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PubMed1977

Surgery and the progression of the occlusive process in patients with peripheral vascular disease.

The angiograms and clinical records of 42 patients with arteriosclerosis obliterans who underwent repeat angiography were analyzed in order to correlate the effects of surgery with progression of the occlusive process in native vessels. Occlusive disease progressed significantly faster in operated limbs (77%) than in nonoperated limbs (44%). When progression occurred, it was more likely to take the form of occlusion in operated limbs (85%) than in nonoperated limbs (61%). Graft closure was associated with a 93% incidence of disease progression, but even limbs with patent grafts had a more rapid progression than the nonoperated limbs (62% vs. 44%). There was a good correlation between the presence of symptoms and the angiographic progression.

Aged↗
PubMed1978

[The effect of varicocele on male fertility with particular consideration of progressive motility (author's transl)].

Two-hundred patients with varicocele were examined for fertility, which was found to have diminished in 75% of the cases because of a decreased sperm count (less than 40 million/ml); 40% of these, the largest group (categorized only with regard to oligospermia), had a sperm count of 21--40 million/ml. The most remarkable finding was restrained fertility in 90% of the cases because of decreased progressive motility (speed of forward progression). Here, the largest group (nearly 50%) was in the category of 21--30%. Decreased progressive motility was mostly combined with a diminished sperm count to an oligoasthenospermia. In 20% of the cases, however, fertility was restrained only by decreased progressive motility in the sense of an asthenospermia. The first effect, due to varicocele, is seen in decreased progressive motility. However, because spermatozoa acquire their progressive motility by means of maturation in the epididymis, the varicocele causes the first damage to the epididymis.

Cell Count↗
PubMed1977

Hormonal control of growth and progression in tumors of Nb rats and a theory of action.

A continuation of previous studies of hormone-dependent tumors in various organs in Nb rats concerns the effects of removal of the hormone stimulus from animals with growing tumors. Tumor regression usually followed this procedure, and in various models it was associated with an increased survival of the animal. A regressed tumor could be caused to grow at any time by estrogen treatment, and the resulting tumor remained hormone dependent, although some progression might occur. Continuous breeding rarely affected the growth or progression of transplanted adrenal or breast carcinomas. When spontaneous regrowth of tumors took place following removal of the estrogen stimulus all types of tumors (except leiomyomas of the uterus, showed progression usually to autonomy, and in the case of male rats bearing breast carcinomas it was inevitable. The substitution of pellets containing a reduced level of estrone to determine which prevented regression and allowed uninterrupted growth offered an assessment of the type or amount of hormone required for the growth of different tumors. By means of such a model of breast cancer in male rats, it was possible to demonstrate that a reduction in hormone levels sufficient to prevent advancing tumor growth, but adequate to reduce the extent of regression, also reduced the frequency or prevented the development of autonomous change. Although regression per se was not a prerequisite for autonomous change, the paradox was evident that progression towards autonomous growth was accelerated with procedures expected to check tumor growth and was minimal with procedures that accelerated it. Liver metastases of hormone-dependent adrenal carcinomas continued growth and could not be influenced by removal of estrogen, although the primary transplant regressed. When such metastases were transplanted, they were not found to have progressed to autonomy but retained a hormone-dependent status. Some tumors, when maintained in estrogen-conditioned hosts, apparently showed a reversion to a more hormone-dependent cell type rather than the expected progression towards autonomy. A theory is suggested to explain the experiments findings on the development and control of estrogen-responsive tumors.

Adrenal Gland Neoplasms↗
PubMed2026

Prion disease mimicking rapidly progressive Alzheimer disease: case series and systematic review.

