A puzzle: where was the airgun pellet?
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Humans↗
Biomedical subjects
A Huang
Publications and source records attributed to A Huang.
[Significance and detection of interleukin-8 in human nasal polyps].
OBJECTIVE: To investigate the distribution and content of immunoreaction interleukin-8(IL-8) antigen in the human nasal polyps. METHODS: Twenty-two cases of nasal polyp and 10 cases of normal inferior turbinate were studied with immunohistochemical SABC method and ELISA method. RESULTS: Immunohistochemical results demonstrated that IL-8 antigen staining occurred predominantly within inflammatory and epithelium cell plasm. The level of IL-8 in nasal polyp tissue was higher than in normal control specimens. The value in nasal polyp tissue was in 322.06-2091.41 pg/ml, but in normal with a range of 29.31-332.19 pg/ml. The results demonstrated a remarkable difference between the two groups (P < 0.001). CONCLUSION: These data demonstrated the presence of IL-8 antigen in nasal polyps. Thus IL-8 likely plays a significant role in the pathogenesis of this disease process. There is an important significance of finding a potential treatment method.
Adolescent↗
Treatment of hypertension with ascorbic acid.
In a randomised, double-blind, placebo-controlled study we showed that treatment of hypertensive patients with ascorbic acid lowers blood pressure. Further studies of ascorbic acid to treat hypertension, with clinical endpoints, are warranted.
Adult↗
Early switch from intravenous to oral antibiotics and early hospital discharge: a prospective observational study of 200 consecutive patients with community-acquired pneumonia.
UNLABELLED: To determine the proportion of patients who can be treated with early switch to oral antibiotics and early discharge, to evaluate clinical outcome and patient satisfaction for patients treated with early switch and early discharge, and to define the factors that interfere with early discharge for some of the patients who underwent early switch to oral antibiotic therapy. DESIGN: Prospective study. PARTICIPANTS: Two hundred consecutive hospitalized patients with community-acquired pneumonia. MAIN OUTCOME MEASURES: Number of days needed to switch to oral therapy and length of hospital stay. Clinical outcome and satisfaction with care were evaluated for those patients treated with early switch and early discharge. RESULTS: Early switch to oral antibiotics (within the first 3 days of hospitalization) was performed in 133 patients (67%). Clinical failure was documented in 1 patient. Early switch and early discharge was performed in 88 patients (44%). The mean length of hospital stay for this group was 3.4 days. The most common reason for prolonged hospitalization after the switch to oral antibiotics was the need for diagnostic workup. More than 95% of patients were satisfied with the care they had received. CONCLUSIONS: Using simple clinical and laboratory criteria, a significant proportion of hospitalized patients with community-acquired pneumonia (44%) can be treated with early switch and early discharge. This model did not affect patient outcome, decreased the length of hospitalization, and was associated with a high level of patient satisfaction.
Administration, Oral↗
Enhanced release of prostaglandins contributes to flow-induced arteriolar dilation in eNOS knockout mice.
Nitric oxide and prostaglandins were shown to contribute to the endothelial mediation of flow-induced dilation of skeletal muscle arterioles of rats. Thus, we hypothesized that flow-induced dilation and its mediation are altered in gracilis muscle arterioles of mice deficient in the gene for endothelial nitric oxide synthase (eNOS-KO) compared with control wild-type (WT) mice. Gracilis muscle arterioles ( approximately 80 micrometer) of male mice were isolated, then cannulated and pressurized in a vessel chamber. The increases in diameter elicited by increases in perfusate flow from 0 to 10 microq/min were similar in arterioles from eNOS-KO (n=28) and WT (n=22) mice ( approximately 20 micrometer at 10 microL/min flow). Removal of the endothelium eliminated flow-induced dilations in vessels of both strains of mice. N(omega)-nitro-L-arginine (L-NNA, 10(-4) mol/L) significantly inhibited flow-induced dilation in arterioles of WT mice by approximately 51% but had no effect on responses of arterioles from eNOS-KO mice. Indomethacin (INDO, 10(-5) mol/L) inhibited flow-induced dilation of WT mice by approximately 49%, whereas it completely abolished this response in arterioles of eNOS-KO mice. Simultaneous administration of INDO and L-NNA eliminated flow-induced responses in arterioles of WT mice. Dilations to carbaprostacyclin were similar at concentrations of 10(-8) and 3x10(-8) mol/L but decreased significantly at 10(-7) mol/L in arterioles of eNOS-KO compared with those of WT mice. These findings demonstrate that, despite the lack of nitric oxide mediation, flow-induced dilation is close to normal in arterioles of eNOS-KO mice because of an enhanced release of endothelial dilator prostaglandins and suggest that this vascular adaptation may contribute to the regulation of peripheral resistance in eNOS-KO mice.
