Infection control measures for public transportation derived from the flow dynamics of obstructed cough jet.

During the COVID-19 pandemic, WHO and CDC suggest people stay 1 m and 1.8 m away from others, respectively. Keeping social distance can avoid close contact and mitigate infection spread. Many researchers suspect that suggested distances are not enough because aerosols can spread up to 7-8 m away. Despite the debate on social distance, these social distances rely on unobstructed respiratory activities such as coughing and sneezing. Differently, in this work, we focused on the most common but less studied aerosol spread from an obstructed cough. The flow dynamics of a cough jet blocked by the backrest and gasper jet in a cabin environment was characterized by the particle image velocimetry (PIV) technique. It was proved that the backrest and the gasper jet can prevent the front passenger from droplet spray in public transportation where maintaining social distance was difficult. A model was developed to describe the cough jet trajectory due to the gasper jet, which matched well with PIV results. It was found that buoyancy and inside droplets almost do not affect the short-range cough jet trajectory. Infection control measures were suggested for public transportation, including using backrest/gasper jet, installing localized exhaust, and surface cleaning of the backrest.

Airborne infection risk of nearby passengers in a cabin environment and implications for infection control.

BACKGROUND: Expiratory droplets cause high infection risk to nearby passengers via airborne route. METHODS: We built a two-row four-seat setup to simulate a public transport cabin. A cough generator and a nebulizer were used to simulate the cough and talk processes respectively. Exposure and infection risk of nearby passengers was studied. The effect of gasper jet and backrest on risk mitigation was investigated. RESULTS: For the activity of coughing, the front passenger has much higher infection risk, which was around four times of that of other passengers, because of the concentration surge in the inhalation zone. For talking, the nearby passengers have similar infection risk because nearby passengers were all exposed to concentration surges with similar peak value. Gasper jet of the infected passenger and higher backrest can extinguish or reduce the concentration surge of front passengers and reduce the infection risk due to coughing and talking droplets. CONCLUSION: The passengers near the infected passenger have very high infection risk. The overhead gasper and a higher backrest can reduce the exposure and mitigate the risk of infection. It is believed that the control measures to protect nearby passengers are urgently needed in public transport cabins.

Dataset on critical parameters of dispersion stability of Cu/Al2O3 nanofluid and hybrid nanofluid for various ultra-sonication times.

The data presented in this data article comprises the critical parameters of dispersion stability such as the particle effective diameter, zeta potential, sedimentation velocity and stability factor for Cu/Al2O3 single particle nanofluid and hybrid nanofluid samples at various ultra-sonication times, that is, 0.5 h, 1.0 h, 2.0 h and 3.0 h. The data for effective diameter and zeta potential was generated using the particle size analyser and zeta potential analyser respectively. The measured data for effective diameter and zeta potential was processed to generate the data for sedimentation velocity and stability factor. The ultra-sonication time with maximum value of stability factor was used for sample preparation of Cu/Al2O3 single particle nanofluid and hybrid nanofluid in the related research article "On trade-off for dispersion stability and thermal transport of Cu-Al2O3 hybrid nanofluid for various mixing ratios" (Siddiqui et al., 2019) [1].

Airborne particles in indoor environment of homes, schools, offices and aged care facilities: The main routes of exposure.

It has been shown that the exposure to airborne particulate matter is one of the most significant environmental risks people face. Since indoor environment is where people spend the majority of time, in order to protect against this risk, the origin of the particles needs to be understood: do they come from indoor, outdoor sources or both? Further, this question needs to be answered separately for each of the PM mass/number size fractions, as they originate from different sources. Numerous studies have been conducted for specific indoor environments or under specific setting. Here our aim was to go beyond the specifics of individual studies, and to explore, based on pooled data from the literature, whether there are generalizable trends in routes of exposure at homes, schools and day cares, offices and aged care facilities. To do this, we quantified the overall 24h and occupancy weighted means of PM10, PM2.5 and PN - particle number concentration. Based on this, we developed a summary of the indoor versus outdoor origin of indoor particles and compared the means to the WHO guidelines (for PM10 and PM2.5) and to the typical levels reported for urban environments (PN). We showed that the main origins of particle metrics differ from one type of indoor environment to another. For homes, outdoor air is the main origin of PM10 and PM2.5 but PN originate from indoor sources; for schools and day cares, outdoor air is the source of PN while PM10 and PM2.5 have indoor sources; and for offices, outdoor air is the source of all three particle size fractions. While each individual building is different, leading to differences in exposure and ideally necessitating its own assessment (which is very rarely done), our findings point to the existence of generalizable trends for the main types of indoor environments where people spend time, and therefore to the type of prevention measures which need to be considered in general for these environments.

