Everything below concerns Peptide mapping. We keep the language plain, cite what the science says, and separate well-supported claims from open questions.
Updated 2026-06-08. Numbers and descriptions here follow the published literature rather than marketing material.
Semax is a synthetic heptapeptide with the sequence Met-Glu-His-Phe-Pro-Gly-Pro. It is described in the literature as an analogue of the ACTH(4–10) fragment, a short N-terminal portion of adrenocorticotropic hormone that retains some neurotropic activity without the full hormonal effects of the parent peptide. The molecule carries a methionine residue at the N-terminus and two proline residues near the C-terminus, features that shape both its interactions with receptor systems and its chemical stability. The free peptide corresponds to the formula C37H51N9O10S and a molecular mass near 813.9 Da.
The compound was developed in the 1980s at the Institute of Molecular Genetics in Moscow, where it emerged from research on short ACTH fragments and their effects on the central nervous system. Russian pharmaceutical listings describe it as a nootropic and neuroprotective agent, most often formulated as nasal drops. It is not a marketed medicine in the United States or the European Union, and no pharmacopoeial monograph covers it. Consequently, most published clinical experience with the substance originates from a small number of research centres, mainly in Russia and neighbouring countries.
The mechanisms attributed to semax are inferred from animal and cell studies rather than traced to one confirmed target. The most frequently cited pathway involves increased expression of brain-derived neurotrophic factor and nerve growth factor in hippocampal and cortical tissue. Some work points to engagement of melanocortin receptors, particularly MC4, which the parent ACTH fragment can activate. Effects on dopaminergic and serotonergic signalling have also been reported. No single account explains all observed results, and the relative weight of each pathway remains unsettled.
Published studies examine a fairly narrow set of endpoints. Rodent experiments commonly measure maze learning, infarct volume after induced ischemia, and tissue levels of neurotrophic factors. Clinical reports from Russian centres describe attention, memory and recovery scores in patients after stroke or transient ischemic attack. Most of those human studies are small and few have been repeated by independent groups. Outcome measures differ between studies, which limits direct comparison.
| Property | Value | Notes |
|---|---|---|
| Molecular formula | C37H51N9O10S | Free acid form of the heptapeptide; depends on terminal groups |
| Molecular mass | About 813.9 g/mol | Average mass used for mass spectrometry confirmation |
| Appearance | White to off-white solid | Supplied as a lyophilised powder; hygroscopic |
| Solubility class | Freely soluble in aqueous media | Water, saline, and phosphate buffers; limited organic solubility |
| Typical storage temperature | -20 degrees Celsius | Long term and dry; short working periods may use 2 to 8 degrees Celsius |
Semax 是一种人工合成的七肽，氨基酸序列为 Met-Glu-His-Phe-Pro-Gly-Pro，单字母缩写记作 MEHFPGP。它被归类为促肾上腺皮质激素片段 ACTH(4-10) 的结构类似物，但并不天然存在于生物体内。母体片段 ACTH(4-10) 的序列为 Met-Glu-His-Phe-Arg-Trp-Gly，Semax 替换了中间两个残基，并在羧基端延长了 Pro-Gly-Pro 三肽。这种延长被普遍认为能提升分子对肽酶的耐受性。
该化合物于二十世纪八十年代在俄罗斯被开发，相关工作由俄罗斯科学院分子遗传学研究所的研究团队主导。开发目标并非复制 ACTH 的完整激素活性，而是寻找保留其神经作用方向、同时去除促肾上腺皮质激素释放效应的短肽片段。研究记录显示，这一方向促成了多个相关短肽的合成与筛选，而 Semax 是其中被研究最广泛的一个。当地文献常以 Семакс 这一名称指代它。
Identity and purity of semax are established with reversed-phase high-performance liquid chromatography coupled to ultraviolet detection, usually at 214 nanometres. Mass spectrometry, most often electrospray ionisation in positive mode, confirms the molecular mass and reveals truncated sequences. Amino acid analysis and peptide mapping after enzymatic digestion provide additional structural confirmation. Laboratories typically report purity as the percentage area of the main peak, a figure that does not capture isomeric or oxidised variants unless the method resolves them.
The peptide is prone to several degradation pathways. Oxidation of the methionine residue produces a sulfoxide that elutes close to the parent peak in many chromatographic systems. Hydrolysis of peptide bonds and deamidation of susceptible residues in related sequences also reduce purity over time. Lyophilised material kept dry at minus twenty degrees Celsius and shielded from light is the most stable form commonly described in laboratory practice.
