Journal articles: 'Inheritance of loss'

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Cheuse, Alan, and Kiran Desai. "The Inheritance of Loss." World Literature Today 80, no. 4 (2006): 36. http://dx.doi.org/10.2307/40159138.

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Goldsmith, Jo, and Helena Cowen. "The inheritance of loss." Journal of Child Psychotherapy 37, no. 2 (June 30, 2011): 179–93. http://dx.doi.org/10.1080/0075417x.2011.581473.

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Xu, Shiyin. "Cultural Trauma in the Inheritance of Loss." Review of Educational Theory 3, no. 4 (November 4, 2020): 64. http://dx.doi.org/10.30564/ret.v3i4.2414.

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Cultural trauma appears when a collectivity of human beings suffers sudden and rapid social change, touching the core of their inner sense. This paper analyzes cultural trauma in the precise time in that novel according to a classification of the Cultural Trauma theory and presents various strategies to cope with trauma. The whole process of cultural trauma reveals the complicated background then. Confronting ethic problems in displacement, tackling pertinent issues of the globalizing world and struggling with the lingering colonial effects of Britain in India, the novel depicts a special historical scene, implying the ways of living and enlightening today’s loss during the period of inheritance.

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Abraham, Abraham Panavelil. "Postcolonial dilemmas in Kiran Desai’s The Inheritance of Loss." IJOHMN (International Journal online of Humanities) 3, no. 5 (October 25, 2017): 15. http://dx.doi.org/10.24113/ijohmn.v3i5.37.

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The paper will try to analyze Kiran Desai’s Booker winning novel The Inheritance of Loss as story dealing primarily about the problems of migration faced by her characters, their tensions and dilemmas. One of the major concerns of diasporic literature is the problem of exile, displacement and the resulting consequences. Uprooting from one’s own home land is an agonizing process that brings numerous material and emotional traumas in the process of re-rooting in an alien land. The characters are often victims of circumstances and by the time they realize the problems, they are exhausted, miserable and frustrated. Even when they come back after their traumatic experiences, like the Judge in the novel, they often develop a sense of distrust and anger. They are in a state of confusion from which they find it difficult to come out. The paper will focus on the experiences of some of the characters in the novel – Jemubhai Patel, the Judge, and Biju, the son of Judge’s cook who is the central character of the novel. The book seems to suggest that true happiness does not lie in material wealth or comforts, but in one’s own dignity, identity and sense of belonging. In the novel, the characters especially Biju has to undergo number of traumatic experiences that brought a lot of material loss, but he has a spiritual gain- the realization of what brings true joy in life. Keywords: Alienation, Assimilation, Diaspora, Hybridization, , Identity, Immigrant, , Postcolonial

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Wenzel, W. G. "The inheritance of percentage moisture loss in sorghum leaves." South African Journal of Plant and Soil 5, no. 2 (January 1988): 111–13. http://dx.doi.org/10.1080/02571862.1988.10634265.

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Sabo, Oana. "Disjunctures and diaspora in Kiran Desai’sThe Inheritance of Loss." Journal of Commonwealth Literature 47, no. 3 (August 14, 2012): 375–92. http://dx.doi.org/10.1177/0021989412450697.

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Di Tullio, Maria Camilla. "Traditional Hindu Elements in Kiran Desai’s The Inheritance of Loss." Le Simplegadi, no. 18 (November 2018): 180–90. http://dx.doi.org/10.17456/simple-106.

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Adriana, Selma Valeska, and Ira Rasikawati. "TRANSCULTURALISM AS CONVEYED IN KIRAN DESAI’S THE INHERITANCE OF LOSS." Journal of Language and Literature 18, no. 1 (April 9, 2018): 57–68. http://dx.doi.org/10.24071/joll.2018.180108.

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Spielman, David Wallace. "“Solid Knowledge” and Contradictions in Kiran Desai'sThe Inheritance of Loss." Critique: Studies in Contemporary Fiction 51, no. 1 (January 2010): 74–89. http://dx.doi.org/10.1080/00111610903249872.

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Alkhodairy, Batool. "A Postcolonial Reading of Kiran Desai's The Inheritance of Loss." Arab World English Journal, no. 220 (November 15, 2018): 1–32. http://dx.doi.org/10.24093/awej/th.220.

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Hasanthi, D. R. "The Mimic Man in Kiran Desai’s The Inheritance of Loss." Shanlax International Journal of English 9, no. 2 (March 1, 2021): 48–57. http://dx.doi.org/10.34293/english.v9i2.3737.

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Spread over continents, countries and cultures, Kiran Desai’s The Inheritance of Loss (2006) takes us on a tour de force into the realms of multiculturalism and hybridity in Indian culture. It focuses on the changing face of India, amidst East - West encounter, globalization and glocalization. The novel as a postcolonial text puts forth, the authority politics of cultural imperialism, even after the independence of India. This paper appraises the novel using Homi. K. Bhabha’s theory of mimicry, hybridity and ambivalence. It concentrates on the mimic man of the novel Judge Jemubhai Patel. This paper focuses on the hybridization of culture along with the making of reformed hybrids who are in a constant conflict with their identity, language and culture on account of the praxis between the culture of the colonized and the colonizer during and after colonization of the colonized. This paper recommends proper mapping of mimicry and hybridity with indigenous culture, values and ethics. It advocates sowing and stringing in cultural amalgamation and westernization in indigenous Indian culture and ethos for a better life and better Indian society.

