Use of a titanium cutting guide to assist raising the composite radial forearm free flap.

The use of composite radial free tissue transfer has been overtaken by other composite flaps. This is due to donor site morbidity and the poor volume of bone yielded. The advantages and potential complications of composite radial flaps are well described. Use of the composite radial forearm free flap has been largely superseded in mandible reconstruction, but applications such as a salvage option still exist. Additionally it may be used in the reconstruction of midface defects. The use of a cutting guide to reduce the donor site complications and yet produce a maximal yield of bone is described herein. With the use of a skilled maxillofacial laboratory, the planning allows precise cuts and placement of the free flap and allows accurate prophylactic plating of the radius. A precise titanium cutting guide and custom distal radius plate are used. Details of three cases where these techniques have been implemented are described. The paper demonstrates the significant advantages of using laboratory-based technology to assist in performing composite radial free flaps. This paper reveals that composite radial free tissue transfer still has a place in the reconstruction of very selective defects of the head and neck. In particular, its use in reconstruction of Class 5 and 6 maxillary defects (Brown classification) is illustrated. Correct case selection and planning results in increased confidence to use this flap.

The age-specific incidence of admission to the intensive care unit for acute myocardial infarction in Antigua and Barbuda

This study was done to assess the age-specific incidence of admission for acute myocardial infarction in Antigua and Barbuda from 1990 to 2001. A retrospective review of Intensive Care Unit admissions for possible acute myocardial infarction was performed. Data obtained included age, gender, country of residence, electrocardiogram, creatine kinase results and intensive care unit outcome. There were, 250 admissions, 194 (78%) having data available for review. Acute myocardial infarction was found in 107/194 (55.2%) patients, age 59.9 +/- 13.7 years, 28% female, 70% from Antigua and Barbuda, 90/107 (85%) were between 35 and 75 years old. The incidence would be 7.5 per year or 9.7 per year if the confirmation rate documented was similar for all admissions. With a yearly population of 9555 men age 35 to 75 years in Antigua and Barbuda, with men accounting for 72% of acute myocardial infarctions, the incidence rate was 0.57 (confirmed) to 0.73 (all admissions) per year per 1000 men. For women, the yearly population was 10822 age 35 to 75 years, and the incidence rate was 0.19 to 0.24 per year per 1000 women. The mortality rate was 12/107 (11.2%), with women being older (67 vs 57 years, p = 0.001) and dying more often (17% vs 9%) compared with men. The mortality rate in the Intensive Care Unit was 0.07 per year for men, 0.04 per year for women per 1000 aged 35 to 75 years. In the United States of America (USA), the admission rate is 4.1 for men and 1.8 for women per year per 1000 aged 35 to 75 years; the mortality rate is 1.0 for men and 0.5 for women per year per 1000 aged 35 to 75 years. Rates of admission to the Intensive Care Unit for acute myocardial infarction in Antigua and Barbuda are 20%, and mortality rates are 10% of those reported in the USA.

The age-specific incidence of admission to the intensive care unit for acute myocardial infarction in Antigua and Barbuda.

This study was done to assess the age-specific incidence of admission for acute myocardial infarction in Antigua and Barbuda from 1990 to 2001. A retrospective review of Intensive Care Unit admissions for possible acute myocardial infarction was performed. Data obtained included age, gender, country of residence, electrocardiogram, creatine kinase results and intensive care unit outcome. There were, 250 admissions, 194 (78%) having data available for review. Acute myocardial infarction was found in 107/194 (55.2%) patients, age 59.9 +/- 13.7 years, 28% female, 70% from Antigua and Barbuda, 90/107 (85%) were between 35 and 75 years old. The incidence would be 7.5 per year or 9.7 per year if the confirmation rate documented was similar for all admissions. With a yearly population of 9555 men age 35 to 75 years in Antigua and Barbuda, with men accounting for 72% of acute myocardial infarctions, the incidence rate was 0.57 (confirmed) to 0.73 (all admissions) per year per 1000 men. For women, the yearly population was 10822 age 35 to 75 years, and the incidence rate was 0.19 to 0.24 per year per 1000 women. The mortality rate was 12/107 (11.2%), with women being older (67 vs 57 years, p = 0.001) and dying more often (17% vs 9%) compared with men. The mortality rate in the Intensive Care Unit was 0.07 per year for men, 0.04 per year for women per 1000 aged 35 to 75 years. In the United States of America (USA), the admission rate is 4.1 for men and 1.8 for women per year per 1000 aged 35 to 75 years; the mortality rate is 1.0 for men and 0.5 for women per year per 1000 aged 35 to 75 years. Rates of admission to the Intensive Care Unit for acute myocardial infarction in Antigua and Barbuda are 20%, and mortality rates are 10% of those reported in the USA.

