Intestinal pseudo-obstruction: An important diagnostic challenge

We present the case of a 72-year-old patient admitted on various occasions with symptoms of intestinal pseudo-obstruction. Extensive diagnostic tests eventually found that the patient had small-cell lung cancer associated with high anti-HU antibody titres, which pointed to a probable paraneoplastic intestinal obstruction syndrome associated with small-cell lung cancer. A paraneoplastic syndrome causing abnormal changes in gastrointestinal motility can be the first signs of small cell lung cancer. These syndromes improve with treatment of the underlying disease, as seen in our patient, who stopped having episodes of intestinal pseudo-obstruction after administration of chemotherapy

Intestinal pseudo-obstruction: An important diagnostic challenge

We present the case of a 72-year-old patient admitted on various occasions with symptoms of intestinal pseudo-obstruction. Extensive diagnostic tests eventually found that the patient had small-cell lung cancer associated with high anti-HU antibody titres, which pointed to a probable paraneoplastic intestinal obstruction syndrome associated with small-cell lung cancer. A paraneoplastic syndrome causing abnormal changes in gastrointestinal motility can be the first signs of small cell lung cancer. These syndromes improve with treatment of the underlying disease, as seen in our patient, who stopped having episodes of intestinal pseudo-obstruction after administration of chemotherapy

Role of SODC protein in antineoplastic drug resistance

Cells need homeostasis to survive, therefore, they use the different pathways available to obtain it. The SODC protein overexpression, which is implicated in this process, suggests that could be implicated in the process of acquisition resistance during chemotherapy.Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech

Proteins involved in carbon metabolism induce bleomycin resistance

S. cerevisiae acquires bleomycin resistance after a long-term exposure to this drug which causes overexpression of TPIS protein. It could be involved in the resistance process. For this reason, it could be good candidates as bleomycin chemo-resistance biomarker. Knowing of the homologous gene in humans facilitates more studies of the expression of this protein in tumors.Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech

Experimental transmission to a calf of an isolate of Spanish classical scrapie

Multiple theories exist regarding the origin of bovine spongiform encephalopathy (BSE). An early and prominent theory proposed that BSE was the result of the adaptation of sheep scrapie to cattle. The reports to date indicate that the distribution of the pathological prion protein (PrPSc) in experimental bovine scrapie is largely restricted to the central nervous system (CNS). Here, we describe pathological findings in a calf intracerebrally inoculated with a Spanish classical scrapie isolate. While clinical disease was observed 30 months after inoculation and PrPSc was detected in the CNS, the corresponding phenotype differed from that of BSE. Immunohistochemistry and PMCA also revealed the presence of PrPSc in the peripheral nerves, lymphoid tissues, skeletal muscle and gastrointestinal tract, suggesting centrifugal spread of the scrapie agent from the brain. To the best of our knowledge, this is the first report describing the detection of PrPSc in tissues other than the CNS after experimental transmission of scrapie to cattle

Incidence, hospitalization, mortality and risk factors of COVID-19 in long-term care residential homes for patients with chronic mental illness

Long-term care residential homes (LTCRH) for patients with chronic mental illness have suffered the enormous impact of COVID-19. This study aimed to estimate incidence, hospitalization, mortality, and risk factors of COVID-19 to prevent future epidemics. From March 2020 to January 2021 and before vaccination anti-SARS-CoV-2 begins, cumulate incidence rate (CIR), hospitalization rate (HR), mortality rate (MR), and risk factors of COVID-19 in the 11 LTCRH of two Health Departments of Castellon (Spain) were studied by epidemiological surveillance and an ecological design. Laboratory tests confirmed COVID-19 cases, and multilevel Poisson regression models were employed. All LTCRH participated and comprised 346 residents and 482 staff. Residents had a mean age of 47 years, 40% women, and suffered 75 cases of COVID-19 (CIR = 21.7%), five hospitalizations (HR = 1.4%), and two deaths (MR = 0.6%) with 2.5% fatality-case. Staff suffered 74 cases of the disease (CIR = 15.4%), one hospitalization (HR = 0.2%), and no deaths were reported. Risk factors associated with COVID-19 incidence in residents were private ownership, severe disability, residents be younger, CIR in municipalities where LTCRH was located, CIR in staff, and older age of the facilities. Conclusion: COVID-19 incidence could be prevented by improving infection control in residents and staff and modernizing facilities with increased public ownership

Recurrent NOMO1 gene deletion is a potential clinical marker in early-onset colorectal cancer and is involved in the regulation of cell migration

