Search PubMed⌕ Search

Biomedical subjects

R Berger

Publications and source records attributed to R Berger.

At least 181 records · Page 10Linked to original sources
PubMed1998

Occupational upper extremity disorders in the federal workforce. Prevalence, health care expenditures, and patterns of work disability.

Upper extremity disorders (UEDs) account for a significant number of work-related illnesses in the US workforce. Little information exists on the distribution of UEDs, their associated health care and indemnity costs, or patterns of work disability. The study presented is an analysis of upper extremity claims within the federal workforce. In this study, the universe consisted of all claims accepted by the US Department of Labor, Office of Workers' Compensation Programs (OWCP), from October 1, 1993, through September 30, 1994. A total of 185,927 claims of notices of injury were processed during the study period, and of these, 8,147 or 4.4% had an UED diagnosis coded according to the International Classification of Diseases, Clinical Modification (ICD-9-CM). 5,844 claims involved a single UED diagnosis and were the only claims field by these employees between October 1, 1990, and September 30, 1994. These single claims with single diagnoses comprised the sample for further analysis. Mononeuritis and enthesopathies of the upper limb were the most common diagnoses, accounting for 43% and 31% of the claims, respectively. Women had a higher proportion of carpal tunnel syndrome, "unspecified" mononeuritis, and "unspecified" enthesopathies. The majority of claimants for both the mononeuritis- and enthesopathy-related diagnoses were between 31 and 50 years of age, received only health care benefits, and did not incur wage loss. Health care costs for mononeuritis and enthesopathy claims were $12,228,755 (M = $2,849). Carpal tunnel syndrome (CTS) and enthesopathy of the elbow were the most costly diagnoses, accounting for 57% and 16% of the total, respectively. Surgical services represented the highest expenditures in CTS claims. Physical therapy accounted for the majority of health care costs for enthesopathy cases. The mean number of workdays lost for CTS and enthesopathy claims were 84 and 79, and the average indemnity costs were $4,941 and $4,477, respectively. These findings indicate that while UEDs represent a relatively small percentage of all workers' compensation cases, the health care and indemnity costs are considerable. Also mean duration and pattern of work disability revealed that these disorders can result in chronic work disability similar to that observed in low back pain. The results highlight the need to determine whether interventions that account for the majority of costs significantly impact long-term outcomes. There is also a need to identify risk factors for prolonged disability in those who experience problems with delayed recovery.

Adolescent↗
PubMed1998

Relationship between the upper limit of vulnerability determined in normal sinus rhythm and the defibrillation threshold in patients with implantable cardioverter defibrillators.

The upper limit of vulnerability is the strength above which ventricular fibrillation is no longer inducible with a shock delivered during the vulnerable phase of the cardiac cycle. It has been demonstrated that the upper limit of vulnerability correlates with the defibrillation threshold in a paced rhythm. The purpose of this study is to evaluate the correlation of the upper limit of vulnerability determined in normal sinus rhythm with the defibrillation threshold using a simplified protocol in patients undergoing placement of an ICD. We studied 28 patients who underwent ICD implantation. CPI generators and Endotak leads were used in all patients. Device-based testing was used to determined the defibrillation threshold and the upper limit of vulnerability. The upper limit of vulnerability was tested with three shocks delivered at 0, 20, and 40 ms before the peak of the T wave during normal sinus rhythm. The defibrillation threshold was determined by a simple step up-down protocol. The upper limit of vulnerability (9.0 +/- 4.5 J) did not significantly differ from the defibrillation threshold (9.9 +/- 4.0 J), P = NS. A close correlation was present, correlation coefficient = 0.75, P < 0.0001. The upper limit of vulnerability was within 5 J of the defibrillation threshold in 27 (96%) of the 28 patients. The upper limit of vulnerability underestimated the defibrillation threshold by 10 J in one patient who had a defibrillation threshold of 15 J. The upper limit of vulnerability determined in normal sinus rhythm correlates significantly with the defibrillation threshold in patients undergoing ICD implantation. The protocol is simple and easily implemented clinically.

Anti-Arrhythmia Agents↗
PubMed1998

Unusual locations for adenosine-sensitive accessory atrioventricular pathways with decremental conduction.

