Miracle-dz/UniFAR-FTUs huggingface dataset:
Respiratory health and lung function in Chinese restaurant kitchen workers

Objectives To measure air pollutant concentrations in Chinese restaurant kitchens using different stove types and assess their influence on workers' respiratory health. Methods 393 kitchen workers from 53 Chinese restaurants were surveyed over 16 months: 115 workers from 21 restaurants using only electric stoves and 278 workers from 32 restaurants using only gas stoves. Workers were interviewed about their respiratory symptoms and had their lung function tested. Concentrations of nitric oxide (NO), nitrogen dioxide (NO2), carbon monoxide (CO), carbon dioxide (CO2), methane (CH4), non-methane hydrocarbons (NMHC), total volatile organic compounds (TVOC) and fine particulate matter (PM2.5) were measured using portable monitors and air-bag sampling. Temperature and noise levels were assessed. Results Median concentrations of NO, NO2 and CO were 7.4, 1.5 and 1.6 times higher in gas-fuelled kitchens than in electric ones and average concentrations of PM2.5 and TVOC were 81% and 78% higher, respectively. Differences were smaller for CH4 and NMHC. Electricity-run kitchens were 4.5°C cooler and 9 dBA less noisy than gas-fuelled ones. Workers using electric cookers had significantly better lung function than their gas-using counterparts and their mean FEV1 and FVC values were 5.4% and 3.8% higher, respectively, after adjustment for confounders. Wheeze, phlegm, cough and sore throat were more prevalent in workers using gas. The adjusted OR for having phlegm regularly was significantly higher. Conclusions The poorer lung function and higher prevalence of respiratory symptoms among workers in gas-fuelled kitchens compared to those in electricity-powered kitchens may be associated with exposure to higher concentrations of toxic air pollutants generated during gas cooking.
Sonographic Depiction of Trigger Fingers in Acromegaly

Objective. The purpose of this study was to compare the prevalence of trigger fingers in patients with acromegaly versus an unaffected control group. Methods. This study was performed with Institutional Review Board approval, and informed written consent was obtained from each patient and control participant. The diagnosis was made by a combination of clinical symptoms and sonographically measured thickening of the first annular (A1) pulley. The A1 pulley thickness was measured in 40 patients and 40 control participants by means of a 17–5 MHz high‐resolution transducer. Thickening of the A1 pulley and abnormalities of the underlying flexor tendons associated with the clinical sign were diagnostic for a trigger finger. The acromegalic patients were divided into groups according to disease activity and therapy. The study was performed at the baseline and at a follow‐up after 1 year. Results. At the baseline, clinical and sonographic findings were consistent with trigger fingers in 25% of patients (6 at presentation and 4 with uncontrolled disease). After 1 year, the trigger fingers recovered in the patients who were not receiving any treatment at the beginning of the study. In patients with uncontrolled disease, the condition remained unchanged. The A1 pulley thickness was greater in the acromegalic patients than control participants (mean ± SD, 0.44 ± 0.19 versus 0.24 ± 0.05 mm; P < .05). In the patients treated for acromegaly, the trigger fingers disappeared, and a reduction in the A1 pulley thickness was noted (P < .05) at the follow‐up. Conclusions. Trigger fingers were observed in 25% of the acromegalic patients but in none of the control participants. The A1 pulley was significantly thicker in the acromegalic patients and normalized after 1 year in some who were treated for the disease.
Lesbians' sexual history with men: implications for taking a sexual history.

BACKGROUND Health care providers may not solicit a comprehensive sexual history from lesbian patients because of provider assumptions that lesbians have not been sexually active with men. We performed this study to assess whether women who identify themselves as lesbians have a history of sexual activities with men that have implications for receipt of preventive health screening. OBJECTIVE To convey the importance for health care providers to know their patients' sexual history when making appropriate recommendations for preventive health care. METHODS A survey was printed in a national news magazine aimed at homosexual men, lesbians, and bisexual men and women. The sample included 6935 self-identified lesbians from all 50 US states. The outcomes we measured were respondents' number of lifetime male sexual partners and partners during the past year, their lifetime history of specific sexual activities (e.g., vaginal intercourse, anal intercourse), their lifetime condom use, and their lifetime history of sexually transmitted diseases. RESULTS Of respondents, 77.3% had 1 or more lifetime male sexual partners, 70.5% had a lifetime history of vaginal intercourse, 17.2% had a lifetime history of anal intercourse, and 17.2% had a lifetime history of a sexually transmitted disease. Exactly 5.7% reported having had a male sexual partner during the past year. CONCLUSION These findings reinforce the need for providers to know their patients' sexual history regardless of their reported sexual orientation, especially with regard to recommendations for Papanicolaou smears and screening for sexually transmitted diseases.
Transition from reversible to irreversible attachment during biofilm formation by Pseudomonas fluorescens WCS365 requires an ABC transporter and a large secreted protein

