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Biomedical subjects

S Adler

Publications and source records attributed to S Adler.

At least 37 records · Page 2Linked to original sources
PubMed2001

Brief clinical report: duodenal laceration presenting as massive hematemesis and multiple intraabdominal abscesses after laparoscopic cholecystectomy.

SUMMARY: Laparoscopic cholecystectomy is considered the gold standard for gallstone disease. Nevertheless, possible severe complications must not be underestimated. Bowel injuries are uncommon, but they are one of the most lethal technical complications of laparoscopic surgery. These injuries were commonly unrecognized at the time of procedures and were diagnosed later when the patients experienced sepsis, peritonitis, intraabdominal abscess, or enterocutaneous fistula. Although duodenal lacerations have been reported with laparoscopic cholecystectomies, they seem to be rare; approximately 30 such cases have been documented previously in the English literature. We report the case of a patient with thermal duodenal injury caused by elective laparoscopic cholecystectomy at an outside center presenting as massive hematemesis and multiple intraabdominal abscesses on the ninth postoperative day. The diagnosis and management of this rare complication of laparoscopic cholecystectomy are described, and the literature is reviewed.

Abdominal Abscess↗
PubMed2001

Endothelial nitric oxide synthase plays an essential role in regulation of renal oxygen consumption by NO.

Nitric oxide (NO) regulates renal O2 consumption, but the source of NO mediating this effect is unclear. We explored the effects of renal NO production on O2 consumption using renal cortex from mice deficient (-/-) in endothelial (e) nitric oxide synthase (NOS). O2 consumption was determined polarographically in slices of cortex from control and eNOS-/- mice. NO production was stimulated by bradykinin (BK) or ramiprilat (Ram) in the presence or absence of an NOS inhibitor. Basal O2 consumption was higher in eNOS-/- mice than in heterozygous controls (919 +/- 46 vs. 1,211 +/- 133 nmol O(2). min(-1). g(-1); P < 0.05). BK and Ram decreased O2 consumption significantly less in eNOS-/- mice [eNOS-/-: BK -19.0 +/- 2.8%, Ram -20.5 +/- 3.3% at 10(-4) M; control: BK -29.5 +/- 2.5%, Ram -34 +/- 1.6% at 10(-4) M]. The NO synthesis inhibitor nitro-L-arginine methyl ester (L-NAME) attenuated this decrease in control but not eNOS-/- mice. An NO donor inhibited O2 consumption similarly in both groups independent of the presence of L-NAME. These results demonstrate that NO production by eNOS is responsible for regulation of renal O2 consumption in mouse kidney.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

Simvastatin reverses impaired regulation of renal oxygen consumption in congestive heart failure.

Nitric oxide (NO) production by endothelial nitric oxide synthase (eNOS) regulates renal O(2) consumption. This mechanism is impaired in heart and kidney of dogs with heart failure (CHF). Simvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl-CoA reductase, increases eNOS expression in the endothelium. Therefore, we studied whether simvastatin treatment could restore the regulation of renal O(2) consumption by stimulators of NO production in dogs with CHF. Renal O(2) consumption was measured after stimulation of NO production with bradykinin, ramiprilat, or amlodipine or the NO donor S-nitroso-N-acetylpenicillamine (SNAP). Simvastatin delayed the time to euthanasia in dogs with CHF (35 +/- 1.0 vs. 29 +/- 1.2 days; P < 0.01). In normal dogs, bradykinin (10(-4) M), ramiprilat (10(-4) M), amlodipine (10(-5) M), and SNAP (10(-4) M) significantly reduced O(2) consumption in the renal cortex (-31.8 +/- 0.9, -30.3 +/- 1.1, -30.1 +/- 2.0, -46.9 +/- 1.0%) and renal medulla (-29.7 +/- 2.1, -33.0 +/- 2.7, -30.8 +/- 2.2, -46.8 +/- 1.1%). Responses to bradykinin, ramiprilat, and amlodipine were significantly attenuated in CHF but were partially or completely restored by simvastatin. Responses to SNAP were unaffected. These data demonstrate that treatment with simvastatin improves renal production of NO in CHF, restoring the normal regulation of renal O(2) consumption by NO.

