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Inclusion body myositis (IBM) [my-oh-SIGH-tis] (sometimes called sporadic inclusion body myositis, sIBM) is the most common inflammatory muscle disease in older adults.^[1] The disease is characterized by slowly progressive weakness and wasting of both distal and proximal muscles, most apparent in the fingerflexors and kneeextensors.^[2] IBM is often confused with an entirely different class of diseases, called hereditary inclusion body myopathies (hIBM).^[3][4] The 'M' in hIBM is an abbreviation for 'myopathy' while the 'M' in IBM is an abbreviation for 'myositis'. These diseases should not be confused with each other. In IBM, two processes appear to occur in the muscles in parallel, one autoimmune and the other degenerative. Inflammation is evident from the invasion of muscle fibers by immune cells. Degeneration is characterized by the appearance of holes, deposits of abnormal proteins, and filamentous inclusions in the muscle fibers.^[5] sIBM is a rare disease, with a prevalence ranging from 1 to 71 individuals per million.^[6][7]

Weakness comes on slowly (over months to years) in an asymmetric manner and progresses steadily, leading to severe weakness and wasting of arm and leg muscles. IBM is more common in men than women.^[8] Patients may become unable to perform activities of daily living and most require assistive devices within 5 to 10 years of symptom onset.^[9] sIBM is not considered a fatal disorder, but the risk of serious injury due to falls is increased. Death in IBM is sometimes related to malnutrition and respiratory failure.^[10] There is no effective treatment for the disease.

• 2Causes
• 3Diagnosis

Signs and symptoms[edit]

How sIBM affects individuals is quite variable as is the age of onset (which generally varies from the forties upwards). Because sIBM affects different people in different ways and at different rates, there is no 'textbook case.'

Eventually, sIBM results in general, progressive muscle weakness. The quadriceps and forearm muscles are usually affected early on. Common early symptoms include frequent tripping and falling, weakness going up stairs and trouble manipulating the fingers (including difficulty with tasks such as turning doorknobs or gripping keys). Foot drop in one or both feet has been a symptom of IBM and advanced stages of polymyositis (PM).

During the course of the illness, the patient's mobility is progressively restricted as it becomes hard for him or her to bend down, reach for things, walk quickly and so on. Many patients say they have balance problems and fall easily, as the muscles cannot compensate for an off-balanced posture. Because sIBM makes the leg muscles weak and unstable, patients are very vulnerable to serious injury from tripping or falling down. Although pain has not been traditionally part of the 'textbook' description, many patients report severe muscle pain, especially in the thighs.

When present, difficulty swallowing (dysphagia) is a progressive condition in those with inclusion body myositis and often leads to death from aspiration pneumonia. Dysphagia is present in 40 to 85% of IBM cases.^[11]

IBM can also result in diminished capacity for aerobic exercise. This decline is most likely a consequence of the sedentary lifestyle that is often associated with the symptoms of IBM (i.e. progressive muscle weakness, decreased mobility, and increased level of fatigue). Therefore, one focus of treatment should be the improvement of aerobic capacity.^[12]

Patients with sIBM usually eventually need to resort to a cane or a walker and in most cases, a wheelchair eventually becomes a necessity.

In addition to plans and instructions for building your own, he includes excellent instructions on how to use it, especially for direct and indirect indexing (the most common kinds). Gingery dividing head pdf.

'The progressive course of s-IBM leads slowly to severe disability. Finger functions can become very impaired, such as for manipulating pens, keys, buttons, and zippers, pulling handles, and firmly grasping handshakes. Arising from a chair becomes difficult. Walking becomes more precarious. Sudden falls, sometimes resulting in major injury to the skull or other bones, can occur, even from walking on minimally-irregular ground or from other minor imbalances outside or in the home, due to weakness of quadriceps and gluteus muscles depriving the patient of automatic posture maintenance. A foot-drop can increase the likelihood of tripping. Dysphagia can occur, usually caused by upper esophageal constriction that often can be symptomatically improved, for several months to years, by bougie dilation per a GI or ENT physician. Respiratory muscle weakness can sometimes eventuate.'^[13]

Causes[edit]

The cause of IBM is unknown. IBM likely results from the interaction of a number of genetic and environmental factors.^[14]

