Miracle-dz/UniFAR-FTUs huggingface dataset:
Physician-Assisted Suicide and Other Forms of Euthanasia in Islamic Spiritual Care

The muteness in the Qur’an about suicide due to intolerable pain and a firm opposition to suicide in the hadith literature formed a strong opinion among Muslims that neither repentance nor the suffering of the person can remove the sin of suicide or mercy ‘killing’ (al-qatl al-rahim), even if these acts are committed with the purpose of relieving suffering and pain. Some interpretations of the Islamic sources even give advantage to murderers as opposed to people who commit suicide because the murderers, at least, may have opportunity to repent for their sin. However, people who commit suicide are ‘labeled’ for losing faith in the afterlife without a chance to repent for their act. This paper claims that Islamic spiritual care can help people make decisions that may impact patients, family members, health care givers and the whole community by responding to questions such as ‘What is the Islamic view on death? ’, ‘What is the Islamic response to physician-assisted suicide and other forms of euthanasia? ’, ‘What are the religious and moral underpinnings of these responses in Islam? ’
Malignancy arising in cystic ovarian teratomas.

Summary. Twenty‐four cases with a malignant change involving one of the elements of an ovarian dermoid cyst are reported. The patients were older than those with benign ovarian dermoid cysts. Squamous carcinoma was most frequent with adenocarcinoma, undifferentiated carcinoma and a fibrosarcoma also occurring. Survival time after diagnosis was less than 1 year in 75% of the cases.
Campylobacter jejuni-Induced Activation of Dendritic Cells Involves Cooperative Signaling through Toll-Like Receptor 4 (TLR4)-MyD88 and TLR4-TRIF Axes

ABSTRACT Campylobacter jejuni is an important cause of human enteritis and has been linked to the development of autoimmune diseases. Recently we showed that infection of murine dendritic cells (DCs) with C. jejuni resulted in DC activation and induction of Campylobacter-specific Th1-effector responses. Toll-like receptor (TLR) signaling through myeloid differentiation factor 88 (MyD88) and/or Toll-interleukin 1 (IL-1) receptor domain-containing adaptor-inducing beta interferon (IFN-β) (TRIF) is critical in inducing immunity against pathogens. In this study, we investigated the role of TLR2, TLR4, MyD88, and TRIF signaling in C. jejuni-induced inflammatory activation of DCs. DC upregulation of major histocompatibility complex class II and costimulatory molecules after C. jejuni challenge was profoundly impaired by TLR2, TLR4, MyD88, and TRIF deficiencies. Similarly, C. jejuni-induced secretion of IL-12, IL-6, and tumor necrosis factor alpha was significantly inhibited in TLR2−/−, TLR4−/−, MyD88−/−, and TRIF−/− DCs compared to that in wild-type DCs; however, the magnitude of inhibition was greater in MyD88−/−, TRIF−/−, and TLR4−/− DCs than in TLR2−/− DCs. Furthermore, C. jejuni induced interferon regulatory factor 3 phosphorylation and IFN-β secretion by DCs in a TLR4-TRIF-dependent fashion, further demonstrating activation of this pathway by C. jejuni. Importantly, TLR2, TLR4, MyD88, and TRIF deficiencies all markedly impaired the Th1-priming ability of C. jejuni-infected DCs. Thus, our results show that cooperative signaling through the TLR4-MyD88 and TLR4-TRIF axes represents a novel mechanism mediating C. jejuni-induced inflammatory responses of DCs. To our knowledge, such a mechanism has not been demonstrated previously for an intact bacterium.
Site-Dependent Recruitment of Inflammatory Cells Determines the Effective Dose of Leishmania major