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Longhitano, Silvia Bragagnolo, and Décio Brunoni. "Genetic hearing loss: a study of 228 Brazilian patients." Genetics and Molecular Biology 23, no. 1 (March 2000): 25–27. http://dx.doi.org/10.1590/s1415-47572000000100004.

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We studied 228 patients, with suspected or confirmed genetic hearing loss, in order to determine the clinical and genetic diagnoses and etiology of each case. Deafness with no associated abnormalities was found in 146 patients (64%) belonging to 112 families. Syndromic deafness was diagnosed in 82 patients (36%) belonging to 76 families. The genetic etiology was as follows: autosomal recessive inheritance in 40.8% of syndromics and non-syndromics, autosomal dominant inheritance in 13.2% and X-linked recessive in 1.3%. In 44.7% of the cases, the etiology of the hearing loss could not be determined. Monogenic causes are the most possible etiology in the latter cases. Parental consanguinity was found in 22.4% of the cases, and deafness was bilateral, profound and neurosensorial in 47.4% of the patients. An early onset of hearing loss (< 2 years of age) occurred in 46.5% of the cases. These results are similar to previous literature reports.

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R, Sumathi, and Midhun Leo James. "MULTICULTURALISM AND ASPECTS OF GLOBALISATION IN KIRAN DESAI’S INHERITANCE OF LOSS." Kongunadu Research Journal 6, no. 1 (June 30, 2019): 8–11. http://dx.doi.org/10.26524/krj277.

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Indian English Literature pertains to the body of work by writers from India, who pen strictly in the English language and whose native or co-native language could be one of the numerous regional and indigenous language of India. English literature in India is also intimately linked with the works of associates of the Indian Diaspora. Among other writers, Kiran Desai is one of the most renowned writers in the Indian English Literature. With Kiran Desai, a literary tradition is reborn. One of the major themes in the novel is multiculturalism. Multiculturalism relates to communities containing multiple cultures. The term is used in two broad ways, either descriptively or normatively. As a descriptive term it usually refers to the simple fact of cultural diversity. It is generally applied to the demographic make-up of a specific place, sometimes at the organizational level, eg: school, businesses, cities, or nations. As a normative term, it refers to ideologies or policies that promote this diversity or its institutionalization. In this sense, multiculturalism is a society at ease with the rich tapestry of human life and the desire amongst people to express their own identity in the manner they see as fit. Such ideologies or policies vary widely, including country to country. Another major theme in the novel is globalization, which is a process of international integration arising from the interchange of world views, products, and other aspects of culture. Advances in transportation and telecommunications infrastructure, including the rise of the telegraph and its posterity the Internet, are majorfactors in globalization, generating further interdependence of economic and cultural activities. The term globalization has been increasing use since the mid-1980s and especially since the mid-1990s. The term globalization is derived from the word globalize, which refers to the emergence of an international network ofsocial and economic systems. This paper attempts to analyze Kiran Desai’s novel The Inheritance of Loss to bring out the various aspects of multicultural clashes and globalization.

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Yoo-Kyeong Won. "Kiran Desai’s The Inheritance of Loss: A Critical Reflection on Globalization." Jungang Journal of English Language and Literature 57, no. 2 (June 2015): 207–30. http://dx.doi.org/10.18853/jjell.2015.57.2.010.

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Cremers, Cor W. R. J. "Meatal atresia and hearing loss. Autosomal dominant and autosomal recessive inheritance." International Journal of Pediatric Otorhinolaryngology 8, no. 3 (March 1985): 211–13. http://dx.doi.org/10.1016/s0165-5876(85)80081-1.

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Thies, C., M. Handrock, K. Sperling, and A. Rcis. "Possible autosomal recessive inheritance of progressive hearing loss with stapes fixation." Journal of Medical Genetics 33, no. 7 (July 1, 1996): 597–99. http://dx.doi.org/10.1136/jmg.33.7.597.

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Jackson, Elizabeth. "Globalization, Diaspora, and Cosmopolitanism in Kiran Desai’s The Inheritance of Loss." ariel: A Review of International English Literature 47, no. 4 (2016): 25–43. http://dx.doi.org/10.1353/ari.2016.0031.

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Singh, Nitin. "Post Colonial Dilemma in Kiran Desai’s Novel “The Inheritance Of Loss”." SMART MOVES JOURNAL IJELLH 6, no. 12 (December 28, 2018): 6. http://dx.doi.org/10.24113/ijellh.v6i12.9854.

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The research paper sheds light on the problems, difficulties and hurdles faced by the migrant people to the different parts of the world. The novel “the Inheritance of Loss” written by Kiran Desai. She is a diasporic writer. Basically diasporic writers are those who are not living in their birthplace countries but still connect with their birthplace through their writings. So the foremost concerns of the diasporic literature is to explore the problems of displaced people, their exile, and the consequences.

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Vaidya, Dr Varsha, and Mr Siddharth Patil. "A Story of Scattered Hearts: Kiran Desai’s The Inheritance of Loss." SMART MOVES JOURNAL IJELLH 8, no. 2 (February 28, 2020): 10. http://dx.doi.org/10.24113/ijellh.v8i2.10414.

