Biomonitoring of airborne trace elements using transplanted lichens around a paper industry (Morelia, Mexico).

The deposition of trace elements around a pulp and paper industry in Morelia, Mexico, was evaluated using two lichen species as biomonitors. Samples of the foliose lichen Flavopunctelia praesignis and the fruticose lichen Usnea ceratina were collected in two remote areas and transplanted at different distances and directions from the pollution source. Lichen samples were exposed for 4 months (1) around the industrial area and (2) in their native habitats (control sites). We investigated the bioaccumulation of 11 trace elements in lichen thalli, and we compared the response of the two lichen species. To identify possible common sources, we evaluated the relationships between trace elements by correlations and cluster analyses. Our results showed that Cd was a good tracer for air pollution from the pulp and paper mills. In samples of Usnea ceratina exposed around the industrial area, Cd was significantly higher than in the remote area. Within the study area, trace element contents increase with the distance from the source, and they showed high depositions in the direction of prevailing winds. Moreover, we were able to detect groups of elements with similar behavior and common origins. Our results indicated that Flavopunctelia praesignis showed a higher capacity to accumulate trace elements than Usnea ceratina.

Helicobacter pylori infection downregulates the DNA glycosylase NEIL2, resulting in increased genome damage and inflammation in gastric epithelial cells.

Infection with the Gram-negative, microaerophilic bacterium Helicobacter pylori induces an inflammatory response and oxidative DNA damage in gastric epithelial cells that can lead to gastric cancer (GC). However, the underlying pathogenic mechanism is largely unclear. Here, we report that the suppression of Nei-like DNA glycosylase 2 (NEIL2), a mammalian DNA glycosylase that specifically removes oxidized bases, is one mechanism through which H. pylori infection may fuel the accumulation of DNA damage leading to GC. Using cultured cell lines, gastric biopsy specimens, primary cells, and human enteroid-derived monolayers from healthy human stomach, we show that H. pylori infection greatly reduces NEIL2 expression. The H. pylori infection-induced downregulation of NEIL2 was specific, as Campylobacter jejuni had no such effect. Using gastric organoids isolated from the murine stomach in coculture experiments with live bacteria mimicking the infected stomach lining, we found that H. pylori infection is associated with the production of various inflammatory cytokines. This response was more pronounced in Neil2 knockout (KO) mouse cells than in WT cells, suggesting that NEIL2 suppresses inflammation under physiological conditions. Notably, the H. pylori-infected Neil2-KO murine stomach exhibited more DNA damage than the WT. Furthermore, H. pylori-infected Neil2-KO mice had greater inflammation and more epithelial cell damage. Computational analysis of gene expression profiles of DNA glycosylases in gastric specimens linked the reduced Neil2 level to GC progression. Our results suggest that NEIL2 downregulation is a plausible mechanism by which H. pylori infection impairs DNA damage repair, amplifies the inflammatory response, and initiates GC.

Analysis of the quality of anticoagulation with vitamin K antagonists in three clinical scenarios in Mexico.

INTRODUCTION: Vitamin K antagonists (VKA) are a therapeutic alternative in patients with venous thromboembolic disease; however, numerous factors affect their pharmacology. OBJECTIVE: To evaluate the quality of VKA anticoagulation at three different time periods in Mexico. METHODS: Prospective study, nested in patient cohorts at three different clinical scenarios between 2013 and 2019. Outpatients with indication for treatment with VKAs for at least 12 months were included. Patients were managed according to the criteria of the treating physician. RESULTS: Patient general characteristics were similar between groups, except for the VKA indication. The results of 4,148 patients and 38,548 INR assessments were analyzed. The times in therapeutic range during the three phases of the study and pooled data were significantly higher for the anticoagulation clinic. Only the number of patient visits was significantly associated with the results, unlike age, gender, and type of VKA. CONCLUSIONS: VKAs are widely used, but it is difficult for therapeutic goals to be achieved, especially in non-specialized clinical services. Creation of anticoagulation clinics is an urgent need for the Mexican health system.