Amlodipine↗
PubMed2001

High remission rate in acute myeloblastic leukemia with only two days of chemotherapy.

Twenty five patients with AML who had neither a history of toxic exposure or myelodysplasia were treated with a remission induction regimen consisting of two pulses of chemotherapy separated by 96 hrs. Each pulse consisted of cytarabine 2gm/m(2) (at t=0 and t=12 hrs) with mitoxantrone [30mg/m(2) ] administered immediately after the second cytarabine administration. Amifostine was administered three times a week [on Monday, Wednesday, and Friday] until the outcome of therapy was known. This regimen induced complete remissions in 15 of 17 patients less than 70 years of age and in 5 of 8 patients older than 70 years.

Adult↗
PubMed2001

IgM anticardiolipin antibodies are associated with stenosis of vascular access in hemodialysis patients but do not predict thrombosis.

AIM: The prevalence of anticardiolipin antibodies (ACA) is elevated amongst hemodialysis patients as compared with the general population. Previous studies have disagreed as to whether the presence of ACA represents a risk factor for access thrombosis. Other risk factors for access thrombosis (decreased blood flow, elevated venous pressure) have also been described. MATERIALS AND METHODS: We performed a combination retrospective and prospective cohort study of a single outpatient dialysis unit to assess the association between these potential risk factors and access thrombosis. ACA, access blood flow, presence of stenosis, and venous pressures were measured in 100 patients. Information on episodes of access thrombosis was gathered for 12 months prior to and 12 months after ACA measurement. RESULTS: ACA were present in 19% of patients with equal numbers of IgG- and IgM-ACA. The presence of IgM-ACA was significantly associated with the use of aspirin and the presence of stenosis by Doppler at the time of ACA testing (p < 0.05). A logistic regression model was used to estimate the association between clinical factors and access thrombosis. In this multivariate analysis, the presence of access stenosis and a history of access thrombosis were both significantly associated with the development of access thrombosis. Adjusted for these variables, neither IgG- nor IgM-ACA was significantly associated with access thrombosis. The presence of an ACA was not associated with episodes of access thrombosis in either the prospective or retrospective analyses. CONCLUSION: Further investigation is required to determine if the association between aspirin use and IgM-ACA, or of IgM-ACA and access stenosis, has implications for underlying pathogenetic mechanisms of access stenosis.

Adult↗
PubMed2000

Measurement of direct photon emission in K+-->pi(+)pi(0)gamma decay

We have performed a measurement of the K+-->pi(+)pi(0)gamma decay and have observed 2x10(4) events. The best fit to the decay spectrum gives a branching ratio for direct photon emission of (4.7+/-0.8+/-0. 3)x10(-6) in the pi(+) kinetic energy region of 55 to 90 MeV and requires no component due to interference with inner bremsstrahlung.

Journal Article↗
PubMed2000

Measurement of structure-dependent K+ --> &mgr;(+)nu(&mgr;)gamma decay

We report the first measurement of a structure-dependent component in the decay K+-->&mgr;(+)nu(&mgr;)gamma. Using the kinematic region where the muon kinetic energy is greater than 137 MeV and the photon energy is greater than 90 MeV, we find that the absolute value of the sum of the vector and axial-vector form factors is |F(V)+F(A)| = 0.165+/-0.007+/-0.011. This corresponds to a branching ratio of B(SD+) = (1.33+/-0.12+/-0.18)x10(-5). We also set the limit -0. 04<F(V)-F(A)<0.24 at 90% C.L.

Journal Article↗
PubMed2000

Further search for the decay K+-->pi(+)nunu;

A search for additional evidence for the rare kaon decay K+-->pi(+)nunu; has been made with a new data set comparable in sensitivity to the previous exposure that produced a single event. No new events were found in the pion momentum region examined, 211 pi(+)nunu;) = 1.5(+3.4)(-1.2)x10(-10).

