Miracle-dz/UniFAR-FTUs huggingface dataset:
Neonatal sepsis: a review with a study of 50 cases.

Neonatal spesis data is presented on 50 cases of this condition admitted to Mayo Hospital in the 2nd 1/2 of 1983. Escherichia coli and group B Streptococci together account for 50-70% of cases at most medical centers in the US. Of the 50 cases in Lahore India the bacterial pathogen was Escherichia coli in 12 cases (24%) leading to 100% mortality. Klebsiella was the pathogen in 6 cases (12%) leading to 50% mortality. Other causes cited such as Pseudomonas Salmonella and Citro Bacter all caused 100% mortality. Traditional birth attendants or others in the house may transmitt pathogens from their own or the mothers person to the newborn. Urinary tract infection coitus within 2 weeks before delivery delay after rupture of membranes premature delivery and absence of specific humoral antibody against pathogens in the mother are factors which increase the risk of infection of the amniotic fluid. In neonates the deficient supply of neutrophils decrease in bactericidal activities of leukocytes impairment of chemotaxis of neutrophils and monocytes and deficiency of complement (C3) in low birth weight infants all constitute a generally inadequate host defense mechanism. For diagnosis cultures of blood and cerebrospinal fluid (CSF) are carried out. Antimicrobial therapy for neonatal sepsis should be continued for 10-14 days or 5-7 days after symptoms have subsided. In meningitis the duration of therapy is 3 weeks. Mortality for neonatal sepsis is 10-40% and for meningitis 15-50%.
Intrasplenic pancreatic pseudocysts.

A 48-year-old man presented with severe left flank pain. He had been a known alcoholic for 20 years. On physical examination, he was afebrile and normotensive. Laboratory values were as follows: leukocytes, 14,700/mm (reference values: 3,900-9,800/mm); lactate dehydrogenase, 190 IU/L (reference values: 120-230 IU/L); amylase, 89 IU/L (reference values: 40-123 IU/L); and C-reactive protein, 7.9 mg/dL (reference values: 0-0.27 mg/dL). A contrast-enhanced CT scan (Image 1) demonstrated pseudocysts of the pancreatic tail extending into the splenic hilum (white arrow) and splenic parenchyma (black arrow). Intrasplenic pancreatic pseudocysts associated with chronic alcoholic pancreatitis were diagnosed. His symptoms and laboratory values improved with conservative treatment including the intravenous administration of antibiotics. Follow-up imaging studies showed that the pseudocyst extension was markedly reduced. The patient remains asymptomatic. As the pancreas and the spleen are located in close proximity, splenic complications may occur in the course of acute and chronic pancreatitis [1]. Although very rare (2%), splenic involvement of the pancreatitis includes splenic vascular injury, intrasplenic pseudocysts, abscess, hematoma, infarction, necrosis, and rupture [2, 3]. Among the above, intrasplenic pseudocysts are the most frequent. The most consistent symptom is abdominal pain in the upper left quadrant. Amylase levels may be normal in some cases [1]. These complications may be lifethreatening; therefore, patients should be closely monitored with imaging studies. Most cases can be managed conservatively; however, surgical interventions, such as splenectomy, distal pancreatectomy and percutaneous drainage, are indicated mainly as a result of clinical findings in order to avoid aggressive outcomes [3]. In conclusion, patients with the risk of chronic pancreatitis should be monitored for splenic complications.
Lipids, lipid domains and lipid-protein interactions in endocytic membrane traffic.