TGF-ß1 activation in human hamstring cells through growth factor binding peptides on polycaprolactone surfaces.

The administration of soluble growth factors (GFs) to injured tendons and ligaments (T/L) is known to promote and enhance the healing process. However, the administration of GFs is a complex, expensive and heavily-regulated process and only achieved by employing supraphysiological GF concentrations. In addition, for proper healing, specific and spatial immobilization of the GFs (s) is critical. We hypothesized that biomaterials functionalized with GF-binding peptides can be employed to capture endogenous GFs in a spatially-controlled manner, thus overcoming the need for the exogenous administration of supraphysiological doses of GFs. Here we demonstrate that the modification of films of polycaprolactone (PCL) with transforming growth factor ß1 (TGF-ß1)-binding peptides allows GFs to be captured and presented to the target cells. Moreover, using a TGF-ß reporter cell line and immunocytochemistry, we show that the GFs retained their biological activity. In human primary tendon cells, the immobilized TGF-ß1 activated TGF-ß target genes ultimately lead to a 2.5-fold increase in total collagen matrix production. In vivo implantation in rats clearly shows an accumulation of TGF-ß1 on the polymer films functionalized with the TGF-ß1-binding peptide when compared with the native films. This accumulation leads to an increase in the recruitment of inflammatory cells at day 3 and an increase in the fibrogenic response and vascularization around the implant at day 7. The results herein presented will endow current and future medical devices with novel biological properties and by doing so will accelerate T/L healing. STATEMENT OF SIGNIFICANCE: Our study describes the possibility to deliver hTGF-ß1 to human derived hamstring cells using a non-covalent bioactive strategy. The significance of our results in vivo with our functionalized biomaterial with TGF-ß1-binding peptides lies in the fact that these materials can now be employed to capture endogenous TGF-ß1 in a spatially-controlled manner, overcoming the need for exogenous administration of supra-physiological TGF-ß1 doses. Our method is different from current solutions that rely on global TGF-ß1 administration, soaking the devices with TGF-ß1, etc. Therefore we believe that our method is a significant change from current state-of-the-art in the types of devices that are used for ligament/tendon repair and that following our method can endow current and future medical devices with TGF-ß1 binding properties.

Increased risk of hepatocellular carcinoma in chronic hepatitis C patients with new onset diabetes: a nation-wide cohort study.

BACKGROUND: The impact of diabetes for hepatocellular carcinoma (HCC) development in chronic hepatitis C (CHC) patients remains controversial. AIM: To investigate the risk of HCC in CHC patients who develop new onset diabetes. METHODS: We conducted a nation-wide cohort study by using Taiwanese National Health Insurance Research Database, which comprised of data from >99% of entire population. Among randomly sampled one million enrollees, 6251 adult CHC patients were identified from 1997 to 2009. Diabetes was defined as new onset in the patient who was given the diagnosis in the years 1999-2009 but not in 1997-1998. The cohorts of CHC with new onset diabetes (n = 1100) and 1:1 ratio age-, gender-, and inception point (onset date of diabetes) matched nondiabetes (n = 1087) were followed up from the inception point until the development of HCC, withdrawal from insurance, or December 2009. RESULTS: After adjustment for competing mortality, patients with new onset diabetes had a significantly higher cumulative incidence of HCC (Relative Risk = 1.544, 95% CI = 1.000-2.387, modified log-rank test, P = 0.047) as compared to those without. After adjustment for age, gender, cirrhosis, hyperlipidaemia, CHC treatment, diabetes treatment, comorbidity index, obesity and statins therapy by Cox proportional hazard model, diabetes was still an independent predictor for HCC (hazard ratio (HR) = 1.906, 95% CI = 1.102-3.295, P = 0.021). The risk for HCC was increased in those who were 40-59 years old, independent of other variables (HR = 3.086, 95% CI = 1.045-9.112, P = 0.041), and after adjustment for competing mortality (modified log-rank test, P = 0.009). CONCLUSION: Chronic hepatitis C patients who develop diabetes are at an increased risk of hepatocellular carcinoma over time.