Journal Article↗
PubMed2000

Absolute structure determination of the highly biologically active bisdehydrodoisynolic acids.

In a project designed to relate the unexpected in vivo and in vitro properties exhibited by (+)- and (-)-bisdehydrodoisynolic acid with their absolute stereochemical structure, an X-ray crystal-structure analysis was undertaken of the highly estrogenic, poorly binding (-) enantiomer. (1) and (13)C NMR spectra are also reported for the first time. The crystal structure shows the cis juxtaposition of the carboxyl and ethyl groups, which are separated by a large torsion angle, and that only the carbon atom holding the carboxyl group is out of the plane in which the remainder of the fused three-ring moiety lies. The crystal structure, which unequivocally characterizes the (-) enantiomer as cis-13(S),14(R) and, implicitly, the (+) enantiomer as cis-13(R),14(S), will be useful in continued studies aimed at explaining the selective estrogen receptor modulation (SERM) of these enantiomers which, in some cases, produces significantly different end-organ effects compared to those of estradiol, in both males and females, affording the promise of a variety of therapeutic and pharmacologic applications.

Crystallography, X-Ray↗
PubMed2000

Changes in cerebral blood flow and distribution associated with acute increases in plasma sodium and osmolality of chronic hyponatremic rats.

The cause of the osmotic demyelination syndrome that follows too rapid correction of chronic hyponatremia (CHN) is unknown. Recently, we reported in CHN rats an association between blood-brain barrier (BBB) disruption occurring as early as 3 h into correction and subsequent demyelination. Given the changes in brain water and blood volume which occur during correction of CHN, we hypothesized that the same correction protocol that causes demyelination might alter cerebral blood flow (CBF) during correction, thereby possibly contributing to BBB disruption and demyelination. Ten CHN rats were given hypertonic sodium intraperitoneally and its effect on CBF was continuously monitored for 3 h by magnetic resonance flow imaging. Over the subsequent 3 h, plasma sodium rose from 110.8 to 127.6 mEq/liter (P < 0.001) but neither mean arterial blood pressure nor arterial CO(2) tension changed significantly. By 30 min, CBF increased by 50% in cortical and subcortical areas (P < 0.001) and remained elevated for the next 60 min. After 2 h, cortical flow was no longer elevated significantly and by 3 h it had returned to control values. Subcortical flow, however, significantly exceeded control values throughout the 3 h so that after 2 h the ratio of cortical to subcortical blood flow had fallen from 1.17 to 0.91 (P < 0.05). Although the mechanism by which increased plasma sodium and osmolality alters CBF is uncertain, the results suggest that changes in CBF may be part of a cascade of cerebrovascular disturbances including endothelial or parenchymal damage, mechanical events, metabolic disturbances, or cytokine release which eventually lead to BBB disruption and subsequent demyelination.

Animals↗
PubMed2000

Blood-brain barrier disruption and complement activation in the brain following rapid correction of chronic hyponatremia.

In previous studies we developed a rat model in which demyelination is reproducibly produced following rapid correction of chronic hyponatremia and demonstrated that the development of demyelination in this model is strongly associated with NMR indices of blood-brain barrier (BBB) disruption. Because complement is toxic to oligodendrocytes, we evaluated the hypothesis that BBB disruption precipitated by correction of hypoosmolality is followed by an influx of complement into the brain, which then contributes to the demyelination that occurs under these conditions. We studied four groups of rats with immunocytochemical analysis using primary antibodies to IgG and the C3d split-fragment of activated complement: (1) normal rats; (2) rats in which hyponatremia was maintained for 7 days; (3) chronically hyponatremic rats in which the plasma [Na(+)] was rapidly corrected with hypertonic saline administration 20 h prior to perfusion; and (4) chronically hyponatremic rats in which the plasma [Na(+)] was rapidly corrected with hypertonic saline administration 5 days prior to perfusion. In normonatremic and uncorrected hyponatremic rats only background staining was observed in areas lacking a BBB and in blood vessel walls, whereas marked increases in IgG and C3d staining were seen in the brains of rats both 20 h and 5 days after rapid correction of hyponatremia. The staining intensity was significantly correlated with the degree of neurological impairment. These results provide evidence for functional BBB disruption following rapid correction of hyponatremia and support the hypothesis that complement activation may be involved in the pathogenesis of osmotic demyelination.

