tbuckley/cabot-search huggingface dataset:
T‐cell chronic lymphocytic leukemia with a helper/inducer membrane phenotype: A distinct clinicopathologic subtype with a poor prognosis
Authors: Thomas E. Witzig, Robert L. Phyliky, Chin‐Yang Li, Henry A. Homburger, Gordon W. Dewald, Barry S. Handwerger
Journal: American Journal of Hematology (1986)

Abstract T‐cell chronic lymphocytic leukemia (T‐CLL) accounts for about 2% of the various types of CLL and can be subtyped into helper/inducer (h/i) and cytotoxic/suppressor (c/s) cell membrane phenotypes. Seven patients with CLL were shown to have T‐CLL with a h/i cell membrane phenotype; four with monoclonal antibody reagents and three by demonstration of the E‐rosette receptor and focal acid alpha naphthyl acetate esterase activity. The clinical courses, treatment responses, and laboratory findings of these seven patients were reviewed to determine the prognosis and unique clinicopathologic features of this subtype. Two patients presented with skin rashes, and five were diagnosed during evaluation for other medical problems. Initially, four patients had splenomegaly and two had lymphadenopathy, but none of the patients had hepatomegaly. Morphologic examination revealed uniform, small lymphocytes in three patients, and the lymphocytes had nuclear indentations in four patients. Sera from the three patients tested were negative for antibody to the human T‐cell leukemia/lymphoma virus I. Peripheral blood mononuclear cells from one patient showed normal interleukin‐2 production and lacked antibody‐dependent cell‐mediated cellular cytotoxicity and natural killer activity. Cytogenetic analysis was done on one patient, revealing an abnormal clone with several chromosomal abnormalities, including an X; 14 translocation with a break point at 14q11. All patients required chemotherapy, and all died a median of 21 months from the time of diagnosis. The findings in these patients, in addition to those in 31 patients described in the literature, indicate that h/i T‐CLL is associated with a poor prognosis and has distinct clinical and pathologic features that separate it from c/s T‐CLL, adult T‐cell leukemia/lymphoma, the cutaneous T‐cell lymphomas, and B‐CLL.
Biology and Physiology Session: Summary of Discussion
Authors: William C. Dewey
Journal: Cancer Research (1984)

whether there is any clear evidence that heat radiosensitizes doses as low as 200 rads. Dewey mentioned that this apparently has been seen in the clinic with conventional doses this low, and H. I. Robins indicated that he had seen this in mice at 150 rads. Dewey further stated that data in vitro indicate that, with doses as low as 200 rads, part of the shoulder on the radiation survival curve can be removed by heat. T. C. Cetas questioned whether there would be any reason to have a probe in the tumor to measure pH at the same time and in the same place that the temperature is being measured during clinical hyperthermia. Dewey stated that ideally he would like to see measurements of temperature, oxygen concentration, and pH all at the same time within the different areas of the tumor. But then, Cetas questioned the value of this, since one-half a degree of fluctuation in temperature apparently eliminates the selective sensitization by low pH. Dewey said that, since hypoxic cells are radioresistant, one would like to know if the pH were lower in all the hypoxic cells in order to expect a selective heat sensitization of all the hypoxic cells and, possibly, of some of the oxygenated cells in the tumor. Thus, one would also like to know the oxygen concentration. However, J. M. C. Bull questioned whether the oxygen concentration measurements would mean anything, since there is an apparent difference in heat sensitivity between acute hypoxia and chronic hypoxia. Obviously, the usefulness of these measurements would depend on the sensi tivity of the measurements. G. M. Hahn mentioned that they have observed that some of the heat sensitivity is lost after maintaining cells for a consider able period of time at low pH. After C. W. Song's paper, R. B. Roemer questioned the
Continuously infused carboplatin used as radiosensitizer in locally unresectable non-small-cell lung cancer: a multicenter phase III study
Authors: H.J.M. Groen, A.H.W. van der Leest, E. Fokkema, P.R. Timmer, G.D. Nossent, W.J.G.M. Smit, J. Nabers, H.J. Hoekstra, J. Hermans, R. Otter, J.W.G. van Putten, E.G.E. de Vries, N.H. Mulder
Journal: Annals of Oncology (2004)
Association of a Germ-Line Copy Number Variation at 2p24.3 and Risk for Aggressive Prostate Cancer
Authors: Wennuan Liu, Jishan Sun, Ge Li, Yi Zhu, Scott Zhang, Seong-Tae Kim, Jielin Sun, Fredrik Wiklund, Kathleen Wiley, Sarah D. Isaacs, Pär Stattin, Jianfeng Xu, David Duggan, John D. Carpten, William B. Isaacs, Henrik Grönberg, S. Lilly Zheng, Bao-Li Chang
Journal: Cancer Research (2009)