There are two major theories about how sIBM is caused. One hypothesis suggests that the inflammation-immune reaction, caused by an unknown trigger – likely an undiscovered virus or an autoimmune disorder– is the primary cause of sIBM and that the degeneration of muscle fibers and protein abnormalities are secondary features.^[15] Despite the arguments 'in favor of an adaptive immune response in sIBM, a purely autoimmune hypothesis for sIBM is untenable because of the disease's resistance to most immunotherapy.'^[16]

The second school of thought advocates the theory that sIBM is a degenerative disorder related to aging of the muscle fibers and that abnormal, potentially pathogenic protein accumulations in myofibrils play a key causative role in sIBM (apparently before the immune system comes into play). This hypothesis emphasizes the abnormal intracellular accumulation of many proteins, protein aggregation and misfolding, proteosome inhibition, and endoplasmic reticulum (ER) stress.^[13]

One review discusses the 'limitations in the beta-amyloid-mediated theory of IBM myofiber injury.'^[17]

Dalakas (2006) suggested that a chain of events causes IBM—some sort of virus, likely a retrovirus, triggers the cloning of T cells. These T cells appear to be driven by specific antigens to invade muscle fibers. In people with sIBM, the muscle cells display “flags” telling the immune system that they are infected or damaged (the muscles ubiquitously express MHC class I antigens) and this immune process leads to the death of muscle cells. The chronic stimulation of these antigens also causes stress inside the muscle cell in the endoplasmic reticulum (ER) and this ER stress may be enough to cause a self-sustaining T cell response (even after a virus has dissipated). In addition, this ER stress may cause the misfolding of protein. The ER is in charge of processing and folding molecules carrying antigens. In IBM, muscle fibers are overloaded with these major histocompatibility complex (MHC) molecules that carry the antigen protein pieces, leading to more ER stress and more protein misfolding.^[15]

A self-sustaining T cell response would make sIBM a type of autoimmune disorder. When studied carefully, it has not been impossible to detect an ongoing viral infection in the muscles. One theory is that a chronic viral infection might be the initial triggering factor setting IBM in motion. There have been a handful of IBM cases—approximately 15—that have shown clear evidence of a virus called HTLV-1. The HTLV-1 virus can cause leukemia, but in most cases lies dormant and most people end up being lifelong carriers of the virus. One review says that the best evidence points towards a connection with some type of retrovirus and that a retroviral infection combined with immune recognition of the retrovirus is enough to trigger the inflammation process.^[15]

• amyloid protein
• The hypothesis that beta amyloid protein is key to IBM has been supported in a mouse model using an Aβ vaccine that was found to be effective against inclusion body myositis in mouse models. Although this vaccine is likely not safe for human use, it still shows that attacking Aβ has efficacy in mice against IBM.^[18]
• Following up on earlier leads, the Greenberg group report finding that the protein TDP-43 is a very prominent and highly sensitive and specific feature of IBM. This protein is normally found within the nucleus but in IBM is found in the cytoplasm of the cell. This important advance should help develop a new screening technique for IBM and may provide clues in terms of a therapeutic approach^[19]

Genetics[edit]

sIBM is not inherited and is not passed on to the children of IBM patients. There are genetic features that do not directly cause IBM but that appear to predispose a person to getting IBM — having this particular combination of genes increases one's susceptibility to getting IBM. Some 67% of IBM patients have a particular combination of human leukocyte antigen genes in a section of the 8.1 ancestral haplotype in the center of the MHC class II region. sIBM is not passed on from generation to generation, although the susceptibility region of genes may be.^[15]

There are also several rare forms of hereditary inclusion body myopathy that are linked to specific genetic defects and that are passed on from generation to generation. Since these forms do not show features of muscle inflammation, they are classified as myopathies rather than forms of myositis. Because they do not display inflammation as a primary symptom, they may in fact be similar, but different diseases to sporadic inclusion body myositis. There are several different types, each inherited in different ways. See hereditary inclusion body myopathy.

