tbuckley/cabot-search huggingface dataset:
DNA-based immunization produces Th1 immune responses to hepatitis delta virus in a mouse model
Authors: Yi-Hsiang Huang, Jaw-Ching Wu, Mi-Hua Tao, Wan-Jr Syu, Sheng-Chieh Hsu, Wei-Kuang Chi, Full-Young Chang, Shou-Dong Lee
Journal: Hepatology (2000)

Hepatitis delta virus (HDV) superinfection is one of the major causes of fulminant hepatitis in endemic areas of hepatitis B virus (HBV) infection. Currently, there is no effective treatment or vaccine against HDV superinfection. DNA-based immunization is a promising antiviral strategy to prevent or treat persistent viral infections. In this study, we investigated the immunological effects of DNA vaccines against HDV in BALB/c mice. Plasmid (pD) encoding large hepatitis D antigen (L-HDAg), or plasmid (pS/pD) coexpressing hepatitis B surface antigen (HBsAg) and L-HDAg, were injected into mice intramuscularly. The seroconversion rate, anti-HBs levels, anti-HDV titers, T-cell proliferation responses, and T-helper (Th)-release cytokine profiles were analyzed. Mice immunized with plasmids, pS/pD or pD, produced low, but significant, titers of anti-HDV antibodies. In contrast, pS/pD induced much stronger anti-HBs titers in the immunized animals. Interestingly, splenic lymphocytes derived from pS/pD-inoculated mice demonstrated significant proliferation responses to recombinant HBsAg and HDAg, and resulted in a Th1-like immune response as suggested by the production of interferon gamma (INF-gamma) and interleukin-2 (IL-2), but not IL-4. The splenic lymphocyte derived from the pD-inoculated mice showed a similar Th1 response to the stimulation of HDAg, but not to HBsAg. In conclusion, our results suggest that DNA vaccines against HDV can induce significant cellular immune responses with a Th1 preference. HBV and HDV coimmunization can be performed by DNA vaccines. These results are promising for the future development of prophylactic and therapeutic HDV vaccines.
VASCULAR NAEVI AND THEIR TREATMENT
Authors: REGINALD T. BRAIN, CHARLES D. CALNAN
Journal: British Journal of Dermatology (1952)

Journal Article VASCULAR NAEVI AND THEIR TREATMENT Get access REGINALD T. BRAIN, M.D., F.R.C.P., REGINALD T. BRAIN, M.D., F.R.C.P. Search for other works by this author on: Oxford Academic Google Scholar CHARLES D. CALNAN, M.D., M.R.C.P. CHARLES D. CALNAN, M.D., M.R.C.P. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 64, Issue 4, 1 April 1952, Pages 147–153, https://doi.org/10.1111/j.1365-2133.1952.tb16178.x Published: 01 April 1952
TREATMENT OF URETHRAL STRICTURE IN THE MALE.Read in the Section on Surgery and Anatomy, at the Forty-fifth Annual Meeting of the American Medical Association, held in San Francisco, June 5-8, 1894.
Authors: JULIUS ROSENSTIRN
Journal: JAMA (1894)

To give you an elaborate description of all the different devices to relieve suffering man from strictures of his urethral canal would be very tiresome indeed. Fortunately, the ten minute limit precludes any such wild desire on my part, and I shall give you simply a brief aphoristical record of my personal views and conclusions, drawn from a rather ample experience. Urethral strictures are attacked either by gradual dilatation, rapid dilatation, divulsion, electrolysis, internal or external urethrotomy or both combined, either the perineal or high section or urethrectomy with or without urethroplasty. The treatment of strictures varies according to their size. Strictures of large caliber as over No. 14 or 15 French, (a French measure that is the only rational one and should be universally adopted) should nearly always be treated by gradual dilatation. Metallic sounds are the best for the purpose. Use antiseptic precautions. Clean the glans and prepuce
Optimization of dietary folate or low-dose folic acid supplements lower homocysteine but do not enhance endothelial function in healthy adults, irrespective of the methylenetetrahydrofolate reductase (C677T) genotype
Authors: Catherine H Pullin, Pauline A.L Ashfield-Watt, Michael L Burr, Zoë E Clark, Malcolm J Lewis, Stuart J Moat, Robert G Newcombe, Hilary J Powers, Jenny M Whiting, Ian F.W McDowell
Journal: Journal of the American College of Cardiology (2001)
Consent Policies and Rates of HIV Testing
Authors: Enrico Girardi, Vincenzo Puro, Gabriella De Carli, Nicoletta Orchi, Giuseppe Ippolito
Journal: JAMA (2007)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Calmodulin, zinc, and calcium in cellular and membrane regulation: An interpretive review
Authors: George J. Brewer
Journal: American Journal of Hematology (1980)

