[Application of a universal system of epitesis fixation in the rehabilitation of patients with maxillofacial defects]. / Proizvodstvo i primenenie universal'noi sistemy fiksatsii epitezov pri reabilitatsii patsientov s defektami litsa.

OBJECTIVE: The aim of the study was the creation of a universal epithesis fixation system that increases the reliability of its functioning in prosthetics of patients with maxillofacial defects of various genesis. MATERIAL AND METHODS: After the surgical preparation of patients, in accordance with the indications of the underlying disease, epithesis was made from rigid silicone elastomers using CAD/CAM technologies. For the production of attachments, the VT1-0 titanium alloy common in medicine was used. RESULTS: A universal epithesis fixation system was used for prosthetics of various parts of the patient's face. Depending on the clinical situation and the size of the prosthetics area, an intermediate lattice plate (mesostructure) of the appropriate size and configuration was selected. Two types of attachments were used to fix epithets: magnetic with a counterpart and non-magnetic mushroom-shaped. The universal epithesis attachment system is distinguished by the possibility of using each hole of the lattice, both for attaching it to the bone structure and for installing attachments, which makes it easy to fix the lattice to residual bone fragments and center the position of the transition elements and attachments depending on the aesthetic and functional needs of the structure in whole. CONCLUSION: The success of prosthetics largely depends on the epithesis attachment system. The proposed universal epithesis fixation system allows its use in various clinical situations and also reduces the cost of prosthetics for patients with maxillofacial defects.

Newly generated dentate granule cells from epileptic rats exhibit elongated hilar basal dendrites that align along GFAP-immunolabeled processes.

Previous studies showed that neurogenesis occurs in the dentate gyrus of the adult rodent. Recent evidence suggests that the resulting newly born neurons integrate into pre-existing hippocampal circuitry. Newly born neurons in the developing and adult dentate gyrus exhibit a transient basal dendrite. In adult pilocarpine-induced epileptic rats, basal dendrites persist and are ectopically located in the hilus where they receive synaptic input from mossy fiber axons. We hypothesize that these hilar basal dendrites are derived from newly born neurons that are born after the pilocarpine-induced seizures. To test this hypothesis, the length of basal dendrites from epileptic rats was compared with that from control rats using doublecortin immunocytochemistry, which labels newly born neurons and their processes for up to 3 weeks after their genesis. The data on hilar basal dendrites in pilocarpine animals indicate that those from newly born neurons are significantly longer than those found in the control rats. We also demonstrate that 20% of newly born neurons in the epileptic rat have a basal dendrite that enters the hilus at an angle greater than 30 degrees from its cell body as compared with <2% in the control rats. Lastly, we provide evidence that the hilar basal dendrites in the epileptic rats are adjacent to glial fibrillary acidic protein-labeled astrocytic processes in the hilus and suggest that an ectopic glial scaffold in the hilus is involved with the formation of hilar basal dendrites. In conclusion, the data show that newly born neurons from epileptic rats have longer hilar basal dendrites and their formation might relate to gliosis which occurs as a result of hilar neuronal cell loss after status epilepticus.

Increase in serotonin-1A autoreceptors in the midbrain of suicide victims with major depression-postmortem evidence for decreased serotonin activity.

It has been hypothesized that a deficit in serotonin may be a crucial determinant in the pathophysiology of major depression. Serotonin-1A receptors are located on serotonin cell bodies in the midbrain dorsal raphe (DR) nucleus, and the activation of these receptors inhibits the firing of serotonin neurons and diminishes the release of this neurotransmitter in the prefrontal cortex. Repeated treatment with some antidepressant medications desensitizes serotonin-1A receptors in the rat midbrain. The present study determined whether the binding of [3H]8-hydroxy-2-(di-n-propyl)aminotetralin (8-OH-DPAT), an agonist at serotonin-1A receptors, is altered in the midbrain of suicide victims with major depression. Radiolabeling of the serotonin-1A receptor in the DR varied significantly along the rostral-to-caudal extent of the human midbrain. The binding of [3H]8-OH-DPAT to serotonin-1A receptors was increased significantly in the midbrain DR of suicide victims with major depression as compared with psychiatrically normal control subjects. In suicide victims with major depression, the increase in the binding of [3H]8-OH-DPAT to serotonin-1A receptors was detected in the entire DR and specifically localized to the dorsal and ventrolateral subnuclei. Enhanced radioligand binding of an agonist to inhibitory serotonin-1A autoreceptors in the human DR provides pharmacological evidence to support the hypothesis of diminished activity of serotonin neurons in suicide victims with major depression.

