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Biomedical subjects

P Lebowitz

Publications and source records attributed to P Lebowitz.

At least 19 recordsLinked to original sources
PubMed2001

Scheduling a delay between different surgeons' cases in the same operating room on the same day using upper prediction bounds for case durations.

UNLABELLED: At some surgical suites, elective cases are only scheduled if they can be completed during regularly scheduled hours. At such a surgical suite, a surgeon may be scheduled to perform one or more cases in an operating room (OR), to be followed by another surgeon who will perform one or more cases. Scheduling a delay between the two surgeons' cases will improve the likelihood that the second surgeon's case(s) will start on time. We show that the mathematics of calculating a scheduled delay between the different surgeons' cases in the same OR on the same day is that of calculating an upper prediction bound for the duration of the second surgeon's case(s). We test an analytical expression for the upper prediction bound for the last one case of the day in an OR, and a Monte Carlo simulation method for the last two cases. We show that these 90% upper prediction bounds are at least as long as the actual durations for 90% +/- 0.2% of single cases and 92% +/- 0.6% of pairs of cases. We conclude that our methodology can be used to calculate an appropriate, and reasonably accurate, scheduled delay between two surgeons' cases in the same OR on the same day. IMPLICATIONS: We show how to use a statistical analysis of historical case duration data to calculate an appropriate and accurate scheduled delay between two surgeons' cases in the same operating room on the same day.

Algorithms↗
PubMed1996

Trimethaphan versus sodium nitroprusside for the control of proximal hypertension during thoracic aortic cross-clamping: the effects on spinal cord ischemia.

Sodium nitroprusside (SNP) has been used to control the proximal hypertension associated with thoracic aortic cross-clamping (TACC) during thoracic aortic surgery. It worsens neurologic outcome, presumably by further decreasing distal arterial pressure and increasing cerebrospinal fluid (CSF) pressure, thereby worsening the spinal cord perfusion pressure (SCPP). Trimethaphan does not increase CSF pressure. Therefore, the present study investigates the effect of trimethaphan versus SNP to control proximal hypertension during TACC on neurologic outcome. Two groups, each with eight mongrel dogs, were studied. All animals underwent descending TACC for 45 min. The mean proximal aortic blood pressure was maintained at 95-100 mm Hg by the use of SNP or trimethaphan. Distal aortic pressure was allowed to vary. The dogs were neurologically evaluated 24 and 48 h later by a blinded observer. During cross-clamping, there was no difference in mean proximal aortic pressure between groups. After 10 min of cross-clamping, distal aortic pressure was higher (P < 0.01), CSF pressure was lower (P < 0.01), and SCPP was higher (P < 0.005) in the trimethaphan group as compared with the SNP group (group effect). Neurologic outcome as assessed by Tarlov's score was better at 24 and 48 h in the trimethaphan group (P < 0.05). Histopathologic injury trended with worsened neurologic outcome. We conclude that 1) trimethaphan produced higher SCPP than SNP, and 2) neurologic outcome was better in the trimethaphan group.

Animals↗
PubMed1995

Propofol reduces the incidence of vomiting after tonsillectomy in children.

We compared the effect of a propofol-based anaesthetic to an isoflurane-based anaesthetic on the incidence of postoperative vomiting in children following tonsillectomy. Thirty-nine children were enrolled in the study and randomized to receive one of the proposed anaesthetics. All patients underwent a mask induction with halothane, nitrous oxide, and oxygen. Intravenous access was established and all children received fentanyl (2-4 micrograms.kg-1) i.v., mivacurium (0.3 mg.kg-1) i.v. and acetaminophen (10-15 mg.kg-1) p.r. Following tracheal intubation, patients received either isoflurane (0.8-1.6%) or propofol (120-180 micrograms.kg-1 min-1) i.v. with nitrous oxide 70%/oxygen 30% for maintenance of anaesthesia. Vital signs were maintained within 20% of baseline. All patients were extubated in the operating room. PACU nursing staff recorded episodes of vomiting for 4-6 h prior to discharge. A telephone interview the following day was also used for data recovery. Age, sex, and duration of the procedure were not significantly different between the two study groups. Of 19 patients who received propofol, four vomited (21%); in contrast, of the 20 patients who received isoflurane, 11 vomited (55%). This difference is significant (P = 0.048 two-tailed Fisher's Exact Test). These data suggest that using propofol for anaesthesia can diminish the incidence of vomiting following tonsillectomy.