The incidence of early-onset colorectal cancer (EOCRC; age younger than 50 years) has been progressively increasing over the last decades globally, with causes unexplained. A distinct molecular feature of EOCRC is that compared with cases of late-onset colorectal cancer, in EOCRC cases, there is a higher incidence of Nodal Modulator 1 (NOMO1) somatic deletions. However, the mechanisms of NOMO1 in early-onset colorectal carcinogenesis are currently unknown. In this study, we show that in 30% of EOCRCs with heterozygous deletion of NOMO1, there were pathogenic mutations in this gene, suggesting that NOMO1 can be inactivated by deletion or mutation in EOCRC. To study the role of NOMO1 in EOCRC, CRISPR/cas9 technology was employed to generate NOMO1 knockout HCT-116 (EOCRC) and HS-5 (bone marrow) cell lines. NOMO1 loss in these cell lines did not perturb Nodal pathway signaling nor cell proliferation. Expression microarrays, RNA sequencing, and protein expression analysis by LC–IMS/MS showed that NOMO1 inactivation deregulates other signaling pathways independent of the Nodal pathway, such as epithelial–mesenchymal transition and cell migration. Significantly, NOMO1 loss increased the migration capacity of CRC cells. Additionally, a gut-specific conditional NOMO1 KO mouse model revealed no subsequent tumor development in mice. Overall, these findings suggest that NOMO1 could play a secondary role in early-onset colorectal carcinogenesis because its loss increases the migration capacity of CRC cells. Therefore, further study is warranted to explore other signalling pathways deregulated by NOMO1 loss that may play a significant role in the pathogenesis of the disease.This study was supported by the health research program of the Instituto de Salud Carlos III (Spanish Ministry of Economy and Competitiveness, PI20/01569 and PI20/0974), co-funded by FEDER funds, and Mutua Madrileña Foundation (FMM20/001). A.M.-M was supported by a predoctoral research grant from the Dr. Moraza Fundation (FMoraza18/001). P.G.V and N.G.-U were supported by a predoctoral research grant from the Consejería de Educación—Junta de Castilla y León. A.N.H. was supported by the National Institutes of Health K12 HD043483 from the Eunice Kennedy Shriver National Institute of Child Health and Human Development

Evidence for the decay B0S→K¯∗0μ+μ−

A search for the decay B0S→K¯∗0μ+μ− is presented using data sets corresponding to 1.0, 2.0 and 1.6 fb−1 of integrated luminosity collected during pp collisions with the LHCb experiment at centre-of-mass energies of 7, 8 and 13 TeV, respectively. An excess is found over the background-only hypothesis with a significance of 3.4 standard deviations. The branching fraction of the B0S→K¯∗0μ+μ− decay is determined to be B(B0s→K¯∗0μ+μ−)=[2.9±1.0(stat)±0.2(syst)±0.3(norm)]×10−8, where the first and second uncertainties are statistical and systematic, respectively. The third uncertainty is due to limited knowledge of external parameters used to normalise the branching fraction measurement.S

Measurement of D ±s production asymmetry in pp collisions at √s=7 and 8 TeV

The inclusive D ±s production asymmetry is measured in pp collisions collected by the LHCb experiment at centre-of-mass energies of √s=7 and 8 TeV. Promptly produced D ±s mesons are used, which decay as D ±s → ϕπ±, with ϕ → K+K−. The measurement is performed in bins of transverse momentum, pT, and rapidity, y, covering the range 2.5 < pT < 25.0 GeV/c and 2.0 < y < 4.5. No kinematic dependence is observed. Evidence of nonzero D ±s production asymmetry is found with a significance of 3.3 standard deviations.S

Measurement of the CKM angle γ using B± → DK± with D → K0Sπ+π−, K0SK+K− decays

A binned Dalitz plot analysis of B± → DK± decays, with D → K 0Sπ+π− and D → K 0SK+K−, is used to perform a measurement of the CP-violating observables x± and y±, which are sensitive to the Cabibbo-Kobayashi-Maskawa angle γ. The analysis is performed without assuming any D decay model, through the use of information on the strong-phase variation over the Dalitz plot from the CLEO collaboration. Using a sample of proton-proton collision data collected with the LHCb experiment in 2015 and 2016, and corresponding to an integrated luminosity of 2.0 fb−1, the values of the CP violation parameters are found to be x− = (9.0 ± 1.7 ± 0.7 ± 0.4) × 10−2, y− = (2.1 ± 2.2 ± 0.5 ± 1.1) × 10−2, x+ = (−7.7 ± 1.9 ± 0.7 ± 0.4) × 10−2, and y+ = (−1.0 ± 1.9 ± 0.4 ± 0.9) × 10−2. The first uncertainty is statistical, the second is systematic, and the third is due to the uncertainty (on the strong-phase measurements. These values are used to obtain γ = (87 + 11− 12)∘, rB = 0.086 + 0.013− 0.014, and δB = (101±11)°, where rB is the ratio between the suppressed and favoured B-decay amplitudes and δB is the corresponding strong-interaction phase difference. This measurement is combined with the result obtained using 2011 and 2012 data collected with the LHCb experiment, to give γ = (80 + 10− 9)∘, rB = 0.080 ± 0.011, and δB = (110 ± 10)°.S