Male accessory gland inflammation or infection （MAGI） is a potentially underdiagnosed complication of type 2 diabetes （DM2）; specifically, we reported in a recent study that the frequency of MAGI was 43% among DM2...Male accessory gland inflammation or infection （MAGI） is a potentially underdiagnosed complication of type 2 diabetes （DM2）; specifically, we reported in a recent study that the frequency of MAGI was 43% among DM2 patients. In previous studies, we have demonstrated that diabetic autonomic neuropathy （DAN） is associated with a peculiar ultrasound characterization of the seminal vesicles （SVs） in DM2 patients. The aim of the present study was to evaluate the frequency of MAGI in two different categories of DM2 patients （i.e. patients with and without symptoms that possibly reflect DAN） and the respective ultrasound characterizations. Sixty DM2 patients with a mean （± s.e.m.） age of 42.0 ± 6.0 years （range： 34-47 years） were classified according to the presence or the absence of symptoms that could possibly reflect DAN （group A： DM2 with symptoms possibly reflecting DAN, n = 28 patients and group B： DM2 without symptoms possibly reflecting DAN, n = 32 patients）. The patients in Group A exhibited a significantly higher frequency of MAGI compared with those in group B patients （P 〈 0.05）; moreover, the Group A patients exhibited a significantly higher frequency of ultrasound signs suggestive of vesiculitis （P 〈 0.05）. Finally, the concentrations of lymphocytes but not the concentrations of the leukocytes in the semen were significantly higher （P 〈 0.05） in group A compared with group B.展开更多
Infection remains an universal important cause of morbidity and mortality,with the highest mortality rate for bloodstream infections（20%-70%）.[1,2]Fortunately,most community acquired infections,
Members of the tumor-necrosis factor-α(TNF-α) and TNF-α receptor(TNFR) superfamilies of proteins(TNFSF and TNFRSF, respectively) play important roles in the function of the immune system. Decoy receptor 3(Dc R3, TN...Members of the tumor-necrosis factor-α(TNF-α) and TNF-α receptor(TNFR) superfamilies of proteins(TNFSF and TNFRSF, respectively) play important roles in the function of the immune system. Decoy receptor 3(Dc R3, TNFRSF6b) is a decoy receptor that binds to three TNFSF ligands, Fas L, LIGHT and TL1 A. Association to these ligands competes with the corresponding functional receptors and blocks downstream signaling, leading to immunomodulatory effects, including the prevention of apoptosis. Dc R3 lacks a transmembrane region and exists only as a secreted protein, which is detectable in biological fluids. Recent studies have shown that Dc R3 is upregulated and may be pathogenetically implicated in several and diverse chronic inflammatory diseases. The strongest associations have been described for rheumatological diseases, mainly systemic lupus erythematosus and rheumatoid arthritis, inflammatory bowel disease, and serious infectious conditions, including systemic inflammatory response syndrome. In the majority of these conditions, Dc R3 m RNA and protein expression is elevated both at the target tissues as well as in the systemic circulation. Dc R3 concentration in the serum is untraceable in the majority of healthy individuals but can be detected in patients with various inflammatory diseases. In mostsuch cases, soluble Dc R3 correlates with disease severity, as patients with severe forms of disease have significantly higher levels than patients with milder or no activity. In addition, effective anti-inflammatory treatment leads to the disappearance of soluble Dc R3 from the circulation. Taken together, current evidence suggests that serum Dc R3 may become a useful biomarker for chronic inflammatory disorders, as it is upregulated in response to inflammatory stimuli, and may serve both as a prognostic marker for disease severity and as a surrogate indicator of response to treatment.展开更多
Pain and itch are unpleasant sensations that often accompany infections caused by viral, bacterial, parasitic, and fungal pathogens. Recent studies show that sensory neurons are able to directly detect pathogens to me...Pain and itch are unpleasant sensations that often accompany infections caused by viral, bacterial, parasitic, and fungal pathogens. Recent studies show that sensory neurons are able to directly detect pathogens to mediate pain and itch. Nociceptor and pruriceptor neurons respond to pathogen-associated molecular patterns, including Toll-like receptor ligands, N-formyl peptides, and bacterial toxins. Other pathogens are able to silence neuronal activity to produce analgesia during infection. Pain and itch could lead to neuronal modulation of the immune system or behavioral avoidance of future patho- gen exposure. Conversely, pathogens could modulate neuronal signaling to potentiate their pathogenesis and facilitate their spread to other hosts. Defining how pathogens modulate pain and itch has critical implications for sensory neurobiology and our understanding of host- microbe interactions.展开更多