A 2007 review concluded there is no indication that the genes responsible for the familial or hereditary conditions are involved in sIBM.^[20]

Diagnosis[edit]

Elevated creatine kinase (CK) levels in the blood (at most ~10 times normal) are typical in sIBM but affected individuals can also present with normal CK levels. Electromyography (EMG) studies usually display abnormalities.^[vague] Muscle biopsy may display several common findings including; inflammatory cells invading muscle cells, vacuolar degeneration, inclusions or plaques of abnormal proteins. sIBM is a challenge to the pathologist and even with a biopsy, diagnosis can be ambiguous.

A diagnosis of inclusion body myositis was historically dependent on muscle biopsy results. Antibodies to cytoplasmic 5'-nucleotidase (cN1A; NT5C1A) have been strongly associated with the condition. In the clinical context of a classic history and positive antibodies, a muscle biopsy might be unnecessary.

Differential diagnosis[edit]

IBM is often initially misdiagnosed as polymyositis. A course of prednisone is typically completed with no improvement and eventually sIBM is confirmed. sIBM weakness comes on over months or years and progresses steadily, whereas polymyositis has an onset of weeks or months. Other forms of muscular dystrophy (e.g. limb girdle) must be considered as well.

Classification[edit]

• The common type is sIBM; it strikes individuals apparently at random.^[21]
• There is a type that has been observed in multiple siblings in the same generation in several families, termed familial inflammatory sIBM, but it is not passed on from generation to generation.^[15]
• There are also several very rare forms of hereditary inclusion body myopathy (hIBM) that are linked to specific genetic defects and that are passed on from generation to generation, each inherited in different ways.^[22]

Treatment[edit]

There is no standard course of treatment to slow or stop the progression of the disease. sIBM patients do not reliably respond to the anti-inflammatory, immunosuppressant, or immunomodulatory medications. Management is symptomatic. Prevention of falls is an important consideration. Specialized exercise therapy may supplement treatment to enhance quality of life. Physical therapy is recommended to teach the patient a home exercise program, to teach how to compensate during mobility-gait training with an assistive device, transfers and bed mobility.

Other related disorders[edit]

When sIBM was originally described, the major feature noted was muscle inflammation. Two other disorders were also known to display muscle inflammation, and sIBM was classified along with them. They are dermatomyositis (DM) and polymyositis (PM) and all three illnesses were called idiopathic (of unknown origin) myositis or inflammatory myopathies.

It appears that sIBM and polymyositis share some features, especially the initial sequence of immune system activation, however, polmyositis comes on over weeks or months, does not display the subsequent muscle degeneration and protein abnormalities as seen in IBM, and as well, polymyositis tends to respond well to treatments, IBM does not. IBM is often confused with (misdiagnosed as) polymyositis. Polymyositis that does not respond to treatment is likely IBM.^[23]

Dermatomyositis shares a number of similar physical symptoms and histopathological traits as polymyositis, but exhibits a skin rash not seen in polymyositis or sIBM. It may have different root causes unrelated to either polymyositis or sIBM.

Mutations in valosin-containing protein (VCP) cause multisystem proteinopathy (MSP), which can present (among others) as a rare form of inclusion body myopathy.

References[edit]

