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PubMed1995

Increased detection of specific tyrosine phosphoproteins correlates with tumor progression of Abelson virus-infected lymphocytes.

Leukemias induced with the v-abl or BCR/ABL oncogene undergo a process of tumor progression which suggests that the ABL oncogene is required but not sufficient for full transformation. In order to identify cellular changes that correlate with progression to full transformation in v-abl transformed lymphoblasts Abelson virus (A-MuLV)-infected murine bone marrow was plated over a pre-established stromal feeder layer. Shortly after A-MuLV infection, transformed lymphoblasts were poorly oncogenic, but over time, progressed in a stepwide manner to a more oncogenic state. The transformants first acquired the ability to grow efficiently in agar, but only over the feeder layer. They next progressed to efficient feeder-independent growth in liquid culture, and then to efficient feeder-independent growth in soft agar. Cell lines that reached the advanced stage of feeder-independent agar growth showed increased detection by antiphosphotyrosine Western blot of the GAP-associated p62 phosphoprotein as well as of a 55 kDa phosphoprotein while detection of the P160 v-abl phosphoprotein remained constant throughout all stages of progression. Although the identity of the p55 phosphoprotein and the mechanism by which detection of p55 and p62 phosphoproteins change on the Western blots during tumor progression are unknown, the data demonstrate that these changes strongly correlate with the stage of progression of v-abl-transformed cells and raise the possibility that these changes may play a role in tumor progression in this model.

3T3 Cells↗

PubMed1993

Myopia and myopic progression among schoolchildren: a three-year follow-up study.

PURPOSE: To discuss the factors that might explain the rate of myopic progression and the degree of myopia after a 3-year follow-up among schoolchildren with myopia. METHODS: Myopic progression among 238 schoolchildren was followed up in a randomized clinical trial of myopia treatment. The associations between the explanatory factors and myopic progression and the final value of the spherical equivalent after the follow-up were studied by analysis of variance and regression analysis. RESULTS: Myopia progressed faster among girls than boys. According to the regression models for the boys, 25% of the variation of myopic progression and 57% of the final spherical equivalent could be explained by initial spherical equivalent, age at receiving first spectacles, time spent on sports and outdoor activities, and on reading and close work. Among the girls, 30% of myopic progression could be explained by age at receiving first spectacles, time spent on reading and close work, and reading distance. Similarly, 49% of the final spherical equivalent could be explained by age at receiving first spectacles, initial spherical equivalent, time spent on reading and close work, and reading distance. The rest of the variations could not be explained by the variables measured in this study. CONCLUSIONS: The factors with the most significant relationships to myopic progression were sex, age of onset, and degree of myopia at the beginning of the follow-up. Myopic progression and final myopia were related to time spent on reading and close work and to reading distance but not, however, to accommodation stimulus.

Accommodation, Ocular↗

PubMed1998

[Anisometropia and presbyopia: prescription of progressive lenses, a new approach].

OBJECTIVE OF THE STUDY: To show that anisometropia does not absolutely preclude the prescription of progressive lenses. MATERIALS AND METHODS: Forty-one anisometropes and presbyopes were selected for a prolonged trial of visual correction using progressive lenses. The congenital or acquired type of their anisometropia and its particular form were also studied. Each patient was submitted to a protocol comprising of a series of ophthalmologic and orthoptic tests so as to evaluate the patient's subjective far and near refraction, with measurement of phorias and of horizontal and vertical ductions, visual acuity, and the quality of binocular vision while looking in different directions. A preliminary trial of correction in actual situation was done in order to check fusion in near vision. The entire range of tests was repeated two months after the patient was provided with the lenses. The tolerance for progressive lenses during the different activities of daily life was evaluated after the second and the sixth months. RESULTS: Seven patients presenting an associated strabismus were not provided with the lenses because the initial pre-lens trial revealed a total inability to read within the near-vision zone. Among the 34 patients provided with the lenses, 21 constantly wore their progressive lenses and said that they were satisfied, 6 wore their progressive lenses during daily activities but preferred to use their unifocal lenses for prolonged reading, and 7 abandoned their progressive lenses because they could not tolerate them. Association with a strabismus is not synonymous with an initial impossibility or with abandonment because of the 27 patients who constantly wore their progressive lenses 9 were strabismic. The best results were obtained in the age range of 45 to 52 years old, for visual acuity for > 20/40, and in cases of congenital anisometropia with intermittent or permanent unilateral neutralization. On the other hand, patients presenting an acquired anisometropia, particularly postoperative, proved to be poor candidates. CONCLUSION: Weak and strong anisometropia does not absolutely preclude the prescription of progressive lenses except for certain strabismic subjects with an abnormal lateral-oriented posture.

