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In many electrically non-excitable cells, Ca2+ entry is mediated predominantly by the store-operated Ca2+ influx pathway. The best-characterised store-operated Ca2+ current is the Ca2+ release-activated Ca2+ current (ICRAC). It is generally believed that high concentrations of intracellular Ca2+ buffer are required to measure ICRAC, due to Ca2+-dependent inactivation of the channels. Recently, we have recorded robust ICRAC in rat basophilic leukaemia (RBL-1) cells at physiological levels of Ca2+ buffering when stores were depleted by inhibition of the sarcoplasmic/ endoplasmic reticulum Ca2+-activated adenosine triphosphatase (SERCA) pumps. However, the second messenger inositol 1,4,5-trisphosphate (InsP3) was not able to evoke the current under such conditions, despite inducing substantial Ca2+ release. We have therefore suggested that a threshold exists within the Ca2+ stores which has to be overcome for macroscopic ICRAC to activate. To establish whether this is a specific feature of ICRAC in RBL-1 cells or whether it is a more general phenomenon, we investigated whether a threshold is also seen in other cell-types used to study store-operated Ca2+ entry. In Jurkat-T lymphocytes, ICRAC is activated weakly by InsP3 in the presence of low concentrations of Ca2+ buffer, whereas the current is large when SERCA pumps are blocked simultaneously, as in RBL-1 cells. Although the electrophysiological properties of ICRAC in the Jurkat cell are very similar to those of RBL-1 cells, the Na+ conductance in the absence of external divalent cations is quite different. Unexpectedly, we failed consistently to record any store-operated Ca2+ current in macrovascular pulmonary artery endothelia whereas robust ICRAC was seen under the same conditions in RBL-1 cells. Our results show that ICRAC has a similar profile of activation in the presence of physiological levels of Ca2+ buffering for Jurkat T-lymphocytes and RBL-1 cells, indicating that the threshold mechanism may be a general feature of ICRAC activation. Because ICRAC in pulmonary artery endothelia is, at best, very small, additional Ca2+ influx pathways may also contribute to agonist-induced Ca2+ entry. 相似文献
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Rashi Jain Rinkee Kumari Sushmita Chakraborty Dipendra K. Mitra Anant Mohan Vijay Hadda Karan Madan Randeep Guleria 《European journal of immunology》2023,53(10):2250255
Sarcoidosis is a systemic inflammatory disorder characterized by tissue infiltration due to mononuclear phagocytes and lymphocytes and associated noncaseating granuloma formation. Pulmonary sarcoidosis (PS) shares a number of clinical, radiological, and histopathological characteristics with that of pulmonary tuberculosis (PTB). Due to this, clinicians face issues in differentiating between PS and PTB in a substantial number of cases. There is a lack of any specific biomarker that can diagnose PS distinctively from PTB. We compared T-cell-based signature cytokines in patients with PS and PTB. In this study, we proposed a serum biomarker panel consisting of cytokines from cells: T helper (Th) 1 [interferon-gamma (IFN-γ); tumor necrosis factor-alpha (TNF-α)], Th9 [interleukin (IL)-9], Th17 [IL-17], and T regulatory (Treg) [IL-10; transforming growth factor-beta (TGF-β)]. We performed the principal component analysis that demonstrated that our serum cytokine panel has a significant predictive ability to differentiate PS from PTB. Our results could aid clinicians to improve the diagnostic workflow for patients with PS in TB endemic settings where the diagnosis between PS and PTB is often ambiguous. 相似文献
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Patankar T Krishnan A Patkar D Kale H Prasad S Shah J Castillo M 《Skeletal radiology》2000,29(7):392-396
Objective. To review imaging studies of isolated involvement of the sacrum due to tuberculosis and determine the role of imaging in
the diagnosis and management of these patients.
Design and patients. A retrospective analysis of 15 cases of isolated sacral tuberculosis imaged with MR imaging was performed. The CT images
were also reviewed where available, and the various lesion characteristics were identified. We also reviewed the medical records
in an attempt to determine the impact of the imaging studies on the management of these patients.
Results. Fifteen patients (5 male, 10 female) presented with symptoms of 3–15 months’ duration. Chronic localized backache with muscle
spasm was the commonest presenting symptom; discharging sinuses with abscess formation was found in six patients, five of
whom were children. MR imaging of the sacrum revealed a hypointense marrow signal on T1-weighted images and hyperintense signal
on T2-weighted images in 14 of 15 patients, the S2 vertebra being always involved. CT revealed osteolytic changes in the sacrum
in all the five patients in whom CT was performed. All patients showed marked clinical improvement within 1 year of anti-tuberculous
chemotherapy.
Conclusion. Isolated tuberculosis of the sacrum is uncommon but should be suspected in patients presenting with chronic low backache
or children with discharging sinuses/abscesses and showing sacral destruction on CT or MR imaging. MR imaging can identify
cases and enables early institution of anti- tuberculous chemotherapy.
Received: 31 August 1999 Revision requested: 1 November 1999 Revision received: 27 March 2000 Accepted: 14 April 2000 相似文献
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Cerebral microbleeds have emerged as an important new imaging marker of cerebral small vessel disease. With the development of MRI techniques that are exquisitely sensitive to paramagnetic blood products, such as T2*-weighted gradient-recalled echo and susceptibility-weighted sequences, microbleeds have been detected in ever-increasing numbers of patients in stroke and cognitive clinics, as well as in healthy older people and in a variety of other rarer diseases and syndromes. Detection of cerebral microbleeds has clinical implications with respect to the diagnosis of the underlying small vessel disease, the safety of antithrombotic use, and the risk of symptomatic intracerebral haemorrhage, cognitive impairment and dementia. This article provides a guide to the detection and clinical relevance of cerebral microbleeds in different conditions based on a comprehensive review of the literature and own findings in research and clinical practice. 相似文献
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Daniel Bakowski Charmaine Nelson Anant B. Parekh 《Pflügers Archiv : European journal of physiology》2012,464(1):27-32
Plasma membrane store-operated Ca2+ release-activated Ca2+ (CRAC) channels are a widespread and conserved Ca2+ influx pathway, driving activation of a range of spatially and temporally distinct cellular responses. Although CRAC channels are activated by the loss of Ca2+ from the endoplasmic reticulum, their gating is regulated by mitochondria. Through their ability to buffer cytoplasmic Ca2+, mitochondria take up Ca2+ released from the endoplasmic reticulum by InsP3 receptors, leading to more extensive store depletion and stronger activation of CRAC channels. Mitochondria also buffer Ca2+ that enters through CRAC channels, reducing Ca2+-dependent slow inactivation of the channels. In addition, depolarised mitochondria impair movement of the CRAC channel activating protein STIM1 across the endoplasmic reticulum membrane. Because they regulate CRAC channel activity, particularly Ca2+-dependent slow inactivation, mitochondria influence CRAC channel-driven enzyme activation, secretion and gene expression. Mitochondrial regulation of CRAC channels therefore provides an important control element to the regulation of intracellular Ca2+ signalling. 相似文献