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Biomedical subjects

E A Woltering

Publications and source records attributed to E A Woltering.

At least 73 records · Page 4Linked to original sources
PubMed1987

Role of peptide radioimmunoassay in understanding peptide-peptide interactions and clinical expression of gastroenteropancreatic endocrine tumors.

Peptide radioimmunoassay has become an important clinical and research tool in understanding the role of peptides in the pathophysiology of gut endocrine tumor syndromes. A gut peptide radioimmunoassay laboratory has been established for the diagnosis and clinical monitoring of endocrine tumors of the gastroenteropancreatic (GEP) system. Radioimmunoassay has enhanced our awareness that co-occurring peptide interactions may modify and ultimately influence the clinical expression of these tumors. Furthermore, it has helped develop a rationale for the use of prototype peptides such as somatostatin and its long-acting analogue Sandostatin (SMS 201-995) in the management of GEP tumors. This group's experience, as well as the experience of other investigators, is presented, and the clinical utility of peptide radioimmunoassay in the field of gut endocrinology is demonstrated.

Adult↗
PubMed1987

The mechanism of hormone-sensitive breast cancer progression on antiestrogen therapy. Implications for treatment and protocol planning.

Fifteen patients whose tumors progressed while they received tamoxifen citrate therapy were studied by serial determinations of serum levels of estrone (E1), estradiol (E2), and dehydroepiandrosterone (DHEA) obtained during progression after withdrawal from tamoxifen therapy and total endocrine ablation or suppression. Discontinuation of tamoxifen therapy resulted in reductions of DHEA, E1, and E2 levels by 44%, 49%, and 42%, respectively. Ablation or suppression reduced sex steroids to minimal levels and produced responses in all patients. Elevations of DHEA, E1, and E2 could be provoked by readministering tamoxifen to hypophysectomized and oophorectomized, but not adrenalectomized, patients, indicating that the adrenal gland is the source of these sex steroids. We conclude that tamoxifen stimulates adrenal production of DHEA, which is aromatized to E1 and E2. Buildup of E1 and E2 overwhelms the competitive binding of tamoxifen to the estrogen receptor, resulting in tumor progression.

Adrenal Glands↗
PubMed1987

Hepatic resection for primary and secondary neoplasms of the liver.

Fifty consecutive major hepatic resections were performed for primary and secondary malignant neoplasms of the liver. There were 7 children and 9 adults with primary neoplasms and 34 patients with secondary neoplasms. The mortality rate was 0 percent and the morbidity rate, 14 percent. Postoperative morbidity correlated with operative blood loss. The 5 year survival rates for children and adults with primary neoplasms were 42 percent and 22 percent, respectively, and the 5 year survival rate for adults with secondary neoplasms was 15 percent. Factors such as disease-free interval, number of metastases, and stage of metastases did not influence the postoperative survival rate. Also, there was no difference in survival rate between patients whose metastases were resected by lobectomy or segmentectomy and those whose metastases were resected by wedge resection.

Adenoma, Bile Duct↗
PubMed1986

Characterization of the in vivo and in vitro inhibition of gastrin secretion from gastrinoma by a somatostatin analogue (SMS 201-995).

Earlier experiments characterized the effect of SMS 201-995 on gastrin secretion from gastrinoma in vivo. The results showed that the somatostatin analogue inhibits basal as well as secretin- and calcium-stimulated gastrin secretion. The current study examined the effect of SMS 201-995 on gastrin secretion from gastrinoma in vitro. Gastrinoma cells were prepared in cell culture or acute cell dispersion to study basal gastrin release. In cell culture, SMS 201-995 at 10(-9) M, 10(-8) M, and 10(-7) M significantly stimulated gastrin secretion (basal medium gastrin, 157 +/- 7.9 pg/ml; with SMS 201-995 10(-9) M, 786 +/- 62 pg/ml; with SMS 201-995 10(-8) M, 569 +/- 72 pg/ml; and with SMS 201-995 10(-7) M, 258 +/- 26 pg/ml). In contrast, in acute cell dispersion, the somatostatin analogue inhibited gastrin secretion (basal medium gastrin, 12.8 +/- 1.3 ng/ml; with SMS 201-995 10(-9) M, 9.0 +/- 0.1 ng/ml; with SMS 201-995 10(-8) M, 8.4 +/- 1.5 ng/ml; and with SMS 201-995 10(-7) M, 7.9 +/- 0.2 ng/ml). Gastrinoma cells were prepared in cell culture to study the effect of SMS 201-995 on gastrin secretion stimulated by secretin and by post-receptor increases in adenosine cyclic nucleotide. The somatostatin analogue inhibited gastrin secretion stimulated by secretin (10(-6) M) (797 +/- 48 pg/ml for secretin alone, compared with 396 +/- 9.4 pg/ml for secretin plus SMS 201-995). SMS 201-995 did not inhibit gastrin secretion stimulated by dibutyryl cyclic AMP (10(-7) M) (617 +/- 62 pg/ml for dibutyryl cyclic AMP alone, compared with 778 +/- 55 pg/ml for the two together). In vitro, SMS 201-995 inhibits basal gastrin secretion from gastrinoma prepared in acute cell dispersion, but not gastrinoma in cell culture, probably due to differences in basal secretory rates. The effect in vitro is less than that in vivo. SMS 201-995 does not inhibit postreceptor increases in adenosine nucleotide. This indirectly supports the hypothesis that SMS 201-995 acts in gastrinoma cells to inhibit gastrin secretion by inhibition of adenylate cyclase activity.

