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Objective: Validate the full-PIERS model in predicting adverse maternal outcomes in women with early-onset preeclampsia with severe features in our population., Methods: Retrospective cohort study. We applied the full-PIERS model on 130 women with severe early-onset preeclampsia who were treated at a second-level hospital in Nuevo León, México. We validated the full-PIERS model in its ability to discriminate through the AUROC., Results: The full-PIERS model applied to the data obtained in our study had good discrimination, revealing an AUC of 0.718 (95% CI 0.515-0.921; P = 0.017). A cut-off of 7.95 was identified as the cut-off point with the best diagnostic performance, with the highest Youden index, presenting a sensitivity of 54.5% and specificity of 99.2% for the development of complications., Conclusion: The full-PIERS model can predict adverse maternal outcomes in women admitted to our hospital with severe early-onset preeclampsia within 48 hours of admission., Competing Interests: The authors declare that they have no conflicts of interest., (Copyright © 2024 Eduardo Ponce Nájera et al.)

β-Cell replacement by in situ reprogramming of non-β-cells is a promising diabetes therapy. Following the observation that near-total β-cell ablation in adult mice triggers the reprogramming of pancreatic α-, δ-, and γ-cells into insulin (INS)-producing cells, recent studies are delving deep into the mechanisms controlling adult α-cell identity. Systematic analyses of the α-cell transcriptome and epigenome have started to pinpoint features that could be crucial for maintaining α-cell identity. Using different transgenic and chemical approaches, significant advances have been made in reprogramming α-cells in vivo into INS-secreting cells in mice. The recent reprogramming of human α-cells in vitro is an important step forward that must now be complemented with a comprehensive molecular dissection of the mechanisms controlling α-cell identity., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Rocky Mountain spotted fever (RMSF) is a tick-borne infection caused by Rickettsia rickettsii. We present a series of two cases of pregnant patients who showed up at the emergency room of a hospital in Nuevo León, Mexico. Both patients lived in environments where R. rickettsii is endemic and they presented with several days of symptoms, including fever. Both patients developed a rash and had stillbirths during their hospital stay. Treatment with doxycycline was delayed, with fatal results in both patients. Diagnosis of RMSF was confirmed via polymerase chain reaction assay postmortem. The need to link epidemiological clues with clinical data is critical in the diagnosis and early treatment of RMSF to prevent maternal deaths.

Generation of surrogate cells with stable functional identities is crucial for developing cell-based therapies. Efforts to produce insulin-secreting replacement cells to treat diabetes require reliable tools to assess islet cellular identity. Here, we conduct a thorough single-cell transcriptomics meta-analysis to identify robustly expressed markers used to build genesets describing the identity of human α-, β-, γ- and δ-cells. These genesets define islet cellular identities better than previously published genesets. We show their efficacy to outline cell identity changes and unravel some of their underlying genetic mechanisms, whether during embryonic pancreas development or in experimental setups aiming at developing glucose-responsive insulin-secreting cells, such as pluripotent stem-cell differentiation or in adult islet cell reprogramming protocols. These islet cell type-specific genesets represent valuable tools that accurately benchmark gain and loss in islet cell identity traits., (© 2022. The Author(s).)

Background: Loss of pancreatic insulin-secreting β-cells due to metabolic or autoimmune damage leads to the development of diabetes. The discovery that α-cells can be efficiently reprogrammed into insulin-secreting cells in mice and humans has opened promising avenues for innovative diabetes therapies. β-cell loss triggers spontaneous reprogramming of only 1-2% of α-cells, limiting the extent of regeneration. Most α-cells are refractory to conversion and their global transcriptomic response to severe β-cell loss as well as the mechanisms opposing their reprogramming into insulin producers are largely unknown. Here, we performed RNA-seq on FAC-sorted α-cells to characterize their global transcriptional responses at different time points after massive β-cell ablation., Results: Our results show that α-cells undergo stage-specific transcriptional changes 5- and 15-days post-diphtheria toxin (DT)-mediated β-cell ablation. At 5 days, α-cells transiently upregulate various genes associated with interferon signaling and proliferation, including Interferon Induced Protein with Tetratricopeptide Repeats 3 (Ifit3). Subsequently, at 15 days post β-cell ablation, α-cells undergo a transient downregulation of genes from several pathways including Insulin receptor, mTOR and MET signaling., Conclusions: The results presented here pinpoint novel markers discriminating α-cells at different stages after acute β-cell loss, and highlight additional signaling pathways that are modulated in α-cells in this context., (© 2021. The Author(s).)

