[Real-time ultrasonic diagnosis of metastatic tumor thrombus in the inferior vena cava].
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Biomedical subjects
Publications and source records attributed to J He.
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A series of 748 patients with lung cancer as treated by surgery from 1961 to 1984 is reported. Regular lobectomy was done in 445 (74%) patients, bronchoplastic lobectomy in 67 (11.2%), segmental or wedge excision in 15 (2.5%) and pneumonectomy in 74 (12.3%) in which the ratio of left to right pneumonectomy was 2.9:1. Overall resection rate was 80.4% (601/748) and resection mortality was 1.2% (7/601) (death within 30 days of operation). Overall 5 year survival rate was 42% (169/402). The 5 year survival rate was 35.3% for pneumonectomy, 54.1% for bronchoplastic lobectomy, 42.3% for regular lobectomy and 16.7% for segmental or wedge excision. In this analysis, emphasis is laid to the therapeutic validity of the different modes of surgery. Statistical data show that only when the indication of different surgical interventions are strictly adhered to and the reasonable procedures are carried out, could better results be obtained. In surgical treatment of lung cancer, it is an important principle to eradicate the tumor and its metastatic foci as thorough as possible and to conserve the respiratory function as much as possible. Regular lobectomy has now become the "standard" and first choice operation. Pneumonectomy should be reserved for the patients with absolute necessity due to the extent of the lesion, adequate cardiopulmonary function and possibility of a permanent cure. Pneumonectomy is substituted by bronchoplastic lobectomy to a certain degree, preserving more of the lung function and improving the living quality after operation and long term results. Extensive practice of this surgical modality is advised.
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CONTEXT: Lowering low-density lipoprotein cholesterol (LDL-C) is known to reduce risk of recurrent coronary heart disease in middle-aged men. However, this effect has been uncertain in elderly people and women. OBJECTIVE: To estimate the risk reduction of coronary heart disease and total mortality associated with statin drug treatment, particularly in elderly individuals and women. DATA SOURCES: Trials published in English-language journals were retrieved by searching MEDLINE (1966-December 1998), bibliographies, and authors' reference files. STUDY SELECTION: Studies in which participants were randomized to statin or control treatment for at least 4 years and clinical disease or death was the primary outcome were included in the meta-analysis (5 of 182 initially identified). DATA EXTRACTION: Information on sample size, study drug duration, type and dosage of statin drug, participant characteristics at baseline, reduction in lipids during intervention, and outcomes was abstracted independently by 2 authors (J.H. and S.V.) using a standardized protocol. Disagreements were resolved by consensus. DATA SYNTHESIS: Data from the 5 trials, with 30 817 participants, were included in this meta-analysis. The mean duration of treatment was 5.4 years. Stati n drug treatment was associated with a20% reduction in total cholesterol, 28% reduction in LDL-C, 13% reduction in triglycerides, and 5% increase in high-density lipoprotein cholesterol. Overall, statin drug treatment reduced risk 31 % in major coronary events (95% confidence interval [CI], 26%-36%) and 21 % in all-cause mortality (95% CI, 14%-28%). The risk reduction in major coronary events was similar between women (29%; 95% Cl, 13 %-42 %) and men (31 %; 95% CI, 26%-35%), and between persons aged at least 65 years (32%; 95% CI, 23%-39%) and persons younger than 65 years (31 %; 95% CI, 24%-36%). CONCLUSIONS: Our meta-analysis indicates that reduction in LDL-C associated with statin drug treatment decreases the risk of coronary heart disease and all-cause mortality. The risk reduction was similar for men and women and for elderly and middle-aged persons.
