Intelligence gene, “Enhancement of memory formation is increased in mice given vorinostat, or by genetic knockout of the HDAC2 gene in mice”

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Treon Verdery

Oct 4, 2022, 4:07:59 AMOct 4
Intelligence genes: There are genes that effect the amount of phosphatidylserine, as well as phosphatidylethanolamine that is produced at the brain, SNPs of these (or gene copy number variations) could be characterized as to their effects on g at humans, and mice engineered to have and make the human highest phosphatidylserine and phosphatidylethanolamine production SNPs (or gene copy number variations) could be measured as to cognitive advantage compared with non genetically modified mice; notably there are numerous items at making phosphatidylserine, described online as a nootropic: production of phosphatidylethanolamine and phosphatidylcholine amounts effect the actual phosphatidylserine amount; diethylaminoethanol is a nootropic, so genes that make phosphatidylethanolamine could have g (like iq) cognitive ability heightening effects complementary or of different kind, or measurably beneficially different than greater phosphatidylserine production

A person blenderizing lkyophilized royal jelly and dissolving the 10HDA in a solvent at the blender could use an evaporable solvent compatible with the 10HDA, a paper online says, “A Quantity of 2000 g of fresh RJ with a moisture content of ∼67% was first extracted with 4000 ml of ethanol by stirring for 2 h at room temperature and then filtered to separate the resulting extract into soluble and insoluble fractions. Another 4000 ml of ethanol was then added to the insoluble fraction and stirred for a further 2 h at room temperature. Insoluble precipitates were removed by filtration, and the supernatant was combined with the soluble fraction from the first extraction and evaporated to dryness. The resulting material (385 g) was then extracted with 2000 ml of water : chloroform (1 : 1). After stirring vigorously for 10 min, the mixture was separated into water and chloroform layers. The chloroform layer was collected and evaporated to dryness (72 g) and extracted with 1000 ml of n-hexane. After stirring vigorously for 10 min, the mixture was separated into hexane-soluble and insoluble fractions by centrifugation and each fraction was evaporated to dryness (yield of each fraction was 5.32 g and 66 g, respectively). 5.32 g of the hexane-soluble fraction was dissolved in n-hexane, applied to a column (41 × 300 mm) of silica gel (BW320MH; Fuji Silysia Chemical Ltd, Aichi, Japan) and then successively eluted with 400 ml of n-hexane and 900 ml of chloroform to yield 10 fractions.” To make 10DHA is it possible to just do the ethanol extraction part if I am willing to put up with 19.25% active material, with some of it (like 6/19.25ths) being 10HDA? Is there a physiologically beneficial alternative to chloroform and hexane? A ketone possibly, I read acetone is physiologically noncompatible, methyl acetate? ethyl acetate, What is most physiologically compatible at 1/100th solvent still at the liposomes?

It is possible that compared with a liposome at royal jelly as well as 10HDA, 10H2DA that a physiological availability heightener could be even more effective, “quercetin, genistein, naringin, sinomenine, piperine, glycyrrhizin and nitrile glycoside have demonstrated capability to enhance the bioavailability”

If royal jelly is completely absent effects on plants, then the 60% of the human genome shared with a plant is an area different than that which royal jelly ingredients cause published longevity, wellness, healthspan benefits, if royal jelly does effect plants, then it is possible a range of libraries of royal jelly chemicals could be screened on plants amplifying affordability and ease of characterization, and providing large n

A screenable library: the first leaves, cotyledons, of plants that are nondifferentiated to my perception are from physiochemically young tissue, noting plants have 60% homologous (same) genes as humans, then it is possible youthification chemicals, that could effect human genetic receptors and phenotypic structures could be at the first leaves, cotyledons, of plants; Getting a bunch of first leaves of plants, from a variety of species, including plants that 96 well plate fish and c elegans often live near, then protein extracting them, solvent extracting them, and water extracting them and screening those proteins, lipids, and water soluble things as libraries at fish and c elegans to find longevity, wellness, and healthspan drugs is a possible longevity technology. A person with $40 experiment would be to grow (sprout) a few hundred cotyledon plants, grind up the cotyledons, and just feed those to c elegans as a % of food, then enumerate the longevity of the c elegans at microsoft office

