Malikpierce9543

Most of death cases were children less than 1-year-old with average age of 7 months. Causes of death were subdural hematoma with skull and ribs fracture.

Identifying risk factors for repeated child abuse help in recognizing child at risk to provide prompt intervention. This study found two factors associated with higher risk of abuse recurrence child age 1-10 years old and abusive parents. PF-4708671 in vitro Children who presented with these risk factors should be recognized and intensively monitored.

Identifying risk factors for repeated child abuse help in recognizing child at risk to provide prompt intervention. This study found two factors associated with higher risk of abuse recurrence child age 1-10 years old and abusive parents. Children who presented with these risk factors should be recognized and intensively monitored.Objective The aim is to assess the effectiveness of a biodegradable antireflux ureteral stent with heparin coating in a comparative study (BraidStent®-H) in an animal model for the treatment of iatrogenic ureteral perforation. Materials and Methods A total of 24 female pigs underwent initial endoscopic, nephrosonographic, and contrast fluoroscopy assessment of the urinary tract. Afterward, unilateral iatrogenic perforation in proximal ureter model was performed. Then the animals were randomly assigned to Group-I, in which a double-pigtail stent was placed for 6 weeks, or Group-II, in which a BraidStent-H a biodegradable heparin-coated stent was placed. Follow-up assessments were performed at 1 and 6 weeks and 5 months. Results In terms of therapeutic effectiveness, complete resolution was observed in 95.8% of Group-I animals and 87.5% in Group-II. No animals in Group-II showed vesicoureteral reflux (VUR) during the study; statistical significance was observed at 1 and 6 weeks versus Group-I. All stents in Group-II degraded without producing obstructive fragments and allowed distal ureteral peristalsis. Heparin coating was not efficient to reduce asymptomatic bacteriuria between groups. Pathologic assessment did not show any significance in the global score, but did in the "fibrosis in muscular layer" parameter, at the ureteral perforation healing area; Group-II showed higher healing quality. Conclusions The biodegradable intraureteral BraidStent®-H is highly effective for the minimally invasive treatment of ureteral perforation, since it displays controlled and predictable degradation, avoiding the development of VUR as well as irritation of the bladder trigone. Unfortunately, heparin coating was not effective in avoiding stent-associated bacteriuria.

Prophylactic trimethoprim-sulfamethoxazole (TMP-SMX) prevents pneumocystis jirovecii infection in SLE on immunosuppression. Its role in preventing other major infections in immuno suppressed SLE patients is unknown.

A non-concurrent cohort study was conducted on patients of SLE fulfilling SLICC and/or ACR 1997 criteria, who received tapering dose of steroid starting with ≥0.5 mg/kg/day of prednisolone or equivalent dose of deflazacort and mycophenolate mofetil ≥1 g/day (or equivalent dose of mycophenolate sodium) at least for the preceding 1 year. Interviewing patients & documenting relevant data from hospital electronic Medical records (EMR), followed by comparison of Incidence densities of major infections between those on prophylactic Trimethoprim 160 mg + Sulfamethoxazole 800 mg and those not on it, was done by student 't' test. Multivariate logistic regression was performed for independent risk of any major infection between the two groups.

Of 228 patients, 162 did not receive TMP-SMX prophylaxis, and 66 had received. The incidence density of major infection was found to be significantly lower in TMP-SMX group (1.25 per 100 person year) as compared to those not on TMP-SMX group (11.201 per 100 person year); P < 0.001 (95% CI 0.027 - 0.449) and odds ratio of 0.03 (CI 0 - 0.24).

Cotrimoxazole prophylaxis in SLE patients on immunosuppression prevents major infections.

Cotrimoxazole prophylaxis in SLE patients on immunosuppression prevents major infections.

To examine the impact of cumulative smoking in pack-years on systemic lupus erythematosus (SLE) cutaneous manifestations and damage.

Our cohort study included 632 adult SLE patients at an academic center, meeting 1997 ACR or 2012 SLICC classification criteria. Outcomes were (1) cutaneous SLICC Damage Index (SDI), (2) ACR and SLICC criteria. Smoking exposure was defined as low (<5 pack-years), medium (5-10), and high (>10), compared to non-smokers. Analysis used multivariable logistic regression to calculate odds ratios and confidence intervals (OR, (95% CI)).

Among 632 SLE patients, mean age 42 ± 14, 91% were female, 82% White, and 40% were ever smokers. Black patients were more likely to have smoked (51% vs. 41% White, 11% Other). Chronic SLICC and SDI cutaneous criteria showed linear pack-year trends, meeting significance with high smoking exposure (OR 2.2, (1.2, 4.2); OR 4.2, (1.9, 9.2)). Those with medium exposure were more likely to meet acute SLICC cutaneous criteria (OR 2.3, (1.1, 5.1)). Low exposure predicted any cutaneous SLICC and ACR criteria (OR 3.7, (1.3, 10.6); OR 2.0 (1.03, 3.8)). Patients of color had more chronic SLICC cutaneous criteria (Other Race OR 3.6 (1.6, 8.1)) and SDI skin damage (Black OR 2.6 (1.1, 5.9)) even controlling for smoking exposure.

Smoking was an independent risk factor for cutaneous SLE. High pack-year exposure and non-White race increased chronic skin manifestations and SDI damage. Findings suggested a dose relationship between smoking and cutaneous SLE damage, making cessation messaging important to potentially improve outcomes and reduce some disparities.

Smoking was an independent risk factor for cutaneous SLE. High pack-year exposure and non-White race increased chronic skin manifestations and SDI damage. Findings suggested a dose relationship between smoking and cutaneous SLE damage, making cessation messaging important to potentially improve outcomes and reduce some disparities.

We aimed to identify transcriptional gene signatures predictive of clinical response, for pharmacodynamic evaluation, and to provide mechanistic insight into JNJ-55920839, a human IgG1κ neutralizing mAb targeting IFN-α/IFN-ω, in participants with systemic lupus erythematosus (SLE).

Blood samples were obtained from SLE participants at baseline and up to Day 130, who received six 10 mg/kg IV doses of JNJ-55920839/placebo every 2 weeks. Participants with mild-to-moderate SLE who achieved clinical responses using SLE Disease Activity Index 2000 Responder Index 4-point change were considered responders. Transcriptional signatures from longitudinally collected blood were generated by RNA-Seq; signatures were generated by microarray from baseline blood samples exposed

to JNJ-55920839 versus untreated.

Two gene signatures (IFN-I Signaling and Immunoglobulin Immune Response) exhibited pharmacodynamic changes among JNJ-55920839 responders. The Immunoglobulin signature, but not the IFN-I signature, was elevated at baseline in JNJ-55920839 responders.