The short version of elevated plus maze fits in a sentence. The long version — which is the one that helps — is below.
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Most published work on selank originates from a small number of research groups in the Russian Federation. A large share of that record appears in Russian-language journals, which limits access for readers who rely on English-indexed databases. Independent replication by laboratories outside the original research network is sparse in publicly available sources. This concentration of origin and language is a frequently noted feature when the compound is summarized in broader reviews of synthetic peptides.
Reported pharmacological effects center on reduced anxiety-like behavior in animal models and on measures of memory and learning. Proposed contributing mechanisms include modulation of GABAergic signaling, shifts in monoamine turnover, and changes in the activity of enzymes that degrade neuropeptides. Effects on the expression of genes linked to neuroplasticity have also been described. No single molecular target is widely accepted, and whether the behavioral findings arise from one pathway or several remains an open question.
Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro. It was designed as a stabilized analogue of tuftsin, a naturally occurring tetrapeptide fragment derived from the immunoglobulin heavy chain. The additional Pro-Gly-Pro segment at the carboxyl terminus is intended to slow enzymatic cleavage. The compound is usually described in the literature as a synthetic peptide with anxiolytic and cognitive-related activity, a label that reflects a research context rather than an approved therapeutic category.
Regulatory treatment varies by jurisdiction. In Russia the compound is a registered prescription product, while in the European Union and the United States it is generally handled as a research chemical without a marketing authorization. Suppliers therefore operate outside pharmaceutical oversight, and buyers rely on supplier documentation for purity and identity claims. Chain of custody and third-party testing are the main verification tools. Analysts note that the absence of a pharmacopoeial monograph for research-grade material limits standardization across vendors.
Purity assessment relies mainly on reverse-phase high-performance liquid chromatography with ultraviolet detection. Because the peptide lacks a strong chromophore, detection often uses backbone absorbance near 214 nm. Identity is confirmed by mass spectrometry, typically electrospray ionization or matrix-assisted laser desorption, comparing the measured mass against the expected value. Amino acid analysis can verify composition after acid hydrolysis. Diastereomer content and residual counterions are reported less often, although both can influence biological assays.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C33H57N11O9 | Derived from the seven-residue sequence |
| Molecular weight | About 751.9 g/mol | Average mass; the monoisotopic value is slightly lower |
| Residue count | Seven amino acids | Thr-Lys-Pro-Arg-Pro-Gly-Pro |
| Parent compound | Tuftsin (Thr-Lys-Pro-Arg) | Selank extends tuftsin at the C-terminus |
| Compound class | Synthetic short peptide | Studied in a research setting; not a licensed drug in most markets |
Reported activity for Selank centers on anxiolytic and nootropic effects. Russian clinical reports describe use in anxiety and in cognitive or attention-related complaints. Most of this evidence comes from studies conducted by the same research groups that developed the peptide. Independent replication in other countries remains limited, and no major Western regulatory agency has approved the compound for any indication. The gap between local reports and external verification is a recurring point in discussions of the peptide.
Tuftsin, the parent structure, is a naturally occurring immunomodulatory tetrapeptide released from the Fc region of immunoglobulin G by spleen enzymes. Selank extends this four-residue sequence with three additional amino acids. The stated rationale is that the added tail slows enzymatic breakdown and may influence receptor interactions. How the full heptapeptide behaves at the molecular level is not firmly established, and proposed mechanisms often involve indirect modulation of neurotransmitter or immune signaling rather than a single defined target.
Proposed mechanisms centre on the GABAergic system. Animal and tissue studies report changes in GABA-A receptor expression and reduced activity of GABA transaminase, the enzyme that degrades GABA. Effects on monoamine turnover, including serotonin and dopamine pathways, are also described, and a separate line of work links the peptide to increased expression of brain-derived neurotrophic factor in hippocampal tissue. Most of these findings come from rodent models and cell preparations. How the individual observations combine into a single coherent mode of action is not settled.