We report the identification of an ATP‐binding cassette (ABC) transporter and an associated large cell‐surface protein that are required for biofilm formation by Pseudomonas fluorescens WCS365. The genes coding for these proteins are designated lap for large adhesion protein. The LapA protein, with a predicted molecular weight of ∼900 kDa, is found to be loosely associated with the cell surface and present in the culture supernatant. The LapB, LapC and LapE proteins are predicted to be the cytoplasmic membrane‐localized ATPase, membrane fusion protein and outer membrane protein component, respectively, of an ABC transporter. Consistent with this prediction, LapE, like other members of this family, is localized to the outer membrane. We propose that the lapEBC‐encoded ABC transporter participates in the secretion of LapA, as strains with mutations in the lapEBC genes do not have detectable LapA associated with the cell surface or in the supernatant. The lap genes are conserved among environmental pseudomonads such as P. putida KT2440, P. fluorescens PfO1 and P. fluorescens WCS365, but are absent from pathogenic pseudomonads such as P. aeruginosa and P. syringae. The wild‐type strain of P. fluorescens WCS365 and its lap mutant derivatives were assessed for their biofilm forming ability in static and flow systems. The lap mutant strains are impaired in an early step in biofilm formation and are unable to develop the mature biofilm structure seen for the wild‐type bacterium. Time‐lapse microscopy studies determined that the lap mutants are unable to progress from reversible (or transient) attachment to the irreversible attachment stage of biofilm development. The lap mutants were also found to be defective in attachment to quartz sand, an abiotic surface these organisms likely encounter in the environment.
Genetic susceptibility to carbamazepine-induced cutaneous adverse drug reactions

The anticonvulsant carbamazepine (CBZ) frequently causes cutaneous adverse drug reactions (cADRs), including maculopapular eruption (MPE), hypersensitivity syndrome (HSS), Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). We reported that SJS/TEN caused by CBZ is strongly associated with the HLA-B*1502 gene in Han Chinese. Here, we extended our genetic study to different types of CBZ-cADRs (91 patients, including 60 patients with SJS/TEN, 13 patients with hypersensitivity syndrome and 18 with maculopapular exanthema versus 144 tolerant controls). We used MALDI-TOF mass spectrometry to screen the genetic association of 278 single nucleotide polymorphisms (SNPs), which cover the major histocompatibility complex (MHC) region, tumor necrosis factor-alpha, heat shock protein and CBZ-metabolic enzymes, including CYP3A4, 2B6, 2C8, 2C9, 1A2 and epoxide hydrolase 1. In addition, we genotyped 20 microsatellites in the MHC region and performed HLA-typing to construct the recombinant map. We narrowed the susceptibility locus for CBZ-SJS/TEN to within 86 kb flanking the HLA-B gene on the extended B*1502 haplotype, and confirmed the association of B*1502 with SJS/TEN [Pc=1.6×10−41, odds ratio (OR)=1357; 95% confidence interval (CI)=193.4–8838.3]. By contrast to CBZ-SJS/TEN, HLA-B*1502 association was not observed in the MPE or HSS groups: MPE was associated with SNPs in the HLA-E region and a nearby allele, HLA-A*3101 (Pc=2.2×10−3, OR=17.5; 95% CI=4.6–66.5), and HSS with SNPs in the motilin gene (Pc=0.0064, OR=7.11; 95% CI=3.1–16.5) located terminal to the MHC class II genes. No SNPs in genes involved in CBZ metabolism were associated with CBZ-induced cADRs. Our data suggest that HLA-B*1502 could contribute to the pathogenesis of CBZ-SJS/TEN, and that genetic susceptibility to CBZ-induced cADRs is phenotype-specific.
Improved Survival Rates With Increased Neurodevelopmental Disability for Extremely Low Birth Weight Infants in the 1990s

