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Biomedical subjects

M Schwartz

Publications and source records attributed to M Schwartz.

At least 127 records · Page 7Linked to original sources
PubMed2000

Anterior ischemic optic neuropathy: a complication after systemic inflammatory response syndrome.

BACKGROUND: Patients are surviving previously fatal injuries. Unique morbidities are occurring in these survivors. Anterior ischemic optic neuropathy represents a previously unrecognized cause of blindness in the trauma victim. We hypothesize that this phenomenon is caused by unique characteristics of optic edema/ pressure or decreased blood flow associated with massive resuscitation. METHODS: Between November of 1991 and August of 1998, there were 18,199 admissions to our trauma center. Of this group, 350 patients required massive volume resuscitation (>20 liters infused over first 24 hours). Patients having closed head injuries, facial fractures or direct orbital trauma were excluded from study. The following variables were studied: demographics, injury severity (Injury Severity Score, highest lactate, worst base deficit, and lowest pH) crystalloid and transfusion requirements, ventilator requirements (PEEP) RESULTS: Of the 350 patients with massive resuscitation, 9 patients were diagnosed with anterior ischemic optic neuropathy (2.6%). Of these, seven patients required celiotomy (78%). Six of the seven celiotomy patients had damage control celiotomies and abdominal compartment syndrome (86%). One patient had a repair of a subclavian artery; one had a complex acetabular repair. Blindness was unilateral in five patients and bilateral in four. All nine patients had evidence of global hypoperfusion, systemic inflammatory response, massive resuscitation, and high ventilatory support; one patient required cardiopulmonary resuscitation. CONCLUSION: Prone positioning is known to be associated with an increased intraocular pressure. We postulate that the combination of massive resuscitation and prone positioning will increase the incidence of anterior ischemic optic neuropathy. As such, we recommend that prone positioning for adult respiratory distress syndrome be reserved for only those patients at risk of death.

Adolescent↗
PubMed2000

Neuroprotection: a new treatment modality for glaucoma?

It is now commonly accepted that glaucoma is a neurodegenerative disease of the optic nerve. Thus, at any given time, there are neurons that, though still viable, are vulnerable to the hostile extracellular milieu and are therefore amenable to neuroprotective therapy. Neuroprotection refers to any intervention, either external to the optic nerve or internally, that will lead to an intracellular change in the balance between survival and death signals in favor of survival. Several potential sites and modalities for such intervention may exist. When designing neuroprotective therapy, ways must be sought to recruit the physiologic self-repair mechanisms awakened by the primary or secondary risk factors. These mechanisms appear to be insufficiently effective when in their natural state, but they may be simulated or boosted by appropriate therapeutic compounds or cells.

Animals↗
PubMed2000

Beneficial autoimmune T cells and posttraumatic neuroprotection.

Injuries of the central nervous system (CNS) lead to an inevitable and irreversible loss of function because of the lack of neurogenesis, poor regeneration, and the spread of degeneration. In most tissues, protection and repair are the function of the immune system. It has long been thought that this does not apply to the CNS, where--because of its immune-privileged character--any immune activity was assumed to be detrimental. We have recently proposed, however, that provided care is taken to avoid the attendant risks, both repair and protection of injured CNS neurons can benefit from immune intervention. In the following I will summarize the data that led to this concept and describe the evidence supporting it.

Animals↗
PubMed2000

Preserved male fertility despite decreased androgen sensitivity caused by a mutation in the ligand-binding domain of the androgen receptor gene.

Mutations in the androgen receptor gene are considered as incompatible with preservation of fertility and have been suggested as a cause of male infertility. Two adult brothers, referred because of gynecomastia and hormonal levels in serum indicating androgen insensitivity (high sex hormone-binding globulin, and LH levels, despite extremely high testosterone concentration), turned out to be relatives to a third young man, referred independently of the two others and exhibiting identical clinical and hormonal stigmata. In all three men, we found a C-->A substitution at position 2470 (exon 7) in the androgen receptor gene, leading to a Gln824Lys mutation in the ligand-binding domain of the receptor. Exploring the family history revealed that their grandfathers, on their mothers' side, were brothers; and the Gln824Lys mutation was also found in the one of them who was still alive. Binding studies with the mutant receptor in transfected COS-7 cells, with mibolerone as ligand, exhibited equal Kd (0.7 vs. 1.0 nmol/ L), IC50 (0.8 vs. 1.1 nmol/L), and maximum binding (7.1 vs. 8.9 fmol/ 10(6) cells), as compared with the wild-type (WT) receptor. In a chloramphenicol acetyl transferase trans-activation assay, the activity of the mutant receptor was identical to that of the WT, when the synthetic androgen R1881 was'used as a ligand; but with dihydrotestosterone, in concentrations up to 10 nmol/L, the activity of Gln824Lys mutated receptor was 10-62% of the WT variant. Thus, Gln824Lys mutation was found, both in vivo and in vitro, to cause slight impairment of receptor function but was compatible with preservation of male fertility. The patients inherited the mutation from their grandfathers through their mothers, and one of the young men possessing the mutation has fathered a daughter.