Pharmacokinetic data are sparse and largely derived from animal work. After intranasal administration the peptide appears in plasma within minutes, and reported half-lives are short, on the order of minutes to tens of minutes. Degradation proceeds through ordinary proteolytic cleavage into constituent amino acids and smaller fragments. Direct evidence that intact Selank reaches brain tissue in meaningful amounts is limited, and the extent of blood-brain barrier penetration is debated. Some authors argue that fragments, not the parent peptide, carry much of the observed activity.
Laboratory work relies on standard behavioral paradigms. Rodents are tested in the elevated plus maze, open field, and passive avoidance tasks, with outcomes compared against diazepam or vehicle controls. Intranasal dosing is used most often because it bypasses first-pass metabolism, though intraperitoneal and intravenous routes also appear in published protocols. Biochemical endpoints include tissue BDNF concentrations, cytokine levels, and monoamine metabolites. Human data are limited to small Russian trials reporting reduced anxiety scores; most were not prospectively registered, and few employed independent outcome assessment.
Measuring peptide exposure inside the brain is technically difficult. Selank is degraded rapidly in plasma, and assays must separate intact peptide from fragments, which favors targeted mass spectrometry over immunoassays alone. Reported half-lives are short, on the order of minutes, so effects observed hours later are attributed to downstream signaling rather than to the parent compound. Blood-brain barrier permeability is debated and rarely quantified directly. Gaps include absent dose-response characterization, inconsistent reporting of purity, and almost no pharmacokinetic data from human participants.
Selank is studied chiefly as an animal-model anxiolytic with proposed secondary effects on memory and immune signaling. Reported mechanisms include modulation of the GABA-A receptor complex, inhibition of enkephalin-degrading enzymes, and shifts in monoamine turnover within limbic structures. Some experiments describe increased expression of brain-derived neurotrophic factor in the hippocampus after repeated dosing. No single molecular target has been confirmed, and the peptide does not bind any receptor with the selectivity typical of a conventional small-molecule drug. Mechanism therefore remains a set of hypotheses rather than an established pathway.
Outside its country of origin the compound is generally handled as a research chemical rather than an approved medicine. No regulatory approval from the United States Food and Drug Administration or the European Medicines Agency has been granted for human use. Identity and purity are normally checked by reverse-phase high-performance liquid chromatography, with mass spectrometry used to confirm the molecular mass. Lyophilised material is stored cold and desiccated, and repeated freeze-thaw cycles are avoided.
Published work on this peptide almost always uses intranasal delivery, with drops or a spray applied to the nasal mucosa. Some animal experiments have used subcutaneous or intraperitoneal injection, and a smaller number have compared routes directly. Oral administration is not a focus of the literature, because short peptides of this size are broken down by digestive enzymes and cross intestinal barriers poorly. How much of an intranasal dose reaches the bloodstream intact in humans remains an open question.
Animal studies have examined behaviour in tests of anxiety, memory retention and stress response, and several report changes in neurotrophic or neurotransmitter-related markers. The human evidence base is much smaller, consisting mainly of short trials conducted in Russia with limited reporting in English-language journals. Sample sizes are modest and outcome measures vary between studies, so the findings are best described as preliminary. Independent replication under modern trial standards has not been widely reported.
Emotion focused therapy/Emotionally focused therapy (EFT), not to be confused with Emotional Freedom Techniques, was initially informed by humanistic–phenomenological and Gestalt theories of therapy. "Emotion Focused Therapy can be defined as the practice of therapy informed by an understanding of the role of emotion in psychotherapeutic change. EFT is founded on a close and careful analysis of the meanings and contributions of emotion to human experience and change in psychotherapy. This focus leads therapist and client toward strategies that promotes the awareness, acceptance, expression, utilization, regulation, and transformation of emotion as well as corrective emotional experience with the therapist. The goals of EFT are strengthening the self, regulating affect, and creating new meaning". Similarly to some Psychodynamic therapy approaches, EFT pulls heavily from attachment theory. Pioneers of EFT are Les Greenberg and Sue Johnson. EFT is often used in therapy with individuals, and may be especially useful for couples therapy. Founded in 1998, Sue Johnson and others lead the International Centre for Excellence in Emotion Focused Therapy (ICEEFT) where clinicians can find EFT training internationally. EFT is also a commonly chosen modality to treat clinically diagnosable trauma.