Abstract A considerable amount of work in recent years has indicated that the intracellular effects of calcium are mediated primarily by calcium‐binding proteins. One of the most important of these proteins is a 17,000‐molecular weight protein–calmodulin. Calmodulin, when activated by calcium, has the potential to activate many enzymes and to stimulate many intracellular events. While calcium is required for many types of cellular activations, zinc tends to be a cellular inhibitor. It appears that zinc is antagonistic to calcium, tending to inhibit the same cellular reactions triggered by an influx of intra‐cellular calcium. Recent investigations have led us to hypothesize that the zinc‐calcium antagonism mentioned above may be the result of inhibitory effects of zinc on calmodulin‐stimulated functions. This inhibition may operate through binding of zinc to the target proteins of calmodulin or through binding of zinc to calmodulin after the calmodulin is complexed to protein. This area will be reviewed in the first part of this paper. In the erythrocyte, excessive intracellular calcium causes hemoglobin retention by erythrocyte membranes and causes erythrocyte shrinkage. Both of these events may occur in sickle erythrocytes because of sickling‐induced calcium accumulation. Recent studies suggest that excessive calcium‐activated calmodulin may be responsible for both hemoglobin retention by the membrane and for erythrocyte shrinkage. On the other hand, trifluoperazine — a phenothiazine drug that inhibits the action of calmodulin — causes erythrocyte swelling (membrane expansion). These observations have led us to hypothesize that calmodulin is intimately involved with regulation of the erythrocyte membrane expansion/shrinkage state. The possible role of excessive calcium‐activated calmodulin in inducing abnormalities in the sickle membrane may lead to a more rational therapy aimed at the membrane lesion in this disease. This therapy might involve a combination of inhibitory agents such as zinc and a phenothiazine. In the last part of the review, we present a model for the regulation of membrane shrinkage by calmodulin in equilibrium with membrane expansion by spectrin‐actin phosphorylation. Whether or not this model is right in its basic elements, we hope it will provoke some additional thinking and experimental work. In fact, this entire review should be viewed as interpretive. That is, observations from diverse sources have been put together in an attempt to make sense out of them and, in particular, to provoke thinking and stimulate experimental work in these areas.
Exocrine Pancreatic Function in Tropical Fibrocalculous Pancreatic Diabetes
Authors: Viswanathan Mohan, Chamukuttan Snehalatha, Mohamed Riazuddin Ahmed, Nagendram Madanagopalan, Suresh Chari, Venkatraman Jayanthi, Sathyasekaran Malathi, Ambady Ramachandran, Moopil Viswanathan
Journal: Diabetes Care (1989)

Exocrine pancreatic function was studied by fecal chymotrypsin test in three groups of diabetic patients seen in southern India. Exocrine pancreatic insufficiency, as shown by low fecal chymotrypsin levels, was seen in 87.5% of patients with fibrocaiculous pancreatic diabetes (FCPD), in 23.5% of insulindependent diabetes mellitus patients, and in 4.5% of non-insulin-dependent diabetes mellitus patients. There was no correlation between fecal chymotrypsin levels and serum amylase, serum lipase, age, body mass index, duration of diabetes, fasting plasma glucose, or glycosylated hemoglobin levels. The fecal chymotrypsin test is a useful additional investigation for the diagnosis of FCPD found in tropical countries.
Woman in persistent vegetative state can die, rules judge
Authors: Clare Dyer
Journal: BMJ (2006)

A woman in a persistent vegetative state is to have artificial nutrition and hydration withdrawn to allow her to die with “dignity” after failing to respond to a drug which is said to have woken up some unconscious patients. 

