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D Teague

Publications and source records attributed to D Teague.

17 recordsLinked to original sources
PubMed1998

Interaction of gemcitabine with paclitaxel and cisplatin in human tumor cell lines.

We have used clonogenic survival assays and flow cytometry of human lung A549, breast MCF7 and pancreas adenocarcinoma P-SW cell lines to examine the effects of gemcitabine (2'-deoxy-2', 2'-difluorocytidine) in combination with cisplatin, paclitaxel or radiation. Additive cell killing was observed for all cell lines when they were treated with cisplatin for 1 h followed by varying concentrations of gemcitabine for 24 h. Likewise, additive cell killing was noted in all cell lines when treated with gemcitabine for 24 h followed by varying doses of radiation. When A549 cells were exposed to gemcitabine for 24 h followed by a 1 h exposure to cisplatin, synergistic effects were noted. Using the latter regimen, MCF7 cells demonstrated additive cell kill, while the P-SW cells showed a more complex relationship with additive killing below 50 nM gemcitabine and less than additive effect above 50 nM gemcitabine. All three cell lines were also tested with various gemcitabine/paclitaxel combinations. When gemcitabine and paclitaxel were incubated concurrently, gemcitabine antagonized the cell kill produced by paclitaxel. All cell lines showed less than additive killing when either gemcitabine incubation preceded the paclitaxel incubation or the paclitaxel incubation preceded the gemcitabine incubation. Our results show that gemcitabine acts as a radiation sensitizer to increase the effects of radiation. Likewise, we demonstrate that the only uniformly beneficial drug combination schedule in all three cell lines was when cisplatin incubation preceded gemcitabine incubation. The gemcitabine/paclitaxel combinations were much more disturbing with respect to potential clinical trials. Our results would caution any planned clinical trials combining paclitaxel with gemcitabine to be reconsidered because of the potential for less than additive and even antagonistic effects of the combination.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1996

Convenient colorimetric and fluorometric assays for S-nitrosothiols.

S-nitrosothiols have been shown to affect a number of physiological functions. Several techniques have been used to detect these species in biological systems, primarily by methods utilizing chemiluminescence. Since the apparatus required for measurement of chemiluminescence are not readily available in most laboratories, methods employing more conventional techniques such as uv-vis and fluorescence spectroscopy may be of greater use. Herein, we report the development of colorimetric and fluorometric methods for the reliable quantitation of S-nitrosothiols. Solutions containing sulfanilamide/N-(1-naphthyl)- ethylenediamine dihydrochloride or 2,2'-azinobis (3-ethylbenzthiazoline-6-sulfonic acid), when exposed to S-nitrosoglutathione (GSNO), S-nitrosocysteine, or S-nitrosoacteylpenicillamine, resulted in no absorbance changes in the range of 400-800 nm. Exposure to HgCl2 or Cu(acetate)2 resulted in release of nitric oxide (NO) from the S-nitrosothiols. The liberated NO reacted subsequently with oxygen and formed a chemical species which reacted with either analysis solution, resulting in an increase in absorption between 400 and 800 nm. A plot of RSNO versus absorbance was linear for both mercury(II) and copper(II) ions where the slope in the presence of mercury ion was significantly greater than that for copper ion. The sensitivity was as low as 5 microM RSNO using HgCl2. The fluorometric method using 2, 3-diaminonaphthalene as the scavenger of the NOsolidusO2 products gave a sensitivity of 50 nM for GSNO. In addition, S-nitrosylated proteins were quantitated using the fluorometric technique. These methods provide accurate determination of low concentrations of S-nitrosothiols, utilizing conventional spectroscopic techniques available in most laboratories.

Benzothiazoles↗
PubMed1996

Early complications with external fixation of pediatric femoral shaft fractures.