ABSTRACT The route of pathogen inoculation by needle has been shown to influence the outcome of infection. Employing needle inoculation of the obligately intracellular parasite Leishmania major, which is transmitted in nature following intradermal (i.d.) deposition of parasites by the bite of an infected sand fly, we identified differences in the preexisting and acute cellular responses in mice following i.d. inoculation of the ear, subcutaneous (s.c.) inoculation of the footpad, or inoculation of the peritoneal cavity (intraperitoneal [i.p.] inoculation). Initiation of infection at different sites was associated with different phagocytic populations. Neutrophils were the dominant infected cells following i.d. , but not s.c. or i.p., inoculation. Inoculation of the ear dermis resulted in higher frequencies of total and infected neutrophils than inoculation of the footpad, and these higher frequencies were associated with a 10-fold increase in early parasite loads. Following inoculation of the ear in the absence of neutrophils, parasite phagocytosis by other cell types did not increase, and fewer parasites were able to establish infection. The frequency of infected neutrophils within the total infected CD11b+ population was higher than the frequency of total neutrophils within the total CD11b+ population, demonstrating that neutrophils are overrepresented as a proportion of infected cells. Employing i.d. inoculation to model sand fly transmission of parasites has significant consequences for infection outcome relative to that of s.c. or i.p. inoculation, including the phenotype of infected cells and the number of parasites that establish infection. Vector-borne infections initiated in the dermis likely involve adaptations to this unique microenvironment. Bypassing or altering this initial step has significant consequences for infection.
Novel Pneumocystis Antigen Discovery Using Fungal Surface Proteomics

ABSTRACT Pneumonia due to the fungus Pneumocystis jirovecii is a life-threatening infection that occurs in immunocompromised patients. The inability to culture the organism as well as the lack of an annotated genome has hindered antigen discovery that could be useful in developing novel vaccine- or antibody-based therapies as well as diagnostics for this infection. Here we report a novel method of surface proteomics analysis of Pneumocystis murina that reliably detected putative surface proteins that are conserved in Pneumocystis jirovecii. This technique identified novel CD4+ T-cell epitopes as well as a novel B-cell epitope, Meu10, which encodes a glycosylphosphatidylinositol (GPI)-anchored protein thought to be involved in ascospore assembly. The described technique should facilitate the discovery of novel target proteins for diagnostics and therapeutics for Pneumocystis infection.
Role of the Aryl Hydrocarbon Receptor in the Immune Response Profile and Development of Pathology during Plasmodium berghei Anka Infection

ABSTRACT Infection with Plasmodium falciparum may result in severe disease affecting various organs, including liver, spleen, and brain, resulting in high morbidity and mortality. Plasmodium berghei Anka infection of mice recapitulates many features of severe human malaria. The aryl hydrocarbon receptor (AhR) is an intracellular receptor activated by ligands important in the modulation of the inflammatory response. We found that AhR-knockout (KO) mice infected with P. berghei Anka displayed increased parasitemia, earlier mortality, enhanced leukocyte-endothelial cell interactions in the brain microvasculature, and increased inflammation in brain (interleukin-17 [IL-17] and IL-6) and liver (gamma interferon [IFN-γ] and tumor necrosis factor alpha [TNF-α]) compared to infected wild-type (WT) mice. Infected AhR-KO mice also displayed a reduction in cytokines required for host resistance, including TNF-α, IL-1β, and IFN-γ, in the brain and spleen. Infection of AhR-KO mice resulted in an increase in T regulatory cells and transforming growth factor β, IL-6, and IL-17 in the brain. AhR modulated the basal expression of SOCS3 in spleen and brain, and P. berghei Anka infection resulted in enhanced expression of SOCS3 in brain, which was absent in infected AhR-KO mice. These data suggest that AhR-mediated control of SOCS3 expression is probably involved in the phenotype seen in infected AhR-KO mice. This is, to our knowledge, the first demonstration of a role for AhR in the pathogenesis of malaria.
Bronquiolite obliterante pós-infecciosa: aspectos clínicos e exames complementares de 48 crianças

