Miracle-dz/UniFAR-FTUs huggingface dataset:
Macroecological patterns of sexual size dimorphism in turtles of the world

Sexual size dimorphism (SSD) is a well‐documented phenomenon in both plants and animals; however, the ecological and evolutionary mechanisms that drive and maintain SSD patterns across geographic space at regional and global scales are understudied, especially for reptiles. Our goal was to examine geographic variation of turtle SSD and to explore ecological and environmental correlates using phylogenetic comparative methods. We use published body size data on 135 species from nine turtle families to examine how geographic patterns and the evolution of SSD are influenced by habitat specialization, climate (annual mean temperature and annual precipitation) and climate variability, latitude, or a combination of these predictor variables. We found that geographic variation, magnitude and direction of turtle SSD are best explained by habitat association, annual temperature variance and annual precipitation. Use of semi‐aquatic and terrestrial habitats was associated with male‐biased SSD, whereas use of aquatic habitat was associated with female‐biased SSD. Our results also suggest that greater temperature variability is associated with female‐biased SSD. In contrast, wetter climates are associated with male‐biased SSD compared with arid climates that are associated with female‐biased SSD. We also show support for a global latitudinal trend in SSD, with females being larger than males towards the poles, especially in the families Emydidae and Geoemydidae. Estimates of phylogenetic signal for both SSD and habitat type indicate that closely related species occupy similar habitats and exhibit similar direction and magnitude of SSD. These global patterns of SSD may arise from sex‐specific reproductive behaviour, fecundity and sex‐specific responses to environmental factors that differ among habitats and vary systematically across latitude. Thus, this study adds to our current understanding that while SSD can vary dramatically across and within turtle species under phylogenetic constraints, it may be driven, maintained and exaggerated by habitat type, climate and geographic location.
Mixed evidence for early bursts of morphological evolution in extant clades

Macroevolutionary theory predicts high rates of evolution should occur early in a clade's history as species exploit ecological opportunity. Evidence from the fossil record has shown a high prevalence of early bursts in morphological evolution, but recent work has provided little evidence for early high rates in the evolution of extant clades. Here, I test the prevalence of early bursts in extant data using phylogenetic comparative methods. Existing models are extended to allow a shift from a background Brownian motion (BM) process to an early burst process within subclades of phylogenies, rather than an early burst being applied to an entire phylogenetic tree. This nested early burst model is compared to other modes of evolution that can occur within subclades, such as evolution with a constraint (Ornstein‐Uhlenbeck model) and nested BM rate shift models. These relaxed models are validated using simulations and then are applied to body size evolution of three major clades of amniotes (mammals, squamates and aves) at different levels of taxonomic organization (order, family). Applying these unconstrained models greatly increases the support for early bursts within nested subclades, and so early bursts are the most common model of evolution when only one shift is analysed. However, the relative fit of early burst models is worse than models that allow for multiple shifts of the BM or OU process. No single‐shift or homogenous model is superior to models of multiple shifts in BM or OU evolution, but the patterns shown by these multirate models are generally congruent with patterns expected from early bursts.
Three-Dimensional Cephalometric Study of Upper Airway Space in Skeletal Class II and III Healthy Patients

Because the pharynx and the dentofacial structures have close relationship, a mutual interaction can be expected to occur between them. The literature presents skeletal malocclusion as etiology for airway morphology changes and/or vice versa. The present three-dimensional cephalometric study from computed tomography scans was carried out to investigate upper airway space in normal nasal breathing patients presenting skeletal pattern of classes II and III. In addition, the statistical analysis was done according to gender criterion. The results revealed that the majority of the airway measurements have not been affected by type of malocclusion. The three-dimensional technology used in this study also allowed the volume and surface area calculations, and no statistical significance was found. The retroglossal width and posterior nasal cavity height mean were larger in males than females in the class II group, but volume and cross-section area were not statistically significant. However, in class III group, although the differences in linear and angular measures means were not significant, the retropalatal volume and retroglossal volume and cross-section area were larger in males. The authors highlight that the evaluation of upper airway space should be an integral part of diagnosis and treatment planning to achieve functional balance and stability of the results.
TNF‐α increases αvβ3 integrin expression and migration in human chondrosarcoma cells

