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DNA double-strand breaks (DSBs) are common events that were recognized as one of the most toxic lesions in eukaryotic cells. DSBs are widely involved in many physiological processes such as V(D)J recombination, meiotic recombination, DNA replication and transcription. Deregulation of DSBs has been reported in multiple diseases in human beings, such as the neurodegenerative diseases, with which the underlying mechanisms are needed to be illustrated. Here, we reviewed the recent insights into the dysfunction of DSB formation and repair, contributing to the pathogenesis of neurodegenerative disorders including Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD) and ataxia telangiectasia (A-T).

Alzheimer's disease (AD) is one of the most prevalent neurodegenerative diseases that is characterized by progressive memory loss and two main pathological hallmarks, including the extracellular amyloid plaques and intracellular neurofibrillary tangles. The microtubule-related protein tau is involved in the pathogenesis of many neurological diseases commonly known as tauopathies and is found to be abnormally hyperphosphorylated in AD and accumulated in neurons. Besides hyperphosphorylation, tau also undergoes abnormal glycosylation, ubiquitination, glycation, and other posttranslational modifications. These abnormalities lead to the aberrant aggregation of tau in the synaptic loci in AD. In this review, we highlighted the most recent studies about how tau is abnormally regulated and how those abnormalities play important roles in the pathogenesis of AD.

Aims. We aimed to investigate whether LCZ696 protects against pathological cardiac hypertrophy by regulating the Sirt3/MnSOD pathway. Methods. In vivo, we established a transverse aortic constriction animal model to establish pressure overload-induced heart failure. Subsequently, the mice were given LCZ696 by oral gavage for 4 weeks. After that, the mice underwent transthoracic echocardiography before they were sacrificed. In vitro, we introduced phenylephrine to prime neonatal rat cardiomyocytes and small-interfering RNA to knock down Sirt3 expression. Results. Pathological hypertrophic stimuli caused cardiac hypertrophy and fibrosis and reduced the expression levels of Sirt3 and MnSOD. LCZ696 alleviated the accumulation of oxidative reactive oxygen species (ROS) and cardiomyocyte apoptosis. Furthermore, Sirt3 deficiency abolished the protective effect of LCZ696 on cardiomyocyte hypertrophy, indicating that LCZ696 induced the upregulation of MnSOD and phosphorylation of AMPK through a Sirt3-dependent pathway. Conclusions. LCZ696 may mitigate myocardium oxidative stress and apoptosis in pressure overload-induced heart failure by regulating the Sirt3/MnSOD pathway.

The genus-level recognition of monophyletic short-legged toads ( Brachytarsophrys) has been recently implicated in the taxonomic debate of Megophrys sensu lato. In the present study, Brachytarsophrys is reasonably regarded as a distinct genus based on significant morphological differentiations and recent molecular analyses. Furthermore, a comprehensive review of this genus is performed, with two species groups proposed based on morphological differences and phylogenetic relationships. Particularly, Brachytarsophrys platyparietus is removed as a synonym of Brachytarsophrys carinense and considered a valid species due to significant genetic divergence and distinct morphological differences. In addition, a new species, Brachytarsophrys orientalis sp. nov., is described based on a series of specimens collected from southeastern China. This work takes the member species of the genus Brachytarsophrys to seven, suggesting that the diversity of Brachytarsophrys is underestimated. In addition, the genus levels of other monophyletic groups within the subfamily Megophryinae are discussed.

