Habitat: Cultivated largely in Uttar Pradesh, Punjab, Rajasthan and Bihar.
English: Ash Gourd, White Gourd, Wax Gourd, White Pumpkin.Ayurvedic: Kuushmaanda, Kuush- maandaka, Kuushmaandanaadi.Unani: Pethaa, Mahdabaa, Kaddu- e-Roomi.Siddha/Tamil: Ven-poosani, Saambalpushani.Action: Leaves—cooling, juice rubbed on bruises. Fruit decoction—laxative, diuretic, nutritious, styptic (given for internal haemorrhages and diseases of the respiratory tract.) Juice of fruit— used for treating epilepsy, insanity and other nervous diseases. The ash of fruit rind—applied on painful swellings. Seeds—anthelmintic.
The fruits contain lupeol, beta-sitos- terol, their acetates and several amino acids. The fruit juice produces tran- quilizing activity and mild CNS depressant effect in mice.The roots of mature plant contain a pentacyclic triterpene, which exhibits antiallergic activity against both homologous passive cutaneous ana- phylaxis and delayed hypersensitivity in mice. The fruit beverage contains pyrazine compounds.Isomultiflorenol acetate, a penta- cyclic triterpene, has been isolated as the major constituent of wax coating of fruits.Dosage: Dried pieces of the fruit— 5-10 g (API Vol. IV.) Fruit juice— 10-20 m (CCRAS.)... benincasa hispidaTwo types of sperm cells are produced: one contains 22 autosomes and a Y sex chromosome (see SEX CHROMOSOMES); the other, 22 autosomes and an X sex chromosome. All the ova, however, produced by normal meiosis have 22 autosomes and an X sex chromosome.
Two divisions of the NUCLEUS occur (see also CELLS) and only one division of the chromosomes, so that the number of chromosomes in the ova and sperms is half that of the somatic cells. Each chromosome pair divides so that the gametes receive only one member of each pair. The number of chromosomes is restored to full complement at fertilisation so that the zygote has a complete set, each chromosome from the nucleus of the sperm pairing up with its corresponding partner from the ovum.
The ?rst stage of meiosis involves the pairing of homologous chromosomes which join together and synapse lengthwise. The chromosomes then become doubled by splitting along their length and the chromatids so formed are held together by centromeres. As the homologous chromosomes – one of which has come from the mother, and the other from the father – are lying together, genetic interchange can take place between the chromatids and in this way new combinations of GENES arise. All four chromatids are closely interwoven and recombination may take place between any maternal or any paternal chromatids. This process is known as crossing over or recombination. After this period of interchange, homologous chromosomes move apart, one to each pole of the nucleus. The cell then divides and the nucleus of each new cell now contains 23 and not 46 chromosomes. The second meiotic division then occurs, the centromeres divide and the chromatids move apart to opposite poles of the nucleus so there are still 23 chromosomes in each of the daughter nuclei so formed. The cell divides again so that there are four gametes, each containing a half number (haploid) set of chromosomes. However, owing to the recombination or crossing over, the genetic material is not identical with either parent or with other spermatozoa.... meiosis
Dominant genes A dominant characteristic is an e?ect which is produced whenever a gene or gene defect is present. If a disease is due to a dominant gene, those affected are heterozygous – that is, they only carry a fault in the gene on one of the pair of chromosomes concerned. A?ected people married to normal individuals transmit the gene directly to one-half of the children, although this is a random event just like tossing a coin. HUNTINGTON’S CHOREA is due to the inheritance of a dominant gene, as is neuro?bromatosis (see VON RECKLINGHAUSEN’S DISEASE) and familial adenomatous POLYPOSIS of the COLON. ACHONDROPLASIA is an example of a disorder in which there is a high frequency of a new dominant mutation, for the majority of affected people have normal parents and siblings. However, the chances of the children of a parent with the condition being affected are one in two, as with any other dominant characteristic. Other diseases inherited as dominant characteristics include spherocytosis, haemorrhagic telangiectasia and adult polycystic kidney disease.
Recessive genes If a disease is due to a recessive gene, those affected must have the faulty gene on both copies of the chromosome pair (i.e. be homozygous). The possession of a single recessive gene does not result in overt disease, and the bearer usually carries this potentially unfavourable gene without knowing it. If that person marries another carrier of the same recessive gene, there is a one-in-four chance that their children will receive the gene in a double dose, and so have the disease. If an individual sufferer from a recessive disease marries an apparently normal person who is a heterozygous carrier of the same gene, one-half of the children will be affected and the other half will be carriers of the disease. The commonest of such recessive conditions in Britain is CYSTIC FIBROSIS, which affects about one child in 2,000. Approximately 5 per cent of the population carry a faulty copy of the gene. Most of the inborn errors of metabolism, such as PHENYLKETONURIA, GALACTOSAEMIA and congenital adrenal hyperplasia (see ADRENOGENITAL SYNDROME), are due to recessive genes.
