Observation of the short-term curative effect of using SuperPATH approach to treat elderly femoral neck fractures with schizophrenia.

As China enters an aging society, the incidence of femoral neck fractures is increasing year by year. For some patients, total hip arthroplasty (THA) is the treatment of choice for displaced femoral neck fractures. Schizophrenia is a common combination of elderly patients with femoral neck fractures, and there are few reports on the treatment. This study describes the short-term efficacy of the supercapsular percutaneously assisted (SuperPATH) approach in the treatment of patients suffered with displaced femoral neck fractures combined with schizophrenia. A retrospective analysis of 20 elderly patients with displaced femoral neck fractures combined with schizophrenia who underwent THA using the SuperPATH approach. Record demographic data, postoperative reexamination of X-ray film to observe the position and the loosening condition of the prosthesis, the length of hospitalization, complications in the hospital and after discharge. The Harris score of hip joint function was used to evaluate postoperative hip joint function. The average age of the 20 patients was 73.1 years. All patients were followed up by outpatient clinic or telephone. The follow-up time was 3-12 months, with an average of 9.2 months. There was no incision infection, no tissue structure damage such as important nerves and blood vessels, and no complications such as early dislocation, loosening of the joint prosthesis, and deep vein thrombosis of lower extremities. The efficacy of the last follow-up was evaluated according to the Harris score of hip joint function: an average of 91 points (78-98 points); 13 cases were excellent, 5 cases were good, and 2 cases were fair. The SuperPATH approach has the advantages of less surgical damage, shorter recovery time, good surgical safety, preserving the normal tension of the muscles around the hip joint, and reducing the incidence rate of early postoperative dislocation of the joint prosthesis. The THA of the SuperPATH approach can treat patients with displaced femoral neck fractures combined with schizophrenia safely and effectively.

Transient up-regulation of gamma-aminobutyric acid(A) receptor binding by lubeluzole after neocortical specify lesion in rats.

The effect of the neuroprotective drug lubeluzole on cortical receptor binding was investigated in animals with photothrombotic ischemic lesions. Control animals were treated with the inactive stereoisomer of the drug. Lubeluzole was applied intravenously as a single bolus (0.31 mg/kg) followed by a 1-h infusion of 0.31 mg/kg. Lubeluzole selectively increased gamma-amino-butyric acid(A) (GABA(A)) receptor binding but had no significant and/or consistent effects on N-methyl-D-aspartate (NMDA), (+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), and kainate receptors. Lubeluzole caused a significant up-regulation of GABA(A) receptor binding in the lesioned area as well as in unimpaired cortical areas of both hemispheres. This effect appeared in the hours following the lesion and peaked at 24 h. Our findings suggest that reduced cortical excitability brought about by increased binding capacities of GABA(A) receptors may contribute to the neuroprotective effect of lubeluzole.

Widespread up-regulation of N-methyl-D-aspartate receptors after focal photothrombotic lesion in rat brain.

Following focal brain lesions, complex adaptive processes take place in remote intact areas. The present study examines changes in NMDA (N-methyl-D-aspartate), AMPA ((+/-)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) and kainate receptors following focal photothrombotic ischemic lesions using quantitative receptor autoradiography. Increases in binding density of NMDA receptors were seen in both hemispheres for up to 30 days. In the contralateral hemisphere, this increase of NMDA receptors occurred as early as 4 h after lesion whereas it appeared with a delay for 14 days on the lesioned side. Binding density of [3H]AMPA and [3H]kainate was unchanged. We suggest that the translational process is differentially regulated by spreading depressions. The delayed up-regulation of NMDA receptor binding on the lesioned side may be due to a translation block similar to that previously described for GABA(A) receptor subunits.

Changes in GABA(A) and GABA(B) receptor binding following cortical photothrombosis: a quantitative receptor autoradiographic study.