An excessive amount of adipose tissue surrounding the blood vessels (perivascular adipose tissue, also known as PVAT) is associated with a high risk of cardiovascular disease. ADSCs derived from different adipose tissues show distinct features, and those from the PVAT have not been well characterized. In a recent study, we reported that some ADSCs in the periaortic arch adipose tissue (PAAT) descend from the neural crest cells (NCCs), a transient population of migratory cells originating from the ectoderm. In this paper, we describe a protocol for isolating red fluorescent protein (RFP)-labeled NCCs from the PAAT of Wnt-1 Cre+/-;Rosa26RFP/+ mice and inducing their adipogenic differentiation in vitro. Briefly, the stromal vascular fraction (SVF) is enzymatically dissociated from the PAAT, and the RFP+ neural crest derived ADSCs (NCADSCs) are isolated by fluorescence activated cell sorting (FACS). The NCADSCs differentiate into both brown and white adipocytes, can be cryopreserved, and retain their adipogenic potential for ~3-5 passages. Our protocol can generate abundant ADSCs from the PVAT for modeling PVAT adipogenesis or lipogenesis in vitro. Thus, these NCADSCs can provide a valuable system for studying the molecular switches involved in PVAT differentiation.

Neurotoxicity is one of the major pathological changes in multiple neurological disorders, including Alzheimer's disease (AD) and Parkinson's disease (PD), the second popular neurodegenerative disease in aged people. It is known that the AD and PD share the similar neuropathological hallmarks, such as the oxidative stress, loss of specific neurons, and aggregation of specific proteins. However, there are no effective therapeutic drugs for both AD and PD yet. Oxytocin (OXT) is a small peptide with 9 amino acids that is neuroprotective to many neurological disorders. Whether OXT administration confers neuroprotection to 1-methyl-4-phenyl-1, 2, 3, 6- tetrahydropyridine (MPTP)-induced neurotoxicity in mice are still not known. In this study, we first found that the OXT levels are decreased in MPTP mice. Supplementation with OXT effectively rescues the locomotor disabilities and anxiety-like behaviors in MPTP mice. OXT also alleviates the hyperphosphorylation of α-synuclein at S129 site and the loss of dopaminergic neurons in the substantia nigra pars compacta, as well as the oxidative stress in the MPTP mice, and alleviates both oxidative stress and cell cytotoxicity in vitro. Furthermore, we found that OXT could inhibit the miR-26a/DAPK1 signal pathway in MPTP mice. In summary, our study demonstrates protective effects of OXT in MPTP mice and that miR-26a/DAPK1 signaling pathway may play an important role in mediating the protection of OXT.

Cardiovascular diseases (CVDs) are considered as the major reason for mortality and morbidity worldwide. Substantial evidence suggests that increased oxidative stress plays a significant role in the pathogenesis of CVDs, including atherosclerosis, hypertension, vascular endothelial dysfunction and ischemic heart disease. Cellular oxidative stress results in the release of toxic free radicals by endothelial cells and vascular smooth muscle cells that interact with cell components such as protein, DNA or lipid resulting in cardiovascular pathology. Silymarin has antioxidant activities against CVDs and offers protection against oxidative stress-induced hypertension, atherosclerosis and cardiac toxicity. We present a comprehensive review regarding the oxidative stress and protective effects of silymarin in CVDs management. We also aim to provide mechanistic insight of the mechanisms of silymarin action in oxidative stress-induced CVDs.

Reproductive dysfunction associated with obesity is increasing among women of reproductive age, including infertility and increasing risk of miscarriage. In females, reproductive disorders are linked to declining quality of oocytes. Using a model of diet-induced obesity, we have investigated the possible effects of obesity on oocyte quality, including metabolism, lipid accumulation, ROS levels, meiosis and changes in spindle structure in Metaphase II. Our study showed that obesity induced by a high fat diet can impair oocyte meiosis, destroy spindle assembly, and promote oxidative stress and abnormal mitochondrial distribution. With the addition of resveratrol, the negative impact of diet-induced obesity on the quality of oocytes was alleviated to some extent. In addition, we found that obesity causes mouse oocytes to soften, and resveratrol can restore the zona pellucida of oocytes to the same state as the control group. In conclusion, resveratrol can reverse the adverse effects of obesity on oocytes, which is beneficial for subsequent embryonic development.