1. ^Ahmed, Mhoriam; Machado, Pedro M; Miller, Adrian; Spicer, Charlotte; Herbelin, Laura; et, al (March 23, 2016). 'Targeting protein homeostasis in sporadic inclusion body myositis'. Science Translational Medicine. 8 (331): 331ra41. doi:10.1126/scitranslmed.aad4583. PMC5043094. PMID27009270.
2. ^Jackson, CE; Barohn, RJ; Gronseth, G; Pandya, S; Herbelin, L; and, The Muscle Study Group (April 2008). 'Inclusion body myositis functional rating scale: a reliable and valid measure of disease severity'. Muscle and Nerve. 37 (4): 473–476. doi:10.1002/mus.20958. PMID18236463.
3. ^IBMmyositis.com
4. ^cureibm.org
5. ^Machado, P; Dimachkie, MM; Bahron, RJ (October 2014). 'Sporadic Inclusion Body Myositis: new insights and potential therapy'. Current Opinion in Neurology. 27 (5): 591–598. doi:10.1097/WCO.0000000000000129. PMC4248565. PMID25159931.
6. ^Machado, P; Brady, S; Hanna, MG (2013). 'Update in inclusion body myosities'. Current Opinion in Rheumatology. 25 (763–771): 763–771. doi:10.1097/01.bor.0000434671.77891.9a. PMC4196838. PMID24067381.
7. ^'Sporadic Inclusion Body Myositis'.
8. ^'Inclusion Body Myositis. IBM information; Age Related illness'.
9. ^'Understanding IBM'.
10. ^Cox, FM; Titulaer, MJ; Sont, JK; Wintzen, AR; et, al (November 1, 2011). 'A 12-year follow-up in sporadic inclusion body myositis: an end stage with major disabilities'. Brain. 134 (11): 3167–3175. doi:10.1093/brain/awr217. PMID21908393.
11. ^Oh TH, Brumfield KA, Hoskin TL, Kasperbauer JL, Basford JR (2008). 'Dysphagia in inclusion body myositis: clinical features, management, and clinical outcome'. Am J Phys Med Rehabil. 87 (11): 883–9. doi:10.1097/PHM.0b013e31818a50e2. PMID18936555.
12. ^Johnson LG, Collier KE, Edwards DJ, et al. (June 2009). 'Improvement in aerobic capacity after an exercise program in sporadic inclusion body myositis'. J Clin Neuromuscul Dis. 10 (4): 178–84. doi:10.1097/CND.0b013e3181a23c86. PMID19494728.
13. ^ ^abAskanas V, Engel WK (2006). 'Inclusion-body myositis: a myodegenerative conformational disorder associated with Abeta, protein misfolding, and proteasome inhibition'. Neurology. 66 (2 Suppl 1): S39–S48. doi:10.1212/01.wnl.0000192128.13875.1e. PMID16432144.
14. ^'Inclusion Body Myositis (IBM)'. Retrieved 7 May 2017.
15. ^ ^abcdeDalakas MC (2006). 'Sporadic inclusion body myositis--diagnosis, pathogenesis and therapeutic strategies'. Nat Clin Pract Neurol. 2 (8): 437–447. doi:10.1038/ncpneuro0261. PMID16932602.
16. ^Inclusion Body Myositis at eMedicine
17. ^Greenberg SA. (2009). 'Inclusion body myositis: review of recent literature'. Curr Neurol Neurosci Rep. 9 (1): 83–89. doi:10.1007/s11910-009-0013-x. PMID19080758.
18. ^Kitazawa M, Vasilevko V, Cribbs DH, LaFerla FM (13 May 2009). 'Immunization with amyloid-β attenuates inclusion body myositis-like myopathology and motor impairment in a transgenic mouse model'. The Journal of Neuroscience. 29 (19): 6132–41. doi:10.1523/JNEUROSCI.1150-09.2009. PMC3049190. PMID19439591. Lay summary. Inclusion body myositis..features include T-cell mediated inflammatory infiltrates and aberrant accumulations of proteins, including amyloid-β (Aβ), tau, ubiquitinated proteins, apolipoprotein E, and β-synuclein in skeletal muscle. .. active immunization markedly reduces intracellular Aβ deposits and attenuates the motor impairment compared with untreated mice..Aβ oligomers contribute to the myopathy process as they were significantly reduced in the affected skeletal muscle from immunized mice. In addition, the anti-Aβ antibodies produced in the immunized mice blocked the toxicity of the Aβ oligomers in vitro, providing a possible key mechanism for the functional recovery.
19. ^Salajegheh, M, Pinkus, JL, Taylor, JP, Amato, AA, Nazareno, R, Baloh, RH, Greenberg, SA. (2009). 'Sarcoplasmic redistribution of nuclear TDP-43 in inclusion body myositis'. Muscle Nerve. 40 (1): 19–31. doi:10.1002/mus.21386. PMC2700211. PMID19533646.CS1 maint: multiple names: authors list (link)
20. ^Needham M, Mastaglia FL, Garlepp MJ (2007). 'Genetics of inclusion-body myositis'. Muscle Nerve. 35 (5): 549–561. doi:10.1002/mus.20766. PMID17366591.
21. ^Karpati G, O'Ferrall EK (Jan 2009). 'Sporadic inclusion body myositis: Pathogenic considerations'. Ann Neurol. 65 (1): 7–11. doi:10.1002/ana.21622. PMID19194875.
22. ^Broccolini A.; Mirabella M. (2014). 'Hereditary inclusion-body myopathies'. Biochim. Biophys. Acta. 1852 (4): 644–650. doi:10.1016/j.bbadis.2014.08.007. PMID25149037.
23. ^When myositis doesn't respond to treatment Retrieved 20 April 2015.