Serotonin receptors in suicide victims with major depression.

Serotonin1A (5-HT1A) and serotonin2A (5-HT2A) receptors in the brain have been implicated in the pathophysiology of suicide. Brain samples were collected at autopsy from suicide victims with a current episode of major depression and matched comparison subjects who died of natural or accidental causes. Retrospective psychiatric assessments were collected from knowledgeable informants for all suicide victims and most of the comparison subjects. Psychiatric diagnoses were determined according to DSM-III-R criteria. Any subjects with current psychoactive substance use disorders were excluded. Quantitative receptor autoradiography was used in serial sections of the right prefrontal cortex (area 10) and hippocampus to measure the binding of [3H]8-hydroxy-2-(di-n-propyl)-aminotetralin ([3H]8-OH-DPAT) to 5-HT1A receptors and [3H]ketanserin to 5-HT2A receptors. Analysis of covariance was used to compare control subjects and suicide victims with major depression. The age of subjects, the time from death to freezing the tissue (postmortem interval), and the storage time of tissues in the freezer were used as covariates in the analyses. There were no significant differences between suicide victims with major depression and comparison subjects in 5-HT1A or 5-HT2A receptors in area 10 of the right prefrontal cortex or the hippocampus. The current results suggest that the number of 5-HT1A and 5-HT2A receptors in the right prefrontal cortex (area 10) or hippocampus are not different in suicide victims with major depression.

Quantitative subregional distribution of serotonin1A receptors and serotonin transporters in the human dorsal raphe.

Subregional distributions of serotonin1A receptors and serotonin transporters within the human dorsal raphe nucleus (DR) were determined by quantitative autoradiographic analyses of radioligand binding in tissue sections. [3H]8-Hydroxy-2-(di-n-propyl)aminotetralin (8-OH-DPAT) and [3H]paroxetine were used to label, respectively, serotonin1A receptors and serotonin transporters in the subnuclei of the DR, which were delineated on the basis of tryptophan hydroxylase (TrpOH) immunoreactivity. [3H]8-OH-DPAT binding was coextensive with the TrpOH-immunoreactive cell bodies and fibers but was distributed unevenly among the subnuclei. In contrast, [3H]paroxetine binding was present throughout the central gray matter, with relatively homogeneous labeling across the subnuclei of the DR. In rostral sections, [3H]8-OH-DPAT binding (fmol/mg protein) in the dorsal subnucleus was lower than that in the ventral or the interfascicular subnucleus. Within the interfascicular subnucleus, [3H]8-OH-DPAT binding decreased progressively in a rostral-to-caudal fashion. The highest levels of [3H]8-OH-DPAT binding were found in the ventrolateral subnucleus at the level of the caudal extent of the trochlear nucleus. The influence of age and postmortem interval on radioligand binding was also examined. These data in the human DR indicate that serotonin1A receptors are differentially distributed among the subnuclei and along the rostro-caudal axis of the midbrain raphe, and serotonin transporters appear to be relatively evenly distributed throughout the DR. Subregional analyses of such serotonergic markers may prove useful in evaluating the role that serotonin may play in depression, schizophrenia, and suicide.

The effect of chronic treatment with a novel aryl-piperazine antipsychotic on monoamine receptors in rat brain.