Chondrosarcoma is a type of highly malignant tumour with a potent capacity to invade locally and cause distant metastasis. Chondrosarcoma shows a predilection for metastasis to the lungs. Tumour necrosis factor (TNF)‐α is a key cytokine involved in inflammation, immunity, cellular homeostasis and tumour progression. Integrins are the major adhesive molecules in mammalian cells and have been associated with metastasis of cancer cells. However, the effects of TNF‐α in migration and integrin expression in chondrosarcoma cells are largely unknown. In this study, we found that TNF‐α increased the migration and the expression of αvβ3 integrin in human chondrosarcoma cells. Activations of MAPK kinase (MEK), extracellular signal‐regulating kinase (ERK) and nuclear factor‐κB (NF‐κB) pathways after TNF‐α treatment were demonstrated, and TNF‐α‐induced expression of integrin and migration activity was inhibited by the specific inhibitor and mutant of MEK, ERK and NF‐κB cascades. Taken together, our results indicated that TNF‐α enhances the migration of chondrosarcoma cells by increasing αvβ3 integrin expression through the MEK/ERK/NF‐κB signal transduction pathway. J. Cell. Physiol. 226: 792–799, 2011. © 2010 Wiley‐Liss, Inc.
[Obstructive sleep apnea-hypopnea syndrome: association with gender, obesity and sleepiness-related factors].

OBJECTIVE To study the effects that gender and obesity have on excessive daytime sleepiness (EDS) in individuals with obstructive sleep apnea-hypopnea syndrome (OSAHS), as well as to identify factors associated with EDS in such individuals. METHODS A total of 300 consecutive patients who completed the clinical evaluation satisfactorily and whose polysomnography showed an apnea-hypopnea index (AHI) > 10 events/hour of sleep were selected from a sleep clinic population for inclusion in the study. RESULTS Mean age was 47 +/- 11 years, and mean AHI was 52.1 +/- 29.2 events/hour of sleep. Females presented higher mean age, lower EDS scores and less time in apnea. Mean EDS score was 14.7 +/- 7.2. The EDS score correlated better with body movements (r = 0.43; p < 0.01), respiratory events during sleep (r = 0.40; p < 0.01), duration of apnea (r = 0.40; p < 0.01), peripheral oxygen saturation (SpO2; r = -0.38; p < 0.01) and AHI (r = 0.37; p < 0.01). Mean body mass index (BMI) was 30.2 +/- 5.3 kg/m(2). Overweight, obesity and morbid obesity were observed in 41, 44 and 5.3% of cases, respectively. Disease severity correlated most strongly with BMI (r = 0.51; p < 0.01). CONCLUSIONS Higher mean age, lower EDS scores and less time spent in sleep apnea time in apnea were associated with being female. Fragmented sleep, number/duration of respiratory events during sleep, SpO2 levels and obesity were associated with sleepiness. The BMI had a significant effect on OSAHS severity.
MicroRNA‐26a is a novel regulator of vascular smooth muscle cell function

Aberrant smooth muscle cell (SMC) plasticity has been implicated in a variety of vascular disorders including atherosclerosis, restenosis, and abdominal aortic aneurysm (AAA) formation. While the pathways governing this process remain unclear, epigenetic regulation by specific microRNAs (miRNAs) has been demonstrated in SMCs. We hypothesized that additional miRNAs might play an important role in determining vascular SMC phenotype. Microarray analysis of miRNAs was performed on human aortic SMCs undergoing phenotypic switching in response to serum withdrawal, and identified 31 significantly regulated entities. We chose the highly conserved candidate miRNA‐26a for additional studies. Inhibition of miRNA‐26a accelerated SMC differentiation, and also promoted apoptosis, while inhibiting proliferation and migration. Overexpression of miRNA‐26a blunted differentiation. As a potential mechanism, we investigated whether miRNA‐26a influences TGF‐β‐pathway signaling. Dual‐luciferase reporter assays demonstrated enhanced SMAD signaling with miRNA‐26a inhibition, and the opposite effect with miRNA‐26a overexpression in transfected human cells. Furthermore, inhibition of miRNA‐26a increased gene expression of SMAD‐1 and SMAD‐4, while overexpression inhibited SMAD‐1. MicroRNA‐26a was also found to be downregulated in two mouse models of AAA formation (2.5‐ to 3.8‐fold decrease, P < 0.02) in which enhanced switching from contractile to synthetic phenotype occurs. In summary, miRNA‐26a promotes vascular SMC proliferation while inhibiting cellular differentiation and apoptosis, and alters TGF‐β pathway signaling. MicroRNA‐26a represents an important new regulator of SMC biology and a potential therapeutic target in AAA disease. J. Cell. Physiol. 226: 1035–1043, 2011. © 2010 Wiley‐Liss, Inc.
High glucose alters apoptosis and proliferation in HEK293 cells by inhibition of cloned BKCa channel

