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Relationship of age and biomedical risk factors to progression of coronary artery disease.

The relationship between age, biomedical risk factors and the progression of occlusive disease of the coronary arteries was studied in 176 patients (age range, 27-66 years) who had undergone at least two cine angiograms. The biomedical risk factors of interest were serum concentrations of cholesterol and triglycerides, smoking, hypertension, diabetes mellitus, family history of coronary disease, electrocardiographic abnormalities, obesity, and age. The findings did not reveal any significant differences in mean lipid levels between patients showing progression of disease and those who did not. However, the distribution of serum cholesterol values indicated more hypercholesterolemic patients among the disease-progression group, and more patients with ideal cholesterol levels among the no-progression group. The other biomedical variables did not appear to be related to the progression of coronary disease. Among the older patients, hypercholesterolemia and diabetes mellitus were related to disease progression. Among the younger patients, smoking was related to progression.

Adult

Respiratory frequency response to progressive isocapnic hypoxia.

1. Ventilatory, tidal volume and frequency responses to progressive isocapnic hypoxia have been measured in twenty-nine healthy subjects by a rebreathing technique. 2. A strong correlation was found between ventilatory response to hypoxia (deltaVI/DELTASaO2) and frequency response to hypoxia (deltaf/deltaSaO2) (r=0-82, P less than 0-001). There was a lesser correlation between deltaV1/deltaSaO2 and tidal volume response (deltaVT/deltaSaO2) (r=0-50, P less than 0-01). These findings suggest that the wide range of ventilatory response to hypoxia among subjects is mainly determined by differences in frequency response and contrast with previous findings in studies of the response to progressive hypercapnia. 3. The breathing pattern during progressive hypoxia and hypercapnia was compared in ten subjects. Ventilation/tidal volume plots were constructed and patterns of response were further analysed in terms of inspiratory duration (TI), expiratory duration (TE) and mean inspiratory flow rate (VI). 4. Increments in ventilation during hypoxia were achieved with a greater respiratory frequency and a smaller tidal volume than during hypercapnia in eight of the ten subjects studied. In two subjects no difference in breathing pattern during hypoxia and hypercapnia was observed. 5. Changes in respiratory frequency during progressive hypoxia were achieved in all subjects by a progressive shortening of TI and TE. By contrast, TI remained constant during hypercapnia until VT had increased to 3-5 times the eupnoeic value; during hypercapnia the increase in frequency was achieved mainly by a progressive shortening of TE. 6. It is concluded that different mechanisms may be involved in altering respiratory frequency when ventilation is driven progressively by these different chemical stimuli.

Carbon Dioxide

Progression from minimal or focal to diffuse proliferative lupus nephritis.

Histologic classification of renal glomerular lesions in 46 patients with systemic lupus erythematosus revealed 17 as having either focal proliferative (10 patients) or minimal mesangial proliferative (7 patients) glomerulonephritis. Six of the 17 have progressed to a diffuse proliferative glomerular lesion on subsequent renal biopsies, 9 months to 5 years later. Five had clinical deterioration at the time of follow-up biopsies; currently one is undergoing hemodialysis and four others have decreased renal function. Although a comparison of those who progressed with those who are stable revealed greater proteinuria in some of those who progressed, no other clinical features of the initial illness were different in the two groups, nor were differences between the two groups noted on light microscopic examination of initial renal biopsies. However, ultrastructurally, electron-dense deposits, especially those subendothelial in location, were noted along glomerular capillary basement membranes more frequently and in greater number in those who progressed. These findings suggest that lupus patients with a mild proliferative glomerulonephritis may have clinical and histologic progression of the renal disease, and those who progress cannot be clearly defined by clinical or light microscopic features. Ultrastructural demonstration of subendotheial deposits suggests a greater likelihood of subsequent progressive disease.

Adolescent

[Heridity of progressive chronic polyarthritis - study of the course].