Increased risk of hepatocellular carcinoma in chronic hepatitis B patients with new onset diabetes: a nationwide cohort study.

BACKGROUND: Diabetes increases the risk of hepatocellular carcinoma (HCC), however, the time-relationship between hepatitis B virus and diabetes for the development of HCC remains unclear. AIM: To explore the risk of HCC in chronic hepatitis B patients with newly diagnosed diabetes. METHODS: We conducted a nationwide cohort study by using Taiwanese National Health Insurance Research Database, which covers over 99% of entire population. Among randomly sampled one million enrollees, 14 523 chronic hepatitis B patients were diagnosed in years 1997-2009. We defined new onset diabetes as patients who were given the diagnosis in the years 1999-2009, but not in 1997-1998. The cohorts of chronic hepatitis B with new onset diabetes (n = 2099) and 1:1 ratio age-, gender- and inception point (onset date of diabetes)- matched nondiabetes (n = 2080) were followed up from the inception point until development of HCC, withdrawal from insurance or December 2009. RESULTS: After adjustment for competing mortality, patients with new onset diabetes had a significantly higher cumulative incidence of HCC [relative risk = 1.628, 95% confidence interval (CI) = 1.114-2.378, modified log-rank test, P = 0.012] as compared to nondiabetes patients. After adjustment for age, gender, hyperlipidaemia, chronic hepatitis B treatment, statins therapy, cirrhosis, comorbidity index and obesity, diabetes was still an independent predictor for HCC (hazard ratio = 1.798, 95% CI = 1.194-2.707, P = 0.005). CONCLUSION: Chronic hepatitis B patients with newly diagnosed diabetes have an increased risk of hepatocellular carcinoma over time.

Limb Idleness Index (LII): a novel measurement of pain in a rat model of osteoarthritis.

OBJECTIVES: Mechanical allodynia during ambulation in osteoarthritis (OA) animal models can be assessed as decreased extent of loading or decreased duration of loading. We propose to measure gait adaptation to pain by both mechanisms with the development of Limb Idleness Index (LII) in a rat model of knee OA. METHODS: Rats were assigned to anterior cruciate ligament transection (ACLT), Sham, or Normal group (n = 6). Gait data were collected at pre-injury, 1, 2, 3 and 6 months post-injury. Ratios of target print intensity, anchor print intensity, and swing duration were combined to obtain LII. The association of gait changes with pain was assessed by buprenorphine treatment at 3 and 6 months post-injury. At 6 months, OA-related structural changes in knee joints were examined by µCT and results from histological scoring were correlated with LII. RESULTS: As compared to pre-injury level (range 0.75-1.20), LII in ACLT group was increased at 6 months post-injury, which was significantly higher than that in Sham and Normal groups (P = 0.024). The increase in LII in ACLT group was effectively reversed by buprenorphine treatment (P = 0.004). ACLT group exhibited a significantly higher maximum Osteoarthritis Research Society International (OARSI) score as compared to Sham (P = 0.005) and Normal (P = 0.006) groups. Significant correlation was found between LII and side-to-side difference in OARSI score (r = 0.893, P < 0.001). CONCLUSIONS: LII presents a good measurement for OA-related knee pain in rat model.

Tendon adhesion measured by a video-assisted gliding test in a chicken model.

