Apparent diffusion coefficient measurements of the pancreas, pancreas carcinoma, and mass-forming focal pancreatitis

Background Mass-forming focal pancreatitis (FP) may mimic pancreatic cancer (PC) on magnetic resonance (MR) imaging, and the preoperative differential diagnosis is often difficult. Recently, the usefulness of diffusion-weighted imaging (DWI) in the diagnosis of pancreatic cancer has been reported in several studies. Purpose To investigate if apparent diffusion coefficient (ADC) measurements based on diffusion-weighted echo-planar imaging (DW-EPI) may distinguish between normal pancreas parenchyma, mass-forming focal pancreatitis, and pancreas carcinoma. Material and Methods MRI was performed on 64 patients: 24 with pancreas carcinoma (PC), 20 with mass-forming focal pancreatitis (FP), three patients with other focal pancreatic disease as well as 17 controls without any known pancreatic disease. Diffusion-weighted sequence with ADC maps and T2-weighted sequence for anatomical information was performed. Apparent diffusion coefficient (ADC) maps were automatically created and analyzed using a dedicated user interface. In the group with pancreas disease the abnormal parenchyma was detected by using T1- and T2-weighted images and the region of interest (ROI) was transferred exactly to the ADC map and the coefficients were registered. In the control group the ROI was set to the head of the pancreas followed by a similar registration of the ADCs. Results ADC values for mass-forming FP and PC differed significantly from ADC values for normal pancreas parenchyma (P = 0.001/P = 0.002). Mean ADC values for mass-forming FP were 0.69 ± 0.18 × 10−3 mm2/s. ADC values for PC were 0.78 ± 0.11 × 10−3 mm2/s, compared to ADC values of 0.17 ± 0.06 × 10−3 mm2/s in the control group. However there was no significant difference in ADCs between PC and mass-forming FP (P = 0.15). Conclusion ADC measurements clearly differentiated between normal pancreatic tissue and abnormal pancreas parenchyma (PC and mass-forming FP). However there is an overlap in values of PC and mass-forming FP, with the consequent problem of their correct identification

SIGLEC1 (CD169): a marker of active neuroinflammation in the brain but not in the blood of MS patients

OBJECTIVE: We aimed to evaluate SIGLEC1 (CD169) as a biomarker in Multiple Sclerosis (MS) and Neuromyelitis optica spectrum disorder (NMOSD) and to evaluate the specificity of SIGLEC1+ myeloid cells for demyelinating diseases. METHODS: We performed flow cytometry-based measurements of SIGLEC1 expression on monocytes in 86 MS patients, 41 NMOSD patients and 31 healthy controls. Additionally, we histologically evaluated the presence of SIGLEC1+ myeloid cells in acute and chronic MS brain lesions as well as other neurological diseases. RESULTS: We found elevated SIGLEC1 expression in 16/86 (18.6%) MS patients and 4/41 (9.8%) NMOSD patients. Almost all MS patients with high SIGLEC1 levels received exogenous interferon beta as an immunomodulatory treatment and only a small fraction of MS patients without interferon treatment had increased SIGLEC1 expression. SIGLEC1+ myeloid cells were abundantly present in active MS lesions as well as in a range of acute infectious and malignant diseases of the central nervous system, but not chronic MS lesions. CONCLUSION: In our cohort, SIGLEC1 expression on monocytes was – apart from those patients receiving interferon treatment – not significantly increased in patients with MS and NMOSD, nor were levels associated with more severe disease. The presence of SIGLEC1+ myeloid cells in brain lesions could be used to investigate the activity in an inflammatory CNS lesion

SIGLEC1 (CD169): a marker of active neuroinflammation in the brain but not in the blood of multiple sclerosis patients