Adult↗
PubMed1986

Somatostatin-like peptides alter calcium but not secretin sensitivity of gastrinoma cells.

The provocation of gastrin release by calcium or secretin is accepted as a method to differentiate the hypergastrinemia of the Zollinger-Ellison syndrome from that of other causes. We have previously shown that calcium and secretin failed to provoke gastrin release from acutely dispersed gastrinoma cells. This disparity between the in vivo and in vitro effects of these two provocative agents suggests that intermediates may be necessary for calcium- or secretin-induced gastrin release. In an acute cell dispersion, serum-free model, two gastrinomas with low levels of endogenous somatostatin (SRIF) and other peptides failed to respond to calcium or secretin provocation. Conversely, a third tumor containing high levels of endogenous SRIF-like peptides and low levels of other gut peptides did respond to calcium, but not to secretin provocation in vitro. We suggest that in vivo, SRIF modulation of gastrin release is a prerequisite for calcium-simulated gastrin secretion.

Animals↗
PubMed1986

The response of a non-functional VIP- and somatostatin-containing tumour to tolbutamide in vitro.

A patient with a tumour containing clinically non-expressive somatostatin (SRIF) and vasoactive intestinal peptide (VIP) was studied in vivo with basal and tolbutamide-provoked SRIF and VIP measurements and failed to respond to tolbutamide infusion. An acute cell dispersion model was used to study this tumour after resection. Incubation of tumour cells in tolbutamide (2 mg/ml) resulted in increases in intracellular SRIF but not in the levels of SRIF released into the incubating medium. In contrast, incubation of tumour cells with tolbutamide decreased supernatant (extracellular) and total (intracellular) VIP by 50%, suggesting a local peptide-peptide modulation of VIP release by high intracellular levels of SRIF or, alternatively, suppression of VIP synthesis and/or release by tolbutamide. Failure of 'nonfunctional' tumours to produce symptoms or abnormal plasma peptide levels may be due to defects in peptide release or complex paracrine peptide-peptide interactions.

Aged↗
PubMed1986

Observations on the effect of a somatostatin analog in the Zollinger-Ellison syndrome: implications for the treatment of apudomas.

Somatostatin is known to inhibit hormone release and gastrointestinal secretion and hence may be useful in the treatment of amine precursor uptake, decarboxylase tumors. Clinical application has been limited by the short half-life, potency, and specificity of the natural hormone. Our study evaluated the effect of a synthetic analog of somatostatin, SMS 201-995 (Sandoz, Inc., E. Hanover, N.J.) on basal and stimulated gastrin release and gastric acid secretion in 10 patients with the Zollinger-Ellison syndrome. In experiment 1, H2-receptor antagonists were discontinued for 48 hours; SMS 201-995, 1 microgram/kg, was given subcutaneously; gastrin and SMS levels in plasma were determined by radioimmunoassay; and gastric secretion was measured and titrated at 0, 1, 2, 3, 4, 5, 6, 8, 10, 12, 14, 16, and 18 hours. The mean +/- SEM baseline gastrin level (1526 +/- 733 pg/ml) was significantly inhibited for 16 hours (p less than 0.05, paired t test). Gastric secretion was neutralized for as long as 18 hours (p 0.05). In experiment 2, three patients received either a secretin (2 U/kg) or a calcium stimulation test (2 mg/kg) with or without pretreatment with SMS 201-995, 1 microgram/kg, subcutaneously. The mean +/- SEM interpreted change in gastrin (ng X 60 min/ml) without SMS 201-995, 36.8 +/- 11 (secretin), and 129 +/- 30 (calcium) were reduced with SMS 201-995 to -1.1 +/- 0.76 (secretin) and -29 +/- 28 (calcium) (p less than 0.05). In the Zollinger-Ellison syndrome, SMS 201-995 caused significant and long-lasting inhibition of both tumor gastrin release and gastric acid secretion, probably by direct action on both the gastrinoma and the stomach. SMS 201-995 blocks acid secretion and secretin- and calcium-stimulated gastrin release, indicating that SMS 201-995 inhibits peptide secretion by postreceptor mechanisms. SMS 201-995 will be useful in the palliative treatment of apudomas.