We searched for deletions in the germ-line genome among 498 aggressive prostate cancer cases and 494 controls from a population-based study in Sweden [CAncer of the Prostate in Sweden (CAPS)] using Affymetrix SNP arrays. By comparing allele intensities of approximately 500,000 SNP probes across the genome, a germ-line deletion at 2p24.3 was observed to be significantly more common in cases (12.63%) than in controls (8.28%); P = 0.028. To confirm the association, we genotyped this germ-line copy number variation (CNV) in additional subjects from CAPS and from Johns Hopkins Hospital (JHH). Overall, among 4,314 cases and 2,176 controls examined, the CNV was significantly associated with prostate cancer risk [odds ratio (OR), 1.25; 95% confidence interval (95% CI), 1.06-1.48; P = 0.009]. More importantly, the association was stronger for aggressive prostate cancer (OR, 1.31; 95% CI, 1.08-1.58; P = 0.006) than for nonaggressive prostate cancer (OR, 1.19; 95% CI, 0.98-1.45; P = 0.08). The biological effect of this germ-line CNV is unknown because no known gene resides in the deletion. Results from this study represent the first novel germ-line CNV that was identified from a genome-wide search and was significantly, but moderately, associated with prostate cancer risk. Additional confirmation of this association and functional studies are warranted.
Dermal cylindromas originate from the eccrine sweat gland
Authors: D. W. K. COTTON, S. G. BRAYE
Journal: British Journal of Dermatology (1984)

Ten dermal cylindromas have been studied using histological, ultrastructural and immunocytochemical techniques. The clinical data from the ten patients have also been reviewed. The results indicate histogenesis from the intradermal coiled duct region of the eccrine sweat gland.
High-Dose Methotrexate in Osteosarcoma: Let the Questions Surcease—Time for Final Acceptance
Authors: Norman Jaffe, Richard Gorlick
Journal: Journal of Clinical Oncology (2008)

