Miracle-dz/UniFAR-FTUs huggingface dataset:
Optimization of the Working Conditions for Magnetic Nanoparticle-Enhanced Microwave Diagnostics of Breast Cancer

Magnetic nanoparticle-aided microwave imaging is recently gaining an increasing interest as a potential tool for breast cancer diagnostics. This is due to the peculiar features of magnetic nanoparticles, which are biocompatible, can be selectively targeted to the tumor, and may change their microwave magnetic response when modulated by a polarizing magnetic field. This latter aspect is particularly appealing, as it enables the physical separation of the microwave signal due the malignancy, targeted by the nanoparticles, from that due to healthy tissue. This increases the specificity of the diagnostic tool, in principle allowing a diagnosis based solely on the detection of the signal due to the nanoparticles response. In this respect, a proper choice of the polarizing field modulation can remarkably increase the detection performances. This paper deals with this issue, by providing the mathematical framework for such an optimization and a procedure for estimating the required quantities from a set of proper measurements. The procedure is then experimentally demonstrated by applying it to a recently developed ultrawideband radar system for the magnetic nanoparticle-aided detection of breast cancer. For such a system, the optimal magnetic field modulation is determined.
FUNCTIONALIZATION AND CROSSLINKING OF MICROCRYSTALLINE CELLULOSE IN AQUEOUS MEDIA: A SAFE AND ECONOMIC APPROACH

Cellulose is the most abundant biopolymer in nature and has a broad range of applications in the pharmaceutical, food and biomedical fields. This review article describes the functionalization conditions, crosslinking agents, reaction pathways and the resulting physicochemical and mechanical properties of functionalized cellulose derivatives. The discussion is focused on aqueous reactions and crosslinking agents that render a material of low toxicity and better biodegradability with a broad range of applications. Crosslinking agents such as dialdehydes (glyoxal and glutaraldehyde), acetals (1,1,4,4-tetramethoxybutane and 1,1,5,5tetramethoxybutane), polycarboxylic acids (acrylic, maleic, polymaleic, succinic polyitaconic and citric acids), phosphorus derivatives (phosphoric acid and triethyl phosphate), silica derivatives (tetraethoxysilane), epichlorohydrin and polyepichlorohydrin were selected for the discussion since they present a low toxicity risk and are able to react efficiently with cellulose rendering products with unique properties.
Role of pili in Haemophilus influenzae adherence and colonization

s of the 30th Interscience Conference on Antimicrobial Agents and Chemotherapy. American Society for Microbiology, Washington, D.C. 27. Hacker, J. 1990. Genetic determinants coding for fimbriae and adhesins of extraintestinal Escherichia coli. Curr. Top. Microbiol. Immunol. 151:1–27. 28. Holmgren, A. , M. J. Kuehn, C. I. Branden, and S. J. Hultgren. 1992. Conserved immunoglobulin-like features in a family of periplasmic pilus chaperones in bacteria. EMBO J. 11:1617–1622. 29. Hultgren, S. J., F. Lindberg, G. Magnusson, J. Khilberg, J. M. Tennent, and S. Normark. 1989. The papG adhesin of uropathogenic Escherichia coli contains separate regions for receptor binding and for the incorporation into the pilus. Proc. Natl. Acad. Sci. USA 86:4357–4361. 30. Jackson, A. D. , P. J. Cole, and R. Wilson. 1996. Comparison of Haemophilus influenzae type b interaction with respiratory mucosa organ cultures maintained with an air interface or immersed in medium. Infect. Immun. 64:2353– 2355. 31. Johnson, P. D. , F. Oppedisano, V. Bennett-Wood, G. L. Gilbert, and R. M. Robins-Browne. 1996. Sporadic invasion of cultured epithelial cells by Haemophilus influenzae type b. Infect. Immun. 64:1051–1053. 32. Kar, S. , S. C. -M. To, and C. C. Brinton, Jr. 1990. Cloning and expression in Escherichia coli of LKP pilus genes from a nontypeable Haemophilus influVOL. 65, 1997 MINIREVIEW 3001
Down‐regulation of the β‐chemokine receptor CCR6 in dendritic cells mediated by TNF‐α and IL‐4

