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Biomedical subjects

S B Jiang

Publications and source records attributed to S B Jiang.

At least 37 records · Page 2Linked to original sources
PubMed1999

Extracorporeal photochemotherapy for cutaneous T-cell lymphoma: a 9.7-year experience.

Cutaneous T-cell lymphoma (CTCL) is an indolent lymphoma usually of CD4+ T lymphocytes in which the aggressive treatment for the advanced stages does not increase survival. Photopheresis has been established as an alternative modality for the therapy of erythrodermic CTCL and reportedly improves survival in patients with advanced stages of the disease. The objective of this study is to review the experience of treating patients with erythrodermic CTCL with extracorporeal photochemotherapy (ECP) at the New York Veteran Affairs Medical Center/NYU Medical Center between September 1987 and April 1997. Forty-one patients with erythrodermic CTCL (stages III and IV) received photopheresis; 25 of them fulfilled the inclusion criterion, i.e., the completion of greater than or equal to 6 cycles of photopheresis. Skin score was defined as a product of severity and percentage of involved surface area. Complete clinical response was defined as disappearance of measurable disease for at least one month, and partial response was defined as greater than or equal to 50% clearance of measurable disease for at least one month. The profile of the patients was: 20 men, 5 women; average age: 64.2 years; 17 patients had stage III disease, and 8 had stage IV disease. Five of the 25 patients (20%) achieved complete clinical response, another 15 (60%) had partial response, and 5 (20%) had no response. The mean time (+/- SD) to achieve complete clinical clearance was 12.6 +/- 10 months (range: 4-30 months) and the mean time (+/- SD) to obtain partial clinical response, including complete response, was 9.7 +/- 5.3 months (range: 4-17 months). Remission duration ranged from 9 to 67 months. The median survival time from the time of initiation of photopheresis is estimated at 70 months. The complete responder group had a lower median CD4/CD8 ratio compared to the non-responders at baseline (3.8 vs 7.2, respectively), although the difference was not statistically significant (P = 0.40). At the time of maximal response, the CD4/CD8 ratio of the complete responder group decreased towards normal values (median = 1.2), whereas this ratio increased among the non-responders (median = 11.0; P = 0.04). Side effects were minimal. Extracorporeal photochemotherapy is an effective and safe treatment for erythrodermic CTCL. In some of these patients, it can induce a long-term and complete clinical remission.

Female↗
PubMed1998

Do we need Monte Carlo treatment planning for linac based radiosurgery? A case study.

The accuracy of conventional empirical and semi-empirical dose calculation algorithms for radiation therapy treatment planning is limited. The main problem is that these algorithms fail to adequately consider the lateral transport of radiation. Most conventional algorithms use measured dose distribution data as input. These data induce an added inaccuracy to stereotactic radiosurgery dose calculations due to the difficulty of acquiring accurate dosimetric data for very small beams; however, since multiple arcs of large solid angles are usually used in stereotactic radiosurgery, the errors introduced by conventional dose algorithms are quite likely to be diluted. The use of Monte Carlo treatment planning for stereotactic radiosurgery has been investigated and described in the present paper. The OMEGA Monte Carlo code system is used as the dose engine in an in-house developed radiosurgery treatment planning system. The Monte Carlo treatment plans are done for two typical clinical cases. In one case, the collimator of 20 mm diameter is used and the lesion is located in the peripheral part of the brain. In the other case, the collimator diameter is 30 mm and the lesion is in the central part of the brain. The resultant dose distributions are compared with those calculated with a conventional dose algorithm which is based on the standard Tissue Maximum Ratio (TMR)/Off Axis Ratio (OAR) formalism. Without the inhomogeneity correction, the conventional algorithm yields accurate relative dose distributions for both cases compared with the Monte Carlo calculations. The absolute dose at the isocenter may be overestimated by the conventional algorithm by 1.5% for the first case and 2.6% for the second case; however, using the method of ratio of TMRs for inhomogeneity correction, the overestimation can be greatly reduced for both cases. The inclusion of the inhomogeneity correction into the conventional dose algorithm does not alter the relative dose distributions. Based on the clinical cases studied, it may be concluded that the conventional dose algorithm is sufficient for radiosurgery treatment planning and the Monte Carlo based radiosurgery treatment planning is unwarranted.

