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LPI 101-500 : LPIC-1 test 101 Exam

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Exam Number : 101-500
Exam Name : LPIC-1 test 101
Vendor Name : LPI
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101-500 test Format | 101-500 Course Contents | 101-500 Course Outline | 101-500 test Syllabus | 101-500 test Objectives

Course Outline: LPIC-101 Certified Linux Administrator

This course prepares students to take the 101 test of the LPI level 1 certification. The Linux Professional Institute (LPI) is the go to certification body for vendor independent Linux certifications. This course covers fundamental Linux skills such as file management and manipulation, text processing, command line use, package management, filesystems, hardware, and many more. Students will feel confident taking the LPI LPIC-1 101 test with in classroom assessments and practice exams.

Module 1: Work on the command line
=> Role of command shell
=> Shells
=> Gathering system info
=> Identifying the shell
=> Changing the shell
=> Shell prompts
=> Bash: bourne-again shell
=> Navigating the filesystem
=> Help from commands and documentation
=> Getting help within the graphical desktop
=> Getting help with man $ info
=> Bash: command line history
=> Bash: command editing
=> Bash: command completion
=> Shell and environment variables
=> Key environment variables Lab tasks
=> Help with commands
=> Linux shells
=> Shell variables
=> Bash history
=> Aliases
Module 2: Use streams, pipes, and redirects
=> File redirection
=> Piping commands together
=> Filename matching
=> File globbing and wildcard patterns
=> Brace expansion
=> General quoting rules
=> Nesting commands
=> Gotchas: maximum command length
Lab tasks
=> Redirection and pipes
=> Wildcard file matching
=> Shell meta-characters
=> Command substitution
Module 3: Manage file permissions and ownership
=> Filesystem hierarchy standard
=> Displaying directory contents
=> Filesystem structures
=> Determining disk usage with df and du
=> File ownership
=> Default group ownership
=> File and directory permissions
=> File creation permissions with umask
=> Changing file permissions
=> Suid and sgid on files
=> Sgid and sticky bit on directories
=> User private group scheme
Lab tasks
=> Navigating directories and listing files
=> Disk and filesystem usage
=> File and directory ownership and permissions
Module 4: Create, delete, find, and display files
=> Directory manipulation
=> File manipulation
=> Deleting and creating files
=> Physical unix file structure
=> Filesystem links
=> File extensions and content
=> Which and type
=> Whereis
=> Searching the filesystem
=> Alternate search method
=> Manually installed shared libraries
Lab tasks
=> Manipulating files and directories
Module 5: Work with archives and compression
=> Archives with tar
=> Archives with cpio
=> The gzip compression utility
=> The bzip2 compression utility
=> The xz compression utility
=> The pkzip archiving/compression format
Lab tasks
=> Archiving and compression
=> Using tar for backups
=> Using cpio for backups
Module 6: Process text streams using filters
=> Producing file statistics
=> The streaming editor
=> Replacing text characters
=> Text sorting
=> Duplicate removal utility
=> Extracting columns of text
=> Displaying files
=> Prepare text for display
=> Previewing files
=> Displaying binary files
=> Combining files and merging text
Lab tasks
=> Text processing
=> Processing text streams
Module 7: Search text files using regular expressions
=> Searching inside files
=> Regular expression overview
=> Regular expressions
=> Re character classes
=> Regex quantifiers
=> Re parenthesis
Lab tasks
=> Pattern matching with regular expressions
=> Extended regular expressions
=> Using regular expressions with sed
Module 8: Perform basic file editing operations using vi
=> Text editing
=> Vi and vim
=> Learning vim
=> Basic vi
=> Intermediate vi
Lab tasks
=> Text editing with vim
Module 9: Create, monitor, and kill processes
=> What is a process=>
=> Process lifecycle
=> Process states
=> Viewing processes
=> Signals
=> Tools to send signals
=> Managing processes
=> Tuning process scheduling
=> Job control overview
=> Job control commands
=> Nohup and disown
=> Uptime
=> Persistent shell sessions with screen
=> Using screen
=> Advanced screen
Lab tasks
=> Job control basics
=> Process management basics
=> Screen basics
=> Using screen regions
Module 10: Use rpm, yum, and debian package management
=> Managing software
=> Rpm architecture
=> Working with rpms
=> Querying and verifying with rpm
=> Installing debian packages
=> Querying and verifying with dpkg
=> The alien package conversion tool
=> Managing software dependencies
=> Using the yum command
=> Yumdownloader
=> Configuring yum
=> The dselect $ apt frontends to dpkg
=> Aptitude
=> Configuring apt
Lab tasks
=> Working with rpms on ubuntu
=> Querying the rpm database
Module 11: Work with partitions, filesystems, and disk quotas
=> Partition considerations
=> Logical volume management
=> Filesystem planning
=> Partitioning disks with fdisk $ gdisk
=> Resizing a gpt partition with gdisk
=> Partitioning disks with parted
=> Filesystem creation
=> Filesystem support
=> Unix/linux filesystem features
=> Swap
=> Selecting a filesystem
=> Filesystem maintenance
=> Mounting filesystems
=> Mounting filesystems
=> Managing an xfs filesystem
=> Nfs
=> Smb
=> Filesystem table (/etc/fstab)
=> Configuring disk quotas
=> Setting quotas
=> Viewing and monitoring quotas
Lab tasks
=> Hot adding swap
=> Accessing nfs shares
=> Setting user quotas
Module 12: Linux boot process
=> Booting Linux on pcs
=> Grub 2
=> Grub 2 configuration
=> Grub legacy configuration
=> Boot parameters
=> Init
=> Linux runlevels aliases
=> Systemd and
=> Runlevel implementation
=> System boot method overview
=> Systemd system and service manager
=> Systemd targets
=> Using systemd
=> Shutdown and reboot
=> System messaging commands
=> Controlling system messaging
Lab tasks
=> Command line messaging
=> Messaging with talkd
=> Boot process
=> Grub command line
=> Basic grub security
Module 13: Determine and configure hardware settings
=> Managing Linux device files
=> Hardware discovery tools
=> Configuring new hardware with hwinfo
=> Pc architecture and bus
=> Dma $ irq
=> Usb devices
=> Usb configuration
=> Configuring kernel components and modules
=> Kernel modules
=> Handling module dependencies
=> Configuring the kernel via /proc/
=> Kernel hardware info /sys/
=> /sys/ structure
=> Random numbers and /dev/random
Lab tasks
=> Adjusting kernel options
Module 14: linux fundamentals
=> Unix and its design principles
=> Fsf and gnu
=> Gpl general public license
=> The linux kernel
=> Components of a distribution
=> Red hat linux products
=> Suse linux products
=> Debian
=> Ubuntu
=> Logging in
=> Got root=>
=> Switching user contexts
Gathering login session info
Lab tasks
=> Login and discovery
=> Switching users with su

