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B Herman

Publications and source records attributed to B Herman.

At least 73 records · Page 4Linked to original sources
PubMed1986

Identification of the cellular mechanisms responsible for platelet-derived growth factor induced alterations in cytoplasmic vinculin distribution.

Exposure of quiescent density arrested BALB/c-3T3 cells (clone A31) to platelet-derived growth factor (PDGF; 6-12 ng/ml) results in a rapid, reversible, time- and dose-dependent removal of vinculin from adhesion plaques (Herman and Pledger, 1985). Potential cellular mechanisms involved in PDGF-induced removal of vinculin from adhesion plaques were examined. Removal of vinculin from adhesion plaques following exposure of cells to PDGF was temperature dependent, occurred in many fibroblast cell lines, and could be mimicked by 12-tetradecanoyl phorbol-13-acetate (TPA; 5-125 nM) or melittin (0.35 microM). Unlike the effect of PDGF, TPA- or melittin-induced vinculin disruption was not reversible. The removal of vinculin from adhesion plaques was inhibited by trifluoroperazine (TFP; 2.5 microM). 8-(N,N-diethylamino) octyl-3,4,5-trimethoxy benzoate (TMB-8; 1.0 microM), mepacrine (220 microM), n-alpha-p-tosyl-L-lysine chloromethylketone (TLCK; 100 microM), phenylmethoxysulphonylfluoride (PMSF; 500 microM), and epsilon-aminocaproic acid (epsilon-ACA; 100 microM); however, amiloride (100 microM), A23187 (20 microM), and chloroquine (1 mM) were unable to inhibit this effect. Melittin disruption of vinculin was inhibited by (in order of decreasing effectiveness) mepacrine greater than TMB-8 greater than TFP greater than leupeptin greater than PMSF, whereas A23187 and amiloride had no effect. The return of vinculin to adhesion plaques following PDGF treatment required de novo mRNA transcription and protein synthesis and was associated with PDGF-stimulated synthesis of vinculin. The observation that both PDGF- and melittin-induced removal of vinculin from adhesion plaques is inhibited by mepacrine suggests that phospholipase activation may be an early and important step in PDGF-induced disruption of vinculin from adhesion plaques. In addition, TFP, TMB-8 and protease inhibitor inhibition of both the PDGF and melittin effects on vinculin distribution, coupled with the finding that TPA can mimic the PDGF or melittin response, suggests that Ca2+, calmodulin, protein kinase C, and/or proteolysis may play an important role(s) in the removal of vinculin from adhesion plaques following PDGF addition. The lack of effect of A23187 addition on vinculin distribution suggests that alterations in cellular Ca2+ is necessary but not sufficient for vinculin removal from adhesion plaques.

Amiloride↗
PubMed1986

Analysis of deoxyribonucleic acid distribution in noncleaving oocytes from patients undergoing in vitro fertilization.

The purpose of this study was to describe the quantity and distribution of deoxyribonucleic acid (DNA) in oocytes that did not fertilize or did fertilize and failed to cleave, from patients who underwent in vitro fertilization. Patients were selected with at least one cleaving egg, so that the sperm population was known to be fertile, and failure of fertilization or cleavage in the remaining oocytes could be attributed to nonspermatozoan factors. The noncleaving oocytes were classified into five categories, the majority of which (71%) lacked a polar body and any morphologically identifiable nucleus or germinal vesicle. Three general defects were found: failure to replicate the DNA properly; failure to package the DNA properly; and failure to organize the nuclear material properly after sperm penetration. It is concluded that either altered stimulation protocols or altered in vitro maturation conditions are needed to increase the average number of normal embryos available for transfer.

Cleavage Stage, Ovum↗
PubMed1985

Binding and internalization of heparin by vascular smooth muscle cells.

Previous work from our laboratory has demonstrated that heparin specifically inhibits the proliferation of vascular smooth muscle cells in vivo and in vitro. In this paper, we examine the binding and mode of internalization of heparin by smooth muscle cells. For these studies, radiolabeled and fluoresceinated (FITC) heparin probes were synthesized that retained their antiproliferative capacity. Binding of 3H-heparin to these cells occurs via specific, high-affinity binding sites (Kd = 10(-9) M, 100,000 binding sites per cell). Approximately 80% of the heparin bound to the cell surface was shed into the culture medium within 2 hr. The heparin that was left on the cell surface was internalized with biphasic kinetics. Approximately 50% of the bound material was internalized within 2 hr. After this initial rapid uptake, the rate slowed substantially, with the remaining heparin requiring 1-2 days to be internalized. Binding and uptake of FITC heparin was monitored using video image intensification fluorescence microscopy. When smooth muscle cells were exposed to FITC heparin at 4 degrees C, a diffuse surface staining pattern was observed. After warming the cells to 37 degrees C, intensely fluorescent vesicles were seen superimposed over the diffuse surface staining within 2 min. After 15 min at 37 degrees C, numerous large punctate vesicles were seen inside the cell. After 2 hr these vesicles had concentrated in the perinuclear region. This pattern of uptake, when considered along with the presence of specific, high-affinity binding sites and the initial rapid uptake of 3H-heparin, suggests that heparin enters smooth muscle cells by both receptor-mediated and other endocytic pathways.