INTRODUCCIÓN: Los antagonista de la vitamina K (AVK) son una alternativa terapéutica en los pacientes con enfermedad tromboembólica venosa; sin embargo, numerosos factores afectan su farmacología. OBJETIVO: Evaluar la calidad de la anticoagulación AVK durante tres diferentes periodos en México. MÉTODOS: Estudio prospectivo, anidado en cohortes de pacientes en tres escenarios clínicos entre los años 2013-2019. Se incluyeron pacientes no hospitalizados con indicación para recibir AVK por al menos 12 meses, quienes fueron manejados de acuerdo con el criterio del médico tratante. RESULTADOS: Las características generales de los pacientes fueron similares entre los grupos, excepto por la indicación para usar los AVK. Se analizaron los resultados de 4148 pacientes y 38 548 evaluaciones de INR. Los tiempos en rango terapéutico durante las tres fases del estudio y los datos acumulados fueron significativamente mayores en la clínica de anticoagulación. Solo el número de visitas de control de los pacientes se asoció significativamente con los resultados, a diferencia de la edad, el sexo y el tipo de AVK. CONCLUSIONES: Los AVK se utilizan ampliamente, pero es difícil alcanzar la meta terapéutica, sobre todo en servicios clínicos no especializados. La creación de clínicas de anticoagulación es una necesidad urgente en el sistema mexicano de salud.

Helicobacter pylori Deregulates T and B Cell Signaling to Trigger Immune Evasion.

Helicobacter pylori is a prevalent human pathogen that successfully establishes chronic infection, which leads to clinically significant gastric diseases including chronic gastritis, peptic ulcer disease (PUD), and gastric cancer (GC). H. pylori is able to produce a persistent infection due in large part to its ability to hijack the host immune response. The host adaptive immune response is activated to strategically and specifically attack pathogens and normally clears them from the infected host. Since B and T lymphocytes are central mediators of adaptive immunity, in this chapter we review their development and the fundamental mechanisms regulating their activation in order to understand how some of the normal processes are subverted by H. pylori. In this review, we place particular emphasis on the CD4+ T cell responses, their subtypes, and regulatory mechanisms because of the expanding literature in this area related to H. pylori. T lymphocyte differentiation and function are finely orchestrated through a series of cell-cell interactions, which include immune checkpoint receptors. Among the immune checkpoint receptor family, there are some with inhibitory properties that are exploited by tumor cells to facilitate their immune evasion. Gastric epithelial cells (GECs), which act as antigen-presenting cells (APCs) in the gastric mucosa, are induced by H. pylori to express immune checkpoint receptors known to sway T lymphocyte function and thus circumvent effective T effector lymphocyte responses. This chapter reviews these and other mechanisms used by H. pylori to interfere with host immunity in order to persist.

von Willebrand Disease and other hereditary haemostatic factor deficiencies in women with a history of postpartum haemorrhage.

INTRODUCTION: Postpartum haemorrhage (PPH) is the main cause of maternal morbidity and mortality globally, but it is far more important in non-developed countries. PPH represents 25% of all maternal deaths worldwide. Women with von Willebrand disease (VWD) and other inherited haemorrhagic disorders are at increased risk of PPH. Our aim was to establish a probable association of severe PPH in women with a history of haemostatic abnormalities. METHODS: An observational, controlled study of adult women with a one or more episodes of severe PPH requiring treatment in an intensive care unit or >10 units of blood products during the 24-hour period after diagnosis and their controls. The tests performed were blood cell count, blood group, renal, viral, liver function and haemostatic tests, fibrinogen, activity of the plasma factors and specific test to diagnose and classify VWD. RESULTS: We included 124 women with 133 PPH events and their controls. The median age at the first event was 25.5 years old. Results were significantly different between the groups in terms of fibrinogen concentration, VWF:Ag, VWF:RCo and FVIII. A specific diagnosis was established in 69 (55.6) and 4 (3.2%) patients in the PPH group and controls, respectively. Of 61 patients with VWD, 57 had type 1, two had type 2A, and another two had type 2B. CONCLUSION: Our results show a relationship between PPH and inherited haemostatic disorders. VWD was the most frequent diagnosis. Appropriate and opportune diagnosis before pregnancy of inherited haemostatic disorders may be important to effectively prevent and treat PPH.

Subtle metabolic alterations in adolescents with obesity and polycystic ovarian syndrome. / Alteraciones metabólicas sutiles en adolescentes con obesidad y síndrome de ovario poliquístico.

