Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0599766 (functional recovery)
 13,441 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Apoptotic cell death is a fundamental and highly regulated biological process in which a cell is instructed to participate actively in its own demise. This process of cellular suicide is activated by developmental and environmental cues and normally plays an essential role in eliminating superfluous, damaged, and senescent cells of many tissue types. In recent years, a number of experimental studies have provided evidence of widespread neuronal and glial apoptosis following injury to the central nervous system (CNS). These studies indicate that injury-induced apoptosis can be detected from hours to days following injury and may contribute to neurological dysfunction. Given these findings, understanding the biochemical signaling events controlling apoptosis is a first step towards developing therapeutic agents which would target this cell death process. This review will focus on the molecular cell death pathways responsible for generating the apoptotic phenotype, summarize what is currently known about apoptotic signals activated in the injured CNS, and what potential strategies might be pursued to reduce this cell death process as a means to promote functional recovery.
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PMID:Caspase-3 apoptotic signaling following injury to the central nervous system. 1138 52

Bipolar disorder is a lifelong illness with a course that is usually chronic or recurrent. Severity of complications is generally proportionate to the number of episodes, especially depression. In addition to potentially preventing episodes, effective treatment reduces mortality. This article reviews long-term treatment strategies for bipolar disorder, focusing on depressive episodes, and discusses treatment studies, including problems in design. Treatment effectiveness, including reduction of suicide risk, is enhanced if patients and physicians collaboratively recognize and treat prodromal symptoms, preventing the emergence of episodes. Strategies for treatment differ as one progresses from obtaining syndromal recovery in the acute episode, to functional recovery during continuation treatment, to stability during maintenance treatment. Successful long-term treatment of bipolar disorder requires integrated pharmacologic and nonpharmacologic treatments combined with a therapeutic alliance that facilitates a proactive, preventive approach to the illness.
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PMID:Long-term treatment in bipolar disorder. 1569 46

Apoptotic cell death is a fundamental and highly regulated biological process in which a cell is instructed to actively participate in its own demise. This process of cellular suicide is activated by developmental and environmental cues and normally plays an essential role in eliminating superfluous, damaged, and senescent cells of many tissue types. In recent years, a number of experimental studies have provided evidence of widespread neuronal and glial apoptosis following injury to the central nervous system (CNS). These studies indicate that injury-induced apoptosis can be detected from hours to days following injury and may contribute to neurological dysfunction. Given these findings, understanding the biochemical signaling events controlling apoptosis is a first step towards developing therapeutic agents that target this cell death process. This review will focus on molecular cell death pathways that are responsible for generating the apoptotic phenotype. It will also summarize what is currently known about the apoptotic signals that are activated in the injured CNS, and what potential strategies might be pursued to reduce this cell death process as a means to promote functional recovery.
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PMID:Apoptotic cell death following traumatic injury to the central nervous system. 1624 74

Neurotensin (NT)-polyplex is a nonviral system for the targeted gene delivery to cells that express and internalize the high-affinity NT receptor (NTSR1). In hemiparkinsonian rats, we previously demonstrated the morphological and functional recovery from dopaminergic neurodegeneration using the NT-polyplex as a vehicle to transfect a neurotrophic gene. The main objective of this work was to demonstrate the feasibility of NT-polyplex to transfect reporter or therapeutic genes into neuroblastoma tumors through the blood stream or by intratumoral injection. N1E-115 cells known to express NTSR1 were allografted into athymic mice to generate the neuroblastoma tumor model. Both routes of administration allowed the NT-polyplex to reach and transfect tumoral cells. A low transgene expression was also detected in intestinal tract cells only after the injection into the blood stream. The transfection of the thymidine kinase (HSVTK) suicide gene followed by ganciclovir (GCV) treatment decreased the size and weight of neuroblastoma tumors by 30-50% and increased apoptosis compared to controls. This study shows the potential of the NT-polyplex as specific gene-transfer system for NTSR1 cancer cells.
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PMID:NT-polyplex: a new tool for therapeutic gene delivery to neuroblastoma tumors. 1918 Jan 42

Advances in the field of stem cell research have raised hopes of creating novel cell replacement therapies for Parkinson disease (PD), although double-blinded clinical trials have met with controversial success in patients implanted with fetal midbrain tissue and autopsy results have shown that some of the grafted fetal neurons displayed pathological changes typical of PD. Dopaminergic neurons have been efficiently derived from stem cells using various methods, and beneficial effects after transplantation have been demonstrated in animal models of PD. Some obstacles remain to be overcome before stem cell therapy can be routinely and safely used to treat PD in humans. A widely used prodrug/suicide gene therapy would be applied to stem cells to reduce risk of tumor formation. Since grafts were transplanted ectopically into the striatum instead of the substantia nigra in most current protocols, surviving dopaminergic neurons would not have to be the same subtype as the nigral cells. If the main mechanism underlying any functional recovery achieved by cell therapies is restoration of dopaminergic neurotransmission, then viral vector-mediated gene delivery of dopamine-synthesizing enzymes represents a more straightforward approach. Future targets for cell therapy should include some types of Parkinsonism with degeneration of striatal neurons.
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PMID:[Cell therapy for Parkinson disease]. 2003 Feb 40