In an analytic epidemiological study 30 relations of patients with progressive chronic polyarthritis with positive rheumatoid factor and 127 relations with negative rheumatoid factor were after-examined concerning their clinical and serological behaviour 6 years after the primary recognition with the aim of an evidence concerning the hypothesis of an hereditary causal factor in progressive chronic polyarthritis. It was revealed that only in 14 of 30 persons with positive primary rheumatoid factor the rheumatoid factor could further be proved, on the other hand 14 relations who had at first a negative rheumatoid factor now, however, reacted with a positive rheumatoid factor. It could be confirmed, that the seropositive forms of the progressive chronic polyarthritis have a stronger hereditary trend to the formation of the rheumatoid factor than the seronegativeones and that after the 50th year of life there exists a significant persistence of the seropositivity. In the group of relations who were seropositive 6 years ago developed a definitive and probable progressive chronic polyarthritis each as well as a further probable progressive chronic polyarthritis in the group of relations who became seropositive only in the period of observation. On account of the changing seropositivity and the only rare appearance of a progressive chronic polyarthritis on the basis of this investigation of hypothesis of the rheumatoid factor as first (premorbid) symptom of a progressive chronic polyarthritis is to be refused.

Adult

Effect of rapid glycemic control on progression of diabetic retinopathy.

The effect of the start of glycemic control on the progression of retinopathy was investigated by a case-control study. The changes in glycosylated hemoglobin (HbA1) were compared between a case group, diabetic cases showing progression of retinopathy (Group 1), and a control group, diabetic cases showing no progression of retinopathy (Groups 2-A and 2-B). Group 2-A was matched with Group 1 on the basis of the grade of retinopathy at the first examination and other clinical data. Group 2-B was matched with Group 1 in terms of HbA1 value and methods of control, but had no retinopathy or background retinopathy. The retrospective follow-up period for the three groups was 24 months. On the basis of the respective matching factors, Groups 1 and 2-A were divided into 9 blocks of homogeneous subjects, and Groups 1 and 2-B were similarly divided into 6 blocks. The resulting data was evaluated block by block, using the analysis of variance (ANOVA) and a conditional logistic regression analysis. In Group 1, the HbA1 value decreased rapidly 10-6 months before the progression of retinopathy, but the HbA1 value did not change in Groups 2-A and 2-B during the 24-month follow-up. The difference in the estimated mean HbA1 value between 10-9 months and 1-0 month before the progression of retinopathy was 2.46% greater in Group 1 than in Group 2-A, as determined by ANOVA. The relative risks of a 1, 2 and 3% increase in HbA1 value for 7-6 months were estimated as 1.6, 2.4 and 3.8, respectively, by conditional logistic regression analysis. These findings indicate that the decrease in HbA1 value during any 6-month period should be limited to less than 2% in order to prevent the progression of retinopathy. It is also evident that too rapid a decrease at the initiation of glycemic control could cause severe or transient exacerbation of the progression of retinopathy.

Analysis of Variance

NeuroOmics-Net: An interpretable multimodal deep learning framework for Alzheimer's disease diagnosis and progression prediction using neuroimaging, EEG, and genomic data.

