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Biomedical subjects

Y Goldberg

Publications and source records attributed to Y Goldberg.

At least 19 recordsLinked to original sources
PubMed2007

Placental shelf - a common, typically transient and benign finding on early second-trimester sonography.

OBJECTIVE: Placental shelves are believed to represent circumvallate placentae. It is thought that circumvallate placenta may be associated with adverse perinatal outcome when present at delivery. The objective of this study was to determine the prevalence, persistence and significance of placental shelves detected in the early second trimester. METHODS: In 152 consecutive anomaly scans performed between 13 and 16 weeks of gestation, special attention was directed to placental structure and the presence of a placental shelf. When present, a mid-gestation scan was performed to verify if the finding persisted. If so, a third-trimester scan was performed. Delivery charts were reviewed for all cases initially diagnosed with a placental shelf, recording any placenta-related complications. RESULTS: In 17 of 152 (11.2%) early second-trimester scans a placental shelf was detected. In three of these 17 cases the shelf persisted to the 20-22-week scan. In the two cases that presented for the third-trimester scan the shelf was no longer present. In all 17 cases the perinatal outcome was good. CONCLUSIONS: In our study group early second-trimester placental shelves rarely persisted to mid-gestation and never to the third trimester. There were no placenta-related perinatal problems. Early second-trimester placental shelf appears to be a common, benign and transient sonographic finding.

Abruptio Placentae↗
PubMed2006

Exosomes are released by cultured cortical neurones.

Accumulating evidence shows that several cell types have the capacity to secrete membrane proteins by incorporating them into exosomes, which are small lipid vesicles derived from the intralumenal membranes of multivesicular bodies (MVBs) of the endocytic pathway. Exosomes are expelled in the extracellular space upon fusion of the MVB with the plasma membrane. Exosomal release is a way of secreting membrane proteins meant to be discarded, or to be passed on to other cells. Here, we demonstrate, using primary cortical cultures, that neurones and astrocytes can secrete exosomes. We find that exosomes released by cortical neurones contain the L1 cell adhesion molecule, the GPI-anchored prion protein, and the GluR2/3 but not the NR1 subunits of glutamate receptors. We also show that exosomal release is regulated by depolarisation. Our observation suggests that exosomes may have a regulatory function at synapses and could also allow intercellular exchange of membrane proteins within the brain.

Animals↗
PubMed2001

Parameters of red blood cell aggregation as correlates of the inflammatory state.

To identify clinically relevant parameters of red blood cell (RBC) aggregation, we examined correlations of aggregation parameters with C-reactive protein and fibrinogen in unstable angina (UA), acute myocardial infarction (AMI), and bacterial infection (BI). Aggregation parameters were derived from the distribution of RBC population into aggregate sizes (cells per aggregate) and changing of the distribution by flow-derived shear stress. Increased aggregation was observed in the following order: UA, AMI, and BI. The best correlation was obtained by integration of large aggregate fraction as a function of shear stress. To differentiate plasmatic from cellular factors in RBC aggregation, we determined the aggregation in the presence and absence of plasma and formulated a "plasma factor" (PF) ranging from 0 to 1. In AMI the enhanced aggregation was entirely due to PF (PF = 1), whereas in UA and BI it was due to both plasmatic and cellular factors (0 < or = PF < or = 1). It is proposed that clinically relevant parameters of RBC aggregation should express both RBC aggregate size distribution and aggregate resistance to disaggregation and distinguish between plasmatic and cellular factors.

Acute-Phase Reaction↗
PubMed2000

[Brief preoperative radiotherapy reduces local recurrences and improves survival in rectal cancer].