Hepatitis E virus (HEV) causes sporadic and epidemic acute viral hepatitis in many developing countries. In Africa, hepatitis E has been documented by virus detection (reverse transcriptase polymerase chain reaction, RT-PCR) in Egypt, Chad, Algeria, Morocco and Tunisia. Cases of presumptive hepatitis E also have been documented by detection of antibody to HEV in the Sudan, Kenya, Ethiopia, Somalia, Djibouti and South Africa. Recently, we reported the recovery of 9 isolates of HEV from feces collected during an outbreak of jaundice in Namibia. These specimens were stored frozen for many years at the South African Institute for Medical Research awaiting new methods to determine the etiology of jaundice. HEV genomic sequences were detected by antigen-capture RT-PCR with primers that amplified 2 independent regions of the HEV genome (ORF-2 and ORF-3). To further characterize the HEV 83-Namibia isolates, we determined the nucleotide (nt) sequence of the 3' end of the capsid gene (296 of 1, 980 nt in ORF-2) and ORF-3 for 1 isolate. The capsid gene sequence shared 86% identity with the prototype Burma strain and up to 96% identity with other African strains at the (nt) level, and 99% identity with Burma or other Africa strains at the amino acid level. A 188 (nt) fragment amplified from ORF-3 was also highly homologous to other HEV but was too short for meaningful comparison. Phylogenetic analysis indicated that HEV 83-Namibia is closely related to other African isolates, and differs from Burmese, Mexican and Chinese HEV. These data link the HEV causing the 1983 Namibia outbreak to more recent HEV transmission in northern and sub-Saharan Africa, suggesting this subgenotype of HEV is firmly established throughout the continent.
Injection of an expression vector pJHEV containing hepatitis E virus (HEV) structural protein open reading frame 2 gene generates a strong antibody response in BALB/c mice that can bind to and agglutinate HEV. In this study, we tested for immunologic memory in immunized mice whose current levels of IgG to HEV were low or undetectable despite 3 doses of HEV DNA vaccine 18 months earlier. Mice previously vaccinated with vector alone were controls. All mice were administered a dose of HEV DNA vaccine to simulate an infectious challenge with HEV. The endpoint was IgG to HEV determined by ELISA. Ten days after the vaccine dose, 5 of 9 mice previously immunized with HEV DNA vaccine had a slight increase in IgG to HEV. By 40 days after the vaccine dose, the level of IgG to HEV had increased dramatically in all 9 mice (108-fold increase in geometric mean titer). In contrast, no control mice became seropositive. These results indicate that mice vaccinated with 3 doses of HEV DNA vaccine retain immunologic memory. In response to a small antigenic challenge delivered as DNA, possibly less than delivered by a human infective dose of virus, mice with memory were able to generate high levels of antibody in less time than the usual incubation period of hepatitis E. We speculate that this type of response could protect a human from overt disease.
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PURPOSE: To test the reliability and performance of two physical diagnosis algorithms for use in physical examination of vascular access grafts. MATERIALS AND METHODS: Grafts were assessed in 39 patients by means of physical examination performed by four observers. Grafts were characterized as having a thrill, pulse, or indeterminate examination at three locations (arterial, midpoint, venous). Findings with this algorithm were compared with those from ultrasound (US) with volume flow measurements. RESULTS: Patients with a thrill at all three locations of the graft all had volume flows greater than 450 mL/min (negative predictive value = 100%). Of patients with a pulse at any of three locations, only 28% (positive predictive value) had a volume flow of 450 mL/min or less. CONCLUSION: Physical examination is a good screening test for ruling out the low flows associated with impending access graft failure, thereby eliminating the need for routine US for many patients.