Objective: To evaluate the frequency of some subtle metabolic alterations in a group of adolescents with obesity and polycystic ovary syndrome (PCOS). Materials and Methods: A cross-sectional, comparative study was conducted in a group of adolescents with obesity, and characterized as with or without PCOS according with the Rotterdam Consensus. Medical history, anthropometry, gynecologic pelvic ultrasound (to evaluate ovarian volumes, number of antral follicles and endometrial width), as well as serum glucose, insulin, lipoproteins, interleukin-6, tumor necrosis factor alpha, total testosterone, dehydroepiandrosterone, sexual hormones binding globulin, leptin, adiponectin and insulin-like growth factor 1, the free-androgen index, free and available testosterone, and homeostatic model assessment index were calculated. For statistics, mean and standard deviation, or median and ranges were used for description as appropriate. Likewise, Student t-test or Mann-Whitney test were used for comparisons. Results: From a sample of 180 adolescents, 47 attached to selection criteria. Mean age was 13.5 year and Z-score 2.5. Eighty percent of adolescents presented central distribution of body fat and 95% hyperinsulinemia. The more frequent dyslipidemias were hypertriglyceridemia in 57% and hypercholesterolemia in 12.8%; 25.5% of adolescents presented two out of three criteria for polycystic ovary syndrome (PCOS). Body mass index and insulin were correlated with free testosterone, but the multivariate analysis demonstrated that the magnitude of the association was significantly higher in SOP patients. Conclusions: The metabolic alterations detected in obese adolescents with SOP suggest that the clinical manifestations that accompany the syndrome characterize the PCOS as a metabolic disease, which carry important health risks at short, medium and long term. Therefore, they merit intervening actions to prevent, diagnose and provide timing treatment in order to limit the damage in the course of the natural history of PCOS.

TLR4 activation enhances the PD-L1-mediated tolerogenic capacity of colonic CD90+ stromal cells.

Signaling via programmed death ligand-1 (PD-L1) and PD-L2 is crucial for maintaining peripheral tolerance. CD90(+) myofibroblasts/fibroblasts (CMFs) are major programmed cell death-1 (PD-1) ligand-expressing cells in normal human colonic mucosa. CMFs suppress activated CD4(+) T cell proliferation via PD-1 ligands. It is not known whether signaling through TLRs contribute to the regulation PD-1 ligands on CMFs upon colonic mucosal tolerance. In this study, we demonstrated that stimulation of TLR4 on human CMFs upregulates PD-L1, but not PD-L2, and reinforces CMF-mediated suppression of CD4(+) T cell proliferation and IFN-γ production. TLR4-mediated upregulation of PD-L1 on CMFs involved NF-κB pathways and was JAK2 and MyD88 dependent. MyD88-dependent stimulation of TLR1/2 and TLR5 also upregulated PD-L1 expression on CMFs in culture. PD-L1 expression was drastically decreased in vivo in the colonic mucosa of mice devoid of MyD88. Induction of MyD88 deficiency in CMFs in fibroblast-specific MyD88 conditional knockout mice resulted in a strong increase in a mucosal IFN-γ expression concomitantly with the abrogation of PD-L1 expression in CMFs under homeostasis and epithelial injury induced by dextran sodium sulfate. Together, these data suggest that MyD88-dependent TLR stimulation of CMFs in the normal colonic mucosa may reinforce these cells' anti-inflammatory capacity and thus contribute to the maintenance of mucosal tolerance.

CagA-dependent downregulation of B7-H2 expression on gastric mucosa and inhibition of Th17 responses during Helicobacter pylori infection.

Gastric epithelial cells (GECs) are the primary target for Helicobacter pylori infection and may act as APCs regulating local T cell responses. We previously reported that H. pylori infection of GECs induces the expression of the T cell coinhibitory molecule B7-H1 on GECs. This process contributes to the hyporesponsiveness of CD4(+) effector T cells and accumulation of regulatory T cells. In the present study, we investigated the impact of H. pylori cytotoxin-associated gene A (CagA) on the modulation of the expression of the T cell costimulator B7-H2 by GECs. B7-H2 is involved in promoting Th17 type responses. H. pylori infection downregulates B7-H2 expression by GECs in a CagA-dependent manner. IFN-γ, which is increased in the H. pylori-infected gastric mucosa, synergizes with H. pylori in downregulating B7-H2 expression by GECs. CagA-mediated modulation of B7-H2 on GECs involves p70 S6 kinase phosphorylation. The CagA-dependent B7-H2 downregulation in GECs correlates with a decrease in Th17 type responses in vitro and in vivo. Furthermore, CagA-dependent modulation of Th17 responses was inversely correlated with the H. pylori colonization levels in vivo. Our data suggest that CagA contributes to the ability of H. pylori to evade Th17-mediated clearance by modulating expression of B7-H2 and, thus, to the establishment of the H. pylori chronic infection.

