Acrocephalosyndactylia ; pathology ; Fetus ; pathology ; Humans

Objective To investigate the relationship between interleukin (IL)-34 and bone erosions in psoriatic arthritis (PsA) patients.Methods Forty PsA patients,20 psoriasis (Ps) patients and 20 healthy volunteers were recruited into this study.The levels of IL-34 and osteoclast related cytokines [including tumor necrosis factor (TNF)-α,receptor activator of nuclear factor-κB ligand (RANKL),osteoclast precursors (OPG)] were detected in the serum samples of all subjects.The correlations among IL-34,the number of osteoclast precursors (OCP),disease activity and imaging scores were analyzed.All data were analyzed by graphpad prism 6.Differences between groups was analyzed with One-way analysis of variance,q tests,and Spearman's correlation was used to explore the relation between disease activity/radiographic scores and laboratory results and followed by linear regressions.Results The serum level of IL-34 in patients with PsA [(328±476) pg/ml] was higher than that in Ps [(33±52) pg/ml,q =3.92,P＜0.01] and healthy controls [(32±32) pg/ml,q =3.93,P＜0.01],the erosive PsA group were higher than the non-erosive PsA group [(449±527) pg/ml and (47±24) pg/ml,q=4.04,P＜0.01].The levels of TNF-α,RANKL and OCP in patients with PsA [(125±79) pg/ml,(488± 475) pg/ml and (17.7±4.8) 5 sigh views] were higher than those in PS [(40±22) pg/ml,(26±3) pg/ml and (5.2± 0.8),q=7.32,6.14 and 2.94,P＜0.01] and healthy controls [(41±19) pg/ml,(65±8) pg/ml and (6.2±1.8),q=6.67,5.62 and 2.71,P＜0.01],whereas the OPG/RANKL ratio in PsA patients (0.5±0.4) was significantly lower than Ps patients (4.3±2.7,q=-3.30,P＜0.01) and healthy controls (1.8±0.6,q=-1.72,P＜0.01).IL-34,TNF-α and RANKL levels were all positively correlated with OCP (r=0.10,P＜0.05;r=0.12,P＜0.05;r=0.13,P＜0.(5,respectively).Conclusion The level of IL-34 is not only high in patients with PsA but also positively correlates with the number of OCP.In PsA,IL-34 is probably related to the OCP and osteoclast differentiation,and further participates in the process of bone destruction.Therefore,IL-34 is promising to become a new target or alternative choice for the treatment of PsA.

Objective To investigate the protective effects and molecular mechanism of peroxisome proliferate-activated receptor α(PPARα) activation on acute myocardial damage induced by isoproterenol (Iso) in rats. Methods Thirty male Wistar rats, weighting 160～180 g, were randomly divided into control group, Iso group, fenafibrate(FF) group(each n=10) according to physique quantity. Acute myocardial injury caused by Iso abdomen cavity injection induced ischemia was established and the protective effects of peroxisome proliferate-activated receptor α activation were accessed by the level of ereatine kinase(CK), lactic dehydrogenase(LDH) in serum as well as the activities of myoperoxidase(MPO) in myocardium, and the protein expressions of PPABα in myocardium by Western blot. Results The level of serum CK in control group, lso group and FF group, was (62.41±9.47),(101.71±11.05),(75.64±11.73)kU/L, respectively(F= 34.34, P<0.01). Whereas the level of serum CK in Iso group and FF group was higher than that in control group(P<0.01 or<0.05), the level of serum CK in FF group was lower than that in Iso group(P<0.01). The levels of LDH in these three groups were (5912.20±204.44), (6365.78±137.10), (6089.76±169.60) U/L, respectively(F= 17.54, P<0.01). Compared with the control group, the levels of LDH in Iso and Fir groups were significantly increased(P<0.01 or<0.05). But the level of LDH in FIr group was decreased compared with that in Iso group(P<0.01). The activities of myocardial MPO in these three groups were (1.95±0.10),(3.89±0.17),(2.49±0.19)U/g, espectively(F=391.68,P< 0.01). The activities of myocardial MPO in Iso and FF groups were higher than that in the control group (all P< 0.01), while the activities of myocardial MPO in FIr group were lower than that in lso group(P<0.01). The protein expressions of PPARα in myocardium of these three groups were 251.57±10.95,191.97±10.74,215.08±9.61, respectively(F=82.69, P<0.01). Conclusion PPARα activation by its actor FF can exert protective effects on the acute myocardial ischemia injury induced by lso in rats through inhibiting the release of inflammatory cell factors.

Objective To assess the impact of intervention with Insulin therapy management unit program in the poorly controlled type 2 diabetic patients in a community of Shanghai.Methods There were 55 patients with type 2 diabetes with poorly controlled hyperglycemia (HbA1C ≥ 8％) enrolled in this study.They were divided at random into 2 groups:intensive care group and standard care group.The subjects in intensive care group were provided with a glucose meter and required to monitor their blood glucose levels at least 2 or 3 times per day.Community health provider acquired information of blood glucose level,episodes of hypoglycemia,and dosage of insulin every week by cell phone.Standard care patients received diabetes care from the same provider in outpatient clinic every month.Results By the end of 6 months of intervention,the intensive care group showed a significant difference in HbA1C as compared to the standard care group (7.40％ ±0.91％ vs 8.65 ％ ± 1.28％,P＜0.01).The frequency of self-monitoring of blood glucose (SMBG) was 4 times per month in both groups at baseline.After intervention,the frequency of SMBG in intensive care group was greatly increased compared to standard care group (50times per month vs 5 times per month,P＜0.01).The frequency of self-reported hypoglycemia in intensive care group was increased compared to standard care group (3 times per month vs once per month,P＜0.01).The average daily dose of insulin in intensive care group was increased 6 units by the end of the present study(P＞0.05).Conclusion After 6 months of intervention,the glycemic control was obviously improved in type 2 diabetic patients treated with insulin and the daily dose of insulin was not increased significantly.TheInsulin therapy management unit is effective and safe.