Experimental cortical photothrombosis leads to pronounced alterations in the binding density of [3H]muscimol and [3H]baclofen to GABA(A) and GABA(B) receptors, both in the lesioned and the structurally intact cortex. The binding density of [3H]muscimol to GABA(A) receptors was markedly increased in the "core" of the lesion during the first week, reaching a maximum on the third day post-lesion. Simultaneously, it dropped in the exofocal primary somatosensory cortex. Reductions in the binding density of [3H]muscimol were also found in remote cortical areas of the contralateral hemisphere and lasted for several weeks. In contrast to the down-regulation of apparent binding density of [3H]muscimol, a long-lasting up-regulation of that of [3H]baclofen to GABA(B) receptors was measured in the exofocal primary somatosensory cortex and in remote cortical areas of both hemispheres. The greatest increase in the binding density of [3H]baclofen was seen on the seventh day in the surroundings of the lesion. Our findings indicate that widespread alterations in the concentrations of GABA(A) and GABA(B) receptors are induced in remote cortical areas by a focal ischaemic lesion. Since GABA(A) receptor affinity is regulated by nitric oxide, we suggest that the observed down-regulation of GABA(A) receptors may be correlated with a lesion-induced increase in nitric oxide, whereas the up-regulation of GABAB receptors might be caused by other mechanisms, e.g., compensatory processes. In the centre of the lesion, however, a GABA(A) receptor-mediated mechanism, which limits the spread of lesion-induced hyperexcitability, is thought to be involved.

Exposure to threshold doses of nicotine in utero: III. Augmentation of the prolactin and ACTH response to 8-OH DPAT by desipramine treatment is compromised in adult male offspring.

Gravid female rats were injected subcutaneously with saline (SAL) or nicotine (3.0 mg/kg and 0.05 mg/kg, bid) from days 14-21 of gestation. Adult 105-day old male offspring from each of the three groups were treated daily with saline or desipramine (DMI) (10 mg/kg, sc) for 14 days. Twenty-four hours after the last injection, animals were challenged with saline or 8-hydroxy-2- (di-n-propylamino) tetralin (8-OH DPAT) (0.1 mg/kg, sc), a serotonin IA(5-HT(IA)) agonist, and plasma prolactin and ACTH concentrations were measured 15 minutes later. DMI treatment augmented both the prolactin and ACTH responses to 8-OH DPAT in the SAL controls. Neither the prolactin nor the ACTH response was augmented significantly in the animals exposed prenatally to either nicotine dosage regimen, although there was a strong trend for the augmentation to occur in the low-dose nicotine exposed animals. The results indicate the capacity of 5-HT systems to adapt normally to DMI administration, as manifested by neuroendocrine responsivity to 8-OH DPAT, was compromised in adult animals exposed to nicotine in utero.

Prenatal stress prevents the desensitization of the corticosterone response to TFMPP by desmethylimipramine, but not by phenelzine, in adult male offspring.

Gravid female rats were subjected to one hour of restraint stress twice daily or left undisturbed from days 14-21 of gestation. Adult 105-day old male non-stressed (NS) and stressed (S) offspring were treated once daily with saline, desipramine (DMI) (10 mg/kg, sc) or phenelzine (5.0 mg/kg, sc) for 14 days. Twenty-four hours after the last injection, animals were challenged with saline or 1-(m-trifluoromethylphenyl)piperazine (TFMPP) (5.0 mg/kg, sc), a serotonin1B/2C (5-HT1B/2C) agonist, and plasma prolactin and corticosterone concentrations were measured one hour later. As compared to acute saline administration, TFMPP significantly increased prolactin and corticosterone concentrations in all groups. In NS offspring, both DMI and phenelzine treatment augmented the prolactin response, but blunted the corticosterone response, to TFMPP. In S offspring, the prolactin response to TFMPP also was augmented by phenelzine or DMI treatment, whereas the corticosterone response to TFMPP was blunted during phenelzine treatment. However, DMI treatment was not able to desensitize the corticosterone response to TFMPP in the S rats. The results indicate the adaptive capacity of 5-HT systems to DMI administration was compromised in adult animals exposed to stress in utero.