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Biomedical subjects

J Lynch

Publications and source records attributed to J Lynch.

At least 109 records · Page 6Linked to original sources
PubMed1998

Effects of milk somatic cell count on cottage cheese yield and quality.

Eight Holstein cows in midlactation were selected for low milk somatic cell count (SCC) and the absence of the pathogens that cause mastitis. Milk collection and cottage cheese manufacture from low SCC milk were replicated on each of 4 d (control period). Each cow was infused with 1000 cfu of Streptococcus agalactiae. One week after infusion, milk from the same eight cows was collected and commingled. On each of 4 d, cottage cheese was made from milk with high SCC (treatment period). A mass-balance protocol, accounting for protein and total solids, was used to determine recoveries in whey, wash water, and uncreamed curd. Actual yields, yields adjusted for composition, and theoretical yields of uncreamed curd were calculated. Mean milk SCC for the periods with the low SCC (control) and the high SCC (treatment) were 83 x 10(3) and 872 x 10(3) cells/ml, respectively. The recovery of protein in the uncreamed curd was higher during the low SCC period than during the high SCC period (75.85% vs. 74.35%). High SCC and the associated higher proteolytic activity caused higher protein loss in the whey and wash water and more curd fines. The percentage of total solids recovery in uncreamed curd was higher for high SCC milk because the lactose content of the high SCC milk was 0.27% lower than that of the low SCC milk. The moisture content of the curd was higher for the high SCC milk (82.75% vs. 83.81%). Proteolysis during refrigerated storage was faster in cottage cheese made from high SCC milk. The yield efficiency of uncreamed curd, adjusted for composition based on 81% moisture, was 4.34% lower for the cottage cheese curd made from high SCC milk.

Animals↗
PubMed1998

Increased expression of HDJ-2 (heat shock protein 40) and heat shock protein 70 in biopsy specimens of transplanted human lungs.

BACKGROUND: Heat shock proteins are expressed during several forms of stress and inflammation. This study was done to determine whether the expression of heat shock protein HDJ-2 (heat shock protein 40), heat shock protein 60, and heat shock protein 70 are increased during rejection in human pulmonary allografts. METHODS: Thirty-five transbronchial biopsy specimens were obtained from adult lung transplant recipients. Histologic analysis and assessment of heat shock protein HDJ-2, heat shock protein 60, and heat shock protein 70 mRNA expression was performed. Total RNA was extracted, reverse transcribed, and amplified by polymerase chain reaction with oligonucleotide primers specific for the heat shock proteins. The identity of the amplified message was verified by Southern blot and slot blot analysis. RESULTS: The expression of heat shock protein HDJ-2 was significantly higher in samples from lung transplant recipients undergoing rejection when compared with recipients without rejection or infection. Heat shock protein 70 expression was also increased in rejection. Expression of heat shock protein 60 did not show any increase in recipients with no evidence of rejection and infection or transplant recipients with rejection or infection. Serial analysis of heat shock protein HDJ-2 and heat shock protein 70 obtained in biopsy specimens during and after rejection showed a decrease of heat shock protein HDJ-2 and heat shock protein 70 expression after resolution of lung rejection. CONCLUSION: Our data demonstrate that the expression of heat shock protein HDJ-2 and heat shock protein 70 increases during lung rejection. However, only heat shock protein HDJ-2 was able to differentiate between rejection and infection. Measurement of heat shock protein HDJ-2 in transbronchial biopsy specimens may assist in the differential diagnosis between rejection and infection in lung transplant recipients.

Carrier Proteins↗
PubMed1998

Genetics and ovarian carcinoma.