Somewhat novel to me: is there an edible surfactant, which can dissolve something like 10HDA as well as 10H2DA in water, then have a chemical put at it to “unsurfactantize” it causing a little blob of lipid soluble material at the top

Also, this suggests that at royal jelly, a solvent extraction finds more of something called 10H2DA than 10HDA: “The active fractions assessed by ER binding assay were pooled, evaporated to dryness and dissolved in a small amount of chloroform, followed by recrystalization five times using methanol. The resulting crystal was identified as 24-methylenecholesterol (24MET) by NMR analysis. The solution remaining after isolation of the crystallized material was evaporated to dryness, dissolved in chloroform and then applied to a column (34 × 240 mm) of Sephadex LH-20 (Amersham Bioscience Corp., NJ, USA). The column was eluted with 300 ml of chloroform to yield seven fractions. The active fractions were pooled, evaporated to dryness and identified as 2DEA by NMR analysis. Five grams of the evaporated hexane-insoluble fraction was dissolved in 40% methanol and applied to a column (50 × 280 mm) of ODS (Chromatorex; Fuji Silysia Chemical Ltd). The column was eluted with 40% methanol containing 0.1% trifluoroacetic acid to generate seven fractions. We obtained two active fractions and identified the active compound within these fractions as 10H2DA and 10HDA by NMR analysis. The yields of 24MET, 2DEA, 10H2DA and 10HDA were 1.2 g, 3 mg, 1.65 g and 0.53 g, respectively.” So as I perceive what this says, they solvent extracted 2000 grams of fresh royal jelly and got three times as much 10H2DA as 10 HDA; That has longevity drug development opportunities as mice fed either 10H2DA or 10HDA could have different longevity increases, up from the published 25 (27%), and it is even possible that plant sources of the dfifferently preferrable 10H2DA or 10HDA could be found, bees that make a larger amount of the more longevizing of the two chemicals could be bred; and things like the c elegans 46%/18% longevity increase from 10HDA could be characterized at 10H2DA as well; Notably one of them has a c=c, and the other a c-c, “10HDA is saturated whereas 10H2DA and 2DEA are both unsaturated fatty acids”, that suggests many possible new molecules

I read that 10HDA causes longevity at c elegans from a calorie restriction similar effect, although the c elegans got to eat as much as they liked, they could find out if screening a library of 10H2DA as well as 10HDA variants has an even greater calorie restriction mechanism-possible longevity effect, with different amounts of things like autophagy produced; notably the possibility of making a variety of multiunsaturated, multi c=c at each molecule versions could be beneficial to making this library, and screening it with 96 well plates on the 46% greater longevity c elegans as well as the 18% greater longevity C elegans as well as the unmodified c elegans; That data could then be used to find which new HDA library variants to feed to mice to find out if the published 25(27%) longevity heightening at mice from oral royal jelly, which I now perceive as being at about a 1 part 10HDA to 3 parts 10 H2DA; as previously described, the longevity effects of acetylated HDA, library screened variants, as well as possibly autophagy producing optimized forms of the HDA molecule could be quantified to find acetylated HDA molecule variants that pass the blood brain barrier much more effectively, and mice could be utilized to verify this was cognitively and emotionally, and wellness, and healthspan, and possibly also longevity beneficial from the greater activity at the brain (CNS)

Thre is also the possibility of a completely new drug, some colorants have a bunch of c=c-c=c, and the HDA molecule is linear, it is possible that a non =O variation on 10HDA (or 10 H2DA) that is longevizing could exist. Or if the =O is function-producing, S, Se, or P or N could be tried where the =O is; Also, a person could like comparing the effects of say a 10 C alkane with an OH on a distal part, with a OH(O=c)c=c molecule of any length to find out if the two distal parts of the 10HDA molecule have an separate longevity effects. If it is the OH(O=C)-C=C part then they could just attach that to metformin or rapamycin to make a longevity drug more effective than rapamycin’s 60% increase of longevity; if, just possibly, a 10 C alkane with an OH on it distally is actually longevizing then it is an outside possibility that this could be produced at a yeast culture solution, causing 25-27% or larger amounts of greater longevity at an automatically produced beverage;