INTRODUCTION: Accessory AV pathways with decremental conduction are uncommon and, in particular, are thought not to occur at the anterior portion of the mitral annulus. METHODS AND RESULTS: This report describes successful catheter ablation in three patients with accessory AV pathways that were adenosine sensitive and showed decremental conduction properties. The pathways were located at the anteroseptal, anteroparaseptal, and anterolateral aspects of the mitral annulus. CONCLUSION: Accessory pathways with decremental conduction do occur anywhere around the mitral annulus, even in the area of fibrous continuity between the aortic leaflet of the mitral valve and the aortic valve itself.

Adenosine↗
PubMed1998

Molecular analysis of a gene encoding a cell-bound esterase from Streptomyces chrysomallus.

A gene (estA) encoding a 42-kDa cell-bound esterase, EstA, was found to be located 75 bp upstream of the cyclophilin A gene (cypA) of Streptomyces chrysomallus. Western blot analysis revealed the presence of EstA (42 kDa) in cell extracts of S. chrysomallus X2 and Streptomyces lividans. EstA specifically hydrolyzes short-chain p-nitrophenyl esters. EstA formation starts at the end of growth phase, and its activity level remains constant throughout stationary phase. Expression of estA from the melanin (mel) promoter in plasmid pIJ702 led to a substantial increase of total esterase activity in streptomycetes.

Amino Acid Sequence↗
PubMed1998

Low dose flunarizine protects the fetal brain from ischemic injury in sheep.

Flunarizine, a calcium channel blocker, reduced cerebral damage caused by hypoxic-ischemic insults in neonatal rats and in fetal sheep near term. However, the high dose regimen used in these studies produced cardiovascular side effects that might have counteracted the neuroprotective properties of flunarizine. Therefore, the neuroprotective effect was tested in a low dose protocol (1 mg/kg estimated body weight). Twelve fetal sheep near term were instrumented chronically. Six fetuses were pretreated with 1 mg of flunarizine per kg of estimated body weight 1 h before ischemia, whereas the remainder (n=6) received solvent. Cerebral ischemia was induced by occluding both carotid arteries for 30 min. To exclude the possibility that the neuroprotective effects of flunarizine were caused by cerebrovascular alterations we measured cerebral blood flow by injecting radiolabeled microspheres before (-1 h), during (3 min and 27 min) and after (40 min, 3 h, and 72 h) cerebral ischemia. At the end of the experiment (72 h) the ewe was given a lethal dose of sodium pentobarbitone and saturated potassium chloride i.v., and the fetal brain was perfused with formalin. Neuronal cell damage was assessed in various brain structures by light microscopy after cresyl violet/fuchsin staining using a scoring system: 1, 0-5% damage; 2, 5-50% damage; 3, 50-95% damage; 4, 95-99% damage; and 5, 100% damage. In 10 other fetal sheep effects of low dose flunarizine on circulatory centralization caused by acute asphyxia could be excluded. In the treated group neuronal cell damage was reduced significantly in many cerebral areas to varying degrees (range for control group, 1.03-2.14 versus range for treated group, 1.00-1.13; p < 0.05 to p < 0.001, respectively). There were only minor differences in blood flow to the various brain structures between groups. We conclude that pretreatment with low dose flunarizine protects the brain of fetal sheep near term from ischemic injury. This neuroprotective effect is not mediated by changes in cerebral blood flow. We further conclude that low dose flunarizine may be clinically useful as a treatment providing fetal neuroprotection, particularly because the fetal cardiovascular side effects are minimal.

Animals↗
PubMed1998

A new case of translocation t(6;11)(q21;q23) in a therapy-related acute myeloid leukemia resulting in an MLL-AF6q21 fusion.

A new case of translocation t(6;11)(q21;q23) in a patient with therapy-related acute myeloblastic leukemia is reported. The translocation results in fusion of the MLL and AF6q21 genes. The breakpoint with AF6q21 is located within the sequences encoding the AF6q21 fork head motif. The similar location of the localization of the chromosome 6 breakpoints in the present case and in the first case reported suggests their nonrandom localization. In addition, treatment for Hodgkin's disease prior to leukemia in both t(6;11)(q21;q23) cases suggests an association of this translocation with therapy-related leukemias, as reported for the recently described.

Adult↗
PubMed1997

Long-term survival of patients with acute myeloid leukemia: a third follow-up of the Fourth International Workshop on Chromosomes in Leukemia.