Ovarian cancer is a disease that will affect approximately 1% of American women during their lifetime, and contributes to more than 14,000 deaths annually. If not detected early, this disease has a 5-year survival rate of less than 20%. Ovarian cancer develops predominantly from the malignant transformation of a single cell type, the surface epithelium. Although the biological mechanisms of transformation remain unclear, it is probably a multistep process requiring an accumulation of genetic lesions in a number of different gene classes. Several proto-oncogenes, such as AKT2 and Ki-RAS, are activated during ovarian cancer development, with putative oncogene-containing chromosomal regions showing imbalances and DNA amplifications. A number of chromosomal regions are also lost in ovarian tumors, indicating that the inactivation of tumor suppressor genes, such as TP53, may also contribute to cancer development. An important recent advancement in the field of ovarian cancer research is the identification of the breast/ovarian cancer susceptibility genes, BRCA1 and BRCA2. Mutations in these two tumor suppressor genes are responsible for the majority of heritable forms of epithelial ovarian cancers. A second class of genes involved in DNA mismatch repair (MMR) are responsible for most cases of hereditary nonpolyposis colorectal cancer (HNPCC). HNPCC or Lynch II cancer syndrome patients are also at an increased risk for developing ovarian cancer. Individuals in cancer-prone kindreds are currently being screened for germline mutations in BRCA1, BRCA2, and several MMR genes (eg, MSH2, MLH1), and mutant allele carriers counseled for cancer risks. Issues related to counseling and management of women at high risk for developing ovarian cancer are discussed. Although BRCA1, BRCA2, and a number of MMR genes have been identified, many more genes involved in gynecologic malignancies remain to be discovered and the clinical significance of the cancer genes already known is still in its infancy.

BRCA1 Protein↗
PubMed1997

Workplace demands, economic reward, and progression of carotid atherosclerosis.

BACKGROUND: Characteristics of the work environment have been associated with cardiovascular morbidity and mortality, but it is unclear whether these factors are associated with preclinical manifestations of disease. METHODS AND RESULTS: We investigated the association between job demands, economic reward, and the 4-year progression of carotid atherosclerosis in a population-based sample of 940 Finnish men. Data from the Kuopio Ischemic Heart Disease Risk Factor Study were used to estimate changes in plaque height, maximum and mean intima-media thicknesses across combinations of job demands, and income. Associations were examined in relation to atherosclerotic risk factors and were stratified by baseline levels of atherosclerosis and prevalent ischemic heart disease. Men who had jobs with high demands and low economic rewards had significantly greater 4-year progression of plaque height (0.33 mm, P = .008) and maximum intima-media thickness (0.32, P = .03) than men with low-demand, high-income jobs. The magnitude of these differences was not greatly attenuated by risk factor adjustment and did not differ when examined by the level of workplace resources, social support, or employment status. Larger differences were observed in a subsample of men who had more advanced atherosclerosis at baseline. CONCLUSIONS: These results show that men with demanding work that produces little economic reward have significantly greater progression of carotid atherosclerosis than more advantaged men. The relationship between job demands and health should be understood in a broad framework of interacting economic conditions, social circumstances, and behaviors that cascade over the life course and may ultimately contribute to socioeconomic inequalities in morbidity and mortality.

Arteriosclerosis↗
PubMed1997

Loss of low-affinity nerve growth factor receptor during malignant transformation of the human prostate.

BACKGROUND: The low-affinity nerve growth factor receptor (LNGFR) exhibits an inverse association of epithelial expression with the degree of differentiation of prostate adenocarcinoma tissue. However, the stage at which loss of LNGFR expression is first manifested in the malignant prostate has not been determined. METHODS: In order to characterize loss of LNGFR expression in the clinically localized malignant prostate of untreated patients, the pattern of expression of the LNGFR was examined in nonmalignant tissues, consisting of normal and prostatic intraepithelial neoplastic tissues, and in malignant tissues that had been graded by Gleason's scores and categorized into well, moderately, and poorly differentiated adenocarcinomas. In order to determine whether there was an inverse correlation between LNGFR expression and prostate-specific antigen (PSA) secretion, preoperative concentrations of PSA in the serum were also analyzed in relation to the differentiative state of the adenocarcinomas. RESULTS: Premalignant prostate tissues exhibited expression of the LNGFR on all epithelia, whereas in malignant prostate tissues a proportion of epithelia exhibited loss of expression of the LNGFR. An increase in Gleason score of the adenocarcinoma tissue was associated with an increase in the proportion of epithelia that exhibited loss of expression of the LNGFR. Moreover, the proportion of epithelia expressing the LNGFR was inversely correlated with an increase in the concentration of serum PSA. The loss of LNGFR expression was first manifested in epithelia that occurred toward the center of adenocarcinoma tissue. Furthermore, extensive loss of expression of the LNGFR of approximately 63% occurred in well-differentiated adenocarcinomas. CONCLUSIONS: These observations demonstrate that loss of LNGFR expression is first observed in well-differentiated malignant epithelia. Hence, loss of the LNGFR may be indicative of the initial stages of malignant transformation of prostate epithelia, as well as all subsequent stages of prostate adenocarcinomas.