England's senior family judge, Sir Mark Potter, ruled last week that doctors could lawfully withdraw all life sustaining treatment from the 53 year old mother, named only as J, who has been in a persistent vegetative state for more than three years after she had a brain haemorrhage on a family holiday in August 2003. 

Her …
SOME LEGAL PHASES OF THE "PATENT MEDICINE" QUESTION.
Authors: CHARLES H. WILLIAMS
Journal: JAMA (1907)

Taking the expert testimony, which has been presented on the question under consideration, to be a substantially correct statement of the facts, and conceding, in fairness to the prisoners at the bar, the "patent medicine" men, that these witnesses, filled with zeal as to the merit of their case, have perhaps gone further than the court, in the impartiality incident to its position, would go in its findings of fact, there can be no question, in the minds of those untrammeled by self-interest, that the "patent medicine" business, as exploited to-day, is a serious evil. That the methods frequently employed for the purpose of inducing the public to buy these remedies are positively dishonest and fraudulent, and that the remedies themselves are in many instances of no medicinal value, can not be questioned. Leaving for the moment the more serious phase of the question, the harmful physiologic effects which naturally
Sendai virus infection changes the subcellular localization of tryptase Clara in rat bronchiolar epithelial cells
Authors: K Sakai, T Kohri, M Tashiro, Y Kishino, H Kido
Journal: European Respiratory Journal (1994)

Tryptase Clara activates the infectivity of Sendai and influenza viruses proteolytically. In this study, we investigated changes in the subcellular localization of tryptase Clara in rat bronchioles with progression of Sendai virus infection. Tryptase Clara and Sendai virus F2 antigen were localized by light and electron immunohistochemical studies. In the uninfected rat lung, tryptase Clara was specifically localized in the secretory granules of respiratory bronchiolar epithelial nonciliated cells, but not in bronchiolar ciliated, or alveolar cells. In the initial stage of Sendai virus infection with slight pathological changes, however, anti-tryptase Clara was highly reactive in luminal peripheral membranes of both nonciliated and ciliated epithelial cells of the bronchioles together with some Sendai virus envelope glycoprotein, F2 antigen. In the progressed stage, tryptase Clara was hard to detect, with heavy accumulation of F2 antigen in the epithelial cells. These immunohistochemical results support our previous findings that in the bronchial lavage fluid tryptase Clara is significantly increased both in amount and activity after viral infection. These results suggest that Sendai virus stimulates the secretion of tryptase Clara from nonciliated bronchiolar epithelial cells to the airway lumen. Accumulation of tryptase Clara on the luminal surface of the bronchiolar epithelial cells and/or in the airway lumen may produce favourable conditions for proteolytic viral activation and multiplication.
Re: Florian Jentzmik, Carsten Stephan, Kurt Miller, et al. Sarcosine in Urine After Digital Rectal Examination Fails as a Marker in Prostate Cancer Detection and Identification of Aggressive Tumours. Eur Urol 2010;58:12–8
Authors: Amitha K Hewavitharana
Journal: European Urology (2010)
Impact of Artemisinin-Based Combination Therapy and Insecticide-Treated Nets on Malaria Burden in Zanzibar
Authors: Achuyt Bhattarai, Abdullah S Ali, S. Patrick Kachur, Andreas Mårtensson, Ali K Abbas, Rashid Khatib, Abdul-wahiyd Al-mafazy, Mahdi Ramsan, Guida Rotllant, Jan F Gerstenmaier, Fabrizio Molteni, Salim Abdulla, Scott M Montgomery, Akira Kaneko, Anders Björkman
Journal: PLoS Medicine (2007)

