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S C Jacobs

Publications and source records attributed to S C Jacobs.

At least 109 records · Page 6Linked to original sources
PubMed1990

Genetic determinants modulating the pathogenic phenotype of tick-borne orbiviruses.

Genetic studies have been carried out on orbiviruses in the Great Island (GI) antigenic subgroup of the Kemerovo serogroup (Orbivrus, Reoviridae) to elucidate the functions of the 10 genomic double-stranded RNA segments. Such studies have shown that segment 4 is the major genetic determinant of neurovirulence (P.A. Nuttall, S.R. Moss, L.D. Jones, and D. Carey, 1989, Virology 172, 428-434), whereas segment 5 of Wexford (WEX) virus and segment 6 of GI virus are the major determinants of serotype specificity (S.R. Moss, C.M. Ayres, and P.A. Nuttall, 1987, Virology 157, 137-144; S.R. Moss, C.M. Ayres, and P.A. Nuttall, 1988, J. Gen. Virol. 69, 2721-2727). In studies with reassortants isolated following dual infection of cell cultures with WEX and GI viruses, the gene combination W4G6 (i.e., viruses deriving segment 4 from WEX virus and segment 6 from GI virus) resulted in nonpathogenic reassortants. Unlike the parental viruses, the avirulent reassortants did not produce clinical evidence of infection in inoculated 2-day-old mice although, suprisingly, they replicated in the brains of the mice. The alternate heterotypic gene combination, G4W5, resulted in typical neurovirulent reassortants. The results indicate that segment 6 of GI virus is able to modulate the phenotypic expression of segment 4 of WEX virus, but not vice versa. Modulation probably results from interactions between the products of these two genomic segments, possibly at the level of virion structure.

Animals↗
PubMed1990

Enhanced prostaglandin synthesis after ultraviolet injury is mediated by endogenous histamine stimulation. A mechanism for irradiation erythema.

Acute ultraviolet light B (UVB) injury is associated with dermal mast cell histamine release. The possibility that histamine-stimulated prostaglandin (PG) synthesis could be a mechanism for irradiation erythema was therefore examined using human skin explants. Explants responded to UV irradiation (120 mJ/cm2) with a fivefold increase in synthesis of prostaglandins E2, F2 alpha and 6-keto PGF1 alpha. Incubating explants with the H1 antihistamines brompheniramine (50 microM) or pyrilamine (30 microM) inhibited PG release from irradiated explants 63 +/- 4.9% (mean +/- SEM) 6 h after UV exposure. Antihistamines did not affect PG synthesis in control explants. Irradiation increased the histamine concentration in explant conditioned medium only 50% over basal values, suggesting that irradiation enhanced histamine responsiveness. Explants were therefore incubated with exogenous histamine. In irradiated explants, PG synthesis was stimulated threefold by 3 microM histamine. Unirradiated explants' PG synthesis was unaffected by histamine. Enhanced histamine sensitivity was also examined in epidermal cell cultures. In irradiated cultures, histamine sensitivity was again markedly potentiated: as little as 1 microM histamine stimulated significant PGE2 release and the response to 10-30 microM histamine was increased six to eight times compared with that of unirradiated cultures. These studies demonstrate that endogenous histamine stimulates PG synthesis in human skin after UV injury by potentiation of histamine-induced prostaglandin release. Potentiated agonist responses induced by UV exposure may contribute to the effects of UVB irradiation injury and in particular to irradiation erythema.

Animals↗
PubMed1989

Intraarterial cisplatin infusion in the management of transitional cell carcinoma of the bladder.