A retrospective study of 27 pediatric patients with femoral shaft fractures treated by external fixation was made to identify complications and evaluate outcomes. The average age at the time of injury was 8 years, 9 months (range 5 years, 6 months to 13 years, 2 months). Sixteen fractures were isolated, and nine were associated with polytrauma. There was only one open fracture. Data obtained from chart review (n = 27), radiographs (n = 27), physical exam (n = 16), and questionnaire (n = 21) identified eight major complications (30%) in six patients and 29 minor complications (107%) in 20 patients. The major complications included two refractures, two fractures through pin sites, one postimmobilization supracondylar femoral fracture, one persistent pin-tract infection requiring early fixator removal, one malreduction, and one loss of reduction. Both the patient with malreduction and the one who lost reduction had > 10 degrees of varus deformity before adjustment of their frames. Five of the eight major complications (64%) were secondary to errors in operative technique or postoperative treatment. Only one major complication was noted among the 16 patients with isolated injuries. Of the patients with minor complications, 14 had pin-tract infections requiring oral antibiotics, five refused to go to school with the fixator in place, five were dissatisfied with scar appearance, and five had clinically insignificant malunions. A clinically insignificant malunion was considered to be angulation > or = 5 degrees varus or valgus or > or = 10 degrees procurvatum or recurvatum deformity that did not affect the patient's function. The minor complications were considered intrinsic to the procedure and difficult to avoid. Despite these problems, all patients with isolated injuries, except one with a slipped capital femoral epiphysis, had excellent function at the time of final review. If external fixation is chosen as the method of treatment for a pediatric femur fracture, careful attention must be paid to operative technique and postoperative treatment in order to minimize complications.

Adolescent↗
PubMed1994

Treatment of locally advanced cancer of the head and neck with 5'-iododeoxyuridine and hyperfractionated radiation therapy: measurement of cell labeling and thymidine replacement.

BACKGROUND: The halogenated pyrimidines 5'-iododeoxyuridine (IdUrd) and 5'-bromodeoxyuridine (BrdUrd) are under active study as radiation sensitizers for a variety of malignancies. Head and neck neoplasms may also be suitable for halogenated pyrimidine-mediated sensitization; previous regimens using intra-arterial BrdUrd delivery, however, were poorly tolerated. PURPOSE: A pilot study was undertaken with the use of intravenous IdUrd with hyperfractionated radiotherapy to assess tolerance. In addition, serial tumor biopsy specimens were obtained to determine the kinetics of IdUrd labeling and incorporation. METHODS: Twelve patients with squamous cell carcinomas of the head and neck (one patient had stage II cancer, one had stage III, and 10 had stage IV) were treated with hyperfractionated radiation therapy at a dose of 1.2 or 1.5 Gy twice a day, to a total dose in the range of 70-76 Gy. IdUrd (1000 mg/m2 per day) was infused for a maximum of 14 days at the beginning and then again during the middle of the radiotherapy. A tumor biopsy specimen was obtained from 11 patients following initiation of treatment with IdUrd. Eight patients consented to serial biopsy to allow the study of IdUrd-labeling indices and thymidine replacement over time. Incorporation of IdUrd into tumor DNA was determined by high-performance liquid chromatography, and cell labeling was determined with the use of an anti-BrdUrd/IdUrd monoclonal antibody in conjunction with flow cytometry. Patients continue to be followed to assess local control. RESULTS: A plot of corrected IdUrd replacement as a function of infusion time suggests the possibility of a plateau after 5-7 days of infusion at 7.5%-8%. The average rate of replacement from days 1 to 5 was 1.3% per day and was determined by linear regression analysis. Acute toxic effects, especially mucositis, were severe enough to require delays in the radiation therapy. Eleven of 12 patients treated had complete clinical remissions. Seven of these patients remain clinically free of local disease at the time of death or most recent follow-up. CONCLUSIONS: The level of IdUrd incorporation and cell labeling should be adequate to produce sensitization. However, the treatment as prescribed in this study (two 14-day infusions of IdUrd during radical radiotherapy with only one planned split) was not completed in a single patient because of either dose-limiting hematologic toxicity or severe mucositis necessitating treatment break. Since this particular regimen is not tolerable, future protocols will have shorter exposures to IdUrd. IMPLICATIONS: Previous regimens using halogenated pyrimidine radiosensitizers have generally used protracted drug delivery schedules. In this study, a high level of IdUrd labeling was measured after 5-7 days of drug infusion. The halogenated pyrimidines deserve further study with the use of repetitive short courses to reduce toxicity and possibly improve efficacy.

Adult↗
PubMed1994

Changes in radiation survival curve parameters in human tumor and rodent cells exposed to paclitaxel (Taxol).