Osteosarcoma is the most common primary malignant bone tumor affecting children and adults. The etiology is unknown, although a higher incidence occurs in patients with bilateral retinoblastoma, Paget’s disease of bone, the Li Fraumeni syndrome, and those who have received therapeutic radiation. The biologic behavior is consistent with the premise that silent pulmonary micrometastases are present in at least 80% of patients at diagnosis. These metastases are not visible on imaging studies, but in the absence of effective systemic therapy, they generally surface 6 to 9 months after surgical ablation of the primary tumor. If untreated, they will be responsible for the patients demise within 2 to 3 years of their appearance. Historical controls reveal a survival of 5% to 20%. There are currently four major classes of chemotherapeutic agents with established efficacy that are used in the therapy of this malignancy: doxorubicin, cisplatin, ifosfamide/high-dose cyclophosphamide, and high-dose methotrexate with leucovorin rescue (MTXL). Doxorubicin and MTX-L were discovered first in the early 1970s. Doxorubicin, and the other agents when discovered later, were accepted without query; not so for MTX-L. It was initially subjected to intense scrutiny, 1,2 rebuffed intermittently, 3 and later incorporated with variable degrees of indifference or enthusiasm into therapeutic regimens seemingly for want of a more effective agent. During this interminable period of probation (still extant 4 ), support for its efficacy and confirmation of its activity emanated from various publications. It was shown to be effective in eliminating overt pulmonary metastases, improving the opportunity for limb salvage, healing pathologic fractures, and enhancing the effect of radiation therapy for palliation and control of inoperable tumors. 5 When administered postoperatively as the sole agent after ablation of the primary tumor, it increased survival to 40%, 6 and in combination with other agents (pre- and postoperative therapy), it increased survival to 65% to 75%. 6-12
Early recovery from cow's milk allergy is associated with decreasing IgE and increasing IgG4 binding to cow's milk epitopes
Authors: Emma M. Savilahti, Ville Rantanen, Jing S. Lin, Sirkku Karinen, Kristiina M. Saarinen, Marina Goldis, Mika J. Mäkelä, Sampsa Hautaniemi, Erkki Savilahti, Hugh A. Sampson
Journal: Journal of Allergy and Clinical Immunology (2010)
Importance of local versus systemic effects of non-steroidal anti-inflammatory drugs in increasing small intestinal permeability in man.
Authors: I Bjarnason, B Fehilly, P Smethurst, I S Menzies, A J Levi
Journal: Gut (1991)

Increased small intestinal permeability caused by non-steroidal anti-inflammatory drugs (NSAIDs) is probably a prerequisite for NSAID enteropathy, a source of morbidity in patients with rheumatoid arthritis. This increased small intestinal permeability may be a summation of a local effect during drug absorption, a systemic effect after absorption, and a local effect of the drug excreted in bile, but the relative contribution made by these factors is unknown. We assessed the effect of indomethacin and nabumetone on intestinal permeability. The principal active metabolite of nabumetone, 6-methoxy-2-naphthylacetic acid, is not subject to appreciable enterohepatic recirculation. Twelve volunteers were studied before and after one week9s ingestion of indomethacin (150 mg/day) and nabumetone (1 g/day) with a combined absorption/permeability test. Neither drug had a significant effect on the permeation of 3-0-methyl-D-glucose, D-xylose, and L-rhamnose. Indomethacin increased the permeation of radioactive 51chromium ethylenediaminetetra-acetic acid (51Cr EDTA) significantly from baseline (mean (SEM) 0.63 (0.09)% v 1.20 (0.14)%, p less than 0.01) but nabumetone did not (0.70 (0.10)% p greater than 0.1). These results were supported by the 51Cr EDTA/L-rhamnose urine excretion ratios, which reflect changes in intestinal permeability. They suggest that NSAIDs increase intestinal permeability during absorption or after biliary excretion and that the systemic effect is of minor importance.
Oligoclonality of human intestinal intraepithelial T cells.
Authors: C Van Kerckhove, G J Russell, K Deusch, K Reich, A K Bhan, H DerSimonian, M B Brenner
Journal: The Journal of Experimental Medicine (1992)

T cells bearing the T cell receptor alpha/beta (TCR-alpha/beta) are the predominant lymphocyte population in the human intestinal epithelium. To examine if normal intestinal intraepithelial lymphocytes (IEL) have a TCR repertoire distinct from the TCR-alpha/beta repertoire in peripheral blood lymphocytes (PBL), comparative analysis of relative V beta gene usage in IEL and PBL was performed by quantitative polymerase chain reaction. In each of the six individuals examined, one to three V beta families made up more than 40% of the total V beta transcripts detected in the IEL, whereas there was a more even distribution of V beta gene usage in the paired PBL. The predominant V beta families, especially V beta 1, V beta 2, V beta 3, and V beta 6, were frequently shared among IEL of different individuals. PCR cloning and sequence analysis of the predominant V beta 6 family in two individuals revealed an identical V-D-J-C sequence in 13 of 21 clones obtained from one donor, and a different repeated sequence in 18 of 27 clones examined in the second donor. These data suggest that the V beta skewing in IEL is due to an oligoclonal T cell expansion and may reflect the response of the intestinal mucosal immune system to a restricted set of as yet undefined antigens present in the gut.
Blunt injury of the radial and ulnar arteries in volley ball players. A report of three cases of the antebrachial-palmar hammer syndrome.
Authors: S. Kostianen, S. Orava
Journal: British Journal of Sports Medicine (1983)