Locoregional recurrence of rectal cancer ranges between 20%-50% following apparently radical surgery. Radiation has the potential of reducing this high rate of recurrence and residual disease. A retrospective analysis of 78 patients with locally advanced, biopsy proven, adenocarcinoma of the rectum treated between 1980-1987 was conducted. 28 (36%) were treated by surgery alone (surgery); 29 (37%) by surgery and postoperative radiotherapy (post-op); and 21 (27%) by surgery and preoperative radiotherapy (pre-op). 41 were females and 37 males. The median age was 62 years (range 25-90). All tumors were resectable. 42 patients (54%) underwent abdomino-perineal resection and 36 (46%) anterior resection [8 patients Dukes B1 (10%); 37 B2 (47%); 2 C1 (3%); 31 C2 (40%)]. Local recurrences were verified by transanal or ultrasound guided needle biopsy. The 5-year actuarial survival rates by the Kaplan-Meier method for 75 evaluated patients was 55%. Overall 5-year actuarial survival was significantly higher (p = 0.001) in pre-op radiotherapy (95%) compared to surgery alone (45%), or surgery with postoperative radiotherapy (32%). The data were significant (p = 0.006) for patients with stage B tumors, but not stage C. This trend of improved survival held also at 8-year follow-up (80% pre-op; 32% post-op; 27% surgery). The 5-year actuarial local control was significantly better (p = 0.03) for the pre-op irradiated patients (22%), compared with surgery only (56%) and post-op radiotherapy (38%). Local control was better (p = 0.02) for Dukes B tumors in the preoperative group, but not Dukes C tumors. Actuarial 5-year survival of those without distant metastases was 87% for pre-op patients, 62% for surgery alone and 48% for post-op radiotherapy. As all patients were clinically classified as advanced rectal tumors, tumor downstaging by preoperative radiotherapy seems to be paramount for local control. Improved local control translates into a significant advantage in overall actuarial survival.

Adult↗
PubMed2000

Internal jugular vein blood flow in normal and growth-restricted fetuses.

OBJECTIVE: To assess internal jugular vein blood flow patterns during the second half of pregnancy in normal and growth-restricted fetuses. METHODS: We did Doppler ultrasound studies of internal jugular veins and the inferior vena cavas longitudinally on 21 normal singleton fetuses from 20 weeks to term, and on eight growth-restricted fetuses with absent end-diastolic flow at the umbilical artery (UA). The three components of the venous flow velocity waveforms were used to calculate peak velocity ratio: Peak systolic velocity (S wave) minus reverse peak velocity (R wave) divided by peak velocity during early diastole (D wave) and velocity time integral ratio: systolic velocity time integral minus reverse velocity time integral divided by velocity time integral during early diastole. Statistical analysis of longitudinal measurements used K-related samples Friedman test; groups were compared with Mann-Whitney U test and chi(2) test. RESULTS: In normal fetuses we found significant increases in peak velocity ratio and velocity time integral ratio of internal jugular veins and the inferior vena cavas throughout gestation. The mean +/- standard deviation (SD) of the internal jugular veins peak velocity ratio (1.12 +/- 0.4 versus 1.46 +/- 0.15, P <.05) and velocity time integral ratio (1.1 +/- 0.2 versus 1.55 +/- 0.17, P <.05) were significantly lower in growth-restricted fetuses compared with normal fetuses at 28-32 weeks' gestation but inferior vena cava indices were not. None of the eight growth-restricted fetuses had umbilical venous pulsations or changes in inferior vena cava or ductus venosus blood flow patterns. All had arterial pH above 7.15 at birth. CONCLUSION: Growth-restricted fetuses with absent end-diastolic velocity in the UA have changes in internal jugular vein blood flow patterns that probably indicate increased cerebral blood flow, more evidence of redistribution of blood flow in growth-restricted fetuses that can be used to maintain them.

Adult↗
PubMed2000

First trimester diagnosis of conjoined twins in a triplet pregnancy after IVF and ICSI: case report.

A case of conjoined twins in a triplet pregnancy after in-vitro fertilization and intracytoplasmic sperm injection is described. The diagnosis was made by high-resolution vaginal sonography, as early as the eighth week of gestation. The third fetus, of different chorionicity, was normal. Selective termination was successfully done at 12 weeks. The possible association between assisted reproduction and conjoined twinning is discussed. The importance of expert early vaginal sonography of pregnancy resulting from assisted reproduction technology is emphasized.

Adult↗
PubMed2000

Fatal pulmonary artery thrombosis in a patient with Behçet's disease, activated protein C resistance and hyperhomocystinemia.

Behçet's disease (BD) is known for its tendency for thromboembolism, which is thought to be due to vascular injury. The important role of inherited thrombophilias is now becoming increasingly clear. However, conflicting data exist in terms of the contribution of these factors to the thrombotic risk in BD. In this case report, we describe a patient with BD who presented with severe cor pulmonale due to recurrent chronic venous thromboembolism and pulmonary artery thrombosis. The biochemical evaluation revealed that the patient was homozygotic for the factor V Leiden (R506Q) mutation and had increased levels of homocysteine. His condition deteriorated despite adequate anticoagulation treatment, and he died suddenly after 7 months of follow-up. We assume that the presence of thrombophilic risk factors augments and synergizes with the hypercoagulable state already existing in BD, leading to fatal thrombosis in this patient.

