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Background: In the 1990s, transjugular intrahepatic portosystemic shunts (TIPS) were performed using bare metal stents, and stent-induced hemolysis was a complication noted in 10% of patients. This was due to the mechanical stress created by turbulent flow from the uncovered interstices. Polytetrafluoroethylene (PTFE) stents came into regular use in the early 2000s becoming the standard equipment for TIPS placements, which are predominately covered. Due to this, stent-induced hemolysis has become a rare phenomenon., Case Presentation: We describe a case of TIPS-induced hemolysis in a 53-years-old Caucasian female patient without cirrhosis. The patient had a history of heterozygous factor 5 Leiden mutation and abnormal lupus anticoagulant profile with development of a portal vein thrombus. She had undergone previous TIPS placement complicated by a TIPS thrombosis 3 years after initial placement requiring venoplasty and extension of the stent. Within one month, the patient developed hemolytic anemia with extensive evaluation that did not yield an alternative cause. Due to temporal association and clinical symptoms, the hemolytic anemia was attributed to the recent TIPS revision., Conclusion: This particular case of TIPS-induced hemolysis in a patient who does not have cirrhosis has not been previously described in the literature. Our case highlights that TIPS-induced hemolysis should be considered in anyone who could have potential underlying red blood cell dysfunction, not just those with cirrhosis. Further, the case demonstrates an important point that mild hemolysis (i.e., not requiring blood transfusion) can likely be managed conservatively, without stent removal., (© 2023. The Author(s).)

Introduction: Recent studies have demonstrated that the protective effect of colonoscopy against colorectal cancer is lower in the proximal colon. Proximal serrated polyps, including sessile serrated adenomas and proximal hyperplastic polyps, can be frequently missed and pose a risk of interval cancers., Aim: To investigate the overall adenoma detection rate (ADR) and the proximal serrated polyp detection rate (PSPDR) among academic gastroenterologists, community gastroenterologists, and colorectal surgeons from a single institution, all of whom have received formal training in colonoscopy during their fellowship., Methods: All complete screening colonoscopies for patients aged 50 or older with a good to excellent bowel preparation performed by different endoscopists at Medstar Washington Hospital Center (Washington, DC) from July 2015 to December 2017 were reviewed. Pathology reports of the resected polyps were manually reviewed., Results: A total of 2850 screening colonoscopies meeting the inclusion criteria were performed by 18 endoscopists (6 academic, 7 community, and 5 colorectal surgeons). There was no significant difference in the mean ADR among the three groups of endoscopists: academic gastroenterologists, community gastroenterologists, and colorectal surgeons (40.3% vs 36.0% vs 39.6%, respectively). However, academic gastroenterologists had a significantly higher PSPDR compared to community gastroenterologists or colorectal surgeons (12.3% vs 5.4% vs 4.5%, respectively, ANOVA p = 0.006)., Conclusion: Our novel data show that academic gastroenterologists had a significantly higher PSPDR compared to community gastroenterologists or colorectal surgeons despite a comparable overall ADR among the three groups. PSPDR may be considered as an important quality indicator for colonoscopy, apart from ADR.

Many physical implementations of qubits-including ion traps, optical lattices and linear optics-suffer from loss. A nonzero probability of irretrievably losing a qubit can be a substantial obstacle to fault-tolerant methods of processing quantum information, requiring new techniques to safeguard against loss that introduce an additional overhead that depends upon the loss rate. Here we present a scalable and platform-independent protocol for estimating the average loss rate (averaged over all input states) resulting from an arbitrary Markovian noise process, as well as an independent estimate of detector efficiency. Moreover, we show that our protocol gives an additional constraint on estimated parameters from randomized benchmarking that improves the reliability of the estimated error rate and provides a new indicator for non-Markovian signatures in the experimental data. We also derive a bound for the state-dependent loss rate in terms of the average loss rate.

