Influencia de la cáscara de maracuyá y papa en la reducción de contaminantes de lixiviados del botadero de la Municipalidad Provincial de Chupaca en el año 2021

El objetivo del trabajo de investigación es analizar cómo influirá la cáscara de maracuyá y la cáscara de papa en la reducción de contaminantes de lixiviados del botadero municipal de la Provincia de Chupaca. El método utilizado fue cuantitativo del tipo hipotético–deductivo, el diseño que se trabajó fue experimental del tipo factorial. La población trabajada fueron los lixiviados del botadero. El instrumento de recolección de dato estuvo compuesto por el monitoreo en laboratorio y la elaboración de reportes de los análisis. Luego de haber realizado el análisis, se ha encontrado que la caracterización fisicoquímica de los lixiviados tuvo valores de DQO de 7639 mg/L, DBO5 de 4984 mg/L y turbidez de 285 NTU. Se trabajó a una dosis de adsorbente de 1 g, 1.5 g y 2 g y un pH de 5.0, 6.0 y 7.0, donde a una dosis de 2 g y pH de 5 se tiene la mayor reducción de los contaminantes de los lixiviados, donde predomina la cáscara de maracuyá para restringir los contaminantes de DQO con 81.59%, DBO5 de 83.83% y la turbidez de 97.87% y la influencia de la cáscara de papa reduce contaminantes de DQO en 79.88 %, DBO5 de 83.90% y la turbidez de 97.54 %. De esta manera, se puede determinar que la influencia en la reducción de contaminantes de lixiviados en la cáscara de maracuyá es mayor que la influencia de la cáscara de papa. Además de ello, se entiende que, al ser un producto natural, el impacto ambiental del coagulante de mayor efectividad es nulo

Common genetic variants in the CLDN2 and PRSS1-PRSS2 loci alter risk for alcohol-related and sporadic pancreatitis

Pancreatitis is a complex, progressively destructive inflammatory disorder. Alcohol was long thought to be the primary causative agent, but genetic contributions have been of interest since the discovery that rare PRSS1, CFTR, and SPINK1 variants were associated with pancreatitis risk. We now report two significant genome-wide associations identified and replicated at PRSS1-PRSS2 (1×10-12) and x-linked CLDN2 (p < 1×10-21) through a two-stage genome-wide study (Stage 1, 676 cases and 4507 controls; Stage 2, 910 cases and 4170 controls). The PRSS1 variant affects susceptibility by altering expression of the primary trypsinogen gene. The CLDN2 risk allele is associated with atypical localization of claudin-2 in pancreatic acinar cells. The homozygous (or hemizygous male) CLDN2 genotype confers the greatest risk, and its alleles interact with alcohol consumption to amplify risk. These results could partially explain the high frequency of alcohol-related pancreatitis in men – male hemizygous frequency is 0.26, female homozygote is 0.07

A novel Alzheimer disease locus located near the gene encoding tau protein

This is the author accepted manuscript. The final version is available from the publisher via the DOI in this recordAPOE ε4, the most significant genetic risk factor for Alzheimer disease (AD), may mask effects of other loci. We re-analyzed genome-wide association study (GWAS) data from the International Genomics of Alzheimer's Project (IGAP) Consortium in APOE ε4+ (10 352 cases and 9207 controls) and APOE ε4- (7184 cases and 26 968 controls) subgroups as well as in the total sample testing for interaction between a single-nucleotide polymorphism (SNP) and APOE ε4 status. Suggestive associations (P<1 × 10-4) in stage 1 were evaluated in an independent sample (stage 2) containing 4203 subjects (APOE ε4+: 1250 cases and 536 controls; APOE ε4-: 718 cases and 1699 controls). Among APOE ε4- subjects, novel genome-wide significant (GWS) association was observed with 17 SNPs (all between KANSL1 and LRRC37A on chromosome 17 near MAPT) in a meta-analysis of the stage 1 and stage 2 data sets (best SNP, rs2732703, P=5·8 × 10-9). Conditional analysis revealed that rs2732703 accounted for association signals in the entire 100-kilobase region that includes MAPT. Except for previously identified AD loci showing stronger association in APOE ε4+ subjects (CR1 and CLU) or APOE ε4- subjects (MS4A6A/MS4A4A/MS4A6E), no other SNPs were significantly associated with AD in a specific APOE genotype subgroup. In addition, the finding in the stage 1 sample that AD risk is significantly influenced by the interaction of APOE with rs1595014 in TMEM106B (P=1·6 × 10-7) is noteworthy, because TMEM106B variants have previously been associated with risk of frontotemporal dementia. Expression quantitative trait locus analysis revealed that rs113986870, one of the GWS SNPs near rs2732703, is significantly associated with four KANSL1 probes that target transcription of the first translated exon and an untranslated exon in hippocampus (P≤1.3 × 10-8), frontal cortex (P≤1.3 × 10-9) and temporal cortex (P≤1.2 × 10-11). Rs113986870 is also strongly associated with a MAPT probe that targets transcription of alternatively spliced exon 3 in frontal cortex (P=9.2 × 10-6) and temporal cortex (P=2.6 × 10-6). Our APOE-stratified GWAS is the first to show GWS association for AD with SNPs in the chromosome 17q21.31 region. Replication of this finding in independent samples is needed to verify that SNPs in this region have significantly stronger effects on AD risk in persons lacking APOE ε4 compared with persons carrying this allele, and if this is found to hold, further examination of this region and studies aimed at deciphering the mechanism(s) are warranted