Aged↗
PubMed1998

Dose perturbation caused by high-density inhomogeneities in small beams in stereotactic radiosurgery.

The influence of high-density tissue heterogeneities in small-diameter beams used in stereotactic radiosurgery has been investigated. Dose perturbation immediately behind aluminium sheets, used to simulate a high-density tissue inhomogeneity such as bone, was studied in a solid water phantom. Dose reduction factors (DRFs), which are the ratios of the dose in the presence of the inhomogeneity to dose in a uniform density solid water phantom, were measured with a diamond detector for three thicknesses of aluminium. DRFs exhibit dependence on both the inhomogeneity thickness and the beam diameter. The DRF decreases with inhomogeneity thickness. The DRF initially decreases with increase in the beam diameter from 12.5 to 25 mm. For fields greater than 25 mm, the DRFs are nearly constant. The commonly used algorithms such as the TAR ratio method underestimate the magnitude of the measured effect. A good agreement between these measurements and Monte Carlo calculations is obtained. The influence of the high-density inhomogeneity on the tissue maximum ratio (TMR) was also measured with the inhomogeneity at a fixed depth dmax from the entrance surface. The TMR is reduced for all detector-inhomogeneity distances investigated. The dose build-up phenomenon observed in the presence of low-density air inhomogeneity is absent in the presence of a high-density inhomogeneity. The beam width (defined by 50% dose points) immediately beyond the inhomogeneity is unaffected by the high-density inhomogeneity. However, the 90%-10% and 80%-20% dose penumbra widths and the dose outside the beam edge (beyond the 50% dose point) are reduced. This reduction in dose outside the beam edge is caused by the reduced range of the secondary radiation (photons and electrons) in the high-density medium.

Data Interpretation, Statistical↗
PubMed1998

On compensator design for photon beam intensity-modulated conformal therapy.

Recently the compensator has been shown to be an in expensive and reliable dose delivery device for photon beam intensity-modulated radiation therapy (IMRT). The goal of IMRT compensator design is to produce an optimized primary fluence profile at the patient's surface obtained from the optimization procedure. In this paper some of the problems associated with IMRT compensator design, specifically the beam perturbations caused by the compensator, are discussed. A simple formula is derived to calculate the optimal compensator thickness profile from an optimized primary fluence profile. The change of characteristics of a 6 MV beam caused by the introduction of cerrobend compensators in the beam is investigated using OMEGA Monte Carlo codes. It is found that the compensator significantly changes the energy spectrum and the mean energy of the primary photons at the patient's surface. However, beam hardening does not have as significant an effect on the percent depth dose as it does on the energy spectrum. We conclude that in most situations the beam hardening effect can be ignored during compensator design and dose calculation. The influence of the compensator on the contaminant electron buildup dose is found to be small and independent of the compensator thickness of interest. Therefore, it can be ignored in the compensator design and included as a correction into the final dose distribution. The scattered photons from the compensator are found to have no effect on the surface dose. These photons produce a uniform low fluence distribution at the patient's surface, which is independent of compensator shape. This is also true for very large fields and extremely asymmetric and nonuniform compensator thickness profiles. Compared to the primary photons, the scattered photons have much larger angular spread and similar energy spectrum at the patient's surface. These characteristics allow the compensator thickness profile and the dose distribution to be calculated from the optimized fluence profile of primary photons, without considering the scattered photons.

Calibration↗
PubMed1997

A fast numerical algorithm for electron mean energy calculation in radiation therapy.