An NMR signal from a sample in a constant stray field of a portable NMR sensor is sensitized to vibrations. The CPMG sequence is synchronized to vibrations so that the constant gradient becomes an "effective" square-wave gradient, leading to the vibration-induced phase accumulation. The integrating nature of the spot measurement, combined with the phase distribution due to a non-uniform gradient and/or a wave field, leads to a destructive interference, the drop in the signal intensity and changes in the echo train shape. Vibrations with amplitudes as small as 140 nm were reliably detected with the permanent gradient of 12.4 T/m. The signal intensity depends on the phase offset between the vibrations and the pulse sequence. This approach opens the way for performing elastometry and micro-rheology measurements with portable NMR devices beyond the walls of a laboratory. Even without synchronization, if a vibration frequency is comparable to 1/2TE of the CPMG sequence, the signal can be severely affected, making it important for potential industrial applications of stray-field NMR., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Smoking causes endothelial cell (EC) injury; however, neither the components of cigarette smoke nor the mechanisms responsible for this injury are understood. The nitrosated derivative of nicotine, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), has been implicated in the carcinogenic effects of tobacco; however, the effects of NNK on the cardiovascular system are largely unknown. NNK binds to beta1- and beta2-adrenergic receptors. Because beta-adrenergic receptor activation causes arachidonic acid (AA) release and cellular injury, we postulated that NNK causes EC injury by a mechanism that involves beta-adrenergic-mediated release of AA. NNK stimulated [3H]AA release from ECs, and this effect was mediated by both beta1- and beta2-adrenergic receptors because pretreatment with atenolol or ICI 118,551 inhibited the response. NNK also induced EC apoptosis, as measured by terminal deoxyribonucleotide transferase-mediated dUTP nick-end labeling and annexin V staining. NNK-mediated apoptosis was attenuated by pretreatment with atenolol or ICI 118,551. Furthermore, depletion of cellular AA by incubation with eicosapentaenoic acid abolished the apoptotic effect of NNK. These data suggest that NNK causes EC apoptosis by a mechanism that involves beta1- and beta2-adrenergic receptor-mediated release of AA.

Objective: To determine effects of commonly used ophthalmic antibiotics on cellular morphologic characteristics and migration of canine corneal epithelium in cell culture., Sample Population: Corneal epithelial cells harvested from corneas of 12 euthanatized dogs and propagated in cell culture., Procedure: Cells were treated with various antibiotics after a defect was created in the monolayer. Cellular morphologic characteristics and closure of the defect were compared between antibiotic-treated and control cells., Results: Cells treated with ciprofloxacin and cefazolin had the greatest degree of rounding, shrinkage, and detachment from plates. Cells treated with neomycin-polymyxin B-gramicidin and gentamicin sulfate had rounding and shrinkage but with less detachment. Cells treated with tobramycin and chloramphenicol grew similarly to control cells. On the basis of comparisons of defect circumference between control cells and cells exposed to antibiotics, tobramycin affected cellular migration the least., Conclusions and Clinical Relevance: Effects of ciprofloxacin and cefazolin on morphologic characteristics of canine corneal epithelial cells in vitro should be taken into consideration before using these antibiotics for first-line of treatment for noninfected ulcers. Of the antibiotics tested that have a primarily gram-negative spectrum of coverage, gentamicin inhibited corneal epithelial cell migration and had greater cytopathologic effects than tobramycin did. For antibiotics with a gram-positive coverage, chloramphenicol had no cytopathologic effects on cells in comparison to cefazolin, which caused most of the cells to shrink and detach from the plate. Polymyxin B-neomycin-gramicidin was midrange in its effects on cellular morphologic characteristics and migration.

The objective of this study was to examine the role of ion transport mechanisms in clinical anticancer drug resistance. Reduction in intracellular accumulation of cisplatin is believed to be an early change in cisplatin-resistant cells, and may be dependent on the concentration of intracellular chloride (Cl-) ions and intracellular pH. The primary aim of this study was to describe the modifying effects of NHMA (5-N,N hexamethylene; amiloride), a Na+/H+ antiport inhibitor, and/or SITS (4-acetamido-4';isothiocyanostilbene-2,2'-disulfonic acid), a HCO3-/Cl- transport inhibitor, in bicarbonate-containing or bicarbonate-free media on cisplatin (cis-diamminedichloroplatinum(II); CDDP) toxicity between known cisplatin-sensitive (COS31) and cisplatin-resistant (COS31/rCDDP) canine osteosarcoma cells. This study has shown that cell survival can be influenced by the inhibition of the Na(+)-dependent HCO3-/Cl- exchanger using SITS. The addition of SITS increases the intracellular Cl- concentration in canine osteosarcoma cells cultured in a bicarbonate-containing media. In a bicarbonate-free media, the addition of SITS results in a decrease in the cytotoxic action of cisplatin.