Activities of Daily Living↗

PubMed2026

Longitudinal progression, metrics, age-dependence, and modifiers of ataxia severity in SCA27B: a multicentre study of 219 patients.

BACKGROUND: Spinocerebellar Ataxia 27B (SCA27B) is a novel, frequent and likely treatable late-onset autosomal-dominant ataxia caused by GAA repeat-expansions in FGF14. For understanding disease evolution and imminent trial planning, metrics of the most widely used clinical outcome assessment (Scale for the Assessment and Rating of Ataxia/SARA), longitudinal progression and modifiers thereof are warranted. METHODS: Multicentre intercontinental observational study (2015-2024) of 661 assessments from 219 patients with SCA27B (age: 68 ± 10 years; SARA: 9 ± 6 points) with item-level distribution-based analyses to characterise SARA metrics relative to ageing-related impairment in 390 healthy controls; and linear mixed-effects modelling to determine longitudinal progression and demographic or genetic modifiers. FINDINGS: Ataxia severity in SCA27B as assessed by SARA was primarily attributable to gait, stance, and lower-limb impairment; other ataxia domains scored ≤1 SARA point in 79-94% of patients. Discrimination of SCA27B motor performance from controls decreased with age due to ageing-related motor variability captured by SARA, thus limiting potential metric response windows for symptomatic treatments. Disease progression was faster in the presence of interfering ageing-related comorbidities in 14 (6%) patients. Overall longitudinal progression of SCA27B was 0.54 SARA points/year [95% CI: 0.37-0.71]. Expansions of (GAA)> 180 repeats were frequent also on the shorter allele (n = 18 (8%), range: 196-348 repeats), and associated with faster progression (+1.6 SARA points/year, [95% CI: 0.9-2.2]), including also otherwise less affected ataxia domains speech and sitting. INTERPRETATION: Disease progression in SCA27B is characterised by mild progression, ageing-related motor variabilities and comorbidities, and associated with repeat size on both alleles. FUNDING: Else-Kröner-Fresenius-Stiftung, EU, DFG, BMBF, CIHR, NAF, Ataxia-UK, CSC.

Humans↗

PubMed2001

Proteinuria as a modifiable risk factor for the progression of non-diabetic renal disease.

BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors reduce urine protein excretion and slow the progression of renal disease. The beneficial effect in slowing the progression of renal disease is greater in patients with higher urine protein excretion at the onset of treatment. We hypothesized that the greater beneficial effect of ACE inhibitors on the progression of renal disease in patients with higher baseline levels of proteinuria is due to their greater antiproteinuric effect in these patients. METHODS: Data were analyzed from 1860 patients enrolled in 11 randomized controlled trials comparing the effect of antihypertensive regimens, including ACE inhibitors to regimens not including ACE inhibitors on the progression of non-diabetic renal disease. Multivariable linear regression analysis was used to assess the relationship between the level of proteinuria at baseline and changes in urine protein excretion during follow-up. The Cox proportional hazards analysis was used to assess the relationship between changes in urine protein excretion during follow-up and the effect of ACE inhibitors on the time to doubling of baseline serum creatinine values or onset of end-stage renal disease. RESULTS: Mean (median) baseline urine protein excretion was 1.8 (0.94) g/day. Patients with higher baseline urine protein excretion values had a greater reduction in proteinuria during the follow-up in association with treatment with ACE inhibitors and in association with lowering systolic and diastolic blood pressures (interaction P < 0.001 for all). A higher level of urine protein excretion during follow-up (baseline minus change) was associated with a greater risk of progression [relative risk 5.56 (3.87 to 7.98) for each 1.0 g/day higher protein excretion]. After controlling for the current level of urine protein excretion, the beneficial effect of ACE inhibitors remained significant [relative risk for ACE inhibitors vs. control was 0.66 (0.52 to 0.83)], but there was no significant interaction between the beneficial effect of ACE inhibitors and the baseline level of urine protein excretion. CONCLUSIONS: The antiproteinuric effects of ACE inhibitors and lowering blood pressure are greater in patients with a higher baseline urine protein excretion. The greater beneficial effect of ACE inhibitors on renal disease progression in patients with higher baseline proteinuria can be explained by their greater antiproteinuric effects in these patients. The current level of urine protein excretion is a modifiable risk factor for the progression of non-diabetic renal disease. ACE inhibitors provide greater beneficial effect at all levels of current urine protein excretion.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2005