19 genes have been discovered that cause α-DG-related dystrophies, with a wide range of phenotypic effects observed, characterized by brain malformations along with muscular dystrophy. Walker-Warburg syndrome (WWS) is the most severe dystroglycanopathy phenotype, with the POMT1 gene as the first reported causative gene, although there have been 11 additional genes implicated in WWS. These genes include POMT2, FKRP, FKTN, ISPD, CTDC2, TMEM5, POMGnT1, B3GALnT2, GMPPB, B3GnT1, and SGK196, many of which have been identified as involved in other dystroglycanopathies. Patients display muscle weakness and cerebellar and ocular malformations, with a life expectancy of less than 1 year. In 2024, a high-throughput functional assay was developed to measure glycosylation levels and assess the functional impact of variants in the enzymes responsible for the glycosylation of α-DG. An additional dystroglycanopathy phenotype is Fukuyama congenital muscular dystrophy (FCMD) caused by a mutation in the Fukutin (FKTN) gene, which is the second most common type of muscular dystrophy in Japan after Duchenne muscular dystrophy. The founder mutation of FCMD is a 3- kilo base pair retrotransposon insertion in the noncoding region of FKTN, leading to muscle weakness, abnormal eye function, seizures, and intellectual disability. While the exact function of FKTN is unknown, FKTN mRNA is expressed in fetuses in the developing CNS, muscles, and eyes, and is likely necessary for normal development since complete inactivation leads to embryonic death at 7 days.
Loose connective tissue, also known as areolar tissue, is a cellular connective tissue with thin and relatively sparse collagen fibers. They have a semi-fluid matrix with lesser proportions of fibers. Its ground substance occupies more volume than the fibers do. It has a viscous to gel-like consistency and plays an important role in the diffusion of oxygen and nutrients from the capillaries that course through this connective tissue as well as in the diffusion of carbon dioxide and metabolic wastes back to the vessels. Moreover, loose connective tissue is primarily located beneath the epithelia that cover the body surfaces and line the internal surfaces of the body. It is also associated with the epithelium of glands and surrounds the smallest blood vessels. This tissue is thus the initial site where pathogenic agents, such as bacteria that have breached an epithelial surface, are challenged and destroyed by cells of the immune system. In the past, the designations areolar tissue, adipose tissue, and reticular tissue have been listed as subsets of loose connective tissue. However, they are no longer considered subsets of loose connective tissue. Loose connective tissue is a subset of connective tissue proper. Furthermore, areolar tissue is the same as loose connective tissue, adipose tissue is a subset of specialized connective tissue, and reticular tissue is the presence of reticular fibers and reticular cells together forming the stroma of hemopoietic tissue (specifically the red bone marrow) and lymphatic tissue organs (lymph nodes and spleen but not the thymus).
specific heat capacity (cp) Also massic heat capacity. The heat capacity of a sample of a substance divided by the mass of the sample. Informally, it is the amount of heat that must be added to one unit of mass of the substance in order to cause an increase of one unit in temperature. The SI unit of specific heat capacity is joule per kelvin per kilogram (J/K/kg). Specific heat capacity often varies with temperature and with each state of matter.
Sources: en.wikipedia.org
=== SEIR model === For many important infections, there is a significant latency period during which individuals have been infected but are not yet infectious themselves. During this period the individual is in compartment E (for exposed).
24 June – Dunedin Airport receives its first international flight—a Jetstar flight from Gold Coast Airport—since the start of the COVID-19 pandemic in 2020. 25 June – Nelson Hospital switches from coal to landfill gas as part of a nationwide decarbonisation shift. 26 June: A state of emergency is declared in the Wairau-Awatere Ward of Marlborough due to heavy rain. 32 Māori land trusts (representing over 150,000 landowners, hapu (sub-groups) and iwi (tribes) file legal proceedings against the New Zealand Crown at the High Court urging the Government to stop the degradation of fresh water, honour the Treaty of Waitangi and Māori rights over water and geothermal resources. The New Zealand Government passed legislation designating the Independent Children's Monitor as an independent Crown entity, dissolving the Children and Young People's Commission and reinstating the Children's Commissioner. 27 June: A state of emergency is declared in Nelson and Tasman due to heavy rain and flooding . Residents of parts of Spring Creek are asked to evacuate in response to concerns that heavy overnight rain could cause the Wairau River to flood. New Zealand First list Member of Parliament Tanya Unkovich resigns to concentrate on work in the private sector. 28 June – A tornado in Waitara damages 11 homes. 29 June — The Government's sentencing reforms, which reduces sentencing discounts and encourages cumulative sentencing, comes into effect. 30 June – Oji Fibre Solutions ceases paper production operations at its Kinleith Mill in Tokoroa, affecting 230 jobs.