BACKGROUND: Prion disease and Alzheimer disease (AD) are common causes of rapidly progressive dementia (RPD). Although most patients with prion disease are distinguished by MRI and CSF findings, selected cases mimic rapidly progressive AD. We characterized AD-prion disease mimics within a prospective cohort and the extant literature to identify the clinical features and tests that support accurate diagnoses in these patients. METHODS: Patients with prion disease initially diagnosed as rapidly progressive AD were identified from a prospective cohort study at Mayo Clinic (February 2020-June 2026) and through systematic review of MEDLINE and Embase. RESULTS: Of 204 patients with RPD, five (2.5%) were initially diagnosed with clinically probable AD but ultimately determined to have prion disease. Systematic review identified 10 additional cases (n=15, median age-at-onset, 59 years; 67% male). Presentations reproduced amnestic (53%), dysexecutive (27%), primary progressive aphasia (13%), and posterior cortical atrophy (7%) AD phenotypes; median time from AD diagnosis to consideration of prion disease was 2 months. Diffusion-weighted MRI abnormalities were absent in Mayo Clinic cases and absent/equivocal (n=2) or overlooked (n=8) in published cases. CSF biomarkers were consistent with AD in 6/9 tested patients, with elevated total tau levels in 11/13 patients and total-tau/p hosphorylated-tau181 ratios in 5/9 patients. Real-time quaking-induced conversion assays for prions were positive in the CSF of 9/12 patients. Prion disease was confirmed by neuropathology (n=7), genetics (n=2), or real-time quaking-induced conversion (n=6) assays. CONCLUSIONS: Prion disease may rarely mimic rapidly progressive AD. Disproportionate elevations in CSF total-tau levels or total-tau/p hosphorylated-tau181 ratios should prompt consideration of prion disease.

Humans↗
PubMed2025

A MGMT Enhancer Variant is Associated with Glioma Susceptibility and Progression.

The O6-methylguanine-DNA methyltransferase (MGMT) plays a significant role in the pathogenesis and progression of glioma. Numerous enhancer variants, including those within the MGMT gene region and adjacent gene regions, have been found to be associated with cancer development and progression. We investigated the significance of enhancer variants located in the intergenic spacer far from the MGMT gene in relation to glioma susceptibility and progression. We recruited 402 glioma patients and 654 controls for this investigation using Sequenom MassARRAY genotyping. We identified a significantly elevated risk of glioma among carriers with the rs11016629 TG genotype compared to those with the GG genotype (OR = 1.41, 95% CI 1.03-1.93; P = 0.034). Subgroup analyses revealed that rs11016629 was significantly associated with glioma risk in subjects with WHO grade IV tumor (OR = 1.59, 95% CI 1.07-2.38; P = 0.023) and high-grade glioma (OR = 1.57, 95% CI 1.11-2.21; P = 0.011). Patients who underwent gross total resection with TG/TT genotypes exhibited a 2.66-fold higher risk of disease progression than GG carriers (HR = 2.66, 95% CI 1.23-5.79; P = 0.014). The study demonstrates that a MGMT enhancer variant rs11016629 contributes to both glioma susceptibility and progression.

Humans↗
PubMed2025

Integrative metabolomic and proteomic analysis of diabetic kidney disease progression with younger-onset type 2 diabetes.

AIM: Younger-onset type 2 diabetes (YT2D) confers a disproportionately high risk of diabetic kidney disease (DKD), yet early biomarkers and underlying mechanisms remain poorly defined. We aimed to identify metabolites associated with DKD progression and integrate metabolomic and proteomic data to elucidate pathways involved in a multi-ethnic Asian cohort. MATERIALS AND METHODS: In this prospective study, 787 YT2D patients (diagnosed at ≤ age 40) were followed for a median of 5.7 years. DKD progression was defined as an annual decline in estimated glomerular filtration rate (eGFR) of ≥3 mL/min/1.73 m2 or ≥ 40% reduction in eGFR from baseline. Plasma metabolites were measured by nuclear magnetic resonance spectroscopy. Multivariable regression analysis was performed in a discovery (N = 550) and internal validation cohort (N = 237). Integrative metabolomic-proteomic analysis (N = 428) was performed using sparse partial least squares discriminant analysis (sPLS-DA). RESULTS: Ninety-eight metabolites were differentially expressed between DKD progressors and non-progressors, of which total branched-chain amino acids (BCAAs) (OR = 0.60, 95% CI 0.46-0.79), valine (OR = 0.62, 95% CI 0.48-0.81), and leucine (OR = 0.56, 95% CI 0.43-0.74) associated with DKD progression, independent of metabolic risk factors. Integrative analysis identified three components comprising 23 proteins and 30 metabolites, involved in the citrate cycle and apoptosis, which improved prediction of DKD progression beyond clinical risk factors (AUC 0.69-0.83). CONCLUSION: Lower plasma BCAA levels are independently associated with DKD progression in YT2D. Integrative multi-omics analysis highlights disruptions in metabolic and apoptotic pathways, providing insights into DKD pathophysiology and potential biomarkers for early risk stratification.