A numerical algorithm for calculating the mean energy of radiotherapy electron beams has been developed. This algorithm is fast and accurate which makes it suitable for routine clinical use. First, a Gaussian distribution of the electron energy spectrum is derived from the linear Boltzmann equation. Based on this Gaussian spectrum, and after introducing a correction to the CSDA mean energy, a recursive-iterative algorithm for the mean energy calculation is developed. The multiple-scattering correction is taken into account using Yang's pathlength distribution theory. Numerical results of the present algorithm are compared with the results obtained through Monte Carlo simulation as well as Harder's formula. Good agreement with Monte Carlo simulation is achieved. Also the new algorithm is much more accurate than the commonly-used empirical formula of Harder.

Algorithms↗
PubMed1995

Efficacy of ultraviolet B phototherapy for psoriasis in patients infected with human immunodeficiency virus.

To evaluate the efficacy of ultraviolet B (UVB) phototherapy for the treatment of psoriasis in patients infected with human immunodeficiency virus (HIV), the response of 14 patients was compared to that of matched seronegative control individuals. All patients were evaluated prior to treatment (baseline) and after 21 treatments for the extent of total body surface area (TBSA) involvement and the quantification of scale, erythema, and thickness of plaques using a scale of 0 (absent) to 4 (severe). The only concomitant medication allowed was salicylic acid in petrolatum. The cumulative score for scale, erythema, and thickness improved 1.9 +/- 0.5 [mean +/- standard error of mean (SEM)] in the HIV group and 2.4 +/- 0.3 in controls. There was 40.9 +/- 7.3% reduction of TBSA involvement in the former and 38.4 +/- 7.6% reduction in the latter group. None of the differences was statistically significant. There was no statistically significant difference in the response to therapy among various stages of immunosuppression in the HIV group. There was also no deterioration of immune status in this group. UVB phototherapy is an effective treatment for psoriasis in patients infected with HIV. The response is identical to that of matched control individuals.

Administration, Cutaneous↗
PubMed1994

Effects of tubeimoside-1 on HIV core protein p24 and cytopathogenesis in vitro.

Tubeimoside-1 (Tub) is a triterpenoid saponin first isolated in China from Bolbostemma paniculatum (Maxim) Franquet, Cucurbitaceae. To find out whether Tub has any anti-infective activity on human immunodeficiency virus (HIV), we tested its effects on HIV core protein p24 (with an ELISA) and HIV-mediated cytopathogenesis (using a colorimetric assay). The results showed that Tub inhibited both p24 production and cytopathogenesis mediated by HTLV-IIIB, and the median effective concentrations (EC50) were 24.1 and 22.9 micrograms.ml-1, respectively. Tub also effectively neutralized the infection of 2 other isolates, HTLV-IIIRF and HTLV-IIIMN. It is concluded that Tub had an inhibitory action on the infection of HIV-1 isolates and would be a promising candidate for treatment of AIDS.

Antiviral Agents↗
PubMed1991

Enhancement of human immunodeficiency virus type 1 infection by antisera to peptides from the envelope glycoproteins gp120/gp41.

Human immunodeficiency virus type 1 (HIV-1) envelope glycoproteins (gp120 and gp41) elicit virus-neutralizing antibodies (VNAB) and also antibodies enhancing HIV-1 infection (EAB). Several epitopes eliciting VNAB have been defined, the principal virus-neutralizing determinant being assigned to the V3 loop of gp120. To provide a background for a rational design of anti-HIV vaccines, it also appears important to define domains eliciting EAB. This was accomplished by screening antisera against synthetic peptides covering almost the entire sequence of gp120/gp41 for their enhancing effects on HIV-1 infection of MT-2 cells, a continuous T cell line. Many (16/30) of the antisera significantly enhanced HIV-1 in the presence of human complement. Antibodies to complement receptor type 2 (CR2) abrogated the antibody-mediated enhancement of HIV-1 infection. Antisera to V3 hypervariable loops of 21 distinct HIV-1 isolates were also tested for their enhancing effects on HIV-1IIIB infection. 11 of these sera contained VNAB and 10 enhanced HIV-1IIIB infection. All antisera with virus-enhancing activity contained antibodies crossreactive with the V3 loop of HIV-1IIIB, and the virus-enhancing activity increased with increasing serological crossreactivity. These results suggest that immunization with antigens encompassing V3 loops may elicit EAB rather than protective antibodies if epitopes on the immunogen and the predominant HIV-1 isolate infecting a population are insufficiently matched, i.e., crossreactive serologically but not at the level of virus neutralization.