Hypertension is considered as the most common risk factor for cardiovascular diseases, also is regarded as a leading cause of the mortality and morbidity worldwide. The mechanisms underlying the pathological process of hypertension are not completely explained. However, there is growing evidence that increased oxidative stress plays an important role in the pathophysiology of hypertension. Several preclinical studies and clinical trials have indicated that antioxidant therapy is important for management of hypertension, using antioxidants compounds such as alpha tocopherol (Vit E) and ascorbic acid (Vit C), polyphenols with others and some antihypertensive drugs that are now in clinical use (e.g. ACEIs, ARBs, novel B-blockers, dihydropyridine CCBs) which have antioxidative pleiotropic effects. The purpose of this review is to highlight the importance of antioxidant therapy for management of oxidative stress induced hypertension. Furthermore, we review the current knowledge in the oxidative stress and its significance in hypertension.

Histone deacetylase 2 (HDAC2) plays a major role in the epigenetic regulation of gene expression. Previous studies have shown that HDAC2 expression is strongly increased in Alzheimer’s disease (AD), a major neurodegenerative disorder and the most common form of dementia. Moreover, previous studies have linked HDAC2 to Aβ overproduction in AD; however, its involvement in tau pathology and other memory-related functions remains unclear. Here, we show that increased HDAC2 levels strongly correlate with phosphorylated tau in a mouse model of AD. HDAC2 overexpression induced AD-like tau hyperphosphorylation and aggregation, which were accompanied by a loss of dendritic complexity and spine density. The ectopic expression of HDAC2 resulted in the deacetylation of the hepatocyte nuclear factor 4α (HNF-4A) transcription factor, which disrupted its binding to the miR-101b promoter. The suppression of miR-101b caused an upregulation of its target, AMP-activated protein kinase (AMPK). The introduction of miR-101b mimics or small interfering RNAs (siRNAs) against AMPK blocked HDAC2-induced tauopathy and dendritic impairments in vitro. Correspondingly, miR-101b mimics or AMPK siRNAs rescued tau pathology, dendritic abnormalities, and memory deficits in AD mice. Taken together, the current findings implicate the HDAC2/miR-101/AMPK pathway as a critical mediator of AD pathogenesis. These studies also highlight the importance of epigenetics in AD and provide novel therapeutic targets.

Background Gut microbes can contribute to their hosts in food digestion, nutrient absorption, and inhibiting the growth of pathogens. However, only limited studies have focused on the gut microbiota of freshwater snails. Pomacea canaliculata is considered one of the worst invasive alien species in the world. Elucidating the diversity and composition of the microbiota in the gut of P. canaliculata snails may be helpful for better understanding the widespread invasion of this snail species. In this study, the buccal masses, stomachs, and intestines were isolated from seven P. canaliculata snails. The diversity and composition of the microbiota in the three gut sections were then investigated based on high-throughput Illumina sequencing targeting the V3-V4 regions of the 16S rRNA gene. Results The diversity of the microbiota was highest in the intestine but lowest in the buccal mass. A total of 29 phyla and 111 genera of bacteria were identified in all of the samples. In general, Ochrobactrum, a genus of putative cellulose-degrading bacteria, was the most abundant (overall relative abundance: 13.6%), followed by Sediminibacterium (9.7%), Desulfovibrio (7.8%), an unclassified genus in the family Aeromonadaceae (5.4%), and Cloacibacterium (5.4%). The composition of the microbiota was diverse among the different gut sections. Ochrobactrum (relative abundance: 23.15% ± 7.92%) and Sediminibacterium (16.95 ± 5.70%) were most abundant in the stomach, an unclassified genus in the family Porphyromonadaceae (14.28 ± 7.29%) and Leptotrichia (8.70 ± 4.46%) were highest in the buccal mass, and two genera in the families Aeromonadaceae (7.55 ± 4.53%) and Mollicutes (13.47 ± 13.03%) were highest in the intestine. Conclusions The diversity and composition of the microbiome vary among different gut sections of P. canaliculata snails. Putative cellulose-degrading bacteria are enriched in the gut of P. canaliculata.