Humans↗
PubMed2026

Characteristics of early-onset, rapidly progressive scoliosis in spinal muscular atrophy type I treated with disease-modifying therapy -a multicenter retrospective study conducted in Japan.

In the era of disease-modifying therapy (DMT), almost all patients with spinal muscular atrophy (SMA) type I treated after onset, but before 6 months of age, develop early-onset, rapidly progressive scoliosis by 2 years of age, despite improvements in their motor function. Seven symptomatic patients with SMA type I who were treated before the age of 6 months were included in this retrospective observational study. Scoliosis had developed in all patients by 27 months of age. Among them, the patients who could stand with support or independently (standing patients; n = 3) tended to present with more progressive scoliosis than the sitters (n = 4). All standing patients demonstrated thoracic hyperkyphosis before or at the time of their scoliosis diagnosis. Despite receiving DMT, these patients continued to show residual key manifestations of SMA type I. Chronic difficulty maintaining posture due to trunk muscle weakness in the lying, sitting, or standing position was considered to be the main contributor to the development and progression of the scoliosis. The development and progression of such scoliosis, which begins in infancy, may be related to inappropriate postural management, which is not currently recognized as such by clinicians, caregivers, or guardians. In this population, it is important to closely monitor patients for such scoliosis from soon after the diagnosis of SMA. As this type of scoliosis progresses rapidly during the early developmental stage, when surgery is not possible, it is necessary to establish a proactive non-surgical management strategy for it.

Humans↗
PubMed2026

Apolipoprotein E promotes papillary thyroid carcinoma progression by activating PINK1/Parkin-mediated mitophagy.

BACKGROUND: Increasing evidence supports a progression-related role of apolipoprotein E (APOE) in papillary thyroid carcinoma (PTC), yet a clear mechanistic explanation for this association is still lacking. Considering the pivotal role of mitochondrial homeostasis in tumorigenesis, the potential role of APOE in promoting PTC progression through mitophagy regulation was investigated. Additionally, the involvement of the PINK1/Parkin-associated pathway in this process was examined to provide insights into its contribution to tumor progression. METHODS: APOE in thyroid carcinoma was characterized in terms of its expression profile, diagnostic relevance, and potential biological functions, based on integrative evidence derived from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets. APOE and mitophagy-related protein expression were further examined in PTC tissues by immunohistochemistry. Further evaluation of APOE in PTC cell lines focused on its association with proliferation, apoptosis, and mitophagy, with bidirectional functional perturbation serving as the basis for assessment. Pharmacological inhibitors were used to assess the involvement of mitophagy-related signaling in the observed APOE-dependent phenotypes. Additionally, the in vivo impact of APOE on PTC tumor growth and mitophagy was further investigated through a nude mouse xenograft model, providing insight into its potential role in tumor progression. RESULTS: A significant upregulation of APOE was observed in thyroid carcinoma tissues and PTC cell lines, supporting its potential relevance as a diagnostic biomarker. The modulation of APOE expression significantly influenced PTC cell proliferation and apoptosis, with overexpression promoting cell proliferation and inhibiting apoptosis, while knockdown led to the opposite effects. Mechanistically, APOE overexpression increased AMP-activated protein kinase (AMPK) phosphorylation and decreased mammalian target of rapamycin (mTOR) phosphorylation, accompanied by increased PINK1 and Parkin expression and mitophagy-related changes, including altered mitochondrial membrane potential, reduced overall reactive oxygen species levels, and increased autophagosome formation. Pharmacological inhibition of mitophagy attenuated the proliferative and antiapoptotic effects of APOE. CONCLUSIONS: These findings demonstrate that APOE promotes PTC progression in association with PINK1/Parkin-related mitophagy and modulation of the AMPK/mTOR axis. The APOE-associated mitophagy axis may provide a rationale for future preclinical investigation in PTC.

Apolipoprotein E (APOE)↗
PubMed2026

An individualized nomogram for predicting progression-free survival in systemic anaplastic large cell lymphoma: a multicenter, retrospective, and internally validated study.