Adult↗
PubMed2000

Treatment of whiplash associated neck pain [corrected] with botulinum toxin-A: a pilot study.

OBJECTIVE: Up to 87% of patients with whiplash associated disorder (WAD) have some degree of muscle spasm that is contributory to both pain and dysfunction. Botulinum toxin A (BTX-A) produces prolonged muscle relaxation that is dose-dependent and can be easily targeted to affected muscles. BTX-A therapy may be an effective form of therapy offering an alternative or adjunct to conventional modalities. We investigated BTX-A as therapy in patients with WAD. METHODS: This randomized, double blind, placebo controlled study compares outcome measures in 26 patients with chronic neck pain (WAD-II chronic) subsequent to a motor vehicle accident. One-half of the patients received 100 units BTX-A, diluted in 1 ml saline, while the other half received just saline (1 ml). Five trigger points received 0.2 ml each of injectant via a 30 gauge needle. Outcome measures included total subjective neck, shoulder, and head pain based on visual analog scales; objective total range of neck motion (ROM), and the Vernon-Mior subjective function index. Followup assessments were carried out at 2 and 4 weeks post-treatment. RESULTS: Fourteen subjects receiving BTX-A and 12 receiving saline completed the study. The treatment group showed a trend toward improvement in ROM and reduction in pain at 2 weeks post-injection. At 4 weeks post-injection the treatment group was significantly improved from preinjection levels (p < 0.01). The placebo group showed no statistically significant changes at any post-treatment time. The Vernon-Mior scale revealed a trend to improvement for both groups. CONCLUSION: BTX-A treatment of subjects with chronic WAD II neck pain resulted in a significant (p < 0.01) improvement in ROM and subjective pain compared to a placebo group, but only a trend to improvement in subjective functioning.

Adult↗
PubMed2000

Successful thrombolytic therapy for massive pulmonary embolism.

The use and scope of thrombolytic therapy in the management of pulmonary embolism (PE) continues to evolve. The results of small studies suggest that thrombolytic therapy might have an impact on survival in massive PE with cardiogenic shock; however, no large studies to further this notion exist. Furthermore, the expanded application of thrombolytic therapy to patients with PE and right ventricular dysfunction (RVD) but without overt hemodynamic collapse remains controversial. We report successful use of the thrombolytic agent tissue plasminogen activator (tPA) in the management of life-threatening PE with RVD without overt cardiovascular collapse. We present evidence for the meritorious use of thrombolytic therapy in this category of PE patients. We believe that a broadened application of thrombolytic therapy to patients with PE and RVD but without cardiogenic shock, especially in younger patients, is beneficial and worth the risk.

Adult↗
PubMed2000

Absence of correlation between X chromosome inactivation pattern and plasma concentration of factor VIII and factor IX in carriers of haemophilia A and B.

Haemophilia A and B are X-linked disorders which are due to a reduced activity of coagulation factor VIII or IX, respectively. Female carriers have a wide range of plasma concentration of factor VIII or factor IX, and may in rare cases have an affected phenotype. In order to investigate if this variation is related to X chromosome inactivation, we determined the X inactivation pattern in 31 haemophilia A and 15 haemophilia B carriers, using a PCR in the androgen receptor locus in blood DNA. Seven of the haemophilia A carriers and none of the haemophilia B carriers had a skewed pattern (> or =80:20). One of the skewed haemophilia A carriers had a low plasma concentration of factor VIII (0.15 U/ml), but the remaining 6 carriers did not differ in factor VIII concentration from that of carriers with a random X inactivation pattern. One carrier with a high factor VIII concentration (2.0 U/ml) did not have a skewed pattern. Similarly, for the haemophilia B carriers, there was no tendency to a more skewed X inactivation pattern in the carriers with low or high factor IX concentrations. In addition, we analysed a female with haemophilia B who was heterozygous for the mutation R180W in the factor IX gene. She had a random X chromosome inactivation pattern. We conclude that the wide range in plasma concentration of factor VIII and factor IX in haemophilia A and B carriers cannot in general be explained by the X chromosome inactivation pattern in peripheral blood cells.