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Human beings are so fragile and impatient that they are easily subjected on emotional basis. It is in human nature that they empathise everything that emotionally attach with them. Emotion plays a vital role in the entire world of human relationship. It is not inept to note here that our thoughts are often forms the core of our actions. It reflects the framework of our psychology greatly. There are instances in the world of living where one work affects because of the mood of a person. Deliberately, the writers across the world develop and circle their thoughts around emotional balance of human beings in various points. They successfully stress the effect of a particular crisis and it’s outcomes on human mind. The present research paper deals with the effects of such crisis on the lives of human being who are deeply engulfed in their normal life. The study is a sincere endeavour to bring to the fore a serious effect of Nepali-a politically motivated-uprising on the common man living peacefully, amicably in harmony with nature.

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Noben-Trauth, Konrad, and Kenneth R. Johnson. "Inheritance patterns of progressive hearing loss in laboratory strains of mice." Brain Research 1277 (June 2009): 42–51. http://dx.doi.org/10.1016/j.brainres.2009.02.012.

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Mambrol, Nasrullah. "Disorientation, Dislocation and Displacement in Kiran Desai's the Inheritance of Loss." SMART MOVES JOURNAL IJELLH 9, no. 2 (February 27, 2021): 158–63. http://dx.doi.org/10.24113/ijellh.v9i2.10917.

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The Inheritance of Loss is more a book about the migrant experience. The plot is essentially about disorientation as a result of dislocation and displacement and the accompanying lack of sympathy resulting in feeling of being dispossessed. The characters feel the pull of the margin all the time thereby struggling to decide between the choice of moving out or remaining there. A sense of alienation and loss is always the immigrant's lifelong companion though they left their shores for a sense of economic or social or professional fulfillment.

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Kokitsu-Nakata, Nancy Mizue, Maria Leine Guion-Almeida, and Antonio Richieri-Costa. "Clinical Genetic Study of 144 Patients With Nonsyndromic Hearing Loss." American Journal of Audiology 13, no. 2 (December 2004): 99–103. http://dx.doi.org/10.1044/1059-0889(2004/013).

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Hearing loss constitutes an important category of congenital defects that can be isolated or part of the phenotypic spectrum of several syndromes. A clinical genetic study was performed on a sample of 144 patients with nonsyndromic hearing loss, establishing the sex distribution, type, degree, symmetry, laterality, progression, etiology, and, when possible, inheritance pattern.

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De Leenheer, Els M. R., Anne-Marie Kuijpers-Jagtman, Rob C. A. Sengers, Grétel G. Oudesluijs, Gudrun A. Rappold, and Cor W. R. J. Cremers. "Congenital Conductive Hearing Loss in Dyschondrosteosis." Annals of Otology, Rhinology & Laryngology 112, no. 2 (February 2003): 153–58. http://dx.doi.org/10.1177/000348940311200208.

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Conductive hearing loss was detected in a boy with a previous diagnosis of dyschondrosteosis. Dyschondrosteosis is a rare inherited condition characterized by mesomelic dwarfism and Madelung's deformity. The syndrome can be caused by mutations in the SHOX gene, and in that case, the pattern of inheritance is pseudoautosomal dominant. Indeed, SHOX mutation analysis in our patient revealed a deletion. The combination of dyschondrosteosis and conductive hearing loss has been reported in 2 previous cases. In our patient, exploratory tympanotomy revealed ankylosis of the stapes and a malformed incus. A substantial gain in hearing threshold was obtained by a stapedectomy in combination with a malleovestibulopexy.

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Berger, Karen H., and Michael P. Yaffe. "Prohibitin Family Members Interact Genetically with Mitochondrial Inheritance Components in Saccharomyces cerevisiae." Molecular and Cellular Biology 18, no. 7 (July 1, 1998): 4043–52. http://dx.doi.org/10.1128/mcb.18.7.4043.

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ABSTRACT Phb2p, a homolog of the tumor suppressor protein prohibitin, was identified in a genetic screen for suppressors of the loss of Mdm12p, a mitochondrial outer membrane protein required for normal mitochondrial morphology and inheritance in Saccharomyces cerevisiae. Phb2p and its homolog, prohibitin (Phb1p), were localized to the mitochondrial inner membrane and characterized as integral membrane proteins which depend on each other for their stability. In otherwise wild-type genetic backgrounds, null mutations in PHB1 andPHB2 did not confer any obvious phenotypes. However, loss of function of either PHB1 or PHB2 in cells with mitochondrial DNA deleted led to altered mitochondrial morphology, and phb1 or phb2 mutations were synthetically lethal when combined with a mutation in any of three mitochondrial inheritance components of the mitochondrial outer membrane, Mdm12p, Mdm10p, and Mmm1p. These results provide the first evidence of a role for prohibitin in mitochondrial inheritance and in the regulation of mitochondrial morphology.

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Higuchi-Sanabria, Ryo, Joseph K. Charalel, Matheus P. Viana, Enrique J. Garcia, Cierra N. Sing, Andrea Koenigsberg, Theresa C. Swayne, et al. "Mitochondrial anchorage and fusion contribute to mitochondrial inheritance and quality control in the budding yeast Saccharomyces cerevisiae." Molecular Biology of the Cell 27, no. 5 (March 2016): 776–87. http://dx.doi.org/10.1091/mbc.e15-07-0455.