Three cases of the antebrachial-palmar hammer syndrome are described in volley ball players. They all suffered from a decreased blood perfusion of their right hand and fingers due to the repeated ball and floor impacts during the volley ball training and playing. The vascular lesions of the radial and ulnar arteries were reversible. The patients recovered spontaneously during the rest from excessive physical activity by their hands. The vascular lesions of this kind are rare but seem to be typical to volley ball players.
Role of Noninvasive Testing in the Clinical Evaluation of Women With Suspected Ischemic Heart Disease
Authors: Jennifer H. Mieres, Martha Gulati, Noel Bairey Merz, Daniel S Berman, Thomas C. Gerber, Sharonne N. Hayes, Christopher M. Kramer, James K. Min, L. Kristin Newby, J.V. (Ian) Nixon, Monvadi B. Srichai, Patricia A. Pellikka, Rita F. Redberg, Nanette K. Wenger, Leslee J. Shaw
Journal: Circulation (2014)
Mechanisms of tertiary lymphoid organ formation during lymphoid neogenesis are involved in lymphoid follicle formation in chronic obstructive pulmonary disease
Authors: Maria Tsoumakidou, Eleni Litsiou, Katerina Tsoutsa, Panagiota Kara, Dimitra Rontogianni, Charalambos Zisis, Ion Belenis, Spyros Zakynthinos
Journal: European Respiratory Journal (2011)

Tertiary lymphoid organs (TLOs) are aggregates of B and T cells formed in response to chronic immune responses. TLOs are the result of lymphoid neogenesis and are formed via production of lymphoid-organizing chemokines (CXCL13, CCL19 and CCL21), in response to signaling from lymphotoxin α (LTα) via TNFR1, TNFR2 and LTR. Stromal cells and antigen presenting cells (APCs), i.e. dendritic cells (DCs), secrete lymphoid chemokines, which attract B cells, T cells and DCs via CCR7 (receptor for CCL19/21) and CXCR5 (receptor for CXCL13). Lymphoid follicles are frequently found in the peripheral lungs of patients with Chronic Obstructive Pulmonary Disease (COPD). Whether they are the result of lymphoid neogenesis remains elusive. Here, we have identified 18 patients with COPD and lymphoid follicles and used immunohistochemistry to analyze the expression of LTa and lymphoid chemokines. Flow cytometry was applied to study expression of their receptors. LTα is abundantly expressed by alveolar macrophages and lung stromal cells and CXCL13 is strongly expressed inside the follicles. HLA-DR+ve cells (APCs), but not CD45-ve stromal cells, strongly express TNFR1 (43% of APCs), TNFR2 (47%) and LTR (38%). CXCR5 is expressed by B cells (96% of B cells), DCs (74% of DCs) and T cells (24% of T cells). CCL19, CCL21 and CCR7 are rarely expressed. In conclusion, molecular mechanisms underlying TLO formation might be involved in lymphoid follicle formation in COPD as follows: stromal cells and macrophages secrete LTa, which induces CXCL13 production by lung APCs, driving the accumulation of CXCR5 bearing B cells, T cells and DCs to sites of TLO. Funded by the Hellenic Thoracic Society.
Treatment Advances for Cocaine-Induced Ischemic Stroke: Focus on Dihydropyridine-Class Calcium Channel Antagonists
Authors: Bankole A. Johnson, Michael D. Devous, Pedro Ruiz, Nassima Ait-Daoud
Journal: American Journal of Psychiatry (2001)

