932 research outputs found
Personalised medicine in the UK: challenges of implementation and impact on healthcare system
The role of salivary gland histopathology in primary Sjogren's syndrome:promises and pitfalls
The role of salivary gland histopathology in primary Sjogren's syndrome:promises and pitfalls
Blood Pressure in Patients with Intermittent Claudication Increases Continuously During Walking
ObjectivesThe purpose of this study was to compare the circulatory responses to walking in patients with peripheral atherosclerotic disease (PAD) and healthy controls.MethodsThe participants were eleven patients with diagnosed PAD, and a control group of six healthy age-matched adults. Blood pressure, heart rate (HR), and acral skin perfusion were recorded continuously before, during and after a walking exercise on a treadmill.ResultsThe patients walked to maximum claudication distance (MCD) on a treadmill, median walking distance 103 (34–223) metres [median (range)], at 3.3 (1.0–4.5) km/h. There was a steep increase in HR and mean arterial pressure (MAP) while the patients were walking. At claudication the median rise in MAP was 46.6 (10.3–61.3) mmHg, systolic blood pressure (SP) increased by 84.9 (31.4–124.9) mmHg, and diastolic blood pressure (DP) by 21.7 (−2.1–31.7) mmHg. HR increased by 34.9 (12.9–48.1) beats/min. The control group walked for 5 minutes at 3.2 (3.0–3.3) km/h. In the control group the blood pressure initially increased moderately but stabilised thereafter. Median rise in MAP during walking was 8.5 (5.6–14.6) mmHg, SP increased by 30.9 (6.6–41.5) mmHg, and DP was reduced by −1.4 (−5.4–1.5) mmHg. HR increased by 27.1 (18.8–34.9) beats/min. We found no significant differences in acral skin perfusion during walking exercise between the patients and control group.ConclusionsIn patients with PAD, blood pressure increased continuously and significantly when walking to MCD (dynamic exercise). The level of increase in blood pressure was similar to that caused in response to isometric exercise
Distribution and Longevity of Pratylenchus penetrans in the Red Raspberry Production System
One of the major constraints on the production of red raspberries in the Pacific Northwest is the presence of the rootlesion nematode Pratylenchus penetrans. Current management of this nematode relies heavily on preplant soil fumigation; however, regulations have made the practice more difficult and expensive. Additional issues with soil fumigation include lack of efficacy at deeper soil depths and potential inability to penetrate raspberry root material that remains in the field during fumigation which may harbor P. penetrans. To address these issues, two field experiments were conducted in northwestern Washington. In the first experiment, the residency time of P. penetrans in root material from the previous raspberry crop, which was terminated with or without the use of herbicides, was monitored over time. Pratylenchus penetrans was found in root material from 6 to 8 mon after the crop was terminated, and herbicide application did not reduce P. penetrans residency time compared to untreated root material. In a second experiment, the vertical distribution of P. penetrans at three different times during the field establishment process (pre- and postfumigation, and at planting) was determined at two locations. Both locations had detectable prefumigation P. penetrans populations at all depths. However, postfumigation populations showed a different distribution pattern between locations. The location with coarser soil had populations located mainly at shallower depths with a maximum of 44 P. penetrans/100 g soil at 16 to 30 cm deep, whereas the location with finer soil had populations located mainly at deeper depths with a maximum of 8 P. penetrans/100 g soil at 76 to 90 cm deep. At planting, distribution tended to equilibrate among depths at both locations, but the overall population pattern across depth at each location was similar to that observed at postfumigation. Understanding more about the residency time and distribution of this nematode may provide growers with information that can be used to more effectively target P. penetrans
Undernutrition and sarcopenic obesity:underrecognised conditions in patients with Sjögren's syndrome?
Undernutrition and sarcopenic obesity:underrecognised conditions in patients with Sjögren's syndrome?
Checkpoint inhibition-induced sicca:a type II interferonopathy?
The advent of immune checkpoint inhibitor (ICI) therapy for treatment of cancers is unfortunately coupled with a broad panoply of side effects, related to non-specific activation of the immune system. One such side effect is the development of sicca complaints. This culminates in a proportion of patients who, according to the ACR-EULAR 2016 criteria, can be classified as suffering from the autoimmune disease primary Sjögren's syndrome (pSS). Although salivary gland (SG) loss of function is often seen after ICI therapy, the similarities with 'classical' pSS patients would appear to end there. Despite the presence of focal lymphocytic sialadenitis typical for SS in salivary gland biopsies from patients receiving ICI therapy, the nature of the immune infiltration (foci) following ICI use (T-cell dominated) is starkly different to that in pSS (B-cell dominated). The SG parenchyma post-ICI use does not present with germinal centres, lymphoepithelial lesions or IgG plasma cells, which are frequently found in the SG in pSS. Here we review the functional deterioration of SGs following ICI use, the SG parenchyma phenotype associated with this, and ultrasound abnormalities. We conclude by suggesting that ICI-induced SG dysfunction may represent a new interferonopathy, driven by IFNγ, and that this 'pSS' patient cohort may require a different management than classical pSS patients
Checkpoint inhibition-induced sicca:a type II interferonopathy?
The advent of immune checkpoint inhibitor (ICI) therapy for treatment of cancers is unfortunately coupled with a broad panoply of side effects, related to non-specific activation of the immune system. One such side effect is the development of sicca complaints. This culminates in a proportion of patients who, according to the ACR-EULAR 2016 criteria, can be classified as suffering from the autoimmune disease primary Sjögren's syndrome (pSS). Although salivary gland (SG) loss of function is often seen after ICI therapy, the similarities with 'classical' pSS patients would appear to end there. Despite the presence of focal lymphocytic sialadenitis typical for SS in salivary gland biopsies from patients receiving ICI therapy, the nature of the immune infiltration (foci) following ICI use (T-cell dominated) is starkly different to that in pSS (B-cell dominated). The SG parenchyma post-ICI use does not present with germinal centres, lymphoepithelial lesions or IgG plasma cells, which are frequently found in the SG in pSS. Here we review the functional deterioration of SGs following ICI use, the SG parenchyma phenotype associated with this, and ultrasound abnormalities. We conclude by suggesting that ICI-induced SG dysfunction may represent a new interferonopathy, driven by IFNγ, and that this 'pSS' patient cohort may require a different management than classical pSS patients
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