OBJECTIVES: To develop an individualized nomogram for predicting disease progression risk in systemic anaplastic large cell lymphoma (sALCL). METHODS: Independent predictors of progression-free survival (PFS) were identified using Cox regression in a multicenter retrospective cohort of 109 sALCL patients (2010-2022). These were incorporated into a three-factor nomogram, evaluated via bootstrapped internal validation (1000 resamples), ROC analysis, C-index, decision curve analysis (DCA), and clinical impact curve (CIC). RESULTS: A total of 29 PFS events occurred during a median follow-up of 31 months. Multivariable modelling selected serum β2-microglobulin elevation, extranodal disease, and front-line chemotherapy choice (CHOP versus CHOPE or BV+CHP) as autonomous progression drivers. Upon internal bootstrap validation, the nomogram yielded strong prognostic accuracy, achieving AUCs of 0.81, 0.85 and 0.87 for 1-, 3- and 5-year progression-free survival, alongside a corrected C-index of 0.779 (95% CI: 0.699 - 0.861). Calibration plots showed close agreement between predicted and observed outcomes, while DCA confirmed superior net clinical benefit versus conventional IPI or Ann Arbor stratification across multiple decision thresholds. CONCLUSION: This first sALCL-specific nomogram integrates clinical and treatment variables to provide personalized PFS risk estimation. While internally validated, this exploratory, observation-based tool requires external validation and recalibration in prospective cohorts before clinical implementation.

Humans↗
PubMed1977

Trabeculectomy and the progression of glaucomatous visual field loss.

Twenty-four eyes of 20 patients with chronic open angle glaucoma who had a trabeculectomy were studied retrospectively. Trabeculectomy resulted in a significant lowering of mean intraocular pressures and improvement of pressure control for the group. Progression of visual field defects occurred in all 24 eyes preoperatively, while postoperatively, the fields of 14 eyes showed no change, but the other ten showed further progression. A comparison of the pressures of the eyes showing continued progression after surgery with the eyes showing no further progression revealed no significant difference in the mean preoperative or postoperative pressure or the mean pressure reduction after surgery. Measurements of the quality of the control, however, showed that the quality of pressure control was significantly better in the eyes that did not show progression of field loss postoperatively. Careful postoperative follow-up observation of the visual field remains necessary even after successful surgical pressure reduction.

Adult↗
PubMed2026

A refined MASH-HCC model identifies macrophage Gadd45b as a key orchestrator of inflammation-driven neoplastic progression.

Metabolic dysfunction-associated steatohepatitis (MASH) is emerging as a leading driver of hepatocellular carcinoma (HCC), yet the molecular mechanisms linking metabolic stress, chronic inflammation and tumorigenesis remain poorly understood. Here we established a metabolically relevant, time-efficient MASH-to-HCC model in C57BL/6N mice by combining a MASH diet with controlled CCl4 administration, enabling stepwise recapitulation of MASH-associated neoplastic progression. Using this model, we identified growth arrest and DNA damage 45b (Gadd45b) as a novel MASH-derived protumorigenic regulator selectively activated under metabolic stress. Integrated analyses of human bulk and single-cell transcriptomic datasets and mouse transcriptomic deconvolution revealed concordant macrophage remodeling and GADD45B/Gadd45b expression dynamics during MASH-to-HCC progression. Mechanistically, fatty acids and TNFα preferentially induced Gadd45b in macrophages, where it amplified TNFα-NF-κB signaling. Macrophage-derived inflammatory signals subsequently induced Gadd45b and NF-κB activation in hepatocytes, establishing a feed-forward inflammatory loop that promoted fibrogenic and partial EMT-like programs and tumor spheroid formation. Importantly, temporal profiling during spheroid formation and progression revealed transient induction of Gadd45b during early spheroid establishment, but not during later progression, indicating that Gadd45b-mediated inflammatory signaling primarily promotes tumor initiation rather than subsequent growth. Consistent with human data, Gadd45b expression increased with disease severity and positively correlated with inflammatory factors in the MASH-HCC model, whereas pharmacological inhibition attenuated the Gadd45b-inflammation signaling axis. Collectively, our findings establish macrophage Gadd45b as a key orchestrator linking metabolic stress, chronic inflammation, and neoplastic transformation during MASH-to-HCC progression. Our refined MASH-HCC model provides a robust platform for mechanistic studies and preclinical evaluation of inflammation-targeted therapies.

