SILICON WIRES FOR NERVE GAP MANAGEMENT: ROLE OF SURFACE PROPERTIES IN NERVE REGENERATION.

Up to 15% of combat trauma cases are accompanied by neuroinjuries with nerve gap formation that need to be bridged using various techniques and materials. Both with this prevalence of limb loss, especially traumatic amputations, tends to grow. Loosed limbs must be prosthetized by modern functional mind-controlled prosthesis based on nerve- or brain-computer interfaces. This study aimed at morphological evaluation of interaction between nerve fibers and silicon wires with different surface properties using peripheral nerve injury and grafting model. Experiment was performed on 50 male Wistar rats, weighing 180-250 g. Rats from experimental groups underwent sciatic nerve injury Sunderland 5 degree with a 10 mm gap formation that was subsequently filled with conduit consisting of decellularized aorta, carboxymethylcellulose gel and a set of longitudinally oriented p-type silicon wires 2-20 µm in diameter. We used silicon wires with native oxide in group Ia, with hydrogen-cleaned surface in group Ib and thermally grown oxide in group Ic. The gap in control groups was filled with decellularized aorta with gel alone (group II) or by autoneurograft (group III). 6 weeks postoperatively the conduit site was harvested and light microscopy performed. Implantation of conduit with native oxide on silicon wires surface resulted in more complete and equal neurotization of the conduit site with close adherence between the newly-formed nerve fibers and silicon wires, in comparison with groups where wires with other surface properties have been used. P-type silicon wires with native oxide are seems to be more suitable than other types of wires for further electrode preparation as a part of regenerative implants.

DYNAMICS OF MORPHOLOGICAL CHANGES OF RATS' ADENOHYPOPHYSIS IN BURN DISEASE.

The article presents data relating to structural changes in rat adenohypophysis in experimental burn disease and its treatment. Experimental studies were conducted for defining peculiarities of structural changes in rats' adenohypophisis without and after skin burn injuries (in 7-14 and 21-30 days) alongside its correction with 0.9% NaCl solution. Application of DNA-cytometry allowed defining subtle mechanisms of pathogenic influence of burn injuries on the organism in general and the cells in particular.

[REACTIVE CHANGES IN SPINAL CORD MOTONEURONS AFTER SCIATIC NERVE INJURY AFTER HIGH-FREQUENCY ELECTROSURGICAL INSTRUMENT APPLICATION].

A new experimental model for tissues connection at peripheral nerve injury site in form of tissues welding was designed. In current study we investigated motoneuron state 1, 3, 6 and 12 weeks after peripheral nerve injury and surgical repair with high-frequency electrosurgical technology. Spinal cord sections was stained by Nissl method and observed with light microscopy. We found that postoperative period in animals from experimental groups characterized by qualitative changes in neurons from spinal motor centers that can be interpreted as compensatory processes as response to alteration. In animals from group with high-frequency electrosurgical technology usage stabilization processes passes more quickly comparatively to animals with epineural sutures. High-frequency electrosurgical technology usage provides less harmful effects on motoneurons than epineural suturing.

Immunohistochemical Analysis of the Structure of Injured Peripheral Nerve Neuroma after Electrosurgical Welding Intervention.

Immunohistochemical analysis of changes in neuroma after surgical treatment of damaged peripheral nerve with the use of high frequency electrosurgical device for high frequency current welding of soft tissues was carried out. No adverse effects of this technology and the bipolar instrument on degeneration and regeneration of damaged nerve stem were detected.

Lactate-mediated glia-neuronal signalling in the mammalian brain.

Astrocytes produce and release L-lactate as a potential source of energy for neurons. Here we present evidence that L-lactate, independently of its caloric value, serves as an astrocytic signalling molecule in the locus coeruleus (LC). The LC is the principal source of norepinephrine to the frontal brain and thus one of the most influential modulatory centers of the brain. Optogenetically activated astrocytes release L-lactate, which excites LC neurons and triggers release of norepinephrine. Exogenous L-lactate within the physiologically relevant concentration range mimics these effects. L-lactate effects are concentration-dependent, stereo-selective, independent of L-lactate uptake into neurons and involve a cAMP-mediated step. In vivo injections of L-lactate in the LC evokes arousal similar to the excitatory transmitter, L-glutamate. Our results imply the existence of an unknown receptor for this 'glio-transmitter'.

Rostral ventromedial medulla and the control of cutaneous vasoconstrictor activity following i.c.v. prostaglandin E(1).

Neurones within the rostral ventromedial medulla project to the intermediolateral cell column of the spinal cord where they may influence sympathetic preganglionic neuronal activity controlling cutaneous vascular beds. Here we assess whether such neurones contribute to cutaneous sympathetic vasoconstrictor activity in a fever-like state induced by i.c.v. injection of E-series prostaglandin. In urethane-anaesthetised rats, we recorded population sympathetic activity to the tail (an index of vasoconstrictor discharge regulating cutaneous thermoregulatory circulations). A survey of the effects of GABA microinjections (200 mM; 60-80 nl; 111 sites in 57 rats) demonstrated that those into the rostral ventromedial medulla (in the region of raphe pallidus and magnus; approximately bregma -10 to -12 mm) markedly decreased (51%-100%) population sympathetic cutaneous vasoconstrictor activity during "normothermic control." In contrast, injections at sites dorsal and lateral to this region tended to produce either a smaller decrease or have no effect. In heat-clamp (nine animals: body temperature 40-41 degrees C) cutaneous vasoconstrictor activity was decreased by 83+/-5%. I.c.v. prostaglandin E(1) (100 ng and above) restored activity to, or above, control levels in these animals and where body temperature was maintained at control levels (12 animals: body temperature 35.5-36.5 degrees C). The depressant action of GABA was sustained in both conditions. GABA did not significantly influence concurrently recorded splanchnic nerve activity and heart rate in any condition although both were increased following i.c.v. prostaglandin E(1) (500 ng). This study is the first to demonstrate that inhibition of neuronal activity within the rostral ventromedial medulla decreases sympathetic cutaneous vasoconstrictor activity during normothermic control and following i.c.v. prostaglandin E(1) (both with and without heat-clamp). Therefore, sympathetic premotor neurones in this area contribute to vasoconstrictor drive in these conditions. In contrast, we were unable to demonstrate that the same area had a substantial involvement in the control of splanchnic nerve activity or heart rate, even when these were enhanced following i.c.v. prostaglandin E(1).