Thirty patients with bulky T3 or T4 transitional cell carcinoma of the bladder, clinically determined to be without nodal or distant metastases, were treated with a 48-hour hypogastric artery infusion of cisplatin (CDDP) 75-150 mg/m2 1 month before tumor resection. Complications of the CDDP infusions were milder than those with intravenous (IV) infusion or rapid intraarterial (IA) infusion, although three lower extremity neuropathies were seen. The CDDP infusions reduced the primary bladder mass effectively, and seven of 16 cystectomy specimens were rendered PO. However, patient survival was clearly predicted by the nodal status. Of 15 T3-4N + MO patients, 11 died at 15 +/- 3 months. Methotrexate, vinblastine, doxorubicin, and cisplatin (M-VAC) chemotherapy was given if residual transitional cell carcinoma was found after IA CDDP. Of 12 P3NOMO patients undergoing cystectomy, eight are alive with no evidence of disease (NED) at 28 +/- 8 months and no patient has died of transitional cell carcinoma. IA CDDP can effectively reduce bulky bladder cancer masses, but has no demonstrable effect on survival in N+ disease. It appears that adjuvant IA CDDP favorably affects survival in T3NOMO transitional cell carcinoma of the bladder.

Carcinoma, Transitional Cell↗
PubMed1989

Complications of hypogastric artery cisplatin infusions.

In an attempt to increase the therapeutic index of Cisplatin (CDDP), 29 continuous 48 hour intra-arterial (IA) infusions of 100-150 mg/m2 CDDP were given to 26 patients with bulky stage T3-T4 bladder cancer. Hypogastric artery catheters were placed distal (n = 42) or proximal (n = 7) to the origin of the superior gluteal artery. Atherosclerosis (n = 5) or aneurysm (n = 2) prevented successful IA catheter placement. Catheter maintenance resulted in no bleeding or thromboembolic episodes. Urethral catheters caused two urinary tract infections. Systemic toxicity was mild with on 4/29 infusions resulting in WBC less than 3,000, 3/29 infusions resulting in creatinine elevation, and 1/29 in peripheral neuropathy. Local effects of the IA CDDP included gluteal pain and ecchymosis (n = 1) and moderately disabling lower extremity neuropathies (n = 3). Systemic side effects of CDDP can be diminished by use of IA route of administration and slow continuous infusion.

Aged↗
PubMed1989

Cultured human prostate-derived fibroblasts produce a factor that stimulates their growth with properties indistinguishable from basic fibroblast growth factor.

Fibrostromal proliferation is believed to be important in the development of benign prostatic hyperplasia (BPH). We found that a mitogen for cultured mesodermal-derived cells was present in extracts of BPH tissue. The mitogen was identified as basic fibroblast growth factor (bFGF). Previous studies did not determine the cell population(s) responsible for bFGF production in the prostate. This information is important to the understanding of the role of bFGF in the etiology of BPH. Human prostate-derived fibroblasts (PF) were initiated in culture. Recombinant bFGF and PF lysates stimulated tritiated thymidine uptake by quiescent PF cells. Greater than 90% of the mitogen in PF lysates bound to heparin-Sepharose and had the same elution profile and apparent molecular weight as bFGF isolated from BPH tissue. The growth factor in PF lysates competed with recombinant iodinated bFGF for binding to antiserum to (1-24)bFGF. Cultured PF incorporated 35S-methionine into protein that was precipitated by antiserum to bFGF. The apparent molecular weight of the radiolabeled protein, about 17,000, was similar to authentic bFGF. The observations are consistent with the interpretation that cultured PF synthesize a growth factor that stimulates their growth with properties that are indistinguishable from bFGF.

Cell Survival↗
PubMed1989

Autonomic control of acid phosphatase exocrine secretion by the rat prostate.

In vivo prostatic secretion was collected from retired breeder Sprague Dawley rats using a method for isolated perfusion of the rat prostatic urethra. Enzymatic acid phosphatase determination was performed on the collected effluent. Control acid phosphatase secretion was 24.2 +/- 2.7 nm over 30 minutes. Intravenous phenylephrine 5 mg/kg stimulated a 10 fold increase in acid phosphatase secretion. The secretion seen with phenylephrine was dose dependent and could be blocked with prazosin, but not yohimbine, atropine, or propranolol. Intravenous beta-adrenergic agonist isoproterenol caused no increase in the secretion of rat prostatic acid phosphatase. Intravenous administration of the cholinergic agonist pilocarpine also resulted in a dose dependent rise in acid phosphatase secretion. The stimulation seen could be blocked by atropine but not phentolamine or propranolol. The stimulation of acid phosphatase secretion seen with alpha 1 adrenergic or cholinergic agonists was not additive. Intravenous vasoactive intestinal peptide did not stimulate acid phosphatase secretion nor did it augment the secretion induced by alpha 1 adrenergic or cholinergic agonists. Release of acid phosphatase into rat prostatic exocrine secretion is under both alpha 1 adrenergic and cholinergic control.