The natural history of primary progressive MS in British Columbia, Canada.

BACKGROUND: Primary progressive multiple sclerosis (PPMS) has a distinct clinical phenotype and has historically been understudied with few longitudinal natural history studies spanning a reasonable time period. The authors examined patient characteristics, disease progression, and associated risk factors in the PP population of British Columbia, Canada. METHOD: The authors report on the PP population from an upcoming publication of the natural history study of definite MS in British Columbia, Canada. The main outcome was sustained progression to Expanded Disability Status Scale (EDSS) 6, secondary outcome time to EDSS 8. Risk factors for progression included sex, onset age, onset symptoms, and for time to EDSS 8, time to EDSS 6. RESULTS: Of the 2,837 patients with definite MS in the original study, 352 (12.4%) had PPMS. Mean disease duration was 17.2 years (0.3 to 49.6 years), mean onset age was 40.1 years (SD 11.5), and 53% (187) were female. One-quarter of the population had reached EDSS 6 after 7.3 years from onset, yet another 25% still did not require a cane after 25 years. Sex, onset age, and onset symptoms did not predict progression (p > 0.05). A shorter time to EDSS 6 predicted a shorter time to EDSS 8 (p < 0.0005). DISCUSSION: Progression of disability was slower than found in previous primary progressive multiple sclerosis natural history studies. However, considerable variation existed, with few predictors, other than "sooner to cane, sooner to wheelchair."

Adult↗

PubMed2001

Final analysis of the European multicenter trial on IFNbeta-1b in secondary-progressive MS.

BACKGROUND: Based on a prospectively planned interim analysis, the European study of interferon beta-1b (IFNbeta-1b) provided evidence that the treatment delays neurologic deterioration in patients with secondary progressive MS (SPMS). The authors analyzed all data collected until closure of the double-blind study to further scrutinize the consistency of the findings. METHODS: The multicenter, double-blind, randomized, placebo-controlled trial treated patients for up to 36 months. The primary and all secondary endpoints of this study were evaluated using the data set at study termination, with a mean follow-up under double-blind conditions of 1054 +/- 199 and 1068 +/- 176 days for the placebo and IFNbeta-1b group. Alternative and more demanding definitions of disease progression were explored. Confirmed progression was analyzed in subgroups according to baseline demographics and baseline indicators of disease activity. RESULTS: Forty-eight of 358 placebo and 40 of 360 IFNbeta-1b-allocated patients were lost to follow-up. Time to confirmed 1.0-point Expanded Disability Status Scale (EDSS) progression for patients receiving IFNbeta-1b was delayed (p = 0.007). The proportion of patients with a confirmed 2.0-point EDSS progression was approximately 27% lower for the group treated with IFNbeta-1b, both including and excluding EDSS data collected during relapses. The proportion of patients with either progression or relapses decreased by nearly 30% in patients treated with IFNbeta-1b compared with placebo. Analysis of subgroups suggests that patients with higher prestudy disease activity (more than two relapses or EDSS progression by more than 1.0 point or both) seem to have a more pronounced treatment effect. CONCLUSION: Analysis of the data set at study termination including additional post hoc outcome measures is consistent with the original findings, thus supporting the conclusion that treatment with IFNbeta-1b is effective in patients with SPMS fulfilling the inclusion criteria of this study.

Adjuvants, Immunologic↗

PubMed1996

Significant progression of white matter lesions and small deep (lacunar) infarcts in patients with stroke.

