Rapidly progressive interstitial lung disease combined with pneumocystis jiroveci pneumonia in a patient with single anti-TIF-1γ antibody positive dermatomyositis in the context of an underlying tumor.

BACKGROUND: Interstitial lung disease (ILD) is a frequently observed comorbidity in autoimmune diseases such as dermatomyositis/polymyositis (DM/PM), and it is significantly associated with specific autoantibody types. One unique antibody type is the anti-transcription intermediate factor-1γ antibody (anti-TIF-1γ Ab), which has a positive rate of only 7%. It is often found in combination with malignancy and rarely with ILD, particularly rapidly progressive ILD (RPILD). In some cases, the presence of ILD in individuals with DM may indicate a paraneoplastic syndrome. Pneumocystis jiroveci pneumonia (PJP) typically occurs due to intensive immunosuppressive therapy, human immunodeficiency virus (HIV) infection, or malignancy, and rarely as an isolated condition. CASE PRESENTATION: A 52-year-old man with a history of rapid weight loss but non-HIV infected and not immunosuppressed who presented with fever, cough, dyspnea, weakness of the extremities, characteristic rash and mechanic's hand. Pathogenic tests suggested PJP, laboratory tests suggested a single anti-TIF-1γ Ab positive DM, imaging suggested ILD, and pathology revealed no malignancy. RPILD and acute respiratory distress syndrome (ARDS) developed after anti-infection and steroid hormone therapy. After mechanical support therapy such as Extracorporeal Membrane Oxygenation (ECMO), the patient developed late-onset cytomegalovirus pneumonia (CMVP), complicated bacterial infection, and ultimately death. Additionally, we discuss the potential causes of rapid weight loss, the mechanisms by which anti-TIF-1γ Ab may lead to ILD, and the possible connection between anti-TIF-1γ Ab positivity, rapid weight loss, immune abnormalities, and opportunistic infections. CONCLUSIONS: This case emphasizes the importance of early recognition of malignant tumors and pulmonary lesions, assessment of the body's immune status, prompt initiation of immunosuppressive treatment, and prevention of opportunistic infections in individuals with single anti-TIF-1γ Ab positive DM presenting with rapid weight loss.

Plasma junctional adhesion molecule C levels are associated with the presence and severity of coronary artery disease.

BACKGROUND: Junctional adhesion molecule C (JAM-C) is a novel cell adhesion molecule that belongs to the immunoglobulin superfamily. Previous studies have demonstrated the up-regulation of JAM-C in atherosclerotic vessels in human and in spontaneous early lesions of apoe-/- mice. However, insufficient research is currently available on the association of plasma JAM-C levels with the presence and severity of coronary artery disease (CAD). OBJECTIVES: To explore the relationship between plasma JAM-C levels and CAD. DESIGN AND METHODS: Plasma JAM-C levels were examined in 226 patients who underwent coronary angiography. Unadjusted and adjusted associations were assessed using logistic regression models. ROC curves were generated to examine the predictive performance of JAM-C. C-statistics, continuous net reclassification improvement (NRI) and integrated discrimination improvement (IDI) were obtained to assess the incremental predictive value of JAM-C. RESULTS: Plasma JAM-C levels were significantly higher in patients with CAD and high GS. Multivariate logistic regression analysis showed that JAM-C was independent predictor for the presence and severity of CAD [adjusted OR (95% CI): 2.04(1.28-3.26) and 2.81 (2.02-3.91), respectively]. The optimal cutoff value of plasma JAM-C levels for predicting the presence and severity of CAD was 98.26 pg/ml and 122.48 pg/ml, respectively. Adding JAM-C to the baseline model improved the global performance of the model [C-statistic increased from 0.853 to 0.872, p = 0.171; continuous NRI (95% CI): 0.522 (0.242-0.802), p < 0.001; IDI (95% CI): 0.042 (0.009-0.076), p = 0.014]. CONCLUSIONS: Our data showed that plasma JAM-C levels are associated with the presence and severity of CAD, suggesting that JAM-C may be a useful marker for the prevention and management of CAD.

Construction and sustained release of konjac glucomannan/naringin composite gel spheres.

Objective: To improve the bioavailability of active substances and reduce the toxic and side effects on the human body, natural biological macromolecules are used to load active substances and control their release speed in different environments of the human body. In this study, mesoporous silica (MSN) was combined with konjac glucomannan (KGM) and sodium alginate (AC) to prepare pH-sensitive konjac glucomannan/sodium alginate-mesoporous silica loaded naringin gel spheres (KS/MSN). On this basis, the structure, morphology, and release properties of the composite gel spheres were characterized. The results showed that the cumulative release rates of both simulated gastric fluid (SGF) and Simulated colonic fluid (SCF) were lower than that of simulated small intestinal fluid (SIF), which indicated that the prepared composite gel spheres were pH-sensitive to SIF and obtained the best release rate of about 70% under SIF environment. Methods: The pH-sensitive konjac glucomannan/sodium alginate composite gel spheres (KGM/SA) were prepared by combining inorganic nano-materials mesoporous silica (MSN) with natural macromolecular polysaccharides konjac glucomannan (KGM) and sodium alginate (SA) and characterized. Results: The results showed that there was a process of ionic crosslinking and entanglement between konjac glucomannan (KGM) and sodium alginate (SA). Naringin (NG) and mesoporous silica (MSN) were successfully compounded and had good compatibility. The gel microstructure diagram showed that the addition of MSN improved the gel properties of KGM, and KGM and SA gel spheres (KGM/SA) had good compatibility with mesoporous silica/naringenin nanoparticles (NG/MSN). The study of the simulated digestive environment of the gastrointestinal release medium showed that Konjac glucomannan/sodium alginate-mesoporous silica loaded naringin gel spheres (KS/NM) composite gel spheres had the best slow-release effect and the highest final-release completion degree in SIF. The release of NG from KS/NM composite gel spheres showed a slow upward trend. The results showed that KS/NM composite gel spheres were pH-sensitive. Conclusion: The KS/NM composite gel spheres showed obvious pH sensitivity to the release of NG, and the gel spheres had a good sustained release effect on NG.

Devazepide suppresses cell proliferation and migration, and induces apoptosis in bladder carcinoma.

BACKGROUND: This study aimed to examine the effects of devazepide on the proliferation, migration, and apoptosis of human bladder cancer (BC) 5637 cells, and its mechanism. METHODS: A cell counting kit-8 (CCK-8) for cell viability assays, a colony formation assay, and immunofluorescence were applied to detect the effects of devazepide on the proliferation of 5637 cells. Cell cycle assay, cell apoptosis assay and wound healing assay were performed to detect the effects of devazepide on the cell cycle, apoptosis, and migration of 5637 cells. The protein expression of CyclinD1, Bcl-2-associated X protein (Bax), poly ADP-ribose polymerase 1 (PARP1), and Cleaved Caspase-3 in 5637 cells was detected by a western blot assay. RESULTS: The proliferation of 5637 cells was significantly inhibited (P<0.001) after incubation with 12, 25, and 50 µM devazepide for 48 and 72 h. A treatment of 25 µM devazepide for 48 h induced G1-S cell cycle arrest and apoptosis (P<0.01), and inhibited cell migration (P<0.05). By western blot assay, we found that devazepide can down-regulate CyclinD1 expression, and up-regulate Bax, PARP1, and Cleaved Caspase-3 expression. CONCLUSIONS: Devazepide inhibits the migration and proliferation of human BC 5637 cells by arresting the G1-S cell cycle, and induces cell apoptosis.