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Higher-functioning mitochondria that are more reduced and have less ROS are anchored in the yeast bud tip by the Dsl1-family protein Mmr1p. Here we report a role for mitochondrial fusion in bud-tip anchorage of mitochondria. Fluorescence loss in photobleaching (FLIP) and network analysis experiments revealed that mitochondria in large buds are a continuous reticulum that is physically distinct from mitochondria in mother cells. FLIP studies also showed that mitochondria that enter the bud can fuse with mitochondria that are anchored in the bud tip. In addition, loss of fusion and mitochondrial DNA (mtDNA) by deletion of mitochondrial outer or inner membrane fusion proteins (Fzo1p or Mgm1p) leads to decreased accumulation of mitochondria at the bud tip and inheritance of fitter mitochondria by buds compared with cells with no mtDNA. Conversely, increasing the accumulation and anchorage of mitochondria in the bud tip by overexpression of MMR1 results in inheritance of less-fit mitochondria by buds and decreased replicative lifespan and healthspan. Thus quantity and quality of mitochondrial inheritance are ensured by two opposing processes: bud-tip anchorage by mitochondrial fusion and Mmr1p, which favors bulk inheritance; and quality control mechanisms that promote segregation of fitter mitochondria to the bud.

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Leone, Maria Pia, Pietro Palumbo, Rocco Ortore, Stefano Castellana, Orazio Palumbo, Salvatore Melchionda, Teresa Palladino, et al. "Putative TMPRSS3/GJB2 digenic inheritance of hearing loss detected by targeted resequencing." Molecular and Cellular Probes 33 (June 2017): 24–27. http://dx.doi.org/10.1016/j.mcp.2017.03.001.

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Cerundolo, R., D. H. Lloyd, and H. G. Pidduck. "Studies on the inheritance of hair loss in the Irish water spaniel." Veterinary Record 145, no. 19 (November 6, 1999): 542–44. http://dx.doi.org/10.1136/vr.145.19.542.

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Mr.Chandramani, Mr Chandramani. "“Kiran Desai’s The Inheritance of Loss: Elements of American Dream and Globalization.”." IOSR Journal of Humanities and Social Science 11, no. 2 (2013): 79–81. http://dx.doi.org/10.9790/0837-1127981.

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Viswamohan, Aysha. "Home, Immigration, and Fractured Identities in Kiran Desai's The Inheritance of Loss." South Asian Review 32, no. 2 (November 2011): 259–73. http://dx.doi.org/10.1080/02759527.2011.11932839.

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Van Heurck, Roxane, Maria Teresa Carminho-Rodrigues, Emmanuelle Ranza, Caterina Stafuzza, Lina Quteineh, Corinne Gehrig, Eva Hammar, et al. "Benefits of Exome Sequencing in Children with Suspected Isolated Hearing Loss." Genes 12, no. 8 (August 20, 2021): 1277. http://dx.doi.org/10.3390/genes12081277.

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Purpose: Hearing loss is characterized by an extensive genetic heterogeneity and remains a common disorder in children. Molecular diagnosis is of particular benefit in children, and permits the early identification of clinically-unrecognized hearing loss syndromes, which permits effective clinical management and follow-up, including genetic counselling. Methods: We performed whole-exome sequencing with the analysis of a panel of 189 genes associated with hearing loss in a prospective cohort of 61 children and 9 adults presenting mainly with isolated hearing loss. Results: The overall diagnostic rate using exome sequencing was 47.2% (52.5% in children; 22% in adults). In children with confirmed molecular results, 17/32 (53.2%) showed autosomal recessive inheritance patterns, 14/32 (43.75%) showed an autosomal dominant condition, and one case had X-linked hearing loss. In adults, the two patients showed an autosomal dominant inheritance pattern. Among the 32 children, 17 (53.1%) had nonsyndromic hearing loss and 15 (46.7%) had syndromic hearing loss. One adult was diagnosed with syndromic hearing loss and one with nonsyndromic hearing loss. The most common causative genes were STRC (5 cases), GJB2 (3 cases), COL11A1 (3 cases), and ACTG1 (3 cases). Conclusions: Exome sequencing has a high diagnostic yield in children with hearing loss and can reveal a syndromic hearing loss form before other organs/systems become involved, allowing the surveillance of unrecognized present and/or future complications associated with these syndromes.

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Verdura, Edgard, Carme Fons, Agatha Schlüter, Montserrat Ruiz, Stéphane Fourcade, Carlos Casasnovas, Antonio Castellano, and Aurora Pujol. "Complete loss of KCNA1 activity causes neonatal epileptic encephalopathy and dyskinesia." Journal of Medical Genetics 57, no. 2 (October 5, 2019): 132–37. http://dx.doi.org/10.1136/jmedgenet-2019-106373.