Matrix metalloproteinase synthesis and expression in isolated LV myocyte preparations.

In several cardiac disease states, alterations in myocyte and extracellular matrix (ECM) structure occur with left ventricular (LV) remodeling and are associated with changes in matrix metalloproteinase (MMP) activity. Although nonmyocyte cell types have been implicated as sites for synthesis and expression of MMPs within the ECM, whether the LV myocyte itself expresses specific types and active forms of MMPs remains unknown. Accordingly, isolated Ca(2+)-tolerant LV porcine myocytes (10(5) cells/ml) in which selective disaggregation and resuspension was performed (13 independent experiments) were plated on basement membrane substrates including Matrigel, collagen IV, laminin, and fibronectin as well as poly-L-lysine. After 24-h incubation, LV myocyte conditioned media were subjected to zymography, a specific MMP-2 proteolytic capture assay, immunoblotting, and ELISA for detection of MMP activity and relative content of the 72-kDa gelatinase MMP-2. Although robust zymographic activity [(pixels. mm(2))/cell] was observed in conditioned media from LV myocytes plated on collagen IV (1,673 +/- 297), fibronectin (1,530 +/- 281), and poly-L-lysine (2,545 +/- 560), proteolytic activity appeared to be lower in conditioned media from LV myocytes plated on Matrigel (842 +/- 83) and laminin (1,329 +/- 238). MMP-2 proteolytic activity was increased by approximately eightfold in conditioned media taken from LV myocytes plated on poly-L-lysine compared with that of Matrigel. With respect to each of the adhesion substrates, MMP-2 content was at least 50% lower in LV myocyte conditioned media taken from Matrigel and laminin. Immunofluorescent labeling of LV myocytes yielded a strong signal for MMP-2 within the myocyte and along the sarcolemmal surface. In conclusion, this study demonstrated for the first time that adult LV myocytes synthesize and express members of the MMP family and thus may potentially participate in the LV remodeling process through synthesis and secretion of MMPs.

Chronic dual inhibition of angiotensin-converting enzyme and neutral endopeptidase during the development of left ventricular dysfunction in dogs.

Angiotensin-converting enzyme (ACE) inhibition as well as neutral endopeptidase (NEP) inhibition was demonstrated to influence hemodynamics in various cardiac disease states. However, specific effects of chronic combined ACE and NEP inhibition on left ventricular (LV) and myocyte geometry and function remain unclear. In this study, a dual-acting metalloprotease inhibitor (DMPI), which possesses both ACE and NEP inhibitory activity, was used in a rapid-pacing model of LV dysfunction. LV and myocyte geometry and function were examined in control dogs (n = 6), in dogs with pacing-induced LV dysfunction (216 +/- 2 beats/min, 28 days, n = 7), and in dogs with DMPI treatment during rapid pacing (10 mg/kg p.o., b.i.d., n = 6). With chronic rapid pacing, LV end-diastolic volume increased (84 +/- 4 vs. 49 +/- 3 ml), and LV ejection fraction decreased (38 +/- 3% vs. 68 +/- 3%) compared with control (p < 0.05). DMPI concomitantly administered during long-term rapid pacing did not change LV ejection fraction (35 +/- 3%), but LV end-diastolic volume was reduced (70 +/- 5 vs. 84 +/- 4 ml; p < 0.05) when compared with rapid pacing only. With long-term rapid pacing, myocyte cross-sectional area was decreased (278 +/- 5 vs. 325 +/- 5 microm2), and resting length increased (178 +/- 2 vs. 152 +/- 1 microm) when compared with control (p < 0.05). With DMPI concomitantly administered during rapid pacing, myocyte cross-sectional area (251 +/- 5 microm2) and resting length (159 +/- 4 microm) were reduced when compared with rapid pacing only (p < 0.05). Myocyte velocity of shortening decreased from control values with long-term rapid pacing (39.3 +/- 3.9 vs. 73.2 +/- 5.9 microm/s; p < 0.05) but improved with DMPI treatment during rapid pacing when compared with rapid pacing only (58.9 +/- 6.7 microm/s; p < 0.05). Myocyte velocity of shortening with beta-adrenergic-receptor stimulation (25 nM isoproterenol) was reduced from controls with rapid pacing (125 +/- 12 vs. 214 +/- 30 microm/s; p < 0.05) but was improved with DMPI treatment during rapid pacing when compared with rapid pacing only (178 +/- 12 microm/s; p < 0.05). In a model of rapid pacing-induced LV failure, concomitant DMPI treatment significantly reduced the degree of LV dilation with no apparent effect on LV pump function. At the level of the LV myocyte, long-term DMPI treatment with rapid pacing improved myocyte performance and beta-adrenergic response. Thus the improvement in isolated myocyte contractile function was not translated into improved global LV-pump performance. The mechanisms by which improved myocyte contractility was not translated into a beneficial effect on LV-pump function with DMPI treatment during rapid pacing remain speculative, but likely include significant changes in LV remodeling and loading conditions.