OBJECTIVE: To investigate whether the extent of white matter lesions (WMLs) and the number of small deep infarcts and territorial infarcts progress over time in patients with stroke and to test the hypothesis that WMLs are associated with small deep infarcts. DESIGN: Computed tomographic follow-up study in a cohort of 107 patients with ischemic stroke (median follow-up, 3.0 years). SETTING: Primary and referral care center. PATIENTS: Sixty-three of 144 registered patients with a first-ever symptomatic lacunar stroke and 44 of 155 with a territorial stroke entered this study. Forty-seven (33%) of the nonparticipating patients with a lacunar stroke and 54 (35%) of those with a territorial stroke died, and 34 (24%) and 57 (37), respectively, refused computed tomographic follow-up. MAIN OUTCOME MEASURES: The extent of the WMLs and the number of small deep and territorial infarcts on computed tomographic scans at study entry and at follow-up. RESULTS: Progression of WMLs occurred in 26 patients (26%), and multivariate regression analysis showed that it was associated with symptomatic lacunar stroke at study entry (adjusted odds ratio [aOR], 5.0; 95% confidence interval [CI], 1.2-20.3), silent small deep infarcts at study entry (aOR, 6.0, 95% CI, 1.0-34.6), old age (aOR, 5.5; 95% CI, 1.3-23.1), and longer follow-up (aOR, 12.7; 95% CI, 1.8-89.0). We found progression of small deep infarcts in 41 patients (38%). The progression was associated with symptomatic lacunar stroke at study entry (aOR, 27.7; 95% CI, 6.3-120.9) and longer follow-up (aOR, 7.7; 95% CI, 1.4-41.3). Progression of both WMLs and small deep infarcts, which occurred in 16 patients (16%), was associated with symptomatic lacunar stroke at study entry (aOR, 34.1; 95% CI, 2.5-471.7), silent small deep infarcts at study entry (aOR, 12.5; 95% CI, 1.4-112.0), and longer follow-up (aOR, 29.7; 95% CI, 1.8-501.0). The number of territorial infarcts increased in 14 patients (13%). The increase was associated with symptomatic territorial stroke at study entry (aOR, 7.9; 95% CI, 1.5-40.8) and a history of ischemic heart disease (aOR, 6.6; 95% CI, 1.3-34.8). CONCLUSIONS: The marked progression of WMLs and small deep infarcts that occurred mainly in patients with lacunar stroke suggests that both WMLs and small deep (lacunar) infarcts are caused by a similar vasculopathy that affects small vessels, which is progressive despite standard stroke treatment.

Adult↗

PubMed2002

The natural history of the syndrome of primary progressive freezing gait.

BACKGROUND: Primary progressive freezing gait disorder is considered to be a distinct clinical entity that manifests predominantly as a progressive freezing gait disorder without accompanying abnormalities. However, confusion remains about its clinical presentation, natural history, and classification. OBJECTIVE: To examine the natural history, clinical and brain imaging characteristics, and response to dopaminergic medications of primary progressive freezing gait (PPFG) disorder. DESIGN/METHODS: Review of medical records, videotape examinations, and computed tomographic and magnetic resonance imaging of the brain and results of neurological evaluations, including the Unified Parkinson's Disease Rating Scale, in patients with PPFG. RESULTS: Thirty patients (16 male) were diagnosed as having PPFG (mean age at onset, 72.2 years; mean duration of disease, 5 years). Gait disorder was the initial complaint in 27 patients. Freezing gait was the initial manifestation in 18 and was present within the first year in 27. Natural history included 25 patients falling within 3 years of onset, 20 experiencing retropulsion within 4 years, and 16 requiring wheelchairs by 5 years. On neurological examination, bradykinesia was present in 29 patients, muscle rigidity in 15, and postural tremor in 11. Other features included speech abnormalities in 10, hyperreflexia without clonus in 17, and dementia in 8. Extraocular movement abnormalities and dysphagia were rare. All 30 patients were treated with levodopa with minimal effect. Eighteen were treated with a dopamine agonist with no notable effect. Of the 23 patients with magnetic resonance imaging scans, results were normal in 9 and included minor nonspecific changes in 14. The computed tomographic scans obtained in 12 patients showed similar results. One patient underwent fluorine F ((18)F) labeled deoxyglucose positron emission tomography, which showed mild reduction in medial frontal glucose metabolism. CONCLUSIONS: Primary progressive freezing gait appears to be a clinically distinct progressive neurological disorder that primarily affects gait, initially resulting in freezing and later in postural instability. A wheelchair-bound state often develops within 5 years. It is accompanied by other parkinsonian features, particularly bradykinesia, but is unresponsive to dopaminergic medications. It progresses in a fairly stereotyped manner. Primary progressive freezing gait disorder should be a unifying term for this disorder that has gone by many names in the literature and should be classified as a Parkinson-plus disorder.