OBJECTIVE: The authors reviewed the pathogenesis of cocaine-related cerebral ischemia, appraised current knowledge of its sequelae, and assessed the role of putative therapeutic agents, particularly dihydropyridine-class calcium channel antagonists. METHOD: The authors performed an OVID-based literature review of all indexed journals between 1966 and 2000. RESULTS: Cocaine abuse significantly increases the risk of ischemic stroke. The principal mechanism of cocaine-induced cerebral ischemia is vasospasm of large cranial arteries or within the cortical microvasculature. Increased levels of extracellular monoamines, particularly dopamine, mediate vasospasm. Neuroanatomical and labeling studies also have shown that dopamine-innervated neurons may regulate cerebral blood flow. Indeed, dopamine-rich brain regions appear to be relatively specific targets for cocaine-induced cerebral ischemia. Neuroimaging studies show that cocaine-induced hypoperfusion can persist even after 6 months of abstinence. Hypoperfusion can result in deficits on complex and simple psychomotor tasks but perhaps not on memory or attention. Severe cerebral ischemia can directly precipitate neuronal death and degradation, a condition exacerbated by liberation of the excitatory amino acid glutamate. Dihydropyridine-class calcium channel antagonists inhibit cocaine-mediated dopamine release on neurons involved in vasospasm and the control of cortical circulation. Other causes of cerebral ischemia include thrombogenesis and vasculitis. Although antithrombotic agents have potential in alleviating cocaine's neurotoxic effects, their use may be limited by the risk of spontaneous hemorrhage. CONCLUSIONS: Cocaine abuse can result in stroke, neuroischemia, and cognitive deficits that can persist even after prolonged abstinence. Dihydropyridine-class calcium channel antagonists, such as isradipine, show promise as therapeutic agents for preventing cocaine-induced cerebral ischemia.
Endogenous prostacyclin biosynthesis and platelet function during selective inhibition of thromboxane synthase in man.
Authors: G A FitzGerald, A R Brash, J A Oates, A K Pedersen
Journal: Journal of Clinical Investigation (1983)

The consequences of inhibiting the metabolism of prostaglandin G2 to thromboxane A2 in man were studied by using an inhibitor of thromboxane synthase, 4-[2-(IH-imidazol-1-yl)ethoxy] benzoic acid hydrochloride (dazoxiben). Single doses of 25, 50, 100, and 200 mg of dazoxiben were administered to healthy volunteers at 2-wk intervals in a randomized, placebo-controlled, double-blind manner. Serum thromboxane B2 and aggregation studies in whole blood and platelet-rich plasma were measured before dosing and at 1, 4, 6, 8, and 24 h after dosing. Both serum thromboxane B2 and the platelet aggregation response to arachidonic acid (1.33 mM) were reversibly inhibited in a dose-dependent manner. Aggregation induced by 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (0.4 and 4.0 microM) in platelet-rich plasma as well as both aggregation and nucleotide release induced by collagen (95 micrograms/ml) in platelet-rich plasma and whole blood were unaltered by dazoxiben. Additional evidence for a platelet-inhibitory effect of the compound was a significant prolongation of the bleeding time at 1 h after administration of the highest dose (200 mg) of dazoxiben. Endogenous prostacyclin biosynthesis was assessed by measurement of the major urinary metabolite of prostacyclin, 2,3-dinor-6-keto-PGF1 alpha (PGI-M). PGI-M excretion was increased by dazoxiben; it rose a mean 2.4-fold from predosing control values at 0-6 h after administration of the highest dose studied (200 mg).
Efficacy assessement of home mechanical ventilation: Comparison of ventilator software data with home respiratory poligraphy (pilot study)
Authors: Joaquim Moreira, Célia Freitas, Tiago Pinto, Miguel Gonçalves, Anabela Marinho, Marta Drummond, João Carlos Winck
Journal: European Respiratory Journal (2013)

Background. Domiciliary bi-level ventilators have specific software that estimates residual Apnea-Hypopnea Index (AHI). The accuracy of this data is important to achieve optimal ventilatory parameters.