MicroRNAs have been implicated in diverse physiological and pathological processes. We previously reported that aberrant microRNA-124 (miR-124)/non-receptor-type protein phosphatase 1 (PTPN1) signaling plays an important role in the synaptic disorders associated with Alzheimer's disease (AD). In this study, we further investigated the potential role of miR-124/PTPN1 in the tau pathology of AD. We first treated the mice with intra-hippocampal stereotactic injections. Then, we used quantitative real-time reverse transcription PCR (qRT-PCR) to detect the expression of microRNAs. Western blotting was used to measure the level of PTPN1, the level of tau protein, the phosphorylation of tau at AD-related sites, and alterations in the activity of glycogen synthase kinase 3β (GSK-3β) and protein phosphatase 2 (PP2A). Immunohistochemistry was also used to detect changes in tau phosphorylation levels at AD-related sites and somadendritic aggregation. Soluble and insoluble tau protein was separated by 70% formic acid (FA) extraction to examine tau solubility. Finally, behavioral experiments (including the Morris water maze, fear conditioning, and elevated plus maze) were performed to examine learning and memory ability and emotion-related behavior. We found that artificially replicating the abnormalities in miR-124/PTPN1 signaling induced AD-like tau pathology in the hippocampus of wild-type mice, including hyperphosphorylation at multiple sites, insolubility and somadendritic aggregation, as well as learning/memory deficits. We also found that disruption of miR-124/PTPN1 signaling was caused by the loss of RE1-silencing transcription factor protein, which can be initiated by Aβ insults or oxidative stress, as observed in the brains of P301S mice. Correcting the deregulation of miR-124/PTPN1 signaling rescued the tau pathology and learning/memory impairments in the P301S mice. We also found that miR-124/PTPN1 abnormalities induced activation of glycogen synthase kinase 3 (GSK-3) and inactivation of protein phosphatase 2A (PP2A) by promoting tyrosine phosphorylation, implicating an imbalance in tau kinase/phosphatase. Thus, targeting the miR-124/PTPN1 signaling pathway is a promising therapeutic strategy for AD.

To explore the effect of electrical stimulation at auricular points (EAS) combined with sound masking on the expression of cAMP-response element binding protein (CREB), brain-derived neurotrophic factor (BDNF) and tyrosine receptor kinase B (TrkB) in the auditory cortex of tinnitus rats.A total of 27 adult male SD rats were randomly divided into a control group, a model group and an EAS group. The rats in the model group and the EAS group were intervened with intraperitoneal injection of sodium salicylate to induce tinnitus model, while the rats in the control group were intervened with injection of 0.9% NaCl solution. After the model was successfully established, the rats in the EAS group were treated with electrical stimulation at "Shenmen" (TF① Compared with the control group, the GPIAS values in 12 kHz, 16 kHz, 20 kHz and 28 kHz were significantly decreased in the model group (allEAS could improve the GPIAS values of high-frequency background sound in tinnitus rats, which may be related with the upregulation of the BDNF/TrkB/CREB signaling pathway in the auditory cortex, leading to the reversion of the maladaptive plasticity.

To understand the current research focus and trends in the field of snail intestinal flora.The literature focusing on snail intestinal flora and published from 1998 to 2017 were retrieved from the core database of Web of Science. The quantitative analysis of literature was then conducted by using CiteSpace software based on the bibliometricsmethod.The research trends were then summarized systematically, and the potential research fronts and focuses were explored.Totally 139 articles were identified in the field of snail intestinal flora. The top three countries with highest publications included the United States of American, Brazil, and South Korea; while the top three institutions were Kyung Hee University, Osvaldo Cruz Foundation, and Oxford University. Five terms were identified as the key words in this field, including diversity, cellulose,The current research focuses on intestinal flora of snails include the diversity, function and application of intestinal flora.［