Activated Protein C Resistance↗
PubMed1999

Protein phosphatase 2A: who shall regulate the regulator?

Protein phosphatases are responsible for keeping the signaling output of stimulus-activated protein kinases in check; but protein phosphatases are also themselves targets and conveyors of biological signals. Among the major serine/threonine phosphatases, protein phosphatase 2A (PP2A) appears to play a privileged role in the regulation of cell growth and division. How PP2A is regulated is an intriguing question. This review will focus on the role of local protein-protein interactions in PP2A control. Work from a number of laboratories has shown that the catalytic activity, substrate specificity, and subcellular targeting of PP2A are regulated by a remarkably diverse range of regulatory subunits and enzyme inhibitors. On the pathological side, DNA tumor viruses subvert PP2A function by producing proteins that compete with specific regulatory subunits. By interfering with PP2A, these viral proteins can elicit changes in the activity of specific signal transduction pathways, such as the mitogen-activated protein kinase cascade. Recent data indicate that besides classical holoenzyme forms, a fraction of PP2A molecules are associated with novel partners implicated in signal transduction. PP2A biochemically and genetically interacts with the Tap42/alpha4 protein, which is part of a rapamycin-sensitive pathway that connects extracellular stimuli to the initiation of mRNA translation. PP2A also binds to CK2alpha, the catalytic subunit of CK2 (formerly casein kinase 2), and binding is sensitive to mitogenic signaling. The potent effect of quantitatively minor PP2A partners might be explained by a general requirement for docking interactions with substrates under intracellular conditions.

Animals↗
PubMed1999

The appearance of L-selectin(low) polymorphonuclear leukocytes in the circulating pool of peripheral blood during myocardial infarction correlates with neutrophilia and with the size of the infarct.

BACKGROUND: It is assumed that not only leukocytosis, but also the activation of white blood cells (WBC) may play a role in the pathogenesis and prognosis of patients with myocardial infarction (MI). Activation of WBC includes upregulation of CD11b/CD18 and downregulation of CD62L (L-selectin) antigens. HYPOTHESIS: The activation of WBC is associated with the appearance of a larger MI. METHODS: CD11b/CD18 and CD62L were measured on the surface of WBC on Day 1 and Day 3 from the onset of MI. The size of the infarct with estimated by calculating the area under the curve of the creatine kinase enzyme, which was measured every 6 h. RESULTS: A negative correlation was noted between the absolute polymorphonuclear count and the availability of the CD62L on these cells during Day 1 (r = -0.46, p = 0.003) and Day 3 (r = -0.35, p = 0.05). There was a positive correlation between the size of MI and the WBC count (r = 0.46, p = 0.004) and a negative correlation with CD62L on polymorphonuclears (r = -0.35, p = 0.03). During Day 3, the CD11b/CD18 on the polymorphonuclears increased despite a decrement in the absolute number of these cells. CONCLUSION: The neutrophilia during the early phases of acute MI correspond to the appearance of the L-selectin(low) population of polymorphonuclear leukocytes. There is a correlation between the appearance of this population and the size of the infarct.

Aged↗
PubMed1999

CK2alpha-protein phosphatase 2A molecular complex: possible interaction with the MAP kinase pathway.

Despite its wide range of known substrates, the signaling function of protein kinase CK2 is still enigmatic. Mounting evidence suggests that CK2alpha, the catalytic subunit of holoenzymic CK2, may exist free of its usual regulatory partner CK2beta, raising the possibility that 'free' CK2alpha has regulation and function distinct from those of the holoenzyme. We previously reported that CK2alpha could bind to the core dimer of protein phosphatase 2A, and indirectly cause down-regulation of the PP2A substrate MEK1, possibly via activation of PP2A and/or targeting of PP2A to some element of the Ras/Raf/MEK pathway. Here, these results are confirmed and extended. By using transfection experiments and immune kinase assays, we show that endogenous PP2Ac and CK2beta are the only major substrates associating with epitope-tagged CK2alpha, and that expression of activated Raf results in disruption of the CK2alpha-PP2A association. Such disruption might be a necessary step for maximal activation of the MAP kinase pathway by Raf. In keeping with this idea, overexpression ofCK2alpha dose-dependently inhibits the mitogen-induced activation of cotransfected, epitope-tagged MAP kinase. We suggest that the CK2beta free form of CK2alpha is both a target and a regulator of Raf/MAPK signaling.