Studies of the neurobiology of suicidal behavior have become an important and integral part of psychiatric research. Over the past several years, studies of the role of brain-derived neurotrophic factor (BDNF) in the pathophysiology of suicidality have attracted significant interest of researchers. Multiple lines of evidence including studies of levels of BDNF in blood cells and plasma of suicidal patients, postmortem brain studies in suicidal subjects with or without depression, and genetic association studies linking BDNF to suicide suggest that suicidal behavior may be associated with a decrease in BDNF functioning. Studies of the BDNF function are important for suicide research and prevention because of the multiple reasons including the following: (i) BDNF plays a role in the pathophysiology of depression, post-traumatic stress disorder, substance use disorders and other conditions associated with suicidal behavior. Treatment-induced enhancements of BDNF can facilitate neural integrity and recovery of function in psychiatric disorders, and consequently prevent suicidal behavior; (ii) abnormal BDNF function may be associated with elevated suicidality independently of psychiatric diagnoses. It is possible that treatment-induced improvement in the BDNF function prevents suicidal behavior independently of improvement in psychiatric disorders; (iii) BDNF may be a biological marker of suicidal behavior in certain patient populations. It is to be hoped that the studies of the neurobiology of suicidal behavior will lead to the development of new methods of suicide prevention.
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PMID:Brain-derived neurotrophic factor and suicidal behavior. 2105 76

Depression is the most common neuropsychiatric complication of a stroke (Post Stroke DepressionPSD) and has been shown to impede the recovery and rehabilitation of these patients. Prevalence rates of PSD vary between 6% and 79%. Direct comparison between studies is limited due to their different methodology. Etiology of PSD is determined by biological and psychosocial factors. Symptoms of PSD appear in three areas: affective, somatic and cognitive. Differential diagnosis includes post-stroke fatigue and pseudo-depressive manifestations of ischemic infarctions (apathy, aprosody, athymhormia, pseudobulbar palsy). Mortality in post-stroke patients is higher than in non-depressed stroke patients and suicide ideation is observed in 6.6-11.3% of stroke patients. Selective serotonin reuptake inhibitors (SSRI) are considered as the first choice treatment of PSD. Other therapeutic approaches include cognitive and functional rehabilitation. PSD is a potentially treatable condition, yet under-diagnosed, and has a negative effect on functional recovery and survival of stroke patients.
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PMID:[Post-stroke depression: recognition and treatment interventions]. 2197 Nov 99

Neuropsychiatric manifestations are common post stroke. Depression has a prevalence rate of 9% to 34% in the initial 3 to 6 months following stroke and is the most common neuropsychiatric sequel of stroke. Poststroke depression (PSD) has a significant adverse impact on the course of rehabilitation following stroke, resulting in overall impaired functional outcome. An increased risk of suicide and increased mortality have been reported. The association of depression and stroke is well established, highly complex, and multifactorial in origin, and the etiology of PSD involves size, location and number of lesions, stroke subtype, stroke severity, social handicap, and family support. Additionally, depression itself is an independent risk factor for stroke. In this article, we review the complex pathogenesis of PSD and summarize pharmacological treatment options. Because of recent important results that may relate to underlying cellular restorative processes, we focus on early prophylactic treatment, particularly as it involves selective serotonin uptake inhibitors (SSRIs). There is a recently recognized synergy between functional recovery and depression prophylaxis. New evidence that antidepressants, and SSRIs in particular, can make a substantial contribution to stroke recovery is explored.
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PMID:Poststroke depression: a review emphasizing the role of prophylactic treatment and synergy with treatment for motor recovery. 2361 55

The epidemic of heart failure has stimulated interest in understanding cardiac regeneration. Evidence has been reported supporting regeneration via transplantation of multiple cell types, as well as replication of postmitotic cardiomyocytes. In addition, the adult myocardium harbors endogenous c-kit(pos) cardiac stem cells (eCSCs), whose relevance for regeneration is controversial. Here, using different rodent models of diffuse myocardial damage causing acute heart failure, we show that eCSCs restore cardiac function by regenerating lost cardiomyocytes. Ablation of the eCSC abolishes regeneration and functional recovery. The regenerative process is completely restored by replacing the ablated eCSCs with the progeny of one eCSC. eCSCs recovered from the host and recloned retain their regenerative potential in vivo and in vitro. After regeneration, selective suicide of these exogenous CSCs and their progeny abolishes regeneration, severely impairing ventricular performance. These data show that c-kit(pos) eCSCs are necessary and sufficient for the regeneration and repair of myocardial damage.
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PMID:Adult c-kit(pos) cardiac stem cells are necessary and sufficient for functional cardiac regeneration and repair. 2434 20

We report our experience with a case of attempted suicidal hanging presenting with dysphagia, in which rehabilitation approaches resulted in improvement. A 36-year-old man was discovered collapsed at home. From the finding of a broken cord nearby, attempted suicide by hanging was suspected. He was transported to hospital after 40 minutes, and regained consciousness after emergency treatment. There were no noteworthy findings on brain magnetic resonance imaging, cervical spine computed tomography, or vocal cord examination. There were no noteworthy psychiatric disorders or cognitive abnormalities. On hospital day 10, he showed signs of dysphagia. Videofluoroscopic examination of swallowing revealed piriform sinuses residue and aspiration after ingestion of jelly in any posture. Rehabilitation approaches were started based on the diagnosis of dysphagia due to impaired transit through the piriform sinuses. The patient achieved independent oral intake by 40 days after the injury. In this case, dysphagia was considered attributable to compression of the vagus nerves running along the lateral aspects of the neck by the cord used in the hanging. If compression is brief, full functional recovery can be expected. Implementation of rehabilitation approaches is also important in this situation.
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PMID:Rehabilitation approaches to dysphagia that was developed for a patient who attempted to commit suicide by hanging: a case report. 2433 46


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