Myocardial matrix metalloproteinase activity and abundance with congestive heart failure.

The left ventricular (LV) myocardial collagen matrix has been proposed to participate in the maintenance of LV geometry. Thus alterations in the composition of the LV myocardial collagen matrix may influence LV function. The matrix metalloproteinases (MMPs) are a family of enzymes that contribute to extracellular remodeling in several disease states. However, the types of MMPs expressed in the normal and congestive heart failure (CHF) state and the relation to MMP activity remained unclear. Accordingly, after 3 wk of pacing (240 beats/min), changes in LV function, substrate-specific MMP activity, and MMP subclass abundance were measured in comparison with control pigs (n = 6). Changes in LV function and geometry were measured by echocardiography; LV end-diastolic dimension increased (3.6 +/- 0.1 vs. 6.0 +/- 0.1 cm, P < 0.05) and LV fractional shortening decreased (47 +/- 1 vs. 15 +/- 1%, P < 0.05) compared with controls. Degradation of fibrillar collagen is achieved through the combined action of interstitial collagenase (MMP-1), gelatinase A (MMP-2), and stromelysin (MMP-3) (He, C., S. Wilheilm, A. Pentland, B. Marmer, G. Grant, A. Eisen, and G. Goldberg. Proc. Natl. Acad. Sci. USA 86:2632-2636, 1989; Woessner, J. FASEB J. 5: 2145-2154, 1991). Accordingly, the relative abundance of specific MMPs (MMP-1, MMP-2, and MMP-3) was examined by immunoblotting. With pacing CHF, the relative abundance for MMP-1 increased to 319 +/- 94%, MMP-2 increased to 194 +/- 31%, and MMP-3 increased to 493 +/- 159% (all P < 0.05). With pacing CHF, LV myocardial zymographic activity for the substrate gelatin increased by 119% (P < 0.05) and for the substrate collagen III by 153% (P < 0.05) over controls. Caseinolytic activity also increased with pacing CHF by 139% (P < 0.05) over controls. In conclusion, LV myocardial MMP activity and abundance increased with pacing-induced CHF. These findings demonstrate that pacing-induced CHF leads to changes in myocardial MMP activity and expression that may be responsible for LV remodeling in CHF.

Increased matrix metalloproteinase activity and selective upregulation in LV myocardium from patients with end-stage dilated cardiomyopathy.

BACKGROUND: One of the hallmarks of dilated cardiomyopathy (DCM) is left ventricular (LV) remodeling. The matrix metalloproteinases (MMPs) are a family of enzymes that contribute to extracellular remodeling in several disease states. Additionally, a family of inhibitors called tissue inhibitors of MMPs (TIMPs) has been shown to exist and to tightly regulate MMP activity. However, the types of MMPs and TIMPs expressed within the normal and DCM LV myocardium and the relation to MMP activity remain unexplored. METHODS AND RESULTS: Relative LV myocardial MMP activity was determined in the normal (n=8) and idiopathic DCM (n=7) human LV myocardium by substrate zymography. Relative LV myocardial abundance of interstitial collagenase (MMP-1), stromelysin (MMP-3), 72 kD gelatinase (MMP-2), 92 kD gelatinase (MMP-9), TIMP-1, and TIMP-2 were measured with quantitative immunoblotting. LV myocardial MMP zymographic activity increased with DCM compared with normal (984+/-149 versus 413+/-64 pixels, P<.05). With DCM, LV myocardial abundance of MMP-1 decreased to 16+/-6% (P<.05), MMP-3 increased to 563+/-212% (P<.05), MMP-9 increased to 422+/-64% (P<.05), and MMP-2 was unchanged when compared with normal. LV myocardial abundance of TIMP-1 and TIMP-2 increased by >500% with DCM. A high-molecular-weight immunoreactive band for both TIMP-1 and TIMP-2, suggesting a TIMP/MMP complex, was increased >600% with DCM. CONCLUSIONS: This study demonstrated increased LV myocardial MMP activity and evidence for independent regulatory mechanisms of MMP and TIMP expression with DCM. These findings suggest that selective inhibition of MMP species within the LV myocardium may provide a novel therapeutic target in patients with DCM.