Chemokines are involved in the control of dendritic cell (DC) trafficking, which is critical for the immune response. We have generated DC from human umbilical cord blood CD34+ progenitors cultured with granulocyte‐macrophage colony‐stimulating factor, tumor necrosis factor α (TNF‐α), and stem cell factor. Using an anti‐CCR6 monoclonal antibody, we observed that these cells showed maximum expression of this β‐chemokine receptor when they were immature, as determined by their relatively low expression of several DC maturation markers such as CD1a, CD11c, CD14, CD40, CD80, and CD83. Immature DC responded strongly to macrophage inflammatory protein‐3α (MIP‐3α), the CCR6 ligand, in migration and calcium mobilization assays. CCR6 expression decreased in parallel with the DC maturation induced by prolonged TNF‐α treatments. Interleukin‐4 was also able to decrease CCR6 protein levels. Our findings suggest that the MIP‐3α/CCR6 interaction plays an important role in the trafficking of immature DC to chemokine production sites such as injured or inflamed peripheral tissues, where DC undergo maturation on contact with antigens. J. Leukoc. Biol. 66: 837–844; 1999.
Acute melioidosis in a soldier home from South Vietnam.

A fatal case of acute melioidosis occurred in a soldier who had recently returned from Vietnam. Pseudomonas pseudomallei was identified by culture of blood specimens taken before and after death, animal inoculation, and fluorescent antibody tests. Chloramphenicol is the drug of choice in this disease.
Prognosis of congestive heart failure in patients with normal versus reduced ejection fractions: results from a cohort of 2,258 hospitalized patients.

BACKGROUND Patients with congestive heart failure have an annual mortality of 10% to 20% depending on disease severity. Though one third of these patients have normal left ventricular (LV) ejection fraction (EF), their natural history is poorly defined. Small population-based studies have suggested a more benign prognosis for patients with preserved LVEF. However, prognosis in hospitalized patients, who form a higher risk group, is not known. METHODS We investigated the survival patterns of 2,258 patients with a primary hospital discharge diagnosis of congestive heart failure between 1990 and 1999. Survival was analyzed and patients with normal and reduced LVEF were compared. RESULTS Their age was 71 +/- 11 years, and 97% were men. There were 1,535 deaths over a mean follow up of 786 days. Of these, 963 (43%) patients had a normal LVEF (>/=55%). Patients with normal LVEF were of the same age as those with reduced LVEF, but had a lower prevalence of atrial fibrillation (20 versus 26%, P =.03), left bundle branch block (2 versus 12%, P <.0001), significant mitral regurgitation (5 versus 31%, P <.0001) and electrocardiographic evidence of myocardial infarction (38 versus 60%, P <.0001). Despite lesser comorbidities, they had a higher mortality hazard, with a 5-year survival of 22% compared with 28% for those with systolic heart failure (P =.007). Proportional hazards model showed presence of normal EF as a categoric variable to be an independent predictor of mortality in those with heart failure after correcting for age and rhythm. CONCLUSIONS Prognosis of hospitalized patients with congestive heart failure and normal LVEF is worse than those with reduced EF despite lesser comorbidities. Studies addressing optimal management of these patients are warranted.
Emerging drugs to reduce abnormal β-amyloid protein in Alzheimer’s disease patients

ABSTRACT Introduction: Currently available drugs against Alzheimer’s disease (AD) target cholinergic and glutamatergic neurotransmissions without affecting the underlying disease process. Putative disease-modifying drugs are in development and target β-amyloid (Aβ) peptide and tau protein, the principal neurophatological hallmarks of the disease. Areas covered: Phase III clinical studies of emerging anti-Aβ drugs for the treatment of AD were searched in US and EU clinical trial registries and in the medical literature until May 2016. Expert opinion: Drugs in Phase III clinical development for AD include one inhibitor of the β-secretase cleaving enzyme (BACE) (verubecestat), three anti-Aβ monoclonal antibodies (solanezumab, gantenerumab, and aducanumab), an inhibitor of receptor for advanced glycation end products (RAGE) (azeliragon) and the combination of cromolyn sodium and ibuprofen (ALZT-OP1). These drugs are mainly being tested in subjects during early phases of AD or in subjects at preclinical stage of familial AD or even in asymptomatic subjects at high risk of developing AD. The hope is to intervene in the disease process when it is not too late. However, previous clinical failures with anti-Aβ drugs and the lack of fully understanding of the pathophysiological role of Aβ in the development of AD, put the new drugs at substantial risk of failure.
Stromelysin-1 (MMP-3) is a target and a regulator of Wnt1-induced epithelial-mesenchymal transition (EMT)