Accurate diagnosis and progression prediction of Alzheimer's disease (AD) remain challenging due to the heterogeneous nature of the disease, which involves structural brain degeneration, electrophysiological dysfunction, and molecular dysregulation. Most existing deep learning approaches rely on a single modality or limited multimodal combinations, thereby failing to capture the complex cross-domain interactions underlying AD progression. Furthermore, the scarcity of large-scale datasets containing synchronized neuroimaging, electrophysiological, and genomic measurements restricts the development of comprehensive multimodal diagnostic systems. To address these challenges, this study proposes NeuroOmics-Net, a multimodal deep learning framework for Alzheimer's disease analysis that integrates structural magnetic resonance imaging (sMRI), electroencephalography (EEG), and gene expression data. The proposed framework combines a Hierarchical Multi-View Encoder (HME) for modality-specific feature extraction, a Cross-Omics Attention Fusion (CAF) module for adaptive integration of complementary biomarkers, and a Disease Progression Graph Learning (DPGL) module for modeling progression-related relationships across biological domains. To facilitate cross-modal integration from independent cohorts, Regularized Canonical Correlation Analysis (RCCA) is employed to align heterogeneous feature representations within a shared latent space. Experiments were conducted using publicly available datasets from ADNI, PhysioNet, and GEO repositories comprising 1120 diagnosis-aligned samples. The proposed framework achieved 94.3% classification accuracy and an AUC of 0.975 for distinguishing normal controls (NC), mild cognitive impairment (MCI), and Alzheimer's disease subjects, while attaining 93.7% accuracy for predicting conversion from stable mild cognitive impairment (sMCI) to progressive mild cognitive impairment (pMCI). However, a fairness sensitivity analysis using stratified demographic reweighting revealed accuracy ranging from 90.8% (low-education, high-comorbidity proxy subgroup) to 96.1% (low-risk, high-reserve proxy subgroup), a demographic parity gap of 5.3 percentage points, indicating that overall accuracy reflects a performance ceiling in a relatively homogeneous research cohort rather than a realistic estimate for demographically diverse clinical populations. Comparative evaluations demonstrated consistent improvements over state-of-the-art unimodal and multimodal deep learning models. Interpretability analysis further identified clinically relevant biomarkers, including hippocampal and entorhinal atrophy, theta-alpha EEG alterations, and APOE-associated molecular pathways. Because sMRI, EEG, and gene expression data were sourced from separate, unpaired cohorts with no subjects possessing all three synchronized measurements, all reported cross-modal associations reflect population-level statistical correspondence across diagnosis-matched groups rather than within-subject physiological coupling; no claim of intra-individual causal cross-modal interaction is made. These findings demonstrate that NeuroOmics-Net provides an effective computer-aided framework for multimodal biomedical data processing and Alzheimer's disease analysis. By integrating neuroimaging, electrophysiological, and genomic information, the proposed approach enables accurate diagnosis, progression prediction, and biologically interpretable decision support for clinical and translational applications.

Humans

Prognostic effect of serum glial fibrillary acidic protein and neurofilament light chain for predicting progression independent of relapse activity in multiple sclerosis: A systematic review.

BACKGROUND: Progression independent of relapse activity (PIRA) is increasingly appreciated as one of the important factors contributing to disability accumulation in MS. sGFAP and sNfL could represent markers reflecting two separate biological processes related to relapse-independent progression in MS. OBJECTIVE: To perform a systematic review of the literature on blood GFAP and/or NfL measured in relation to PIRA or other similar relapse-independent progression endpoints in people with MS. METHODS: PubMed, Scopus, and Web of Science databases were searched from inception to 1 June 2026. The eligible studies were original human studies measuring blood GFAP and/or NfL concentrations in serum, plasma, or any other type of blood-derived material and assessing PIRA, PIRMA, CDP/CDW without relapses, relapse-free EDSS progression, non-inflammatory progression, or comparable relapse-independent disability worsening outcomes. Methodological quality was assessed according to the Newcastle-Ottawa scale and the QUIPS instrument for bias detection in the body of evidence on prognostic factors. Due to heterogeneity of outcomes, biomarker measurements and effect estimates, results were synthesized qualitatively rather than quantitatively. RESULTS: After removing duplicates, 1206 records were screened, followed by full-text review of 120 reports. A total of 18 reports were included. Overall, sGFAP was associated more frequently with PIRA or PIRA-like disability progression, particularly in cohorts with suppressed or limited overt inflammatory activity. Evidence for sNfL was more variable and context-dependent: several studies reported associations with PIRA-like or relapse-independent disability worsening when acute inflammatory activity was absent, suppressed, or analytically separated, whereas other studies reported negative or inconclusive findings. Negative or inconclusive results were reported by several articles, particularly when broad outcomes were evaluated or the study population was small. CONCLUSION: Blood GFAP and NfL give complementary but non-interchangeable information concerning PIRA in MS patients. The existing evidence base does not allow us to perform meta-analysis because of heterogeneity in terms of outcomes, standardization of biomarkers, and treatment context. Further prospective investigations with uniform criteria will be necessary for their use as biomarkers of PIRA in clinical settings.

Humans

Clinicogenomic predictors of survival and intracranial progression after stereotactic radiosurgery for colorectal cancer brain metastases.