Animals↗
PubMed1991

Hepatitis B virus DNA in sera of virus carriers positive exclusively for antibodies to the hepatitis B core antigen.

The prevalence of serum HBV DNA in individuals positive for anti-HBc alone was determined by the polymerase chain reaction in two groups with endemic HBV infection from Canton (group A) and Hainan (group B), provinces of China. Twenty-one out of 294 individuals in group A (7.2%) and 193 out of 1995 in group B (9.7%) were positive for anti-HBc but negative for other markers of ongoing or past HBV infection (HBsAg and anti-HBs). HBV DNA was detected in 6/21 sera in group A (28.6%) and 68/193 in group B (35.2%) in their initial serum specimen. One of the six HBV-DNA-positive individuals in group A became negative after 6 months and four of the 58 positive in group B became negative at 4 years of follow-up. All of the individuals remained positive for anti-HBc and negative for anti-HBs, but one of them became positive for HBsAg on follow-up. None of the anti-HBc- and HBV-DNA-positive subjects had symptoms of liver diseases. They were, therefore, defined as chronic asymptomatic HBV carriers with undetectable HBsAg. This type of carrier should be added to the typical HBsAg-positive carrier, who constitutes about 10-15% of the general Chinese population, to give a more complete estimate of asymptomatic HBV carriers in China.

Adolescent↗
PubMed1991

Cytoplasts from cytotoxic T lymphocytes are resistant to perforin-mediated lysis.

Cytotoxic T lymphocytes (CTL) contain a potent cytolytic pore-forming protein (PFP, perforin or cytolysin) localized in their cytoplasmic granules. In the presence of calcium, perforin lyses a variety of target cells (TC) non-specifically. CTL, however, are generally resistant to the lytic effect of perforin. In this work, cytoplasts from CTL and susceptible TC were made by centrifuging cells on a Ficoll density gradient in the presence of cytochalasin B. Characterization by electron microscopy and a serine esterase assay established that both CTL and TC cytoplasts were completely devoid of nuclei and CTL cytoplasts contained essentially no granules. CTL cytoplasts are just as resistant to perforin-mediated lysis as the intact CTL, and both TC and their corresponding cytoplasts are very sensitive to lysis. Furthermore, CTL cytoplasts are less effective than TC cytoplasts in inhibiting hemolysis, a property shared by the respective intact cells. These results indicate that soluble granular components do not confer resistance on CTL, and suggest that the protective agent(s) acts by impeding perforin binding to the CTL membrane.

Animals↗
PubMed1990

Resistance of cytolytic lymphocytes to perforin-mediated killing. Inhibition of perforin binding activity by surface membrane proteins.

The mechanism whereby cytolytic lymphocytes protect themselves from killing mediated by their own cytotoxic protein, perforin, was studied. By using a competition assay, we demonstrated that the resistance of cells to perforin-mediated cytolysis is inversely correlated with their ability to absorb perforin, with tumor cells and noncytotoxic lymphocytes that are susceptible to perforin-mediated lysis being able to absorb perforin from the supernatant much better than CTL. The evidence implies that there is molecule on cytolytic lymphocytes that interferes with perforin-binding activity, resulting in the inability of perforin to lyse these cells. The molecule is most likely a surface protein or complex of proteins because its activity decreases after CTL treatment with the proteolytic enzymes trypsin and papain, and the activity can be recovered by incubation of the treated CTL cells at 37 degrees C for 6 h. The recovery can be blocked by emetine, cycloheximide, and actinomycin D, inhibitors of protein and RNA/DNA synthesis. The protein contains carbohydrate groups that play an important role in the function of the protein, as indicated by the fact that inhibition of glycosylation by tunicamycin and cleavage of sialic acid from the protein with neuraminidase result in a significant increase of perforin binding to CTL. Cross-linkage of CTL membrane proteins with glutaraldehyde and formaldehyde and blockage of the functional domains of the protein with an antiserum against CTL also inhibit the activity of this protein. Temperature-dependence studies that allow for a dissociation of the binding and pore-forming stages of perforin-mediated hemolysis suggest that the protective protein interferes at the perforin-binding stage.