We developed a video-assisted gliding test to evaluate the gliding force and the flexion angle with unrestricted joint motion. Tendon adhesion was induced in a chicken model of flexor digitorum profundus (FDP) injury at the annular pulley region of the long toe. The chicken feet were harvested immediately after injury, and 2 weeks and 6 weeks after injury. During the gliding test, the injured FDP was pulled for 15 mm then returned to its initial position. The test was recorded using a video camera and registered to the gliding test mechanical data. The maximum flexion angle and gliding resistance were calculated. The maximum flexion angle was significantly decreased from 78 (SD 10) in controls to 42 (SD 22) in tendons with injury, while gliding resistance was significantly increased in week 2 (0.06, SD 0.05) and week 6 (0.07, SD 0.01) after injury.

Supplementation-time dependence of growth factors in promoting tendon healing.

Growth factors potentially promote tendon healing. Understanding the right time to administer growth factors and the dosage of growth factors are prerequisites for designing effective cytokine therapy. We investigated the supplementation-time dependence of the effects of platelet-derived growth factor isoform B at various dosages on tendon healing, and the temporal responsiveness of healing tendon toward platelet-derived growth factor. Platelet-derived growth factor isoform B at various dosages (0, 10, 100, or 1000 ng) was delivered into the gap wound of rat patellar tendons via microsyringe injection on Day 3 or Day 7 after injury. Tendon specimens were harvested on Day 14 for measurement of cell proliferation, pyridinoline content, and mechanical properties. We found increased proliferative response only when the growth factor was supplemented on Day 3 after injury, whereas supplementation on Day 7 resulted in greater peak load, cross-sectional area, and pyridinoline content. The ultimate stress did not change. Our findings suggest supplementation of platelet-derived growth factor isoform B at Day 7 benefits the mechanical properties and maturation of healing tendons. We also found platelet-derived growth factor receptor beta expressing cells at the remodeling site as much as 6 months after injury, suggesting healing tendon also may be responsive to long-term delivery of platelet-derived growth factor.

Total flavones of Hippophae rhamnoides promotes early restoration of ultimate stress of healing patellar tendon in a rat model.

Traditional Chinese herbal medicine has long been used for treatment of tendon injuries. Comparing to the modern way of treatments, Traditional Chinese medicine also stresses on strategies to promote the inherent healing capacity of tendons. Hippophae rhamnoides, known as Shaji, is one of Chinese herbal drugs that are traditionally used to promote tendon and ligament injuries. The total flavones of H. rhamnoides (TFH), with major constituents including quercetin, isorhamnetin and kaempferol, have been demonstrated with most of the bioactive properties of Shaji. In the present study, we evaluated the potential effect of TFH in the restoration of ultimate stress of healing patellar tendon in a well-established gap wound model in rats. A 0.1 mg TFH was injected to wound 1 day after the injury, and the ultimate stress of the healing tendon was measured at day 14 post-injury. The results showed that the ultimate stress of the healing tendon was significantly promoted by injection of TFH, increasing from 30 to 50% as compared to saline control. Excessive fibrotic response was not found in TFH-treated animals, but an enhanced collagen deposition and a better fibre alignment were observed. The results suggest that TFH may improve the ultimate stress of healing tendons at early stages, which implies possible earlier rehabilitation programme and better recovery.

Induction of cortical cataracts in cultured mouse lenses with H-89, an inhibitor of protein kinase A.