Adenocarcinoma↗
PubMed1997

[The current standing of obstetrical analgesia and anesthesia. A survey of North Rhein-Westfalia].

BACKGROUND: The purpose of this study was to determine obstetrical pain management practices for labour for spontaneous and operative vaginal deliveries since there were no comparative German data available for the past 10 years. METHODS: A mail survey was sent to the chief anaesthetists of all hospitals in North Rhine-Westfalia designated to have obstetrical beds. The confidential and standardised questionnaire consisted of 24 mainly multiple-choice questions relating to general issues and methods of analgesia and anaesthesia for vaginal deliveries. RESULTS: In all, 118 completed replies to 258 sent questionnaires were received, giving a response rate of 46%. Among the 118 hospitals there were 79,157 vaginal deliveries annually. All participating hospitals practiced either systemic analgesics/spasmolytics and/or regional-anaesthetic methods (Table 2). Perineal local infiltration (23.7% of vaginal deliveries, in 99% of cases performed by the obstetrician) and epidural analgesia (23.2% of vaginal deliveries, in 81% of cases performed by an anaesthetist) were the commonest regional-anaesthetic methods. Pudendal nerve blocks were performed in 18.5% of vaginal deliveries (Table 1). Of all participating hospitals, 97% provided a 24-h epidural service. The method of epidural anaesthesia was widely homogeneous in all 118 hospitals (Table 3). Other methods of regional analgesia (i.e., epidural infusions or patient-controlled epidural analgesia) were performed only rarely. CONCLUSIONS: The methods of obstetrical analgesia and anaesthesia are on a high level and show a broad homogeneity in all hospitals. Overall, the results indicate, in comparison to former studies and in common with other countries, steadily increasing use of regional anaesthesia performed by anaesthetists in contrast to decreasing numbers of local infiltrations performed by obstetricians.

Analgesia, Obstetrical↗
PubMed1997

Management of blunt splenic trauma: significant differences between adults and children.

BACKGROUND: Although highly successful in children, nonoperative management of blunt splenic injury in adults is less defined. The purpose of this study was to determine whether mechanism of injury, grade of splenic injury, associated injuries, and pattern of injury differ between adults and children (younger than 15 years of age). METHODS: Four hundred eleven patients (293 adults and 118 pediatric patients) with blunt splenic injury were admitted to an affiliated adult/pediatric trauma program from 1989 to 1994. Computed tomography (CT) scans were interpreted in a blinded fashion. Mechanism of injury was significantly different for adults versus children (p < 0.05): motor vehicle crash (66.9% versus 23.7%), motorcycle (8.8% versus 0.8%), sports (2.4% versus 16.9%), falls (8.8% versus 25.4%), pedestrian/automobile (4.4% versus 11.0%), bicycle (1.4% versus 9.3%), and other (7.3% versus 12.7%). RESULTS: Higher injury severity scores, lower Glasgow Coma Scales, and higher mortality indicated that the adults were more severely injured than the children. Fifty-nine percent of the adults and 7% of the children required immediate laparotomy for splenic injury. Both CT grade and quantity of blood on CT predicted the need for exploration in adults but not in children. An injury severity score above 15 and high-energy mechanisms correlated with the need for operative intervention. CONCLUSIONS: Rather than children simply being physically different, they are injured differently than adults, hence the high rate of nonoperative management.

Accidents, Traffic↗
PubMed1997

An update of HNPCC (Lynch syndrome).

Genetic epidemiology studies of colorectal cancer (CRC) can identify persons who are at inordinately high risk and who thereby might benefit from targeted early detection and primary prevention programs, inclusive of prophylactic surgery in selected cases. The discipline of molecular genetics has identified germline mutations that include APC in familial adenomatous polyposis (FAP) and mutator genes, namely MSH2, MLH1, PMS1, and PMS2 in hereditary nonpolyposis colorectal cancer (HNPCC). These discoveries have significantly enhanced our ability to identify individuals whose cancer destiny can literally be determined at birth. This review updates HNPCC's differential diagnosis, heterogeneity, tumor spectrum, newly found evidence of accelerated colonic adenoma to CRC, survival advantage, and currently available surveillance and management programs. Emphasis has been on how knowledge of the genetics and natural history of HNPCC can be used effectively to promote early diagnosis or prevention of cancer.

Adenomatous Polyposis Coli↗
PubMed1997

The genetics and natural history of hereditary colon cancer.