The effects of chronic treatment of rats with RWJ 37796, a novel aryl-piperazine containing antipsychotic drug, on brain monoamine receptors were studied. Rats were treated daily with RWJ 37796 (1.3 mg/kg), the typical antipsychotic haloperidol (1 mg/kg) or vehicle (control) for 21 days, and were sacrificed 3 days after the last injection. Binding of [3H]Sch-23390 and [3H]spiperone to D1 and D2 dopamine receptors, respectively, and [3H]8-hydroxy-2-(di-n-propylamino)-tetralin ([3H]8OH-DPAT) to 5-HT1A receptors were measured in various brain regions using quantitative autoradiography. Binding to D2 dopamine receptors was significantly elevated in the caudate-putamen of rats treated with haloperidol or RWJ 37796 as compared to controls. However, the magnitude of the increase in D2 binding was significantly greater in haloperidol-treated (+38%) compared to RWJ 37796-treated (+21%) rats. Haloperidol treatment also increased binding (+35%) to D2 dopamine receptors in the nucleus accumbens, where RWJ 37796 treatment had a considerably smaller effect (+12). No changes in D1 dopamine or 5-HT1A receptor binding were detected following either antipsychotic treatment in any brain regions studied. Thus, at comparable doses, the novel antipsychotic RWJ 37796 produces less up-regulation of D2 dopamine receptor binding in the striatum than does the typical antipsychotic haloperidol.

Repeated treatment with ascorbate or haloperidol, but not clozapine, elevates extracellular ascorbate in the neostriatum of freely moving rats.

Acute administration of neuroleptic drugs alters the extracellular level of ascorbate in the neostriatum, and increasing evidence suggests a role for this vitamin in the behavioral, and possibly therapeutic, effects of these drugs. To shed further light on this issue, extracellular ascorbate was recorded in the neostriatum and nucleus accumbens of awake, behaving rats following chronic treatment with either classical (haloperidol) or atypical (clozapine) neuroleptics or ascorbate itself. Electrochemically modified, carbon-fiber microelectrodes were lowered in place the day after the last of 21 daily injections of either haloperidol (0.5 mg/kg, SC), clozapine (20 mg/kg, IP), sodium ascorbate (500 mg/kg, IP) or vehicle. Voltammetric measurements were obtained during quiet rest and following administration of d-amphetamine (2.5 mg/kg). Repeated treatment with either haloperidol or ascorbate elevated basal extracellular ascorbate and potentiated the amphetamine-induced increase in ascorbate release in neostriatum but not nucleus accumbens. Both treatment groups also showed a significant increase in amphetamine-induced sniffing and repetitive head movements compared to vehicle-treated animals. In contrast, repeated clozapine had no effect on extracellular ascorbate in either neostriatum or nucleus accumbens, but increased the locomotor response to an amphetamine challenge. Thus, to the extent that increases in neostriatal ascorbate exert neuroleptic-like effects, such effects are likely to parallel haloperidol rather than clozapine.

[The effect of phenobarbital, ionol and cAMP on the activity of glutathione metabolism enzymes in rodents]. / Vliianie fenobarbitala, ionola i cAMP na aktivnost' fermentov metabolizma glutationa u gryzunov.

The phenobarbital and ionol administration to rats and mice increases considerably the glutathione transferase, glutathione reductase and gamma-glutamyl transferase activities in the liver. The induction of these enzymes has been observed in a number of experiments in the heart and kidney but it was less pronounced. A correlation was established between the induction of glutathione transferase, glutathione reductase and gamma-glutamyl transferase, their changes in mice and rats, phenobarbital and ionol effects. The stimulatory effect of cAMP on glutathione transferase in the liver (and in a number of experiments in the heart) increased against a background of the both agents. The cAMP-dependent activation of glutathione peroxidase was retained in the heart but in some series experiments it disappeared in the liver and kidney. Mechanisms of the long-term (induction) and short-term (cAMP) elevation of the glutathione transferase and glutathione peroxidase activities functioned independently and often in concord. It is suggested that induction of glutathione metabolism enzymes may play an important role in biological effects of ionol.

[The changes in the enzymatic activity of glutathione metabolism in immobilization stress and their possible significance]. / Izmeneniia aktivnosti fermentov metabolizma glutationa pri immobilizatsionnom stresse i ikh vozmozhnoe znachenie.

Immobilization of rats for 20 minutes and for 4 hours activates glutathione peroxidase in the heart, liver, and kidneys and glutathione transferase in the heart and liver, but inhibits gamma-glutamyl transferase in the liver and kidneys. Most of these changed values become normalized one hour after cessation of 4-hour stress. Propranolol completely prevents activation of glutathione peroxidase and glutathione transferase by stress. The changes in the activity of the glutathione metabolism enzymes are evidently of a protective character in relation to lipid peroxidation.