OBJECTIVE: Brain metastases (BM) from colorectal cancer (CRC) are associated with dismal prognosis. When BM-directed therapy is considered, better methods are needed to identify patients at risk of poor oncological outcomes in order to optimize patient selection for closer surveillance or escalated therapy. The authors sought to identify clinicogenomic predictors of survival and intracranial disease progression after CRC BM have been treated with stereotactic radiosurgery (SRS). METHODS: Patients with newly diagnosed CRC BM treated with SRS between 2009 and 2022 who had next-generation genomic sequencing data available were included. Frameless SRS was delivered in 1-5 fractions, alone or after neurosurgical resection. Outcomes included overall survival (OS) and intracranial progression (IP), evaluated per patient treated with SRS, and local progression (LP), evaluated per BM. Associations between baseline clinicogenomic features and outcomes were evaluated with Cox regression and competing risk regression, with death as a competing risk. RESULTS: This analysis included 123 patients with 299 BM. At BM diagnosis, 111 patients (90%) had progressive extracranial disease, and 79 patients (64%) had ≥ 3 sites of extracranial metastasis. The median (IQR) number of BM was 2 (1-3) per patient. The median (IQR) biologically effective dose (BED) was 51.3 (51.3-65.1) Gy, corresponding to a prescription of 27 Gy in 3 fractions. OS, IP, and LP estimates at 1 year after SRS were 36%, 55%, and 12%, respectively. OS was independently associated with progressive extracranial disease (HR 4.26, 95% CI 1.63-11.2, p = 0.003) and ≥ 3 extracranial metastatic sites (HR 1.84, 95% CI 1.12-3.01, p = 0.02). LP was less likely when BM received BED ≥ 51.3 Gy (HR 0.24, 95% CI 0.07-0.78, p = 0.02), independent of BM diameter (HR 1.21/cm, 95% CI 0.8-1.84, p = 0.4). IP was independently associated with genomic alterations; TP53 driver alterations were associated with higher risk of IP (HR 2.71, 95% CI 1.26-5.79, p = 0.01), whereas MYC pathway alterations were associated with lower risk (HR 0.15, 95% CI 0.03-0.68, p = 0.01). CONCLUSIONS: The authors identified clinicogenomic features associated with adverse outcomes after SRS for CRC BM. Progressive and extensive extracranial metastases predicted worse OS. Insufficient SRS doses predicted greater risk of LP. Wild-type TP53 and alterations in the MYC pathway were independently associated with lower risk of IP. Patients at high risk of IP may be considered for closer surveillance or escalated therapy.

Humans

An Integrative Proteomic Approach to Reveal Altered Signaling Modules During Alzheimer's Disease Progression in PS19 Tauopathy Mice.

Alzheimer's disease (AD) is a slowly progressive neurodegenerative disease that is characterized by cognitive, functional, and behavioral impairments. These changes occur owing to the progressive accumulation of extracellular amyloid-beta plaques and intracellular neurofibrillary tangles of hyperphosphorylated tau protein. AD is associated with the dysfunction of several essential neurotransmitter systems, such as dopamine, and impaired neurotransmission. Despite the association of neurotransmitter changes within the brain and AD pathology, in-depth profiling studies on neurotransmitters and their related proteomic changes are limited. This study was conducted to profile and integrate the proteomes and neurotransmitters in seven brain regions of PS19 (Tau P301S) mice according to AD progression between 4 and 7 months. Proteomic analysis revealed significantly altered canonical pathways in various brain regions, including metabolic abnormalities. In the neurotransmitter profile, we found significant alterations in the levels of six neurotransmitters-dopamine, serotonin, homovanillic acid, norepinephrine, 3-methoxytyramine, and 3,4-dihydroxyphenylacetic acid-during AD progression. Using an integrative approach between proteome and neurotransmitter profiles, we found that AD progression-dependent dopamine- and serotonin-related signaling modules are closely related to neurotransmitter changes, especially in the hippocampus and cerebellum. This integrative approach could provide new signaling modules to help understand AD progression and thereby enable improved treatment and clinical outcomes.

Animals

From genes to trajectories: mapping genetic influences on Huntington's disease progression.