Animals↗
Temporal kinetics and cellular phenotype of TNF p55/p75 receptors in experimental allergic encephalomyelitis.
TNF-alpha and LT-alpha are thought to be involved in the immunopathology of CNS demyelinating diseases. Both cytokines induce cellular effects through 55-kDa type-1 receptors (R1) and 75-kDa type-2 receptors (R2). To date, no study has specifically identified the various cell populations that express TNF receptors (TNFR) in the inflammatory and demyelinating mouse model, EAE. Phenotyping the TNFR positive cells is important in determining when and where the ligands may be acting and playing a role in disease pathology. We observed an upregulation of TNF R1 and R2 mRNA in high endothelial venules (HEVs) in the lymph node and CNS before the onset of EAE (preclinical phase). This upregulation of TNFR expression in HEVs was followed by a rapid increase in leukocytes within the CNS after the onset of clinical disease. The temporal kinetics of these data suggest that HEVs become activated early, probably through the release of pro-inflammatory cytokines originating from circulating leukocytes. An increase in TNFR on HEVs would make these cells more susceptible to TNF-induced changes, such as increasing cellular adhesion molecules, thereby further facilitating the trafficking of leukocytes into the CNS parenchyma.
Animals↗
More males seek treatment for eating disorders.
OBJECTIVE: This study compares males and females with DSM-IV-defined eating disorders who were admitted to the inpatient eating disorders service at The New York Hospital, Cornell between 1984 and 1987. METHODS: During this period, 51 males and 693 females presented for their first admission. Demographic information, questionnaires, and SCID interviews were used to compare the male and female samples. RESULTS: Males were significantly more likely than females to have a later onset of their eating disorder (20.56 vs. 17.15 years), and to be involved in an occupation or sport in which weight control influences performance. There were no significant gender differences in other characteristics or comorbid diagnoses. Males constituted an increasing percentage of total admissions between 1984 and 1997 (r = .692, p = .009). DISCUSSION: The similarities of core eating disorder psychopathology and comorbid illness in male and female patients encourage the continued use of similar detection and treatment strategies with both groups.
Adolescent↗
FGF-19, a novel fibroblast growth factor with unique specificity for FGFR4.
We have identified a novel fibroblast growth factor, FGF-19, the most distant member of the FGF family described to date. FGF-19 is a high affinity, heparin dependent ligand for FGFR4 and is the first member of the FGF family to show exclusive binding to FGFR4. Human FGF-19 maps to chromosome 11 q13.1, a region associated with an osteoporosis-pseudoglioma syndrome of skeletal and retinal defects. FGF-19 message is expressed in several tissues including fetal cartilage, skin, and retina, as well as adult gall bladder and is overexpressed in a colon adenocarcinoma cell line.
Adenocarcinoma↗
A multi-centre randomized phase II study of nolatrexed versus doxorubicin in treatment of Chinese patients with advanced hepatocellular carcinoma.
PURPOSE: A multi-centre randomized phase II study of single agent nolatrexed dihydrochloride versus doxorubicin was undertaken in Chinese patients with advanced hepatocellular carcinoma (HCC) to study and compare the clinical efficacy of the two drugs. METHODS: Fifty-four patients with clinical or histological diagnosis of HCC were randomized in a 2:1 ratio to receive nolatrexed or doxorubicin. Nolatrexed 725 mg/m(2)/day was given by continuous infusion via a central venous device for 5 days and doxorubicin 60 mg/m(2) was given as a rapid intravenous infusion every 3 weeks. RESULTS: No objective responses were observed in either treatment arm. Two patients in the nolatrexed arm and none in the doxorubicin arm had >50% decline in serum alpha-fetoprotein. The median survival for the patients in the nolatrexed and doxorubicin arms was 139 days and 104 days, respectively. Moderate toxicities including leukopenia, thrombocytopenia, mucositis and skin rash were observed in both treatment arms. CONCLUSION: Nolatrexed and doxorubicin are minimally active in the treatment of advanced HCC. Given the small sample size, no difference is observed between the two drugs.