Even though increased accumulations of radiolabeled antisense DNAs compared to control DNAs are becoming a routine observation in cultured tumor cells, trustworthy evidence of tumor targeting in vivo by an antisense mechanism remains elusive. The goal of this study was to obtain convincing evidence of antisense tumor targeting in nude mice by using two different tumors and both intratumoral (i.t.) and intravenous (i.v.) administration of radiolabeled antisense and control sense DNAs. Both the MDR++ cell line KB-G2 and its parent MDR+ cell line KB-31 were used in this study. The antisense (AS) DNA was directed against the AUG start codon of the MDR1 mRNA and, along with the sense (S) control DNA, was a uniform phosphorothioate administered naked. In previous cell culture studies from our laboratories, the accumulation of this AS DNA was strikingly high in KB-G2 cells and only average in KB-31 cells, a fact we attribute to the 1000-fold higher expression by RT-PCR of MDR1 mRNA in the former cell line. In this study, both DNAs were radiolabeled with (99m)Tc via MAG3 and administered i.t. or i.v. at 1 microg (100 microCi) per animal 24 h prior to sacrifice and dissection in mice bearing thigh tumors of about 1 g. Following i.t. administration, no statistically significant differences (Student's t test, p < 0.05, N = 4) between the AS and S DNA biodistributions in normal tissues were observed except in the KB-G2 mice in which muscle levels were lower for the S control. In contrast, tumor levels in the KB-G2 animals were significantly higher for the AS DNA vs S DNA (14.7 vs 8.5% ID/g) while this difference (8.6 vs 4.3% ID/g) was insignificant in the KB-31 animals. The whole body images obtained just prior to sacrifice clearly show improved targeting of AS DNA vs S DNA in the KB-G2 but not the KB-31 animals. Calculations based on these results show that about 60 000 AS DNAs accumulated specifically (i.e. AS DNA - S DNA) per KB-G2 tumor cell following i.t. administration. When administered i.v. rather than i.t., higher tumor levels in KB-G2 animals compared to KB-31 were not observed, most likely because of the lower dosage reaching the tumors. When the KB-G2 and KB-31 results are combined, no statistically significant differences between the AS and S DNA biodistributions in normal tissues were observed except in blood in which S DNA levels were higher and in spleen in which they were lower. In contrast, tumor levels were significantly higher for the AS DNA vs S DNA (0.100 vs 0.063% ID/g). Calculations based on these results show that about 400 AS DNAs accumulated specifically per tumor cell following i.v. administration. Therefore evidence for tumor targeting in vivo by an antisense mechanism has been obtained in that statistically higher tumor accumulations of the (99m)Tc-AS DNA were observed compared to the control (99m)Tc-S DNA both following i.t. and i.v. administrations. The successful localization of AS DNA in tumor demonstrates that in vivo AS targeting of tumor is feasible although improvements in tumor delivery and normal tissue clearance are needed for practical antisense imaging.
The distribution of Candida species was examined using 1114 yeasts isolated from various clinical specimens. The isolates were identified by germ tube test, hyphal/pseudohyphae and chlamydoconidia production and carbohydrate assimilation test using ten carbohydrates (glucose, sucrose, trehalose, cellobiose, arabinose, galactose, mannitol, raffinose, lactose and maltose). Among the 1114 isolates studied, 9 species of Candida were identified and the relative frequency of isolation was C. albicans (44.2%), C. parapsilosis (26.0%), C. tropicalis (17.7%), C. glabrata (9.6%), C. krusei (1.2%), C. rugosa (0.6%), C. guilliermondii (0.2%), C. lusitaniae (0.08%) and C. kefyr (0.08%). Non-C. albicans was the most common Candida species isolated from blood, respiratory system, urine and skin. The isolate from vaginal swabs was predominantly C. albicans. 82.2% of C. glabrata and 64.2% of C. krusei isolated in this study were from vaginal swabs.
The pyrazolo[3,4-d]pyrimidine-4,6-diamine nucleosides 2b-d stabilize the dA-dT base pair significantly when the dA-residue is replaced. Oligonucleotide duplexes incorporating 2b-d show a 4-6 degrees C Tm increase per modification. The 7-bromo compound 2b harmonizes the stability of the dA-dT vs. the dG-dC pair. According to this the stability of such duplexes depends no longer on the base pair composition of a DNA molecule.