The cellular identity of pancreatic polypeptide (Ppy)-expressing γ-cells, one of the rarest pancreatic islet cell-type, remains elusive. Within islets, glucagon and somatostatin, released respectively from α- and δ-cells, modulate the secretion of insulin by β-cells. Dysregulation of insulin production raises blood glucose levels, leading to diabetes onset. Here, we present the genetic signature of human and mouse γ-cells. Using different approaches, we identified a set of genes and pathways defining their functional identity. We found that the γ-cell population is heterogeneous, with subsets of cells producing another hormone in addition to Ppy. These bihormonal cells share identity markers typical of the other islet cell-types. In mice, Ppy gene inactivation or conditional γ-cell ablation did not alter glycemia nor body weight. Interestingly, upon β-cell injury induction, γ-cells exhibited gene expression changes and some of them engaged insulin production, like α- and δ-cells. In conclusion, we provide a comprehensive characterization of γ-cells and highlight their plasticity and therapeutic potential., (© 2021. The Author(s).)

Binder jet additive manufacturing (BJAM) is capable of fabricating complex three-dimensional components from a variety of material classes. Understanding the fundamentals of BJAM, including spreading of thin layers of powder, powder-binder interactions, and post-processing is critical to develop robust process parameters for BJAM. Toward meeting these needs, this work presents the design, fabrication, and qualification of a testbed for modular, mechanized, BJAM. The testbed seeks to replicate the operating conditions of commercial AM equipment and features fully programmable motion control including powder spreading using a precision roller mechanism, powder supply via a vibrating hopper, and gantry positioning of an inkjet printhead. The inkjet deposition system allows for the use of variable nozzle diameters, the exploration of novel binder compositions, and full control of jetting parameters. Validation of the accuracy and repeatability of the machine and its subsystems, as well as the fabrication of exemplary stainless steel components, are described. The precision engineered testbed can therefore enable the study of the BJAM process, exploration of novel binder compositions, and processing of custom powders to further scientific research and industrial applicability of BJAM., Competing Interests: Conflict of interest/Competing interest Not applicable.

The β-cell regeneration field has shown a strong knowledge boost in the last 10 years. Pluripotent stem cell differentiation and direct reprogramming from other adult cell types are becoming more tangible long-term diabetes therapies. Newly generated β-like-cells consistently show hallmarks of native β-cells and can restore normoglycemia in diabetic mice in virtually all recent studies. Nonetheless, these cells still show important compromises in insulin secretion, cell metabolism, electrical activity, and overall survival, perhaps due to a lack of signal integration from other islet cells. Mounting data suggest that diabetes is not only a β-cell disease, as the other islet cell types also contribute to its physiopathology. Here, we present an update on the most recent studies of islet cell heterogeneity and paracrine interactions in the context of restoring an integrated islet function to improve β-cell replacement therapies., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Bru-Tari, Oropeza and Herrera.)

Aluminum alloy 7075 (Al 7075) with a T73 heat treatment is commonly used in aerospace applications due to exceptional specific strength properties. Challenges with manufacturing the material from the melt has previously limited the processing of Al 7075 via welding, casting, and additive manufacturing. Recent research has shown the capabilities of nanoparticle additives to control the solidification behavior of high-strength aluminum alloys, showcasing the first Al 7075 components processed via casting, welding, and AM. In this work, the properties of nanoparticle-enhanced aluminum 7075 are investigated on welded parts, overlays and through wire-based additive manufacturing. The hardness and tensile strength of the deposited materials were measured in the as-welded and T73 heat-treated conditions showing that the properties of Al 7075 T73 can be recovered in welded and layer-deposited parts. The work shows that Al 7075 now has the potential to be conventionally welded or additively manufactured from wire into high-strength, crack-free parts.