BACKGROUND: In 1982, the Fourth International Workshop on Chromosomes in Leukemia reviewed data prospectively collected on 716 patients with acute myeloid leukemia (AML) diagnosed between 1980 and 1982. The present study examined the extended follow-up on these patients. METHODS: The analyses included cytogenetic and clinical data, with a median follow-up of 14.7 years, from 54 patients with treatment-associated AML and 628 with de novo AML. Of these patients, 291 received induction therapy that would be considered standard by today's criteria; no patient received high-dose cytarabine (HiDAC) intensification. RESULTS: Among the patients with treatment-associated AML, the only long-term survivor in retrospect appears to have had de novo AML. Among the patients with de novo AML, achievement of complete remission and survival varied significantly based on cytogenetic classification among all 628 patients as well as among those who did and did not receive standard induction therapy. The remission rate and survival were significantly better with standard induction therapy for patients with t(15;17) and normal cytogenetics. Multivariate analyses showed that karyotype was an independent predictor of survival for all patients and those receiving standard induction therapy. Only 8.9% of patients were alive 5 years following diagnosis, but 5 years of continuous remission was synonymous with cure. Even among 5-year survivors who had suffered a previous relapse, 41% appeared to be cured. Survival among patients in continuous remission for > or = 10 years varied significantly by cytogenetic classification. In the absence of HiDAC intensification, no complete responders with t(8;21) and only 7% with normal cytogenetics survived continuously 10 years disease free. CONCLUSIONS: Cure of AML following specific therapies must be evaluated in the context of cytogenetics. A meta-analysis incorporating cytogenetic data is indicated for patients with > or = 10 years of follow-up.

Acute Disease↗
PubMed1997

A TEL-JAK2 fusion protein with constitutive kinase activity in human leukemia.

The Janus family of tyrosine kinases (JAK) plays an essential role in development and in coupling cytokine receptors to downstream intracellular signaling events. A t(9;12)(p24;p13) chromosomal translocation in a T cell childhood acute lymphoblastic leukemia patient was characterized and shown to fuse the 3' portion of JAK2 to the 5' region of TEL, a gene encoding a member of the ETS transcription factor family. The TEL-JAK2 fusion protein includes the catalytic domain of JAK2 and the TEL-specific oligomerization domain. TEL-induced oligomerization of TEL-JAK2 resulted in the constitutive activation of its tyrosine kinase activity and conferred cytokine-independent proliferation to the interleukin-3-dependent Ba/F3 hematopoietic cell line.

Amino Acid Sequence↗
PubMed1997

AF6q21, a novel partner of the MLL gene in t(6;11)(q21;q23), defines a forkhead transcriptional factor subfamily.

Fusion genes implicating the MLL gene have been recently demonstrated in various 11q23 chromosomal abnormalities in human hematopoietic malignancies. We analyzed a t(6;11)(q21;q23) translocation detected in a secondary acute myeloblastic leukemia. This translocation results in fusion of the MLL gene on 11q23 to a previously unknown gene on chromosome 6 that differs from the previously reported MLL partner gene AF6q. The novel gene, named AF6q21, encodes a forkhead (FH) protein with strong similarities to the two FH family members whose genes are already known to be involved in chromosomal translocations of human malignancies, AFX and FKHR. Strikingly, in these translocations the breakpoints are located at the same position within the FH domains. Therefore, AF6q21, AFX, and FKHR could define a new FH subfamily particularly involved in human malignancies.

Amino Acid Sequence↗
PubMed1997

Safety and effectiveness of placement of pacemaker and defibrillator leads in the axillary vein guided by contrast venography.

Despite evidence of an increased incidence of lead fracture, the infraclavicular subclavian approach remains the dominant approach for placement of pacemaker and implantable defibrillator leads. Although this complication can be prevented by lead placement in the cephalic vein or by recently described approaches for lead placement in the axillary vein, these approaches have not gained widespread acceptance. The purpose of this study was to evaluate the safety and efficacy of an alternative technique for lead placement that uses contrast-guided venipuncture of the axillary vein with a 5Fr micropuncture introducer set. A total of 50 patients underwent an attempt at placement of pacemaker or implantable defibrillator leads via the axillary vein using this new technique. Patients were randomized into 2 groups based on whether the initial attempt at axillary vein access was performed medial or lateral to the rib cage margin. Lead placement was successfully accomplished in 49 of the 50 patients using this technique. Initial success was achieved in each of 25 patients randomized to the medial approach compared with 18 of 24 patients randomized to the lateral approach to the axillary vein (75%). In each of the 6 patients in whom the initial technique failed, lead placement was subsequently achieved with the medial approach. In addition to a higher initial success rate, the medial approach was determined to be preferable as evidenced by a shorter lead placement time, a smaller number of contrast injections, and a reduced requirement for additional micropuncture guidewires. There were no major complications associated with either approach. Contrast-guided venipuncture of the axillary vein is a safe and effective approach to placement of endocardial leads.