Cutaneous sympathetic motor rhythms during a fever-like response induced by prostaglandin E(1).

Neuronal population discharges within the CNS and in somatic and sympathetic motor nerves often display oscillations. Peripheral oscillations may provide a window into central mechanisms, as they often show coherence with population activity of subsets of central neurones. The reduction in heat loss through the cutaneous circulation during fever may be mediated via sympathetic premotor neurones not utilised during normal temperature regulation. Consequently, here we assessed, in anaesthetised rats, whether the frequency signature of population sympathetic discharge observed in neurones innervating the tail (thermoregulatory) circulation changed during a fever-like response induced by intracerebroventricular injection of prostaglandin E(1). We found that when core temperature was raised to 38.8-40.5 degrees C sympathetic activity was abolished. Following administration of prostaglandin (400 ng or 1 microg per rat), activity was restored to levels seen prior to heating (154+/-53.5%; n=10). Injection of vehicle had no effect (n=7). Prior to heating when most animals were in central apnoea (14/18) two peaks were observed in autospectra of sympathetic activity: one at 0.68-0.93 Hz (T-peak) and another at the frequency of ventilation (2 Hz). Central respiratory drive was recruited during hyperthermia where it was 1:2 locked to the frequency of ventilation and following prostaglandin administration, an additional peak in sympathetic autospectra was seen at this frequency. Time-evolving spectra indicated that this peak resulted from the dynamic locking of the 'T-peak' to central respiratory drive. Our data show that during a fever-like response the dominant oscillations in sympathetic activity controlling a thermoregulatory circulation and their dynamic coupling to respiratory-related inputs are similar to those seen under normal conditions. Therefore, during this fever-like response, the neural substrate(s) underlying the oscillations is not reconfigured and remains capable of sculpturing the pattern of sympathetic neuronal discharge that may be regulated by several descending pathways.

Role of capsaicin-sensitive afferents in fever and cytokine responses during systemic and local inflammation in rats.

OBJECTIVE: Peripheral afferents play an important role in fever. In the present study, we investigated the role of capsaicin-sensitive afferents in fever and cytokine responses during systemic (induced by intraperitoneal lipopolysaccharide, LPS) and local (induced by injection of Freund's incomplete adjuvant, FIA, into the paw) inflammation. METHODS: Fevers in rats (8-10 weeks of age) whose capsaicin-sensitive afferents were depleted by neonatal capsaicin (50 mg/kg) treatment were compared to those of rats treated as neonates with vehicle. To investigate a possible involvement of cytokines, plasma levels of interleukin-6 (IL-6) and tumor necrosis factor (TNF) were measured during LPS- and FIA-induced fever in rats after capsaicin-induced desensitization. Body temperature was measured by biotelemetry. IL-6 and TNF bioactivities in plasma were determined using bioassays. RESULTS: The initial but not the late phase of LPS (50 microg/kg)-induced fever was markedly higher (approximately 1.0 degree C) in rats whose capsaicin-sensitive neurons were destroyed by neonatal capsaicin treatment. Capsaicin-induced desensitization also resulted in significantly higher plasma levels of IL-6 and TNF 1 but not 4 h after LPS challenge. In contrast, the day after injection with FIA (0.1 ml), rats treated with capsaicin had significantly lower body temperatures compared with vehicle-treated animals. No differences were found in plasma levels of IL-6 and TNF between capsaicin- and vehicle-treated animals in response to FIA. CONCLUSIONS: These data indicate that the role of capsaicin-sensitive afferents in fever depends on the type of inflammatory response. During systemic inflammation, capsaicin-sensitive afferents may be involved in modulating fever by regulating the levels of pyrogenic cytokines. During local inflammation, the late phase of fever is partially mediated via capsaicin-sensitive afferents.

[Experience with the diagnosis and treatment of secondary odontogenic mediastinitis]. / Opyt diagnostiki i lecheniia vtorichnogo odontogennogo mediastinita.

Thirteen patients with acute odontogenic mediastinitis were diagnosed and treated. The authors stress that the disease is a rare (0.89%) complication of odontogenic infection with high rate of lethal outcome (23.1%) due to delayed diagnosis and insufficient surgical intervention despite the severe course of the ailment. With timely performed surgery and intensive care measures, 9 patients had a benign outcome of the disease.

Long-term energy savings hospital's goal.

Using cost/benefit analysis, this hospital has implemented a variety of cost-effective energy conservation projects and is looking into long-term programs for the future.

How to use malpractice data in quality assessment.

Although some may doubt that malpractice claims data are a useful quality assurance device, a recently released volume compiled by the National Association of Insurance Commissioners dispels much of this criticism, according to the author. The article details how the data were derived and suggests how they might be used in the hospital setting.