A peptide biosensor is a type of biosensor that uses peptides or short amino acid fragments as the biorecognition element in detecting a specific analyte. The interaction of the peptide with the analyte generates a measurable signal (optical, electrical or mass-based) which is transformed by an appropriate transducer. Peptide biosensor exploits the affinity or ability of the peptide to bind to the target analyte such as proteins, nucleic acid, and metal ions. Unlike the conventional biosensors that employ antibodies, enzymes, whole cells or polymers, peptide-based biosensors use short and specific peptide sequences that have high affinity to the analyte of interest. This technique provides higher stability, specificity, sensitivity, easier synthesis when compared to the traditional biosensors like enzyme-based and antibody-based. Peptides can serve as an ideal substitute for protein as a biorecognition elements (receptor) in biosensors because they share identical chemical structure. They can be synthesized artificially via solid-phase synthesis to provide a specific sequence or screening library of peptides. Some peptide sequences are specific substrate for enzymes and are crucial for enzymatic assays and inhibitor screening This type of biosensor has been increasingly used in medical diagnostics e.g., detection of cancer markers, pathogens, screening small molecule drug, food testing and bioprocess control. Their compatibility and adaptability with various signal transduction methods enables them valuable technique across research and industry
Patella fossa: Shallow saucer-like concavity anteriorly, in which the lens rests, separated by Berger's space Ligamentum hyaloideocapsulare (Wieger's ligament): Circular thickening of vitreous 8–9mm in diameter, delineates the patella fossa Anterior hyaloid: Vitreous surface anterior to ora serrata. Continuous with and invests in the zonular fibres, and extends forward between the ciliary processes Vitreous base: Denser cortical area of vitreous. Firmly attached to the posterior 2mm of the pars plana, and the anterior 2–4mm of retina Posterior hyaloid surface: Closely applied to retinal internal limiting membrane. Firm attachment sites: Along blood vessels and at sites of retinal degeneration Space of Martegioni: A funnel shaped space overlying the optic disc with condensed edge Cloquet's canal: A 1–2 mm wide canal within the vitreous, from the space of Martegioni to the space of Berger, along an S-shaped course mainly below the horizontal. It is labelled "hyaloid canal" in the above diagram. Mittendorf's dot: A small circular opacity on the posterior lens capsule, which represents the site of attachment of the hyaloid artery before it subsequently regressed. Bergmeister's papilla: A tuft of fibrous tissue at the optic disc, which represents a remnant of the sheath associated with the hyaloid artery before it subsequently regressed. Internal structures of the vitreous
== Structure == The ITGA2 gene is located on chromosome 5q11.2 and encodes the integrin alpha-2 (CD49b) protein. This is a type I transmembrane Glycoprotein that belongs to the integrin alpha chain family. The mature α2 subunit associates non-covalently with the β1 integrin subunit to form the α2β1 integrin receptor. This is a major collagen-binding integrin in vertebrates. Integrin α2 is an integrin alpha subunit, so it is made of a large extracellular domain, a single transmembrane domain, and a short cytoplasmic tail. The extracellular region contains an inserted (I) domain, or the αI domain. This is responsible for recognizing and binding collagen molecules within the extracellular matrix. Binding to collagen needs divalent cations such as magnesium (Mg2+) and manganese (Mn2+). This stabilizes the ligand-binding site and regulates receptor affinity. The α2β1 integrin has inactive and active conformations with different affinity for extracellular ligand. Intracellular signaling may lead to conformational changes of the integrin and increase the affinity to ligands (inside-out signaling), whereas ligand binding initiates signaling pathways that influence cell adhesion, migration, proliferation, and survival (outside-in signaling).