Aged↗

PubMed2007

Qualitative estimates of medial temporal atrophy as a predictor of progression from mild cognitive impairment to dementia.

BACKGROUND: Individuals diagnosed as having mild cognitive impairment (MCI) have a high likelihood of progressing to dementia within 3 to 5 years, but not all individuals with MCI progress to dementia. Prognostic uncertainty suggests the need for additional measures to assist the clinician. OBJECTIVE: To assess the added value of qualitative measures of medial temporal atrophy (MTA) to estimate the relative risk of progressing from MCI to dementia. DESIGN: A 3-year, double-blind, placebo-controlled Alzheimer's Disease Cooperative Study initially designed to evaluate the efficacy of donepezil hydrochloride or vitamin E vs placebo to delay progression of MCI to dementia. SETTING: Memory assessment centers. PATIENTS: A total of 190 individuals with MCI. MAIN OUTCOME MEASURES: Ratings of MTA performed using magnetic resonance images obtained at baseline. Log-rank tests and Cox proportional hazards ratios examining the significance of MTA estimates in predicting progression of MCI to dementia. RESULTS: A mean MTA score greater than 2.0 was associated with a greater than 2-fold increased likelihood of progression to dementia during the observation period (hazards ratio, 2.30; 95% confidence interval, 1.09-4.92; P = .03) after controlling for age, education, sex, and baseline Mini-Mental State Examination score. CONCLUSIONS: Adjusted estimates of MTA were associated with significantly increased risk of developing dementia within 3 years, suggesting that obtaining a magnetic resonance image during the evaluation of MCI may offer additional independent information about the risk of progression to dementia. Given the relatively high prevalence of MCI in the general population, use of this method as part of routine clinical evaluation may help identify individuals who might benefit from increased surveillance and future treatment. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00000173.

Aged↗

PubMed1999

Methodological variations in estimating apparent progressive visual field loss in clinical trials of glaucoma treatment.

OBJECTIVES: To compare methods to estimate the incidence of visual field progression used by 3 large randomized trials of glaucoma treatment by applying these methods to a common data set of annually obtained visual field measurements of patients with glaucoma followed up for an average of 6 years. METHODS: The methods used by the Advanced Glaucoma Intervention Study (AGIS), the Collaborative Initial Glaucoma Treatment Study (CIGTS), and the Early Manifest Glaucoma Treatment study (EMGT) were applied to 67 eyes of 56 patients with glaucoma enrolled in a 10-year natural history study of glaucoma using Program 30-2 of the Humphrey Field Analyzer (Humphrey Instruments, San Leandro, Calif). The incidence of apparent visual field progression was estimated for each method. Extent of agreement between the methods was calculated, and time to apparent progression was compared. RESULTS: The proportion of patients progressing was 11%, 22%, and 23% with AGIS, CIGTS, and EMGT methods, respectively. Clinical assessment identified 23% of patients who progressed, but only half of these were also identified by CIGTS or EMGT methods. The CIGTS and the EMGT had comparable incidence rates, but only half of those identified by 1 method were also identified by the other. CONCLUSIONS: The EMGT and CIGTS methods produced rates of apparent progression that were twice those of the AGIS method. Although EMGT, CIGTS, and clinical assessment rates were comparable, they did not identify the same patients as having had field progression.

Disease Progression↗

PubMed2001

Clinical factors associated with progression of glaucomatous optic disc damage in treated patients.