PURPOSE: Late G2 and M are the most radiosensitive phases of the cell cycle. Cells exposed to paclitaxel develop a cell cycle arrest in G2/M. These studies were performed to assess the in vitro radiosensitization properties of paclitaxel in human tumor and rodent cell lines. METHODS AND MATERIALS: The effect of paclitaxel on the radiation sensitivity of human breast (MCF-7), lung (A549), ovary (OVG-1) adenocarcinoma and Chinese hamster lung fibroblast V79 cells was determined with clonogenic assays. DNA flow cytometry studies were performed to define the cell cycle characteristics of the cells during irradiation. Survival curve parameters for all cell lines were determined with the use of a computer program which represents cell survival after radiation by a linear-quadratic model. RESULTS: All cell lines developed a G2/M block after exposure to paclitaxel for 24 h. However, the degree of radiosensitization produced by paclitaxel varied among the cell lines. The maximal sensitizer enhancement ratio (SER) of paclitaxel was 1.8 in MCF-7 cells, 1.6 in OVG-1 cells, and 1.7 in V79 cells. However, no concentration of paclitaxel was able to enhance the radiation sensitivity of A549 cells. Paclitaxel increased the linear (alpha) component of the radiation survival curves in all cell lines. The quadratic (beta) component was unaffected by paclitaxel in the rodent cells. High concentrations of paclitaxel (> or = 1000 nM) increased beta slightly in the human cell lines but there was considerable variation in the effect of paclitaxel on beta. The cells which were sensitized to radiation by paclitaxel had a relatively small baseline alpha component, while A549 cells had a large alpha component. CONCLUSION: We conclude that paclitaxel is a modest radiosensitizer in some, but not all, human tumor cells. Paclitaxel appears to cause radiosensitization mainly by increasing the alpha component of radiation survival curves. Cells that normally have a relatively small alpha component should exhibit the most radiosensitization in response to paclitaxel while cells with a large alpha component should show little or no radiosensitization after paclitaxel treatment. Because the greatest effect of paclitaxel is on the linear component of radiation survival curves, these results indicate that paclitaxel may be an effective radiation sensitizer in many human tumors treated at clinically relevant radiation doses of 2 Gy or less.

Animals↗
PubMed1994

In vitro studies of Taxol as a radiation sensitizer in human tumor cells.

BACKGROUND: Cells exposed to paclitaxel (Taxol) develop a cell cycle arrest in G2/M. It has long been recognized that late G2 and M are the most radiosensitive phases of the cell cycle. PURPOSE: These studies were performed to assess the in vitro radiosensitization properties of paclitaxel in human tumor cell lines. METHODS: The effect of paclitaxel at concentrations ranging from 0 to 10,000 nM on the radiation sensitivity (from 0 to as much as 10 Gy in certain experiments) of human breast (MCF-7), lung (A549), ovary (OVG-1), and pancreas (PC-Sh) adenocarcinoma cells was determined using clonogenic assays. DNA flow cytometry studies were performed to define the cell cycle characteristics of populations of cells that had been treated for 6-72 hours with 0, 100, 1000, or 10,000 nM paclitaxel. RESULTS: All cell lines developed a G2/M block after exposure to 100-10,000 nM paclitaxel for 24 hours. However, the degree of radiosensitization produced by paclitaxel varied among the cell lines. The sensitizer enhancement ratio (SER) of paclitaxel at 10% survival was 1.8 in MCF-7 cells and 1.6 in OVG-1 cells. However, paclitaxel at any concentration was unable to enhance the radiation sensitivity of A549 cells. PC-Sh cells demonstrated a complex and inconsistent radiosensitization response to paclitaxel. At 10% survival, an SER of 1.5 was observed in PC-Sh cells. However, at 1% survival, no radiosensitization was observed in PC-Sh cells. Maneuvers that prevented paclitaxel from producing a G2/M block, including coincident treatment with cycloheximide or treatment of cells in plateau phase of growth, completely abrogated the radiosensitization afforded by paclitaxel in MCF-7 cells. CONCLUSIONS: Paclitaxel is a modest radiosensitizer in some, but not all, human tumor cells. The degree of radiosensitization that we have observed with paclitaxel is similar to what has been found with other chemotherapeutic agents. The absence of radiosensitization by paclitaxel in MCF-7 cells grown to plateau phase or treated with cycloheximide implies that the development of a G2/M block is a necessary condition for paclitaxel radiosensitization. However, the inability of paclitaxel to radiosensitize A549 cells despite the presence of a G2/M block in those cells demonstrates that a G2/M block is not a sufficient condition for paclitaxel radiosensitization. IMPLICATIONS: Paclitaxel can radiosensitize to a modest degree some, but not all, human cell lines by a mechanism that requires the production of a G2/M cell cycle block. Additional studies are needed to define more clearly the mechanism by which paclitaxel radiosensitizes cells.