External links[edit]

The System/38 was a minicomputer and midrange computerserverplatform manufactured and sold by the IBM Corporation. IBM announced the System/38 in 1978.^[1] The System/38 had 48-bit addressing, which was unique for the time, and a novel integrated database system. It was oriented toward a multi-user system environment. The typical system handled from a dozen to several dozen terminals.

• 2Hardware characteristics

History[edit]

The System/38 was introduced on October 24, 1978 and delivered in 1980. Developed under the code-name 'Pacific', it was made commercially available in August 1979. The system offered a number of innovative features, and was the brainchild of Frank Soltis and Glenn Henry. It had been developed over eight years by IBM's laboratory in Rochester, Minnesota.^[2] The president of IBM's General Systems Division (GSD) said at the time: 'The System/38 is the largest program we've ever introduced in GSD and it is one of the top three or four largest programs ever introduced in IBM.'^[3] The System/38 was nearly called the System/380, and the AS/400 was nearly called the System/40.^{[citation needed]}

The system was designed as a follow-on for the System/3,^[3] but it was not compatible with those computers. The predecessors to the System/38 were the System/3 (1969), System/32 (1975), and System/34 (1977). In 1983 the System/36 was released as a low-end business computer for users who found the System/38 too expensive for their needs. The System/38 was succeeded by the AS/400 midrange computer family in 1988. The AS/400 was designed for OS/400 (today's IBM i). Later, the AS/400 line switched from its earlier System/38-like processors to PowerPC-based processors. It subsequently merged with the IBM RS/6000 family, designed to run AIX, into a single family of server computers–the IBM Power Systems, capable of running either IBM i, AIX, or Linux.

Hardware characteristics[edit]

The IBM 5381 System Unit contained processor, main memory, disk storage, a diskette magazine drive, and a system console with keyboard and a display. 5381 was available in Model 100 and Model 200.

The IBM 5382 System Unit was physically identical to 5381, but had more powerful processors, more memory, and more disk storage. 5382 was available in Models 300, 400, 500, 600, and 700.

In hindsight, the System/38's architecture was probably too demanding of the hardware of the era. When first launched, it struggled under the overhead of the software and operating system, which consumed almost 60 MB on disk, a vast sum at the time, leading some wags to suggest that the pre-announce code name for the series, PACIFIC, was actually an acronym meaning 'Performance Ain't Critical If Function Is Complete.'

Processing unit[edit]

The system included a central processing unit with 512K, 768K, 1024K, 1280K, or 1536K bytes of main storage, It included a memory management unit supporting demand paging, used by the system software to implement a single-level store architecture.

System console keyboard/display[edit]

The System/38 console included a keyboard and a display screen with 16 lines of 64 characters, which was inconsistent with the locally attached 5250 terminals, which were either 12x40 or 24x80, depending on model. The keyboard was used by the system operator when entering Control Language commands.

Diskette magazine drive[edit]

The diskette magazine drive was standard on all models.

Control Program Facility[edit]

The operating system of the System/38 was called CPF, for 'Control Program Facility'. CPF is not related to SSP, the operating system of the IBM System/34 and System/36. CPF objects are files, programs, message queues, userprofiles, and libraries.

The System/38 also has the distinction of being the first commercially available IBM Midrange computer to have a database management system (DBMS) integrated into the operating system.

The operational control language of the System/38 was called CL, for 'Control Language'. CL programs, similar in concept to shell scripts, could be compiled and executed natively.

The System/38 also had security built in as part of its architecture. Each object or library could have access controlled on a user-by-user basis. This has been continued and expanded throughout the AS/400 and iSeries computer lines.

Technology independence[edit]

The System/38 and its descendants are the only commercial computers ever to use a machine interface architecture to isolate the application software and most of the operating system from hardware dependencies, including such details as address size and register size.

