Miracle-dz/UniFAR-FTUs huggingface dataset:
Analysis of Suicide Notes: An experience in Eskişehir City.

INTRODUCTION It is estimated that a million people around the world die by suicide each year. It has been reported that a note was left in 5%-43% of the suicides. In this study, it we aimed to evaluate and discuss suicide notes in our city which is situated in Western Anatolia and where several universities are located. METHOD All forensic deaths in Eskişehir in 10-year period between 2001 and 2011 were evaluated. Forensic investigation files were assessed. After investigation, Out of 399 cases, 168 (42.1%) cases, who were determined to have left a suicide letter, telephone message (sms) or message via social network sites, were included in the scope of the study. RESULTS It was found that 95 (56.5%) of all cases had left a suicide letter, 69 (41.1%) cases had sent a telephone message to a person or more than one person, 4 (2.4%) cases had written notes about suicide and death in social networking sites. CONCLUSION A suicide note is an important finding in suicide cases to clarify the case. However, the note should be confirmed by investigation to be accepted as evidence.
Defective protective capacity of W/Wv mice against Strongyloides vatti infection and its reconstitution with bone marrow cells

Summary The susceptibility of congenitally anemic, and mast cell deficient W/Wv mice to infection with Strongyloides ratti was examined. After a primary infection, W/Wv mice showed greater and more persistent peak larval counts than did normal littermates. Worm expulsion was also slower in W/Wv mice than in +/+ mice. Furthermore, difference in susceptibility was expressed as early as 24 h after infection, suggesting not only that protective mechanisms of the gut but also of the connective tissue were defective in W/Wv mice. Reconstitution with bone marrow or spleen cells from +/+ mice was effective in restoring the protective response in W/Wv mice, whereas thymocytes or mesenteric lymph nodes had no effect. Both connective tissue and mucosal mast cells were repaired in W/Wv mice after marrow reconstitution and infection. Since relatively long incubation period was required for the expression of such reconstituting activities, bone marrow cells seem to contain precursor cells of the effector and/or regulator cells.
Climate Variability and the Occurrence of Human Puumala Hantavirus Infections in Europe: A Systematic Review

Hantaviruses are distributed worldwide and are transmitted by rodents. In Europe, the infection usually manifests as a mild form of haemorrhagic fever with renal syndrome (HFRS) known as nephropathia epidemica (NE), which is triggered by the virus species Puumala. Its host is the bank vole (Myodes glareolus). In the context of climate change, interest in the role of climatic factors for the disease has increased. A systematic review was conducted to investigate the association between climate variability and the occurrence of human Puumala hantavirus infections in Europe. We performed a literature search in the databases MEDLINE, EMBASE and Web of Science. Studies that investigated Puumala virus infection and climatic factors in any European country with a minimum collection period of 2 years were included. The selection of abstracts and the evaluation of included studies were performed by two independent reviewers. A total of 434 titles were identified in the databases, of which nine studies fulfilled the inclusion criteria. The majority of studies were conducted in central Europe (Belgium, France and Germany), while only two came from the north (Sweden) and one from the south (Bosnia). Strong evidence was found for a positive association between temperature and NE incidence in central Europe, while the evidence for northern Europe so far appears insufficient. Results regarding precipitation were contradictory. Overall, the complex relationships between climate and hantavirus infections need further exploration to identify specific health risks and initiate appropriate intervention measures in the context of climate change.
Fine mapping of the keratoconus with cataract locus on chromosome 15q and candidate gene analysis.