Adult↗
Psoriasin (S100A7) expression and invasive breast cancer.
Alteration of psoriasin (S100A7) expression has previously been identified in association with the transition from preinvasive to invasive breast cancer. In this study we have examined persistence of psoriasin mRNA and protein expression in relation to prognostic factors in a cohort of 57 invasive breast tumors, comprising 34 invasive ductal carcinomas and 23 other invasive tumor types (lobular, mucinous, medullary, tubular). We first developed an IgY polyclonal chicken antibody and confirmed specificity for psoriasin by Western blot in transfected cells and tumors. The protein was localized by immunohistochemistry predominantly to epithelial cells, with both nuclear and cytoplasmic staining, as well as occasional stromal cells in psoriatic skin and breast tumors; however, in situ hybridization showed that psoriasin mRNA expression was restricted to epithelial cells. In breast tumors, higher levels of psoriasin measured by reverse transcriptase-polymerase chain reaction and Western blot (93% concordance) were significantly associated with estrogen and progesterone receptor-negative status (P < 0.0001, P = 0.0003), and with nodal metastasis in invasive ductal tumors (P = 0. 035), but not with tumor type or grade. Psoriasin expression also correlated with inflammatory infiltrates (all tumors excluding medullary, P = 0.0022). These results suggest that psoriasin may be a marker of aggressive behavior in invasive tumors and are consistent with a function as a chemotactic factor.
Blotting, Western↗
Epidermoid cyst of the scrotum extending into the true pelvis.
A 9-year-old boy presented with an asymptomatic scrotal mass that was separate from the testes. The workup included a scrotal ultrasound scan and voiding cystourethrogram. On surgical exploration, the mass was solid, separate from the testes, and extended into the pelvis. The mass was removed, and pathologic examination revealed an epidermoid cyst. This is an uncommon scrotal lesion in boys and may represent a monodermal teratoma or abnormal closure of the median raphe. To our knowledge, this is only the second case report of an epidermoid cyst of the scrotum extending into the true pelvis.
Child↗
Lipid hydroperoxides inhibit nitric oxide production in RAW264.7 macrophages.
The effects of oxidatively modified low density lipoprotein (oxLDL) on atherogenesis may be partly mediated by alterations in the production of nitric oxide (NO) by vascular cells. Lipid hydroperoxides (LOOH) and lysophosphatidylcholine (lysoPC) are the major primary products of LDL oxidation. The purpose of this study was to characterize the effects of oxLDL, LOOH and lysoPC on NO production and the expression of inducible nitric oxide synthase (iNOS) gene in lipopolysaccharide (LPS) stimulated macrophages. LDL was oxidized using an azo-initiator 2,2'-azobis (2-amidinopropane) HCl (ABAP) and octadecadienoic acid was oxidized by lipoxygenase to generate 13-hydroperoxyl octadecadienoic acid (13-HPODE). Our study showed that oxLDL markedly decreased the production of NO, the levels of iNOS protein and iNOS mRNA in LPS stimulated macrophages. The inhibition potential of oxLDL on NO production and iNOS gene expression depended on the levels of LOOH formed in oxLDL and was not due to oxLDL cytotoxicity. Furthermore, 13-HPODE markedly reduced NO production and iNOS protein levels, whereas lysoPC showed only slight reduction. The effects of 13-HPODE and lysoPC did not require an acetylated LDL carrier. Our results suggest that 13-HPODE is a much more potent inhibitor of NO production and iNOS gene expression than lysoPC in LPS stimulated RAW264.7 macrophages.
Animals↗
Influence of estrogen receptor variants on the determination of ER status in human breast cancer.