Cell Cycle↗
PubMed1994

The influence of Cremophor EL on the cell cycle effects of paclitaxel (Taxol) in human tumor cell lines.

We have performed DNA flow analysis, mitotic index studies, time-lapse photography, and paclitaxel uptake studies of human tumor cell lines exposed to paclitaxel. DNA flow analysis demonstrated that cells began accumulating in G2/M within 6 hrs of exposure to paclitaxel; by 12 hrs over 50% of cells accumulated in G2/M at all concentrations tested. After 24 hrs of exposure to 10 nM paclitaxel, cells underwent non-uniform mitotic division resulting in multinucleated cells. Of cells treated with 30 nM to 1000 nM paclitaxel, 75% to 85% remained blocked in G2/M for up to 72 hrs. Although a large proportion of cells treated with higher concentrations of paclitaxel (10,000 nM) was blocked in G2/M, a significant proportion (10% to 40%) of these cells was also in G1. Cells exposed to lower concentrations of paclitaxel (10 nM to 1000 nM) in medium containing 0.135% (v/v) Cremophor EL also had a relatively large proportion in G1. Mitotic index studies demonstrated that the paclitaxel-induced G2/M block was initially a mitotic block and that cells remained in mitosis for up to 24 hrs. With additional time of exposure to paclitaxel, mitotic index and time-lapse studies indicated that cells attempted to complete mitosis; however, cytokinesis was inhibited and cells became multinucleated. Time-lapse photography revealed that paclitaxel markedly prolonged the time in mitosis from 0.5 hr to 15 hr. High levels of Cremophor EL (0.135% v/v) markedly reduced the number of cells in mitosis but did not alter the mitotic delay induced by paclitaxel. 3H-paclitaxel uptake studies revealed that high concentrations of Cremophor EL did reduce the rate of uptake of paclitaxel into cells but had little effect on total paclitaxel accumulation. These results confirm that paclitaxel has striking effects on the cell cycle and show that high concentrations of Cremophor EL are capable of inducing a cell cycle block distinct from the mitotic block seen with paclitaxel. These results also demonstrate that cells exposed to paclitaxel for longer than 24 hours attempt to complete mitosis but the process of cytokinesis is inhibited. Together with cytotoxicity data, these results indicate that entry into and exit out of mitosis are prerequisites for paclitaxel cytotoxicity.

Adenocarcinoma↗
PubMed1994

Cycloheximide inhibits the cytotoxicity of paclitaxel (Taxol).

Treatment of human breast (MCF-7) and lung (A549) adenocarcinoma cell lines with 10 micrograms/ml cycloheximide provided substantial protection from paclitaxel-induced cytotoxicity. Addition of cycloheximide to cells at 0, 6, 12 or 18 h into a 24 h exposure to paclitaxel resulted in cytotoxicity similar to that found in cells treated with paclitaxel alone for only 0, 6, 12 or 18 h, respectively. DNA flow cytometry showed that paclitaxel blocked cells in G2/M. Mitotic index studies demonstrated that paclitaxel arrested cells in mitosis and that prolonged exposure to paclitaxel resulted in the development of multiple micronuclei. Concurrent incubation of cells in cycloheximide prevented the development of a G2/M block, mitotic arrest and micronuclei formation. The addition of cycloheximide to cells at 6 or 12 h into a 24 h exposure to paclitaxel reduced the degree of G2/M block to that produced by incubation of cells in paclitaxel alone for only 6 or 12 h. Mitotic index studies confirmed that cells treated with cycloheximide during paclitaxel exposure had a marked reduction in the percentage of cells in mitosis. However, the percentage of paclitaxel-treated cells which had multiple micronuclei was increased in cells treated with cycloheximide. These results indicate that entry into mitosis is a prerequisite for paclitaxel-induced cytotoxicity and that cycloheximide reduces cytotoxicity due to paclitaxel by preventing cells from entering mitosis. However, once cells have entered mitosis in the presence of paclitaxel, protein synthesis is not required for the development of multiple micronuclei and cytotoxicity.