Animals↗
PubMed1985

[Instrumental esophageal perforation--its treatment and results].

The number of oesophagus perforations has increased considerably with the increase in endoscopic, diagnostic and therapeutic procedures. 46 instrumental oesophagus perforations have been observed between 1973 and 1984. The youngest patient was a 2-year-old girl with a benign oesophagus stenosis and the eldest was an 89-year-old man with a neoplasm of the cardia. The average age was 62 years. 26 patients were treated conservatively; 20 patients were treated surgically. In 2 cases the oesophagus was diverted at the cervical level and the cardia detached. 8 months later this was successfully reconstructed. 9 out of 43 patients died. In every case, the cause of death were cardio-pulmonal complications accompanying general sepsis.

Adolescent↗
PubMed1985

Platelet-derived growth factor-induced alterations in vinculin and actin distribution in BALB/c-3T3 cells.

Exposure of BALB/c-3T3 cells (clone A31) to platelet-derived growth factor (PDGF) results in a rapid time- and dose-dependent alteration in the distribution of vinculin and actin. PDGF treatment (6-50 ng/ml) causes vinculin to disappear from adhesion plaques (within 2.5 min after PDGF exposure) and is followed by an accumulation of vinculin in punctate spots in the perinuclear region of the cell. This alteration in vinculin distribution is followed by a disruption of actin-containing stress fibers (within 5 to 10 min after PDGF exposure). Vinculin reappears in adhesion plaques by 60 min after PDGF addition while stress fiber staining is nondetectable at this time. PDGF treatment had no effect on talin, vimentin, or microtubule distribution in BALB/c-3T3 cells; in addition, exposure of cells to 5% platelet-poor plasma (PPP), 0.1% PPP, 30 ng/ml epidermal growth factor (EGF), 30 ng/ml somatomedin C, or 10 microM insulin also had no effect on vinculin or actin distribution. Other competence-inducing factors (fibroblast growth factor, calcium phosphate, and choleragen) and tumor growth factor produced similar alterations in vinculin and actin distribution as did PDGF, though not to the same extent. PDGF treatment of cells for 60 min followed by exposure to EGF (0.1-30 ng/ml for as long as 8 h after PDGF removal), or 5% PPP resulted in the nontransient disappearance of vinculin staining within 10 min after EGF or PPP additions; PDGF followed by 0.1% PPP or 10 microM insulin had no effect. Treatment of cells with low doses of PDGF (3.25 ng/ml), which did not affect vinculin or actin organization in cells, followed by EGF (10 ng/ml), resulted in the disappearance of vinculin staining in adhesion plaques, thus demonstrating the synergistic nature of PDGF and EGF. These data suggest that PDGF-induced competence and stimulation of cell growth in quiescent fibroblasts are associated with specific rapid alterations in the cellular organization of vinculin and actin.

Actins↗
PubMed1985

[Esophagus perforation--treatment and results].

Esophageal perforation is most often caused by instrumental lesion during endoscopy. Mortality is still high; underlying malignant disease, septic complications and cardiopulmonary problems are endangering the patient. In small perforation with poor clinical symptoms, conservative treatment (i.e. antibiotics, gastric suction, parenteral nutrition) should be considered. We could treat in this way more than 50% of our cases. On the other hand, some patients require agressive surgical procedures, e.g. cervical esophagostomy gastrostomy and disconnection of esophageal continuity.

Adolescent↗
PubMed1979

Risk of infection in prolonged central venous catheterization.

Classically, duration of infusion was thought to increase the rate of contamination by catheters. The results of this study show that this is not true and that, to the contrary, there is a definite difference in contamination rates between the basilic and the jugular and subclavian veins. The advantage of the basilic way which exists whatever the pathologic condition must undoubtedly determine the choice of this way of catheterization rather than any other.

Arm↗
PubMed1978

The biology of social attachments: opiates alleviate separation distress.

The possibility that brain opiate systems participate in the control of social affect was assessed by determining capacity of low doses of exogenous opiates (0.125-0.50 mg/kg oxymorphone, and 0.10-0.50 mg/kg morphine sulfate) to reduce distress vocalizations of socially isolated puppies. Low doses of opiates were capable of profoundly reducing crying as well as the motor agitation they exhibit during brief periods of social isolation. Since reductions in crying could be obtained with morphine in the absence of any gross behavioral disturbances, the possibility is entertained that brain opiates may function to control the intensity of emotions arising from social separation. Possible parallels between the biological nature of narcotic addiction and the formation of social bonds are discussed.

Animals↗