Matrix metalloproteinases (MMPs) play a well-defined role in later stages of tumor progression. However, there has been evidence that they also contribute to earlier stages of malignant transformation. The Wnt signaling transduction pathway plays a critical role in development and in the pathogenesis of many epithelial cancers. Here we have used Wnt1-induced epithelial-mesenchymal transition (EMT) in C57MG murine mammary epithelial cells to study the role of MMPs in this early step of malignant progression. Overexpression of Wnt1 in C57MG cells promoted EMT, the translocation of b-catenin from the cell membrane to the nucleus and its transcriptional activity, cell proliferation and cell motility. Simultaneously, we observed an increased expression of stromelysin-1 (MMP-3) and a 5.5-fold increase in MMP-3 promoter activity in C57MG cells expressing Wnt1 compared with C57MG cells. Treatment of Wnt-overexpressing cells with MMP inhibitor AG3340 decreased MMP-3 expression. We also found evidence that MMP-3 and Wnt3a cooperate in enhancing the transcriptional activity of β-catenin in C57MG cells. Consistently, the effects of Wnt1 on EMT, proliferation, and migration were inhibited by MMP inhibitors, or upon downregulation of MMP-3 by siRNA. These results suggest that MMP-3 is both a direct transcriptional target and a necessary contributor of the Wnt/b-catenin signaling pathway.
Cerebral Network Disruption as a Possible Mechanism for Impaired Recovery after Acute Pontine Stroke

Background: Recovery from stroke is presumed to be a function of a widespread cerebral network. Chronic white matter lesions (WML) have been proposed to be a predictor of poor outcome after acute stroke. We tested the hypothesis that the extent of WML has an effect on functional recovery in acute pontine stroke by disrupting the integrity of the supratentorial cerebral network. Methods: Seventeen patients with acute unilateral pontine stroke who had received a standardized stroke workup and additional diffusion tensor imaging (DTI) were studied. After grading the extent of WML according to the Fazekas scale and semiautomated lesion volume calculation, we compared patients with acute pontine infarction and advanced WML to those with absent or minimal WML regarding baseline characteristics, stroke subtype and clinical outcome. In addition, we used tract-based spatial statistics for voxel-wise analysis of the DTI-derived parameter fractional anisotropy in the white matter tracts. Results: The volume of WML ranged between 0.1 and 42.1 cm3 (mean = 15.9) and was graded as follows: 0 in 5.9%, 1 in 35.3%, 2 in 41.2% and 3 in 17.6%. Both patients with Fazekas grades 2–3 (p = 0.014) as well as those with larger WML volumes (p = 0.037) had severer functional deficits at the 3-month follow-up. White matter tracts displaying a significant decrease in fractional anisotropy values were the corpus callosum, the anterior thalamic radiation and the inferior fronto-occipital fasciculus. Conclusions: Chronic WML contribute to a less favorable clinical outcome after pontine stroke depending on (1) the extent of pre-existing WML and (2) the degree of disruption of cerebral connectivity as indicated by reduced tissue integrity in the white matter not affected by WML as detected by DTI and tract-based spatial statistics.
Is Plasminogen Deficiency a Thrombotic Risk Factor ? – A Study on 23 Thrombophilic Patients and their Family Members

Summary The role of plasminogen (plg) deficiency in the pathogenesis of venous thromboembolism is debated in the literature. In the present study we evaluated the prevalence of plg deficiency in our thrombophilia patients and aimed to elucidate the thrombosis risk of plg deficiency as a single defect or in combination with other defects, with special focus on APC resistance. The study cohort included 1192 consecutive patients with a history of clinically or objectively diagnosed venous and/or arterial thromboembolism and/or positive family history who were referred to our department for thrombophilia investigation from 02/1988 to 03/1997. All available family members of patients with plg deficiency were tested for plg, APC resistance and other thrombophilic defects that were established in the propositus. 23/1192 propositi were plg-deficient corresponding to an overall prevalence of 1.9%, i.e. 2.2% in patients with venous thrombosis and 1.4% in those with arterial events. Out of the 23 plg-deficient propositi, 8 showed one or multiple additional thrombophilic defects, and in 4 patients relevant circumstantial risk factors were present. Of the 53 available family members, 28 were plg-deficient including 5 with additional APC resistance, and 4 subjects had isolated APC resistance. Ten of the 53 family members had already suffered thromboembolic events, i.e. 5 (18%) in the plg-deficient group and 5 (20%) in the non-deficient group, both groups showing an almost identical median age at the time of investigation (28.9 years and 27.1 years, respectively). Based on our data, plg deficiency is a rare defect in thrombophilic patients and as a single defect it does not seem to be a strong thrombotic risk factor, as 11 of 23 propositi had additional thrombophilic defects or circumstantial risk factors, and in the family members thrombotic events were equally frequent in the plg-deficient and non-deficient subjects.
P27.14: Fetal cystic hygroma and mid‐trimester maternal serum screening