There are characteristics which may be incompletely recessive – that is, neither completely dominant nor completely recessive – and the heterozygotus person, who bears the gene in a single dose, may have a slight defect whilst the homozygotus, with a double dose of the gene, has a severe illness. The sickle-cell trait is a result of the sickle-cell gene in single dose, and sickle-cell ANAEMIA is the consequence of a double dose.
Sex-linked genes If a condition is sex-linked, affected males are homozygous for the mutated gene as they carry it on their single X chromosome. The X chromosome carries many genes, while the Y chromosome bears few genes, if any, other than those determining masculinity. The genes on the X chromosome of the male are thus not matched by corresponding genes on the Y chromosome, so that there is no chance of the Y chromosome neutralising any recessive trait on the X chromosome. A recessive gene can therefore produce disease, since it will not be suppressed by the normal gene of the homologous chromosome. The same recessive gene on the X chromosome of the female will be suppressed by the normal gene on the other X chromosome. Such sex-linked conditions include HAEMOPHILIA, CHRISTMAS DISEASE, DUCHENNE MUSCULAR
DYSTROPHY (see also MUSCLES, DISORDERS OF – Myopathy) and nephrogenic DIABETES INSIPIDUS.
If the mother of an affected child has another male relative affected, she is a heterozygote carrier; half her sons will have the disease and half her daughters will be carriers. The sister of a haemophiliac thus has a 50 per cent chance of being a carrier. An affected male cannot transmit the gene to his son because the X chromosome of the son must come from the mother; all his daughters, however, will be carriers as the X chromosome for the father must be transmitted to all his daughters. Hence sex-linked recessive characteristics cannot be passed from father to son. Sporadic cases may be the result of a new mutation, in which case the mother is not the carrier and is not likely to have further affected children. It is probable that one-third of haemophiliacs arise as a result of fresh mutations, and these patients will be the ?rst in the families to be affected. Sometimes the carrier of a sex-linked recessive gene can be identi?ed. The sex-linked variety of retinitis pigmentosa (see EYE, DISORDERS OF) can often be detected by ophthalmoscopic examination.
A few rare disorders are due to dominant genes carried on the X chromosome. An example of such a condition is familial hypophosphataemia with vitamin-D-resistant RICKETS.
Polygenic inheritance In many inherited conditions, the disease is due to the combined action of several genes; the genetic element is then called multi-factorial or polygenic. In this situation there would be an increased incidence of the disease in the families concerned, but it will not follow the Mendelian (see MENDELISM; GENETIC CODE) ratio. The greater the number of independent genes involved in determining a certain disease, the more complicated will be the pattern of inheritance. Furthermore, many inherited disorders are the result of a combination of genetic and environmental in?uences. DIABETES MELLITUS is the most familiar of such multi-factorial inheritance. The predisposition to develop diabetes is an inherited characteristic, although the gene is not always able to express itself: this is called incomplete penetrance. Whether or not the individual with a genetic predisposition towards the disease actually develops diabetes will also depend on environmental factors. Diabetes is more common in the relatives of diabetic patients, and even more so amongst identical twins. Non-genetic factors which are important in precipitating overt disease are obesity, excessive intake of carbohydrate foods, and pregnancy.
SCHIZOPHRENIA is another example of the combined effects of genetic and environmental in?uences in precipitating disease. The risk of schizophrenia in a child, one of whose parents has the disease, is one in ten, but this ?gure is modi?ed by the early environment of the child.... genetic disorders
Habitat: Cultivated in Uttar Pradesh, Punjab, Maharashtra and Gujarat.
English: Radish.Ayurvedic: Muulaka, Laghu- muulaka, Muulakapotikaa, Visra, Shaaleya, Marusambhava. Pods— Sungraa, Singri, Mungraa.Unani: Muuli, Turb Fajal.Siddha/Tamil: Mullangi.Action: Radish—preparations are used in liver, gallbladder and urinary complaints. Green leaves— diuretic and carminative. Seeds— diuretic, purgative, expectorant.