Pyrethroid insecticides are commonly used as insecticides and considered to be less toxic to mammals, but may still impair the reproduction of animals and humans. The aim of this research was to evaluate the tendency of deltamethrin induced oxidative stress and its effects on meiosis, apoptosis and autophagy of mouse oocytes in vitro maturation after deltamethrin exposure. Especially, the maturation rate of oocytes decreased significantly after 14 h exposure of deltamethrin in concentration-dependent manners, which was manifested as abnormal spindle morphology and DNA double strand breaks. Oxidative stress was found in mouse oocytes exposed to deltamethrin, as shown by changes in the expression of CAT and SOD2. Our results also show that deltamethrin affects the quality of oocytes by causing abnormal mitochondrial distribution and by decreasing mitochondrial membrane potential. The apoptosis of oocyte regulated by the expression of Bax and Bcl-2 protein was obviously affected by deltamethrin. Compared with the control group, the expression of key regulatory factors in the autophagy pathway, LC3, Atg12, Atg14, and Beclin, increased in the experimental group. In summary, these results revealed that deltamethrin might inhibit the maturation of mouse oocytes and adversely affect the survival of oocytes.

Impairments of dendritic trees and spines have been found in many neurodegenerative diseases, including Alzheimer's disease (AD), in which the deficits of melatonin signal pathway were reported. Melatonin receptor 2 (MT2) is widely expressed in the hippocampus and mediates the biological functions of melatonin. It is known that melatonin application is protective to dendritic abnormalities in AD. However, whether MT2 is involved in the neuroprotection and the underlying mechanisms are not clear. Here, we first found that MT2 is dramatically reduced in the dendritic compartment upon the insult of oligomer Aβ. MT2 activation prevented the Aβ‐induced disruption of dendritic complexity and spine. Importantly, activation of MT2 decreased cAMP, which in turn inactivated transcriptional factor CCAAT/enhancer‐binding protein α(C/EBPα) to suppress miR‐125b expression and elevate the expression of its target, GluN2A. In addition, miR‐125b mimics fully blocked the protective effects of MT2 activation on dendritic trees and spines. Finally, injection of a lentivirus containing a miR‐125b sponge into the hippocampus of APP/PS1 mice effectively rescued the dendritic abnormalities and learning/memory impairments. Our data demonstrated that the cAMP‐C/EBPα/miR‐125b/GluN2A signaling pathway is important to the neuroprotective effects of MT2 activation in Aβ‐induced dendritic injuries and learning/memory disorders, providing a novel therapeutic target for the treatment of AD synaptopathy.

Glyphosate is a high-efficiency, low-toxicity, broad-spectrum herbicide. The residues of glyphosate-based herbicides are frequent pollutants in the environment. However, the effects of glyphosate on oocyte maturation, as well as its possible mechanisms, remain unclear. The present study revealed that mouse oocytes had reduced rates of germinal vesicle breakdown (GVBD) and first polar body extrusion (PBE) after treatment with 500 μM glyphosate. Reactive oxygen species (ROS) were found in mouse oocytes exposed to glyphosate, as shown by changes in the mRNA expression of related antioxidant enzyme genes (cat, sod2, gpx). After 14 h of exposure to glyphosate, metaphase II (MII) mouse oocytes displayed an abnormal spindle morphology and DNA double-strand breaks (DNA-DSBs). Simultaneously, mitochondria showed an aggregated distribution and decreased membrane potential in mouse oocytes exposed to glyphosate. The protein expression levels of apoptosis factors (Bax, Bcl-2) and the mRNA expression levels of apoptosis-related genes (bax, bcl-2, caspase3) were measured by Western blot and qRT-PCR, respectively. Meanwhile, the expression levels of autophagy-related genes (lc3, atg14, mtor) and proteins (LC3, Atg12) were significantly decreased in the glyphosate treatment group compared with the control group. Collectively, our results indicated that glyphosate exposure could interfere with mouse oocyte maturation by generating oxidative stress and early apoptosis.