Both type 1 and type 2 diabetes are associated with hyperglycemia and loss of functional beta cell mass. Inducing proliferation of preexisting beta cells is an approach to increase the numbers of beta cells. In this study, we examined a panel of selected small molecules for their proliferation-inducing effects on human pancreatic beta cells. Our results demonstrated that a small molecule inhibitor of the menin-MLL interaction (MI-2) and small molecule inhibitors of TGF-β signaling (SB431542, LY2157299, or LY364947) synergistically increased ex vivo replication of human beta cells. We showed that this increased proliferation did not affect insulin production, as a pivotal indication of beta cell function. We further provided evidence which suggested that menin-MLL and TGF-β inhibition cooperated through downregulation of cell cycle inhibitors CDKN1A, CDKN1B, and CDKN2C. Our findings might provide a new option for extending the pharmacological repertoire for induction of beta cell proliferation as a potential therapeutic approach for diabetes., Competing Interests: Declaration of Competing Interest The authors declare no competing interest., (Copyright © 2020 Elsevier GmbH. All rights reserved.)

The contribution and impact of combined laser ablation inductively coupled plasma time-of-flight mass spectrometry (LA-ICP-TOF-MS) and laser-induced breakdown spectroscopy (LIBS) were evaluated for the discrimination analysis of different coal samples. This tandem approach allows simultaneous determination of major and minor elements (C, H, Si, Ca, Al, Mg, etc.) and trace elements (V, Ba, Pb, U, etc.) in the coal. The research focused on coal-classification strategies based on principle component analysis (PCA) combined with K-means clustering, partial least-squares discrimination analysis (PLS-DA), and support vector machine (SVM) for analytical performance. Correlation analyses performed from TOF mass and LIBS emission spectra from the coal samples showed that most major, minor, and trace element emissions had negative correlation with the volatile content. Suitable variables for the classification models were determined from these data. The individual TOF data, LIBS data, and combined data of TOF and LIBS as the inputs for different models were analyzed and compared. In all cases, the results obtained with the combined TOF and LIBS data were found to be superior to those obtained with the individual TOF or LIBS data. The nonlinear SVM model combined with TOF and LIBS data provided the best coal-classification performance, with a classification accuracy of up to 98%.

Laser-induced breakdown spectroscopy (LIBS) and laser ablation inductively coupled plasma optical emission spectrometry (LA-ICP-OES) were used simultaneously for the elemental analysis of asphaltene samples using minimum sample pretreatment in combination with low laser energy to reduce the amount of removed particles and avoid carbon deposits in the ablation cell. Quantitative analyses of S, Ni, and V were accomplished with LA-ICP-OES using external calibration with the C line as internal standard. The aromatic/paraffinic nature of the asphaltenes was also obtained throughout the H/C ratio using LIBS and partial least square regression model. The results showed very good agreement (±10%) between the concentration obtained by LA-ICP-OES and microwave-assisted acid digestion values.

Cell-identity switches, in which terminally differentiated cells are converted into different cell types when stressed, represent a widespread regenerative strategy in animals, yet they are poorly documented in mammals. In mice, some glucagon-producing pancreatic α-cells and somatostatin-producing δ-cells become insulin-expressing cells after the ablation of insulin-secreting β-cells, thus promoting diabetes recovery. Whether human islets also display this plasticity, especially in diabetic conditions, remains unknown. Here we show that islet non-β-cells, namely α-cells and pancreatic polypeptide (PPY)-producing γ-cells, obtained from deceased non-diabetic or diabetic human donors, can be lineage-traced and reprogrammed by the transcription factors PDX1 and MAFA to produce and secrete insulin in response to glucose. When transplanted into diabetic mice, converted human α-cells reverse diabetes and continue to produce insulin even after six months. Notably, insulin-producing α-cells maintain expression of α-cell markers, as seen by deep transcriptomic and proteomic characterization. These observations provide conceptual evidence and a molecular framework for a mechanistic understanding of in situ cell plasticity as a treatment for diabetes and other degenerative diseases.