Animals↗
PubMed1990

Perforin binding to cells and lipid membranes determined by a simple competition assay.

Perforin-mediated lysis consists of at least three steps: perforin binding to the target cell, insertion into the plasma membrane, and polymerization to form pores. Perforin binding, the first step, is critical for pore formation. Accordingly, a competition assay was here established for detecting the perforin-binding activities of nucleated cells and lipid membrane vesicles such as cytoplasts or liposomes. The competition assay has certain advantages over the 51Cr release assay, since no isotope and less perforin are needed for the competition assay, and the perforin-binding activity of liposomes and proteolytic enzyme-treated and fixed nucleated cells can also be detected. The competition assay was used to study the mechanism of resistance of cytolytic T lymphocytes (CTL) to perforin-mediated lysis. The results from this assay indicate that perforin-binding activity is not a function of membrane rigidity, and that there is a direct correlation between the ability of cells to bind perforin and their susceptibility to lysis by perforin, i.e., resistant CTL and their corresponding cytoplasts bind perforin much less effectively than susceptible tumor cells and their cytoplasts. A model is proposed whereby a surface molecule or complex of molecules on CTL interferes with perforin-binding activity, thus protecting CTL from perforin-mediated lysis.

Animals↗
PubMed1990

Resistance to the pore-forming protein of cytotoxic T cells: comparison of target cell membrane rigidity.

Cytotoxic T lymphocytes (CTL) release from their granules a 70 kDa protein, called PFP, perforin or cytolysin, which inserts into the target cell plasma membrane in its monomeric form. Here it polymerizes into a macromolecular complex forming pores as large as 20 nm. Although purified PFP/perforin can effectively lyze all target cells tested. CTL are refractory to lysis. The mechanism underlying the resistance of CTL is currently unknown. This study represents a search for membrane structural properties that could confer resistance to CTL against PFP/perforin-mediated lysis. The fluorescent dye merocyanine 540 was used to measure the lipid head group packing of CTL and several target cells, and 1-[4-(trimethylamine)phenyl]-6-phenylhexa-1,3,5-triene was used to estimate the fluidity of the membrane hydrocarbon region. The resistance against PFP/perforin-mediated lysis was determined by the 51Cr release assay. A comparison of the membrane rigidity with cell resistance led to the conclusion that the membrane lipid structure cannot account for the unusually high resistance of CTL. In particular, the resistant CTL line CTLL-2 has a lipid head group packing that is looser than that of Yac-1, and the sensitive target cells Jy-25 and EL-4 have membrane acyl chains that are less fluid than those of the effector CTLL-R8.

Animals↗
PubMed1989

Identification and characterization of a membrane-bound cytotoxin of murine cytolytic lymphocytes that is related to tumor necrosis factor/cachectin.