Compilers for System/38 and its successors generate code in a high-level instruction set (originally called MI for 'Machine Interface', and renamed TIMI for 'Technology Independent Machine Interface' for AS/400). MI/TIMI is a virtual instruction set; it is not the instruction set of the underlying CPU.

Unlike some other virtual-machine architectures in which the virtual instructions are interpreted at runtime (see P-code machine), MI/TIMI instructions are never interpreted. They constitute an intermediate compile time step and are translated into the processor's instruction set as the final compilation step. The MI/TIMI instructions are stored within the final program object, in addition to the executable machine instructions. If a program is moved from a processor with one native instruction set to a processor with another native instruction set, the MI/TIMI instructions will be re-translated into the native instruction set of the new machine before the program is executed for the first time on the new machine.

As a result, it is possible for a program originally developed on a System/38 to run on current IBM i hardware without ever being recompiled. This capability allowed the AS/400 to migrate from CISC (Complex Instruction Set Computer) to RISC (Reduced Instruction Set Computer) in the 1990s. If the MI/TIMI instructions existed in a compiled program, a relatively simple re-translation created a new program native to the new hardware.

Distributed Data Management[edit]

In 1986, System/38 announced support for Distributed Data Management Architecture (DDM). Such a middleware in the context of a distributed system is the software layer that lies between the operating system and applications. Distributed Data Management Architecture defines an environment for sharing data. This enabled System/38 programs to create, manage, and access record-oriented files on remote System/36, System/38, and IBM mainframe systems running CICS. It also allowed programs on remote System/36 and System/38 computers to create, manage, and access files of a System/38.

Programming languages[edit]

Languages supported on the System/38 included RPG III, COBOL, BASIC, and PL/I.

Software[edit]

Decades later, the same software, originally dismissed by some critics^[who?] as a momentary aberration, runs better than ever on many thousands of modern iSeries and IBM/i systems within commercial and government enterprises of all types and sizes.^{[citation needed]}

Successor system[edit]

The System/38 was superseded by the AS/400 (which also supported System/36 data & programs, to a fairly large extent, with some exceptions). The AS/400 was primarily a re-marketing of the System/38, with some updates to the operating system, including the luxurious non-trivial expansion of source and object names from 8 to a new 10 characters maximum. S/38 programs with 'observability' intact, that is source code embedded within the compiled binary executive at the expense of larger compiled object sizes, can still run on the AS/400 and successor systems as the restore option incorporates a recompile for the then back-version source. However, most proprietary vendor application libraries of objects were compiled without such 'observability' and required original vendor replacement and consequent expense when upgrading to an AS/400. Pricing at the time was tiered, the same exact software, but priced based upon the model, its speed and capacity, of the system to be installed upon.

Sales[edit]

IBM sold an estimated 20,000 System/38s within the first five years of availability, according to articles published in industry magazines NEWS 34/38 and Midrange Computing. Although billed as a minicomputer, the S/38 was much more expensive than IBM's established best-selling System/34, and its replacement, the System/36. Of equal importance was the difficulty of upgrading from, say, a System/34 to a S/38. Although the machines had some similarities, such as twinax peripherals and RPGprogramming languages, in reality they were very different. IBM tacitly acknowledged this by bringing out the System/36 – an upgraded System/34 – after the launch of the S/38.

In the marketplace, IBM thus found itself with three overlapping, but incompatible, ranges. The System/34/36, the System/38 and the mainframe /360 architecture (that the System/38 was originally designed to replace). Digital Equipment Corporation, at that time one of IBM's main competitors, was able to exploit this by offering a wide range of products based on a single architecture. IBM's counter to this, the 9370 or 'baby mainframe', was a commercial failure.

References[edit]

1. ^'IBM Archives: 1970s, year 1978'. IBM.
2. ^'IBM Rochester @ 50'(PDF).
3. ^ ^ab'IBM System/38'. IBM Archives.