3T3 Cells↗
PubMed1998

Resistance to activated protein C and the leiden mutation: high prevalence in patients with abruptio placentae.

OBJECTIVE: The Leiden mutation, a point mutation in the gene encoding coagulation factor V, is associated with a high frequency of thromboembolic phenomena. It has recently been connected with adverse outcomes of pregnancy. We carried out this study to define its connection with abruptio placentae. STUDY DESIGN: Twenty-seven women who had abruptio placentae and 29 control subjects matched for age, parity, and ethnic origin were studied. We studied all women for possible hypercoagulation defects. All women demonstrating resistance to activated protein C were studied for the presence of the factor V Leiden mutation. RESULTS: Seventeen of 27 case patients had an activated protein C ratio </=2.5, compared with 5 of 29 control subjects (odds ratio 8.16, 95% confidence interval 3.6-12.75, P =.00125). Participants with activated protein C ratios </=2.5 underwent deoxyribonucleic acid analysis. Eight case patients were found to have the factor V Leiden mutation (5 heterozygous and 3 homozygous, 29.6%), compared with 1 heterozygote among the control subjects who were tested (3.4%). CONCLUSION: Factor V Leiden mutation was found quite frequently in patients with abruptio placentae.

Abruptio Placentae↗
PubMed1998

Role of phosphatidylinositol 3-kinase activation in the hypertrophic growth of adult ventricular cardiomyocytes.

OBJECTIVE: The present study investigated whether activation of phosphatidylinositol 3-kinase (PI3-kinase) is involved in the stimulation of hypertrophic growth of adult ventricular cardiomyocytes under alpha- or beta-adrenoceptor stimulation. METHODS: Adult ventricular rat cardiomyocytes were used either directly after isolation (day 1 culture) or after cultivation for 6 days in presence of 20% fetal calf serum (day 7 culture). PI3-kinase activity was determined in extracts of cardiomyocytes after immunoprecipitation with an antibody against the p85 subunit of PI3-kinase. The influence of PI3-kinase inhibition on myocardial growth was determined using the specific PI3-kinase inhibitors wortmannin and LY294002. RESULTS: In day 1 cultures alpha-adrenoceptor stimulation, but not beta-adrenoceptor stimulation caused activation of PI3-kinase. In response to alpha-adrenoceptor stimulation but not beta-adrenoceptor stimulation an acceleration of protein synthesis (incorporation of 14C-phenylalanine) and an increase in the total masses of cellular protein and RNA was observed. In these cultures inhibition of PI3-kinase attenuated the acceleration of protein synthesis and the increase in cellular masses of protein or RNA in response to alpha-adrenoceptor stimulation. In day 7 cultures alpha- and beta-adrenoceptor stimulation caused activation of PI3-kinase and increased protein synthesis. In these cultures inhibition of PI3-kinase attenuated the growth response to alpha- and beta-adrenoceptor stimulation. CONCLUSIONS: PI3-kinase activation via protein kinase C-dependent or cAMP-dependent pathways is required for hypertrophic growth of adult cardiomyocytes.

Adrenergic alpha-Agonists↗
PubMed1998

Laparoscopic resection of ovarian benign cystic teratomas: experience with 84 cases.

Laparoscopic treatment of benign cystic teratoma of the ovary has been recommended following the study of relatively small numbers of patients. We reviewed our experience with a prospective ongoing protocol for the treatment of benign ovarian teratomas, between January 1990 and December 1996. Sonography established the diagnosis, and biochemical markers were used to screen for possible malignancy. Surgery consisted of resecting the cyst and conserving the ovary if appropriate. The resected cyst was aspirated of its contents following insertion into an EndoCatch bag. Removal was accomplished via the narrowest incision possible by pulling the bag's margins through the incision and grasping the solid parts with conventional surgical instruments. The diameter of the cysts ranged from 2 to 15 cm. Cystectomy was performed in 47, and oophorectomy in 37, patients. Spillage occurred in 11 cases, but none developed peritonitis or fever. The mean duration of post-operative stay was 0.9 days (range 0.5-2). We conclude that laparoscopic resection of benign teratomas of the ovary is safe, well tolerated, and shortens hospital stay.

Adolescent↗
PubMed1998

Intracellular signaling leads to the hypertrophic effect of neuropeptide Y.