Objective: To determine whether serum alpha 1-acid glycoprotein (AGP) concentration was a useful marker of relapse in dogs with lymphoma that were in clinical remission following treatment with doxorubicin., Design: Cohort study., Animals: 12 dogs with lymphoma and 10 healthy dogs., Procedure: Serum AGP concentration was measured in the healthy dogs and in the dogs with lymphoma before treatment, 3 weeks after the first dose of doxorubicin was administered, and every 3 weeks thereafter until relapse (i.e., recurrence of clinically detectable disease such as palpable enlargement of peripheral lymph nodes). Serum AGP concentrations were determined by use of a radial immunodiffusion kit., Results: Mean serum AGP concentration in healthy dogs was significantly less than concentration in dogs with lymphoma prior to treatment. Mean serum AGP concentrations after the first and each subsequent dose of doxorubicin were not significantly different from concentration in healthy dogs. However, mean serum AGP concentrations 3 weeks prior to and at the time of relapse were significantly higher than concentration measured after the first dose of doxorubicin, and were not significantly different from concentration measured before treatment., Clinical Implications: Results suggest that measuring serum AGP concentration may be a useful method of predicting relapse before recurrence of clinically detectable disease in dogs with lymphoma undergoing treatment with doxorubicin.

Background: The objective of this study was to determine if glutathione-S-transferases were detectable in the plasma of dogs and to determine if concentrations of the a- and pi-subtypes were related with tumor response to single agent anthracycline (e.g., doxorubicin) chemotherapy in dogs with lymphoma., Materials and Methods: Plasma was obtained from 10 healthy, normal dogs and from 11 dogs with lymphoma before treatment, 3 weeks after 1 dose of doxorubicin and every 3 weeks thereafter until relapse (the physical detection of recurrent and enlarged peripheral lymph nodes). Plasma concentration of alpha and pi-GST was determined by use of an ELISA technique with well plates pre-coated with IgG[anti-Canine alpha-GST or anti-Human pi-GST]., Results: Mean plasma alpha-GST concentrations did not significantly decline after 1 dose of doxorubicin chemotherapy; however, mean plasma alpha-GST concentrations were markedly increased (p < 0.05) at the time of relapse (the physical detection of recurrent and enlarged peripheral lymph nodes)., Conclusions: In this study we show that a relationship exists between the plasma alpha-GST concentration and the clinical response of dogs with lymphoma to doxorubicin chemotherapy.

Background: In this report we describe the establishment, characterization, and research utility of a cell line derived from a dog having a spontaneously occurring osteosarcoma., Materials and Methods: Tumor samples were collected from a dog with a naturally occurring osteosarcoma and processed for light microscopy, electron microscopy, immunocytochemistry, immunohistochemistry, karyology, and cell culture. Established cells from passage 31 (COS31; canine Qsteosarcoma cells from passage 31) were inoculated subcutaneously between the scapula and in the right abdominal side of athymic nude mice and evaluated similarly., Results: COS31 cells derived in cell culture and in nude mice had morphological and biochemical properties comparable in all respects to the original canine tumor specimen., Conclusions: The ability of COS31 cells to produce tumors in nude mice (i.e. a small animal model) typical of canine osteosarcoma (i.e. a large animal model) with a similar pathological and biological behavior (e.g. alkaline phosphatase and osteocalcin positive immunostaining, osteoid production, rapid growth, and wide spread metastases) demonstrates the potential utility of COS31 cells as a in vitro and in vivo model system in the development of new strategies in the treatment of human osteosarcoma.

Background: In this report we describe the establishment, characterization, and research utility of a cell line derived from a dog having a spontaneously occurring osteosarcoma (COS) made resistant to the cytotoxic effects of cisplatin chemotherapy., Materials and Methods: Established cells from passage 31 (COS31) were exposed to increasing sublethal concentrations of cisplatin in vitro., Results: A 2.2-fold increase in glutathione-S-transferase (GST) activity was found to be induced in this cell line (COS31/rCDDP) compared to parent cells. Furthermore, these cells were 7.8-fold more resistant to the cytotoxic effects of higher concentrations of cisplatin compared to parent cells. Ethacrynic acid was found to inhibit GST enzymatic activity and increase cisplatin cytotoxicity in resistant COS31 (COS31/rCDDP) cells., Conclusions: Inhibiting the function of GST with ethacrynic acid pretreatment in humans and dogs with osteosarcoma may result in more tumor cells than normal cells killed in vivo by cisplatin, thus significantly prolonging lifespan without increasing host toxicity.