Determination of estrogen receptor alpha (ER) status in breast cancer is an important predictive factor for clinical response to endocrine therapy. We have recently shown that discrepancies in ER status determined by immunohistochemical assay (ER-IHA) can occur between amino-terminal (1D5) and carboxyl-terminal (AER-311) targeted ER antibodies and that those tumors which demonstrate discordance are associated with increased expression of truncated ER variant mRNAs. In this study, we have explored this observation to examine if ER variant expression can exert a direct effect on ER-IHA or whether this association is attributable to the characteristics of the antibodies. ER negative cos-1 cells were transfected with expression vectors containing wild type ER (wt-ER) and/or a frequently expressed truncated variant, ER-clone-4 variant. We found that ER-IHA performed with the same N- and C-terminal targeting ER antibodies on cos-1 cells expressing wt-ER alone demonstrated no difference in signals by western blot (P > 0.1). However, co-expression of wt-ER and the truncated ER-clone-4 variant, resulted in discordant IHA results with relatively higher ER-IHA H-scores from N-terminal antibodies (P < 0.03). Furthermore, re-examination of a subset of breast tumors previously studied by ER-IHA showed persistent concordance in 4/5 cases and persistent differences in 3/5 cases with a different pair of ER antibodies. We conclude that the presence of truncated ER variant proteins can interfere with the interpretation of ER status determined by IHA and that this may account for some of the inconsistencies between ER status and response to endocrine therapy.
Antibodies, Neoplasm↗
Development of nitric oxide and prostaglandin mediation of shear stress-induced arteriolar dilation with aging and hypertension.
We hypothesized that during hypertension, the impairment of mediation of shear stress-induced dilation by nitric oxide (NO) is due to the prevailing hemodynamic forces, and that mediation of this response by NO should still be present in young spontaneously hypertensive rats (SHR). Thus, responses to increases in perfusate flow eliciting increases in wall shear stress were investigated in pressurized (80 mm Hg), isolated arterioles ( approximately 70 to 100 microm) of the left or right gracilis muscle obtained from the same WKY and SHR at 4 and 12 weeks of age. Flow-induced dilations were similar in WKY and SHR at 4 weeks (maximum, 26.5+/-1.8 and 24. 2+/-2.0 microm, respectively). Also, the middle of the upward portion of the shear stress-diameter curves was similar in arterioles of the 2 strains. Inhibition of NO synthase with N(omega)-nitro-L-arginine (L-NNA) or inhibition of synthesis of prostaglandins (PGs) with indomethacin elicited an approximately 50% reduction in flow-dependent dilation, whereas their combined administration eliminated the responses in both groups. In arterioles of 12-week-old WKY, flow-induced dilation became significantly greater (maximum, 46.1+/-2.3 microm) than responses of arterioles of 4-week-old WKY and 12-week-old SHR (maximum, 18.3+/-5. 9 microm), which shifted only the shear stress-diameter curve of the 12-week-old WKY significantly to the left. Also, at 12 weeks of age, flow-dependent dilation of arterioles from SHR is mediated solely by PGs. Thus, shear stress-induced arteriolar dilation is mediated by NO and PGs in 4-week-old WKY and SHR. With aging, the release of NO and PGs increases in normotensive rats, whereas the contribution of NO to the regulation of shear stress disappears in 12-week-old SHR, which suggests that this change is probably caused by the increase in intraluminal pressure as hypertension develops.
Aging↗
Immunohistochemical analysis of BCL-2 protein expression in renal cell carcinoma.
PURPOSE: To investigate the incidence, extent, and distribution of bcl-2 protein expression in human renal cell carcinomas. MATERIALS AND METHODS: Using immunohistochemical tissue staining techniques, bcl-2 protein expression was analyzed in archival nephrectomy specimens removed for renal cell carcinoma or trauma and in 3 renal cell carcinoma cell lines. RESULTS: Normal kidneys demonstrated bcl-2 immunopositivity primarily within the cytoplasm of distal tubule cells. Only rare and minor staining of the proximal tubular cells, thought to be the origin of renal cell carcinoma, was noted in histologically normal controls and areas adjacent to tumor. In contrast, bcl-2 protein expression was demonstrated in 70% of renal cell carcinomas and in all 3 experimental cell lines. CONCLUSIONS: Bcl-2 is a proto-oncogene known to regulate apoptosis (programmed cell death). Bcl-2 protein is overexpressed in the majority of renal cell carcinomas examined. Bcl-2 overexpression may have a role in tumorigenesis and may explain the relative resistance of renal cell carcinoma to chemotherapeutic agents and to radiation therapy.
Carcinoma, Renal Cell↗
Ibuprofen combined with antibiotics suppresses renal scarring due to ascending pyelonephritis in rats.