Resting membrane potential The baseline electrical potential across the neuron's membrane when it is not actively sending signals, typically around –70 mV in neurons. Reticular formation A network of nuclei in the brainstem involved in regulating arousal, attention, sleep–wake cycles, and autonomic functions. Retina A thin layer of tissue at the back of the eye that contains photoreceptors and neurons responsible for detecting light and initiating visual processing. Retinotopy An orderly representation of the visual field maintained throughout the visual pathways, including the visual cortex. Retrograde amnesia A type of memory loss where individuals cannot recall past memories prior to a brain injury, while the ability to form new memories may be preserved. Retrograde transport The movement of materials from the axon terminal back to the cell body, typically via dynein motors. Used for recycling vesicles and transporting signals. Rett syndrome A rare neurodevelopmental disorder, primarily affecting females, caused by mutations in the MECP2 gene. Characterized by developmental regression, motor problems, and seizures. Reuptake The process by which neurotransmitters are reabsorbed by the presynaptic neuron after being released, terminating synaptic transmission. Reward system A group of brain structures involved in motivation, pleasure, and reinforcement. Includes the ventral tegmental area, nucleus accumbens, and prefrontal cortex. Rhinal cortex A region of the medial temporal lobe that plays a key role in memory and object recognition.
Sources: en.wikipedia.org
== History == Before the causes of PKU were understood, PKU caused severe disability in most people who inherited the relevant mutations. Nobel and Pulitzer Prize-winning author Pearl S. Buck had a daughter named Carol who lived with PKU before treatment was available, and wrote an account of its effects in a book called The Child Who Never Grew. Many untreated PKU patients born before widespread newborn screening are still alive, largely in dependent living homes/institutions. Phenylketonuria was discovered by the Norwegian physician Ivar Asbjørn Følling in 1934 when he noticed hyperphenylalaninemia (HPA) was associated with intellectual disability. In Norway, this disorder is known as Følling's disease, named after its discoverer. Følling was one of the first physicians to apply detailed chemical analysis to the study of disease. In 1934 at Rikshospitalet, Følling saw a young woman named Borgny Egeland. She had two children, Liv and Dag, who had been normal at birth but subsequently developed intellectual disability. When Dag was about a year old, the mother noticed a strong smell in his urine. Følling obtained urine samples from the children and, after many tests, he found that the substance causing the odor in the urine was phenylpyruvic acid. The children, he concluded, had excess phenylpyruvic acid in the urine, the condition which came to be called phenylketonuria (PKU). His analysis of the urine of the two affected siblings led him to request many physicians near Oslo to test the urine of other affected patients.
==== Reptiles ==== In larger animals, different muscle groups will increasingly require different fiber type proportions within muscle for different purposes. Turtles, such as Trachemys scripta elegans, have complementary muscles within the neck that show a potential inverse trend of fiber type percentages (one muscle has high percentage of fast twitch, while the complementary muscle will have a higher percentage of slow twitch fibers). The complementary muscles of turtles had similar percentages of fiber types.
Ghiorso and co-workers analyzed filter papers which had been flown through the explosion cloud on airplanes (the same sampling technique that had been used to discover 244Pu). Larger amounts of radioactive material were later isolated from coral debris of the atoll, and these were delivered to the U.S. The separation of suspected new elements was carried out in the presence of a citric acid/ammonium buffer solution in a weakly acidic medium (pH ≈ 3.5), using ion exchange at elevated temperatures; fewer than 200 atoms of einsteinium were recovered in the end. Nevertheless, element 99, einsteinium, and in particular 253Es, could be detected via its characteristic high-energy alpha decay at 6.6 MeV. It was produced by the capture of 15 neutrons by uranium-238 nuclei followed by seven beta decays, and had a half-life of 20.5 days. Such multiple neutron absorption was made possible by the high neutron flux density during the detonation, so that newly generated heavy isotopes had plenty of available neutrons to absorb before they could disintegrate into lighter elements. Neutron capture initially raised the mass number without changing the atomic number of the nuclide, and the concomitant beta-decays resulted in a gradual increase in the atomic number:
Sources: en.wikipedia.org
It is described as a synthetic analogue of the ACTH(4–10) fragment, a short segment of adrenocorticotropic hormone. Its sequence differs from that fragment and includes two proline residues, which influence stability and behaviour in solution.
It appears in Russian pharmaceutical listings as a nasal formulation, but it is not an authorised medicine in the United States or the European Union. Outside those markets it is normally encountered as a research chemical rather than a prescription product.
Laboratory and animal work points to melanocortin signalling and changes in neurotrophic factor levels, especially brain-derived neurotrophic factor. The exact receptor targets and the degree to which these findings transfer to humans are still unresolved.
It consists mainly of animal experiments and small clinical reports, with much of the clinical material published in Russian-language journals. Large independent trials are scarce. Separating reliable effects from chance findings is consequently difficult.