Physicochemical, antifungal and antioxidant properties of a pectin - aloe mucilage - candelilla wax - Larrea tridentata polyphenols based bioactive film were evaluated. Antifungal capacity was analyzed against Botrytis cinerea, Colletotrichum gloeosporioides, Fusarium oxysporum and Alternaria alternata . The main antioxidants in Larrea tridentata polyphenols were identified by HPLC-MS. Water vapor permeability (WVP) was measured in the film. Antioxidant capacities for ABTS · + , DPPH · , lipid oxidation inhibition (LOI) and ferric reducing antioxidant power (FRAP) (97, 92, and 57 %, 0.73 mM Fe, respectively) were evaluated. It was possible to determine the MIC 50 for the fungi evaluated at concentrations of 558-612 ppm of polyphenols. Antioxidants identified were nordihydroguaiaretic acid (NDGA), Quercetin, and Kaenpherol. Treatment with 1.1 % of pectin, 0.16 % candelilla wax, 0.3 % glycerol, 5 % AM and 4 % extract of polyphenols showed values of thickness and WVP suitable to be applied on model fruits.

The mechanisms that restrict regeneration and maintain cell identity following injury are poorly characterized in higher vertebrates. Following β-cell loss, 1-2% of the glucagon-producing α-cells spontaneously engage in insulin production in mice. Here we explore the mechanisms inhibiting α-cell plasticity. We show that adaptive α-cell identity changes are constrained by intra-islet insulin- and Smoothened-mediated signalling, among others. The combination of β-cell loss or insulin-signalling inhibition, with Smoothened inactivation in α- or δ-cells, stimulates insulin production in more α-cells. These findings suggest that the removal of constitutive 'brake signals' is crucial to neutralize the refractoriness to adaptive cell-fate changes. It appears that the maintenance of cell identity is an active process mediated by repressive signals, which are released by neighbouring cells and curb an intrinsic trend of differentiated cells to change.

We evaluated the performance of laser ablation analysis techniques such as laser-induced breakdown spectroscopy (LIBS), laser ablation inductively coupled optical emission spectrometry (LA-ICP-OES), and laser ablation inductively coupled plasma mass spectrometry (LA-ICP-MS), in comparison with that of ICP-OES using aqueous solutions for the quantification of sulfur (S) in edible salts from different geographical origins. We found that the laser ablation based sampling techniques were not influenced by loss of S, which was observed in ICP-OES with aqueous solutions for a certain salt upon their dissolution in aqueous solutions, originating from the formation of volatile species and precipitates upon their dilution in water. Although detection of S using direct laser sampling with LA-ICP-MS has well-known isobaric and polyatomic interferences, LIBS and LA-ICP-OES showed good accuracy in the detection of S for all salts. LIBS also provided the ability to identify the dominant chemical form in which S is present in salts. Correlation between S and oxygen, observed in LIBS spectra, provided chemical information about the presence of S 2- or [Formula: see text], which are associated with the origin and quality of edible salts.

Direct solid sampling by laser ablation into an inductively coupled plasma synchronous vertical dual view optical emission spectroscope (LA-SVDV-ICP-OES) was used for the elemental analysis of nutrient elements Ca, B, Mn, Mg, K, and Zn and essential (non-metallic) elements P and S in plant materials. The samples were mixed with paraffin as a binder, an approach that provides better cohesion of the particles in the pellets in addition to supplying carbon to serve as an internal standard (atomic line C I 193.027 nm) as a way to compensate for matrix effects, and/or variations in the ablation process. Precision was in the range of 1-8% relative standard deviation (RSD) with limit of detection in the range of 0.4-1 mg/kg -1 and 25-640 mg/kg -1 for metallic and non-metallic elements, respectively.

