BACKGROUND HIV-1 CRF55_01B was first reported in 2013. At present, no report is available regarding this new clade's polymorphisms in its functionally critical regions protease and reverse transcriptase. OBJECTIVE To identify the diversity difference in protease and reverse transcriptase between CRF55_01B and its parental clades CRF01_AE and subtype B; and to investigate CRF55_01B's drug resistance mutations associated with the protease inhibition and reverse transcriptase inhibition. METHODS HIV-1 RNA was extracted from plasma derived from a MSM population. The reverse transcription and nested PCR amplification were performed following our in-house PCR procedure. Genotyping and drug resistant-associated mutations and polymorphisms were identified based on polygenetic analyses and the usage of the HIV Drug Resistance Database, respectively. RESULTS A total of 9.24 % of the identified CRF55_01B sequences bear the primary drug resistance. CRF55_01B contains polymorphisms I13I/V, G16E and E35D that differ from those in CRF01_AE. Among the 11 polymorphisms in the RT region, seven were statistically different from CRF01_AE's. Another three polymorphisms, R211K (98.3%), F214L (98.3%), and V245A/E (98.3 %.), were identified in the RT region and they all were statistically different with that of the subtype B. The V179E/D mutation, responsible for 100% potential low-level drug resistance, was found in all CRF55_01B sequences. Lastly, the phylogenetic analyses demonstrated 18 distinct clusters that account for 35% of the samples. CONCLUSIONS CRF55_01B's pol has different genetic diversity comparing to its counterpart in CRF55_01B's parental clades. CRF55_01B has a high primary drug resistance presence and the V179E/D mutation may confer more vulnerability to drug resistance. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.OBJECTIVE Ischemia-reperfusion (I/R) injury is a pathological feature of ischemic stroke. This study investigated the regulatory role of miR-485-5p in I/R injury. METHODS SH-SY5Y cells were induced with oxygen and glucose deprivation/reoxygenation (OGD/R) to mimic I/R injury in vitro. Cells were transfected with designated constructs (miR485-5p mimics, miR-485-5p inhibitor, lentiviral vectors overexpressing Rac1 or their corresponding controls). Cell viability was evaluated using MTT assay. The concentrations of lactate dehydrogenase, malondialdehyde, and reactive oxygen species were detected to indicate the degree of oxidative stress. Flow cytometry and caspase-3 activity assay were used for apoptosis assessment. Dual-luciferase reporter assay was performed to confirm that Rac family small GTPase 1 (Rac1) was a downstream gene of miR-485-5p. RESULTS OGD/R resulted in decreased cell viability, elevated oxidative stress, increased apoptosis, and downregulated miR-485-5p expression in SH-SY5Y cells. MiR-485-5p upregulation alleviated I/R injury, evidenced by improved cell viability, decreased oxidative markers, and reduced apoptotic rate. OGD/R increased the levels of Rac1 and neurogenic locus notch homolog protein 2 (Notch2) signaling-related proteins in cells with normal miR-485- 5p expression, whereas miR-485-5p overexpression successfully suppressed OGD/R-induced upregulation of these proteins. Furthermore, the delivery of vectors overexpressing Rac1 in miR485-5p mimics-transfected cells reversed the protective effect of miR-485-5p in cells with OGD/R-induced injury. CONCLUSION This study showed that miR-485-5p protected cells following I/R injury via targeting Rac1/Notch2 signaling, suggesting that targeted upregulation of miR-485-5p might be a promising therapeutic option for the protection against I/R injury. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.The pathogenic mechanisms involved in a disastrous scenario following epidural steroid injections (ESI) remain unclarified. Intra-arterial injection of steroids with needle-penetrating vascular injury would be the culprit a particulate medicine elicited a brain or spinal cord strokelike attack. On the other hand, the limited experimental approaches simulating an accidental steroid intra-arterial injection for ESI conflicted in their results hemorrhage vs. ischemia. This article dissects the potential pathogenic mechanisms at a neurovascular unit. Noticeably, a schematic provides an explanation of how emboli formed by particulate steroids elicit either hemorrhagic or ischemic lesion. In addition, development of a rat model with intravertebral artery steroid injection is a proposal to address the unmet need in evaluating steroids and vascular injury in ESI.  https://www.selleckchem.com/products/jtc-801.html  Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.BACKGROUND Diabetes is a metabolic chronic disorder affecting the central nervous system. A growing body of evidence have depicted that high glucose level leads to the activation of the transient receptor potential melastatin 2 (TRPM2) channels. However, there are no studies targeting TRPM2 channels in diabetes-induced cognitive decline using a pharmacological approach. OBJECTIVE The intent of the present study was to investigate the effects of 2- aminoethoxydiphenyl borate (2-APB), a TRPM2 inhibitor, in diabetes-induced cognitive impairment. METHOD Streptozotocin (STZ, 50 mg/kg, i.p.) was used to induce diabetes in rats. Animals were randomly divided into the treatment group, model group and age-matched control and pre se group. 2-APB treatment was given for three weeks to the animals. After 10-days of treatment behavioural parameters were performed. Animals were sacrificed at 10th-week of diabetic induction and the hippocampus and cortex were isolated. After that, protein and mRNA expression study was perfoc rats. Moreover, 2- APB also down-regulated the expression of TRPM2 mRNA and protein in the hippocampus as well as AchE activity in the cortex of diabetic animals as compared to diabetic animals. Moreover, 2-APB treatment also upregulated the CaMKII (Thr-286), GSK-3β (Ser9), CREB (Ser133), and PSD-95 expression and mRNA levels of parvalbumin, calsequestrin, and BDNF while mRNA level of calcineurin A was down-regulated in the hippocampus of diabetic animals. CONCLUSION This study confirms the ameliorative effect of TRPM2 channel inhibitor in the diabetes-induced cognitive deficits. Inhibition of TRPM2 channels reduces the calcium associated downstream signaling and showed a neuroprotective effect of TRPM2 channels in diabetes-induced cognitive impairment. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.