Adult↗
PubMed1986

Effect of secretin on gastrin release from gastrinoma cells in vitro.

Secretin appears to have a direct effect on gastrinoma cells, which results in a paradoxic increase in the serum gastrin level in patients with the Zollinger-Ellison syndrome. To evaluate this effect, gastrinoma cells were challenged with secretin in acute cell dispersion or after 2 weeks in culture. Acutely dispersed cells were incubated for 15 minutes or 3 hours with and without secretin 10(-6) mol/L. (sec). There was no significant difference in gastrin release between control and sec groups in the two acute incubation periods. At 15 minutes the control value was 47 +/- 1 and the sec value was 54 +/- 1 ng/ml, while at 3 hours the control value was 59 +/- 1 and the sec value was 61 +/- 1 ng/ml. In the cell culture preparation, secretin stimulated gastrin release at all doses (control 463 +/- 85, SEC 10(-10) mol/L 603 +/- 37, sec 10(-8) mol/L 706 +/- 37, sec 10(-6) mol/L 798 +/- 48 pg/ml ([p less than 0.05, Student t test]). These results indicate that secretin stimulates gastrin release directly from cultured gastrinoma cells in a dose-dependent manner but does not stimulate gastrin release from acute cell dispersion. This might be attributed partly to the recovery of secretin receptors in the cultured cells.

Cells, Cultured↗
PubMed1985

Gastrin release from dispersed gastrinoma cells: effects of calcium and calcium ionophore (A23187).

Dispersed single-cell suspensions of human gastrinoma tissue were incubated for 15, 60, and 120 min in a calcium-containing medium, (0.1, 2, 10 mM) in calcium-free medium and in calcium-free medium containing the calcium ionophore A23187 (0.01, 1, and 100 micrograms/ml). Supernatant and pellet (intracellular) gastrin levels were determined by radioimmunoassay. Supernatant gastrin levels remained stable over 120 min in calcium chloride or calcium gluconate containing medium, while intracellular pellet gastrin approximately tripled during the same incubation period. Total gastrin (supernatant plus pellet) approximately doubled during the 2-hr incubation in calcium. However, calcium (0.1, 2, or 10 mM) failed to produce a dose-dependent rise in supernatant, pellet, or total gastrin when compared to calcium-free incubates. Contrary to the expected gastrin response to calcium, supernatant and pellet gastrin levels were higher in incubates in calcium-free medium than in calcium-containing incubates. A23187 (0.01 or 1 mcg/ml) in a calcium-free medium decrease supernatant gastrin while high dose ionophore (100 mcg/ml) increased supernatant gastrin. All doses of ionophore stimulated pellet and total gastrin levels. Thus, it appears that the clinical augmentation of gastrin levels, seen with calcium challenge in vivo may not be solely due to changes in serum calcium.

Adult↗
PubMed1985

Penetrating chest wall and thoracic injuries.

Two hundred seventy patients with penetrating chest wall and thoracic injuries were treated at the Metropolitan Nashville General Hospital in a 5.5-year period ending July 1982. Most (250) were males, and the average age was 29.3 years. One hundred thirty-four injuries were the result of gunshot wounds and 18 patients had sustained shotgun wounds. Stab wounds were the cause of injury in 117 patients. Most patients were successfully treated with closed tube thoracostomy. Twenty-five patients required emergency room thoracotomy, and 27 patients were stable enough to be transported to the operating room for thoracotomy and repair of injuries. Survival in the patients who had emergency room thoracotomy was 12 per cent and 78 percent in patients who had operating room thoracotomy. All but one of the patients who died following operating room thoracotomy died within 1 hour of admission. When thoracotomy is indicated, it frequently must be performed very soon after admission. The indications for emergency thoracotomy must be known and recognized early if it is to be an effective procedure.

Adult↗
PubMed1984

A method for intraoperative identification of the recurrent laryngeal nerve.