Further reading[edit]

• Levy, Henry M. (1984). 'The IBM System/38'(PDF). Capability-Based Computer Systems. Digital Press. ISBN0-932376-22-3.
• Soltis, Frank G.; Hoffman, RL (Spring 1979). Design Considerations for the IBM System/38. Compcon. IEEE. pp. 132–37.
• IBM System/38 Technical Developments(PDF). IBM Product Design and Development, General Systems Division. 1980 [1978]. ISBN0-933186-03-7. G580-0237-1.
  • Henry, GG (1980) [1978]. 'Introduction to IBM System/38 Architecture'. IBM System/38 Technical Developments(PDF). IBM Product Design and Development, General Systems Division. pp. 3–6. ISBN0-933186-03-7. G580-0237-1.
  • Berglund, NC (1980) [1978]. 'Processor Development in the LSI Environment'. IBM System/38 Technical Developments(PDF). IBM Product Design and Development, General Systems Division. pp. 7–10. ISBN0-933186-03-7. G580-0237-1.
  • Curtis, HW (1980) [1978]. 'Integrated circuit design, production, and packaging for System/38'. IBM System/38 Technical Developments(PDF). IBM Product Design and Development, General Systems Division. pp. 11–15. ISBN0-933186-03-7. G580-0237-1.
  • Donofrio, MN; Flur, B; Schnadt, RT (1980) [1978]. 'Memory design/technology for System/38'. IBM System/38 Technical Developments(PDF). IBM Product Design and Development, General Systems Division. pp. 16–18. ISBN0-933186-03-7. G580-0237-1.
  • Hoffman, RL; Soltis, FG (1980) [1978]. 'Hardware organization of the System/38'. IBM System/38 Technical Developments(PDF). IBM Product Design and Development, General Systems Division. pp. 19–21. ISBN0-933186-03-7. G580-0237-1.
  • Houdek, ME; Mitchell, GR (1980) [1978]. 'Translating a large virtual address'. IBM System/38 Technical Developments(PDF). IBM Product Design and Development, General Systems Division. pp. 22–24. ISBN0-933186-03-7. G580-0237-1.
  • Lewis, DO; Reed, JW; Robinson, TS (1980) [1978]. 'System/38 I/O structure'. IBM System/38 Technical Developments(PDF). IBM Product Design and Development, General Systems Division. pp. 25–27. ISBN0-933186-03-7. G580-0237-1.
  • Dumstorff, EF (1980) [1978]. 'Application of a microprocessor for I/O control'. IBM System/38 Technical Developments(PDF). IBM Product Design and Development, General Systems Division. pp. 28–31. ISBN0-933186-03-7. G580-0237-1.
  • Roellinger, Jr, FX; Horn, DJ (1980) [1978]. 'Microprocessor-based communications subsystem'. IBM System/38 Technical Developments(PDF). IBM Product Design and Development, General Systems Division. pp. 32–35. ISBN0-933186-03-7. G580-0237-1.
• Berstis, Viktors (May 6–8, 1980). Security and protection of data in the IBM System/38. 7th Annual symposium on Computer Architecture. La Baule, US: ACM. pp. 245–52. doi:10.1145/800053.801932.
• Sincoskie, W. David; Farber, David ‘Dave’ J. (July 1980). 'SODS/OS: Distributed Operating System for the IBM Series/1'. Operating Systems Review. 14 (3): 46–54. doi:10.1145/850697.850704.
• Houdek, Merle E.; Soltis, Frank G.; Hoffman, Roy L. (1981). IBM System/38 support for capability-based addressing. 8th annual symposium on Computer Architecture. Minneapolis, MN, US: IEEE Computer Society Press. pp. 341–48.
• Soltis, Frank G. (September 1981). 'Design of a Small Business Data Processing System'. Computer. IEEE. 14 (9): 77–93. doi:10.1109/c-m.1981.220610. ISSN0018-9162.
• Phuc, Nguen Hoan; Becker, M; Sevray, P (1983). Dean, SM; Hammersley, P (eds.). Performance Comparison Between B*-Tree and Prefix Binary Tree Index Organizations. 2nd Int'l Conference on Databases. Churchill College, Cambridge: Wiley Heyden.
• Newman, M (1986), The Architecture of the IBM System/38. IBM Small and Medium Systems Infotech State of the Art Report, Oxford: Pergamon

External links[edit]

• 'IBM Archives -- Glossary 3'. IBM.
• Corestore Museum System/38 performing power-up & diagnostic IPL from floppy (video).