Background & Aims: Inefficient fatty acid oxidation in mitochondria and increased oxidative damage are features of non-alcoholic fatty liver disease (NAFLD). In rodent models and patients with NAFLD, hepatic expression of peroxisome proliferator-activated receptor-γ (PPARG) coactivator 1α (PPARGC1A or PGC1A) is inversely correlated with liver fat and disease severity. A common polymorphism in this gene (rs8192678, encoding Gly482Ser) has been associated with NAFLD. We investigated whether reduced expression of PGC1A contributes to development of NAFLD using mouse models, primary hepatocytes, and human cell lines., Methods: HepG2 cells were transfected with variants of PPARGC1A and protein and messenger RNA levels were measured. Mice with liver-specific hemizygous or homozygous disruption of Ppargc1a (Ppargc1a f/+ Alb-cre +/0 and Ppargc1a f/f Alb-cre +/0 mice, respectively) were fed regular chow (control) or a high-fat diet supplemented with 30% d-fructose in drinking water (obesogenic diet) for 25-33 weeks. Liver tissues were analyzed by histology and by immunoblotting. Primary hepatocytes were analyzed for insulin signaling, reactive oxygen species, and estrogen response. Luciferase reporter expression was measured in transfected H2.35 cells expressing an estrogen receptor reporter gene, estrogen receptor 1, and/or PGC1A/B., Results: The serine 482 variant of the human PGC1A protein had a shorter half-life than the glycine 482 variant when expressed in HepG2 cells. Liver tissues from mice with liver-specific hemizygous disruption of Ppargc1a placed on an obesogenic diet expressed increased markers of inflammation and fibrosis and decreased levels of antioxidant enzymes compared with the Ppargc1a +/+ on the same diet. Oxidative damage was observed in livers from Ppargc1a f/+ Alb-cre +/0 mice of each sex, in a cell-autonomous manner, but was greater in livers from the female mice. Expression of PGC1A in H2.35 cells coactivated estrogen receptor 1 and was required for estrogen-dependent expression of genes that encode antioxidant proteins. These findings could account for the increased liver damage observed in female Ppargc1a f/+ Alb-cre +/0 mice; while, compensatory increases in PPARG coactivator 1β could prevent oxidative damage associated with complete loss of PGC1A expression in Ppargc1a f/f Alb-cre +/0 female mice., Conclusions: In mice, loss of estrogen signaling contributes to oxidative damage caused by low levels of PGC1A in liver, exacerbating steatohepatitis associated with diets high in fructose and fat., (Copyright © 2017 AGA Institute. Published by Elsevier Inc. All rights reserved.)

A 55-year-old female patient, born in Ayacucho, with a history of dermatomyositis for 3 years, who received irregular treatment with prednisone. Two months prior to admission, she presented with autoinmune hemolytic anemia and idiopathic thrombocytopenic purpura. The patient received methylprednisolone pulse therapy and packed red blood cells transfusions. Upon admission, she was drowsy, with a poor overall status, marked weight loss, dehydration, with presence of livedo reticularis in her lower extremities, and onychodystrophy and onycholysis on the toes of both feet. Western blot test was positive for human T-lymphotropic virus type 1 (HTLV-1). The patient evolved with recurrent hypoglycemia. Therefore, we report a case of dermatomyositis and Evans syndrome in the context of an HTLV-1 infection.