It has been reported that diabetic vascular dysfunction is associated with impaired function of large conductance Ca2+‐activated K+ (BKCa) channels. However, it is unclear whether impaired BKCa channel directly participates in regulating diabetic vascular remodeling by altering cell growth in response to hyperglycemia. In the present study, we investigated the specific role of BKCa channel in controlling apoptosis and proliferation under high glucose concentration (25 mM). The cDNA encoding the α+β1 subunit of BKCa channel, hSloα+β1, was transiently transfected into human embryonic kidney 293 (HEK293) cells. Cloned BKCa currents were recorded by both whole‐cell and cell‐attached patch clamp techniques. Cell apoptosis was assessed with immunocytochemistry and analysis of fragmented DNA by agarose gel electrophoresis. Cell proliferation was investigated by flow cytometry assays, MTT test, and immunocytochemistry. In addition, the expression of anti‐apoptotic protein Bcl‐2, intracellular Ca2+, and mitochondrial membrane potential (Δψm) were also examined to investigate the possible mechanisms. Our results indicate that inhibition of cloned BKCa channels might be responsible for hyperglycemia‐altered apoptosis and proliferation in HEK‐hSloα+β1 cells. However, activation of BKCa channel by NS1619 or Tamoxifen significantly induced apoptosis and suppressed proliferation in HEK‐hSloα+β1 cells under hyperglycemia condition. When rat cerebral smooth muscle cells were cultured in hyperglycemia, similar findings were observed. Moreover, the possible mechanisms underlying the activation of BKCa channel were associated with decreased expression of Bcl‐2, elevation of intracellular Ca2+, and a concomitant depolarization of Δψm in HEK‐hSloα+β1 cells. In conclusion, cloned BKCa channel directly regulated apoptosis and proliferation of HEK293 cell under hyperglycemia condition. J. Cell. Physiol. 226: 1660–1675, 2011. © 2010 Wiley‐Liss, Inc.
Knockdown of heme oxygenase‐2 impairs corneal epithelial cell wound healing

Heme oxygenase (HO) represents an intrinsic cytoprotective system based on its anti‐oxidative and anti‐inflammatory properties mediated via its products biliverdin/bilirubin and carbon monoxide (CO). We showed that deletion of HO‐2 results in impaired corneal wound healing with associated chronic inflammatory complications. This study was undertaken to examine the role of HO activity and the contribution of HO‐1 and HO‐2 to corneal wound healing in an in vitro epithelial scratch injury model. A scratch wound model was established using human corneal epithelial (HCE) cells. These cells expressed both HO‐1 and HO‐2 proteins. Injury elicited a rapid and transient increase in HO‐1 and HO activity; HO‐2 expression was unchanged. Treatment with biliverdin or CORM‐A1, a CO donor, accelerated wound closure by 10% at 24 h. Inhibition of HO activity impaired wound closure by more than 50%. However, addition of biliverdin or CORM‐A1 reversed the effect of HO inhibition on wound healing. Moreover, knockdown of HO‐2 expression, but not HO‐1, significantly impaired wound healing. These results indicate that HO activity is required for corneal epithelial cell migration. Inhibition of HO activity impairs wound healing while amplification of its activity restores and accelerates healing. Importantly, HO‐2, which is highly expressed in the corneal epithelium, appears to be critical for the wound healing process in the cornea. The mechanisms by which it contributes to cell migration in response to injury may reside in the cytoprotective properties of CO and biliverdin. J. Cell. Physiol. 226: 1732–1740, 2011. © 2010 Wiley‐Liss, Inc.
Collapse and stability of single- and multi-wall carbon nanotubes

The collapse and stability of carbon nanotubes (CNTs) have important implications for their synthesis and applications. While nanotube collapse has been observed experimentally, the conditions for the collapse, especially its dependence on tube structures, are not clear. We have studied the energetics of the collapse of single- and multi-wall CNTs via atomistic simulations. The collapse is governed by the number of walls and the radius of the inner-most wall. The collapsed structure is energetically favored about a certain diameter, which is 4.12, 4.96 and 5.76 nm for single-, double- and triple-wall CNTs, respectively. The CNT chirality also has a strong influence on the collapsed structure, leading to flat, warped and twisted CNTs, depending on the chiral angle.
Skull Indices in a Population Collected From Computed Tomographic Scans of Patients with Head Trauma