Dibucaine acts as a weak protonophore in cytochrome c oxidase proteoliposomes. At low concentrations in the presence of permeant anions, it stimulates turnover and collapses enzyme-generated pH gradients. At higher concentrations, dibucaine inhibits activity of cytochrome c oxidase in proteoliposomes and the isolated enzyme. It also induces a red shift in the resting spectrum, indicating a change at the binuclear centre. This spectroscopic effect is kinetically biphasic. Dibucaine inhibits steady-state oxidase activity, but not the rate of the red shift in the cytochrome a3 Soret band during turnover. It reacts faster with the partially reduced state than with resting enzyme. The inhibition is kinetically biphasic with a noncompetitive Ki approximately 0.5 mM. Excess dibucaine effects a maximal turnover decline of 80%. At low ionic strength only the total Vmax is affected; tight binding of cytochrome c and turnover at the "tight" site are unaffected. Dibucaine may bind to an anionic site in a hydrophobic pocket, modifying electron transfer from cytochrome a and CuA to cytochrome a3 - CuB and the oxidized spectrum of the latter centre. Stimulation of turnover in cytochrome c oxidase in proteoliposomes is due to a separate membrane-dependent proton translocation catalysed by dibucaine in the presence of permeant anions.
To investigate the long-term effect of a topically applied beta-blocker on human corneal epithelium, the corneal epithelial barrier function and the superficial cell area of the corneal epithelium were evaluated. Seventeen normal healthy volunteers (without medication), 7 cataract patients (treated with pyrenoxine eyedrops) and 7 glaucoma or ocular hypertension patients (treated with 0.5% timolol maleate) were assigned to this study. The eyedrops had been used on a daily basis for at least 3 months. In the evaluation of corneal epithelial barrier function, fluorescein uptake was measured using a slitlamp fluorophotometer after application of 3 microl of 0.5% fluorescein for 10 min. In the evaluation of the superficial cell area, the central corneal epithelium was measured by tandem scanning confocal microscopy (TSCM). The healthy control and timolol groups were compared. Corneal fluorescein uptake in the healthy control, pyrenoxine and timolol groups was 20.3 +/- 3.2, 21.5 +/- 4.0 and 76.2 +/- 30.0 ng/ml (mean +/- standard error), respectively. There was a significantly higher fluorescein uptake in the timolol group compared to the pyrenoxine group (p = 0.0088) and the healthy control group (p = 0.0055). TSCM showed no significant difference in the superficial cell areas of the corneal epithelium between the healthy control and timolol groups. beta-Blocker eyedrops decreased the corneal epithelial barrier function. Their application was not accompanied by any biomicroscopic change in the superficial cell area.
Observational epidemiologic studies identify an inverse relationship between dietary fiber and protein intake and blood pressure. This relationship has been demonstrated in both cross-sectional and prospective cohort studies and among various populations. Few randomized trials have examined the effect of dietary fiber and protein supplementation on blood pressure. In general, these intervention studies suggest that dietary fiber intake may lower blood pressure. However, they do not confirm the observational relationship between dietary protein and blood pressure. Furthermore, there are many limitations in the design of these clinical trials. Carefully designed randomized controlled trials with sufficient sample size to recognize a 2-3 mm Hg change in blood pressure using well-characterized dietary fiber and protein preparations are needed to confirm or refute these observed effects.
OBJECTIVES: We investigated the ability of several human neutralizing monoclonal antibodies (mAbs), originally raised against human immunodeficiency virus (HIV) clade B isolates, to neutralize primary clade C isolates as single agents and in combination. STUDY DESIGN/METHODS: HIV clade C isolates from five different countries were tested for susceptibility to neutralization by anti-clade B mAbs in human peripheral blood mononuclear cells. Monoclonal antibody combinations were evaluated for possible synergy. RESULTS: All 20 primary HIV clade C isolates could be neutralized 97.5% to 100% by a quadruple combination of mAbs IgG1b12, 2G12, 2F5, and 4E10. These mAbs recognized conserved epitopes and were highly synergistic, resulting in strong cross-clade neutralization. CONCLUSIONS: In our previous experiment, a synergistic combination of human neutralizing mAbs protected all macaque neonates against oral challenge with a simian-human immunodeficiency virus encoding HIV env. Together, our data suggest that passive immunization with currently available anti-clade B mAbs could play a role in preventing HIV clade C transmission through breastfeeding.