BACKGROUND: Reducing intraocular pressure (IOP) in glaucomatous eyes does not always prevent disease progression. OBJECTIVE: To determine the clinical factors associated with progressive optic disc damage in glaucomatous eyes receiving treatment to reduce IOP. METHODS: Baseline and follow-up optic disc photographs as well as demographic and clinical data were retrospectively studied in 186 eyes of 93 patients with primary open-angle glaucoma, and in 138 eyes of 69 patients with normal-pressure glaucoma. The patients with primary open-angle glaucoma were included in the study only if their treated IOPs during a follow-up period of 5 years were less than 21 mm Hg. The patients with normal-pressure glaucoma were included only if their IOPs were reduced by at least 20% during the follow-up period. The association of progressive optic disc damage with patient- and eye-specific characteristics was examined using multivariate analysis. RESULTS: During the 5-year study period, 141 (43.5%) of the 324 eyes exhibited progressive optic disc damage defined by at least a 5% decrease in the neural rim area-to-disc area ratio. Using multivariate analysis, the following were found to be strongly associated with progressive neural rim damage: a baseline smaller neural rim area-disc area ratio (P<.001); a baseline larger zone beta area-disc area ratio (P =.04); a baseline larger parapapillary atrophy length-disc circumference ratio (P =.05); a diagnosis of normal-pressure glaucoma (P =.01); and combined medical and surgical treatment prior to the study period (P =.01). CONCLUSIONS: Clinical factors other than IOP may be important indicators of subsequent progression of glaucomatous optic disc damage. Our findings suggest that eyes with advanced glaucomatous optic disc damage and normal-pressure glaucoma are more likely to progress despite receiving treatment to reduce IOP.

Aged↗

PubMed2006

Six-year progression of retinopathy and associated risk factors in African American patients with type 1 diabetes mellitus: the New Jersey 725.

OBJECTIVE: To report the 6-year progression of diabetic retinopathy (DR) and associated risk factors among African American patients with type 1 (insulin-dependent) diabetes mellitus. METHODS: Participants from the New Jersey 725 included 483 African American patients with type 1 diabetes who underwent reexamination as part of a 6-year follow-up. Evaluations included a structured clinical interview, ocular examination, 7 stereoscopic fundus photographs, and blood pressure measurements. Severity of DR was determined via masked grading of fundus photographs. Biological evaluation included blood and urine assays. RESULTS: During the 6-year period, 56.1% of patients at risk showed progression of DR; 15.0% showed progression to proliferative DR; and 15.9% developed macular edema. A baseline high glycosylated hemoglobin level and systemic hypertension were significant risk factors for progression of DR, progression to proliferative DR, and incidence of macular edema. Progression to proliferative DR was significantly associated with baseline older age, renal disease, and severity of DR. The incidence of macular edema was significantly associated with baseline older age, low socioeconomic status, severity of DR, and total serum cholesterol level. CONCLUSIONS: Six-year progression of DR is high in African American patients with type 1 diabetes. Improving glycemic and blood pressure control may reduce the ocular morbidity of diabetes in African Americans.

Adolescent↗

PubMed1995

Early progression of ophthalmoplegia in patients with ischemic oculomotor nerve palsies.

OBJECTIVE: To describe the frequency and clinical correlates of early progression of ophthalmoplegia in patients with ischemic oculomotor nerve palsies. DESIGN: Cohort survey, case series. SETTING: Multispecialty clinic providing primary, secondary, and tertiary care in central and northern Wisconsin. PATIENTS: Sixteen patients evaluated within 1 week of the reported onset of ischemic oculomotor nerve palsy were identified and followed up prospectively using a standardized ophthalmoplegia grading scheme. All patients were followed up serially until their ophthalmoplegia resolved. MAIN OUTCOME MEASURES: Descriptive analysis of the temporal course of ophthalmoplegia and frequency of progression of deficits. Comparison between the group that had progression of ophthalmoplegia with the group that did not for age, hematocrit, cholesterol level, and adiposity; presence of diabetes, hypertension, hypercholesterolemia, and coronary artery disease; history of stroke; and tobacco use. RESULTS: Eleven (69%) of 16 patients had progression of ophthalmoplegia. The median time between reported onset and peak severity of ophthalmoplegia was 10 days. The only important difference between the progressive and nonprogressive groups was a shorter time to resolution of ophthalmoplegia for the nonprogressive group. CONCLUSIONS: Early progression of ophthalmoplegia occurs often in patients with ischemic oculomotor nerve palsies. The power to find differences between progressive and nonprogressive groups was limited by the small number of patients available for analysis.

Aged↗

PubMed1997

Parapapillary chorioretinal atrophy in patients with ocular hypertension. II. An evaluation of progressive changes.