Background: It is important to find out the skull's anatomic indices with computed tomography (CT), especially the skull's dimensions according to the patients age and sex, because it can give important results in neurosurgery. We will also describe the skull's parameters among the Kerman population. Method: Of the 2000 CT scans taken after head trauma injury in Kerman province from June 2002 to September 2006, we analyzed 1034 good quality films. The most frequent skull dimensions were measured on each film, and the data were computed and analyzed to assess the cranial indices in various ages and sexes. Two types of classifications were carried out: classic method, which uses cranial indices, and posterior fossa angle dimensions as an alternative method. Skull dimensions were statistically analyzed between groups, and any difference greater than 0.05 was considered significant. Results: Of the 1034 films, 871 films belonged to the men and 184 to the women at age older than 5 years and younger than 70 years. Most of the CT films belonged to the patients with age older than 20 years and younger than 40 years in both sexes. Although the rates of various skull types were different according to the method of classification, the most frequent skull type was dolichocephalic followed by mesocephalic and brachycephalic in both sexes. In addition, in both sexes, the frequency of dolichocephaly was greater in children than adults, but brachycephaly was more frequent in adults than children. Conclusions: With CT scans as an accurate and suitable source of anthropometric evaluation of body dimensions, we found that, in our population, the most frequent skull type is dolichocephalic followed by mesocephalic, which seems to be closer to the Anglo-Saxon population considering the rates of dolichocephaly and mesocephaly.
Epidermal growth factor increases clathrin‐dependent endocytosis and degradation of claudin‐2 protein in MDCK II cells

Epidermal growth factor (EGF) decreases the mRNA and protein levels of claudin‐2 (CLDN2) in Madin–Darby canine kidney (MDCK) II cells. Here we examined whether EGF affects the stability and intracellular distribution of CLDN2 protein. EGF decreased surface and total levels of CLDN2, which was inhibited by U0126, a MEK inhibitor. CLDN2 was co‐localized at the tight junctions (TJs) with ZO‐1, a scaffolding protein. The fluorescence signal for CLDN2 disappeared on treatment with EGF, which was inhibited by U0126. EGF accelerated the decrease in CLDN2 in the presence of cycloheximide, a translation inhibitor, indicating that EGF reduces the stability of the protein. Chloroquine, a lysosomal protease inhibitor, blocked the EGF‐induced decrease in CLDN2 protein and caused the co‐localization of CLDN2 with Lamp‐1, a marker of lysosome. Monodancylcadaverine, an inhibitor of endocytosis, and clathrin siRNA blocked the EGF‐induced decrease in CLDN2 and the translocation of CLDN2 from the TJs to the lysosome. EGF increased the association of CLDN2 with clathrin and adaptin α which was inhibited by U0126. These results suggest that EGF accelerates clathrin‐dependent endocytosis and lysosomal degradation of CLDN2 protein mediated by the activation of a MEK/ERK pathway. J. Cell. Physiol. 226: 2448–2456, 2011. © 2010 Wiley‐Liss, Inc.
Peritoneal Dialysis: A Tool in Veterinary Critical Care

Summary Peritoneal dialysis is an effective modality for the treatment of acute and chronic renal failute, specific intoxications, electrolyte abnormalities, and fluid overload. This review of peritoneal dialysis as it applies to the veterinary critical care setting includes: the indications and contraindications for dialysis; selection and placement of peritoneal catheters; description of the dialysis delivery technique; considerations for monitoring the dialysis patient and treatment of common complications of dialysis therapy. If appropriately applied, peritoneal dialysis is a viable treatment tool in veterinary critical care.
Macrophage‐induced expression and release of matrix metalloproteinase 1 and 3 by human preadipocytes is mediated by IL‐1β via activation of MAPK signaling