Background. Advances in perinatal care have resulted in increased survival rates for extremely low birth weight children. We sought to examine the relative changes in rates of survival and neurodevelopmental impairment at 20 months of corrected age among 500- to 999-g birth weight infants born at our perinatal center during 2 periods, before and after the introduction of surfactant therapy in 1990. Methods. Four hundred ninety-six infants with birth weights of 500 to 999 g were born at our perinatal center during period I (1982–1989) (mean body weight: 762 g; mean gestational age: 25.8 weeks) and 682 during period II (1990–1998) (mean body weight: 756 g; mean gestational age: 25.5 weeks). Rates of death and survival with and without neurodevelopmental impairment at 20 months of corrected age for the 2 periods were compared with logistic regression analyses, with adjustment for gestational age. Results. Survival rates increased from 49% during period I to 67% during period II. Neonatal morbidity rates also increased during period II, including rates of sepsis (from 37% to 51%), periventricular leukomalacia (from 2% to 7%), and chronic lung disease, defined as oxygen dependence at 36 weeks of corrected age (from 32% to 43%). Rates of severe cranial ultrasound abnormalities were similar (22% vs 22%). Among children monitored, the rate of neurologic abnormalities, including cerebral palsy, increased from 16% during period I to 25% during period II and the rate of deafness increased from 3% to 7%. The overall rate of neurodevelopmental impairment (major neurosensory abnormality and/or Bayley Mental Developmental Index score of <70) increased from 26% to 36%. Compared with period I, in period II there were decreased rates of death (odds ratio [OR]: 0.3; 95% confidence interval [CI]: 0.2–0.4) and increased rates of survival with impairment (OR: 2.3; 95% CI: 1.7–3.3) but also increased rates of survival without impairment (OR: 1.7; 95% CI: 1.3–2.2). Compared with period I, for every 100 infants with birth weights of 500 to 999 g born in period II, 18 additional infants survived, of whom 7 were unimpaired and 11 were impaired. Conclusions. The improved survival rates in the 1990s occurred with an increased risk of significant neurodevelopmental impairment. Prospective parents of extremely low birth weight infants should be advised of this substantial risk, to facilitate decision-making in the delivery room.
Carcinogenesis in Rats by Aflatoxins ! , and B 2 l

Aflatoxins Bj, GÃŒ, and B2 of high purity have been prepared from a crude mixture of aflatoxins and have been tested by long-term feeding in drinking water to rats, at concentrations of 1 jug/ml and 3 jug/ml. Aflatoxin B! produced liver tumors in 19 of 30 rats given a total dose of 2 mg each; 3 of 10 animals receiving a total dose of 1 mg developed liver tumors. Aflatoxin GÃŒgave rise to liver tumors in 3 of 30 animals given a total dose of 2 mg and to 1 liver tumor in 10 animals given 1 mg each. However, of 26 rats receiving a total of 6 mg aflatoxin GÃŒ, 21 animals developed liver tumors, and 6 animals had kidney tumors. A number of animals receiving 2 mg of aflatoxin G! also had kidney tumors. There was no sex difference in the incidence of liver tumors, but kidney tumors were seen only in males. The liver tumors were almost all hepatocellular carcinomas. No liver tumors were seen in 10 rats receiving a total dose of 1 mg aflatoxin B2.
Gout Induced by Intoxication of Sodium Bicarbonate in Korean Native Broilers

Gout is a metabolic disorder that results in hyperuricemia and the deposition of positively birefringent monosodium urate crystals in various parts of the body. Intoxication of sodium bicarbonate (SBC) for 35 days in Korean native broilers was investigated. Sixty birds, aged 2 weeks, divided into 5 groups were exposed to excess SBC: 2 g/L (group A), 7.5 g/L (group B), 20 g/L (group C), 40 g/L (group D). Toxicopathological examination of all exposed birds revealed the manifestation of visceral and articular gout in group C, while birds of group D showed acute kidney damage with manifestation of excessive visceral gout. Interestingly, few birds in group D also showed signs of rare condition of acute articular gout. Dose-dependent increments in erythrocytic count, hematocrit values, and hemoglobin levels of the exposed birds were observed. Hypernatremia, hyperuricemia, hypokalemia, and hypochloremia were common findings among exposed birds. Microscopic examination of birds that manifested visceral gout revealed significant urate deposit, tubular necrosis, and tophi formation in renal interstitium. These findings provide a pathophysiological link that SBC intoxication may support hyperuricemia, which is an independent risk factor for gout and other renal dysfunctions. Further study is required to delineate the effect of lowering uric acid on progression of gout and other renal diseases.
Protein kinase C is involved in resistance to myocardial infarction induced by heat stress.