Signal transduction pathways involved in the hypertrophic effect of neuropeptide Y (NPY) were investigated in adult cardiomyocytes. Reduction of transforming growth factor-beta activity in serum-supplemented media abolished the induction of hypertrophic responsiveness to NPY. In responsive cells, NPY (100 nM) increased protein synthesis, determined as incorporation of [14C]phenylalanine, by 35 +/- 15% (P < 0.05, n = 16 cultures). In these cells, NPY activated pertussis toxin (PTx)-sensitive G proteins and phosphatidylinositol (PI) 3-kinase. PTx and inhibition of PI 3-kinase abolished the hypertrophic effect of NPY. NPY also activated protein kinase C (PKC) and mitogen-activated protein (MAP) kinase. Inhibition of these two kinases attenuated the induction of creatine kinase (CK)-BB but not the growth response to NPY. In conclusion, NPY stimulates protein synthesis in adult cardiomyocytes via activation of PTx-sensitive G proteins and PI 3-kinase and it induces the fetal-type CK-BB via activation of PKC and MAP kinase.

Androstadienes↗
PubMed1997

Regulation of protein phosphatase 2A by direct interaction with casein kinase 2alpha.

Timely deactivation of kinase cascades is crucial to the normal control of cell signaling and is partly accomplished by protein phosphatase 2A (PP2A). The catalytic (alpha) subunit of the serine-threonine kinase casein kinase 2 (CK2) bound to PP2A in vitro and in mitogen-starved cells; binding required the integrity of a sequence motif common to CK2alpha and SV40 small t antigen. Overexpression of CK2alpha resulted in deactivation of mitogen-activated protein kinase kinase (MEK) and suppression of cell growth. Moreover, CK2alpha inhibited the transforming activity of oncogenic Ras, but not that of constitutively activated MEK. Thus, CK2alpha may regulate the deactivation of the mitogen-activated protein kinase pathway.

3T3 Cells↗
PubMed1996

The anti-proliferative effect of sulindac and sulindac sulfide on HT-29 colon cancer cells: alterations in tumor suppressor and cell cycle-regulatory proteins.

Nonsteroidal anti-inflammatory drugs lower the incidence of and mortality from colon cancer. Sulindac reduces the number and size of polyps in patients with familial adenomatous polyposis. We have shown that sulindac and sulindac sulfide reversibly reduce the proliferation rate of HT-29 colon cancer cells, alter their morphology, induce them to accumulate in the G0/G1 phase of the cell cycle, and sulindac sulfide induces cell death by apoptosis. In this study we confirmed that sulindac and sulindac sulfide prevent HT-29 cells from progressing from the G0/G1 into the S phase. This block in cell cycle progression is associated with an initial rise, then an abrupt decrease in the levels of p34cdc2 protein. Sulindac and sulindac sulfide decrease the levels of mitotic cyclins, induce the levels of p21WAF-1/cip1, and reduce the total levels of pRB, with a relative increase in the amount of the underphosphorylated form of pRB in a time- and concentration-dependent manner. In addition, these compounds reduce the levels of mutant p53. These responses are not associated with intestinal cell differentiation and occur independent of the ability of these compounds to induce apoptosis. We conclude that sulindac and sulindac sulfide reduce the levels of major components of the molecular cell cycle machinery and alter the levels of several tumor suppressor proteins in a manner consistent with cell cycle quiescence. These mechanisms may be operative in vivo to account, in part, for the anti-neoplastic effects of these compounds.

Adenocarcinoma↗
PubMed1996

Antiphospholipid syndrome manifested by ischemic stroke in a patient with Crohn's disease.

Cerebrovascular accidents are rare but well documented in patients with Crohn's disease. Up to 10% of hypercoagulable state manifestations reported in association with inflammatory bowel disease are ischemic strokes. However, no clear mediating factor has thus far been suggested. A 44-year-old woman with Crohn's disease for 25 years developed a left temporal stroke associated with anticardiolipin antibody and lupus anticoagulant suggesting antiphospholipid syndrome. A thorough evaluation did not reveal any other risk factor for ischemic stroke. No possible sources of emboli were found in the carotids and heart, and no deficiencies of protein C and activated protein C, protein S, and anti-thrombin III leading to hypercoagulable state were present. There may be a possible association between antiphospholipid syndrome and hypercoagulable state in Crohn's disease.

Adult↗