=== Spondylodysplastic === Spondylodysplastic EDS (spEDS) is characterized by short stature (progressive in childhood), muscle hypotonia (ranging from severe congenital to mild later-onset), and bowing of limbs. It can be caused by variations in both copies of the B4GALT7 gene. Other cases can be caused by variations in the B3GALT6 gene. People with variations in this gene can have kyphoscoliosis, tapered fingers, osteoporosis, aortic aneurysms, and problems with the lungs. Other cases can be caused by the SLC39A13 gene. Those with variations in this gene have protuberant eyes, wrinkled palms of the hands, tapering fingers, and distal joint hypermobility.
Sources: en.wikipedia.org
In normal bone, fractures occur when there is significant force applied or repetitive trauma over a long time. Fractures can also occur when a bone is weakened, such as with osteoporosis, or when there is a structural problem, such as when the bone remodels excessively (such as Paget's disease) or is the site of the growth of cancer. Common fractures include wrist fractures and hip fractures, associated with osteoporosis, vertebral fractures associated with high-energy trauma and cancer, and fractures of long-bones. Not all fractures are painful. When serious, depending on the fractures type and location, complications may include flail chest, compartment syndromes or fat embolism. Compound fractures involve the bone's penetration through the skin. Some complex fractures can be treated by the use of bone grafting procedures that replace missing bone portions. Fractures and their underlying causes can be investigated by X-rays, CT scans and MRIs. Fractures are described by their location and shape, and several classification systems exist, depending on the location of the fracture. A common long bone fracture in children is a Salter–Harris fracture. When fractures are managed, pain relief is often given, and the fractured area is often immobilised. This is to promote bone healing. In addition, surgical measures such as internal fixation may be used. Because of the immobilisation, people with fractures are often advised to undergo rehabilitation.
An atrophic scar takes the form of a sunken recess in the skin, which has a pitted appearance. These are caused when underlying structures supporting the skin, such as fat or muscle, are lost. This type of scarring is often associated with acne, chickenpox, other diseases (especially Staphylococcus infection), surgery, certain insect and spider bites, or accidents. It can also be caused by a genetic connective tissue disorder, such as Ehlers–Danlos syndrome.
Connective tissue diseases (also termed connective tissue disorders, or collagen vascular diseases), are medical conditions that affect connective tissue. Connective tissues protect, support, and provide structure for the body's other tissues and structures. They hold the body's structures together. Connective tissues consist of two distinct proteins: elastin and collagen. Tendons, ligaments, skin, cartilage, bone, and blood vessels are all made of collagen. Skin and ligaments also contain elastin. These proteins and the surrounding tissues may suffer damage when the connective tissues become inflamed. The two main categories of connective tissue diseases are (1) a set of relatively rare genetic disorders affecting the primary structure of connective tissue, and (2) a variety of acquired diseases where the connective tissues are the site of multiple, more or less distinct immunological and inflammatory reactions. Diseases in which inflammation or weakness of collagen tends to occur are also referred to as collagen diseases. Collagen vascular diseases can be (but are not necessarily) associated with collagen and blood vessel abnormalities that are autoimmune in nature. Some connective tissue diseases have strong or weak genetic inheritance risks. Others may be due to environmental factors, or a combination of genetic and environmental influences.
=== Membranes === Membranes can be either of connective tissue or epithelial tissue. Connective tissue membranes include the meninges (the three membranes covering the brain and spinal cord) and synovial membranes that line joint cavities. Mucous membranes and serous membranes are epithelial with an underlying layer of loose connective tissue.
Sources: en.wikipedia.org
Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro, designed as a metabolically stabilized analogue of the endogenous tetrapeptide tuftsin. It has been studied mainly against anxiety-related and cognitive endpoints rather than as an approved medicine in most jurisdictions.
Tuftsin contains four residues, while selank carries an additional Pro-Gly-Pro segment at the carboxyl end. That extension is intended to reduce enzymatic cleavage. Comparative pharmacokinetic data in humans remain limited.
No single receptor target is widely accepted as the definitive mediator of the reported effects. Proposed contributors include GABAergic modulation, shifts in monoamine turnover, and altered neuropeptide degradation. The mechanism is treated in the literature as unresolved.
Purity is usually reported as an HPLC area percentage, most often measured at 214 nm. Identity is confirmed separately by mass spectrometry. A certificate of analysis should state both the method and the observed value.