It has long been known that lipids are responsible for the structural integrity of biological membranes, and confer specific dynamic properties to the bilayer. However, they have often been considered as passive components of the membrane, beyond their well-known function as second messengers in signal transduction pathways. Evidence has been accumulating that lipids are sorted along the routes of membrane traffic, and that they are directly involved in the regulation of protein sorting and membrane flow. In this review, we will discuss recent studies on the organization and possible functions of lipids in the endocytic pathway.
Homocysteic Acid as a Putative Excitatory Amino Acid Neurotransmitter: I. Postsynaptic Characteristics at N‐Methyl‐D‐Aspartate‐Type Receptors on Striatal Cholinergic Interneurons

Abstract: The actions of the stereoisomers of homocysteic acid (HCA) were characterized at N‐methyl‐D‐aspartate (NMDA)‐type receptors which mediate excitatory amino acid‐evoked [3H]acetylcholine ([3H]ACh) release from striatal cholinergic interneurons. Like NMDA, l‐HCA and d‐HCA evoked the release of [3H]ACh formed from [3H]choline in striatal slices. The concentration‐response curve for l‐HCA was virtually superimposable on that for NMDA, yielding an equal EC50 value (56.1 μM) and maximal response. However, d‐HCA was weaker, with an EC50 value of 81.1 μM, and an apparently smaller maximal response. l‐HCA‐evoked [3H]ACh release was inhibited by the same categories of compounds which inhibit NMDA‐evoked [3H]ACh release: the divalent ion Mg2+ (IC50= 25.8 μM); competitive NMDA antagonists 2‐amino‐7‐phosphonoheptanoate (IC50= 51.2 μM) and 3‐(2‐carboxypiperazin‐4‐yi)propyl‐1 ‐phosphonic acid (IC50= 20.1 μM); and the dissociative anesthetics tile‐tamine (IC50= 0.59 μM) and MK‐801 (IC50= 0.087 μM). Like NMDA, l‐HCA produced a tachyphylaxis in this system. Tachyphylaxis to NMDA resulted in a decreased response to l‐HCA, and conversely, tachyphylaxis to l‐HCA resulted in a decreased response to NMDA. The results suggest that l‐HCA is an agonist at the NMDA‐type receptor and may represent an endogenous ligand for this excitatory amino acid receptor.
Morphological study of the rostral interstitial nucleus of the medial longitudinal fasciculus in the monkey, Macaca mulatta by Nissl, Golgi, and computer reconstruction and rotation methods

We have studied the morphology of silver‐impregnated neurons (rapid Golgi technique) in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), a center involved in the control of vertical and torsional saccadic eye movements. This morphological study of riMLF neurons in the rhesus monkey was undertaken to further our understanding of the functional circuitry of the oculomotor system. Our study employed Nissl, Golgi, and computer‐ assisted methods. The cytoarchitectonic boundaries of the riMLF and its relationships to neighboring structures were determined in both Nissl and Golgi preparations. Five (I–V) distinct morphological types of riMLF neurons were distinguished in the Golgi impregnations on the basis of soma size, dendritic size, numbers of primary dendrites, number of dendritic branch points, as well as form, number, and distribution of dendritic appendages. Type I neurons impregnated most frequently and had the most extensive and highly branched dendritic tree. Type II neurons displayed thick dendrites with complex dendritic appendages, but the dendritic tree was much more compact than that of type I cells. Type III and type V cells had fusiform somas and relatively unbranched dendritic trees but differed greatly in size as well as dendritic morphology. The type IV cell was the smallest neuron and had many characteristics of the local interneurons found in other thalamic, subthalamic, hypothalamic, and midbrain centers. The type V was the largest neuron, least frequently impregnated, and found only at rostral riMLF levels. Digitized reconstructions of each type of neuron were rotated by the computer, which revealed that the dendritic trees of types I, III, and V occupy a disk‐like compartment in the riMLF neuropil. In contrast, the trees of types II and IV occupy a roughly spherical compartment. We suggest that three of the cell types are well suited for specific purposes: type II cells for receiving, topographically organized inputs that contain spatial information, type I cells for short‐lead burst neuron output to the motor neurons or other premotor centers, and type IV cells for inhibitory inputs to type I cells. © 1994 Wiley‐Liss, Inc.
Self-organization of grafted polyelectrolyte layers via the coupling of chemical equilibrium and physical interactions