MOTIVATION: There are many diseases with established genetic factors, such as Huntington's disease (HD), that are characterized by variable rates of progression. However, beyond the contribution of the known genetic factors - in this case the Huntingtin (HTT) gene - the impact of the full human genome on the natural progression of such diseases throughout a patient's life remains largely unknown. The increased availability of genome wide association (GWA) data in HD gene expansion carriers (HDGECs), combined with the clinical assessment scores on the same set of patients, has provided a perfect opportunity to assess the potentially broader genetic impact on the natural progression of HD. RESULTS: We present a genetics-driven, probabilistic disease progression model designed to identify and investigate the ways in which a range of genetic factors affect the natural progression of HD. When applied to a clinico-genomic HD dataset, our model identified several single nucleotide polymorphisms (SNPs) with previously unreported effects on disease progression that act at distinct stages and with varying magnitudes. This discovery may shed light on the potential mechanistic impact of previously unidentified genes on HD that may have implications for clinical management. As increasing amounts of GWA data become available more generally, we anticipate that this modeling framework will be broadly applicable to other diseases with strong genetic components. AVAILABILITY AND IMPLEMENTATION: The source code for IHDPM is available at https://github.com/BiomedSciAI/IHDPM.

Huntington Disease

Progressive cardiac phenotypes and reduced reversibility from long-term CUGexp RNA expression in a DM1 mouse model.

Myotonic dystrophy type 1 (DM1) is caused by an expanded CTG repeat in the DMPK gene, resulting in mutant transcripts that form expanded CUG (CUGexp) RNA foci and sequester muscleblind-like (MBNL) RNA-binding proteins. DM1 is multisystemic, with progressive worsening of disease manifestations in affected tissues. Disease progression is attributed to somatic expansion of the CTG repeats with age, resulting in production of CUGexp RNA with enhanced intrinsic toxicity due to increased MBNL sequestration. To determine the degree to which cardiac disease progression can occur independently of repeat expansion, we used a transgenic DM1 mouse model with inducible heart-specific expression of a stable, interrupted 960-CUG-repeat RNA. Sustained CUGexp RNA expression caused progressive cardiac enlargement, contractile dysfunction, conduction delay, myocardial fibrosis, and reduced survival, while MBNL-dependent splicing defects remained static, consistent with the stable repeat length. We also determined the degree of reversibility after different periods of CUGexp RNA expression by shutting off the repeat-containing transgene. Suppression of CUGexp RNA expression rescued cardiac abnormalities, but reversibility declined with longer exposure to the toxic RNA. These findings demonstrate that prolonged expression of stable CUGexp RNA drives progressive cardiac pathology, revealing a mechanism of disease progression in DM1 in addition to somatic expansion.

Animals

Multiomic study of cutaneous T-cell lymphoma reveals single-cell clonal evolution in progression and therapy resistance.

Cutaneous T-cell lymphoma (CTCL) remains a challenging disease due to its significant heterogeneity, therapy resistance, and relentless progression. Multiomics technologies offer the potential to provide uniquely precise views of disease progression and response to therapy. Here, we present a comprehensive multiomics view of CTCL clonal evolution, incorporating exome, whole-genome, epigenome, bulk, single-cell T-cell receptor, and single-cell RNA sequencing of 99 clinically annotated serial skin, peripheral blood, and lymph node samples from 34 patients with CTCL. We leveraged this extensive data set to define the molecular underpinnings of CTCL progression in individual patients at single-cell resolution with the goal of identifying clinically useful biomarkers and therapeutic targets. Our studies identified recurrent progression-associated clonal genomic alterations; we highlight mutation of CCR4, phosphoinositide 3-kinase inhibitor signaling, and programmed cell death protein 1 (PD-1) checkpoint pathways as evasion tactics deployed by malignant T cells. We identified a gain-of-function mutation in STAT3 (D661Y) and demonstrated, using cleavage under targets and release using nuclease (CUT&RUN) and RNA sequencing, that it enhances binding to and transcription of genes in Rho GTPase pathways. With our previous work implicating this pathway in histone deacetylase inhibitor-resistant CTCL, these data provide further support for a previously unrecognized role for Rho GTPase pathway dysregulation in CTCL progression. Recurrent progression-associated mutations were common in the epigenetic modifier EZH2, suggesting that EZH2 inhibition may benefit patients with CTCL. Our findings support an approach in which genomic analysis is widely used for improved disease monitoring, biomarker-informed clinical trial design, and genome-guided therapeutic decision-making. Moreover, these molecular changes present new opportunities for therapeutic targeting in this challenging and incurable cancer.