Acid Phosphatase↗
PubMed1988

Exocrine secretion of epidermal growth factor by the rat prostate: effect of adrenergic agents, cholinergic agents, and vasoactive intestinal peptide.

Perfusion of the rat prostatic urethra in vivo provided a means of collecting the rat prostatic secretory product. The secretion of the protein epidermal growth factor (EGF) was investigated by radioimmunoassay (RIA). Baseline secretion of EGF into prostatic fluid was less than .03 +/- .004 SEM ng/min. The alpha-adrenergic agonist phenylephrine caused an increase in EGF to 3.6 +/- .4 SEM ng per 30-min period. The stimulation was blocked completely by prazosin and only partially by yohimbine, indicating primarily alpha 1 control. One mg/kg IV phenylephrine produced a maximal response. The beta-adrenergic agonist isoproterenol caused no increased secretion of EGF. The cholinergic agonist pilocarpine stimulated EGF secretion to 3.2 +/- .6 SEM ng per 30-min period. Atropine blocked the cholinergic stimulation. The combination of phenylephrine and pilocarpine did not result in greater stimulation than either agent alone. Vasoactive intestinal peptide (VIP) did not stimulate EGF secretion, nor did it augment either pilocarpine or phenylephrine-stimulated secretion. EGF secretion into rat prostatic fluid is under both alpha 1-adrenergic and cholinergic control.

Animals↗
PubMed1988

A growth factor in bovine and human testes structurally related to basic fibroblast growth factor.

Homogenates of human testes, epididymides and prostate, and calf testes and epididymides are mitogenic for cultured human foreskin fibroblasts. The growth factors appear similar in that they are inactivated by boiling and acid, but not by treatment with reducing agent. The growth factor in human and bovine testes was partially purified from tissue homogenates, prepared in high ionic strength buffer (pH 7.6) containing protease inhibitors, by ammonium sulfate precipitation and two cycles of heparin-Sepharose chromatography. The growth factor in calf testes was also partially purified from tissue extracted in ammonium sulfate without protease inhibitors, acidified to pH 4.5, and precipitated by ammonium sulfate followed by two cycles of heparin-affinity chromatography. A predominant 17,500 molecular weight (MW) growth factor was identified from alkaline homogenates of human and calf testes by its reactivity with antisera prepared against synthetic peptides whose sequences corresponded to residues 1-12 (amino-terminal), 33-43 (internal) and 136-145 (carboxy-terminal) of bovine basic fibroblast growth factor (bFGF). A slightly smaller 16,600 MW peptide from acidic extracts of calf testes also reacted with antisera to the three synthetic peptides. A 15,500 MW peptide, lacking immunoreactivity with antiserum to the amino-terminal synthetic peptide, was also seen. These findings suggest that a growth factor is present in human and calf testes that is structurally related to bFGF. The structure of the growth factors appears to be altered during the isolation procedure.

Aged↗
PubMed1988

Characterization of growth factors derived from the rat ventral prostate.

