors present thirty-four patients with microgenia operated on by advancement genioplasty. The indications and advantages of this method in improving the facial profile are reviewed and compared with other surgical possibilities described in the literature.

The clinical features of the toxic shock syndrome are well established. It is rapidly developing disease and may be lethal if not recognized and treated in time. Once the syndrome was associated with the use of tampon by menstruating women. Recently this syndrome has been reported as due to Staphylococcus aureus infection. A severe case of toxic shock syndrome in a 18-years-old patient after reduction mammoplasty is reported, and the importance of an early diagnosis is emphasized.

The lateral calcaneal artery flap is an axial flap which comprises also the saphenous vein and the sural nerve. Its use has been reported for coverage of skin loss of the malleolus and calcaneal area. The donor area should be closed by a split thickness skin graft. In the present report, eight patients who had skin loss on the foot were submitted to reconstruction with the lateral calcaneal flap. In seven there were island flaps and in one a bridge of skin similar to that described by Grabb and Argenta. The etiology was trauma in five patients and decubitus ulcer in three. The results were good. The flap was adequate for the cover on the posterior foot area even after submitted to the strain of normal walking. The advantages were simpler technique and consistency of the anatomical landmarks.

We describe a case of advanced chronic renal failure with persisting hypokalemia. The clinical study revealed the simultaneous presence of a salt and potassium loosing nephropathy associated with aldosterone-producing adenoma. This late pathology was revealed as electrolytic changes characteristic of primary hyperaldosteronism became evident as the renal function progressively deteriorated.