Adolescent↗
PubMed2000

Lymphocytes, autoantibodies and psychosis--coincidence versus etiological factor: an update.

Several factors have been suggested in the etiopathology of schizophrenia, including autoimmune factors. Subgroup of schizophrenics have been found to have immunologic abnormalities. Evidence is presented of the role of lymphocytes and cytokine production in psychiatric disorders. Hypersecretion of IL-2 and IL-6 in acute exacerbation or in relapse-prone patients, decreased ratio of CD4+/CD8+, detection of antinuclear, anticytoplasmatic, antiphospholipid antibodies and others in chronic schizophrenic patients and lately the presence of antiphospholipid antibodies in unmedicated psychotic patients are examples of the immunologic abnormalities findings. These results suggest that schizophrenia may result from an immunologic disorder, which is mediated mainly (but probably not only) by lymphocyte dysfunction.

Autoantibodies↗
PubMed2000

RGC death in mice after optic nerve crush injury: oxidative stress and neuroprotection.

PURPOSE: To establish a method for morphometric analysis of retrogradely labeled retinal ganglion cells (RGCs) of the mouse retina, to be used for the study of molecular aspects of RGC survival and neuroprotection in this model; to evaluate the effect of overexpression of Cu-Zn-superoxide dismutase (CuZnSOD) on RGC survival after severe crush injury to the optic nerve, and to assess the effect of the alpha2-adrenoreceptor agonist brimonidine, recently shown to be neuroprotective, on RGC survival. METHODS: A severe crush injury was inflicted unilaterally in the orbital portion of the optic nerves of wild-type and transgenic (Tg-SOD) mice expressing three to four times more human CuZnSOD than the wild type. In each mouse all RGCs were labeled 72 hours before crush injury by stereotactic injection of the neurotracer dye FluoroGold (Fluorochrome, Denver, CO) into the superior colliculus. Survival of RGCs was then assessed morphometrically, with and without systemic injection of brimonidine. RESULTS: Two weeks after crush injury, the number of surviving RGCs was significantly lower in the Tg-SOD mice (596.6 +/- 71.9 cells/mm(2)) than in the wild-type control mice (863. 5 +/- 68 cells/mm(2)). There was no difference between the numbers of surviving RGCs in the uninjured retinas of the two strains (3708 +/- 231.3 cells/mm(2) and 3904 +/- 120 cells/mm(2), respectively). Systemic injections of brimonidine significantly reduced cell death in the Tg-SOD mice, but not in the wild type. CONCLUSIONS: Overexpression of CuZnSOD accelerates RGC death after optic nerve injury in mice. Activation of the alpha2-adrenoreceptor pathway by brimonidine enhances survival of RGCs in an in vivo transgenic model of excessive oxidative stress.

Adrenergic alpha-Agonists↗
PubMed2000

Using the PerioChip in treating adult periodontitis: an interim report.

Multicenter clinical trials have established that the adjunctive use of the subgingival controlled release of chlorhexidine, in the form of the PerioChip, significantly reduces pocket probing depth, improves probing attachment levels, and reduces bleeding on probing compared to scaling and root planing alone, for periods up to 9 months. The purpose of the present study was to report on the adjunctive use of the PerioChip for the long-term management of adult periodontitis for 2 years. A total of 836 patients with adult periodontitis from private dental offices were recruited into the trial. This interim report is on the first 72 patients to have completed the 2-year study. Treatments included initial definitive therapy followed by PerioChip placement in pocket sites with a pocket probing depth of > or = 5 mm after 1 month. Subsequently, the patients received routine periodontal maintenance therapy together with the placement of a PerioChip in pockets with pocket probing depths > or = 5 mm every 3 months. Results indicated that there was a continuous decrease in pocket probing depth over the 2 years (1.26 +/- 0.77 mm). This decrease in pocket probing depth was marked over the first 9 to 12 months, and then appeared to be less marked over the next 12 months. At 2 years, 60% of the patients had at least 2 pockets showing a reduction of 2 mm or more, and only 10% of the patients showed no change or increased pocket probing depth. The results indicate that adjunctive PerioChip use is a clinically effective treatment option for dental professionals and their patients for the long-term management of adult periodontitis.

Adult↗
PubMed2000

Mitochondrial DNA variant 11719G is a marker for the mtDNA haplogroup cluster HV.

Based on sequencing data and results obtained from applying a tailored mismatch polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis, we report that the G allele of the mitochondrial DNA (mtDNA) polymorphism at nucleotide position 11719 is associated with the European mtDNA haplogroup cluster HV, and that 11719A is therefore the ancestral allele.

DNA, Mitochondrial↗