Thyroid and parathyroid surgery is associated with a 1 to 6 percent incidence of injury to the recurrent laryngeal nerve. Electrical stimulation of the recurrent laryngeal nerve produces vocal cord motion that can be monitored by means of a double-cuffed endotracheal tube. Twelve patients underwent prospective evaluation with this monitoring system, and in all 12, the recurrent laryngeal nerve was accurately identified and localized. The nerve could be stimulated from a mean distance of 1.7 cm by a mean amperage of 1.3 mA. Postoperative indirect laryngoscopy demonstrated normal vocal cord function in all patients.

Adolescent↗
PubMed1984

Failure of secretin to stimulate gastrin release and adenylate cyclase activity in gastrinoma in vitro.

It has been hypothesized that secretin may act directly on gastrinoma through the adenylate cyclase system to cause stimulation of gastrin release. We studied gastrinoma cells in vitro to determine whether secretin would stimulate gastrin release directly and whether the gastrinoma cell membrane had a functional secretin receptor adenylate cyclase system. Fresh tumor was prepared in cell suspensions containing 1.5 X 10(6) viable cells and incubated for 2 hours with either 2 mM CaCl2 alone (control) or 2 mM CaCL2 and 0.025 U/ml secretin. The gastrin content of the cells in each incubation chamber and the medium were determined by radioimmunoassay and results were expressed as mean gastrin pg/microgram protein +/- SD. Under basal conditions the cellular gastrin content was 39.9 +/- 6.4 (control) compared with 16.7 +/- 2.1 (secretin). After 2 hours of incubation, cellular gastrin content increased in both groups: 68.5 +/- 11.9 (control) to 68.3 +/- 5.5 (secretin). However, the percent of gastrin released into the medium during incubation decreased by one half in both groups (control 37.3% +/- 4.0% to 22.2% +/- 3.0%; secretin 42.8% +/- 7.0% to 18.9% +/- 1.8%). Adenylate cyclase activity was assessed by measuring cAMP generation in fresh-frozen gastrinoma and cultured gastrinoma cell membranes. Isoproterenol (10(-5) M), PGE1 (10(-4) M), and GppNHp (guanine nucleotide) (10(-5) M) caused fivefold to 25-fold increases in cAMP generation. Secretin did not stimulate adenylate cyclase activity above basal (21.73 +/- 4.07 and 2.29 +/- 1.2 pmol cAMP/mg protein/min) for frozen and cultured gastrinoma, respectively. Secretin failed to stimulate gastrin release and adenylate cyclase in vitro. This suggests that secretin-stimulated gastrin release in vivo may not be due to a direct effect of secretin on the gastrinoma.

Adenylyl Cyclases↗
PubMed1983

ABO (H) cell surface antigens in benign and malignant parotid neoplasms.

Twenty-two inflammatory, benign, or malignant parotid lesions were studied by means of the specific red cell adherence test (SRCA), a modification of the Coombs' mixed cell agglutination reaction. In 22 normal parotid tissues the acinar structures were devoid of red cell agglutination, but it was present in ductal epithelium. Findings were similar in 2 cases of parotitis, 11 benign mixed tumors, and 1 malignant mixed tumor. All lacked red cell agglutination in areas of neoplastic change. Benign Warthin's tumors (4 cases) demonstrated antigenicity in the columnar epithelial component of the tumor, but lacked red cell agglutination in areas of the lymphoid component. One malignant Warthin's tumor showed agglutination in areas of normal columnar epithelium but not in areas of malignant dedifferentiation. Undifferentiated carcinoma (1 case) and adenoid cystic carcinoma (2 cases) did not possess detectable ABO (H) antigens in neoplastic areas of the gland. The absence of ABO antigens in normal acinar glands supports their suggested myoepithelial or mesenchymal derivation, as the absence of antigen in benign and malignant mixed tumors supports their proposed mesenchymal derivation. Ductular epithelium and the epithelial components of benign Warthin's tumors have ABO (H) antigens, while the loss of antigen in the epithelial portion of the malignant Warthin's tumor is characteristic of epithelial neoplastic dedifferentiation. Loss of antigen in adenoid cystic and undifferentiated carcinomas of the parotid supports the concept that antigen is absent in epithelially derived malignant neoplasms.

ABO Blood-Group System↗
PubMed1981

Early versus delayed shoulder motion following axillary dissection: a randomized prospective study.