OBJECTIVES: To provide an overview of the genetics, natural history, surveillance and management of hereditary colorectal cancer with emphasis on hereditary nonpolyposis colorectal cancer (HNPCC). DATA SOURCES: Published research and review articles, clinical summaries, and personal experience. CONCLUSION: Hereditary factors may account for approximately 10% of colorectal cancer cases. Genes responsible for some of these disorders have been identified and cloned, making it possible to test family members for gene carrier status. Identification of individuals at highest risk for cancer could lead to more effective prevention and early detection. However, there are potential medical, psychological, and insurance problems inherent in predisposition testing that must be addressed. IMPLICATIONS FOR NURSING PRACTICE: Nurses can play a key role in identifying patients who may be at high risk for colorectal cancer by recognizing a significant cancer family history. A well-informed nurse can assist in counseling the patient so that he/she can be knowledgeable about all aspects of genetic testing. When a cancer genetic diagnostic has been established, nurses can be emotionally supportive and reinforce the importance for continued surveillance or prophylactic surgery.

Colorectal Neoplasms, Hereditary Nonpolyposis↗
PubMed1997

Strain magnitude related changes in whole bone architecture in growing rats.

Short daily periods of controlled dynamic loading were applied in vivo through the flexed carpus and olecranon to the intact ulna of 240 g male Sprague-Dawley rats. This technique involved neither surgical preparation, nor direct loading of the periosteum at a site close to the region of the bone in which adaptive modeling was subsequently assessed. The animals used their limbs normally between loading episodes, thus approximating to the natural situation, in which short periods of exercise are generally superimposed on longer periods of less strenuous activity. The strain patterns associated with normal activities were established for the rat ulna from strain gauges implanted in vivo. Typical peak strain magnitudes during unrestricted locomotion varied between -0.0007 and -0.0012, with peak strain rates between 0.023 and -0.038 sec-1. Stride frequency was 1.5-4.2 Hz. The adaptive response to a single 10 min period of loading each day, causing peak dynamic strains of -0.002 (1200 cycles at 2 Hz, and a loading/unloading rate of +/-0.03 sec-1), involved modification of the normal growth related medial to lateral modeling drift, simultaneously reducing the rate of lateral periosteal bone deposition and medial bone resorption. This change to the normal modeling pattern reduced the total amount of new bone formation as well as the midshaft curvature of the ulna. At higher peak strain amplitudes (-0.004), adaptive straightening was accompanied by an increase in bone mass, achieved by an increase in the mineral apposition rate on the previously forming lateral face, and arrest of resorption on the medial ulna surface, with reversal to formation. These experiments show that the growing rat ulna underwent adaptive changes in both bone mass and architecture when short daily periods of axial loading, producing strains within the physiological range and with near normal strain distribution, were superimposed on the loading associated with normal activity. At moderate peak strain magnitude (-0.002), modification of drift produced a straighter bone, associated with a reduced periosteal bone formation. At higher strain magnitude (-0.004), adaptive modeling produced a straighter bone associated with increased periosteal bone formation.

Animals↗
PubMed1997

A randomized phase II study of BB-10010: a variant of human macrophage inflammatory protein-1alpha for patients receiving high-dose etoposide and cyclophosphamide for malignant lymphoma and breast cancer.

Macrophage inflammatory protein-1alpha (MIP-1alpha) is a chemokine that can inhibit the cell cycle progression of both primitive haemopoietic and epidermal progenitor cells. This property could potentially be exploited to attenuate both the myelosuppressive effects of chemotherapy as well as mucositis. We evaluated both the biological and clinical effects of BB-10010, a genetically engineered variant of MIP-1alpha, in patients with malignant lymphoma or breast cancer receiving high-dose etoposide (VP 3.6 g/m2) and cyclophosphamide (Cy 200 mg/kg). 52 patients were randomized to one of three cohorts. Cohort A received no BB-10010; cohorts B and C received 10 microg/kg and 100 microg/kg of BB-10010, respectively. All patients received post-chemotherapy G-CSE BB-10010 was well tolerated. There were no significant differences between groups in recovery to an ANC > 0.5 x 10(9)/l, 1 x 10(9)/l or 1.5 x 10(9)/l, the number of days with an ANC < 0.5 x 10(9)/l, days to a platelet count > 50 x 10(9)/l or 100 x 10(9)/l, or the incidence and severity of mucositis. There was no evidence of any effect of BB-10010 on colony-forming cell (CFC) or long-term culture-initiating cell (LTC-IC) mobilization, cycling activity in the marrow or on chemotherapy-induced changes in CFC or LTC-IC number both of which were in the normal range by 22 d after completion of the chemotherapy. To our knowledge this is the first report of a myelointensive regimen having no apparent long-term effect on the LTC-IC compartment. In summary, BB-10010 is safe when used in patients receiving high-dose therapy but has no effect on reducing the toxicity of such therapy.