PURPOSE To report the fine mapping of the keratoconus with cataract locus on chromosome 15q and the mutational analysis of positional candidate genes. METHODS Genotyping of two novel microsatellite markers and a single nucleotide polymorphism (SNP) in the critical region of linkage for keratoconus with cataract on 15q was performed. Positional candidate genes (MORF4L1, KIAA1055, ETFA, AWP1, REC14, KIAA1199, RCN2, FAH, IDH3A, MTHFS, ADAMTS7, MAN2C1, PTPN9, KIAA1024, ARNT2, BCL2A1, ISL2, C15ORF22 (P24B), DNAJA4, FLJ14594, CIB2 (KIP2), C15ORF5, and PSMA4) prioritized on the basis of ocular expression and probable function were screened by PCR-based DNA sequencing methods. RESULTS We report the refinement of the linkage region for keratoconus with cataract to an interval of approximately 5.5 Mb flanked by the MAN2C1 gene and the D15S211 marker on chromosome 15q. Mutational analysis of positional candidate genes detected many sequence variations and single nucleotide polymorphisms. None of the sequence variants were considered pathogenic as they were also found in unaffected family members and normal control DNA samples. CONCLUSIONS Fine mapping of the keratoconus with cataract locus on 15q has reduced the linked region to 5.5 Mb, thereby excluding 28 candidate genes. A further 23 candidate genes were excluded by direct sequencing methods, although a pathogenic genomic rearrangement or exonic deletion would not have been detected.
Human fetal neocortical tissue grafted to rat brain cavities survives, leads to reciprocal nerve fiber growth, and accumulates host IgG

The human‐to‐rat xenograft approach offers possibilities to study aspects of primate cortex development and function without monkeys. Human fetal cortical tissue was grafted to prepared cortical cavities of immunosuppressed host rats. Fetal tissue fragments were collected after routine low‐pressure vacuum aspiration abortions performed in the first trimester of gestation. Human derived neurons and human nerve fiber outgrowth were visualized by immunohistochemistry with antibodies against human neurofilament protein 70 kD (hNFP70). Ingrowth from rat host striatum or cortex into the grafts was analyzed by immunohistochemistry with antibodies against tyrosine hydroxylase. Astrocytes were evaluated by immunohistochemistry with antibodies against glial fibrillary acidic protein. The grafts grew into different sizes (1–10 mm in diameter) and contained large numbers of hNFP70‐positive nerve fibers. All grafts gave rise to outgrowth of hNFP70‐positive fibers into the host with partly a cortical layering; layers III and IV received a majority of the human fibers. In several cases, the graft‐derived nerve fibers entered the host brain at restricted areas, while there was no crossing over of nerve fibers at the rest of the graft‐host interface. Tyrosine hydroxylase‐positive fibers were usually not abundant in the grafts. Interestingly, cases of massive ingrowth occurred from host striatum into the graft in a pattern suggesting “permissive sites” at the graft‐host interface in the same way as outgrowth from graft to host was found. Additionally, tyrosine hydroxylase‐immunoreactive fibers from host cortex were found to grow into the transplant. Glial fibrillary acidic protein immunoreactivity was increased at the interfaces between graft and host cortex or host striatum. Immunohistochemistry using antibodies against rat IgG indicated the presence of rat IgG within the grafts, and in bordering areas of host brain, possibly indicating a defective graft‐host barrier. Taken together, these results show that human cortical‐tissue pieces grafted to cortical cavities of immunosuppressed rats survive grafting and develop, and that reciprocal nerve fiber growth between grafts and hosts occur. Human cortical neurons can grow into the rat host brain in a pattern which is partly determined by host cortical architecture. © Wiley‐Liss, Inc.
Modulating the immune response to genetic immunization

Genetic immunization, also known as DNA or polynucleotide immunization, is a novel strategy for vaccine development in which plasmid DNA encoding either individual or a collection of antigens is directly administered to a host. Such immunization leads to host expression of the delivered foreign gene, resulting in the induction of a specific immune response against the in vivo produced antigen. DNA immunization has been shown to induce protective immune responses in several infectious disease and cancer experimental model systems. Furthermore, DNA vaccines have recently entered the clinic for analysis as both prophylactic and therapeutic agents. Although the mechanisms of immunity to DNA have not yet been fully elucidated, it has become apparent that the immune response achieved by DNA vaccination is quite malleable, and can be manipulated by altering the conditions under which the vaccine is administered. Either through changing the method or location of immunization, altering the number of immunostimulatory sequences in the plasmid, altering the immunization regimen, or coadministering genes for cytokines or costimulatory molecules, one can modulate both the magnitude and orientation of the subsequent immune response. Through maximization of this feature of DNA immunization, we will likely be able to design vaccines and immunotherapeutic agents that are tailored to the correlates of protection for a particular disease, resulting in a new generation of more focused and effective immune stimulating agents. —Cohen, A. D. , Boyer, J. D. , Weiner, D. B. Modulating the immune response to genetic immunization. FASEB J. 12, 1611–1626 (1998)
Restoration of the insulinotropic effect of glucose‐dependent insulinotropic polypeptide contributes to the antidiabetic effect of dipeptidyl peptidase‐4 inhibitors