Time-dependent changes in matrix metalloproteinase activity and expression during the progression of congestive heart failure: relation to ventricular and myocyte function.

The development of congestive heart failure (CHF) is associated with left ventricular (LV) dilation and myocardial remodeling. However, fundamental mechanisms that contribute to this remodeling process with the progression of CHF remain unclear. The matrix metalloproteinases (MMPs) have been demonstrated to play a significant role in tissue remodeling in a number of pathological processes. The present project tested the hypothesis that the LV dilation and remodeling during the progression of CHF is associated with early changes in MMP expression and zymographic activity. LV and myocyte function, collagen content, and MMP expression and zymographic activity were serially measured during the progression of CHF caused by pacing-induced supraventricular tachycardia (SVT) in pigs. After 7 days of SVT, LV end-diastolic dimension and myocyte length both increased by 15% from control values, and LV fractional shortening fell by 20%. At the level of the myocyte, percent shortening fell by 16% after 7 days of SVT, with no change in the steady-state velocity of shortening. Longer durations of SVT caused progressive LV dilation, LV pump failure, and myocyte contractile dysfunction. Specifically, 21 days of SVT resulted in a >50% increase in LV dimension, a 56% fall in LV fractional shortening, and a 33% decline in myocyte velocity of shortening. The decline in LV and myocyte function with 21 days of SVT was accompanied by signs and symptoms of CHF. Thus, SVT causes time-dependent changes in LV geometry and function and the subsequent development of CHF. LV myocardial collagen content and confluence fell by >25% after 7 days of SVT and were accompanied by an 80% increase in LV myocardial MMP zymographic activity against the substrate gelatin. After 14 days of SVT, total LV myocardial collagen content was reduced by 24%, and LV myocardial MMP zymographic activity increased by >100% from control values. Interstitial collagenase (MMP-1), stromelysin (MMP-3), and 72-kD gelatinase (MMP-2) were increased by approximately 2-fold after 7 days of SVT. LV MMP zymographic activity and abundance remained elevated with longer durations of SVT. The results of the present study demonstrated that in this model of CHF, early changes in LV myocardial MMP zymographic activity and protein levels occurred with the initiation and progression of LV dilation and dysfunction. These findings suggest that an early contributory mechanism for the initiation of LV remodeling that occurred in this model of developing CHF is enhanced expression and potentially increased activity of LV myocardial MMPs.

Downstream defects in beta-adrenergic signaling and relation to myocyte contractility after cardioplegic arrest.