Aged↗
PubMed1997

Autosomal recessive liver phosphorylase kinase deficiency caused by a novel splice-site mutation in the gene encoding the liver gamma subunit (PHKG2).

To facilitate mutation analysis of patients with an autosomal recessive form of liver phosphorylase kinase deficiency, the genomic structure of the gene encoding the testis/liver gamma subunit (PHKG2) was established. The gene consist of 10 exons. The translation start site is located in exon 2. Analysis of DNA from two female siblings, affected with liver phosphorylase kinase deficiency, by exon specific amplification followed by direct sequencing, revealed a single donor splice site mutation in the PHKG2 gene, IVS4 + 1(g --> a). The mutation leads to the skipping of exon 4, which results in a frameshift, starting at nucleotide 272, a premature stop codon after 32 additional amino acids, and subsequent loss of the catalytic site. It is concluded that deficiency of phosphorylase kinase in liver of the patients is caused by the IVS4 + 1(g --> a) mutation. In the patients described here, this genotype is associated with development of liver fibrosis.

Amino Acid Sequence↗
PubMed1997

No effect of glutamate on metabolic disturbances in hippocampal slices of mature fetal guinea pigs after transient in vitro ischemia.

The involvement of glutamate in the development of cerebral metabolic disturbances in mature fetuses after transient ischemia was studied using a hippocampal slice model. We investigated the effects of exogenously applied glutamate or glutamate antagonists on the recovery of energy metabolism and protein synthesis rate (PSR) in hippocampal slices of mature guinea pigs after in vitro ischemia. The slices were incubated in a thermostatically controlled flow-through chamber and gassed with carbogen (95% O2/5% CO2). In vitro ischemia was induced by transferring the slices to an aglycemic, artificial cerebrospinal fluid (aCSF) equilibrated with 95% N2/5% CO2. In a first set of experiments slices were exposed to 10 mM glutamate during a 20-40 min period of in vitro ischemia. In a second set slices were incubated in aCSF containing MK-801 (100 microM) or kynurenic acid (0.5 mM) 30 min before, during and 2 h after in vitro ischemia. After a 12 h recovery phase, the concentrations of adenylates in the slices were measured by HPLC after extraction with perchloric acid. PSR was calculated from the rate of incorporation of [14C]leucine into tissue proteins. Neither glutamate nor glutamate antagonists had any effect on the postischemic recovery of energy metabolism and PSR when applied during in vitro ischemia. It is therefore concluded that glutamate does not play a major role in the development of metabolic disturbances in hippocampal slices from mature guinea pig fetuses subjected to transient in vitro ischemia.

Adenosine Triphosphate↗
PubMed1997

A new member of the amphiphysin family connecting endocytosis and signal transduction pathways.

Src homology 3 (SH3) domains are conserved modules which participate in protein interaction by recognizing proline-rich motifs on target molecules. To identify new SH3-containing proteins, we performed a two-hybrid screen with a proline-rich region of human SOS-1. One of the specific SOS-1 interacting clones that were isolated from a mouse brain cDNA library defines a new protein that was named amphiphysin 2 because of its homology to the previously reported amphiphysin. Amphiphysin 2 is expressed in a number of mouse tissues through multiple RNA transcripts. Here, we report the amino acid sequence of a brain form of amphiphysin 2 (BRAMP2) encoded by a 2. 5-kilobase mRNA. BRAMP2 associates in vitro with elements of the endocytosis machinery such as alpha-adaptin and dynamin. On a biosensor surface, the BRAMP2/dynamin interaction appeared to be direct and partly dependent on a proline-rich sequence of dynamin. Association with dynamin was also observed in PC12 cells after cell stimulation with nerve growth factor, suggesting that amphiphysin 2 may be connected to receptor-dependent signaling pathways. This hypothesis is strengthened by the ability of BRAMP2 to interact with the p21(ras) exchange factor SOS, in vitro, as a possible point of interconnection between the endocytic and signaling pathways.