To examine whether 12 weeks of treatment with a dipeptidyl peptidase‐4 (DPP‐4) inhibitor, sitagliptin, influences the insulin secretion induced by glucose, glucose‐dependent insulinotropic polypeptide (GIP) and glucagon‐like peptide‐1 (GLP‐1) during a hyperglycaemic clamp in patients with type 2 diabetes (T2DM).
Properties of single potassium channels in guinea pig hepatocytes

The patch‐clamp technique of cell‐attached and inside‐out configurations was used to study the single potassium channels in isolated guinea pig hepatocytes. The single potassium channels in isolated guinea pig hepatocytes were recorded at different K+ concentrations. A linear single‐channel current‐voltage relationship was obtained at the voltage range of ‐80 to ‐20 mV with slope conductance of 70 ± 6 pS (n = 10). Under symmetrical high K+ concentration of 148 mM in the cell‐attached patch membrane, the I‐V curve exhibited a mild inward rectification at potentials positive to +20 mV. The values of reversal potential was +5 ± 2 mV (n = 10). When the external potassium concentration ([K+]0) was decreased to 74 mM and 20 mM, the slope conductance was decreased to 48 ± 2 pS (n = 4) and 24 ± 3 pS (n = 3), respectively. The reversal potential was changed by 58 mV for a tenfold change in [K+]0, indicating that this channel was highly selective for K+. Open probabilities (P0) of the channel were 73‐93% without apparent voltage dependence. The distributions of open time of the channels were fitted to two exponentials, while those of closed time were fitted to three exponentials, exhibiting no voltage dependence. The success rate of K+ channel activity to be recorded was 28% at room temperature, and there were no increases in the success rate nor in the channel opening probabilities at a temperature of 34‐36°C. P0 in inside‐out patches was not changed by application of 1 μM Ca2+ nor 1 mM Mg2+ to the internal side of patch membranes. It is concluded that a novel type of the K+ channels in guinea pig hepatocytes had different properties of slope conductance, channel kinetics, and sensitivity to [Ca2+]i, from those in other species. © 1994 Wiley‐Liss, Inc.
Changes in coping style following traumatic brain injury and their relationship to productivity status.

The use of maladaptive coping strategies following traumatic brain injury (TBI) is known to be associated with increased depression and a lower productivity status. What is not known is whether coping behaviours change following TBI and if they do change whether these changes account for significant variance in outcome. Seventy-three significant others of TBI survivors were recruited at the time their friend/family member was injured and followed prospectively. They reported on their friend/family member's pre-injury and 6-month coping behaviours using the Coping with Health Injuries and Problems Scale. The use of emotional pre-occupation coping (p = .02) increased significantly and approached significance for distraction coping(p = .08). These changes in coping also accounted for significant variance (22%, p = .02) in productivity status over and above that accounted for by demographics and injury severity. Whether maladaptive coping changes can be prevented with a view to improving outcomes is a question that now needs to be explored.
‘Let's twist again’: surgically induced renewal of left ventricular torsion in ischemic cardiomyopathy

Objectives To test the potential of the heart to be surgically restored at a near-normal global condition, granted that its physiological characteristics are respected (working volumes, chamber geometry, fiber orientation, opposite rotation of apex and base, global torsion and strain). Methods From May 2007 to December 2008, 12 consecutive patients with ischemic cardiomyopathy were included in this study. All patients underwent modified surgical anterior ventricular restoration combined with complete coronary revascularization and, when indicated, mitral anuloplasty. The modified restoration aims to re-approach residual myocardium, redirecting fiber orientation displaced by infarct scar toward a more physiological gross disposition. Patients were studied preoperatively and postoperatively with a complete echocardiographical assessment, including speckle-tracking analysis. Results Standard parameters significantly improved after the operation (end diastolic volume, P < 0.001; end systolic volume, P < 0.001; ejection fraction, P = 0.004), and so did peak systolic apical rotation, peak systolic left ventricular torsion and two-chamber and four-chamber longitudinal strain (P = 0.004, 0.003, 0.05 and 0.01, respectively). Pearson's correlation between apical rotation and longitudinal strain (two-chamber and four-chamber) was −0.877 (P < 0.001) and −0.720 (P = 0.008), respectively, and between torsion and longitudinal strain was −0.845 (P = 0.001) and −0.785 (P = 0.002), respectively. Conclusion This study reveals an unexpected potential of the myocardium to be restored at a near-normal global condition, with regard to all of its physiological characteristics. The concept of fiber-based surgical treatment, supported by an imaging-guided preoperative study, could widen the potential of repairing a failing heart.
The Significance of Serum Urea and Renal Function in Patients With Heart Failure