A new species of the genus Leptolalax is described from the Tengchong Section of Gaoligongshan National Nature Reserve, Tengchong County, Yunnan Province, China. The new species, Leptolalax tengchongensis sp. nov., can be distinguished from its congeners by a combination of the following characters: (1) small size (SVL 23.9-26.0 mm in males, 28.8-28.9 mm in females); (2) dorsal skin shagreened and scattered with fine, round reddish tubercles; (3) toes with rudimentary webbing and narrow lateral fringes; (4) tympanum distinctly discernible, almost entirely black; (5) ventrolateral glands indistinct; (6) flanks with several distinct and large dark blotches; (7) ventral surfaces white, scattered with distinct irregular dark speckling; (8) iris not bicolored, uniformly dark brown and scattered with minute, coppery reticulations throughout. To date, the new species has only been found at its type locality in evergreen broadleaf forests at elevations between 2000-2100 m.

Objective To investigate the effects of probucol on erectile function in streptozotocin-induced diabetic rats and explore the underlying mechanisms. Methods A total of thirty 12-week-old Sprague-Dawley male rats received a 1-time intraperitoneal streptozotocin (60 mg/kg) or vehicle injection after a 12-hour fast. Three days later, the streptozotocin-induced diabetic rats were randomly divided into 2 groups and were treated with daily gavage feedings of probucol at doses of 0 and 500 mg/kg for 12 weeks. A positive control group underwent intraperitoneal injection of saline followed by daily gavage of saline solution. Erectile function was assessed by electrical stimulation of the cavernous nerves with real-time intracavernous pressure measurement. After euthanasia, penile tissue was investigated using immunohistochemistry, Western blot, and ELISA to assess the protein arginine-N-methyltransferase 1/dimethylarginine dimethylaminohydrolase/asymmetric dimethylarginine/nitric oxide synthase metabolism pathway. Superoxide dismutase activity and malondialdehyde levels were detected by colorimetry. We also evaluated penile histological changes such as smooth muscle contents and Masson's trichrome stain. Results Significant recovery of erectile function was observed in the probucol-treated rats than the untreated diabetic rats. The protein expression of dimethylarginine dimethylaminohydrolase and nitric oxide synthase, cyclic guanosine monophosphate concentrations, and superoxide dismutase activity in cavernous tissue of probucol-treated rats were significantly higher than the untreated diabetic rats. The protein expression of protein arginine-N-methyltransferase 1, asymmetric dimethylarginine concentrations, and malondialdehyde levels in cavernous tissue of probucol-treated rats were significantly lower than the untreated diabetic rats. In addition, probucol treatment markedly augments the cavernous smooth muscle content. Conclusion Probucol treatment improves erectile function by restoring endothelial function and preventing cavernous fibrosis in streptozotocin-induced diabetic rats.

A new tree frog species of the genus Liuixalus was described from Heishiding Nature Reserve, Guangdong Province, China based on a combination of morphological characters and molecular phylogenetic analyses. Liuixalus feii sp. nov. is distinguished from its congeners by a combination of following characters: small size (SVL 16.2-17.6 mm in adult males and 18.0-18.7 mm in adult females); snout obtusely pointed; tympanum distinct, about half size of eye diameter; nostril closer to eye than to the tip of snout; fingers free of webbing; toe III longer than toe V; toes weakly webbed; tibiotarsal articulation reaching the naris or loreal; dorsal skin smooth and scattered with fine granulars; a subtle longitudinal median ridge present on dorsum; weak skin folds present on dorsal surface of body and thighs; supratympanic fold distinct and curved; ventral surface dull white with more or less irregular dark spots; iris bicolored. The new species appears to be forest-dependent and to date has only been found on the forest floor in primary forests at elevations between 350-800 m. Based on our molecular analyses, we consider Liuixalus catbaensis as a junior synonym of L. calcarius. Thus, with the description of the new species, the genus Liuixalus hitherto contains five recognized species, four of which are endemic to China.