Anesthesia↗
PubMed1995

An audit of adverse events in children sedated with chloral hydrate or propofol during imaging studies.

We examined records of sedations provided by the paediatric anaesthesiology staff for 455 children (ages 1 mo-17 yr) undergoing MRI or CT scans at our institution over a twelve-month period with regard to the monitoring of adverse events: excessive sedation, agitation, vomiting, hypoxaemia, and major airway compromise. One hundred-and-thirty-one patients (29%) received chloral hydrate; 324 patients (71%) received propofol. All patients were monitored with continuous noninvasive pulse oximetry and received supplemental oxygen via nasal cannulae. Of the patients who received chloral hydrate, 64 (49%) were over one year of age; of the patients who received propofol, 318 (98%) were one year of age or older. In the chloral hydrate group, 23 patients (19%) were deemed excessively sedated and four patients (3%) were agitated; no patients in the propofol group experienced any of the adverse outcomes reviewed. Furthermore, no patients in either group had significant airway compromise and none was admitted to the hospital as a result of the sedation.

Adolescent↗
PubMed1994

Delayed awakening from general anaesthesia in a patient with Hunter syndrome.

Hunter syndrome is one of a heterogeneous group of recessively inherited mucopolysaccharide storage diseases (MPS) with similar biochemical defects manifested by impairments in mucopolysaccharide catabolism with variable but progressive clinical courses. Abnormal accumulation and deposition of mucopolysaccharides in the tissue of several organs to numerous anatomical, musculoskeletal and neurological abnormalities which are known to complicate anaesthetic and airway management. Hunter syndrome has a wide variance of clinical phenotypes ranging from mild to severe. We present a patient having physical and neurological features consistent with a severe clinical presentation of Hunter syndrome (MPS, Type II). Following a seemingly uneventful intraoperative anaesthetic course including isoflurane, nitrous oxide and fentanyl (0.93 microgram.kg-1), resumption of spontaneous ventilation and return to consciousness were delayed until intravenous naloxone (200 micrograms) was administered 110 min after the opioid administration. The cause of delayed recovery from anaesthesia in this patient is unknown.

Anesthesia Recovery Period↗
PubMed1993

Expression of the leukemia-associated gene, p18, in normal and malignant tissues; inactivation of expression in a patient with cleaved B cell lymphoma/leukemia.

p18 is a well conserved gene coding for an 18 kDa cytosolic phosphoprotein. Although the function of p18 is unknown, it is suspected of playing a role in regulation of cell proliferation or the proliferation-differentiation switch. Here we have found p18 mRNA expression highest in testis, brain, thymus and a multipotent hematopoietic stem cell line and lowest in liver. p18 was also expressed vigorously in all but one of 85 diverse tumor cell lines and primary human malignant specimens examined. In five primary tumors, expression was substantially elevated with respect to expression in contiguous normal tissue. Expression in chronic phase chronic myelogenous leukemia cells was far greater than in normal blood cells and increased with progression of disease. In liver material, the highest level of p18 was found in a primary hepatoblastoma, a stem cell tumor, whereas a benign adenoma demonstrated very low level expression. Cells from a cleaved B cell lymphoma/leukemia failed to express p18 whereas 18 specimens from other B lymphoid malignancies, including a second cleaved cell malignancy, expressed p18 at substantial levels. These data are consistent with p18 playing a role in control of cell proliferation in at least certain tissues. The questions arise if high level p18 expression in certain malignancies may play a primary role in driving cell proliferation or, based on chromosomal localization and inactivation of p18 expression in one lymphoma, if p18 may act as a tumor suppressor.

Carcinoma, Hepatocellular↗
PubMed1990

Relationship of bcr breakpoint to chronic phase duration, survival, and blast crisis lineage in chronic myelogenous leukemia patients presenting in early chronic phase.