Abstracts from the 8th International Conference on cGMP Generators, Effectors and Therapeutic Implications

This work was supported by a restricted research grant of Bayer AG

Responsabilidad profesional de enfermería: vigilancia del trabajo de parto que condicionó muerte fetal

Síntesis de la Queja. La paciente refirió que debido a una mala vigilancia en su trabajo de parto y a la falta de atención por parte del personal médico y de Enfermería, su hijo tuvo sufrimiento fetal lo que le condicionó su fallecimiento.Summary of the complaint. The patient reported that due to poor surveillance in her labor and the lack of attention from the medical and nursing staff, her son had fetal distress which conditioned her death

HIV Drug Resistance Surveillance in Honduras after a Decade of Widespread Antiretroviral Therapy.

We assessed HIV drug resistance (DR) in individuals failing ART (acquired DR, ADR) and in ART-naïve individuals (pre-ART DR, PDR) in Honduras, after 10 years of widespread availability of ART.365 HIV-infected, ART-naïve, and 381 ART-experienced Honduran individuals were enrolled in 5 reference centres in Tegucigalpa, San Pedro Sula, La Ceiba, and Choluteca between April 2013 and April 2015. Plasma HIV protease-RT sequences were obtained. HIVDR was assessed using the WHO HIVDR mutation list and the Stanford algorithm. Recently infected (RI) individuals were identified using a multi-assay algorithm.PDR to any ARV drug was 11.5% (95% CI 8.4-15.2%). NNRTI PDR prevalence (8.2%) was higher than NRTI (2.2%) and PI (1.9%, p500 vs. <350 CD4+ T cells/μL. PDR in recently infected individuals was 13.6%, showing no significant difference with PDR in individuals with longstanding infection (10.7%). The most prevalent PDR mutations were M46IL (1.4%), T215 revertants (0.5%), and K103NS (5.5%). The overall ADR prevalence in individuals with <48 months on ART was 87.8% and for the ≥48 months on ART group 81.3%. ADR to three drug families increased in individuals with longer time on ART (p = 0.0343). M184V and K103N were the most frequent ADR mutations. PDR mutation frequency correlated with ADR mutation frequency for PI and NNRTI (p<0.01), but not for NRTI. Clusters of viruses were observed suggesting transmission of HIVDR both from ART-experienced to ART-naïve individuals and between ART-naïve individuals.The global PDR prevalence in Honduras remains at the intermediate level, after 10 years of widespread availability of ART. Evidence of ADR influencing the presence of PDR was observed by phylogenetic analyses and ADR/PDR mutation frequency correlations

PDR in a Honduran HIV-1-infected cohort, April 2013-April 2015 (n = 365).

<p>^a Pre-Antiretroviral Treatment Drug Resistance (PDR) estimated using the WHO HIV transmitted drug resistance surveillance mutation list.</p><p>^b PDR estimated with the Stanford algorithm (v7.0), with a threshold of ≥15 for at least one antiretroviral drug of the specified class. ARV, Antiretroviral; NNRTI, Non-Nucleoside Reverse Transcriptase Inhibitors; NRTI, Nucleoside Reverse Transcriptase Inhibitors; PI, Protease Inhibitors.</p><p>PDR in a Honduran HIV-1-infected cohort, April 2013-April 2015 (n = 365).</p