The competition between chemical equilibrium, for example protonation, and physical interactions determines the molecular organization and functionality of biological and synthetic systems. Charge regulation by displacement of acid-base equilibrium induced by changes in the local environment provides a feedback mechanism that controls the balance between electrostatic, van der Waals, steric interactions and molecular organization. Which strategies do responsive systems follow to globally optimize chemical equilibrium and physical interactions? We address this question by theoretically studying model layers of end-grafted polyacids. These layers spontaneously form self-assembled aggregates, presenting domains of controlled local pH and whose morphologies can be manipulated by the composition of the solution in contact with the film. Charge regulation stabilizes micellar domains over a wide range of pH by reducing the local charge in the aggregate at the cost of chemical free energy and gaining in hydrophobic interactions. This balance determines the boundaries between different aggregate morphologies. We show that a qualitatively new form of organization arises from the coupling between physical interactions and protonation equilibrium. This optimization strategy presents itself with polyelectrolytes coexisting in two different and well-defined protonation states. Our results underline the need of considering the coupling between chemical equilibrium and physical interactions due to their highly nonadditive behavior. The predictions provide guidelines for the creation of responsive polymer layers presenting self-organized patterns with functional properties and they give insights for the understanding of competing interactions in highly inhomogeneous and constrained environments such as those relevant in nanotechnology and those responsible for biological cells function.
Expression of galectins‐1, ‐3 and ‐4 varies with strain and type of experimental colitis in mice

Galectins are increasingly the focus of biomedical research. Although they are involved at different stages in inflammation, data on galectins in colitis remain scarce. The aim of this study was to determine and compare the expression of galectins in acute and chronic experimental colitis in mice. Immunohistochemistry for galectins‐1, ‐3 and ‐4 was performed on colon tissue from C57BL/6 and BALB/c mice with acute dextran sodium sulphate colitis and from 129 Sv/Ev IL‐10 knock‐out (IL‐10−/−) mice. From these three mouse strains, we first detected major differences in galectin expression related to the genetic background in the control animals. With regard to inflammation, chronic colitis in IL‐10−/− mice was associated with increased galectin‐4 expression; in contrast with the two other models, no galectin‐1 and ‐3 alterations were observed in IL‐10−/− mice. Acute colitis in C57BL/6 and BALB/c mice showed increased galectin‐3 expression in the lamina propria and the crypt epithelium, together with a decreased nuclear expression. These results suggest an involvement of galectins in the development and perpetuation of colonic inflammation and illustrate that the choice of the mouse strain for studying galectins might influence the outcome of the experiments.
A New Moduli Set for Residue Number System: {rn 2,rn 1,rn}

In this paper a new moduli set {rn -2,rn -1,rn} is introduced where r = 2k + 1 and k= 1,2,3,. This moduli set includes pair wise relatively prime moduli, so it offers the maximum possible dynamic range. For this moduli set, the related circuits are simply realized in the Multiple Valued Logic (MVL) and arithmetic in this moduli set enjoys very high speed operations and simple reverse/forward conversion (RNS to MVL/MVL to RNS). After introducing the new moduli set, we design its related circuits and converters. Finally, we compare the results to those of similar moduli sets and show that our moduli set significantly improves the time complexity while offers greater dynamic range.
Immunotherapy with Aducanumab Restores Calcium Homeostasis in Tg2576 Mice

Calcium homeostasis plays a major role in maintaining neuronal function under physiological conditions. Amyloid-β (Aβ) initiates pathological processes that include disruption in intracellular calcium levels, so amelioration of the calcium alteration could serve as an indirect functional indicator of treatment efficacy. Therefore, calcium dynamics were used as a measure of functional outcome. We evaluated the effects of the anti-Aβ antibody aducanumab on calcium homeostasis and plaque clearance in aged Tg2576 mice with in vivo multiphoton imaging. Acute topical application of aducanumab to the brain resulted in clearance of amyloid plaques. Although chronic systemic administration of aducanumab in 22-month-old mice did not clear existing plaques, calcium overload was ameliorated over time. Therefore, this antibody likely restores neuronal network function that possibly underlies cognitive deficits, indicating promise as a clinical treatment. In addition, functional readouts such as calcium overload may be a more useful outcome measure to monitor treatment efficacy in models of Alzheimer's disease compared with amyloid burden alone. SIGNIFICANCE STATEMENT Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is currently without a cure. Aducanumab is an anti-amyloid-β antibody being developed for the treatment of AD. Interim analyses of a phase 1b clinical trial have suggested potential beneficial effects on amyloid pathology and cognitive status in patients treated with aducanumab (Sevigny et al., 2016). Here, we show that a murine analog of aducanumab clears amyloid plaques in an acute setting and restores calcium homeostasis disrupted in a mouse model of AD upon chronic treatment. Therefore, we demonstrate that aducanumab reverses a functional outcome measure reflective of neural network activity.
2009 update on the classification of renal epithelial tumors in adults