Introduction: Situs inversus totalis is an uncommon anomaly which exist a complete transposition of organs and it's occasionally associated with congenital heart diseases, such as tetralogy of fallot. Pheochromocytoma is a rare neuroendocrine tumor with an annual incidence of 2-8 cases per million people and for years has been studied its relationship with the hypoxic pathway. Case Report: A 29 year old male with a history of tetralogy of fallot corrected at 10 years and situs inversus totalis. He was admitted to hospital with a progressive story of four months of constipation, palpitations, headache, dyspnea and sweating. Physical examination revealed a thinned man with peripheral cyanosis, clubbing and signs of decompensated congestive heart failure as hepatomegaly, legs edema, multifocal systodiastolic murmurs, abdominal distension and jugular venous distention. The echocardiogram shows severe right ventricular dysfunction and severe pulmonary hypertension. Furthermore, abdominal computed tomography shows right adrenal mass. Elevated metanephrines and catecholamines confirmed the diagnosis of pheochromocytoma. Surgical removal is decided and preoperative management begins with alpha-adrenergic blockade, however the patient had a hemodynamic decompensation with an unfavorable evolution. Discussion: In conclusion, there are few reports of cyanotic congenital heart disease with pheochromocytoma. Several studies show a significant association between both of them due to chronic hypoxia leads sustained hyperresponsiveness in adrenal medulla and it would cause the tumor. Special preoperative management of pheochromocytoma is recommended when there underlying heart disease and congestive heart failure. We present the first international report of tetralogy of fallot and pheochromocytoma in a patient with situs inversus totalis.

There is growing concern over confounding artifacts associated with β-cell-specific Cre-recombinase transgenic models, raising questions about their general usefulness in research. The inducible β-cell-specific transgenic (MIP-CreERT(1Lphi)) mouse was designed to circumvent many of these issues, and we investigated whether this tool effectively addressed concerns of ectopic expression and disruption of glucose metabolism. Recombinase activity was absent from the central nervous system using a reporter line and high-resolution microscopy. Despite increased pancreatic insulin content, MIP-CreERT mice on a chow diet exhibited normal ambient glycemia, glucose tolerance and insulin sensitivity, and appropriate insulin secretion in response to glucose in vivo and in vitro. However, MIP-CreERT mice on different genetic backgrounds were protected from high-fat/ streptozotocin (STZ)-induced hyperglycemia that was accompanied by increased insulin content and islet density. Ectopic human growth hormone (hGH) was highly expressed in MIP-CreERT islets independent of tamoxifen administration. Circulating insulin levels remained similar to wild-type controls, whereas STZ-associated increases in α-cell number and serum glucagon were significantly blunted in MIP-CreERT(1Lphi) mice, possibly due to paracrine effects of hGH-induced serotonin expression. These studies reveal important new insight into the strengths and limitations of the MIP-CreERT mouse line for β-cell research., (© 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.)

Objectives: Peroxisome proliferator-activated receptor γ coactivator 1 (PPARGCA1, PGC-1) transcriptional coactivators control gene programs important for nutrient metabolism. Islets of type 2 diabetic subjects have reduced PGC-1α expression and this is associated with decreased insulin secretion, yet little is known about why this occurs or what role it plays in the development of diabetes. Our goal was to delineate the role and importance of PGC-1 proteins to β-cell function and energy homeostasis., Methods: We investigated how nutrient signals regulate coactivator expression in islets and the metabolic consequences of reduced PGC-1α and PGC-1β in primary and cultured β-cells. Mice with inducible β-cell specific double knockout of Pgc-1α/Pgc-1β (βPgc-1 KO) were created to determine the physiological impact of reduced Pgc1 expression on glucose homeostasis., Results: Pgc-1α and Pgc-1β expression was increased in primary mouse and human islets by acute glucose and palmitate exposure. Surprisingly, PGC-1 proteins were dispensable for the maintenance of mitochondrial mass, gene expression, and oxygen consumption in response to glucose in adult β-cells. However, islets and mice with an inducible, β-cell-specific PGC-1 knockout had decreased insulin secretion due in large part to loss of the potentiating effect of fatty acids. Consistent with an essential role for PGC-1 in lipid metabolism, β-cells with reduced PGC-1s accumulated acyl-glycerols and PGC-1s controlled expression of key enzymes in lipolysis and the glycerolipid/free fatty acid cycle., Conclusions: These data highlight the importance of PGC-1s in coupling β-cell lipid metabolism to promote efficient insulin secretion.