Strong evidence implicates fusion of control elements and 5' sequences of the bcr gene of chromosome 22 with 3' sequences of the c-abl gene of chromosome 9 in the pathogenesis of Ph-positive and certain cases of Ph-negative chronic myelogenous leukemia (CML). Since this fusion gene gives rise to a chimeric tyrosine protein kinase with transforming potential, and since the bcr exon contribution to this chimeric protein is variable, the question has arisen as to whether bcr breakpoint location and bcr exon contribution could influence the clinical course of CML. Prior studies have yielded conflicting results on this point. Here we have looked, in a manner approximating a prospective analysis, at the relation of bcr breakpoint localization to the duration of chronic phase, total survival, and blast crisis phenotype in 81 patients presenting in the chronic phase of CML. We have found no significant differences in chronic phase duration or total survival among patients with breakpoints in the three major subregions of a breakpoint cluster region within the bcr gene. These findings indicate that chronic phase duration and total survival cannot be predicted from bcr breakpoint for CML patients presenting in chronic phase and suggest that unknown oncogenic events determining the onset of blast crisis are the prime determinants of prognosis. Combined analysis of blast crisis cell lineage in our patients and patients presented in a previous study has revealed an overall ratio of myeloid:lymphoid (M:L) crisis of 3.4:1, but a striking predominance of myeloid crisis in patients with breakpoints in subregion 2 (M:L of 9:1), and a lower than expected M:L ratio (1.6:1) among patients with breakpoints in subregion 3 (P for subregion 2 versus 3 = .012; subregions 0,1,2 versus 3 = .012; subregions 0,1,3 versus 2 = .032). The molecular basis for this divergence from the anticipated M:L ratio in patients with breakpoints in bcr subregions 2 and 3 is unknown.

Adult↗
PubMed1987

Polymorphism of the human c-abl gene: relation to incidence and course of chronic myelogenous leukemia.

Abnormalities in structure and expression of the proto-oncogene c-abl have been implicated in the genesis of chronic myelogenous leukemia (CML). We studied leukemic cell DNA from 42 CML patients for evidence of rearrangement and/or amplification of c-abl analogous to that described in the CML cell line K562. Using the enzymes Bgl II, Pst I, Xba I, seven patients demonstrated an atypical Southern blot pattern similar to that found in K562. Analysis of DNA from normal controls and skin fibroblast from one of the seven patients established that the atypical blot pattern was due to a restriction fragment length polymorphism rather than a gene rearrangement. Further analysis revealed that c-abl exists as two alleles, A and B, yielding three genotypes: AA, AB and BB. Inheritance was Mendelian. With respect to allele A, allele B contains a deletion of about 1 kb lying in a intronic region in close proximity to highly repetitive Alu sequences and the sequence coding for phosphotyrosine of the c-abl protein. K562 and the seven patients with similar Southern patterns were identified as AB heterozygotes. In K562, only the A allele was amplified. The frequencies of AA and AB genotypes in 37 Caucasian CML patients were 81.1% and 18.9% and in 57 unrelated normal Caucasian controls 87.7% and 12.3%, not significantly different. The BB genotype was identified in less than 1% of Caucasians. Of note, five AB patients who developed a terminal blast crisis demonstrated a 4:1 lymphoid:myeloid crisis ratio in contrast to a 2:7 lymphoid:myeloid crisis ration in nine AA patients and a similar ratio in mixed AA and AB historical controls. Otherwise, CML patients with AA and AB genotypes manifested similar clinical parameters. No patients demonstrated amplification of c-abl and analysis of four AB patients for loss of one c-abl allele during the course of their disease was negative. Thus, amplification of c-abl and loss of one c-abl allele are both infrequent in CML and do not play a significant role in the course of the disease.

Blast Crisis↗
PubMed1985

Selectivity of interferon action in simian virus 40-transformed cells superinfected with simian virus 40.