Background The Roll Back Malaria strategy recommends a combination of interventions for malaria control. Zanzibar implemented artemisinin-based combination therapy (ACT) for uncomplicated malaria in late 2003 and long-lasting insecticidal nets (LLINs) from early 2006. ACT is provided free of charge to all malaria patients, while LLINs are distributed free to children under age 5 y ("under five") and pregnant women. We investigated temporal trends in Plasmodium falciparum prevalence and malaria-related health parameters following the implementation of these two malaria control interventions in Zanzibar. Methods and Findings Cross-sectional clinical and parasitological surveys in children under the age of 14 y were conducted in North A District in May 2003, 2005, and 2006. Survey data were analyzed in a logistic regression model and adjusted for complex sampling design and potential confounders. Records from all 13 public health facilities in North A District were analyzed for malaria-related outpatient visits and admissions. Mortality and demographic data were obtained from District Commissioner's Office. P. falciparum prevalence decreased in children under five between 2003 and 2006; using 2003 as the reference year, odds ratios (ORs) and 95% confidence intervals (CIs) were, for 2005, 0.55 (0.28–1.08), and for 2006, 0.03 (0.00–0.27); p for trend < 0.001. Between 2002 and 2005 crude under-five, infant (under age 1 y), and child (aged 1–4 y) mortality decreased by 52%, 33%, and 71%, respectively. Similarly, malaria-related admissions, blood transfusions, and malaria-attributed mortality decreased significantly by 77%, 67% and 75%, respectively, between 2002 and 2005 in children under five. Climatic conditions favorable for malaria transmission persisted throughout the observational period. Conclusions Following deployment of ACT in Zanzibar 2003, malaria-associated morbidity and mortality decreased dramatically within two years. Additional distribution of LLINs in early 2006 resulted in a 10-fold reduction of malaria parasite prevalence. The results indicate that the Millennium Development Goals of reducing mortality in children under five and alleviating the burden of malaria are achievable in tropical Africa with high coverage of combined malaria control interventions.
Spread of SARS slows
Authors: J. Parry
Journal: BMJ (2003)

The outbreak of severe acute respiratory syndrome (SARS) has slowed considerably, with only 182 new cases worldwide in the week to 2 June, taking the total to 8384. However, the disease claimed another 45 lives during the week, and the death toll stood at 770 people.

The World Health Organization is cautiously optimistic that the outbreak in China is now under control and that the disease is on the decline in Taiwan, but Canada is experiencing a fresh outbreak linked to four Toronto hospitals.

“As we approach the three month mark since the global alert was issued on 12 March, we are confident that the SARS outbreak is well on its way to being contained globally,” said Peter Cordingley, WHO's spokesman in Manila.

“However, there are still pockets of anxiety, particularly in the more remote provinces of China and possibly Taiwan, and what has happened in Toronto should be a lesson to health authorities everywhere that nobody can afford to let their guard down,” he added.

By 2 June Canada had reported 198 probable cases, and the new outbreak has put Canada back on WHO's list of areas with local transmission, 12 days after it was taken off. The death toll has risen to 31, and autopsies …
Researchers say they will send unpublished alteplase data to UK drug regulator on request
Authors: D. Cohen, H. Macdonald
Journal: BMJ (2015)

Previously unpublished data that could potentially resolve concerns over the safety and efficacy of the acute ischaemic stroke drug alteplase will be made available to the UK drug regulator on request, an email seen by The BMJ has indicated.

Alteplase is the only thrombolytic drug with a licence for the management of acute ischaemic stroke. In some countries in Europe, including the United Kingdom, it is marketed for use within four and a half hours of onset of symptoms, and in the United States it is marketed for use within three hours. 

However, the use of alteplase has been shrouded in controversy almost since the drug was approved (1996 in the US and 2002 in parts of Europe), with some doctors and academics questioning its efficacy and safety and the methodology of some of the trials. 

In August 2014 the UK Medicines and Healthcare Products Regulatory Agency (MHRA) convened a group of experts to review “any new information or concerns about the data that underpin the present marketing authorisation” of alteplase,1 after a letter in the Lancet …
Effect of promoters on incidence of bladder cancer in experimental animal models.
Authors: R M Hicks
Journal: Environmental Health Perspectives (1983)