Multiomics

Targeting super-enhancer-driven SKIL transcription by CDK7 inhibitor THZ1 to suppress gastric cancer progression.

BACKGROUND: Gastric cancer (GC) is a lethal malignancy characterized by high incidence, mortality, and limited treatment options. Transcriptional addiction is a key cancer hallmark that drives tumor pathogenesis, making its inhibition a promising therapeutic strategy for GC. The study aims to investigate the roles and mechanisms of super-enhancer (SE)-driven oncogenic transcriptional addiction in GC progression and to identify novel targetable vulnerabilities. METHODS: We utilized cellular and animal models to assess the effects of THZ1 treatment and CDK7 knockdown on GC progression. RNA sequencing was employed to elucidate the potential molecular mechanism of THZ1 treatment. ChIP-seq was performed to establish SE landscape in GC. Integrative analysis of transcriptomic and SE profiling was used to identify THZ1-targeted oncogenic genes. Rescue experiments were conducted to confirm that THZ1 treatment suppresses GC malignant progression by targeting SE-driven SKIL transcription. RESULTS: GC cells exhibited pronounced sensitivity to THZ1 compared to normal gastric mucosa cells, and the treatment potently suppressed tumor growth and migration in both cellular and animal models. CDK7 was significantly upregulated in GC tissues, and its knockdown inhibited malignant progression in vitro and in vivo, whereas its overexpression accelerated tumor progression. Mechanistically, SE-driven oncogenic transcriptional amplification underlies GC cell susceptibility to THZ1, supported by the identification of novel oncogenic genes such as SKIL. SKIL, a key Hippo pathway regulator, was highly expressed in GC cells, and its elevated expression predicted poor patient prognosis. SKIL silencing attenuated malignant phenotypes, while its overexpression diminished THZ1’s suppression of GC cell proliferation and migration. CONCLUSION: Our findings demonstrate that THZ1 inhibits GC progression by disrupting SE-driven oncogenic transcription, thereby offering CDK7 inhibition as a promising therapeutic intervention for GC.

Stomach Neoplasms

Alpha 1-antitrypsin activity of perilymph. Occurrence during progression of otospongiosis.

Previous studies by the Adams method demonstrated a strong correlation between hydrolytic enzyme activity of perilymph and progression of bone conduction loss two years preceding stapedectomy. Alpha 1-Antitrypsin was chosen since its activity can be very precisely measured by a radical immunodiffusion technique and since it is one of the enzymes identified in perilymph of patients with active otospongiosis. Samples of 3 mul to 5 mul of perilymph removed during 103 stapedectomies and samples of known alpha 1-trypsin activity were placed on slides coated with alpha 1-antitrypsin serum. The zone of diffusion was stained and measured after 38 hours of incubation. Antitrypsin values were lowest in 24 cases, two with no preoperative bone conduction progression, three with moderate progression of 10 to 15 dB, and 19 with rapid progression of more than 20 dB. They were highest in 36 cases with no progression, and in one case with moderate progression. This study confirms previous reports on the enzymatic activity in otospongiotic disease.

Humans

Inflammatory cells in solid murine neoplasms. II. Cell types found throughout the course of Moloney sarcoma regression or progression.