Changes in receptivity epithelial cell markers of endometrium after ovarian stimulation treatments: its role during implantation window.

BACKGROUND: To compare the expression of receptivity markers in epithelial and stromal cells in the endometrium of ovulatory women and infertile with hypothalamic pituitary dysfunction (HPD), untreated or treated with clomiphene citrate (CC), or with recombinant follicle stimulating hormone (rFSH). METHODS: Twelve control ovulatory and 32 anovulatory women, 22 of whom received ovulation induction with CC (n = 12) or rFSH (n = 10). Endometrial biopsies were obtained during the mid-secretory phase. Hormonal secretion was measured by chemiluminescence immunoassay, endometrial dating and cellular expression and distribution of receptivity proteins were evaluated by quantitative immunohistochemistry. RESULTS: CC or rFSH treatments, modified the expression of epithelial receptivity markers, such as Glycodelin A, beta-catenin, CD166/ALCAM and IGF-1R, but not in stromal markers. Also, a change in their cell distribution was observed. CONCLUSIONS: Treatment of infertile women with HPD modified the expression and distribution of receptivity markers in the mid-secretory phase of the endometrium in epithelial but not stromal cells, which can help to explain changes in the receptivity of the endometrium during treatments and suggest an important role of these cells in the receptivity window.

[Interactions between markers of endothelial damage (homocysteine and asymmetric dimethylarginine) and antioxidants and B-vitamins in preeclamptic women]. / Interacción entre los marcadores de daño endotelial (homocisteóna y dimetilarginina asimétrica) con las vitaminas antioxidantes y del grupo B en pacientes con preeclampsia.

BACKGROUND: Preeclampsia is a pregnancy-related pathological condition triggered by an abnormal placentation which produces endothelial dysfunction (ED). ED, in turn, is associated with an increase in homocysteine (hcy) and asymmetric dimethylarginine (ADMA); these molecules are also increased when some of the B-vitamins are deficient. It is unclear whether increases in hcy and ADMA during preeclampsia are the result of ED, or the consequence of a B-vitamin deficiency. OBJECTIVE: To evaluate hcy, ADMA, folic acid (FA), vitamin B6 and B2 concentrations in patients with preeclampsia. METHODS: In a cross-sectional design 19 patients with severe preeclamp- sia (preeclampsia) and 57 with normal pregnancy (no-preeclampsia), paired by gestational age and body mass index, were studied. Plasma hcy, ADMA, FA and vitamins B6 and B12 were determined. Non-parametric statistics was used for between-groups comparisons and regression analyses to evaluate interactions among molecules. RESULTS: 72% of women were vitamin B deficient, 40% were deficient of B12 and 4% of FA. Preeclamptic patients presented hcy and ADMA concentrations higher than no-preeclamptic ones. Inferential analyses demonstrated that: hcy and ADMA are increased during preeclampsia independently from vitamins blood concentration; that the risk for pre- eclampsia is associated with high hcy but not with vitamins deficiency; and that the ratio L-arginine:ADMA decreases the preeclampsia risk. CONCLUSION: In patients with preeclampsia, increases of hcy and ADMA are associated with ED, but not with deficiency of the vitamins involved in their metabolism.

[Contraception in women with chronic diseases]. / Anticoncepción en mujeres con enfermedades crónicas.