Adaptor Protein Complex alpha Subunits↗
PubMed1997

Effects of atenolol as add-on therapy to fosinopril in heart failure.

Several trials have demonstrated functional benefit with beta-blockers in patients with chronic heart failure. The aim of this observational study was to investigate if additional beneficial effects can be obtained from beta-blockade in a heart failure population that is already receiving high-dose ACE-inhibitor therapy. Atenolol is a long-acting cardioselective beta-blocking agent and is devoid of additional vasodilatory properties. Twenty-five male patients with class II or III heart failure and background therapy of digitalis, furosemide and 20 mg fosinopril per day were treated with 40 mg fosinopril per day and additional 75 mg atenolol per day (beta-blocker group) or with 40 mg fosinopril per day alone (control group). At the end of one year, changes in left ventricular function, exercise parameters and plasma neurohumoral variables reflecting vasoconstriction (noradrenaline, big endothelin) were measured and compared in the two treatment groups. Nineteen patients completed the study. Drop-outs were due to death (4 patients) and non-compliance (2 patients) with no significant difference between the groups. There was a beta-blocker related improvement in left ventricular ejection fraction (p < 0.05 between groups) and an increase in peak oxygen consumption in the control group only (p < 0.05 between groups). Thus, in a heart failure population receiving high-dose ACE inhibitor background therapy beta-blockade with atenolol produced additional benefit by reversing left ventricular dysfunction.

Adrenergic beta-Antagonists↗
PubMed1997

JEM-1, a novel gene encoding a leucine-zipper nuclear factor upregulated during retinoid-induced maturation of NB4 promyelocytic leukaemia.

Retinoid-induced proliferation causing hyperleukocytosis is a severe complication of retinoid therapy in t(15;17) acute promyelocytic leukaemia. The molecular basis of this phenomenon is unknown. It is possible that the transiently enhanced cell proliferation results from RA-induction of growth regulatory genes. Using Differential Display of cDNAs from NB4 cells we have identified Jem, a novel gene transcript which is upregulated by retinoids during the early proliferative response in maturating cells but not in resistant cells. A 2.7 kb cDNA was cloned and sequenced. The open reading frame contains a 400 amino acid sequence corresponding to a novel 45 kDa basic protein (pI 8.9). The JEM DNA sequence is detected by FISH on human chromosome 1 at q24. The Jem peptide sequence shows a 'leucine-zipper' dimerisation motif with limited homology to Fos/Jun and ATF/CREB proteins and several putative phosphorylation sites. An atypical basic region may correspond to an unknown DNA-binding domain. The C-terminal end of Jem spans a long stretch featuring a PEST motif. After transfection into COS cells, the Jem protein shows a ponctuated nuclear localisation. We hypothesise that this novel nuclear factor may act as a transcription factor, or a coregulator, involved in either cell growth control and/or maturation.

Amino Acid Sequence↗
PubMed1997

Dispersion of ventricular activation and refractoriness in patients with idiopathic dilated cardiomyopathy.

We sought to evaluate the electrophysiologic substrate for ventricular arrhythmias and sudden cardiac death in patients with idiopathic dilated cardiomyopathy. When compared with controls, patients with cardiomyopathy had prolonged activation times, increased dispersion of activation and recovery, and prolonged duration of monophasic action potential recordings at 70%, but not at 90%, of repolarization.

Cardiac Catheterization↗
PubMed1997

Power spectrum of the QRS complex in patients with panic disorder and normal controls.

We performed spectral analysis on the QRS complex of the electrocardiogram obtained using standard limb leads, sampled at 500 Hz with 12 bit precision in 20 normal subjects and 15 patients with panic disorder. We divided the frequency range of the QRS into two bands based on spectral patterns before and after the postural challenge-mid frequency (MF): 7.8-20 Hz; and high frequency (HF): 21-250 Hz. Postural change from supine to standing produced a significant increase in absolute (P = 0.003) and relative HF power (P = 0.00001). Patients with panic disorder had a significantly decreased QRS HF power (P = 0.003). The increase in QRS HF power may have been due to the shortening of the QRS interval in standing posture. The decreased QRS HF power in patients with panic disorder should be further investigated due to the recent reports of an association of phobic anxiety and fatal coronary heart disease, and the possible association of decreased high frequency components of QRS in myocardial infarction.

Adult↗