Background: Toxoplasma gondii infection has been associated with psychiatric diseases. However, there is no information about the link between this infection and patients with mental and behavioral disorders due to psychoactive substance use., Methods: We performed a case-control study with 149 psychiatric patients suffering from mental and behavioral disorders due to psychoactive substance use and 149 age- and gender-matched control subjects of the general population. We searched for anti-T. gondii IgG and IgM antibodies in the sera of participants by means of commercially available enzyme-linked immunoassays. Seroprevalence association with socio-demographic, clinical and behavioral characteristics in psychiatric patients was also investigated., Results: Anti-T. gondii IgG antibodies were present in 15 (10.1%) of 149 cases and in 14 (9.4%) of 149 controls (P=1.0). Anti-T. gondii IgM antibodies were found in 11 (7.4%) of the 149 cases and in 16 (10.7%) of the 149 controls (P=0.31). No association of T. gondii exposure with socio-demographic characteristics of patients was found. Multivariate analysis of clinical and behavioral characteristics of cases showed that T. gondii seropositivity was positively associated with consumption of opossum meat (OR=10.78; 95% CI: 2.16-53.81; P=0.003) and soil flooring at home (OR=11.15; 95% CI: 1.58-78.92; P=0.01), and negatively associated with suicidal ideation (OR=0.17; 95% CI: 0.05-0.64; P=0.008)., Conclusions: Mental and behavioral disorders due to psychoactive substance use do not appear to represent an increased risk for T. gondii exposure. This is the first report of a positive association of T. gondii exposure with consumption of opossum meat. Further studies to elucidate the role of T. gondii infection in suicidal ideation and behavior are needed to develop optimal strategies for the prevention of infection with T. gondii.

Promoting ectopic development of pancreatic beta cells from other cell types is one of the strategies being pursued for the treatment of diabetes. To achieve this, a detailed outline of the molecular lineage that operates in pancreatic progenitor cells to generate beta cells over other endocrine cell types is necessary. Here, we demonstrate that early transient expression of the endocrine progenitor bHLH protein Neurogenin 3 (Ngn3) favors the promotion of pancreatic beta and delta cell fates over an alpha cell fate, while later transient expression promotes ectopic development of all three endocrine cell fates. We found that short-term activation of Ngn3 in Xenopus laevis endoderm just after gastrulation was sufficient to promote both early and ectopic development of beta and delta cells. By examining gene expression changes 4 h after Ngn3 activation we identified several new downstream targets of Ngn3. We show that several of these are required for the promotion of ectopic beta cells by Ngn3 as well as for normal beta cell development. These results provide new detail regarding the Ngn3 transcriptional network operating in endocrine progenitor cells to specify a beta cell phenotype and should help define new approaches to promote ectopic development of beta cells for diabetes therapy., (Copyright © 2012 Wiley Periodicals, Inc.)

Introduction: Hashimoto's encephalopathy is a neurological disorder of unknown cause associated with thyroid autoimmunity. The disease occurs primarily in the fifth decade of life and may present in two types - a sudden vasculitic type or a progressive subacute type associated to cognitive dysfunction, confusion and memory loss., Case Presentation: We report the case of a 62-year-old Hispanic woman, previously healthy, who developed a subacute onset of declining upper brain function. Serologic studies demonstrated high levels of antithyroid antibodies. Electroencephalographic and magnetic resonance image findings were consistent with Hashimoto's encephalopathy., Conclusion: Hashimoto's encephalopathy is a diagnosis of exclusion. This unusual disorder is often under-recognized because of the multiple and protracted neurocognitive manifestations; therefore, it is important to be aware of the clinical manifestations to make a correct diagnosis.

It is shown three cases of sclerosing peritonitis, two of them related to gastric adenocarcinoma and the other one associated to thecoma. The clinical picture comprised abdominal pain, ascites and intestinal occlusion. Key words: Sclerosing Peritonitis, Adenocarcinoma, Stomach, Signet Ring Cells, Krukenberg's Tumor, Thecoma, Intestinal Occlusion.