PURPOSE: To compare the effects of two serine-threonine protein kinase inhibitors in a mouse lens culture system previously designed to investigate cortical cataracts caused by L-buthionine sulfoximine (BSO), inhibitor of GSH biosynthesis. METHODS: Cataract development in HL-1 medium was evaluated visually or by measurement of lens Na+/K+ ratio through atomic absorption. Protein changes were evaluated by 32P-labeling, 2D-gel electrophoresis, phosphorimaging and mass spectrometry. Results. H-7 (50 microM), inhibitor of protein kinase A (PKA) and protein kinase C (PKC), did not cause cataracts, but inhibited BSO cataract development. By contrast, 25 microM H-89, selective inhibitor of PKA, caused large annular cortical cataracts and 100-fold elevation of Na+/K+ within 30 hr in day 10 lenses, in either the presence or absence of BSO. H-89 cataracts were also seen in day 12 and day 21 lenses. 32P-labeling of day 12 lenses pretreated with H-89 displayed more than 80% decrease in phosphorylation of alphaA crystallin, a known substrate of PKA, in the insoluble protein fraction. 2D-gel electrophoresis of day 12 H-89 cataract lens fractions revealed limited degradation of alpha and beta crystallins, degradation of cytoskeletal proteins, and elevated lens Ca2+ (>4 nmol/mg wet wt.), suggesting Ca2+-activated proteolysis. Conclusions. High Na+/K+ cataracts are induced by H-89, selective inhibitor of PKA, but not by H-7, an inhibitor of both PKA and PKC that impeded BSO-induced Na+/K+ elevation and cataract. These results suggest contrasting effects of PKA and PKC on lens cation transport and cortical cataract development.

Altered patterns of phosphorylation in cultured mouse lenses during development of buthionine sulfoximine cataracts.

Buthionine sulfoximine (BSO), a specific inhibitor of glutathione biosynthesis, induces oxidative cataracts following multiple injections into mice at 1 week of age. Cultures of lenses with (35)S-methionine have previously demonstrated altered patterns of protein biosynthesis that precede and accompany these cataracts. To obtain parallel information about changes in protein phosphorylation during cataract development, lenses from BSO-treated or control mouse pups were cultured for 3 hr at 37 degrees C with (32)P(i), homogenized in phosphate buffer, and resolved by centrifugation into water-soluble (WS) and water-insoluble (WI) fractions. These were characterized by 2D-gel electrophoresis, Coomassie blue staining, phosphorimaging, immunoblotting, and tandem mass spectrometry. Heaviest labelling was in the WI fraction. The labelled 2D-gel spots included: (1) a series of phosphorylated filensins at 95 kDa; (2) a major radioactive spot at 45-50 kDa, slightly anodic to actin and the beaded filament protein, phakinin (CP 49); (3) a phosphorylated betaB1-crystallin, considerably anodic to parent betaB1; (4) an acidic cluster of labelled alphaA-crystallins, phosphorylated in part at serine-148, and (5) a labelled trace alpha crystallin, slightly anodic to alphaB-crystallin. The results confirm previously reported phosphorylations of actin, phakinin, alphaA- and alphaB-crystallin, demonstrate previously unrecognized phosphorylations of filensin and betaB1-crystallin, and provide unequivocal evidence for phosphorylation of alphaA-crystallin at serine-148. The earliest changes in phosphorylation detected after BSO treatment were increased labelling of alphaA- and alphaB-crystallin during cataract stages 1-3, coupled with a general decrease in protein labelling. In stage 5 cataracts, phosphorylated alpha crystallins persisted as the dominant labelled species. However, the major modifications of alphaA-crystallin in advanced BSO cataracts were unlabelled and partially degraded, in contrast to phosphorylated alphaA. It is therefore proposed that phosphorylation of alphaA-crystallin may confer resistance to proteolytic degradation.

Distribution of human lens crystallins and their sulphydryl contents of different age in two-dimension electrophoresis.

PURPOSE: To analyze water-soluble (WS) human lens proteins of fetus, adult and age-related cataract by two-dimensional IEF/SDS-PAGE electrophoresis. METHODS: DACM [N-(7-Dimethylamino-4-methyl-3-coumarinyl) maleimide] was used to determine the lens proteins sulphydryl (SH) content. RESULT: Protein SH contents in WS lens proteins have no significant difference among fetus, adult and age-related cataract lens. This is different from the relative published results obtained in lens proteins of animal cataract model using similar SH detecting methods. CONCLUSIONS: IEF/SDS-PAGE electrophoresis demonstrated that there were much more fragmentation of crystallins during lens development and cataractogenic process. It is suggested that this phenomenon is likely to be due to further conformational changes in the fragmented cyrstallins during aging and cataractogenic process.