Also, what are 10HDA and 10H2DA metabolized into, characterizing those metabolites to find out if they have longevizing effects, different areas of tissue concentration, or completely different drug effects could have longevity technology value, notably there is: cytoplasm metabolism compared with liver metabolism, compared with circulatory system enzyme metabolism each with likely different metabolic products, all of which could be screened for novel higher longevity effects; noting that autophagy happens at the cytoplasm, the 10HDA and 10H2DA cytoplasm metabolites could be particularly likely to be longevity drugs

Royal jelly proteins like royalactin are at a thing I read, published as having a longevity effect, possibly on c elegans, that is different than, and (slightly) contributive to the 10HDA 10H2DA longevity increasing (18-46%) effect (another study possibly, 10-20%); another published paper used a protease to modify royalactin and then (I perceive) measured the effects of the protease treatment on the longevity effects from the modified royalactin, the protease modified royalactin was, to my perception, highly similar to the unmodified royalactin; That brings up doing other modifications to the royalactin protein molecule that could be screened as a library at 96 well plates and the organ9isms like fish and c elegans that I think could live at 96 well plates, aside from the published protease there are numerous ultraffordable enzymes like pepsin, trypsin, chymosin, a variety of others, and notably, vegetable powder treated with alkali tastes different, and to many, more delicious, so there is a range of durable on drying pH modifications to royalactin that could be screened; Also, it could be possible to coat, or react, the outer surface of the royalactin protein with something like an aldehyde that makes it differently reactive, less reactive (possibly more stomach passing), more durable, “rubberier”, online it mentions edible aldehydes, “The aldehyde used should be an edible aldehyde such as vanillin, anisaldehyde or butyraldehyde”; it is possible that like formaldehyde kind of rubberizes, dereactifies and preserves proteins, that the edible aldehydes modfiy royalactin to be stomach passing, enterically functional, as well as have different, quantifiable, longevity, wellness and healkthspan effects; just because the protein goes rubbery is different than it not working as well; screening these edible aldehyde modified royal jelly proteins as both enteric and even direct oral longevity drugs could be beneficial,

Along with liposomes and physiological availability enhancers like piperine, it is possible that gel blobs or easy to make edible jello might heighten absorption of beneficial chemicals and drugs; sodium alginate and calcium chloride combine (2 percent alginate to 98 percent water) to make a gel, it seems possible that there could be jellos, possibly nonprotein jellos, that are still gel at pH 3.5-7.9 that can be poured into a dish and eaten with a spoon, with delicious flavor, while making the drug dissolved in the jello much more physiologically available; this could have application globally as just making some jello might be kind of easy while being a way to distribute and cause to be medically active, a variety of drugs, possibly even antigens, immunizations, and protein or also peptide drugs; edible aldehyde modified protein drugs and antigens for immunization might still be medically functional even though preserved, strengthened, as well as made slightly rubbery with the edible aldhehyde;

A person online basically already thought of it, at fishfood, “A further option would be to include in the pellet mixture material which would effervesce” the recreational fish’ food could contain pH activated colorant that would only be hypervisible to the fish from ph 6.99 to 7, or 7.00 to 7.01, so would harmlessly become transparent at an aquarium, this would though provide a bunch of appetizing visual stimulation to the recreational fish that might then avidly seek and eat the delicious vegetarian or tissue culture based fishfood, I think nonvegetarian food sources are less ethical than vegetarian food sources, and I appreciate and prefer that milk and eggs might be produced with tissue culture technology as well; at humans I strongly support breastfeeding!

Vinyl is C2H3+, it seems like if there were a way to make really hyperaffordable vinyl cations out of either natural ethlene gas or even methane gas that making liquid fuels would be even thriftier;

I can see why a person would make a different, more ordered polymer on purpose and do something with it, but lignosulfates look like you could attach something to them and make a big dendritic chemical, like a catalyst, or a drug at hundreds or thousands or millions of kilogram quantities really fast, “Lignosulfonate have very broad ranges of molecular mass (they are very polydisperse). A range of from 1000–140,000 da has been reported” like, just thinking, if there is a an benzene cycle opener, and online it says there are, that can take apart the benzeneish thing at a lignosulphate then the molecule could do a bunch of new things, an anerobic benzene cycle opening bacterial chemical is published, and aerobic benzene cycle openers are also published, “Aerobic bacteria can break up aromatic rings with oxygenases in a reaction known as oxidative dearomatisation. Such reactions have an excellent thermodynamic, and oxygen atoms from the air are incorporated into the resulting products.”, other benzene cycle openers are also published, so if any of them are ultraffordable enough to use on lignosulphate then that supports the mass production of likely high utility chemicals