Obesity is associated with a chronic low‐grade inflammation and increased macrophage infiltration in adipose tissue. Matrix metalloproteinases (MMPs) are involved in adipose tissue remodeling and inflammatory responses in obesity. This study investigated whether macrophage‐derived factors modulate expression and secretion of MMP1 and MMP3 in human preadipocytes. The potential mediators and signaling pathways were also explored. MMP1 and MMP3 were primarily expressed and secreted by preadipocytes and dramatically reduced post‐differentiation. Preadipocytes were incubated with RPMI 1640 medium (control) or THP‐1 macrophage‐conditioned (MC) medium (25% and 100%) for 24 h. MC medium markedly increased mRNA levels of MMP1 (up to 122‐fold) and MMP3 (up to 59‐fold), as well as protein release of MMP1 (up to 378‐fold) and MMP3 (up to 10‐fold) in a dose‐dependent manner. Treatment with IL‐1β or TNFα, the major products of macrophages, also induced MMP1 and MMP3 secretion by preadipocytes. Neutralizing IL‐1β abolished the induction of MMP1 and MMP3 in preadipocytes by MC medium while the effects of TNFα neutralization were modest. Furthermore, MC medium or IL‐1β led to the phosphorylation of p38, ERK and JNK MAPKs. Inhibition of p38, ERK and JNK reversed the stimulatory effects of MC or IL‐1β on MMP1 and MMP3 production. MC medium and IL‐1β also activated NF‐κB p65 whereas reduced IκBα protein expression in preadipocytes. These results suggest that macrophage accumulation in adipose tissue has a central role in stimulating MMP1 and MMP3 production by preadipocytes, and this is partially mediated by IL‐1β via activation of the MAPK and NF‐κB signaling pathways. J. Cell. Physiol. 226: 2869–2880, 2011. © 2011 Wiley‐Liss, Inc.
Norepinephrine‐induced diastolic dysfunction with aortic valve opening under calcium‐loading in rats

Heart failure associated with a high plasma level of norepinephrine (NE) has an extremely poor prognosis with NE being the most powerful predictor of all‐cause mortality. An increase in the diastolic intracellular calcium level (Ca2+) occurs in left ventricular dysfunction; however, the cause‐and‐effect relationships among Ca2+loading, high plasma NE, and an increase in diastolic ventricular pressure is unclear. Here, we examined the relationship between diastolic dysfunction and NE with and without Ca2+loading in rats. Animals were studied in four groups: Ca2+loading for 45 min (Ca2+group), NE alone for 25 min (30 µg/kg/min NE for 25 min; NE group), Ca2+loading and NE for 25 min after Ca2+loading (Ca2+‐NE group), and a vehicle group. Hemodynamics were examined using a micromanometer‐tipped pressure catheter, and diastolic function was studied using Doppler echocardiography. Significantly increased left ventricular end‐diastolic pressure (LVEDP) and decreased E and Ea waves and deceleration time (DCT) were found in the Ca2+‐NE group, compared with the Ca2+and NE groups. There were no changes in left ventricular pressure (LVP) and LV ejection fraction (EF) among the four groups. NE‐induced diastolic contracture (NEIDC) with aortic valve opening occurred in the diastole when LVP overshot the aortic pressure after co‐administration of NE and Ca2+after Ca2+loading, and pulmonary hemorrhage was observed in all animals of the Ca2+‐NE group. The results support the suggestion that NE may be an important factor in the development of diastolic dysfunction in ischemic heart disease. Drug Dev. Res. 67:511–518, 2006. © 2006 Wiley‐Liss, Inc.
Stereolithography: A Method for Planning the Surgical Correction of the Hypertelorism

Hypertelorism is a deformity characterized by an increase in interorbital distance. The treatment can be orbital mobilization, or if the malformation goes along with occlusal alterations, the indicated treatment is a facial bipartition with hemifacial rotation. The intention of the present study was to describe a surgical planning technique in locating the anatomic points and planes on a stereolithographic model of a patient with 0-14 fissure and its surgical application.
Titin and ryanodine receptor antibodies and neuromuscular involvement in myasthenia gravis

Of sera of patients with myasthenia gravis (MG), 30% contains titin and ryanodine receptor (RyR) antibodies. In early-onset MG (i.e., before 50 years of age), the presence of titin antibodies strongly suggests a thymoma. Late-onset MG comprises one MG group, characterized by a broad antimuscle immune response, including both titin and the acetylcholine receptor (AChR). Another group is preferentially associated with the HLA-A3, B7 and DRw2 antigens, representing a delayed early-onset of the disease that has a selective AChR immune response. The presence of titin and RyR antibodies is associated with more severe disease. Titin antibodies may, in some patients with rippling muscle disease, affect the contractile machinery of myofibers, thereby affecting their mechanical sensitivity. It is not known whether this occurs in MG. RyR antibodies may impair excitation–contraction coupling and contribute to muscle weakness in MG patients. Titin antibodies may serve as tumor markers in early-onset MG patients.