文摘Male accessory gland inflammation or infection （MAGI） is a potentially underdiagnosed complication of type 2 diabetes （DM2）; specifically, we reported in a recent study that the frequency of MAGI was 43% among DM2 patients. In previous studies, we have demonstrated that diabetic autonomic neuropathy （DAN） is associated with a peculiar ultrasound characterization of the seminal vesicles （SVs） in DM2 patients. The aim of the present study was to evaluate the frequency of MAGI in two different categories of DM2 patients （i.e. patients with and without symptoms that possibly reflect DAN） and the respective ultrasound characterizations. Sixty DM2 patients with a mean （± s.e.m.） age of 42.0 ± 6.0 years （range： 34-47 years） were classified according to the presence or the absence of symptoms that could possibly reflect DAN （group A： DM2 with symptoms possibly reflecting DAN, n = 28 patients and group B： DM2 without symptoms possibly reflecting DAN, n = 32 patients）. The patients in Group A exhibited a significantly higher frequency of MAGI compared with those in group B patients （P 〈 0.05）; moreover, the Group A patients exhibited a significantly higher frequency of ultrasound signs suggestive of vesiculitis （P 〈 0.05）. Finally, the concentrations of lymphocytes but not the concentrations of the leukocytes in the semen were significantly higher （P 〈 0.05） in group A compared with group B.
文摘Infection remains an universal important cause of morbidity and mortality,with the highest mortality rate for bloodstream infections（20%-70%）.[1,2]Fortunately,most community acquired infections,
文摘Members of the tumor-necrosis factor-α(TNF-α) and TNF-α receptor(TNFR) superfamilies of proteins(TNFSF and TNFRSF, respectively) play important roles in the function of the immune system. Decoy receptor 3(Dc R3, TNFRSF6b) is a decoy receptor that binds to three TNFSF ligands, Fas L, LIGHT and TL1 A. Association to these ligands competes with the corresponding functional receptors and blocks downstream signaling, leading to immunomodulatory effects, including the prevention of apoptosis. Dc R3 lacks a transmembrane region and exists only as a secreted protein, which is detectable in biological fluids. Recent studies have shown that Dc R3 is upregulated and may be pathogenetically implicated in several and diverse chronic inflammatory diseases. The strongest associations have been described for rheumatological diseases, mainly systemic lupus erythematosus and rheumatoid arthritis, inflammatory bowel disease, and serious infectious conditions, including systemic inflammatory response syndrome. In the majority of these conditions, Dc R3 m RNA and protein expression is elevated both at the target tissues as well as in the systemic circulation. Dc R3 concentration in the serum is untraceable in the majority of healthy individuals but can be detected in patients with various inflammatory diseases. In mostsuch cases, soluble Dc R3 correlates with disease severity, as patients with severe forms of disease have significantly higher levels than patients with milder or no activity. In addition, effective anti-inflammatory treatment leads to the disappearance of soluble Dc R3 from the circulation. Taken together, current evidence suggests that serum Dc R3 may become a useful biomarker for chronic inflammatory disorders, as it is upregulated in response to inflammatory stimuli, and may serve both as a prognostic marker for disease severity and as a surrogate indicator of response to treatment.
基金supported by funding from the National Institutes of Health(NCCIH DP2AT009499 and MAID K22AI114810),USA
文摘Pain and itch are unpleasant sensations that often accompany infections caused by viral, bacterial, parasitic, and fungal pathogens. Recent studies show that sensory neurons are able to directly detect pathogens to mediate pain and itch. Nociceptor and pruriceptor neurons respond to pathogen-associated molecular patterns, including Toll-like receptor ligands, N-formyl peptides, and bacterial toxins. Other pathogens are able to silence neuronal activity to produce analgesia during infection. Pain and itch could lead to neuronal modulation of the immune system or behavioral avoidance of future patho- gen exposure. Conversely, pathogens could modulate neuronal signaling to potentiate their pathogenesis and facilitate their spread to other hosts. Defining how pathogens modulate pain and itch has critical implications for sensory neurobiology and our understanding of host- microbe interactions.
