In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Context: Intraflagellar transport (IFT) is a motility process operating between the ciliary/flagellar (interchangeable terms) membrane and the microtubular axoneme of motile and sensory cilia. Multipolypeptide IFT particles, composed of complexes A and B, carry flagellar precursors to their assembly site at the flagellar tip (anterograde) powered by kinesin, and turnover products from the tip back to the cytoplasm (retrograde) driven by cytoplasmic dynein. IFT is essential for the assembly and maintenance of almost all eukaryotic cilia and flagella, and mutations affecting either the IFT motors or the IFT particle polypeptides result in the inability to assemble normal flagella or in defects in the sensory functions of cilia.', 'We found that the IFT complex B polypeptide, IFT27, is a Rab-like small G protein. Reduction of the level of IFT27 by RNA interference reduces the levels of other complex A and B proteins, suggesting that this protein is instrumental in maintaining the stability of both IFT complexes. Furthermore, in addition to its role in flagellar assembly, IFT27 is unique among IFT polypeptides in that its partial knockdown results in defects in cytokinesis and elongation of the cell cycle and a more complete knockdown is lethal.\Question: Is intraflagellar transport protein 27 a small G protein involved in cell-cycle control?
IFT27, a small G protein, is one of a growing number of flagellar proteins that are now known to have a role in cell-cycle control.

Context: HIV-1-infected and/or immune-activated microglia and macrophages are pivotal in the pathogenesis of HIV-1-associated neurocognitive disorders (HAND). Glutaminase, a metabolic enzyme that facilitates glutamate generation, is upregulated and may play a pathogenic role in HAND. Our previous studies have demonstrated that glutaminase is released to the extracellular fluid during HIV-1 infection and neuroinflammation. However, key molecular mechanisms that regulate glutaminase release remain unknown. Recent advances in understanding intercellular trafficking have identified microvesicles (MVs) as a novel means of shedding cellular contents. We posit that during HIV-1 infection and immune activation, microvesicles may mediate glutaminase release, generating excessive and neurotoxic levels of glutamate.', 'MVs isolated through differential centrifugation from cell-free supernatants of monocyte-derived macrophages (MDM) and BV2 microglia cell lines were first confirmed in electron microscopy and immunoblotting. As expected, we found elevated number of MVs, glutaminase immunoreactivities, as well as glutaminase enzyme activity in the supernatants of HIV-1 infected MDM and lipopolysaccharide (LPS)-activated microglia when compared with controls. The elevated glutaminase was blocked by GW4869, a neutral sphingomyelinase inhibitor known to inhibit MVs release, suggesting a critical role of MVs in mediating glutaminase release. More importantly, MVs from HIV-1-infected MDM and LPS-activated microglia induced significant neuronal injury in rat cortical neuron cultures. The MV neurotoxicity was blocked by a glutaminase inhibitor or GW4869, suggesting that the neurotoxic potential of HIV-1-infected MDM and LPS-activated microglia is dependent on the glutaminase-containing MVs.\Question: Do glutaminase-containing microvesicles from HIV-1-infected macrophages and immune-activated microglia induce neurotoxicity?
These findings support MVs as a potential pathway/mechanism of excessive glutamate generation and neurotoxicity in HAND and therefore MVs may serve as a novel therapeutic target.

Context: BTX-A is the standard treatment for glabellar furrows. However, some individuals have resting glabellar rhytides that are sufficiently deep that they respond poorly to BTX-A alone.', 'To compare the efficacy of BTX-A combined with intradermal Hylan B with the efficacy of BTX-A alone in individuals with moderate to severe glabellar rhytides.', 'This was a retrospective study of 16 subjects with moderate to severe glabellar rhytides. Their response to Hylan B plus BTX-A was compared clinically and photographically to their response to BTX-A alone.', 'All subjects had moderate or severe glabellar rhytides at rest before treatment. After BTX-A alone, none (0%) had achieved no or mild rhytides. After BTX-A and Hylan B injection, only 1 of 16 (6%) had moderate glabellar rhytides, with the remainder (94%) being mild.\Question: Do deep resting glabellar rhytides respond to BTX-A and Hylan B?
Moderate to severe glabellar rhytides were treated better by BTX-A combined with Hylan B injection than by BTX-A alone.