A decoction of dry radish is given orally in piles. Extract of the dry root is given for hiccough, influenza, dysentery, colic and urinary troubles.Key application: In peptic disorders, especially those related to dyskinesia of the bile ducts; and in catarrhs of the upper respiratory tract. (German Commission E.)The Ayurvedic Pharmacopoeia of India recommends the juice of the whole plant in sinusitis; juice of the root in diseases of the throat and sinusitis; and the seed in amenorrhoea, cough and dyspnoea.The fleshy root and seeds contain trans-4-methyl-thiobutenyl isothio- cyanate glucoside (the pungent principle), cyanidin-5-glucoside-3-sophoro- side, pelargonidin diglycoside, cyani- din diglycoside, 5-methyl-L-cysteine- sulphoxide (methiin), steroidal sa- pogenins and sulphorophene.The enzymes present in the radish are phosphatase, catalase, sucrase, amylase, alcohol dehydrogenase and pyruvic carboxylase.Radish contains caffeic acid and fer- ulic acid which exhibit hepatoprotec- tive and choleretic properties. It contains choline which prevents deposition of fat in liver. Amino acids, or- nithine, citrulline, arginine, glutamic acid and asparatic acid remove toxins from the body and urea acumulation.Radish is a good source of ascorbic acid (15-40 mg/100 g), trace elements include aluminium, barium, lithium, manganese, silicon, titanium, also iodine (upto 18 mcg/100 g) and ascor- bigen.Roots, leaves, flowers and pods are active against Gram-positive bacteria.The seeds are reported to contain a broad spectrum antibiotic, machro- lysin, specific against Mycobacterium tuberculosis. Raphanin, extracted from the seeds, is active against Grampositive and Gram-negative bacteria.A purified basic protein, homologous to nonspecific lipid transfer proteins, from seeds showed antifungal activity.Raphanus caudatus Linn., synonym R. sativus var. caudatus, is known as Rat-Tail Radish.A native to Java, it is cultivated in northern and western India. The root is not used; pods, purple or violet in colour, are consumed for properties attributed to Raphanus sp. These are known as Mungraa or Sungraa.Dosage: Whole plant-20-40 ml juice; root—15-30 ml juice. (API, Vol. II.) Seed—1-3 g powder. (API, Vol. III.)... raphanus sativusSometimes during cell division chromosomes may be lost or duplicated, or abnormalities in the structure of individual chromosomes may occur. The surprising fact is the infrequency of such errors. About one in 200 live-born babies has an abnormality of development caused by a chromosome, and two-thirds of these involve the sex chromosomes. There is little doubt that the frequency of these abnormalities in the early embryo is much higher, but because of the serious nature of the defect, early spontaneous ABORTION occurs.
Chromosome studies on such early abortions show that half have chromosome abnormalities, with errors of autosomes being three times as common as sex chromosome anomalies. Two of the most common abnormalities in such fetuses are triploidy with 69 chromosomes and trisomy of chromosome 16. These two anomalies almost always cause spontaneous abortion. Abnormalities of chromosome structure may arise because of:
Deletion Where a segment of a chromosome is lost.
Inversion Where a segment of a chromosome becomes detached and re-attached the other way around. GENES will then appear in the wrong order and thus will not correspond with their opposite numbers on homologous chromosomes.
Duplication Where a segment of a chromosome is included twice over. One chromosome will have too little nuclear material and one too much. The individual inheriting too little may be non-viable and the one with too much may be abnormal.
Translocation Where chromosomes of different pairs exchange segments.
Errors in division of centromere Sometimes the centromere divides transversely instead of longitudinally. If the centromere is not central, one of the daughter chromosomes will arise from the two short arms of the parent chromosome and the other from the two long arms. These abnormal daughter chromosomes are called isochromosomes.
These changes have important bearings on heredity, as the e?ect of a gene depends not only upon its nature but also upon its position on the chromosome with reference to other genes. Genes do not act in isolation but against the background of other genes. Each gene normally has its own position on the chromosome, and this corresponds precisely with the positon of its allele on the homologous chromosome of the pair. Each member of a pair of chromosomes will normally carry precisely the same number of genes in exactly the same order. Characteristic clinical syndromes, due to abnormalities of chromosome structure, are less constant than those due to loss or gain of a complete chromosome. This is because the degree of deletion, inversion and duplication is inconstant. However, translocation between chromosomes 15 and 21 of the parent is associated with a familial form of mongolism (see DOWN’S (DOWN) SYNDROME) in the o?spring, and deletion of part of an X chromosome may result in TURNER’S SYNDROME.
Non-disjunction Whilst alterations in the structure of chromosomes arise as a result of deletion or translocation, alterations in the number of chromosomes usually arise as a result of non-disjunction occurring during maturation of the parental gametes (germ cells). The two chromosomes of each pair (homologous chromosomes) may fail to come together at the beginning of meiosis and continue to lie free. If one chromosome then passes to each pole of the spindle, normal gametes may result; but if both chromosomes pass to one pole and neither to the other, two kinds of abnormal gametes will be produced. One kind of gamete will contain both chromosomes of the pair, and the other gamete will contain neither. Whilst this results in serious disease when the autosomes are involved, the loss or gain of sex chromosomes seems to be well tolerated. The loss of an autosome is incompatible with life and the malformation produced by a gain of an autosome is proportional to the size of the extra chromosome carried.
Only a few instances of a gain of an autosome are known. An additional chromosome 21 (one of the smallest autosomes) results in mongolism, and trisomy of chromosome 13 and 18 is associated with severe mental, skeletal and congenital cardiac defects. Diseases resulting from a gain of a sex chromosome are not as severe. A normal ovum contains 22 autosomes and an X sex chromosome. A normal sperm contains 22 autosomes and either an X or a Y sex chromosome. Thus, as a result of nondisjunction of the X chromosome at the ?rst meiotic division during the formation of female gametes, the ovum may contain two X chromosomes or none at all, whilst in the male the sperm may contain both X and Y chromosomes (XY) or none at all. (See also CHROMOSOMES; GENES.)... sex chromosomes
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