OBJECTIVE: To determine whether parapapillary chorioretinal atrophy in patients with ocular hypertension remained stationary or progressed along with glaucomatous optic nerve damage. METHODS: The morphometric parameters and progression of parapapillary atrophy were retrospectively investigated, using serial photographs, in 350 eyes of 175 patients with ocular hypertension. The association of parapapillary atrophy progression with subsequent glaucomatous conversion and with other baseline patient- and eye-specific characteristics was analyzed. RESULTS: Progression in the area and extension of parapapillary atrophy before noticeable optic disc or visual field changes was observed in 48 (49.0%) of 98 eyes that converted to glaucoma, while parapapillary atrophy progression was noted in 25 (9.9%) of 252 ocular hypertensive eyes that did not develop glaucomatous damage (P<.001). The predictive sensitivity and specificity of this observation were 49% and 90%, respectively. In a logistic multiple regression model, the progression of parapapillary atrophy was associated with a family history of glaucoma (odds ratio, 2.7) and the initial size of zone beta (odds ratio, 1.64, for an increase of 0.10 of the zone beta area-disc area ratio). CONCLUSION: The progression of parapapillary chorioretinal atrophy may be an early glaucomatous finding in some patients with ocular hypertension.

Choroid↗

PubMed2005

Molecular profiling of tumor progression in head and neck cancer.

OBJECTIVE: To assess gene expression changes associated with tumor progression in patients with squamous cell carcinoma of the oral cavity. DESIGN: A microarray containing 17 840 complementary DNA clones was used to measure gene expression changes associated with tumor progression in 9 patients with squamous cell carcinoma of the oral cavity. Samples were taken for analysis from the primary tumor, nodal metastasis, and "normal" mucosa from the patients' oral cavity. SETTING: Tertiary care facility. Patients Nine patients with stage III or stage IV untreated oral cavity squamous cell carcinoma. RESULTS: Our analysis to categorize genes based on their expression patterns has identified 140 genes that consistently increased in expression during progression from normal tissue to invasive tumor and subsequently to metastatic node (in at least 4 of the 9 cases studied). A similar list of 94 genes has been identified that decreased in expression during tumor progression and metastasis. We validated this gene discovery approach by selecting moesin (a member of the ezrin/radixin/moesin [ERM] family of cytoskeletal proteins) and one of the genes that consistently increased in expression during tumor progression for subsequent immunohistochemical analysis using a head and neck squamous cell carcinoma tissue array. CONCLUSION: A distinct pattern of gene expression, with progressive up- or down-regulation of expression, is found during the progression from histologically normal tissue to primary carcinoma and to nodal metastasis.

Carcinoma, Squamous Cell↗

PubMed2026

Prognostic Value of Blood-Based P-Tau217 Levels for Progression to Cognitive Impairment.

IMPORTANCE: Blood-based biomarkers for Alzheimer disease, particularly plasma phosphorylated tau 217 (p-tau217), accurately reflect early Alzheimer disease brain pathology in cognitively unimpaired individuals, but estimates of absolute risk of progression to cognitive impairment across multiple cohorts are needed. OBJECTIVE: To estimate absolute risk of progression to cognitive impairment and rates of cognitive decline based on plasma p-tau217 across cognitively unimpaired older adults. DESIGN, SETTING, AND PARTICIPANTS: Longitudinal cohort study using harmonized data from 2684 cognitively unimpaired older adults (defined within cohort) across 6 observational and clinical trial cohorts based in North America, Japan, and Australia. The earliest enrollment was in 2004, with most recent follow-up in 2025. EXPOSURE: Baseline plasma p-tau217. MAIN OUTCOMES AND MEASURES: The primary outcome was time to progression to cognitive impairment (mild cognitive impairment, dementia, or 2 consecutive global Clinical Dementia Rating scores ≥0.5). The secondary outcome was longitudinal change on the latent Preclinical Alzheimer Cognitive Composite (PACC; higher values indicate better performance). RESULTS: Among the 2684 participants (median [IQR] age, 69.6 [66.2-74.2] years; 1697 [63%] female), there were 478 events of progression to cognitive impairment over a median follow-up of 5.4 years (maximum follow-up of 13.5 years). Each 1-SD increase in baseline p-tau217 level was associated with an increased risk of progression to cognitive impairment (hazard ratio, 1.38 [95% CI, 1.30-1.46]), and the association remained significant after adjustment, including β-amyloid positron emission tomography scan Centiloids (hazard ratio, 1.32 [95% CI, 1.24-1.41]). Participants with high (1.1-2.4 SD) and very high (>2.5 SD) baseline p-tau217 had 24% (95% CI, 20%-28%) and 38% (95% CI, 33%-43%) absolute risk of progression over 5 years, respectively, and risk was markedly higher over 10 years, although longer-term estimates were constrained by limited data. Elevated p-tau217 was also associated with faster cognitive decline based on change in latent PACC score. Among the overall sample, baseline latent PACC scores ranged from -0.8 to 2.7. The 5-year annualized decline for the very high p-tau217 group was -0.07 latent PACC units/y (95% CI, -0.10 to -0.05), relative to 0.03 units/y (95% CI, 0.02-0.04) in the low p-tau217 group. CONCLUSIONS AND RELEVANCE: In a pooled sample of multiple selected cohorts of cognitively unimpaired older adults, higher plasma p-tau217 levels were consistently associated with increased risk of clinical progression and accelerated cognitive decline. By providing time-specific absolute risk estimates, these findings support the potential of p-tau217 for prognostic model development, with direct implications for future trial design. Further validation in unselected populations is needed to inform individual prognosis and clinical decision-making in cognitively unimpaired individuals.