Journal Article↗
PubMed1977

Progression and resolution of changes in pulmonary function and structure due to pulmonary microembolism and blood transfusion.

It was the purpose of this research to define the progression over several days of changes in pulmonary function and structure and to document the phases of recovery following transfusions to dogs of sublethal quantities of stored blood containing microaggregates. Ten dogs underwent partial exchange transfusions averaging 60% of blood volume through standard blood transfusion filters. Average screen filtration pressure (SFP) of the blood was 85 mm Hg. Pulmonary hypertension did not develop, but there were striking decreases in O2 consumption, increases in Qs/Qt and decreases in Do2. Changes became progressively more marked over the first 48 to 72 hours after the transfusions. Pulmonary function of surviving animals returned nearly to normal by the sixth day after transfusions. Pathologic examinations of the lungs of animals sequentially sacrificed over 6 days showed intravascular microemboli, alveolar cell hyperplasia and interstitial and alveolar pulmonary edema. Progressive recovery was associated with progressive resolution of all detrimental changes. In 6 animals exchange transfused 100% of their blood volumes through dacron wool (Swank) filters and in three control animals that were not transfused, there were no significant changes in pulmonary function or structure. These experiments define the progression of deterioration and recovery over 6 days of pulmonary function in dogs after sublethal pulmonary microembolism occurring during blood transfusion.

Animals↗
PubMed2025

Nanopore-based sequencing of active DNA replication reveals key principles of metazoan replication fork progression, origin and termination sites.

Balancing replication fork progression and origin usage is essential to maintain genome stability, but measuring replication fork progression rates and origin usage throughout the genome has been challenging. Here, we use nanopore sequencing combined with DNAscent to measure replication fork progression together with origin and termination site usage with single-molecule precision throughout the Drosophila genome with nearly full genome coverage. We find that replication fork progression rates are not uniform throughout the genome. Rather, fork progression is slowest in euchromatin, and this is not correlated with active transcription. Replication origins are also influenced by chromatin, but the exact position of initiation is highly variable and are often several kilobases away from ORC binding sites. Termination sites lack any chromatin or sequence motifs and appear nearly random throughout the genome. By measuring DNA replication dynamics at near full genome coverage, our work reveals key principles of metazoan replication dynamics.

Journal Article↗
PubMed1976

Progressive cone dystrophies.

Patients with progressive generalized cone dystrophy often present nystagmus (or strabism) and complain of photophobia, decrease in visual acuity or disturbances in colour perception. The most classic fundus abnormality is the bull's eye maculopathy or a pallor of the optic disc. Minimal macular changes are sometimes seen, which may progress to a bull's eye type of macular degeneration. The photopic ERG is always very affected, whereas at first the scotopic ERG seems normal. Progressive deterioration of the visual functions is accompanied by increasing fundus lesions and rod involvement, as suggested by the modifications of the dark adaptation curve and the scotopic ERG. However, the progression of typical generalized cone dysfunction is very slow. On the contrary, in some cases of so-called Stargardt's disease with peripheral participation, a very rapid progression has been observed. In such cases a normal ERG does not necessarily mean that the disease will remain localized to the macular area. No definite prognosis can be made on one single ERG. In 3 cases with sector pigmentary retinopathy the photopic ERG was more affected than the scotopic ERG. However, these cases are probably primary cone-rod dystrophies. Although there is no electrophysiological control, our clinical impression is that the evolution, if possible, is very slow.

Adolescent↗
PubMed1979

Radiographic caries diagnosis. A study of caries progression and observer performance.