Adolescent↗
PubMed1997

A new biological assay for measuring cyanide in blood.

UNLABELLED: Clinical diagnosis of cyanide poisoning is complicated by the lack of an easy, convenient assay for cyanide concentration in blood. Therapy may be delayed with unconfirmed diagnosis because the conventional antidote to cyanide poisoning exposes patients to substantial risks. We developed a new spectrophotometric assay to measure cyanide by extraction into a sodium hydroxide trap, followed by the addition of exogenous methemoglobin as a colormetric indicator. Samples of blood from 15 healthy subjects and 5 patients who had received prolonged nitroprusside infusions were assayed. To optimize assay characteristics, methemoglobin concentrations, pH, temperature, incubation time, and buffer strengths were varied. Duplicate samples were assayed by using the polarographic method for assay validation. Over a range from 300 ng/mL to 7 microg/mL, the correlation between methods was r = 0.983. Interassay and intraassay variability were 5% and 2%, respectively. Samples drawn from the five patients and tested by using both methods yielded a correlation of r = 0.978. This new assay for cyanide in blood may greatly facilitate the diagnosis and treatment of cyanide ingestion. The use of methemoglobin as the colorimetric indicator in the assay contributes to its low cost and ease of use. IMPLICATIONS: Cyanide, an important factor in death from burn-related inhalation injury, is difficult and time-consuming to measure. We developed a new, rapid blood test for cyanide using methemoglobin as a colormetric indicator. A rapid, accessible test for cyanide may speed the diagnosis and treatment of cyanide poisoning.

Adult↗
PubMed1997

Genomic sequencing of DPC4 in the analysis of familial pancreatic carcinoma.

A first-degree relative with pancreatic cancer is found in 5% to 10% of patients with pancreatic carcinomas, suggesting an inherited predisposition for this neoplasm. The recently identified DPC4 tumor suppressor gene is a strong candidate for the gene responsible for the familial form of pancreatic carcinoma. DPC4 was identified in a consensus area of homozygous deletion in pancreatic carcinomas, and it is biallelically inactivated in approximately 50% of sporadic pancreatic carcinomas. The coding sequence of this gene is 1660 nucleotides in length, covering 11 exons. We describe optimized primers and conditions used in polymerase chain reaction and cycle sequencing of the entire DPC4 coding sequence of 25 individuals (eight with pancreatic carcinoma) from 11 kindreds with a familial aggregation of pancreatic carcinoma. No mutations in the coding sequences of the DPC4 gene were found; hence, it appears that germline mutations in DPC4 cannot account for many of the familial aggregations of pancreatic carcinoma.

Carcinoma↗
PubMed1997

Socioeconomic status and progression of carotid atherosclerosis. Prospective evidence from the Kuopio Ischemic Heart Disease Risk Factor Study.

Socioeconomic status (SES) is importantly associated with cardiovascular morbidity and mortality, but no information exists on the relationship between SES and progression of atherosclerotic vascular disease. We investigated the association between education and income and the 4-year progression of carotid atherosclerosis in a population-based sample of Finnish men. Data from the Kuopio Ischemic Heart Disease Risk Factor Study were used to estimate changes in maximum and mean intima-media thickness (IMT) and maximum plaque height across levels of SES in 1022 men. Associations between SES and atherosclerotic progression were examined in relation to risk factors and stratified by baseline levels of atherosclerosis and prevalent ischemic heart disease (IHD). There were significant, inverse, graded relationships between levels of education and income for all three progression measures, which were largely unaffected by risk factor adjustment. For education, the age- and baseline IMT-adjusted maximum progression for those with primary schooling or less was 0.28 mm and for those who graduated from high school, 0.24 mm (P = .05). Compared with the lowest SES group, men with the highest SES had 14% to 29% less atherosclerotic progression, depending on the measure used. Associations of the same magnitude were evident in subgroups without advanced baseline IMT and in men who were free of IHD. These results show that men with poor education and low income have significantly greater progression of carotid atherosclerosis than men with more advantages. The findings strengthen the contention that SES plays a significant role early in the atherosclerotic disease process and that reducing the burden of atherosclerotic vascular disease associated with lower SES will require approaches that focus on all stages of the life course.