The role and timing of physical therapy following axillary dissection for melanoma, or in conjunction with modified radical mastectomy has not been extensively studied. A prospective randomized clinical trial was carried out over an 18-month period in the Surgery Branch, National Cancer Institute (NCI) and Department of Rehabilitation Medicine, Clinical Center, in which patients were assigned to receive one of two postoperative physical therapy regimens. Patients were assigned to receive graduated increases in allowed range of motion (ROM), either beginning on postoperative day 1 (early) or day 7 (delayed). All patients were advanced to full pain-free ROM when the suction catheters were removed. A total of 36 patients with 40 axillary dissections (19 for melanoma, 21 for breast cancer) were included in this study. Patients randomized to receive early motion had more total wound drainage (805 +/- 516 cc vs. 420 +/- 301 cc, p < 0.01), more days of drainage (10.3 +/- 5.3 vs. 6.2 +/- 2.7, p < 0.01), and later postoperative day of discharge (12.8 +/- 5.1 days vs. 9.2 +/- 4.0 days, p < 0.02) than did patients who started motion on day 7. Wound complications including infection and small areas of skin breakdown occurred more frequently in the early group (seven patients vs. one patient, p < 0.02). No significant differences in the per cent of patients achieving functional ROM could be identified between these two groups at one, three or six months after operation. Transient serratus anterior palsy (12 patients) and latissimus dorsi palsy (2 patients) occurred in approximately 30% of all patients, regardless of group (breast vs. melanoma, early vs. delayed), but returned to normal in all patients. The early institution of flexion and abduction exercises following axillary dissection thus appears to have a deleterious effect on wound healing and drainage. Adequate functional ROM is attained in all patients with a minimum of complications when active motion exercises are delayed for up to 7 days after axillary dissection.

Adult↗
PubMed1981

ABO(H) cell surface antigens in parathyroid adenoma and hyperplasia.

Forty-three cases of primary hyperparathyroidism were studied with the specific red cell adherence test (SRCA) to determine the presence or absence of ABO(H) cell surface antigens on abnormal parathyroid tissue. Of the 27 patients with the clinicopathologic diagnosis (CPD) of adenoma, 24 (89%) had lost the ABO(H) cell surface antigen of the abnormal gland. Among the 15 patients with the CPD of hyperplasia, the parathyroid tissue from three (20%) had lost its red cell antigen. In one patient, a metastasis from a parathyroid carcinoma had lost the ABO surface antigen. Several patients in whom conflicting SRCA and CPD were obtained had factors that raised doubts as to the validity of their CPD. The SRCA is a simple test that may aid in the difficult differentiation between parathyroid adenoma and hyperplasia.

ABO Blood-Group System↗
PubMed1980

Detection of human chorionic gonadotropin in fresh and formalin-fixed testicular tumor tissue. Comparison of sensitivity of immunoperoxidase to radioimmunoassay.

Immunmocytochemical techniques for the detection of human chorionic gonadotropin (HCG), such as immunoperoxidase or immunofluorescence, allow detection but not quantification of this hormone. A modification of standard radioimmunoassay (RIA) techniques allows utilization of tissue slurries and yields quantitative data on tissue HCG levels. Tissue slurry RIAs and indirect immunoperoxidase were performed on fresh and formalin-fixed tissue specimens from 15 patients with nonseminomatous testicular tumors. HCG detectability by RIA or immunoperoxidase was markedly decreased by formalin fixation. Tissue specimens with high levels of HCG in the fresh state yielded positive immunoperoxidase and RIA results, while specimens with minimally elevated HCG levels tended to be negative. Results of tissue slurry RIAs correlated well with immunoperoxidase results. The detection of HCG in fixed tissue appears to underestimate the amount of HCG present in fresh specimens. Therefore, a negative RIA on formalin-fixed tissue slurry or negative immunoperoxidase of the formalin-fixed, paraffin-embedded tissue does not rule out the absence of HCG in fresh tissue.

Chorionic Gonadotropin↗
PubMed1980

Evaluation of bupivacaine nerve blocks in the modification of pain and pulmonary function changes after thoracotomy.

Thirty-one patients undergoing thoracotomy were prospectively randomized to receive (1) no nerve blocks (n = 12), (2) placement of percutaneous catheters for intermittent nerve blocks with bupivacaine (Marcaine) (n = 10), or (3) bupivacaine nerve blocks intraoperatively (n = 8). One patient refused postoperative evaluation and was not included in this study. All patients received similar preoperative, intraoperative, and postoperative medications. Comparison of preoperative and postoperative arterial blood gases, assessments of pain and alertness, and chest roentgenograms showed no statistical advantage for any group. Analgesic requirements and pulmonary functions (functional residual capacity, tidal volume, minute ventilation peak flow, or forced expiratory volume) did not differ among the groups. Statistically significant differences were seen in mean respiratory rate and forced vital capacity. These differences, however, indicate that bupivacaine either by intraoperative use or by intermittent percutaneous administration did not improve postoperative increases in respiratory rate or decreases in forced vital capacity.

Bupivacaine↗