Cytotoxic T lymphocytes (CTLs) kill their targets by a contact-dependent mechanism. We investigated the possibility that the CTL membranes themselves could exert direct cytotoxic activity. Murine CTLs that had been fixed with paraformaldehyde retained a slow cytotoxic activity toward various target cells that are also sensitive to another cytokine, tumor necrosis factor (TNF)/cachectin. This cytotoxic activity was neutralized by antibodies specific for TNF. Membrane fractions obtained from CTLs were cytotoxic to TNF-sensitive targets but not to several TNF-resistant cell lines. Immunoblot analysis revealed a membrane protein band of 50-60 kDa from CTLs that reacts with anti-TNF antibodies. The surface localization of this cytokine was further ascertained by flow cytometry, indirect immunofluorescence, and immunoelectron microscopy studies using TNF-specific antibodies. Radioiodination of CTL surface proteins followed by immunoprecipitation with anti-TNF antibodies confirmed the presence of a TNF-related cytokine in the plasma membranes of CTLs that migrated with an apparent molecular mass of 50-60 kDa under disulfide-reducing conditions. This cytokine can be removed from membranes by treatment with detergents but not with high-salt buffers, suggesting that it may be an integral membrane protein.

Animals↗
PubMed1988

Resistance of cytolytic lymphocytes to perforin-mediated killing. Lack of correlation with complement-associated homologous species restriction.

CTL and NK cells resist self-mediated killing and lysis by their own pore-forming protein (PFP; perforin). Perforin, like C, lyses RBC. Efficient C-mediated lysis of RBC occurs when both C and RBC are from different species (homologous species restriction). A protective surface protein (C8-binding protein, homologous restriction factor) has been reported to mediate both homologous species restriction in C-dependent cytolysis and protection of some target cells against perforin-induced lysis. We show here that perforin, unlike C, lyses target cells across a variety of species, including the homologous one, while the same target cell populations resist the attack by homologous C. Perforin-containing extracts of CTL and LAK/NK cells from three species (rat, mouse, and human) and purified mouse perforin were tested against RBC from 10 different species, several nucleated target cell lines, and one primary cell population (thymocytes). While resisting lysis by homologous C, most of these cell types were lysed effectively by perforin without any homologous restriction pattern. CTL and NK cells, like other nucleated targets, are resistant to lysis by homologous but not heterologous C; however, these cell types are resistant to both homologous and heterologous perforin. Together, our results suggest that the protective mechanisms associated with C- and perforin-mediated lysis are distinct.

Animals↗
PubMed1985

[Surface morphologic changes of thymocytes in Ehrlich ascitic carcinoma-bearing mice].

The surface morphologic changes of thymocytes in Ehrlich ascitic carcinoma (EAC)-bearing mice were studied by scanning electronmicroscope. The changes were: marked atrophy of the thymus; rapid loss of surface microvilli; formation of the blebs of various sizes; roughening of cell surface and some twisty cells on day 10 after intraperitoneal injection of EAC (4 X 10(6) cell/mouse). These changes show that the early degeneration of the thymocytes takes place during the EAC development. The significance is discussed in detail.

Animals↗
PubMed1985

Dose finding double-blind clinical trial with praziquantel in schistosomiasis japonica patients.

A double-blind clinical trial with praziquantel was carried out. A total of 400 cases was treated with four different dosages, namely, 60, 50, 40 and 30 mg/kg body weight of praziquantel. The drug was given in one day divided into two doses. Identical placebo tablets were used to make up a total of 60 mg/kg. Tolerance was good in all with the exception of one case suffering from asthmatic attack with papule rashes over large area of the body surface. 394 patients were able to be followed up parasitologically six months post-treatment. 79.8%, 71.7%, 78.8% and 70.1% of the patients were negative in the groups with the total dose of 60, 50, 40 and 30 mg/kg respectively. The cure rates as well as the side effects were similar for the four groups. The efficacy was lower than that reported by other authors and the possibility of reinfection was incriminated. In villages with few snails the negative hatching rates in aforementioned four groups were 89.1%, 91.1%, 88.9% and 81.8%, while in villages with abundant snails the rates were 68.2%, 46.5%, 66.7% and 54.8%. The difference between the two areas was statistically significant. Higher efficacy was observed in adults with an average cure rate of 80.0% than in children under 15 years of age, the average cure rate being 57.1%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