Treatment of African green monkey kidney CV-1 cells with human alpha interferons before infection with simian virus 40 (SV40) inhibited the accumulation of SV40 mRNAs and SV40 T-antigen (Tag). This inhibition persisted as long as the interferons were present in the medium. SV40-transformed human SV80 cells and mouse SV3T3-38 cells express Tag, and interferon treatment of these cells did not affect this expression. SV80 and SV3T3-38 cells which had been exposed to interferons were infected with a viable SV40 deletion mutant (SV40 dl1263) that codes for a truncated Tag. Exposure to interferons inhibited the accumulation of the truncated Tag (specified by the infecting virus) but had no significant effect on the accumulation of the endogenous Tag (specified by the SV40 DNA integrated into the cellular genome). The level of Tag in SV40-transformed mouse SV101 cells was not significantly decreased by interferon treatment. SV40 was rescued from SV101 cells and used to infect interferon-treated and control African green monkey kidney Vero cells. Tag accumulation was inhibited in the cells which had been treated with interferons before infection. Our data demonstrate that even within the same cell the interferon system can discriminate between expression of a gene in the SV40 viral genome and expression of the same gene integrated into a host chromosome.

Animals↗
PubMed1983

The human c-ras1H oncogene: a mutation in normal and neoplastic tissue from the same patient.

The c-ras1H oncogene can be distinguished from its normal cellular counterpart by the loss of a restriction endonuclease site. This sequence alteration is the basis of a rapid screening method for the presence of this oncogene. DNA's from 34 individuals were screened by this method, and all were homozygous for the normal allele. In contrast, DNA from a patient's bladder tumor, as well as DNA from his normal bladder and leukocytes, were heterozygous at that restriction endonuclease site. Further restriction enzyme mapping pinpointed the change in the mutant allele as being one of two nucleotides, either of which would change the 12th amino acid (glycine) in the normal c-ras1H gene product. Point mutations in the codon for this amino acid have previously been described in a bladder tumor cell line and in the viral oncogene v-rasH. These results indicate that the patient carried a c-ras1H oncogene in his germ line, raising the possibility that the c-ras1H oncogene confers a predisposition to neoplasia.

Base Sequence↗
PubMed1983

The HL-60 transforming sequence: a ras oncogene coexisting with altered myc genes in hematopoietic tumors.

The oncogene of the HL-60 human promyelocytic leukemia cell line has been passed serially through NIH/3T3 mouse fibroblasts. Oncogene-specific probes prepared from the resulting tertiary transfectants by molecular cloning have been used to show that loss of the transfected oncogene from NIH/3T3 cells correlates with reversion to nontransformed morphology. Analysis of cells transfected by the oncogenes of other tumors and tumor cell lines indicates that the transforming gene of the HL-60 leukemia cell line is closely related to oncogenes of a Burkitt's lymphoma, an acute myelogenous leukemia, an adenocarcinoma of the colon, a neuroblastoma, and two sarcomas. This oncogene is distantly related to the viral oncogenes of Kirsten and Harvey sarcoma viruses. It has been termed N-ras. The active N-ras oncogene coexists with altered versions of the myc oncogene in the HL-60 and AW Ramos human tumors. This suggests a multistep mechanism involving both ras and myc genes in the creation of these tumors.

Animals↗
PubMed1982

Abnormally spliced messenger RNA in erythroid cells from patients with beta+ thalassemia and monkey cells expressing a cloned beta+-thalassemic gene.

The reduced beta-globin synthesis characterizing the beta+ thalassemia phenotype has been shown to be caused by anomalous processing within the small intervening sequence (IVS1) of the beta-globin mRNA precursor. The beta-globin gene from such patients contains a single base substitution within IVS1, located 22 bp from the 3' junction between IVS1 and exon 2, creating an alternative splice site within IVS1 and resulting in retention of the 3'-terminal 19 bases of IVS1. We have identified this abnormally spliced mRNA in the reticulocyte RNA of two patients with beta+ thalassemia, by S1 nuclease mapping and primer-extension analysis. Moreover, a cloned beta+-thalassemic gene preferentially generated the anomalously spliced RNA when expressed in monkey kidney cells. The anomalously spliced RNA constituted approximately 80%--90%, and normal beta RNA approximately 10%--20%, of the total beta mRNA. In contrast, the small amount of beta mRNA present in reticulocytes from such patients consisted predominantly of normal beta mRNA. These results suggest that the reduced amount of normally functioning beta mRNA present in such patients results from preferential processing at the alternative splice site, with subsequent instability, reduced nuclear processing and/or inadequate cytoplasmic transport of the abnormal RNA species.

Animals↗