The function of the renin-angiotensin-aldosterone system (RAAS) in the mammalian eye remains unclear, although alterations in the concentrations of various pathway components can influence intraocular pressure and the electroretinogram. Angiotensin Converting Enzyme (ACE) has been localized to ocular tissues and fluids. Aqueous humor and serum values of ACE are increased in sarcoid uveitis patients. We used the dog to simultaneously examine the effects of a topically administered ACE inhibitor on the intraocular pressure (IOP), on components of the renin-angiotensin pathway in the serum and aqueous humor, and to monitor any systemic effects of the ACE inhibitor. The novel ACE inhibitor, SCH 33861 (Schering Corporation), decreased IOP in amounts similar to timolol when applied topically to the canine eye. Serum ACE values significantly decreased in SCH 33861 treated dogs, while aqueous ACE values were only slightly decreased. A decrease in heart rate, and systolic and diastolic blood pressure in these dogs during the treatment period indicated probable systemic absorption. Normal values of aqueous humor and serum angiotensin-I were established for the dog. Plasma renin activity and angiotensin-I values were not significantly changed for any of the treatment groups. Topical application of SCH 33861 to the canine eye is a useful model to further evaluate the role of the renin-angiotensin system in the eye.

The histopathologic features of 120 cases of pigmented spindled nevus (PSCN) from the years 1973 through 1988 were reviewed from a consultative practice heavily weighted with difficult nevomelanocytic lesions. The patients' mean age was 25.2 years, and females outnumbered males (68 versus 52). Extremity lesions made up 69.6% of the total, with the thigh the most common site. The lesions were categorized into one of four variants of PSCN, based on the presence or absence of various architectural and cytologic parameters and involvement of the reticular dermis. Thirteen cases (10.8%) were designated typical PSCN, and were characterized by fascicles of uniform pigmented spindle cells without cellular atypia and limited to the epidermis or papillary dermis. Ninety-five cases (79.2%) were classified as atypical PSCN (PSCN with architectural and/or cytologic atypia). Some of the latter also demonstrated substantial numbers of epithelioid cells, thus exhibiting some overlap with Spitz nevus. Eight cases showed striking features of dysplastic nevus. Ten cases had fascicles of pigmented spindle cells involving the reticular dermis ("plexiform" PSCN). Two cases were designated as combined PSCN because of the presence of banal nevus cells in addition to the spindle cell component. Clinical follow-up of a small group of patients has not suggested, to date, any aggressive behavior. Knowledge of PSCN and its atypical variants is important for discrimination from malignant melanoma.

K-562 cells grown in serum-free medium were treated with gamma interferon (IFN-gamma) and they became significantly less susceptible to natural killer (NK) cell-mediated cytolysis. To examine if this loss in susceptibility was related to induced differentiation events, the presence of various antigens was determined after induction. There was a coincident expression of class I HLA common antigen, although it is not clear if this is a direct causal relationship. The level of the constitutively expressed myelomonocytic antigen, reactive with anti-Leu-M1, was not affected by IFN-gamma induction and three normally nonexpressed monocytic antigens, defined by monoclonal antibodies, remained unexpressed. IFN-gamma did induce an enhanced expression of IL-2 receptors on K-562 cells after 2 days of treatment but, thereafter, the expression appeared to be suppressed. Electron microscopy of IFN-gamma-treated cells revealed the development of increased surface blebbing and electron-dense cytoplasmic inclusions. These ultramicroscopic changes could not be correlated with definitive differentiation events. We suggest that IFN-gamma treatment of K-562 cells induces class I HLA expression and morphological changes that may be important to differentiation events that render the cells less susceptible ot NK-mediated cytolysis.

Human interferon-gamma (IFN-gamma), encoded in Escherichia coli by recombinant human DNA, induces the expression of HLA antigens in the pluripotent hematopoietic stem cell line K-562 grown in serum-free growth medium. Expression was noted in 90% of the cells within 4 days and there was a high density of expression per cell, as determined by cytofluorography. Upon subculture, the cells rapidly lose their ability to express HLA, indicating that the continued presence of IFN-gamma is necessary for the expression. Reinduction of expression with IFN-gamma occurs in a high percentage of cells (up to 90%), which is comparable to the induction in freshly treated control cells.