Renal function and urea are frequently abnormal in patients with heart failure (HF) and are predictive of increased mortality. The relative importance of each parameter is less clear. We prospectively compared the predictive value of renal function and serum urea on clinical outcome in patients with HF. Patients hospitalized with definite clinical diagnosis of HF (n = 355) were followed for short-term (1 yr) and long-term (mean, 6.5 yr) survival and HF rehospitalization. Increasing tertiles of discharge estimated glomerular filtration rate (eGFR) were an independent predictor of increased long-term survival (hazard ratio [HR], 0.65; 95% confidence interval [CI], 0.47-0.91; p = 0.01) but not short-term survival. Admission and discharge serum urea and blood urea nitrogen (BUN)/creatinine ratio were predictors of reduced short- and long-term survival on multivariate Cox regression analysis. Increasing tertiles of discharge urea were a predictor of reduced 1-year survival (HR, 2.13; 95% CI, 1.21-3.73; p = 0.009) and long-term survival (HR, 1.93; 95% CI, 1.37-2.71; p < 0.0001). Multivariate analysis including discharge eGFR and serum urea demonstrated that only serum urea remained a significant predictor of long-term survival; however, eGFR and BUN/creatinine ratio were both independently predictive of survival. Urea was more discriminative than eGFR in predicting long-term survival by area under the receiver operating characteristic curve (0.803 vs. 0.787; p = 0.01). Increasing tertiles of discharge serum urea and BUN/creatinine were independent predictors of HF rehospitalization and combined death and HF rehospitalization. This study suggests that serum urea is a more powerful predictor of survival than eGFR in patients with HF. This may be due to urea's relation to key biological parameters including renal, hemodynamic, and neurohormonal parameters pertaining to the overall clinical status of the patient with chronic HF. Abbreviations: ADHF = acute decompensated heart failure, AUC = area under the curve, BUN = blood urea nitrogen, CI = confidence interval, eGFR = estimated glomerular filtration rate, HF = heart failure, HR = hazard ratio, MDRD = Modification of Diet in Renal Disease, ROC = receiver operating characteristic.
The RAS Effector RIN1 Directly Competes with RAF and Is Regulated by 14-3-3 Proteins

ABSTRACT Activation of RAS proteins can lead to multiple outcomes by virtue of regulated signal traffic through alternate effector pathways. We demonstrate that the RAS effector protein RIN1 binds to activated RAS with an affinity (K d , 22 nM) similar to that observed for RAF1. At concentrations close to their equilibrium dissociation constant values, RIN1 and RAF1 compete directly for RAS binding. RIN1 was also observed to inhibit cellular transformation by activated mutant RAS. This distinguishes RIN1 from other RAS effectors, which are transformation enhancing. Blockade of transformation was mediated by the RAS binding domain but required membrane localization. RIN1 recognizes endogenous RAS following transient activation by epidermal growth factor, and a portion of RIN1 fractionates to the cell membrane in a manner consistent with a reversible interaction. RIN1 also binds to 14-3-3 proteins through a sequence including serine 351. Mutation of this residue abolished the 14-3-3 binding capacity of RIN1 and led to more efficient blockade of RAS-mediated transformation. The mutant protein, RIN1S351A, showed a shift in localization to the plasma membrane. Serine 351 is a substrate for protein kinase D (PKD [also known as PKCμ]) in vitro and in vivo. These data suggest that the normal localization and function of RIN1, as well as its ability to compete with RAF, are regulated in part by 14-3-3 binding, which in turn is controlled by PKD phosphorylation.
The Sphingolipid Long-chain Base-Pkh1/2-Ypk1/2 Signaling Pathway Regulates Eisosome Assembly and Turnover*