It is possible that a genetics of neuroanatomy could have a high numeric correlation with things that humans, that is persons, that is people, that is homo sapiens find preferable; one of these thigns is feeling good; it is possible the genetics of a 99th percentile largeness of size of hippocampus has a numerically predictive relation with the simultaneous experience of being of higher g (intelligence) than the majority of the population as well as feeling good, “The hippocampi of patients who suffer from depression are significantly smaller than those of healthy individuals [13]. This may be due to the decreased neurogenesis in depressed individuals, because hippocampal neurogenesis is reduced by stress [12] and increased by antidepressant treatment [14]. The parallel changes in BDNF levels and neurogenesis in response to stress and antidepressant treatment suggest a positive correlation between the BDNF level and hippocampal neurogenesis.”

Royal Jelly and 10HDA effect on subjective well being like behavior at mice: “RJ (250 mg/kg/day), HDEA (100 or 500 μg/kg/day), or fluvoxamine (1000 μg/kg/day), each dissolved in phosphate-buffered saline (PBS), was injected intraperitoneally into mice once a day for 21 days”

that is RJ 17.5 grams a day at a human, or with mouse compensation dosage, 1.46 grams a day

Also, that is 35000 ug per 24 hours of 10HDA, or about 1/3 of 100,000 ug, which is 100 mg, so about 35 mg of 10HDA per day, with mouse compensation dosage, 2.91 mg of 10HDA/24 hours, they call it HDEA though, at 6/100ths 10HDA per gram of royal jelly, that is only like 50mg of royal jelly lyophilized powder’s 10HDA,

Also, “Alternatively, RJ (2.5 g/kg/day) was orally administered” so that is 175 g of royal jelly per 24 hours at a 70kg human, although with the mouse compensation dosage it is about 14g/24 hours

Possible longevity lipid similar to 10HDA at royal jelly, “Previously we found that medium-chain fatty acids with 8–12 carbons and their esters facilitate the activation (phosphorylation) of ERK 1/2 of cultured embryonic cortical/hippocampal neurons [33].” From what I perceive, they are making 8-12 C lipids with some =O on them, kind of like 10HDA, and noting they have the ability to cause neural actions; further, “ In particular, trans-2-decenoic acid ethyl ester (DAEE) has the most potent activity.”, alsdo, “DAEE increases the expression of mRNAs of BDNF and neurotrophin-3 and the protein content of synapse-specific proteins such as synaptophysin, synapsin-1, and syntaxin”, DAEE as an ethyl ester decanoic acid is kind of like a alternate lipid version of 10HDA notably an ethyl ester; this DAEE chemical could be quantified to find out if it makes mice live longer as the people that wrote the paper note it has the highest neurobeneficial activity; notably they call DAEE “trans-2-decenoic acid ethyl ester” which reminds me of a trans-fatty acid, a chemically constructed trans fat, notably trans fats do not occur naturally, so DAEE has a greater rigidity at the “2” area than a natural decanoic acid, suggesting they (the authors) made a rigid trans fat on purpose as part of creating a more effective molecule, a better than royal jelly lipid lipid, on purpose

Also, at another study with DAEE, “DAEE-treatment (100 μg/kg body weight injected at 0.5, 24, 48, 72 h after PMCAO (a mouse model of the cerebral infarction caused by unilateral permanent middle cerebral artery occlusion (PMCAO)) significantly restored the mice from PMCAO-induced neurological deficits including motor paralysis”, “These results suggest that DAEE has a neuro-protective effect on cerebral infarction”

an image of DAEE: 

suggests that a 70kg mammal dose at 100ug/Kg is 7000ug, or about 7 milligrams at a 70 Kg mammal, notably with mouse compensation factor, a human dose of DAEE is just .583 mg per 70 Kg human, they utilized four after event dosages, so either 28 milligrams or about 2.4 milligrams

also, “we developed trans-2-decenoic acid ethyl ester (DAEE) as a stable and small molecule with BDNF-like activities.” that suggests a modification to DAEE with a blood brain barrier passing moiety, connected with an enzymatically degradeable linker or an active transport moeity could pass the blood brain barrier hundreds or thousands of times more, benefitting well brain function , also DAEE, or a modification might be simultaneously enjoyable and physiologically beneficial, “DAEE behaved like an anxiolytic and ameliorated this characteristic anxiety-like symptom, suggesting that DAEE may be a promising candidate for a novel anxiolytic” Notably as DAEE is similar to 10HDA of royal jelly, and royal jelly causes 25/27% greater mouse longevity, DAEE, possibly depending on what part of the brain it goes to, could be a fun (anxiolytic), cognitively beneficial (BDNF) drug that also creates greater longevity