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BackgroundSince 1994, over 50 families affected by the episodic ataxia type 1 disease spectrum have been described with mutations in KCNA1, encoding the voltage-gated K+ channel subunit Kv1.1. All of these mutations are either transmitted in an autosomal-dominant mode or found as de novo events.MethodsA patient presenting with a severe combination of dyskinesia and neonatal epileptic encephalopathy was sequenced by whole-exome sequencing (WES). A candidate variant was tested using cellular assays and patch-clamp recordings.ResultsWES revealed a homozygous variant (p.Val368Leu) in KCNA1, involving a conserved residue in the pore domain, close to the selectivity signature sequence for K+ ions (TVGYG). Functional analysis showed that mutant protein alone failed to produce functional channels in homozygous state, while coexpression with wild-type produced no effects on K+ currents, similar to wild-type protein alone. Treatment with oxcarbazepine, a sodium channel blocker, proved effective in controlling seizures.ConclusionThis newly identified variant is the first to be reported to act in a recessive mode of inheritance in KCNA1. These findings serve as a cautionary tale for the diagnosis of channelopathies, in which an unreported phenotypic presentation or mode of inheritance for the variant of interest can hinder the identification of causative variants and adequate treatment choice.

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Liu, Qiang, and Nan Shi. "Research on the Protection Predicament and Digital Breakthrough Path of Rural Architecture in Shandong." E3S Web of Conferences 236 (2021): 05090. http://dx.doi.org/10.1051/e3sconf/202123605090.

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Rural arechitecture, as an important carrier of rural areas, faces the huge impact of modern life style and construction mode, and there is a crisis of cognitive degradation and loss of skills. with the continuous promotion of rural revitalization, the crisis of its protection and inheritance is increasingly serious, and the disadvantages of the single inheritance mode of oral transmission and personal transmission and personal transmission are also gradually revealed. In this predicament, how to innovate the inheritance of traditional skills has become an urgent problem to be solved. In the era when digital technology has penetrated into every field of modern life and become a technology booster, this paper intends to use digital technology and take the construction technology of rural architecture in Shandong province as the entry point to solve the dilemma faced by rural architecture and study the effective way of its digital inheritance and development.

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Ichinose, Aya, Hideaki Moteki, Mitsuru Hattori, Shin-ya Nishio, and Shin-ichi Usami. "Novel Mutations in LRTOMT Associated With Moderate Progressive Hearing Loss in Autosomal Recessive Inheritance." Annals of Otology, Rhinology & Laryngology 124, no. 1_suppl (March 18, 2015): 142S—147S. http://dx.doi.org/10.1177/0003489415575043.

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Objective: We present a patient who was identified with novel mutations in the LRTOMT gene and describe the clinical features of the phenotype including serial audiological findings. Methods: One hundred six Japanese patients with mild to moderate sensorineural hearing loss from unrelated and nonconsanguineous families were enrolled in the study. Targeted genomic enrichment and massively parallel sequencing of all known nonsyndromic hearing loss genes were performed to identify the genetic cause of hearing loss. Results: Compound heterozygotes with a novel frame-shift mutation and a missense mutation were identified in the LRTOMT gene. The mutated residues were segregated in both alleles of LRTOMT, present within the LRTOMT2 protein coding region. The patient had moderate sloping hearing loss at high frequencies, which progressed at 1000 Hz and higher frequencies over a period of 6 years. Conclusion: Hearing loss caused by mutations in the LRTOMT gene is extremely rare. This is the first case report of a compound heterozygous mutation in a nonconsanguineous family.

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Chen, B. Y., W. K. Heneen, and V. Slmonsen. "Genetics of isozyme loci in Brassica campestris L. and in the progeny of a trigenomic hybrid between B. napus L. and B. campestris L." Genome 33, no. 3 (June 1, 1990): 433–40. http://dx.doi.org/10.1139/g90-065.

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F2 progeny of Brassica campestris crosses were analyzed for single-locus inheritance of glucosephosphate isomerase, leucine aminopeptidase, 6-phosphogluconate dehydrogenase, phosphoglucomutase, and shikimate dehydrogenase enzymes. In most of the F2 families, the observed inheritance data for six polymorphic isozyme loci coincided well with the ratios expected under Mendelian segregation of either codominant alleles or dominant-recessive alleles when a null allele was involved. Complete linkage was observed for one locus pair (Lap-2A/6Pgd-2Ac), with the recombination frequency estimated to be r ≈ 0.000. From isozyme analyses made on resynthesized Brassica napus (AACC) and the actual parents B. campestris (AA) and B. alboglabra (CC) and on a trigenomic hybrid (AAC) between B. napus and B. campestris, it was possible to recognize A and C genome specific isozyme loci through the nonoverlapping electrophoretic mobilities of alleles characteristic of each genome. The trigenomic hybrid was selfed and genetic analyses of the offspring indicated that the A genome specific isozyme loci displayed a normal disomic inheritance. The C genome specific isozyme loci, on the other hand, showed nonrandom loss in the aneuploid offspring, thereby indicating the nonrandom loss of C genome chromosomes. At least 4 of the 8 C genome specific isozyme loci studied were located on separate chromosomes. The apparent occurrence of multiplicates of certain isozyme loci supports the concept that duplication of structural nuclear genes prevails in the diploid Brassica genomes.Key words: isozymes, Brassica, inheritance, trigenomic hybrid (2n = 29, AAC), genome-specific isozyme loci.

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NAWATA, Hiroyuki. "Verbal Inflection, Feature Inheritance, and the Loss of Null Subjects in Middle English." Interdisciplinary Information Sciences 20, no. 2 (2014): 103–20. http://dx.doi.org/10.4036/iis.2014.103.