Regressing and progressing Moloney sarcomas, induced in BALB/c mice by the injection of cultured sarcoma cells (MSC)1, were sampled for histologic analysis and then disaggregated using mixtures of trypsin, collagenase and DNAse or collagenase and DNAse alone. The types of inflammatory cells (IC) found in resultant cell suspensions were determined 6, 11, 14 and 18 days post inoculation. Inflammatory infiltrates were composed almost exclusively of three cell types; neutrophils, T lymphocytes and macrophages. The extent to which each was found in tumors was related to the time post inoculation. Neutrophils were part of an early acute inflammatory response seen in both developing regressing and progressing sarcomas. The onset of regression was associated histologically with the appearance within tumors of a mononuclear inflammatory infiltrate. T lymphocytes and macrophages were the principal constituents. A higher percentage of T lymphocytes was recovered at all sampling times from regressing, compared to progressing, sarcomas. During development of the mononuclear inflammatory infiltrate there were relatively more large T cells in regressing, than in progressing tumors, and the percentage of macrophages was higher. Thereafter, the proportion of macrophages in the recovered cell population was approximately the same for both types of tumor. Such equality was more apparent than real, however, since IC were restricted to the peripheries of progressing sarcomas after the acute inflammatory phase, but continued to be found throughout regressing neoplasms. The effective ratio of macrophages and T lymphocytes to tumor cells therefore was much lower in progressing sarcomas than was suggested by percentage figures. The data presented support the concept that T lymphocytes are instrumental in causing the regression of Moloney sarcomas, possibly through interactions with macrophages.

Animals

Critical review of the models to study the biologic progression of bladder cancer.

For transitional cell carcinoma of the bladder, clinical data indicate that invasive, metastatic tumors can arise through at least two different progression pathways. The majority of invasive, metastatic bladder neoplasms clinically present de novo, i.e., the patients have no history of malignant bladder disease. This implies that the highly malignant tumor cells either arise de novo or have undergone a rapid progression. Alternatively, a considerable fraction of patients with superficial bladder cancer process to invasive disease after a history of relatively benign superficial TCC. The molecular and cell biological basis of tumor progression is only poorly understood. Clearly, a better understanding of this progress could have profound clinical implications, since patients with superficial TCC with a high risk for progression would have to be treated more aggressively. We discuss the problems that are associated with tumor biological studies on early steps in the progression of TCC, especially from a "model system point of view."

Animals

Enhanced rate of progression of coronary artery disease following aortocoronary saphenous vein bypass surgery.

To evaluate the fate of the boronary arteries after aortocoronary bypass, 40 patients underwent serial selective coronary angiographic studies 1 year apart, and the frequency of progression of coronary artery disease was estimated. Thirty-two had saphenous vein bypass surgery after the first procedure, six had Vineberg operations, and two had no interim operation. In each patient, the right, left, anterior descending and circumflex coronary arteries (including their branches) were separately evaluated. Progressive narrowing was evident in 31 of 50 (62 per cent) bypassed vessels and in only 11 to 113 (9.7 per cent) nonbypassed arteries (p less than 0.001). Coronary arteries with moderate to severe obstruction initially (50 to 99 per cent occluded) manifested progressive diseasee more frequently (33 of 70 arteries) than did arteries that were normal or mildly narrowed initially (4 of 71) (p less than 0.001. Considering only those vessels with 50 to 99 per cent obstruction initially, 27 of 35 (77 per cent) of the bypassed arteries and only 6 of 35 (17 per cent) of the nonbypassed arteries showed progression (p less than 0.001). We conclude that moderately or severely narrowed coronary arteries are more likely to show progressive narrowing than normal or mildly obstructed ones and that progression of coronary disease is greater in bypassed vessels than in nonbypassed vessels. In view of potential graft closure, the implications of these findings must be considered in selecting patients for aortocoronary bypass.

Cineangiography

Interaction between verbal and gestural language in progressive aphasia: a longitudinal case study.

The objective of this longitudinal study is to investigate the on-line interaction between praxis and linguistic abilities in a progressive aphasia case. During 3 years of evolution, procedural discourse of a progressive aphasic patient was videotaped five times, allowing us to analyze the progression of both language and gestural production as well as the interaction between these two. We anticipated that, in the absence of apraxia, the patient would compensate for her speech deficit by producing progressively more and more meaningful gestures. Our compensatory hypothesis was confirmed but the compensation was not as efficient as one would expect given the absence of apraxia. With the progression of the speech deficit, the patient could not replace some verbs by pantomimes that were otherwise accompanying her discourse in the preceding testing sessions. We suggest that such a compensatory ability may constitute one important characteristic of the progressive aphasia syndrome.

Aphasia