BACKGROUND: Almost 10% of women in reproductive age had a chronic disease, and contraception is frequently ignored by these patients. The lack of use of contraceptives methods has a higher repercussion in these patients; if pregnant, the risk is increased in morbidity and feto-maternal mortality. OBJECTIVES: to know the contraceptive coverage in women with chronic degenerative diseases, the kind of contraceptive methods and the unsatisfied demand. MATERIAL AND METHODS: A descriptive study was made with the application of a survey from the one elaborated by the IMSS. It explores contraception socio-demographic data, causes of non-protection and also explores Medical Doctor (MD) participation. Sample size was calculated in 385 women in reproductive age with a chronic disease. RESULTS: 428 women about 30-49 years old were interviewed, 53% of them were married, they had various diseases, the contraceptive coverage was 84%. The definitive methods were the most used with 47%, followed by the condom with 20%, intrauterine device with 13% and others in minor proportion. 38.5% of patients with sexual life have risk of pregnancy for lack of use of method or for using one of low effectiveness and continuity. Of 45 (16%) patients with sexual life that did not use methods, 29% because they wish pregnancy, 18% by collateral effects and the rest for other causes. From this same patients 21 wished getting pregnant and 24 did not, this is an unsatisfied demand of 53%. The MD's informed about risks in case of pregnancy of 83.4% of the patients. CONCLUSIONS: The contraceptive coverage is low and the unsatisfied demand is higher than in the general population. It requires the effective participation of health personal in this group of high reproductive risk.

Amniotic fluid-borne hepatocyte growth factor protects rat pups against experimental necrotizing enterocolitis.

Fetal swallowing of amniotic fluid, which contains numerous cytokines and growth factors, plays a key role in gut mucosal development. Preterm birth interrupts this exposure to amniotic fluid-borne growth factors, possibly contributing to the increased risk of necrotizing enterocolitis (NEC) in premature infants. We hypothesized that supplementation of formula feeds with amniotic fluid can provide amniotic fluid-borne growth factors and prevent experimental NEC in rat pups. We compared NEC-like injury in rat pups fed with infant formula vs. formula supplemented either with 30% amniotic fluid or recombinant hepatocyte growth factor (HGF). Cytokines/growth factors in amniotic fluid were measured by immunoassays. Amniotic fluid and HGF effects on enterocyte migration, proliferation, and survival were measured in cultured IEC6 intestinal epithelial cells. Finally, we used an antibody array to investigate receptor tyrosine kinase (RTK) activation and immunoblots to measure phosphoinositide 3-kinase (PI3K) signaling. Amniotic fluid supplementation in oral feeds protected rat pups against NEC-like injury. HGF was the most abundant growth factor in rat amniotic fluid in our panel of analytes. Amniotic fluid increased cell migration, proliferation, and cell survival in vitro. These effects were reproduced by HGF and blocked by anti-HGF antibody or a PI3K inhibitor. HGF transactivated several RTKs in IEC6 cells, indicating that its effects extended to multiple signaling pathways. Finally, similar to amniotic fluid, recombinant HGF also reduced the frequency and severity of NEC-like injury in rat pups. Amniotic fluid supplementation protects rat pups against experimental NEC, which is mediated, at least in part, by HGF.

The 700-1500 cm⁻¹ region of the S1 (ùB2) state of toluene studied with resonance-enhanced multiphoton ionization (REMPI), zero-kinetic-energy (ZEKE) spectroscopy, and time-resolved slow-electron velocity-map imaging (tr-SEVI) spectroscopy.

We report (nanosecond) resonance-enhanced multiphoton ionization (REMPI), (nanosecond) zero-kinetic-energy (ZEKE) and (picosecond) time-resolved slow-electron velocity map imaging (tr-SEVI) spectra of fully hydrogenated toluene (Tol-h8) and the deuterated-methyl group isotopologue (α3-Tol-d3). Vibrational assignments are made making use of the activity observed in the ZEKE and tr-SEVI spectra, together with the results from quantum chemical and previous experimental results. Here, we examine the 700-1500 cm(-1) region of the REMPI spectrum, extending our previous work on the region ≤700 cm(-1). We provide assignments for the majority of the S1 and cation bands observed, and in particular we gain insight regarding a number of regions where vibrations are coupled via Fermi resonance. We also gain insight into intramolecular vibrational redistribution in this molecule.

[Functionality and endometrial changes associated with induction ovulation with citrate of clomifene and recombinant FSH in infertile women]. / Funcionalidad y cambios endometriales asociados con la inducción de ovulación con citrato de clomifeno y FSH recombinante en mujeres con infertilidad.

It has been reported that infertility affects approximately 20% of couples in reproductive age around the world. Although many factors involved, ovulatory dysfunction and particularly the hypothalamus pituitary dysfunction are quite common. The first line treatment for these pathologies consists on the administration of inducing ovulation agents such as recombinant gonadotropins and clomiphene citrate which it was obtained high rates of ovulation but not of pregnancy. So determine the effect of these treatments on the endometrium at morphological and molecular level is very important to understand the female reproductive physiology and optimize clinical strategies to obtain better pregnancy rates after treatments. In this paper we detailed the studies that have reported changes at the molecular and morphological level in human endometrium.