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Gold, Michael, and Isabelle Rapin. "Non-Mendelian mitochondrial inheritance as a cause of progressive genetic sensorineural hearing loss." International Journal of Pediatric Otorhinolaryngology 30, no. 2 (August 1994): 91–104. http://dx.doi.org/10.1016/0165-5876(94)90191-0.

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Pupo, Altair Cadrobbi, Sulene Pirana, Mauro Spinelli, Karina Lezirovitz, Regina C. Mingroni Netto, and Lisandra S. Macedo. "Study of a Brazilian Family Presenting Non-syndromic hearing loss with mitochondrial inheritance." Brazilian Journal of Otorhinolaryngology 74, no. 5 (September 2008): 786–89. http://dx.doi.org/10.1016/s1808-8694(15)31392-6.

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Balciuniene, Jorune, Niklas Dahl, Erik Borg, Eva Samuelsson, Markus J. Koisti, Ulf Pettersson, and Elena E. Jazin. "Evidence for Digenic Inheritance of Nonsyndromic Hereditary Hearing Loss in a Swedish Family." American Journal of Human Genetics 63, no. 3 (September 1998): 786–93. http://dx.doi.org/10.1086/302012.

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Sluder, G., F. J. Miller, K. Lewis, E. D. Davison, and C. L. Rieder. "Centrosome inheritance in starfish zygotes: Selective loss of the maternal centrosome after fertilization." Developmental Biology 131, no. 2 (February 1989): 567–79. http://dx.doi.org/10.1016/s0012-1606(89)80027-2.

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Larsen, Jesper, Anders G. Pedersen, Henrik Christensen, Magne Bisgaard, Øystein Angen, Peter Ahrens, and John E. Olsen. "Evidence for Vertical Inheritance and Loss of the Leukotoxin Operon in Genus Mannheimia." Journal of Molecular Evolution 64, no. 4 (April 2007): 423–37. http://dx.doi.org/10.1007/s00239-006-0065-3.

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Lechowicz, Urszula, Agnieszka Pollak, Dominka Oziębło, and Monika Ołdak. "Pathogenic p.Cys194Metfs*17 variant argues against TMPRSS3/GJB2 digenic inheritance of hearing loss." European Archives of Oto-Rhino-Laryngology 273, no. 5 (September 25, 2015): 1327–28. http://dx.doi.org/10.1007/s00405-015-3782-7.

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Li, Xia, Susan Ferro-Novick, and Peter Novick. "Different polarisome components play distinct roles in Slt2p-regulated cortical ER inheritance in Saccharomyces cerevisiae." Molecular Biology of the Cell 24, no. 19 (October 2013): 3145–54. http://dx.doi.org/10.1091/mbc.e13-05-0268.

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Ptc1p, a type 2C protein phosphatase, is required for a late step in cortical endoplasmic reticulum (cER) inheritance in Saccharomyces cerevisiae. In ptc1Δ cells, ER tubules migrate from the mother cell and contact the bud tip, yet fail to spread around the bud cortex. This defect results from the failure to inactivate a bud tip–associated pool of the cell wall integrity mitogen-activated protein kinase, Slt2p. Here we report that the polarisome complex affects cER inheritance through its effects on Slt2p, with different components playing distinct roles: Spa2p and Pea2p are required for Slt2p retention at the bud tip, whereas Bni1p, Bud6p, and Sph1p affect the level of Slt2p activation. Depolymerization of actin relieves the ptc1Δ cER inheritance defect, suggesting that in this mutant the ER becomes trapped on the cytoskeleton. Loss of Sec3p also blocks ER inheritance, and, as in ptc1Δ cells, this block is accompanied by activation of Slt2p and is reversed by depolymerization of actin. Our results point to a common mechanism for the regulation of ER inheritance in which Slt2p activity at the bud tip controls the association of the ER with the actin-based cytoskeleton.

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Srinivasan, N., J. Westby, E. H. Horn, G. Dolan, and S. Deam. "F X Nottingham and F X Taunton Two Novel Mutations in Factor X Resulting in Loss of Functional Activity and an Interpretation Using Molecular Modelling." Thrombosis and Haemostasis 85, no. 02 (2001): 265–69. http://dx.doi.org/10.1055/s-0037-1615695.

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SummaryWe report two novel mutations in the Factor X gene which result in a bleeding tendency in two unrelated Caucasian families. Although the mutations occur at adjacent codons in exon 8 and result in reduced functional activity with normal antigen levels, the patterns of inheritance appear to be quite distinct. Factor X Nottingham (alanine 404 threonine) appears to be associated with an autosomal recessive pattern of inheritance. In contrast, Factor X Taunton (arginine 405 glycine) results in a mode of inheritance consistent with an autosomal dominant pattern, all five of the heterozygotes in this family being clinically affected. Molecular modelling studies suggest that, in the case of Factor X Nottingham, a drastic conformational change causes major unfolding of the protein. For Factor X Taunton, less extreme conformational changes occur causing loss of functional activity such that substrate binding sites might be maintained. It is proposed that competition with wild type for substrate binding could occur leading to a dominant negative effect.