Some outside of liposome is molecularly active liposomes pass the blood brain barrier, perhaps DAEE could be localized at particular brain areas and transported in larger, oral, amounts with liposomes that have active surface moieties

They made modifications to DAEE that caused greater activity, it is possible making these same modifications tot he 10HDA (and 10H2DA) at royal jelly could cause royal jelly lipids that create even greater longevity increases: “we investigated the protective effect of the ester, thioester, and amide compounds of 2‐decenoic acid derivatives (termed compounds A, B, and C, respectively). The potency of the protective activity against the CORT‐induced depression‐like or anxiety‐like behaviors and the reduction in pERK1/2 level were found to be in the following order: compound B > compound C > compound A.”, also, “treatment with compound B at either 0.3 or 1.5 mg/kg” So it is possible that a thioester or amide of 10HDA could have a greater well being and longevity effect than 10HDA; these are beneficial possible longevity drugs to quantify, also at humans this is a 105 mg/24 hours thioester of deacnoic acid dose, or utilizing mouse compensation factor a 8.3 mg/24 hour human dose;

“Earlier we found that (E)‐2‐ethyl dec‐2‐enoate (trans‐2‐decenoic acid ethyl ester: DAEE” also, based on this: it is possible that a durablized version could actually be a deuterated, mre gradually moving, thus possibly less reactive version, as well as the possibility that a nanosphere or liposome version could omit reacting with all the parts of the body other than the part it was directed to be at, “However, a serious problem has been that the biological activities of DAEE are unstable and influenced by the lot preparation used in experiments (Furukawa S., Iinuma M., Soumiya H., Fukumitsu H. and Furukawa Y. unpubl. results). A primary reason for this instability is thought to be the easy hydrolysis of the ester bond because DAEE has five times higher activity for increasing pERK1/2 levels in vitro than trans‐2‐decenoic acid, the nonester form of DAEE (Hirakawa et al. 2010). DAEE is thought to be a promising lead compound for development of new drugs for treatment of mood disorders; however, it is not considered to be a goal compound.”

Note: I think I saw that there was an April 2019 patent on some variation of DAEE like possibly a thioester, I am really enthused that something that could be a quantitatively mesurable as effective longevity drug might soon be a developed drug;

Nifty thioester as well as amide versions of DAEE, as molecular diagrams, which is kind of like 10HDA at

Note: amazingly, you can just order DAEE online: “Chemical structures of compounds A, B, and C are indicated in Figure 1, as is the structure of (DAEE). DAEE was purchased from Sigma‐Aldrich (St. Louis, MO).”

viewing the images at the paper the thioester and the amide versions of DAEE, although very diferent as molecules are very similar as to anti-stress anxiolytic effect; notably over 14-21 days, at .3 to 1.5 mg/Kg the thioester version of DAEE caused an absence of anxious behavior similar to that of mice who were absent being made anxious

“Healthy animals were not used in the experiments to evaluate the activities of the compounds because (1) 2‐decenoic acid derivatives, which have structures and activities similar to those of compound B, were earlier shown not to affect healthy mice in terms of their depressive or anxious state or level of phosphorylated ERK1/2 in the hippocampus” this could possibly suggest that DAEE as well as things like thioester and amide versions, is absent notable personality modifying effects on well normal mammals, a thing that could be beneficial to some humans; “Each compound (A, B, or C) was orally administered to the mice once a day at a dose of 0.3 or 1.5 mg/kg through a stomach tube.”