We aimed to evaluate SIGLEC1 (CD169) as a biomarker in multiple sclerosis (MS) and Neuromyelitis optica spectrum disorder (NMOSD) and to evaluate the presence of SIGLEC1(+) myeloid cells in demyelinating diseases. We performed flow cytometry-based measurements of SIGLEC1 expression on monocytes in 86 MS patients, 41 NMOSD patients and 31 healthy controls. Additionally, we histologically evaluated the presence of SIGLEC1(+) myeloid cells in acute and chronic MS brain lesions as well as other neurological diseases. We found elevated SIGLEC1 expression in 16/86 (18.6%) MS patients and 4/41 (9.8%) NMOSD patients. Almost all MS patients with high SIGLEC1 levels received exogenous interferon beta as an immunomodulatory treatment and only a small fraction of MS patients without interferon treatment had increased SIGLEC1 expression. In our cohort, SIGLEC1 expression on monocytes was—apart from those patients receiving interferon treatment - not significantly increased in patients with MS and NMOSD, nor were levels associated with more severe disease. SIGLEC1(+) myeloid cells were abundantly present in active MS lesions as well as in a range of acute infectious and malignant diseases of the central nervous system, but not chronic MS lesions. The presence of SIGLEC1(+) myeloid cells in brain lesions could be used to investigate the activity in an inflammatory CNS lesion

Inclusive e+^+e−^- production in collisions of pions with protons and nuclei in the second resonance region of baryons

Inclusive e$^+$e$^-$ production has been studied with HADES in $\pi^-$ + p, $\pi^-$ + C and $\pi^- + \mathrm{CH}_2$ reactions, using the GSI pion beam at $\sqrt{s_{\pi p}}$ = 1.49 GeV. Invariant mass and transverse momentum distributions have been measured and reveal contributions from Dalitz decays of $\pi^0$, $\eta$ mesons and baryon resonances. The transverse momentum distributions are very sensitive to the underlying kinematics of the various processes. The baryon contribution exhibits a deviation up to a factor seven from the QED reference expected for the dielectron decay of a hypothetical point-like baryon with the production cross section constrained from the inverse $\gamma$ n$\rightarrow \pi^-$ p reaction. The enhancement is attributed to a strong four-momentum squared dependence of the time-like electromagnetic transition form factors as suggested by Vector Meson Dominance (VMD). Two versions of the VMD, that differ in the photon-baryon coupling, have been applied in simulations and compared to data. VMD1 (or two-component VMD) assumes a coupling via the $\rho$ meson and a direct coupling of the photon, while in VMD2 (or strict VMD) the coupling is only mediated via the $\rho$ meson. The VMD2 model, frequently used in transport calculations for dilepton decays, is found to overestimate the measured dielectron yields, while a good description of the data can be obtained with the VMD1 model assuming no phase difference between the two amplitudes. Similar descriptions have also been obtained using a time-like baryon transition form factor model where the pion cloud plays the major role.Comment: (HADES collaboration

Genetic Evidence for Involvement of Neuronally Expressed S1P1 Receptor in Nociceptor Sensitization and Inflammatory Pain

Sphingosine-1-phosphate (S1P) is a key regulator of immune response. Immune cells, epithelia and blood cells generate high levels of S1P in inflamed tissue. However, it is not known if S1P acts on the endings of nociceptive neurons, thereby contributing to the generation of inflammatory pain. We found that the S1P1 receptor for S1P is expressed in subpopulations of sensory neurons including nociceptors. Both S1P and agonists at the S1P1 receptor induced hypersensitivity to noxious thermal stimulation in vitro and in vivo. S1P-induced hypersensitivity was strongly attenuated in mice lacking TRPV1 channels. S1P and inflammation-induced hypersensitivity was significantly reduced in mice with a conditional nociceptor-specific deletion of the S1P1 receptor. Our data show that neuronally expressed S1P1 receptors play a significant role in regulating nociceptor function and that S1P/S1P1 signaling may be a key player in the onset of thermal hypersensitivity and hyperalgesia associated with inflammation