Multistage models of carcinogenesis proposed to account for the observed patterns of tumor development in the skin, liver, lung, bladder and other organs involve initiation of neoplastic change in a few cells by a threshold dose of carcinogen followed by conversion of these latent tumor cells into an autonomous cancer by further doses of the same and/or other carcinogens, and/or noncarcinogenic promoting agents. In the rat urinary bladder, neoplastic change can be initiated by a few weeks treatment with low doses of N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) or N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) or by a single, low dose, intravesicular instillation of N-methyl-N-nitrosourea (MNU). Very few animals treated thus will develop bladder cancer unless exposed subsequently to some further regime which will promote tumor growth from the initiated cells. Many different factors will stimulate tumor growth in the initiated rat bladder, including further low doses of complete bladder carcinogens, dietary factors such as metabolites of tryptophan or deficiency of vitamin A, the food additives saccharin and cyclamate and some alkylating agents such as cyclophosphamide and methylmethane sulfonate. New and published evidence is reviewed which supports the belief that these and other factors are promoters or later stage carcinogens in the bladder. The difficulties of defining a promoter and of identifying markers of promotion, i.e., of distinguishing the second from the later stages of carcinogenesis in the urinary bladder, are discussed with reference to the action of promoters in the mouse skin initiation/promotion model. However, in terms of their effect on an initiated population on the risk of developing cancer, it is suggested that such a distinction is largely irrelevant. Since both second and later stage carcinogens accelerate tumor development in an initiated urothelium, they both have the potential to lower the age at which bladder cancer becomes symptomatic. They are thus as important as are initiating carcinogens in determining the patterns of age-related neoplastic disease in any population.
Genetics and halothane hepatitis.
Authors: M J Cousins, G K Gourlay, P Hall, J Adams
Journal: BMJ (1981)

isolation of G vaginalis together with the significantly higher isolation rate among heterosexual men suggests that while gardnerella infection of the male urethra is unlikely, colonisation of this site may be an important factor in the epidemiology of "non-specific" vaginitis.This should be borne in mind when setting up and evaluating trials of therapy for this condition.
Biosynthetic and proliferative characteristics of tubulointerstitial fibroblasts probed with paracrine cytokines
Authors: René J. Alvarez, Mae Jane Sun, Thomas P. Haverty, Renato V. Iozzo, Jeanne C. Myers, Eric G. Neilson
Journal: Kidney International (1992)

Biosynthetic and proliferative characteristics of tubulointerstitial fibroblasts probed with paracrine cytokines.Fibroblasts in parenchymal organs potentially contribute extracellular matrix to local fibrogenic processes.This contribution, in some circumstances, may be initiated by cytokines disseminated from inflammatory lesions.Different populations of fibrobiasts, however, might respond distinctively to this cytokine bath depending on the microenvironment in which they reside.We have begun to explore this issue using syngeneic, low-passage fibroblasts cultured in serum-free media that were derived originally from the dermis (DFBs) and from tubulointerstitium (TFB5) of the kidney.Our findings indicate that, while fibroblasts from each compartment appear similar at the ultrastructural level, there are a variety of functional differences which distinguish their proliferative response, and their collagen secretory response (types I, III, IV, and V) following challenge with various doses of immune-relevant cytokines (TGF/3, EGF, IL-i, IL-2 and yIFN) in culture.DFB5, for example, express more surface EGF receptors than do TFBs, and, as a consequence, exhibit a more robust proliferative response to EGF in serum-free media.Unstimulated DFBs also secrete more collagen types I and III than TFBs, while unstimulated TFBs secrete more types IV and V.The expression of these collagens in TFBs was confirmed by Northern blot hybridization.When these sets of fibroblasts were further stimulated by cytokines, some of the cytokines not only differentially effect the secretion of various species of collagens within the same group of cells, but also between cells from populations which are anatomically distinct.DFBs, furthermore, at mid-level doses of cytokine, demonstrated a general trend towards less secretion of all types of collagen (particularly for TGFf3, EGF, and IL-2), while TFBs seemed less repressive.In TFBs the cytokine-induced responses for collagen types I and III tended to be discordant, and for types I and IV EGF inhibited, while TGFI3 stimulated the secretory process.These findings speak collectively for the presence of a functional heterogeneity among organ-based populations of syngeneic fibroblasts in normal tissues.Fibrosis in parenchymal organs is the pernicious end-product of progressive deposition of extracellular matrix remodelling normal somatic architecture [1-31.Such damage is typically preceded by inflammatory events which activate a variety of tissue resident cells including fibroblasts [4, 51.The fibrogenesis of organs, with its attendant distortion of normal structures, is also frequently the late consequence of autoimmune injury