OBJECTIVE: Transient left ventricular dysfunction can occur after hypothermic, hyperkalemic cardioplegic arrest and is associated with decreased beta-adrenergic receptor responsiveness. Occupancy of the beta-adrenergic receptor activates adenylate cyclase, which phosphorylates the L-type Ca2+ channel-enhancing myocyte contractility. The goal of this study was to identify potential mechanisms that contribute to the defects in the beta-adrenergic receptor signaling cascade after cardioplegic arrest. METHODS: Isolated left ventricular porcine myocytes were assigned to one of two treatment groups: (1) cardioplegic arrest (24 mEq/L K+, 4 degrees C x 2 hours, then 5 minutes in 37 degrees C cell media; n = 130) or (2) normothermic control (cell media, 37 degrees C x 2 hours; n = 222). Myocyte contractility was assessed at baseline and after either beta-adrenergic receptor occupancy (25 nmol/L isoproterenol [INN: isoprenaline]), activation of adenylate cyclase (0.5 mumol forskolin), or direct activation of the L-type Ca(2+)-channel (10 nmol/L or 100 nmol/L (-)BayK 8644). RESULTS: Myocyte velocity of shortening (micron/sec) was increased with beta-adrenergic receptor occupancy or direct adenylate cyclase stimulation compared with baseline in the normothermic group (187.3 +/- 6.9, 181.7 +/- 10.2, and 73.9 +/- 2.9, respectively; p < 0.0001) and after cardioplegic arrest (128.6 +/- 8.9, 124.3 +/- 9.4, and 46.1 +/- 2.6, respectively; p < 0.0001). However, the response after cardioplegic arrest was significantly reduced compared with normothermic values under all conditions (p = 0.012). Direct activation of the L-type Ca(2+)-channel, which eliminates beta-adrenergic receptor-dependent events, increased myocyte contractility in the normothermic group (161.90 +/- 12.0, p < 0.0001) and after cardioplegic arrest (92.78 +/- 6.8, p < 0.0001), but the positive inotropic response appeared reduced compared with normothermic control values (p = 0.003). CONCLUSION: These findings suggest that contributory mechanisms for the reduced beta-adrenergic receptor-mediated response after hypothermic, hyperkalemic cardioplegic arrest lie downstream from these specific components of the transduction pathway and likely include defects in Ca2+ homeostasis, myofilament Ca2+ sensitivity, or both.

A network simulation model of large herringbone and parallel milking parlors.

A network simulation model of herringbone and parallel milking parlors was built. Parlor performance was predicted based on the number of cows milked per hour and the amount of milk harvested per shift. Modeled parlors operated using a task-oriented milking routine. The simulation also modeled milking personnel, milking system vacuum pressure and pulsation ratio, and milk yield per cow per milking. The probability distributions of the model components that were used for validation were fitted from data collected from four dairies with the following parlors: double-16 herringbone, double-20 herringbone, double-35 parallel, and double-40 parallel. All fitted distributions were continuous, non-negative, and skewed to the right. The mean number of cows milked per hour (simulated and observed, respectively) was 1) double-16 herringbone, 164.8 and 164.6;2) double-20 herringbone, 207.6 and 206.6; 3) double-35 parallel, 319.2 and 320.2; and 4) double-40 parallel, 361.6 and 362.5. Mean milk yields harvested per shift were 1) double-16 herringbone, 9020 and 9030 kg; 2) double-20 herringbone, 14,800 and 14,746 kg; 3) double-35 parallel, 20,900 and 20,945 kg; and 4) double-40 parallel, 27,100 and 26,974 kg, for simulated and observed yields, respectively. Differences between simulated and observed means for either variable were not significant.

Factors affecting the performance of simulated large herringbone and parallel milking parlors.

A simulation model of double-16 and double-20 herringbone and parallel milking parlors and double-32 and double-40 parallel milking parlors was used to examine the effects of size, design, operating characteristics of the milking system, management strategies, and milk yield on parlor performance. Analysis of factorial experiments indicated that smaller parlors were more efficient. Turns per hour and milk per stall per hour for double-16, -20, -32, and -40 parallel parlors were 5.87, 5.91, 5.21, and 5.00 turns/h and 56.19, 56.46, 49.66, and 47.94 kg/h, respectively. A wider pulsation ratio (60:40 to 70:30) increased performance measures about 4%, and increased vacuum pressure (46.6 to 50.8 kPa) increased performance measures > 6%. Parallel parlors outperformed herring-bones by nearly 8%. Abbreviated milking procedures resulted in a > 6% increase in performance measures over standard milking procedures. Performance response was significantly diminished when the amount of milking labor exceeded deficit amounts (20 to 32 units per milker) for abbreviated milking procedures or standard amounts (13.3 to 16 units per milker) for standard milking procedures. When milk yield increased, turns per hour decreased, but milk per stall per hour increased.

Simulating individual cow milk yield for milking parlor simulation models.