Tissue homogenates of rat ventral prostate were examined for growth factor activity using a fibroblast mitogenesis assay. G-75 Sephadex gel filtration separated the growth factor activity into two peaks. A broad first peak contained 98% of the protein and several growth factor moieties. A smaller second peak (MW 6,000) contained epidermal growth factor (EGF) as determined by binding in both a competitive receptor binding assay and a radioimmunoassay using anti-mouse epidermal growth factor (anti-mEGF). The broad first peak also contained substantial amounts of EGF-like activity as higher MW forms of EGF. The broad first peak was further fractionated by heparin-Sepharose affinity chromatography. A major fraction with growth factor activity eluted at 1.5 M NaCl and this fraction was shown to contain bFGF by immunostaining with antisera prepared against synthetic peptides corresponding to amino acid sequences 1-12 (amino terminal), 33-43 (internal), and 136-145 (carboxy terminal) of basic fibroblast growth factor (bFGF). EGF-like and bFGF-like molecules account for the major growth factor activity in the rat ventral prostate.

Animals↗
PubMed1988

Use of a prototype 3F electrohydraulic electrode with ureteroscopy for treatment of ureteral calculous disease.

A 3F electrohydraulic electrode was used with flexible ureteroscopy to treat upper urinary tract calculi in 18 patients. Of 21 procedures performed 10 involved retrograde passage of the ureteroscope and 11 consisted of antegrade procedures with percutaneous nephrostomy access. Complete fragmentation was achieved in 19 of the 21 procedures. In 1 patient bilateral renal caliceal diverticular calculi were treated with the electrohydraulic electrode used to open initially the diverticular orifice. Minor complications included retained stone fragments and small ureteral perforations. No serious complications resulted from the lithotripsy and no patient required an open operation. Flexible ureteroscopy, retrograde or antegrade, appears to offer access to upper tract stones not treated reliably with rigid ureteroscopy. Electrohydraulic lithotripsy with this small 3F probe appears to be a safe and effective means to treat upper urinary tract stones.

Adult↗
PubMed1988

Primary renal carcinoid tumor.

A case of primary renal carcinoid tumor in a sixty-seven-year-old man is presented. Radical nephrectomy removed the primary disease, but hepatic metastases developed and the patient subsequently died. Review of the literature disclosed 8 other cases of primary renal carcinoid. Three of these had metastatic spread.

Aged↗
PubMed1987

Prostatic growth factor: purification and structural relationship to basic fibroblast growth factor.

Prostatic growth factor (PrGF) was purified from alkaline homogenates of human benign prostatic hyperplastic tissue by a combination of ammonium sulfate precipitation, heparin affinity chromatography, and cation-exchange chromatography. The 17,600-dalton, basic (pI 10.2) PrGF is related to basic fibroblast growth factor (bFGF) since antisera raised against synthetic peptides with sequence homologies corresponding to an internal peptide and amino- and carboxyl-terminal peptides of bFGF react with the growth factor. The growth factor appears larger than bFGF, suggesting that additional amino-terminal sequences may be present as a result of alkaline extraction in the presence of protease inhibitors.

Amino Acid Sequence↗
PubMed1987

Amino-terminal sequence of a large form of basic fibroblast growth factor isolated from human benign prostatic hyperplastic tissue.

Homogenization of human benign prostatic hyperplastic tissue in high ionic strength alkaline buffer containing protease inhibitors resulted in the isolation of a 17,400 molecular weight growth factor. When tissue was homogenized in ammonium sulfate at pH 4.5 without protease inhibitors a smaller, 16,600 dalton, growth factor was isolated. Both growth factors reacted with antisera against synthetic peptides whose sequences corresponded to the amino-terminal (1-12), Internal (33-43) and carboxyl-terminal (135-145) portions of basic fibroblast growth factor (bFGF). This suggested that the smaller growth factor was not a truncated form of (1-146) bFGF and that the larger growth factor may contain additional sequences. Amino-terminal sequencing showed the larger growth factor to have the sequence: Ala-Ala-Gly-Ser-Ile-Thr-Thr-Leu-Pro-Ala-Leu-Pro-Glu-Asp-Gly-Gly-Ser-Gly- Ala-Phe-Pro-. These results show that the larger growth factor is an 8 amino acid extended from of (1-146) bFGF and it is likely that the smaller growth factor is a proteolytic cleavage product of the larger growth factor produced during the extraction procedure.

Amino Acid Sequence↗