OBJECTIVE To investigate the relationship between maternal serum screening markers and pregnancy outcome in fetuses with cystic hygroma at 15-18 weeks of gestation. STUDY DESIGN We retrospectively reviewed case-notes of 34 consecutive singleton fetuses with cystic hygroma referred at 15-18 weeks of gestation. All cases had maternal blood sampled for triple screening at the time of the ultrasound scan. RESULTS In total, 62% of fetuses with cystic hygroma had abnormal chromosome complements and 80% had a poor outcome. Six fetuses presenting normal values of human chorionic gonadotropin (0.5-2.5 MoM [multiples of the median]), serum alpha-fetoprotein (0.5-2.5 MoM) and unconjugated estriol (>0.5 MoM), normal karyotype and absence of associated structural anomalies had an uneventful outcome. CONCLUSIONS Our data demonstrated that cystic hygroma at 15-18 weeks has a strong association with chromosomal abnormalities. In euploid fetuses, maternal serum screening results may have a role in the diagnostic work-up of the pregnancy.
Expression of nuclear factor-kappa B and I kappa B alpha proteins in prostatic adenocarcinomas: correlation of nuclear factor-kappa B immunoreactivity with disease recurrence.

PURPOSE The nuclear transcription factor nuclear factor-kappa B (NF kappa B) and its inhibitor, I kappa B, regulate the transcription of various genes involved in cell proliferation, adhesion, and survival. The NF kappa B transcription factor complex plays a role in cancer development and progression through its influence on apoptosis. More recently, NF kappa B has been shown to be activated in human and androgen-independent prostate cancer cells. To our knowledge, this is the first study demonstrating the prognostic significance of NF kappa B immunoreactivity in prostate adenocarcinomas (PACs). EXPERIMENTAL DESIGN Using prostatectomy specimens, we performed immunohistochemical staining for NF kappa B and I kappa B alpha (Santa Cruz Biotechnology) on formalin-fixed, paraffin-embedded sections obtained from 136 patients with PAC. Cytoplasmic and nuclear immunoreactivity was scored for intensity and distribution, and results were correlated with preoperative serum prostate-specific antigen, tumor grade, stage, DNA ploidy (Feulgen spectroscopy), and biochemical disease recurrence. RESULTS Forty-nine percent of PACs overexpressed cytoplasmic NF kappa B, and 63% showed decreased I kappa B expression. Cytoplasmic NF kappa B overexpression correlated with advanced tumor stage (P = 0.048), aneuploidy (P = 0.022), and biochemical disease recurrence (P = 0.001). When we compared the means for the NF kappa B-positive and -negative subgroups, NF kappa B overexpression correlated with preoperative serum prostate-specific antigen (P = 0.04) and DNA index (P = 0.05). Fifteen percent of PACs expressed nuclear NF kappa B, which correlated with high tumor grade (P = 0.001) and advanced stage (P = 0.05). Decreased I kappa B alpha expression correlated with high tumor grade (P = 0.015). On multivariate analysis, tumor stage (P = 0.043) and NF kappa B overexpression (P = 0.006) were independent predictors of biochemical recurrence. CONCLUSION These results support a role for NF kappa B pathway proteins in the tumorigenesis of PACs. The findings are also consistent with reported experimental studies suggesting a new strategy of combined chemotherapy and specific NF kappa B blockade in decreasing the rate of disease relapse.
Can Career Advancement and Job Security Act as Collaterals for Commitment? Evidence from the Hotel Industry of Malaysia

 Abstract — This study aims to examine the role of career advancement and job security as predictors of employee commitment to their organization. Data was collected from 580 frontline employees attached to two departments of 29 luxury hotels in Peninsular Malaysia. Statistical results using Partial Least Squares technique provided support for the proposed hypotheses. In view of the findings, theoretical and practical implications are discussed.
Diabetes Associated With Short Survival in Pancreatic Cancer.