Heat stress (HS) is known to protect against mechanical dysfunction and myocardial necrosis in myocardial ischemia-reperfusion models both in vivo and in vitro. However, the mechanisms involved in this form of cardioprotection remain unclear. Protein kinase C (PKC) and tyrosine kinase activation have both been shown to be involved in the delayed phase of protection following ischemic preconditioning, a phenomenon which appears to be analogous to HS-induced protection. Therefore, we investigated the role of PKC and tyrosine kinase in HS-induced resistance to myocardial infarction, in the isolated rat heart. The selective inhibitors chelerythrine (Che) and genistein (Gen) were used to inhibit PKC and tyrosine kinase, respectively. Rats were treated with Che (5 mg/kg, i.p.) or Gen (5 mg/kg, i.p.) or vehicle before they were either heat stressed (42 degrees C for 15 min) or sham anesthetized. Twenty-four h later their hearts were isolated, retrogradely perfused, and subjected to 35-min occlusion of the left coronary artery followed by 120-min of reperfusion. Infarct-to-risk ratio was significantly reduced in HS (19.9+/-1.1%) compared to sham (43.1+/-1.1%) hearts. This reduction in infarct size was abolished in chelerythrine-treated groups (43.8+/-1.9% in HS+Che v 44.9+/-2.0% in sham+Che), but was conserved in genistein-treated groups (17.7+/-0.9% in HS+Gen v 36.4+/-2.8% in sham+Gen). In order to confirm that genistein at this dose was effectively inhibiting tyrosine kinase activity, we observed the ability of the agent to prevent the hypoglycemic responses to insulin in a separate group of anesthetised rats receiving an i.v. insulin infusion. Western blot analysis of the myocardial hsp72 showed a HS-induced increase of this protein, which was modified by neither the PKC inhibitor, chelerythrine, nor the tyrosine kinase inhibitor, genistein. We conclude that the activation of PKC, but not of tyrosine kinase, appears to play a role in the functional cardioprotection associated with the heat stress response. Although protection appears to be dissociated from induction of hsp72, further work is required to explore the importance of hsp72 phosphorylation to cytoprotective activity of the protein.
Two Distinct Sets of NS2A Molecules Are Responsible for Dengue Virus RNA Synthesis and Virion Assembly

ABSTRACT Flavivirus nonstructural protein 2A (NS2A) plays important roles in both viral RNA synthesis and virion assembly. The molecular details of how the NS2A protein modulates the two distinct events have not been defined. To address this question, we have performed a systematic mutagenesis of NS2A using dengue virus (DENV) serotype 2 (DENV-2) as a model. We identified two sets of NS2A mutations with distinct defects during a viral infection cycle. One set of NS2A mutations (D125A and G200A) selectively abolished viral RNA synthesis. Mechanistically, the D125A mutation abolished viral RNA synthesis through blocking the N-terminal cleavage of the NS2A protein, leading to an unprocessed NS1-NS2A protein; this result suggests that amino acid D125 (far downstream of the N terminus of NS2A) may contribute to the recognition of host protease at the NS1-NS2A junction. The other set of NS2A mutations (G11A, E20A, E100A, Q187A, and K188A) specifically impaired virion assembly without significantly affecting viral RNA synthesis. Remarkably, mutants defective in virion assembly could be rescued by supplying in trans wild-type NS2A molecules expressed from a replicative replicon, by wild-type NS2A protein expressed alone, by a mutant NS2A (G200A) that is lethal for viral RNA synthesis, or by a different mutant NS2A that is defective in virion assembly. In contrast, none of the mutants defective in viral RNA synthesis could be rescued by trans-complementation. Collectively, the results indicate that two distinct sets of NS2A molecules are responsible for DENV RNA synthesis and virion assembly. IMPORTANCE Dengue virus (DENV) represents the most prevalent mosquito-borne human pathogen. Understanding the replication of DENV is essential for development of vaccines and therapeutics. Here we characterized the function of DENV-2 NS2A using a systematic mutagenesis approach. The mutagenesis results revealed two distinct sets of NS2A mutations: one set of mutations that result in defects in viral RNA synthesis and another set of mutations that result in defects in virion assembly. trans-Complementation analysis showed that mutants defective in viral RNA synthesis could not be rescued by wild-type NS2A; in contrast, mutants defective in virion assembly could be successfully rescued by wild-type NS2A or even by a mutant NS2A that is incompetent to support viral RNA synthesis. These results support a model in which two distinct sets of NS2A molecules are responsible for DENV RNA synthesis (located in the viral replication complex) and virion assembly (located in the virion assembly/budding site). The study confirms and extends our understanding of the two critical roles of flavivirus NS2A in viral RNA synthesis and virion assembly.
Study of Telomere Length Reveals Rapid Aging of Human Marrow Stromal Cells following In Vitro Expansion