Adult↗
PubMed1997

Workplace conditions, socioeconomic status, and the risk of mortality and acute myocardial infarction: the Kuopio Ischemic Heart Disease Risk Factor Study.

OBJECTIVES: This study investigated whether the association between workplace conditions and the risk of all-cause and cardiovascular mortality and acute myocardial infarction differed by socioeconomic status. METHODS: Prospective data were used to examine these associations in 2297 Finnish men, with adjustment for prevalent diseases and biological, behavioral, and psychosocial covariates, and stratified by employment status and workplace social support. RESULTS: Elevated age-adjusted relative hazards for all-cause mortality were found for men who reported high demands, low resources, and low income; high demands, high resources, and low income; and low demands, high resources, and low income. Similar patterns were found for cardiovascular mortality. In contrast, elevated age-adjusted relative hazards for acute myocardial infarction were observed only in men who reported high demands, low resources, and low income. These results did not differ by level of workplace social support or employment status. CONCLUSIONS: The negative effects of workplace conditions on mortality and of myocardial infarction risk depended on income level and were largely mediated by known risk factors.

Adult↗
PubMed1997

Predictors of disability retirement.

OBJECTIVES: Disability retirement may increase as the work force ages, but there is little information on factors associated with retirement because of disability. This is the first prospective population-based study of predictors of disability retirement including information on workplace, socioeconomic, behavioral, and health-related factors. METHODS: The subjects were 1038 Finnish men who were enrolled in the Kuopio Ischemic Heart Disease Risk Factor Study, who were 42, 48, 54, or 60 years of age at the beginning of the study, and who participated in a 4-year follow-up medical examination. RESULTS: Various job characteristics predicted disability retirement. Heavy work, work in uncomfortable positions, long workhours, noise at work, physical job strain, musculoskeletal strain, repetitive or continuous muscle strain, mental job strain, and job dissatisfaction were all significantly associated with the incidence of disability retirement. The ability to communicate with fellow workers and social support from supervisors tended to reduce the risk of disability retirement. The relationships persisted after control for socioeconomic factors, prevalent disease, and health behavior, which were also associated with disability retirement. CONCLUSIONS: The strong associations found between workplace factors and the incidence of disability retirement link the problem of disability retirement to the problem of poor work conditions.

Adult↗
PubMed1997

Increased concentration of soluble human leukocyte antigen class I levels in the bronchoalveolar lavage of human pulmonary allografts.

BACKGROUND: Human leukocyte antigen (HLA) class I antigens, are glycoproteins expressed on the cell surface and are also secreted (sHLA) into the surrounding fluids. This study investigates whether pulmonary allograft rejection is associated with an increased amount of sHLA class I in the bronchoalveolar lavage (BAL) fluid. METHODS: Enzyme-linked immunosorbant assays were used to measure sHLA class I levels in BAL samples from 66 lung transplant recipients. RESULTS: Analysis of pulmonary allograft recipients revealed that the mean concentration of sHLA class I was significantly higher in samples from recipients with acute rejection than in recipients with no evidence of rejection. Seventy-two percent of the patients with rejection had sHLA levels above the normal range for patients with infection or rejection. Conversely, sHLA levels were within normal limits in 94% of the control population. Time kinetic analysis revealed that in subjects with rejection, sHLA class I levels peaked in the first 2 weeks after transplantation and decreased thereafter. Increased levels of sHLA were found in patients with acute rejection but not in those with chronic rejection. Fifty-nine percent (n = 10) of the patients with infection had sHLA levels within the normal (no infection or rejection) range. The remaining 41% (n = 7) with infection had sHLA above the normal range. Fifty-seven percent (n = 4) of the latter group had cytomegalovirus infection. These results were confirmed in a prospective study carried out by analyzing paired samples obtained during and after rejection. Eight of the nine patients had high BAL sHLA class I during acute rejection, and low BAL sHLA class I levels after resolution of the acute rejection. CONCLUSION: Our data demonstrate that measurement of sHLA class I levels in BAL samples is a sensitive indicator of acute rejection.

Acute Disease↗