Animals↗
PubMed2000

The activation of intracellular tyrosine kinases by interferon-alpha (IFNalpha) correlates with its antiproliferative activity in B-lymphoid cell lines, but not in B-cell chronic lymphocytic leukemia patients.

The response to interferon-alpha (IFNalpha) treatment in leukemias of the B-cell lineage shows a marked heterogeneity. A distinct subset of patients with B-CLL responds to treatment with IFNalpha, while the drug has no therapeutic effect in the majority of patients. The mechanism of this phenomenon is poorly understood. The cellular events induced by this cytokine mediated by a number of specific signaling events. Therefore, we studied the effect of recombinant IFNalpha on tyrosine phosphorylation and proliferation of cytosolic proteins in human cell lines and in freshly isolated B-CLL cells in order to test the potential value of these events as a pretreatment test for IFNalpha in CLL. In human lymphoid cell lines, IFNalpha induced tyrosine phosphorylation of multiple cytosolic proteins in a time- and concentration-dependent manner. This effect correlated with its growth-inhibitory effect in almost all cell lines. In marked contrast, in freshly isolated B-CLL cells IFNalpha seemed to have both stimulatory and inhibitory effects on proliferation, but it consistently stimulated tyrosine phosphorylation. Moreover, the clinical response of B-CLL to IFNalpha did not correlate with the activation of tyrosine kinases nor with the inhibition of cell growth in vitro. Therefore, the assessment of IFNalpha-induced tyrosine phosphorylation of cytosolic phospho-proteins does not allow to predict the treatment response to IFNalpha in CLL patients.

Aged↗
PubMed2000

Alpha-synuclein accumulation in a case of neurodegeneration with brain iron accumulation type 1 (NBIA-1, formerly Hallervorden-Spatz syndrome) with widespread cortical and brainstem-type Lewy bodies.

We studied a 27-year-old woman who died after a 6-year history of progressive dementia, dystonia, ataxia, apraxia, spasticity, choreoathetosis, visual and auditory hallucinations, and optic atrophy. Magnetic resonance imaging showed decreased intensity in the globus pallidus, substantia nigra, and dentate nuclei in T2-weighted images, supporting the clinical diagnosis of neurodegeneration with brain iron accumulation type 1 (NBIA-1; formerly known as Hallervorden-Spatz syndrome). At autopsy the brain showed mild frontotemporal atrophy and discoloration of the globus pallidus and the substantia nigra pars reticularis. Histologically, features typical of NBIA-1 were found including widespread axonal spheroids and large deposits of iron pigment in the discolored regions. Additionally, excessive numbers of Lewy bodies (LBs) were found throughout all examined brain stem and cortical regions. LBs of both types, as well as Lewy neurites in this case of NBIA-1, were strongly labeled by antibodies against alpha-synuclein. These findings give further evidence that accumulation of alpha-synuclein is generally associated with LB formation, i.e., in Parkinson's disease, dementia with Lewy bodies and NBIA-1. The case presented here is particularly notable for its high number of LBs in all areas of the cerebral cortex.

Adult↗
PubMed2000

Poor prognosis acute myelogenous leukemia: 1 - response to treatment with high dose cytarabine/mitoxantrone/ethyol @ (Amifostine).