Human marrow stromal cells (MSCs) can be isolated from bone marrow and differentiate into multiple tissues in vitro and in vivo. These properties make them promising tools in cell and gene therapy. The lack of a specific MSC marker and the low frequency of MSCs in bone marrow necessitate their isolation by in vitro expansion prior to clinical use. This may severely reduce MSC proliferative capacity to the point that the residual proliferative potential is insufficient to maintain long‐term tissue regeneration upon reinfusion. In this study we determined the effect of in vitro expansion on the replicative capacity of MSCs by correlating their rate of telomere loss during in vitro expansion with their behavior in vivo. We report that even protocols that involve minimal expansion induce a rapid aging of MSCs, with losses equivalent to about half their total replicative lifespan.
Intralobar sequestration of the lingula pulmonalis.

Intralobar sequestration of the lingula pulmonalis was noted in a white woman cadaver of 62 years. As the affected tissue was adherent to the pericardium, it received an extrapulmonary arterial supply from both the pericardiophrenic artery and a systemic vessel derived from the aorta. This case was of particular interest as an apparent intermediate condition between intralobar sequestration and accessory lung and because of the unusual situation of the anomaly.
Chromosome allele loss in colorectal liver metastases and its association with clinical features

Molecular genetic changes are better characterized in colorectal carcinoma than in other common adult tumours. Consistent allele losses, or loss of heterozygosity (LOH), on chromosomes 5q, 17p and 18q have been well established. These changes are associated with the prognosis of the disease. Little is known of such changes in liver metastases of colorectal origin. The extent of allelic loss and its association with clinical features were investigated in 19 patients with colorectal liver metastases by using 24 probes to detect restriction fragment length polymorphism. A high frequency of LOH on chromosomes 5q, 17p and 18q was found in these secondary tumours. No consistent loss has so far been shown in any other chromosome. The frequency of allele loss correlated significantly with prognostic features such as the number and size of liver secondaries (P < 0·005), metastasis to the lymph nodes (P < 0·01) and curative or palliative operation (P < 0·02).
Simulated full-waveform lidar compared to Riegl VZ-400 terrestrial laser scans

A 3-D Monte Carlo ray-tracing simulation of LiDAR propagation models the reflection, transmission and ab- sorption interactions of laser energy with materials in a simulated scene. In this presentation, a model scene consisting of a single Victorian Boxwood (Pittosporum undulatum) tree is generated by the high-fidelity tree voxel model VoxLAD using high-spatial resolution point cloud data from a Riegl VZ-400 terrestrial laser scanner. The VoxLAD model uses terrestrial LiDAR scanner data to determine Leaf Area Density (LAD) measurements for small volume voxels (20 cm sides) of a single tree canopy. VoxLAD is also used in a non-traditional fashion in this case to generate a voxel model of wood density. Information from the VoxLAD model is used within the LiDAR simulation to determine the probability of LiDAR energy interacting with materials at a given voxel location. The LiDAR simulation is defined to replicate the scanning arrangement of the Riegl VZ-400; the resulting simulated full-waveform LiDAR signals compare favorably to those obtained with the Riegl VZ-400 terrestrial laser scanner.
A longitudinal study of oral ulcerative mucositis in bone marrow transplant recipients

Background. Few longitudinal studies have investigated the onset, duration, and resolution of ulcerative mucositis in bone marrow transplant recipients. This study prospectively followed a group of such patients on a daily basis to obtain data on the incidence of ulcerative mucositis, location and duration of lesions, severity with different conditioning regimens, and the relationship of such mucositis to the absolute neutrophil count.