PURPOSE: In acute pyelonephritis renal scarring may be decreased by immediate antibiotic therapy. Unfortunately in children there is often a delay in starting treatment, which increases the likelihood of renal scarring. In rodents immediate antibiotic therapy is effective for preventing renal scar formation resulting from experimentally induced pyelonephritis. However, the same treatment beginning 72 hours after infection does not prevent renal scarring in this paradigm. We examined whether delayed administration of the nonsteroidal anti-inflammatory agent ibuprofen only or combined with antibiotics suppresses renal scarring in a model of ascending pyelonephritis in rats. MATERIALS AND METHODS: An inoculum of 5x10(9) organisms per ml. of Escherichia coli strain BH-5 was instilled into the bladder of rats and the urethra was occluded for 4 hours. Groups of animals were and were not treated with 15 mg./kg. cefadroxil or 10 mg./kg. ibuprofen given twice daily for 5 days, or the 2 drugs combined. Treatment began 72 hours after inoculation. In an additional group of rats sterile phosphate buffered saline was instilled into the bladder. In each rat the kidneys were examined grossly and microscopically 6 weeks later. RESULTS: Combined antibiotics and ibuprofen significantly inhibited gross renal scarring compared with no treatment or antibiotics only (p<0.05). No difference in renal scarring was detected in animals that received no treatment versus those that received antibiotics or ibuprofen only (p>0.05). CONCLUSIONS: Renal scarring resulting from acute pyelonephritis in this rat model is not decreased by delayed treatment with antibiotics only. The addition of ibuprofen to antibiotic therapy is effective for decreasing renal scarring due to acute pyelonephritis even when treatment is delayed for 72 hours.
Animals↗
Genomic amplification of a decoy receptor for Fas ligand in lung and colon cancer.
Fas ligand (FasL) is produced by activated T cells and natural killer cells and it induces apoptosis (programmed cell death) in target cells through the death receptor Fas/Apol/CD95. One important role of FasL and Fas is to mediate immune-cytotoxic killing of cells that are potentially harmful to the organism, such as virus-infected or tumour cells. Here we report the discovery of a soluble decoy receptor, termed decoy receptor 3 (DcR3), that binds to FasL and inhibits FasL-induced apoptosis. The DcR3 gene was amplified in about half of 35 primary lung and colon tumours studied, and DcR3 messenger RNA was expressed in malignant tissue. Thus, certain tumours may escape FasL-dependent immune-cytotoxic attack by expressing a decoy receptor that blocks FasL.
Adult↗
Superoxide released to high intra-arteriolar pressure reduces nitric oxide-mediated shear stress- and agonist-induced dilations.
It is thought that elevated levels of reactive oxygen metabolites contribute to the dysfunction of vascular endothelium in hypertension. We hypothesized that high intravascular pressure itself elicits production of superoxide, which then interferes with nitric oxide (NO)-mediated responses of arterioles. Thus, isolated arterioles (approximately 80 microm in diameter) from gracilis muscle of normotensive Wistar rats were cannulated and exposed to 140 mm Hg perfusion pressure for 30 minutes (in the absence of perfusate flow). After high intravascular pressure treatment, dilations to increases in perfusate flow (0 to 30 microL/min) were significantly reduced (from 39+/-2.2 to 19+/-2.1 microm at 30 microL/min), eliciting an increase in wall shear stress from approximately 20 to approximately 60 dyne/cm2. Nomega-nitro-L-arginine (10(-4) mol/L) did not affect, whereas indomethacin eliminated, flow-induced dilations after pressure treatment. In control, substance P (SP, 10(-9) to 5x10(-8) mol/L), sodium nitroprusside (SNP, 10(-8) to 10(-6) mol/L), and adenosine (ADO, 10(-6) to 5x10(-5) mol/L) elicited dilations (SP: 31.5+/-1.9 microm, SNP: 45.6+/-4 microm, and ADO: 37.2+/-4.1 microm, at maximum concentrations, respectively). After pressure treatment, maximum dilations to SP and SNP were significantly reduced (by 49% and 39%, respectively), whereas responses to ADO were not affected. Presence of superoxide dismutase (120 U/mL) and catalase (80 U/mL), but not catalase alone, in the perfusate solution prevented the reduction in dilation of arterioles to flow and agonists after pressure treatment by restoring NO mediation. We conclude that high intravascular pressure per se elicits the release of superoxide, which then interferes with NO, a mechanism that contributes to the elevation of wall shear stress and peripheral resistance in hypertension.
Adenosine↗