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Roeder, Amy D., Greg J. Hermann, Brian R. Keegan, Stephanie A. Thatcher, and Janet M. Shaw. "Mitochondrial Inheritance Is Delayed in Saccharomyces cerevisiae Cells Lacking the Serine/Threonine PhosphatasePTC1." Molecular Biology of the Cell 9, no. 4 (April 1998): 917–30. http://dx.doi.org/10.1091/mbc.9.4.917.

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In wild-type yeast mitochondrial inheritance occurs early in the cell cycle concomitant with bud emergence. Cells lacking thePTC1 gene initially produce buds without a mitochondrial compartment; however, these buds later receive part of the mitochondrial network from the mother cell. Thus, the loss ofPTC1 causes a delay, but not a complete block, in mitochondrial transport. PTC1 encodes a serine/threonine phosphatase in the high-osmolarity glycerol response (HOG) pathway. The mitochondrial inheritance delay in theptc1 mutant is not attributable to changes in intracellular glycerol concentrations or defects in the organization of the actin cytoskeleton. Moreover, epistasis experiments withptc1Δ and mutations in HOG pathway kinases reveal thatPTC1 is not acting through the HOG pathway to control the timing of mitochondrial inheritance. Instead, PTC1may be acting either directly or through a different signaling pathway to affect the mitochondrial transport machinery in the cell. These studies indicate that the timing of mitochondrial transport in wild-type cells is genetically controlled and provide new evidence that mitochondrial inheritance does not depend on a physical link between the mitochondrial network and the incipient bud site.

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Cavalera, Maria Alfonsa, Floriana Gernone, Annamaria Uva, Paola D’Ippolito, Xavier Roura, and Andrea Zatelli. "Clinical and Histopathological Features of Renal Maldevelopment in Boxer Dogs: A Retrospective Case Series (1999–2018)." Animals 11, no. 3 (March 13, 2021): 810. http://dx.doi.org/10.3390/ani11030810.

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Renal maldevelopment (RM) has been proposed to replace the old and sometimes misused term “renal dysplasia” in dogs. Although renal dysplasia has been described in Boxers, hereditary transmission has only been hypothesized. This study reports clinical and renal histological findings in Boxer dogs with RM, proposing a possible mode of inheritance. Medical records of 9 female Boxer dogs, older than 5 months and with a clinical diagnosis of chronic kidney disease prior to one year of age, were retrospectively reviewed. Polyuria and polydipsia (PU/PD), decreased appetite, weight loss, lethargy and weakness were described in all affected dogs. Common laboratory findings were proteinuria, diluted urine, non-regenerative anemia, azotemia, hyperphosphatemia, hypoalbuminemia and hypercholesterolemia. Histopathology of the kidneys revealed the presence of immature glomeruli in all dogs, which is consistent with RM. In 7 related dogs, the pedigree analysis showed that a simple autosomal recessive trait may be a possible mode of inheritance. Renal maldevelopment should be suspected in young Boxer dogs with a history of PU/PD, decreased appetite, weight loss, lethargy, weakness and proteinuria. Due to its possible inheritance, an early diagnosis of RM may allow clinicians to promptly identify other potentially affected dogs among the relatives of the diagnosed case.

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Bradshaw, Laura D., Michael Barrett, and Charles G. Poneleit. "Inheritance of Bentazon Susceptibility in a Corn (Zea mays) Line." Weed Science 42, no. 4 (December 1994): 641–47. http://dx.doi.org/10.1017/s0043174500077080.

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Greenhouse experiments were conducted to determine if the inheritance of bentazon susceptibility in the corn inbred ‘GA209’ is a recessive single gene trait Bentazon was applied at 4.4 kg ai ha-1plus 1% by vol crop oil concentrate in all experiments. This treatment caused 96 and 30% visual injury and 86 and 50% dry weight loss for corn inbreds GA209 and ‘Ky226,’ respectively. Corn inbreds ‘B73,’ ‘T61,’ Mo17,’ ‘Pa91,’ and ‘CI66’ showed less than 18% injury and 10% dry weight loss and were considered tolerant of bentazon. Single crosses and reciprocal single crosses of GA209 with the other inbreds were considered bentazon tolerant with approximately 10% stunting and tissue necrosis and 20% dry weight reduction resulting from bentazon. Bentazon susceptibility was not maternally inherited. Apparent single recessive gene control of bentazon susceptibility of GA209 was observed for F2 and backcross segregations. However, subsequent analyses of F3 and selfed-backcross populations indicated that two genes, probably located on the same chromosome, controlled the bentazon susceptibility. Duplicate dominant epistasis provided the best fit for injury and dry weight reduction segregations in populations derived from the cross of inbreds GA209 and B73.

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Knibb, W. R., J. S. F. Barker, and J. G. Oakeshott. "The genetics of abnormal abdomen, incomplete abdomen, and bobbed in Drosophila buzzatii." Genome 32, no. 5 (October 1, 1989): 754–61. http://dx.doi.org/10.1139/g89-508.

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Five stocks of Drosophila buzzatii with superficially similar abdominal disruptions including partial tergite and sternite loss were isolated by inbreeding. Three of the stocks have indistinguishable phenotypes, the inheritance of which is maternally influenced. This phenotype and its mode of inheritance bear similarities with those of Abnormal abdomen in D. melanogaster. The phenotype in the fourth stock is slightly different and is due to a single autosomal recessive gene, which we denote incomplete abdomen. In the fifth stock the trait is limited to females, and in appearance and mode of inheritance resembles bobbed in D. melanogaster. Furthermore, only in this stock are rDNA deletions evident. The combined frequencies of the three types of abdominal aberration were found to be around 1% in several samples from wild and laboratory populations of D. buzzatii.Key words: Drosophila, abnormal abdomen, ribosomal DNA, selection.