Eisosomes are recently described fungal structures that play roles in the organization of the plasma membrane and endocytosis. Their major protein components are Pil1 and Lsp1, and previous studies showed that these proteins are phosphorylated by the sphingolipid long-chain base-activated Pkh1 and Pkh2 protein kinases in vitro. We show that Pkh1 and Pkh2 phosphorylate Pil1 and Lsp1 in vivo to produce species B, and that heat stress, which activates Pkh1 and Pkh2, generates a more highly phosphorylated species, C. Cells with low Pkh activity lack species B and C and contain abnormally organized eisosomes. To verify that Pil1 phosphorylation is essential for correct eisosome organization, phosphorylated serine and threonine residues were identified and changed to alanines. A variant Pil1 protein lacking five phosphorylation sites did not form eisosomes during log phase growth, indicating that phosphorylation is critical for eisosome organization. We also found that eisosomes are dynamic structures and disassemble when the Ypk protein kinases, which are activated by the sphingolipid-Pkh signaling pathway, are inactivated or when the sphingolipid signal is pharmacologically blocked with myriocin. We conclude that eisosome formation and turnover are regulated by the sphingolipid-Pkh1/2-Ypk1/2 signaling pathway. These data and previous data showing that endocytosis is regulated by the sphingolipid-Pkh1/2-Ypk1/2 signaling pathway suggest that Pkh1 and -2 respond to changes in membrane sphingolipids and transmit this information to eisosomes via Pil1 phosphorylation. Eisosomes then control endocytosis to align the composition and function of the plasma membrane to match demand.
Place of Death for People with Noncancer and Cancer Illness in South Australia: A Population-Based Survey

A large representative population survey of 9,500 households reports the association between place of death, diagnosis (cancer vs. noncancer), and use of palliative care services of terminally ill South Australians. Thirty-one percent (1,920) indicated that someone close to them had died of a terminal illness in the preceding five years; 18% had died of noncancer illness and 82% of cancer. Sixty-two percent of deceased individuals accessed palliative care services. More patients with cancer than noncancer had had palliative care (65% vs. 48%; p<0.0001). Compared with cancer patients, those with noncancer illness had died in hospices less frequently (9% vs. 15%; p=0.0015) and in nursing homes more frequently (15% vs. 5%; p<0.0001). Similar proportions had died in hospital (60%) and at home (16%–20%). Palliative care service involvement did not reduce institutional deaths, but shifted them from hospital to hospice.
A novel toluene-3-monooxygenase pathway cloned from Pseudomonas pickettii PKO1

Plasmid pRO1957, which contains a 26.5-kb fragment from the chromosome of Pseudomonas pickettii PKO1, allows P. aeruginosa PAO1 to grow on toluene or benzene as a sole carbon and energy source. A subclone of pRO1957, designated pRO1966, when present in P. aeruginosa PAO1 grown in lactate-toluene medium, accumulates m-cresol in the medium, indicating that m-cresol is an intermediate of toluene catabolism. Moreover, incubation of such cells in the presence of 18O2 followed by gas chromatography-mass spectrometry analysis of m-cresol extracts showed that the oxygen in m-cresol was derived from molecular oxygen. Accordingly, this suggests that toluene-3-monooxygenation is the first step in the degradative pathway. Toluene-3-monooxygenase activity is positively regulated from a locus designated tbuT. Induction of the toluene-3-monooxygenase is mediated by either toluene, benzene, ethylbenzene, or m-cresol. Moreover, toluene-3-monooxygenase activity induced by these effectors also metabolizes benzene and ethylbenzene to phenol and 3-ethylphenol, respectively, and also after induction, o-xylene, m-xylene, and p-xylene are metabolized to 3,4-dimethylphenol, 2,4-dimethylphenol, and 2,5-dimethylphenol, respectively, although the xylene substrates are not effectors. Styrene and phenylacetylene are transformed into more polar products.