[Insulin resistance frecuency in women's with polycystic ovary syndrome using hyperinsulinemic-euglycemic clamp]. / Frecuencia de resistencia a la insulina en pacientes con síndrome de ovario poliqulstico con el clamp hiperinsulinémico euglucémico.

OBJECTIVE: To assess IR in PCOS patients, using the HE-clamp as the IR gold standard. MATERIAL AND METHODS: A transversal design was done. All patients who accepted to participate provided written informed consent. PCOS was diagnosed according to the 2003 Rotterdam criteria. IR was assessed using the H-clamp, and other IR surrogates such as; fasting plasma insulin (FPI), homeostasis model assessment (HOMA) index and insulin/ glucose rate (I/G rate). Statistical analysis was performed using measures of location and spread was used according to data distribution. RESULTS: 21 patients were included. The mean age of the total group studied was 29.5 +/- 4.8 years, and the body mass index (BMI) was 27.2 +/- 3.08 kg/m2. The 85.7% of the patients met the three Rotterdam criteria for the diagnosis of PCOS. According to the HE clamp 95.2% were IR (M/I value < 6 mg/Kg/min), in contrast the prevalence of IR using sur- rogates was 47.6%, 33.3%, and 66.6% for FPI, G/I rate, and HOMA index respectively. CONCLUSIONS: Our findings show that IR is highly prevalent in patients with PCOS, and that this prevalence is even higher when insulin sensitivity is assessed using the glucose clamp technique. This evidence suggests that IR could be considered diagnostic criteria for PCOS.

[Clinical practice guideline for the diagnosis and treatment of hyperprolactinemia]. / Guía de práctica clínica para el diagnóstico y tratamiento de la hiperprolactinemia.

BACKGROUND: Hyperprolactinemia is a common finding within clinical practice in both endocrinology and general practice fields, amongst other specialties. The general practitioner and other specialists must know the indications and serum prolactin determination parameters in order to, once detected, derive the patient for a correct assessment and begin treatment. OBJECTIVE: Formulate a clinical practice guideline evidence-based for the diagnosis and treatment of hyperprolactinemia. METHOD: It took the participation of eight gynecologists, two pathologists and a pharmacologist in the elaboration of this guideline due their experience and clinical judgement. These recommendations were based upon diagnostic criteria and levels of evidence from treatment guidelines previously established, controlled clinical trials and standardized guides for adolescent and adult population with hyperprolactinemia. RESULTS: During the conformation of this guideline each specialist reviewed and updated a specific topic and established the evidence existent over different topics according their field of best clinical expertise, being enriched by the opinion of other experts. At the end, all the evidence and decisions taken were unified in the document presented here. CONCLUSIONS: It is presented the recommendations established by the panel of experts for diagnosis and treatment of patients with high levels of prolactin; also the level of evidence for the diagnosis of hyperprolactinemia, handling drug-induced hyperprolactinemia and prolactinomas in pregnant and non-pregnant patients.

Factor XII Deficiency in Mexico: High Prevalence in the General Population and Patients with Venous Thromboembolic Disease.

INTRODUCTION: Thrombosis is one of the leading causes of morbidity and mortality worldwide. Venous thromboembolic disease (VTD) is considered a new epidemic. FXII deficiency is supposed to be a cause of thrombosis. To search for unknown causes of thrombosis in our population, our aim was to determine if FXII deficiency can be considered a risk factor for VTD. METHODS: Young adult Mexican patients with at least one VTD episode and healthy controls were included in this prospective, observational, controlled study. Liver and renal function tests, blood cytometry, and blood coagulation assays were performed. Plasma FXII activity and its concentration were evaluated. RESULTS: Over a two-year period, 250 patients and 250 controls were included. FXII activity was significantly lower in the control group compared to patients with VTD (p = 0.005). However, percentage of patients and controls with FXII deficiency was 8.8 and 9.2%, respectively (p = 1.000). No significant association was found between FXII deficiency and VTD (p = 1.0). FXII plasma concentration was lower in controls vs. patients with VTD: 4.05 vs. 6.19 ng/mL (p <0.001). Percentage of patients with low FXII plasma concentration was 1.6% and 6.0% in patients and controls, respectively (p = 0.010). CONCLUSIONS: FXII deficiency is a frequent finding in patients with VTD and controls in Mexico. Some patients with FXII deficiency had normal APTT result, an effect not described above. FXII plasma concentration was lower in patients with low activity.