Adenocarcinoma↗
PubMed1994

Sequence dependence of paclitaxel (Taxol) combined with cisplatin or alkylators in human cancer cells.

Clinical trials combining paclitaxel with other active chemotherapy agents are currently underway. In vitro preclinical studies may assist in the selection of appropriate drug combinations or sequences for clinical investigation. We have used clonogenic cell survival assays and DNA flow cytometry to examine the effect of paclitaxel combined with melphalan, thiotepa, or cisplatin on the survival and cell-cycle parameters of human lung A549 and breast MCF-7 adenocarcinoma cells. A549 and MCF-7 cells were incubated with paclitaxel for 24 h, followed by a 1 h exposure to cisplatin, melphalan, or thiotepa. Both cell types were also incubated with cisplatin or an alkylator for 1 h followed by a 24 h paclitaxel exposure. When the paclitaxel exposure preceded either melphalan, thiotepa, or cisplatin, the cytotoxicity was additive for both cell lines tested. When cisplatin or alkylator exposure was given prior to the paclitaxel, cytotoxicity was also additive in MCF-7 cells. However, cisplatin or alkylators were antagonistic to paclitaxel cytotoxicity when they preceded the paclitaxel exposure in A549 cells (e.g., 2% survival with 100 nM paclitaxel vs. 7% survival with cisplatin and paclitaxel). Cell-cycle analysis revealed that exposure to 100 nM paclitaxel for 24 h blocked a majority of the cells into the G2/M phase (> or = 80% for A549 cells, 60-65% for MCF-7 cells). However, exposure to alkylators before incubation in paclitaxel reduced the proportion of A549 but not MCF-7 cells in G2/M--e.g., exposure to 30 micrograms/ml cisplatin prior to paclitaxel exposure caused only 25% of A549 and 55% of MCF-7 cells to block in G2/M.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1993

Cytotoxic studies of paclitaxel (Taxol) in human tumour cell lines.

The cytotoxicity of paclitaxel against eight human tumour cell lines has been studied with in vitro clonogenic assays. The fraction of surviving cells fell sharply after exposure for 24 h to paclitaxel concentrations ranging from 2 to 20 nM; the paclitaxel IC50 was found to range between 2.5 and 7.5 nM. Increasing the paclitaxel concentration above 50 nM, however, resulted in no additional cytotoxicity after a 24 h drug exposure. Cells incubated in very high concentrations of paclitaxel (10,000 nM) had an increase in survival compared with cells treated with lower concentrations of the drug. Prolonging the time of exposure of cells to paclitaxel from 24 to 72 h increased cytotoxicity from 5 to 200 fold in different cell lines. Exponentially growing cells were more sensitive to paclitaxel than were cells in the plateau phase of growth. Cremophor EL, the diluent in which the clinical preparation of paclitaxel is formulated, antagonised paclitaxel at concentrations of 0.135% (v/v). These data suggest that paclitaxel will be most effective clinically when there is prolonged exposure of tumour to the drug. Further, it appears that modest concentrations (i.e., 50 nM) should be as effective as higher concentrations of paclitaxel. Finally, we have noted that Cremophor EL is a biologically active diluent and, at high concentrations (0.135% v/v), can antagonise paclitaxel cytotoxicity.

Adenocarcinoma↗
PubMed1988

Increasing dextrose concentrations in total parenteral nutrition (TPN) causes alterations in hepatic morphology and plasma levels of insulin and glucagon in rats.

Hepatic steatosis is an ongoing problem in total parenteral nutrition (TPN). The etiology of this deranged hepatic morphology is unclear, but lack of enteral stimulation and excess carbohydrate calories have been suggested as altering the intestinal hormone profile. In this study, adult male Sprague-Dawley rats (n = 28) received internal jugular catheters: group 1 (n = 7) received saline (3 cc/hr) and chow ad libitum; groups 2, 3, and 4 (n = 7) received 15, 20, and 25% dextrose-base TPN solutions, respectively, in quantities matching the caloric intake of paired ad libitum animals. At 7 days portal and peripheral venous blood samples were drawn for insulin and glucagon radioimmunoassay, and livers were removed for histologic examination and determination of total hepatic lipid content. Portal and peripheral insulin levels rose in a linear fashion with increasing dextrose concentration. Lipid content increased with elevated portal venous insulin/glucagon ratio in groups 3 and 4. Periportal fatty infiltration increased with increasing dextrose concentrations. The results suggest that the liver's response to altered portal insulin/glucagon ratio may play an important role in changes of hepatic morphology associated with TPN.