The case of a 23-year old woman with a history of epigastric pain, a palpable tumor that covered the epigastrium and the left hypochondrium, and an episode of acute pancreatitis was reported. The computerized tomography revealed a pancreatic cyst. The CA-125 increased significantly. An exploratory laparotomy was performed, finding an endometrioma. The pathological anatomy showed necrotic tissue, mucus and blood, with a presence of macrophages with hemosiderin phagocytosis. The symptoms and signs, pathogenesis and treatment of the endometriosis of the pancreas are discussed.

Unlabelled: The case of a 22 year old woman from Huaraz is presented herein. She suffered from pain at right hypocondrium, associated to nausea and vomits, which intensified three days prior to admission. Upon examining her, a faded gallbladder murmur was found on the base of the right hemithorax. There is pain in the abdomen when touched at the epigastrium and right hypocondrium. The liver is perceived 3 cm beneath the costal edge: White blood count with severe eosinophilia. Mild cholestasis is observed. Abdominal scan: Heterogeneous hepatic mass, with a 13 cm diameter in the right lobe. CAT scan: Subcapsular 14x8 cm mass. Scintiscan: Liver with a low absorption area showing absence of perfusion to the vascular pool. She undergoes an exploratory laparotomy and an 800 cc subcapsular hematoma is found in segment 6, 7 and 8, which is drained. Evolution evidences the persistence of eosinophilia and positive Arc-2 is obtained for Fasciola. She was administered Triclabendazol and is currently asymptomatic., Conclusion: The invasive stage of human fascioliasis may cause hepatic hematoma as a rare complication. The triad of persisting eosinophilia, painful hepatomegalia and prolonged fever leads to insist in the search of fascioliasis in endemic areas.

The clinical case of one patient with fever of unknown origin, due to granulomatous hepatitis of tuberculous etiology was presented. The patient was a a 50-year-old woman, with 50 days illness characterized by chills, 39 degrees C fever and heavy diaphoresis. She had a record of seven malaria cases. She looked thin and pale at the initial physical examination. During the evolution, she developed pancytopenia, massive hepatosplenomegaly, jaundice, and anasarca. The patient underwent screening tests for infection, neoplasias, collagenosis, and granulomatous diseases. The laboratory tests showed transaminase-alkaline phosphatase dissociation, which led to the final diagnosis of tuberculosis, through the histological examination of the liver parenchyma. The specific treatment against tuberculosis caused remission of fever, ascites, and hepatomegaly and normalization of liver tests, with satisfactory clinical evolution.

We present the clinical case of a patient with vascular compression of the duodenum or superior mesenteric artery compression syndrome.A female, 42 years old, with history of two months' evolution characterized by postprandial epigastric colic, without irradiation, accompanied by nausea and intractable vomiting, weight loss and gastric shaking. A double contrast gastric duodenum x-ray showed the duodenal frame with exaggerated dilatation and stenosis close to the Treitz angle, through which the contrast media barely flowed. The endoscopy revealed duodenal obstruction, gastric retention and erosive esophagitis. The computerized tomography identified a significant dilatation of the duodenal arc, with stenosis on the aorto-mesenteric junction. We performed an exploratory laparotomy, making a latero-lateral duodenojejunal trans-mesocolic anastomosis. Satisfactory evolution and discharge without complications.

Human fasciolasis is an infection caused by the liver fluke Fasciola hepatica that predominantly affects cattle and sheep, man being an accidental host. The epidemiological situation has changed in the last few years, reporting an increase in the number of new cases in different countries around the world. In the majority of cases, diagnosis of infection in the acute or invasive phase or in chronic or state phase, is difficult because the symptoms of both phases overlap or due to the lack of symptoms or the intermittent elimination of eggs by the adult worm. Determining the phase will depend on clinical suspicion and on the selection of adequate serological and coprological methods in the acute or chronic stages, respectively, as well as determining whether the patient comes from an endemic area. In this study, we reported six cases of patients that were hospitalized at the Arzobispo Loayza Hospital in Lima, Peru, from 1990 to 1999, whose diagnoses were different from the final ones and which evidenced diagnosing problems. The important correlation between the place of origin, the physical and laboratory findings to diagnose this parasitic disease were emphasized.