association between long-term diabetes and poor overall survival among patients with diabetes and pancreatic cancer in three longitudinal studies. The authors reported a 40% to 50% increased risk of death for patients with long-term diabetes (duration of 4 years) compared with those without diabetes (P .05) in two prospective cohort studies 2,3 and a clinic-based study. 1 In contrast, no statistically significant association between short-term diabetes (duration of 4 years) and survival was observed. Thus, the authors concluded that there is a link between chronic glucose intolerance and pancreatic cancersurvival,whereasshort-termdiabetesdoesnotportendaworse prognosis among patients with pancreatic adenocarcinoma. We have a concern about the authors’ conclusion regarding the association between short-term diabetes and survival. Because the information on diabetes was collected via a biennial questionnaire in the cohort studies, it is possible that the number of patients with short-term diabetes was greatly underestimated, which may have biased the risk estimate toward null. The prevalence of patients with short-term diabetes was 4.67% (47 of 1,006) and 18.65% (72 of 386), whereas the prevalence of patients with any type of diabetes was 17.99% (181 of 1,006) and 31.35% (121 of 386) in the cohort and the clinic-based studies, respectively. The prevalence of diabetes in the clinic-based study was quite similar to the numbers previously reported by other studies. Short-term diabetes was associated with a nonsignificant but increased risk of death in this clinic series (hazard ratio [HR], 1.22; 95% CI, 0.89 to 1.67). In our recently completed studyof1,328patientswithpathologicallyconfirmedpancreaticductal adenocarcinoma of all stages at MD Anderson Cancer Center, we foundthatshort-termdiabetes(durationof3years)wasassociated with a significantly increased risk of death (HR, 1.23; 95% CI, 1.09 to 1.40). Wehavealsoconductedameta-analysisof29studiesondiabetesandoverallsurvivalofpatientswithpancreaticcancerandfounda reduced survival of patients with diabetes in 25 clinic-based studies (pooled HR, 1.13; 95% CI, 1.02 to 1.25), but not in four cohort studies 4-7 (pooled HR, 1.12; 95% CI, 0.95 to 1.32). The prevalence of patients with diabetes was 28.61% (4,133 of 14,446) and 20.92% (1,124 of 5,372) in the clinic and cohort studies, respectively. These observations suggest that short-term diabetes is associated with a higher risk of death in patients with pancreatic cancer. The inconsistentobservationswithrespecttotheassociationbetweendiabetesand
Retrospective study of papulonodular skin lesions and their clinopathological correlation

Background: Papulonodular lesion of the skin is a more common variety. Various types of diseases manifested with papulonodular lesions surface, for example, infectious diseases, benign neoplastic diseases, and malignant tumors as well as metastatic tumors. Therefore, a brief idea about the clinical history, age, sex, and various sites of lesion is important. Objectives: To evaluate the incidence of different infectious, benign, and malignant diseases manifested with papulonodular lesions. To study the various papulonodular lesions of skin in relation to different age group, sex, and location. To compare our observation with that of other authors and to correlate clinical data with that of histopathological study. Materials and Methods: In the present study, from November 2007 to November 2009, total 75 cases of papulonodular lesions were taken for study from Department of Dermatology and Department of Pathology, BJ Medical College and Civil Hospital, Ahmedabad, Gujarat, India. All lesions were studied with respect to clinical history, physical examination, histopathological examination of biopsy material on HE stain and also on special stains when required. Results: In the present study, 69% of papulonodular lesions of skin were of infectious origin followed by 24% as benign origin and 7% as malignant origin. In infectious lesions, most common is leprosy with incidence of 22.67%, erythema nodosum leprosum 20%, and cutaneous tuberculosis mostly scrofuloderma 8% and Prurigo Nodularis 6.67%. In benign lesions, trichoepithelioma has incidence of 8% and syringoma 5.33%. In malignant lesions, Basal cell carcinoma has incidence of 4% and metastatic carcinoma 2.67%. Clinically, most of infectious lesions are diagnosed and are confirmed by histopathology. In leprosy, clinopathological correlation is 94.12% and in erythema nodosum leprosum, it is 93.33%, while in cutaneous tuberculosis, actinomycosis, and epidermoid cyst, clinopathological correlation is 100% with histopathological diagnosis. Conclusion: Papulonodular lesion of skin is clinically well diagnosed and better correlated with histopathological examination.
A novel motility pattern in quail spermatozoa with implications for the mechanism of flagellar beating

Background information. The spermatozoon of the quail (Coturnix coturnix L., var japonica) has a ‘9+2’ flagellum that is unusually long. When it moves in a viscous medium, near to the coverslip, it develops a meander waveform. Because of the high viscosity, the meander bends are static in relation to the field of view; bend propagation is therefore manifest as the forward movement of the flagellum through the meander shape. At the same time, the origin of the oscillation typically shifts proximally in a stepwise fashion. These movements have been analysed in the hope of contributing to the resolution of problems in flagellar mechanics.