The classification of kidney tumors in adults expands rapidly with new categories recently incorporated. This will result in the modification of the current 2004 World Health Organization (WHO) classification of the adult renal epithelial neoplasms. Emphasis should be placed in defining risk groups categorized as malignant or benign tumors, including a category of tumors with low malignant potential to accommodate recently recognized categories with extremely good prognosis after surgery. Unusual tumors such as familial renal cell carcinoma (RCC), translocation RCC, renal cell carcinoma after neuroblastoma, tubular mucinous and spindle cell carcinoma, and mixed epithelial and stromal tumors are also presented. A number of recently described entities and morphologic variants of classical categories deserve recognition since they can be important in differential diagnosis. This review emphasizes clinical, pathological and genetic features defining renal epithelial tumors in adults.
Role of early and late replication events in induction of apoptosis by baculoviruses

Autographa californica nuclear polyhedrosis virus (AcMNPV) mutants that lack the apoptotic suppressor gene p35 cause apoptosis in Spodoptera frugiperda SF21 cells. To identify a viral signal(s) that induces programmed cell death, we first defined the timing of apoptotic events during infection. Activation of a P35-inhibitable caspase, intracellular fragmentation of host and AcMNPV DNA, and cell membrane blebbing coincided with the initiation of viral DNA synthesis between 9 and 12 h after infection and thus suggested that apoptotic signaling begins at or before this time. Virus entry was required since binding of budded virus to host cell receptors alone was insufficient to induce apoptosis. To therefore determine the contribution of early and late replication events to apoptotic signaling, we used the AcMNPV mutant ts8 with a temperature-sensitive lesion in the putative helicase gene p143. At the nonpermissive temperature at which viral DNA synthesis was conditionally blocked, ts8 caused extensive apoptosis of the SF21 cell line p3576D, which dominantly interferes with anti-apoptotic function of viral P35. Confirming that apoptosis can be induced in the absence of normal viral DNA synthesis, parental SF21 cells also underwent apoptosis when infected with a ts8 p35 deletion mutant at the nonpermissive temperature. However, maximum levels of ts8 p35 deletion mutant-induced apoptosis required a temperature-sensitive event(s) that included the initiation of viral DNA synthesis. Collectively, these data suggested that baculovirus-induced apoptosis can be triggered by distinct early (pre-DNA synthesis) and late replicative events, including viral DNA synthesis or late gene expression.
A HISTOPATHOLOGICAL STUDY OF SMOKING ON FREE GINGIVA IN PATIENTS WITH MODERATE TO SEVERE PERIODONTITIS

Introduction Cigarette smoking has been recognized to be a risk factor for progression of periodontal disease. Due to less inflammation and bleeding in the presence of clinical signs of periodontal disease in smokers than in nonsmokers and given the conflicting results of studies on changes in the epithelium and gingival connective tissue by smoking, this study was performed to evaluate the thickness and keratosis on the epithelium of free and sulcular gingival tissue in smokers and nonsmokers patients with moderate to advanced periodontitis. Methods: In this cross sectional study, biopsies were obtained from palatal gingival of 60 patients with moderate to advanced periodontitis (30 smokers and 30 nonsmokers). These biopsies were histologically processed, serially sectioned at 5 microns, stained with H. E. and examined by image analysis software (analysis-SL-starter), which was used to perform the morphometric evaluation of the outer and inner epithelial thickness, keratosis and vascularity in connective tissue. The data were analyzed with SPSS 17, t-test, Mann-Whitney Test, and Pearson correlation. p 0.001) Conclusions: It seems that the reduction of the clinical signs of inflammation in the gingival tissue of smokers is due to changes in gingival epithelium and connective tissue from smoking.
Treatment of cognitive impairment in patients with multiple sclerosis