A new longevity technology: There are a few ways to think about what they describe, one is that they have located a brain cytoprotein that could be meaningful thoroughout the body, and contribute to longevity effects, like those published about royal jelly, and likely 10HDA; this would be a new longevity protein, and upregulating it, making more of it, creating new longevity genetics with it, finding beneficial SNPs about it, or optimizing gene copy number variations about it could be a new longevity technology; the other possibility is that their decanoic acid thioester DAEE just happens to be anxiolytic, and their protein is just a stress removing thing, “How did 2‐decenoic acid derivatives, including compound B, generate a BDNF‐like signal? Earlier we observed that one of the active 2‐decenoic acid derivatives, DAEE, started increasing the level of phosphorylated ERK1/2 at 15 min after the addition and attained the maximal value at the 2‐h time point when tested on cultured cortical/hippocampal neurons (Makino et al. 2010). Such a gradual increase in activation is unlikely to indicate molecular kinetics produced by a specific interaction between ligand and its specific receptor. We presume that the active compound was incorporated passively into the lipid bilayer of neurons and then interacted with and activated some “protein X” in the neurons. This activated protein X may then have mediated the phosphorylation of particular tyrosine kinases of high‐affinity neurotrophin receptors such as TrkB and TrkC. We have found a candidate of protein X predominantly expressed in neuronal cells and are currently investigating its involvement in the DAEE‐mediated mechanism of actions.”; what the authors think is the protein of action, could also be a new to me longevity gene protein mechanism

Also, there is a patent on DAEE variations: The trans-2-decenoic acid derivative or a pharmaceutically acceptable salt, which is the compound of the present invention, is specifically represented by the general formula (I):

wherein X is a substituent such as a 1-pyrrolidyl, a 3-thiazolizyl, or a piperidino, and the compound is highly useful as a pharmaceutical agent, such as a prophylactic or therapeutic agent for a peripheral nerve disorder

when they say “erk1/2”, “mitogen-activated protein kinases (MAPK)/extracellular signal-regulated kinases (ERK)1/2 [29]. Activated ERK1/2 then passes into the nucleus to activate transcription factors such as cAMP response element binding protein (CREB), leading to regulation of expression of various genes involved in neuronal differentiation, learning, and memory”

In that study we found that (1) DAEE stimulates phosphorylation of ERK1/2 via MEK activation; (2) DAEE activates CREB predominantly through ERK1/2 activation, not through other pathways such as cAMP/protein kinase A; (3) DAEE increases the expression of mRNAs of BDNF and neurotrophin-3 and the protein content of synapse-specific proteins such as synaptophysin, synapsin-1, and syntaxin [33]. From these observations, HDEA was considered to activate ERK1/2 followed by CREB phosphorylation, which might be a common target of BDNF and antidepressants to improve symptoms

Longevity technology: varieties of 10HDA like that at longevizing royal jelly that have 8 or could have 9 C instead, “honeybees (Apis mellifera L.) produce a caste-related blend of functionalized 8-and 10-carbon fatty acids in their mandibular glands”, also, “the resulting 10-carbon hydroxy acids are oxidized in a caste-selective manner, thereby determining many of the functional differences”, so the 8 C versions could possibly have different =O (esters) as well as different -OH locations, these could be tested as to longevity effects on c elegans and vertebrate fish at 96 well plates, then be longevity tested at mice as C8, and also a novel C9 version of the particular versions of the different than 10HDA mandibular gland products bees produce; this could be a few more possible beneficial longevity molecules to screen

Source of a decanoic acid that is bacterial: cis-2-Decenoic acid is a fatty acid made by Pseudomonas aeruginosa. It looks a lot like 10HDA, and makes me think that a slight mutation and winnowing of pseudomonas aeruginosa could produce lots of 10HDA or a variety of other possibly longevizing decanoic acid physiochemicals; also, genetically engineering mammals to produce their own 10DHA or a more effective longevity chemical is a new kind of longevity gene, a modification of C2DA production genetics from P. aeruginosa could be a new longevity chemical producing gene at a variety of organisms and even plants so all those organisms and humans benefit; also, it is possibly a slight variation on this gene could produce the BDNF activity-like, possibly longevizing, 2.9 mg/70Kg human dose DAEE decanoic acid that causes calmness, more effective healing, and exploratory behavior among mice

Longevity drug: Different species of bees make different versions of things like royal jelly, and likely different species of bees have different queen longevity ratios, that suggests there is a longest queen lifespan bee, and she might eat a form of the longest lifespan producing royal jelly; some other bee species and their chemicals are at pherobase,

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