Aged↗

PubMed2004

Effect of intensive compared with moderate lipid-lowering therapy on progression of coronary atherosclerosis: a randomized controlled trial.

CONTEXT: Statin drugs reduce both atherogenic lipoproteins and cardiovascular morbidity and mortality. However, the optimal strategy and target level for lipid reduction remain uncertain. OBJECTIVE: To compare the effect of regimens designed to produce intensive lipid lowering or moderate lipid lowering on coronary artery atheroma burden and progression. DESIGN, SETTING, AND PATIENTS: Double-blind, randomized active control multicenter trial (Reversal of Atherosclerosis with Aggressive Lipid Lowering [REVERSAL]) performed at 34 community and tertiary care centers in the United States comparing the effects of 2 different statins administered for 18 months. Intravascular ultrasound was used to measure progression of atherosclerosis. Between June 1999 and September 2001, 654 patients were randomized and received study drug; 502 had evaluable intravascular ultrasound examinations at baseline and after 18 months of treatment. INTERVENTIONS: Patients were randomly assigned to receive a moderate lipid-lowering regimen consisting of 40 mg of pravastatin or an intensive lipid-lowering regimen consisting of 80 mg of atorvastatin. MAIN OUTCOME MEASURES: The primary efficacy parameter was the percentage change in atheroma volume (follow-up minus baseline). RESULTS: Baseline low-density lipoprotein cholesterol level (mean, 150.2 mg/dL [3.89 mmol/L] in both treatment groups) was reduced to 110 mg/dL (2.85 mmol/L) in the pravastatin group and to 79 mg/dL (2.05 mmol/L) in the atorvastatin group (P<.001). C-reactive protein decreased 5.2% with pravastatin and 36.4% with atorvastatin (P<.001). The primary end point (percentage change in atheroma volume) showed a significantly lower progression rate in the atorvastatin (intensive) group (P =.02). Similar differences between groups were observed for secondary efficacy parameters, including change in total atheroma volume (P =.02), change in percentage atheroma volume (P<.001), and change in atheroma volume in the most severely diseased 10-mm vessel subsegment (P<.01). For the primary end point, progression of coronary atherosclerosis occurred in the pravastatin group (2.7%; 95% confidence interval [CI], 0.2% to 4.7%; P =.001) compared with baseline. Progression did not occur in the atorvastatin group (-0.4%; CI -2.4% to 1.5%; P =.98) compared with baseline. CONCLUSIONS: For patients with coronary heart disease, intensive lipid-lowering treatment with atorvastatin reduced progression of coronary atherosclerosis compared with pravastatin. Compared with baseline values, patients treated with atorvastatin had no change in atheroma burden, whereas patients treated with pravastatin showed progression of coronary atherosclerosis. These differences may be related to the greater reduction in atherogenic lipoproteins and C- reactive protein in patients treated with atorvastatin.

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