Introduction: Identifying and treating cognitive impairment in patients with multiple sclerosis (MS) is increasingly recognized as a crucial step in selecting the most appropriate treatment for the individual. Currently, the neuropsychological tests used to assess patients are time-consuming and require specialist training to administer; consequently, cognitive impairment in MS is underdiagnosed. Many treatments are available for MS, including disease-modifying drugs (DMDs) and symptomatic therapies, but what are their effects on cognitive performance? Areas covered: This article will review published studies describing the cognitive effects of DMDs and symptomatic treatments for MS. Expert opinion: Some DMDs may improve cognitive performance in patients with MS. None of the symptomatic drug treatments reviewed showed positive effects on cognitive performance, with the possible exception of L-amphetamine, which may improve memory in patients with existing deficits, and methylphenidate, on which more data are needed. Cognitive rehabilitation can improve cognitive performance, but experience with these techniques is limited. Treatment for patients with MS and cognitive impairment should, therefore, include a DMD in combination with a pharmacological or perhaps non-pharmacological cognitive-enhancement strategy. However, the methods used to diagnose cognitive impairment, and to assess the effect of treatment on function over time and need to be refined.
Control of lactotrop proliferation by dopamine: Essential role of signaling through D2 receptors and ERKs

Dopamine is thought to exert a negative control on lactotrop cell proliferation and prolactin production. Indeed, mice lacking the D2 receptor develop pituitary tumors of lactotrop origin. Because lactotrops express two isoforms of D2R, D2L, and D2S, in a specific ratio, we decided to explore the physiological importance of their relative abundance in vivo. Thus, we generated transgenic animals overexpressing either D2L or D2S in lactotrops. Increased expression of D2S, but not of D2L, leads to mitogen-activated protein kinase (MAPK) induction, which results in pituitary hypoplasia. On the other hand, levels of phosphorylated MAPKs are drastically reduced in pituitary tumors generated by the absence of D2-dependent signaling. These results underline a critical role of D2-mediated MAPK activation in lactotrop proliferation. Furthermore, whereas D2S overexpression results to a drastic reduction of prolactin, D2L overexpression elevates it. Our findings underscore a different role of the two D2R isoforms in the pituitary gland physiology.
Biodiversity change is uncoupled from species richness trends: Consequences for conservation and monitoring

Global concern about human impact on biological diversity has triggered an intense research agenda on drivers and consequences of biodiversity change in parallel with international policy seeking to conserve biodiversity and associated ecosystem functions. Quantifying the trends in biodiversity is far from trivial, however, as recently documented by meta-analyses, which report little if any net change in local species richness through time. Here, we summarise several limitations of species richness as a metric of biodiversity change and show that the expectation of directional species richness trends under changing conditions is invalid. Instead, we illustrate how a set of species turnover indices provide more information content regarding temporal trends in biodiversity, as they reflect how dominance and identity shift in communities over time. We apply these metrics to three monitoring datasets representing different ecosystem types. In all datasets, nearly complete species turnover occurred, but this was disconnected from any species richness trends. Instead, turnover was strongly influenced by changes in species presence (identities) and dominance (abundances). We further show that these metrics can detect phases of strong compositional shifts in monitoring data and thus identify a different aspect of biodiversity change decoupled from species richness. Synthesis and applications: Temporal trends in species richness are insufficient to capture key changes in biodiversity in changing environments. In fact, reductions in environmental quality can lead to transient increases in species richness if immigration or extinction has different temporal dynamics. Thus, biodiversity monitoring programmes need to go beyond analyses of trends in richness in favour of more meaningful assessments of biodiversity change.