Twenty patients with poor prognosis AML and four patients in the blastic phase of a myeloproliferative disorder were treated with two 'pulses' of therapy each consisting of two doses of high dose araC (separated by 12 h) followed by a single dose of mitoxantrone. The pulses were separated by 96 h. Amifostine was then administered tiw. The median age of the population was 68 years with 88% of patients having had either a prior MDS, MPD or toxic exposure. The acute leukemia of 58% of patients either entered a CR or reverted to preleukemic state. For patients under 70 years of age, treatment produced 62% CRs with a leukemia free decision marrow in 77%. For patients over 70 years the CR rate was 27% with 36% of patients having a leukemia free decision marrow.

Adult↗
PubMed2000

Case reports. Disseminated cryptococcoses without cryptococcal antigen detection.

During the last decade cryptococcoses were most frequently diagnosed in AIDS patients, where serologically high amounts of glucoronoxylomannan (GXM) were detectable. Disseminated cryptococcoses without cryptococcal antigen detection is unusual. Between August and October 1998 disseminated cryptococcoses were diagnosed in three patients consecutively although cryptococcal antigen was not detectable. Only one of the patients was HIV infected.

AIDS-Related Opportunistic Infections↗
PubMed2000

On changing curricula: lessons learned at two dissimilar medical schools.

Two dissimilar U.S. medical schools--the University of Pittsburgh School of Medicine and the University of Texas Medical Branch at Galveston-changed their curricula for the first two years of medical education from ones that were lecture-dominated and departmentally run to ones that are centrally governed, multi-modal, goal-oriented, and fully integrated, with mechanisms to continue curricular change into the last two years of medical education. The change at each school was in response to national education philosophy, the recommendations of the Liaison Committee for Medical Education after the most recent site visit, and faculty's and students' concerns and interests. The change process took place over a three- to four-year period at each school, involved students, faculty, and administration, and utilized task forces and retreats as communication vehicles. The barriers encountered (e.g., belief by some that the curriculum needed no change; concern over loss of departments' control) and the processes employed to overcome them and to radically change the curricula (e.g., commitment of the central administration and dean to the change, involvement of all segments of the school in the change process, appointment of department chairs on task forces, and creation of a strong curriculum committee that gave authority to faculty and students) were essentially identical. The resulting curricula were also largely similar in their main characteristics, but there were notable differences, based on the goals and concerns of the two institutions.

Curriculum↗
PubMed2000

Influence of posture, breathing pattern, and type of exercise on minute ventilation estimation by a pacemaker transthoracic impedance sensor.

Previous studies have shown a high correlation between transthoracic impedance minute ventilation (IMV) determined by a pacemaker sensor and actual minute ventilation (VE) measured by standard methods. We hypothesized that several factors (e.g., posture, breathing pattern, and exercise type) could potentially affect the calibration between IMV and VE. In patients with Medtronic Kappa 400 pacemakers, VE (L/min) was monitored using a standard cardiopulmonary metabolic gas analysis system with simultaneous recording of IMV (ohms/min) using DR-180 extended telemetry monitors. Effects of posture and of breathing pattern at rest (19 patients; age 60 +/- 13 years) were evaluated by monitoring each patient under three conditions: (a) slow breathing, supine, (b) slow breathing, sitting, and (c) shallow breathing, supine. Calibration at rest was defined as the ratio of IMV to VE. Effect of type of exercise on calibration compared treadmill versus graded bicycle ergometer exercise (18 patients; age 62 +/- 14 years). Calibration during exercise was defined as: (a) "Begin" (the IMV to VE ratio at VE = 10 L/min, the typical VE value at beginning of exercise), and (b) slope of the IMV/VE regression line. Calibration of IMV/VE was significantly smaller for sitting versus supine position (0.7130.177, P < 0.001) and for shallow versus slow breathing (0.7210.373, P < 0.001), and larger for treadmill versus bicycle exercise (Begin: 1.240.43, P = 0.018; Slope: 1.260.42, P = 0.013). In conclusion, posture, breathing pattern, and type of exercise affect the IMV estimation of the actual VE, possibly by altering the static or dynamic geometry (thus, the impedance) of the intrathoracic viscera.

Arrhythmias, Cardiac↗