Objectives. Compare the residual AHI from the software of ventilator with the residual AHI obtained by a Domiciliary Respiratory Poligraphy (DRP) in patients with Chronic Respiratory Failure (CRF).

Methods. Patients newly diagnosed with CRF and eligible for Home Mechanical Ventilation (HMV) were included. All patients were treated with BiPAP A30 (Phillips Respironics®). By 3rd month all performed DRP (Alice 5, Phillips Respironics®, 10 channels, including z-Rip (Pro-Tech) and TcCO2 (Sentec®)). The residual AHI obtained from the ventilator software ( EncoreAnywhere , Phillips Respironics®) was compared with the residual AHI from DRP reviewed manually.

Results. Data is presented as median (per 25-75). 16 patients were studied, 9 (56,25%) with restrictive disease and 7 (43,75%) with obstructive disease with a FVC of 68,5 (50-81,1)%, FEV1 of 57,9 (28,3-73)%, PaCO2 of 51,1 (45,4-59,5) mmHg, PaO2 of 63,5 (56,2-71,5) mmHg. SpO2 of 93,5 (91,7-95,3)%. Measured by the DRP baseline AHI improved in all patients (18 (7,8-50,8) vs 2,9 (0,9-8,1), p<0,01) /h. When compared with residual AHI of ventilator software 3,4 (0,8-5,5) /h no significant differences were found (p=0,5).

Conclusion. Although further research is warranted, the results of this pilot study suggest that the AHI obtained by the ventilator software can be used to achieve optimal ventilatory parameters in patients with CRF of varying severity.
Disordered Fat Storage and Mobilization in the Pathogenesis of Insulin Resistance and Type 2 Diabetes
Authors: Gary F. Lewis, André Carpentier, Khosrow Adeli, Adria Giacca
Journal: Endocrine Reviews (2002)

The primary genetic, environmental, and metabolic factors responsible for causing insulin resistance and pancreatic β-cell failure and the precise sequence of events leading to the development of type 2 diabetes are not yet fully understood. Abnormalities of triglyceride storage and lipolysis in insulin-sensitive tissues are an early manifestation of conditions characterized by insulin resistance and are detectable before the development of postprandial or fasting hyperglycemia. Increased free fatty acid (FFA) flux from adipose tissue to nonadipose tissue, resulting from abnormalities of fat metabolism, participates in and amplifies many of the fundamental metabolic derangements that are characteristic of the insulin resistance syndrome and type 2 diabetes. It is also likely to play an important role in the progression from normal glucose tolerance to fasting hyperglycemia and conversion to frank type 2 diabetes in insulin resistant individuals. Adverse metabolic consequences of increased FFA flux, to be discussed in this review, are extremely wide ranging and include, but are not limited to: 1) dyslipidemia and hepatic steatosis, 2) impaired glucose metabolism and insulin sensitivity in muscle and liver, 3) diminished insulin clearance, aggravating peripheral tissue hyperinsulinemia, and 4) impaired pancreatic β-cell function. The precise biochemical mechanisms whereby fatty acids and cytosolic triglycerides exert their effects remain poorly understood. Recent studies, however, suggest that the sequence of events may be the following: in states of positive net energy balance, triglyceride accumulation in "fat-buffering" adipose tissue is limited by the development of adipose tissue insulin resistance. This results in diversion of energy substrates to nonadipose tissue, which in turn leads to a complex array of metabolic abnormalities characteristic of insulin-resistant states and type 2 diabetes. Recent evidence suggests that some of the biochemical mechanisms whereby glucose and fat exert adverse effects in insulin-sensitive and insulin-producing tissues are shared, thus implicating a diabetogenic role for energy excess as a whole. Although there is now evidence that weight loss through reduction of caloric intake and increase in physical activity can prevent the development of diabetes, it remains an open question as to whether specific modulation of fat metabolism will result in improvement in some or all of the above metabolic derangements or will prevent progression from insulin resistance syndrome to type 2 diabetes.