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Crider, David G., Luis J. García-Rodríguez, Pallavi Srivastava, Leonardo Peraza-Reyes, Krishna Upadhyaya, Istvan R. Boldogh, and Liza A. Pon. "Rad53 is essential for a mitochondrial DNA inheritance checkpoint regulating G1 to S progression." Journal of Cell Biology 198, no. 5 (August 27, 2012): 793–98. http://dx.doi.org/10.1083/jcb.201205193.

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The Chk2-mediated deoxyribonucleic acid (DNA) damage checkpoint pathway is important for mitochondrial DNA (mtDNA) maintenance. We show in this paper that mtDNA itself affects cell cycle progression. Saccharomyces cerevisiae rho0 cells, which lack mtDNA, were defective in G1- to S-phase progression. Deletion of subunit Va of cytochrome c oxidase, inhibition of F1F0 adenosine triphosphatase, or replacement of all mtDNA-encoded genes with noncoding DNA did not affect G1- to S-phase progression. Thus, the cell cycle progression defect in rho0 cells is caused by loss of DNA within mitochondria and not loss of respiratory activity or mtDNA-encoded genes. Rad53p, the yeast Chk2 homologue, was required for inhibition of G1- to S-phase progression in rho0 cells. Pif1p, a DNA helicase and Rad53p target, underwent Rad53p-dependent phosphorylation in rho0 cells. Thus, loss of mtDNA activated an established checkpoint kinase that inhibited G1- to S-phase progression. These findings support the existence of a Rad53p-regulated checkpoint that regulates G1- to S-phase progression in response to loss of mtDNA.

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Ruiz-Cruz, M. D., and C. Sanz de Galdeano. "Genetic significance of zircon in orthogneisses from Sierra Nevada (Betic Cordillera, Spain)." Mineralogical Magazine 81, no. 1 (February 2017): 77–101. http://dx.doi.org/10.1180/minmag.2016.080.072.

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AbstractZircon from two types of orthogneisses (inheritance-rich and inheritance-poor) from Sierra Nevada (Betic Cordillera, Spain) was investigated by integrating U–Pb geochronology, cathodoluminescence and back-scattered SEM imaging, laser-ablation inductively coupled plasma mass spectrometry analyses and Raman spectroscopy to examine the conditions of magmatic zircon growth and the variable extent and mechanisms of the Alpine modifications. Zircon from inheritance-rich gneiss consists of two main domains: inherited (Neoproterozoic-to-Early Paleozoic and Devonian) cores and magmatic overgrowths, which provided 206Pb/238U concordant ages of 286 ± 3 Ma. In inheritance-poor gneiss, zircons consist of magmatic cores and very altered rims defining a discordia with an upper intercept with the Concordia at 287 + 21 –22 Ma and a lower intercept at 20.8 + 48.6 –20.8 Ma. Magmatic domains of zircon from inheritance-rich gneiss have lower rare-earth element (REE) contents than magmatic domains from inheritance-poor gneiss, reflecting the less evolved nature of the melt. Altered domains in zircon from inheritance-poor gneisss how greater U concentrations, lower REE concentrations and lower Th/U ratios relative to the cores, interpreted as representing Pb loss from the U-rich magmatic domains during the Alpine event. Morphological changes within single grains and between populations reflects the evolution during magmatic cooling. We show that, whereas classic methods allow two different interpretations for the geodynamic setting of the two types of gneisses, a complete study of composition, morphology and structure of zircon can help to decide that a model based on a common source for the granitic melt better fits the zircon characteristics than a model based on melts generated in two different geotectonic settings.

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Egilmez, Oguz Kadir, and M. Tayyar Kalcioglu. "Genetics of Nonsyndromic Congenital Hearing Loss." Scientifica 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/7576064.

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Congenital hearing impairment affects nearly 1 in every 1000 live births and is the most frequent birth defect in developed societies. Hereditary types of hearing loss account for more than 50% of all congenital sensorineural hearing loss cases and are caused by genetic mutations. HL can be either nonsyndromic, which is restricted to the inner ear, or syndromic, a part of multiple anomalies affecting the body. Nonsyndromic HL can be categorised by mode of inheritance, such as autosomal dominant (called DFNA), autosomal recessive (DFNB), mitochondrial, and X-linked (DFN). To date, 125 deafness loci have been reported in the literature: 58 DFNA loci, 63 DFNB loci, and 4 X-linked loci. Mutations in genes that control the adhesion of hair cells, intracellular transport, neurotransmitter release, ionic hemeostasis, and cytoskeleton of hair cells can lead to malfunctions of the cochlea and inner ear. In recent years, with the increase in studies about genes involved in congenital hearing loss, genetic counselling and treatment options have emerged and increased in availability. This paper presents an overview of the currently known genes associated with nonsyndromic congenital hearing loss and mutations in the inner ear.

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Journal articles on the topic 'Inheritance of loss'

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