BACKGROUND: The clinical evaluation of patients with postinfectious bronchiolitis obliterans (BO) is variable. OBJECTIVE: Substantiate the clinical characteristics, the evolution and the complementary tests of 48 patients with post infectious bronchiolitis obliterans (BO). METHOD: Observational and retrospective study. Diagnosis of BO was based upon clinical criteria, CT scan findings and exclusion of other diseases. History prior to diagnosis and complementary tests were evaluated as well as initial and final values of oxygen saturation. RESULTS: Mean age of patients at the acute stage of the infectious disease was of 9.6 Thirty two of the patients were male. All were hospitalized during the acute stage, 14 of them (29%) in the ICU. Four patients died two years after onset of acute bronchiolitis. During evolution all required emergency care due to exacerbation of the pulmonary condition and 24 (50%) were hospitalized, 2 of them in the ICU. The majority continued presenting cough, wheezing, crackles and hyperinflation, however to a lesser degree. Mean of initial arterial saturation was of 89% and final of 92%. The most common infectious agents in the sputum samples were H. influenzae, S. pneumoniae and M. caterrhalis. Increased serum IgM and IgG were found in 9 and 7 patients respectively. The most frequent findings at thorax CT scan were mosaic perfusion, bronchioectasis, atelectasis and bronchial wall thickening. CONCLUSION: Post infectious BO is a chronic and severe disease with persistent symptoms that in general affect infants. Positive serum cultures and increased serum immunoglobulins are suggestive of a chronic infectious inflammatory condition.
WeiSTARS: A weighted trust-aware relay selection scheme for VANET

Considered as a primordial component of Cooperative Intelligent Transportation Systems (C-ITS), Vehicular Ad Hoc Network (VANET) plays a weighty role to facilitate different on-road applications, most of which primary rely on multi hop communications. To ensure reliability and security of such communication, it is very pertinent to guarantee that the most proper and trustworthy vehicles are selected as relays. This paper takes up this challenge by introducing a weighted probabilistic and trust-aware strategy called WeiSTARS, to ensure high delivery ratios within reduced delays. Simulation results conducted using NS2 tool depicted that our technique enhances the delivery ratio by more than 8% with around 30% less delay compared to both GytAR and GPSR routing protocols even in the presence of high ratios of dishonest vehicles.
INTERLEUKIN‐1β AND INTERFERON‐γ REGULATE INTERLEUKIN‐6 PRODUCTION IN CULTURED HUMAN INTESTINAL EPITHELIAL CELLS

Recent studies suggest that interleukin-6 (IL-6) is produced in the intestinal mucosa during sepsis and endotoxemia and that the enterocyte may be a source of IL-6 in these conditions. The regulation of IL-6 production in the enterocyte is not fully understood. We tested the hypothesis that IL-6 production in the enterocyte is regulated by proinflammatory cytokines. This was done by treating cultured Caco-2 cells, a transformed human intestinal epithelial cell line, with different concentrations of tumor necrosis factor-α (TNF-α), IL-1α, IL-6 or interferon-(IFN-α). IL-6 production by the Caco-2 cells was determined by ELISA. The expression of IL-6 mRNA was determined by reverse-transchptase polymerase chain reaction. IL-6 was not produced in unstimulated Caco-2 cells. Treatment of the Caco-2 cells with IL-1α resulted in a dose- and time-dependent stimulation of IL-6 production with a maximal effect noted at an IL-1α concentration of . 5 ng/mL at 24 h. IFN-α alone did not stimulate IL-6 production but potentiated the effect of IL-1α in a synergistic fashion. Treatment of the Caco-2 cells with IL-1α induced expression of IL-6 mRNA with a response noticed after 30 min. TNF-α and IL-6 did not influence the production of IL-6 in the Caco-2 cells. The results suggest that enterocyte IL-6 production is stimulated by IL-1α and that this effect is potentiated by IFN-α. The regulation of IL-6 production in the enterocyte may be specific for IL-1α, since neither TNF nor IL-6 stimulated IL-6 production.
Requirement for Serratia marcescens Cytolysin in a Murine Model of Hemorrhagic Pneumonia