A method of simulating individual cow milk yield per milking as a function of herd milk yield and month was formulated for milking parlor simulation models. Milk yield per milking was modeled for each month in three herd milk yield categories: 8165, 8845, and 9525 kg/yr of milk per cow. Actual individual cow DHIA test day milk weight data for three Florida dairy herds in each herd milk yield category and month were adjusted to the mean of their respective actual milk shipped per cow on test day then pooled and converted to a basis of three times per day milk yield per milking. After minor truncation, Weibull probability distributions fitted to these data sets adequately modeled milk yield per milking per cow. Analysis of simulation results for milk yield per milking per cow indicated no significant differences between actual and simulated means for any herd milk yield category or month. Simulations of monthly and yearly total herd milk yield for each herd indicated that fitted Weibull distributions also adequately modeled monthly and yearly herd milk yield characteristics and reflected seasonal herd milk yield patterns typical of Florida.

Closure of large spina bifida defects: a simple technique based on anatomical details.

Much has been written about closure of large spina bifida defects. There is an increased demand to close these defects irrespective of the final outcome of the patient. Plastic surgeons may become involved in the closure of large defects. Perforator vessels of the back passing through the latissimus fascia can maintain viability of triangular island flaps. Therefore, such flaps can be used to close the large midline defects of spina bifida. This article reviews the literature and presents a simple technique based on anatomical properties of the region surrounding the defect.

Thymic carcinoma and aplastic anemia: report of a previously undocumented association.

A case of thymic carcinoma documented after a 6-year history of aplastic anemia is reported. The anemia responded initially to steroids and antithymocyte globulin. The carcinoma may have arisen in a previous undetected thymoma; alternatively, an underlying abnormality, presumably immunologic, played a role in the development of the anemia and the thymic carcinoma.

Effects of colchicine on sulfated glycosaminoglycan production and cell detachment in pre-capillary pulmonary endothelial cells.

The effects of colchicine on the morphology, substrate adhesiveness, and production of glycosaminoglycan (GAG) macromolecules by cultured pre-capillary pulmonary endothelial cell were studied. Colchicine-treated cells demonstrated altered morphology and decreased substrate adhesiveness compared to untreated cells. In addition, [35S]sulfate incorporation into glycosaminoglycans was decreased 33% after treatment with colchicine. Spectrophotometric measurement of total cellular GAG revealed a similar GAG reduction in colchicine-treated cells. The composition of [35S]sulfate radiolabelled GAG was similar in cultures with and without colchicine, consisting of approximately 56% chondroitin sulfate and the remainder heparin/heparan sulfate. The results indicate that colchicine influences the biological behavior of pre-capillary endothelial cells, in part by altering the amount of glycosaminoglycan molecules produced.

Primary Hodgkin's disease of the skull following a 3-year history of pseudotumor cerebri.

Hodgkin's disease involving contiguous areas of the skull, overlying soft tissue, and extending to the underlying epidural space, developed in a 29-year-old woman with a 3-year history of pseudotumor cerebri. The patient had been on varying doses of steroids since shortly after the development of headaches and papilledema in 1981. In 1984, following radiation therapy for Hodgkin's disease, the tumor and headaches resolved. Pseudotumor cerebri antedating Hodgkin's disease has not been previously reported. The pseudotumor cerebri may have been an early manifestation of Hodgkin's disease in an unusual location.

Altered glycosaminoglycan production by HL-60 cells treated with 4-methylumbelliferyl-beta-D-xyloside.

Glycosaminoglycans, mainly chondroitin 4-sulfate, are located in the primary granules of human myeloid cells. These polyanionic carbohydrates are believed to play an important role in leukocyte maturation and function. To study the effect of altered chondroitin sulfate metabolism on human promyelocytic leukemia cells, we have treated HL-60 cells with 4-methylumbelliferyl-beta-D-xyloside. beta-D-Xylosides initiate the synthesis of free chondroitin sulfate chains. Cytochemical studies of treated cells demonstrated a marked increase in cytoplasmic granules stained with cationic dyes. This was confirmed by radiolabeled precursor incorporation studies that demonstrated a 344% increase in 35S-sulfate uptake into glycosaminoglycans associated with the cells and a 39% increase in incorporation into glycosaminoglycans released into the media. Chromatographic analyses of these glycosaminoglycans from treated cells demonstrated that the newly formed chondroitin sulfate chains were not attached to protein core and were of shorter length, but of greater charge density than chondroitin sulfate produced by control cells. Thus, beta-D-xyloside appears to alter the protein linkage, chain length, and sulfation of chondroitin sulfate produced by HL-60 cells, and these changes are morphologically evident. These biochemically altered cells may provide important information concerning the role of these macromolecules in myeloid development.