A detailed index and score system was employed in radiographic studies of the progression of proximal caries during a three and a six year interval after the termination of the regular school dental care. It was demonstrated that the score system offers advantages compared with systems for estimating caries progression only taking into account the number of new lesions, since the former also reveals progression of already existing lesions. Most of the new lesions being developed during a six year interval was found in the enamel. The progression of already existing carious lesions was slow. Fewer new lesions and a slower progression of already existing lesions were found with the increasing age of the patients. Wide variations between observers were found at radiographic examinations of extracted teeth. The influence of such variations on the results of epidemiological caries investigations was elucidated. The importance of minimizing the rate of false positive diagnoses in investigations comparing the caries prevalence between different groups of patients was demonstrated. Data from the dental literature were used to estimate the probabilities of clinical cavities at different extents of the radiographically registered carious lesions. These probabilities were lower, the lower the prevalence of cavities and the smaller the extent of the radiographic lesion. Receiver operating characteristic curves based on the extents of the radiographic carious lesions were employed in assessing optimal criteria for restorative treatment, taking into account the prevalence of carious cavities and the costs of errors in the decision-making. The lower the cavity prevalence and the higher the cost of overtreatment, the greater the extent of the radiographic lesion that should be used as criterion for restorative treatment. The results of radiographic examinations of carious lesions were found to be greatly influenced by information given to the examiners and by the opinions of other observers. Such an influence, if occurring in epidemiological investigations, may give misleading results. Different densities in radiographs of different groups of patients to be compared may also give rise to inaccurate results. Ways of minimizing the influence of observer variations are discussed.

Adolescent↗
PubMed1977

[Pathogenesis of progressive forms of tick-borne encephalitis].

An analysis of the pathogenesis of progressive forms of tick-borne encephalitis based on observations of 109 patients revealed the existence of similar amounts of progressive forms in different endemic foci, as well as a dependence of such forms on the syndrome of the acute period. It was possible to demonstrate a transformation of progressive syndromes in dynamics. The outcome of syndromes in a progressive development are phenocopies of the known hereditary diseases of the nervous system. The clinical forms of progressive development are determined mainly by hereditary factors. Their appearance is due to an immune defect which facilitates the development of a persisting infection. Hopeful results are provided by specific and nonspecific vaccinotherapy.

Adult↗
PubMedDate not supplied

Visual field progression in open-angle glaucoma patients presenting with monocular field loss.

Twenty-one patients with primary open-angle glaucoma were followed an average of 4.4 years after developing monocular field loss. Nine of the undamaged fellow eyes developed field loss, while 16 of the 21 eyes presenting with field loss showed progression of field changes. In 13 patients, the presenting eye had a greater progression of field loss than the fellow eye, and asymmetry of pressure control explained this in only five patients. Eleven patients with symmetric pressure control had progressive field changes in one or both eyes, and in seven, the presenting eye showed greater progression than its fellow. This suggests that an eye with field loss may be more susceptible to progression of field changes at similar pressure levels than an eye without previous damage. Furthermore, patients with unilateral field loss have a greater incidence of field loss in the undamaged fellow eye than do patients with bilateral ocular hypertension.

Adult↗
PubMed2025

EIF2B5 promotes malignant progression of hepatocellular carcinoma by activating the PI3K/AKT signaling pathway through targeting RPL6.

Hepatocellular carcinoma (HCC) is a highly aggressive malignancy with limited treatment options and poor prognosis. In this study, we demonstrated the critical role of EIF2B5 in driving HCC progression. We found EIF2B5 expression is significantly upregulated in HCC tumor tissues in several bioinformatics datasets, including The Cancer Genome Atlas, and that high expression of EIF2B5 predicts poor prognosis for HCC patients. Through a series of in vitro cell biology experiments, we found that EIF2B5 knockdown significantly attenuated Hep3B and HepG2 proliferation, migration, and invasion and increased cell cycle arrest, whereas EIF2B5 overexpression promoted HCC progression. Through mass spectrometry and immunoprecipitation validation, we found that EIF2B5 directly interacted with RPL6 and that when EIF2B5 was overexpressed in HCC cells, it promoted the expression of the downstream protein RPL6, which was able to activate the phosphatidylinositol kinase (PI3K)/serine-threonine kinase (AKT)/mammalian target of rapamycin (mTOR) pathway and thereby increase the proliferation and invasion ability of HCC cell lines, as verified by second-generation sequencing analysis and western blot. We further verified these findings using the mouse ectopic tumor assay, and the results showed that EIF2B5 knockdown significantly inhibited tumor progression in HCC mice. The present study suggests that EIF2B5 promotes malignant progression of HCC by interacting with RPL6 and activating the PI3K/AKT/mTOR signaling pathway and may serve as a potential target for the treatment of HCC.

Humans↗