3% vs. 86.4%, p=0.09) and non-Hispanic (72.6% vs. 77.3%, p=0.35). Average annual pertussis incidence was 5.7/100,000 among pregnant and 7.3/100,000 among non-pregnant women. Compared to non-pregnant patients, more pregnant patients reported whoop (41.9% vs. 31.3%), post-tussive vomiting (58.1% vs. 47.9%) and apnea (37.3% vs. 29.0%); however, differences were not statistically significant (p>0.05 for all). A similar proportion of pregnant and non-pregnant patients reported ever having received Tdap (31.6% vs. 32.7%, p=0.84).

Our analysis suggests that pertussis incidence and clinical characteristics of disease are similar among pregnant and non-pregnant women. Continued monitoring is important to further define pertussis epidemiology in pregnant women.

Our analysis suggests that pertussis incidence and clinical characteristics of disease are similar among pregnant and non-pregnant women. Continued monitoring is important to further define pertussis epidemiology in pregnant women.Mounting evidence has shown the involvement of long non-coding RNAs (lncRNAs) during various cancer metastatic events (abbreviated as CMEs, e.g. cancer cell invasion, intravasation, extravasation, proliferation, etc.) that may cooperatively facilitate malignant tumor spread and cause massive patient deaths. The study of lncRNA-CME associations might help understand lncRNA functions in metastasis and present reliable biomarkers for early dissemination detection and optimized treatment. Therefore, we developed a database named ‘lncR2metasta’ by manually compiling experimentally supported lncRNAs during various CMEs from existing studies. LncR2metasta documents 1238 associations between 304 lncRNAs and 39 CMEs across 54 human cancer subtypes. Each entry of lncR2metasta contains detailed information on a lncRNA-CME association, including lncRNA symbol, a specific CME, brief description of the association, lncRNA category, lncRNA Entrez or Ensembl ID, lncRNA genomic location and strand, lncRNA experiment, lncRNA expression pattern, detection method, target gene (or pathway) of lncRNA, lncRNA regulatory role on a CME, cancer name and the literature reference. An easy-to-use web interface was deployed in lncR2metasta for its users to easily browse, search and download as well as to submit novel lncRNA-CME associations. LncR2metasta will be a useful resource in cancer research community. It is freely available at http//lncR2metasta.wchoda.com.Leukoencephalopathy with brain stem and spinal cord involvement and lactate elevation disorder (LBSL) arises from mutations in mitochondrial aspartyl-tRNA synthetase (DARS2) gene. The disease has a childhood or juvenile-onset and is clinically characterized by cerebellar ataxia, cognitive decline and distinct morphological abnormalities upon magnetic resonance imaging. We previously demonstrated that neurons and not adult myelin-producing cells are specifically sensitive to DARS2 loss, hence likely the primary culprit in LBSL disorder. We used conditional Purkinje cell (PCs)-specific Dars2 deletion to elucidate further the cell-type-specific contribution of this class of neurons to the cerebellar impairment observed in LBSL. We show that DARS2 depletion causes a severe mitochondrial dysfunction concomitant with a massive loss of PCs by the age of 15 weeks, thereby rapidly deteriorating motor skills. Our findings conclusively show that DARS2 is indispensable for PC survival and highlights the central role of neuroinflammation in DARS2-related PC degeneration.Peroxisome proliferator-activated receptor gamma (PPARγ) acts as a ligand activated transcription factor and regulates processes, such as energy homeostasis, cell proliferation and differentiation. PPARγ binds to DNA as a heterodimer with retinoid X receptor and it is activated by polyunsaturated fatty acids and fatty acid derivatives, such as prostaglandins. In addition, the insulin-sensitizing thiazolidinediones, such as rosiglitazone, are potent and specific activators of PPARγ. PPARγ is present along the hypothalamic-pituitary-testis axis and in the testis, where low levels in Leydig cells and higher levels in Sertoli cells as well as in germ cells have been found. High amounts of PPARγ were reported in the normal epididymis and in the prostate, but the receptor was almost undetectable in the seminal vesicles. Interestingly, in the human and in pig, PPARγ protein is highly expressed in ejaculated spermatozoa, suggesting a possible role of PPARγ signaling in the regulation of sperm biology. This implies that both natural and synthetic PPARγ ligands may act directly on sperm improving its performance. Given the close link between energy balance and reproduction, activation of PPARγ may have promising metabolic implications in male reproductive functions. In this review, we first describe PPARγ expression in different compartments of the male reproductive axis. Subsequently, we discuss the role of PPARγ in both physiological and several pathological conditions related to the male fertility.

Tofacitinib is an oral, small molecule Janus kinase inhibitor for the treatment of ulcerative colitis (UC). Here, we performed an integrated analysis of malignancy events from the tofacitinib phase 3 UC clinical development program (excluding nonmelanoma skin cancer [NMSC]).

Data (up to May 2019) were pooled from two phase 3 induction studies, a phase 3 maintenance study, and an ongoing, open-label, long-term extension (OLE) study, and analyzed as 3 cohorts induction (N = 1139), maintenance (N = 592), and overall (induction, maintenance, and ongoing OLE study; N = 1124). Proportions and incidence rates (IRs; unique patients with events per 100 patient-years [PY] of exposure) for malignancies confirmed by adjudication were calculated.

The overall cohort consisted of patients who received at least 1 dose of tofacitinib at 5 or 10 mg twice daily, for up to 6.8 years, with an exposure of 2576.4 PY. Of the 1124 overall cohort tofacitinib-treated patients, 20 developed a malignancy (excluding NMSC; IR, 0.75; 95% confidence interval, 0.46-1.16), of which 17 occurred in patients treated with tofacitinib 10 mg twice daily; importantly, more than 80% of patients predominantly received this dose. Furthermore, there was no apparent clustering of malignancy types, and IRs were stable over time.

In the tofacitinib UC clinical development program, malignancy events were infrequent, and rates were comparable with those in the tofacitinib rheumatoid arthritis and psoriatic arthritis clinical development programs, and for biologic UC treatments. NSC 178886 ClinicalTrials.gov NCT01465763, NCT01458951, NCT01458574, and NCT01470612.

In the tofacitinib UC clinical development program, malignancy events were infrequent, and rates were comparable with those in the tofacitinib rheumatoid arthritis and psoriatic arthritis clinical development programs, and for biologic UC treatments. ClinicalTrials.gov NCT01465763, NCT01458951, NCT01458574, and NCT01470612.