Animals↗
PubMed1987

The value of hepatobiliary scans in fasted patients receiving total parenteral nutrition.

Hepatobiliary scanning is considered to be a highly accurate method for the diagnosis of acute cholecystitis. False-positive scans (failure to visualize the gallbladder in the absence of cholecystitis) have been reported to occur in fasted patients receiving total parenteral nutrition (TPN). To determine the prevalence of false-positive scans in this patient population and identify factors that might be associated with scan outcome, hepatobiliary imaging was performed in fasted patients receiving TPN and without clinical evidence of acute cholecystitis. Gallbladder nonvisualization occurred in 18 of 50 (36%) patients. In the group whose gallbladders did not visualize, a significantly higher male to female ratio (15:3 versus 17:15; p = 0.016), alkaline phosphatase (346 +/- 84 IU/L versus 212 +/- 32 IU/L, p less than 0.04), total bilirubin (1.7 +/- 0.3 mg/dl versus 1.0 +/- 0.2 mg/dl, p less than 0.02), and lower serum albumin (2.4 +/- 0.01 gm/dl versus 2.8 +/- 0.2 gm/dl, p less than 0.02) levels were noted. In 18 patients, gallbladder ultrasonography was also performed, and the presence of sludge or a thickened gallbladder wall did not correlate with scan outcome. The prevalence of false-positive hepatobiliary scans in fasted patients receiving TPN is significant and does not always correlate with a syndrome of acute gallbladder inflammation. The results of such scans must therefore be interpreted with caution in these patients.

Adult↗
PubMed1972

Social services.

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Alcoholism↗
PubMedDate not supplied

Early nutrition support modifies immune function in patients sustaining severe head injury.

BACKGROUND: Immunosuppression after severe head injury has been characterized by a depressed CD4 (T-helper/inducer)-CD8 (T-suppressor/cytotoxic) ratio and decreased T-lymphocyte responsiveness. Some investigators propose that this immunocompromized state is the result of an injury-associated hypermetabolic response and inadequate nutrient delivery during the immediate postinjury recovery phase. Previous observations from our institution demonstrated a preserved CD4-CD8 ratio in severe closed-head injury (CHI) patients receiving early parenteral nutrition (PN). It was unclear whether early PN or other aspects of patient care eliminated the characteristic depression in cellular immunity. The purpose of this study was to further investigate the effect of early PN on the immune function of CHI patients. METHODS: Nine patients sustaining severe CHI were prospectively randomized to either early PN (n = 4) at day 1 or delayed PN (n = 5) at day 5. Total nutrient administration was delivered at 2 g of protein/kg per day and 40 nonprotein kcal/kg per day for at least the first 14 days of hospitalization. Analysis for T-lymphocyte expression of CD4 and CD8 cell surface antigens and interleukin-6 was performed on days 1, 3, 7, and 14 of hospitalization. T-lymphocyte activation in response to stimulation by concanavalin A (Con A), phytohemagglutinin (PHA), and pokeweed mitogens (PWM) was also assessed on these days. RESULTS: Significant increases in total CD4 cell counts (2048 +/- 194 to 2809 +/- 129 vs 1728 +/- 347 to 1825 +/- 563, p < .05) and CD4% (42.6 +/- 4.4% to 56.2 +/- 2.6% vs 36.6 +/- 6.6% to 36.6 +/- 11.3%, p < .05) were observed at day 14 in patients receiving early vs delayed PN. An improved lymphocyte response from baseline to day 14 after Con A stimulation was demonstrated in the early PN group (3850 +/- 1596 to 16144 +/- 5024 cpm, p < .05). A significant rise in the CD4-CD8 ratio over baseline to day 14 was also noted in the early PN group (1.43 +/- 0.17 to 2.38 +/- 0.54, p < .05). CONCLUSIONS: The early aggressive nutrition support of CHI patients appears to modify immunologic function by increasing CD4 cells, CD4-CD8 ratios, and T-lymphocyte responsiveness to Con A.

Adolescent↗