ABSTRACT Serratia marcescens, a member of the carbapenem-resistant Enterobacteriaceae, is an important emerging pathogen that causes a wide variety of nosocomial infections, spreads rapidly within hospitals, and has a systemic mortality rate of ≤41%. Despite multiple clinical descriptions of S. marcescens nosocomial pneumonia, little is known regarding the mechanisms of bacterial pathogenesis and the host immune response. To address this gap, we developed an oropharyngeal aspiration model of lethal and sublethal S. marcescens pneumonia in BALB/c mice and extensively characterized the latter. Lethal challenge (>4.0 × 106 CFU) was characterized by fulminate hemorrhagic pneumonia with rapid loss of lung function and death. Mice challenged with a sublethal dose (<2.0 × 106 CFU) rapidly lost weight, had diminished lung compliance, experienced lung hemorrhage, and responded to the infection with extensive neutrophil infiltration and histopathological changes in tissue architecture. Neutrophil extracellular trap formation and the expression of inflammatory cytokines occurred early after infection. Mice depleted of neutrophils were exquisitely susceptible to an otherwise nonlethal inoculum, thereby demonstrating the requirement for neutrophils in host protection. Mutation of the genes encoding the cytolysin ShlA and its transporter ShlB resulted in attenuated S. marcescens strains that failed to cause profound weight loss, extended illness, hemorrhage, and prolonged lung pathology in mice. This study describes a model of S. marcescens pneumonia that mimics known clinical features of human illness, identifies neutrophils and the toxin ShlA as a key factors important for defense and infection, respectively, and provides a solid foundation for future studies of novel therapeutics for this important opportunistic pathogen.
OBSTETRIC PARALYSIS: ITS ETIOLOGY, PATHOLOGY, CLINICAL ASPECTS AND TREATMENT, WITH A REPORT OF FOUR HUNDRED AND SEVENTY CASES

Obstetric paralysis, a paralysis produced during birth, is due to an injury to the nerves of the brachial plexus. The resultant paralysis is characteristic; the arm hangs vertically, the elbow extended, the forearm pronated and the whole arm inwardly rotated. The paralysis is usually flaccid. I shall endeavor in this paper, by a review of all the literature, to give the reader the various theories as to the causes of the paralysis, as well as to offer the conclusions I have reached by a study of 470 cases. Certain experimental work which I have done, with the idea of determining clearly the etiology and pathology, will be described and conclusions drawn therefrom. The pathologic and clinical aspects of the condition will be discussed and analyzed, and the treatment, operative and nonoperative, will be dealt with under appropriate headings. Definite conclusions will be drawn from the study of about 500 cases,
Cytadherence of Mycoplasma pneumoniae Induces Inflammatory Responses through Autophagy and Toll-Like Receptor 4

ABSTRACT Mycoplasma pneumoniae causes pneumonia, tracheobronchitis, pharyngitis, and asthma in humans. The pathogenesis of M. pneumoniae infection is attributed to excessive immune responses. We previously demonstrated that M. pneumoniae lipoproteins induced inflammatory responses through Toll-like receptor 2 (TLR2). In the present study, we demonstrated that M. pneumoniae induced strong inflammatory responses in macrophages derived from TLR2 knockout (KO) mice. Cytokine production in TLR2 KO macrophages was increased compared with that in the macrophages of wild-type (WT) mice. Heat-killed, antibiotic-treated, and overgrown M. pneumoniae failed to induce inflammatory responses in TLR2 KO macrophages. 3-Methyladenine and chloroquine, inhibitors of autophagy, decreased the induction of inflammatory responses in TLR2 KO macrophages. These inflammatory responses were also inhibited in macrophages treated with the TLR4 inhibitor VIPER and those obtained from TLR2 and TLR4 (TLR2/4) double-KO mice. Two mutants that lacked the ability to induce inflammatory responses in TLR2 KO macrophages were obtained by transposon mutagenesis. The transposons were inserted in atpC encoding an ATP synthase F0F1 ε subunit and F10_orf750 encoding hypothetical protein MPN333. These mutants showed deficiencies in cytadherence. These results suggest that cytadherence of M. pneumoniae induces inflammatory responses through TLR4 and autophagy.
Hypertension is Common among HIV-Infected Persons, But Not Associated with HAART

Background: With improved survival after the introduction of highly active antiretroviral therapy (HAART), non-AIDS-related morbidity and mortality have come to the forefront in the management of HIV patients. HAART has been linked to the development of several risk factors for cardiovascular disease including insulin resistance and hyperlipidemia, but its influence on hypertension requires further study. Methods: We performed a cross-sectional study of HIV-infected persons at two large HIV clinics to evaluate the prevalence and factors associated with hypertension. Hypertension was defined by at least two blood pressure measurements >140/90 mmHg or the use of an antihypertensive medication. Statistical analyses included multivariate logistic regression models. Results: We studied 707 HIV-infected adults with a median age of 41 years (IQR 36-46), 92% were male, 49% were Caucasian, and 72% were receiving HAART. The overall prevalence of hypertension was 31% and was similar among those receiving and not receiving HAART (32% vs. 29%, p = 0.47). Factors associated with hypertension in the multivariate model included increasing age, longer duration of HIV, higher body mass index, and diabetes, with a trend for African American ethnicity. Conclusions: Hypertension is common among HIV-infected persons and is associated with established risk factors, but not with HAART use. Given the high prevalence of hypertension and its association with duration of HIV infection, other factors such as virally-mediated endothelial changes or immune activation may play a role. Further investigations are needed.
The Effect of Administrative Resources on Care in Nursing Homes