Protective effect of occlusion on disciform degeneration.

One patient developed disciform degeneration and loss of central vision despite laser application. Sixty-two years before, the contralateral eye had sustained a penetrating steel injury with subsequent scarring and pupillary membrane and cataract formation. This eye, when surgically rehabilitated, showed no signs of macular degeneration. Although alluded to, we know of no other known cases of occluded eyes being spared of senile macular degeneration reported in the literature. We postulate that unfiltered, ambient light may be the cause of macular degeneration and suggest that more emphasis should be placed on prevention of macular degeneration by the use of protective eye wear.

[Regulation by catecholamines and cAMP of enzymes of thiol and disulfide metabolism]. / Issledovanie reguliatsii katekholaminami i cAMP fermentov obmena tiolov i disul'fidov.

In vivo exo- and endogenous catecholamines have no influence on the activities of thioredoxin reductase, glutathione reductase, thiol transferase and nonselenium-dependent glutathione peroxidase. At the same time catecholamines activate via beta-adrenoceptors glutathione S-transferase and selenium-dependent glutathione peroxidase from many tissues and inhibit gamma-glutamyl transferase from kidney. In vitro cAMP has identical effects on the activities of the above enzymes. The possible significance of regulation of glutathione metabolism enzymes is discussed.

[Effect of emotional stress on the activity of enzymes of glutathione metabolism]. / Vliianie émotsional'nogo stressa na aktivnost' fermentov metabolizma glutationa.

Emotional stress during 20 min induced the stimulation of the glutathione peroxidase activity in heart, liver and kidney tissues and the activation of glutathione-S-transferase in heart and liver tissues. gamma-Glutamyl transferase activity was inhibited in liver and kidney tissues. The alterations were gradually decreased in heart greater than or equal to liver greater than kidney. Both catecholamines (in vivo) and cAMP (in vitro) produced the same effects. Close correlation between the stress and cAMP actions on the glutathione metabolizing enzymes was found. No changes of glutathione reductase activity was observed in all the tissues studied.

[Activity of enzymes of glutathione metabolism and regulation by cAMP in human tumors]. / Aktivnost' fermentov metabolizma glutationa i ikh reguliatsiia tsAMF v opukholiakh cheloveka.

Tumors were studied in 38 patients, tissues located far away from tumor being used as control. Breast and stomach tumors revealed relatively high levels of glutathione reductase, glutathione-S-transferase (I) and, particularly, gamma-glutamyl transferase (II). The said changes were not observed in colorectal tumors. Gamma-glutamyl transferase (II) may be used as a marker for breast and stomach malignancies in man but it is not a universal and absolutely specific marker for all tumors. The activity of glutathione peroxidase (III) either did not change or decreased. The activating effect of cAMP on III and I remained generally unchanged in all tumors studied.

Single-injection epidural anesthesia with bupivacaine and morphine for prostatectomy.

In 30 patients having prostatectomies, 15 patients (group I) given single-injection epidural anesthesia using bupivacaine and morphine (4 mg) were compared with 15 patients (group II) given epidural bupivacaine without morphine. Patients in group I had pain relief for a mean duration of 27 hours and did not request additional analgesia. Patients receiving bupivacaine alone had pain relief for an average of 6.2 hours after surgery; all required narcotics postoperatively. It was concluded that the addition of 4 mg of morphine to the local anesthetic for epidural anesthesia in patients having prostatectomies results in excellent postoperative analgesia.

Lipid keratopathy following corneal hydrops.

A case of lipid keratopathy occurred following acute rupture of Descemet membrane. The cause of the hydrops remained undetermined. There was no history of any prior corneal inflammation or vascularization in the initially involved eye. Lipid deposition was observed following resolution of the corneal edema, and its course was followed for the next several months. Histopathologic studies of the specimen showed lipid deposits in the posterior and middle corneal stroma and degenerative changes in the corneal lamellae and Bruch membrane. Laboratory examination disclosed a type IV hyperlipemia, with normal serum cholesterol levels and elevation of pre-beta-lipoproteins and triglycerides. It cannot be determined from our study if this condition was a causative factor.