Species of bent-toed gecko (Cyrtodactylus) in Vietnam have been described at a rate of nearly four species per year since 2007 mostly based on morphological data. A tool that guides species delimitation will accelerate the rate of documentation, and at a time when the recognition of species greatly benefits conservation. We use DNA barcoding using COI (550 bp) to re-examine the levels of genetic divergence and taxonomic status of 21 described species of Vietnamese bent-toed geckos. Tree-based analyses resolve all sampled species and identify potential undescribed taxa. Kimura 2-parameter genetic distances between the described species average 21.0±4.2% and range from 4.3% to 28.7%. Further, our analyses discover two potentially new species from Vietnam, two from Laos and one from China. Herein we describe the new species Cyrtodactylus puhuensis sp. nov. from Vietnam on the basis of both genetics and morphology. Genetically, it differs from the remaining species by an average K2P distance of 24.0±1.8%. Morphologically, the new species is diagnosed by its medium-size (snout-vent length 79.24 mm and tail length 82.59 mm, for the single known individual), in having a series of moderately enlarged transverse subcaudals and a series of moderately enlarged femoral scales that extend from precloacal scales, in possessing femoral scales without pores, with males having five precloacal pores, and in exhibiting 8 supralabials, 10 infralabials, 23 narrow subdigital lamellae on its fourth toe, and 36 transverse ventrals.

The accretion of the Indian subcontinent to Eurasia triggered a massive faunal and floral exchange, with Gondwanan taxa entering into Asia and vice versa. The traditional view on the Indian–Asian collision assumes contact of the continental plates during the Early Eocene. Many biogeographic studies rely on this assumption. However, the exact mode and timing of this geological event is still under debate. Here we address, based on an extensive phylogenetic analysis of rhacophorid tree frogs, if there was already a Paleogene biogeographic link between Southeast Asia and India; in which direction faunal exchange occurred between India and Eurasia within the Rhacophoridae; and if the timing of the faunal exchange correlates with one of the recently suggested geological models. Rhacophorid tree frogs showed an early dispersal from India to Asia between 46 and 57 Ma, as reconstructed from the fossil record. During the Middle Eocene, however, faunal exchange ceased, followed by increase of rhacophorid dispersal events between Asia and the Indian subcontinent during the Oligocene that continued until the Middle Miocene. This corroborates recent geological models that argue for a much later final collision between the continental plates. We predict that the Oligocene faunal exchange between the Indian subcontinent and Asia, as shown here for rhacophorid frogs, also applies for other nonvolant organisms with an Indian–Asian distribution, and suggest that previous studies that deal with this faunal interchange should be carefully reinvestigated.

The bent-toed gecko (Cyrtodactylus wayakonei Nguyen, Kingsada, Rosler, Auer and Ziegler, 2010) has been recorded for the first time in China. Here, we provide descriptions of specimens from Yunnan, China. This species was distinguished from all congeners by the following characteristics: 7-8 supralabials; 9-10 infralabials; dorsal tubercles smooth to slightly keeled; 17-19 rows of dorsal tubercles; 6-8 precloacal pores in both sexes; femoral scales not enlarged; no femoral pores; subcaudals somewhat enlarged and broadened; and tail tubercles flat and smooth.

In order to evaluate the phylogenetic position and validity of Rana altaica, we investigated the phylogeny of brown frogs in Eurasia by Bayesian Inference and Maximum Parsimony analyses of a fragment from the mitochondrial DNA gene Cytochrome b. Both analyses resolved R. altaica as nesting deeply within R. arvalis. Most samples of the nominal R. altaica from the Altai region and specimens from Central Siberia shared a haplotype with R. arvalis based on the network analysis. The matrilineal relationships suggested that R. altaica should be considered as a junior synonym of R. arvalis. Furthermore, our study suggested that the species group division of Chinese brown frogs should be re-evaluated within a phylogenetic context.