This article evaluates whether the hours spent on the job by nursing home administration have an effect on the quality of care. Administration with more hours on the job were expected to be actively involved in developing market strategies, implementing continuous, quality improvement, and in developing stricter facility guidelines for care—all of which contribute to improved care processes. The proportion of residents who were restrained, catheterized, had pressure ulcers, or were given psychoactive drugs and the number of health-related deficiencies and nonhealth-related deficiencies were used as measures of quality in 15,834 nursing facilities. We examined effects separately for facilities that belong to a chain and those that are freestanding. Overall, the results indicate that the quality indicators are associated with the number of full-time equivalent hours of administration in both chain and freestanding facilities. This study provides preliminary evidence that the intensity of facility administration can have an important effect on the quality of care residents receive.
Early Induction of Interleukin-10 Limits Antigen-Specific CD4+ T Cell Expansion, Function, and Secondary Recall Responses during Persistent Phagosomal Infection

ABSTRACT Diverse pathogens have evolved to survive and replicate in the endosomes or phagosomes of the host cells and establish persistent infection. Ehrlichiae are Gram-negative, intracellular bacteria that are transmitted by ticks. Ehrlichiae reside in the endosomes of the host phagocytic or endothelial cells and establish persistent infection in their vertebrate reservoir hosts. CD4+ T cells play a critical role in protection against phagosomal infections. In the present study, we investigated the expansion, maintenance, and functional status of antigen-specific CD4+ T cells during persistent Ehrlichia muris infection in wild-type and interleukin-10 (IL-10)-deficient mice. Our study indicated that early induction of IL-10 led to reduced inflammatory responses and impaired bacterial clearance during persistent Ehrlichia infection. Notably, we demonstrated that the functional production of gamma interferon (IFN-γ) by antigen-specific CD4+ T cells maintained during a persistent phagosomal infection progressively deteriorates. The functional loss of IFN-γ production by antigen-specific CD4+ T cells was reversed in the absence of IL-10. Furthermore, we demonstrated that transient blockade of IL-10 receptor during the T cell priming phase early in infection was sufficient to enhance the magnitude and the functional capacity of antigen-specific effector and memory CD4+ T cells, which translated into an enhanced recall response. Our findings provide new insights into the functional status of antigen-specific CD4+ T cells maintained during persistent phagosomal infection. The study supports the concept that a better understanding of the factors that influence the priming and differentiation of CD4+ T cells may provide a basis to induce a protective immune response against persistent infections.
Efeito dose-resposta de uma formulação de dentifrício com concentração reduzida de fluoreto: estudo in vitro

The utilization of dentifrices with low fluorine concentration, for children under 6 years of age, has been suggested to reduce the risks of dental fluorosis. However, in order to have anticariogenic potential, the dentifrice should form loosely-bound fluorine (CaF2) on dental enamel. Considering that the formation of CaF2 is a function inversely related to pH, dentifrices with pH 5.5, with 275, 550 and 1,100 ppm (NaF/silica) were developed in order to assess dose-response effects. A comparison between those dentifrices, a placebo product and the Crest toothpaste (positive control - standard) was carried out. Furthermore, the bioavailability of dentifrices, in terms of formation of total fluorine (TF), CaF2, and fluorapatite (FA) on human dental enamel, was evaluated. An ion-specific electrode was utilized for the determination of the dosage of fluorine. The results revealed that the dentifrice with 550 ppm was more effective than both the placebo and the dentifrice with 275 ppm, presenting no difference in relation to the positive control (p > 0.05). A dose-effect correlation was observed as to the CaF2 formed. In conclusion, the modified formulation with 550 ppm can be considered as effective as the standard dentifrice with 1,100 ppm, and its utilization would be safer with regard to dental fluorosis.