Pyridinoline in relation to ultimate stress of the patellar tendon during healing: an animal study.

The ultimate stress of the central one-third of the patellar tendon was studied in a gap wound-healing model in the rat. The specimens were also analyzed for collagen and nonreducible crosslinks, as measured by hydroxyproline and pyridinoline content, respectively. Thirty days after injury, the ultimate stress of the healing patellar tendon was restored to an average of 71% of the control value and remained constant over time. The pyridinoline content of the healing tendon was twice the control value by 30 days after injury and reached a plateau; however, the hydroxyproline content did not change significantly over time. Stepwise regression analysis demonstrated that pyridinoline was a better biochemical marker for ultimate stress than was hydroxyproline. The current study provides insights into the functional behaviour of the healing patellar tendon by establishing the relationship between the two biochemical components and the ultimate stress of the healing patellar tendon. This study also suggests the possibility of using pyridinoline content as an indirect marker of the ultimate stress because in vivo assessment is impossible.

Modifications in lens protein biosynthesis signal the initiation of cataracts induced by buthionine sulfoximine in mice.

Cataract induction in preweanling mice by L-buthionine sulfoximine (BSO), an inhibitor of glutathione biosynthesis, was correlated with perturbations in vitro protein biosynthesis. These were detected by incubation of late precataract and early cataract lenses with 35S-labeled amino acids, followed by dissection of lenses into capsule-epithelium and decapsulated fiber fractions, further processing of the fibers into water-soluble, urea-soluble and urea-insoluble fractions, and analysis by 2D electrophoresis and fluorography. Most of the protein labeling in control lenses was in the water-soluble fiber and capsule-epithelium fractions (80% and 14% of total cpm, respectively). Labeling in all three fiber fractions was decreased by cataract induction. The urea-insoluble fraction displayed a transient increase in labeled high molecular weight basic protein, as labeling of polypeptide monomers decreased. Densitometric analysis of fluorograms from the water-soluble and urea-soluble fiber fractions revealed a sharp decrease in fiber gamma-crystallin polypeptide labeling preceding and accompanying early cataract development, a delayed decrease in labeling of alpha A-crystallin and increased relative percentage of several labeled beta-crystallin polypeptides, especially in the urea-soluble fraction. By contrast with diminished labeling of the fiber fractions during cataract initiation, protein labeling of the corresponding capsule-epithelium fraction was stimulated dramatically and persisted at reduced levels during early opacification (stage 3), when nearly all of the protein labeling in the lens was found in capsule-epithelium. Capsule-epithelium polypeptides showing increased labeling during cataract initiation included alpha A-crystallin, several acidic polypeptides of M(r) = 40-50 kDa and a group of neutral to mildly acidic polypeptides of M(r) = 20-28 kDa. this transient activation, which was relatively non-specific, may relate to previously reported observations of polyribosome accumulation in lens epithelium during initial development of BSO cataracts. The labeled capsule-epithelium preparations are known to include newly differentiating fibers near the lens equator as well as epithelial cells. Both of these cell populations survive in mature BSO cataracts. It is suggested that modifications of the normal pattern of gene expression in the lens may be involved in initiation of the mouse BSO cataract and its subsequent pattern of development.

Assessment of sulfhydryl group in individual rat lens protein subunits during galactose cataract development.

A specific reagent DACM [N-(7-Dimethylamino-4-methyl-3-coumarinyl)maleimide] is used to study the -SH groups in lens proteins of normal and galactose cataractous rats. DACM when reacts readily with -SH groups form strong fluorescent adducts. The two -dimensional electrophoresis with DACM pre-labeled proteins is a simple and sensitive method for detecting -SH groups of protein subunit. In the present study, based on IEF/SDS-PAGE electrophoretically characterized soluble crystallins, describes specific changes in -SH groups of protein subunit during the development of galactose cataract. The contents of -SH groups of crystallins are progressively decreased in cataractous (5+) lens, the reduction of -SH content in alpha- and beta- crystallin protein subunits of the normal and cataractous lens proteins is also noticeable.