Adolescent ; Diagnosis, Differential ; Humans ; Male ; Sturge-Weber Syndrome ; pathology

Objective To investigate the potential application of a non-viral gene carrier , TAT-LK15 , for delivering nNOSsiRNAin vivo and to study whether TAT-LK15/siRNA can be a new treatment method for chronic inflammatory pain. Method TAT-LK15 was complexed with nNOSsiRNA or scrambled control siRNA. The expression of nNOS was determined in SCDH of chronic inflammatory pain rats by western-blot assay. Pain control efficacy was evaluated by mechanical withdrawal threshold (MWT) and thermal withdrawal duration (TWD) assays. Results nNOS protein expression was efficiently inhibited by intrathecal injection of TAT-LK15/siRNA complexes , with the reduction of nNOS protein by 52%. Moreover , injection of TAT-LK15/siRNA com-plexes significantly could decrease MWT , but increase TWD in rats with chronic inflammatory pain. Conclusions TAT-LK15 can efficiently deliver nNOSsiRNAin vivo and nNOSsiRNA can relieve chronic inflammatory pain in rats.

Objective To study the effectiveness and safety of lipo-PGE1 on proteinuria in patients with diabetic nephropathy. MethodsForty-eight cases suffering from diabetic nephropathy with proteinuria exceeding 0.5 g/d and stage Ⅱ-Ⅳ of chronic kidney disease were divided into two groups.The basic treatment scheme for all the patients includes insulin and/or oral antidiabetic drugs and anti-hypertension drugs.The patients in the control group were given dipyridamole,and those in the lipo-PGE1-treatment group were managed with lipo-PGE1(alprostadil injection),10 ?g,qd?14 d.Results After the treatment,a decrease in proteinuria and increase in serum albumin were observed in the lipo-PGE1-treatment group,which was superior to the control group(P

Objective To evaluate the changes to mitochondrial ultrastructure in melanocytes of perilesional skin from patients with vitiligo.Methods Skin specimens were obtained from the perilesional area (0.5-1 cm distal to vitiligo lesions) of 10 patients with progressive vitiligo and 10 patients with stable vitiligo,as well as from the normal skin of 10 healthy volunteers.The morphology of melanocytes was observed by using transmission electron microscopy (TEM).Besides,stereological parameters of mitochondria,such as volume density (Vv),surface density (Sv) and numerical density (Nv),were measured.Results In melanocytes from the healthy controls,there were a large number of melanosomes with the number of melanosomes per melanocyte being 28.57± 3.21,which were mainly at stage Ⅲ and Ⅳ; mitochondria with normal structure and densely packed cristae were regularly arranged; autophagosomes were seen occasionally.Compared with the melanocytes from healthy controls,there was an obvious decrease in the number of melanosomes (especially stage Ⅲ melanosomes) in melanocytes from the perilesional skin of patients,with the number of melanosomes per melanocyte being 22.00 ± 6.16 (P ＜ 0.05) and 17.43 ± 6.24 (P ＜ 0.05) in patients with progressive vitiligo and stable vitiligo,respectively.TEM also showed disorganized or disrupted mitochondria in various shapes and sizes,most of which were swelling with obscure cristae and vacuolization,in melanocytes from the perilesional skin,and no autophagy was observed.The three stereological parameters were significantly different between the three groups of tissue specimens (all P ＜ 0.05),with the Nv,Vv and Sv of mitochondria being (7.194 ± 1.434) μm-3,(4.8 ± 1.2) ％,(2.42 ± 0.86) μ m-1 respectively in melanocytes from the healthy controls,(4.055 ± 0.906) μm-3,(7.4 ± 2.1)％,(3.58 ± 1.15)μm-1 respectively from patients with progressive vitiligo,(5.311 ± 0.873) μm-3,(6.5 ± 1.4)％,(2.82 ± 0.94) μm-1 respectively from patients with stable vitiligo.Conclusions Mitochondria are injured in melanocytes from perilesional skin of patients with vitiligo,and the degree of injury is more intense in progressive vitiligo than in stable vitiligo.

Aged ; Humans ; Lower Extremity ; Middle Aged ; Muscle, Skeletal/physiology* ; Vibration

Reactive oxygen species (ROS) is defined as the electron reduction product of oxygen with high reactivity which can maintain normal physiological functions and redox homeostasis. The tumor microenvironment is in a state of oxidative stress. ROS can affect multiple processes of tumor immune response by modulating the phenotype and functions of tumor cells and immune cells. With the rapid development of immunology, ROS-based tumor immunomodulation has been widely concerned and studied. In this review, the mechanism of ROS participating in tumor immune response is elaborated. Meanwhile, the research process and application of ROS in tumor immunomodulation in recent years are reviewed and analyzed.