Vibrations of the low energy states of toluene (X̃ (1)A1 and à (1)B2) and the toluene cation (X̃ (2)B1).

We commence by presenting an overview of the assignment of the vibrational frequencies of the toluene molecule in its ground (S0) state. The assignment given is in terms of a recently proposed nomenclature, which allows the ring-localized vibrations to be compared straightforwardly across different monosubstituted benzenes. The frequencies and assignments are based not only on a range of previous work, but also on calculated wavenumbers for both the fully hydrogenated (toluene-h8) and the deuterated-methyl group isotopologue (α3-toluene-d3), obtained from density functional theory (DFT), including artificial-isotope shifts. For the S1 state, one-colour resonance-enhanced multiphoton ionization (REMPI) spectroscopy was employed, with the vibrational assignments also being based on previous work and time-dependent density functional theory (TDDFT) calculated values; but also making use of the activity observed in two-colour zero kinetic energy (ZEKE) spectroscopy. The ZEKE experiments were carried out employing a (1 + 1(')) ionization scheme, using various vibrational levels of the S1 state with an energy <630 cm(-1) as intermediates; as such we only discuss in detail the assignment of the REMPI spectra at wavenumbers <700 cm(-1), referring to the assignment of the ZEKE spectra concurrently. Comparison of the ZEKE spectra for the two toluene isotopologues, as well as with previously reported dispersed-fluorescence spectra, and with the results of DFT calculations, provide insight both into the assignment of the vibrations in the S1 and D0(+) states, as well as the couplings between these vibrations. In particular, insight into the nature of a complicated Fermi resonance feature at ∼460 cm(-1) in the S1 state is obtained, and Fermi resonances in the cation are identified. Finally, we compare activity observed in both REMPI and ZEKE spectroscopy for both toluene isotopologues with that for fluorobenzene and chlorobenzene.

Interaction of the NO 3pπ Rydberg state with Ar: potential energy surfaces and spectroscopy.

We present the experimental and simulated (2+1) REMPI spectrum of the C(2)Π state of the NO-Ar complex, in the vicinity of the 3p Rydberg state of NO. Two Rydberg states of NO are expected in this energy region: the C(2)Π (3pπ) and D(2)Σ(+) (3pσ) states, and we concentrate on the former here. When the C(2)Π (3pπ) state interacts with Ar at nonlinear orientations, the symmetry is lowered to C(s), splitting the degeneracy of the (2)Π state to yield C((2)A") and C((2)A') states. For these two states of NO-Ar, we calculate potential energy surfaces using second order Møller-Plesset perturbation theory, exploiting a procedure to converge the reference Hartree-Fock wavefunction to describe the excited states, the maximum overlap method. The bound rovibrational states obtained from the surfaces are used to simulate the electronic spectrum, which is in excellent agreement with experiment, providing assignments for the observed spectral lines from the calculated rovibrational wavefunctions.

Helicobacter pylori and Its Role in Gastric Cancer.

Gastric cancer is a challenging public health concern worldwide and remains a leading cause of cancer-related mortality. The primary risk factor implicated in gastric cancer development is infection with Helicobacter pylori. H. pylori induces chronic inflammation affecting the gastric epithelium, which can lead to DNA damage and the promotion of precancerous lesions. Disease manifestations associated with H. pylori are attributed to virulence factors with multiple activities, and its capacity to subvert host immunity. One of the most significant H. pylori virulence determinants is the cagPAI gene cluster, which encodes a type IV secretion system and the CagA toxin. This secretion system allows H. pylori to inject the CagA oncoprotein into host cells, causing multiple cellular perturbations. Despite the high prevalence of H. pylori infection, only a small percentage of affected individuals develop significant clinical outcomes, while most remain asymptomatic. Therefore, understanding how H. pylori triggers carcinogenesis and its immune evasion mechanisms is critical in preventing gastric cancer and mitigating the burden of this life-threatening disease. This review aims to provide an overview of our current understanding of H. pylori infection, its association with gastric cancer and other gastric diseases, and how it subverts the host immune system to establish persistent infection.