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LPI 101 test prep

Molecular analysis of Genetic Iron-overload disorders | 101-500 PDF Dumps and Free PDF

Molecular prognosis of HFE-connected Hemochromatosis (category 1 Hemochromatosis) Molecular, mobile & Pathophysiological historical past

figure 1 offers a top level view of the pathophysiology of category 1 hemochromatosis. category 1 hemochromatosis is attributable to the HFE gene observed on chromosome 6,[3] and most regularly regarding C282Y homozygosity. it's hence a recessive disease, and best C282Y homozygotes can advance clinically enormous iron overload.[4] The average HFE gene probably acts as an iron sensor that interacts with transferrin receptors (TFRs) 1 and a couple of after which prompts a signaling cascade.[5] The C282Y mutation in HFE inhibits a molecular cascade that ends with diminished hepatic production of hepcidin, the iron hormone.[6–9] It is not yet clear at which stage HFE interacts with this cascade, which includes the BMP/SMAD pathway,[10,11] with two proteins taking part in an incredible position physiologically in activating this pathway – hemojuvelin[12] and BMP6.[13–15] in the case of C282Y homozygosity, the ensuing decreased production of hepcidin by using the liver ends up in iron overload. indeed, lowered hepcidin results in intestinal hyperabsorption of iron and better free up of iron from the spleen (this iron comes from the normal degradation of growing older purple blood cells in the body of the physiological erythrophagocytotic manner). as a result of this improved iron arrival into the plasma from two diverse sources, plasma iron rises, leading to accelerated saturation of transferrin, the physiological plasma iron transporter. This enhanced transferrin saturation (>45% and sometimes >eighty%), in flip, generates the appearance of a abnormal species of circulating iron, called non-transferrin-bound iron (NTBI).[16]

determine 1.

Mechanism of iron overload in quantitative hepcidin deficiency (hemochromatosis forms 1, 2 and three). (A) Corresponding HFE and non-HFE mutations result in diminished hepcidin construction; (B) and (C) lowered hepcidinemia raises intestinal iron absorption; (D) and (E) diminished hepcidinemia increases iron unlock from the spleen; (F) the ensuing hypersideremia leads, via non-transferrin-sure iron, to iron deposition within the liver (however additionally the pancreas and the heart). tailored with permission from.[1]

Non-transferrin-bound iron has two important houses. First, it is avidly taken up via the quite a few parenchymal cells (certainly within the liver,[17] the pancreas and the coronary heart), accounting for the building of visceral iron deposition. 2nd, it takes a specific kind, referred to as labile plasma iron (LPI),[18] which seems when transferrin saturation is over 75%.[19] LPI is liable to producing radical oxygen species, leading to its additional designation as reactive plasma iron, and represents the potentially toxic sort of circulating iron. as a result of chronic and predominant extra intracellular iron deposition, cells are steadily damaged and lesions develop in corresponding organs. These deleterious effects explain the leading scientific manifestations of persistent iron-overload disorders.[1,20] The liver raises in quantity (hepatomegaly), releases more transaminases into the plasma (as a result of cytolysis), and develops a scarring manner corresponding to fibrosis that may cause cirrhosis and, afterward, to hepatocellular carcinoma. excessive iron deposition in the pancreas, coronary heart and endocrine glands (pituitary, gonads) can cause insulin-elegant diabetes, cardiac failure and hypogonadism (with impotence in men), respectively. moreover, bone and joints may also be affected, leading to osteoporosis and persistent arthritis, the epidermis turns into hyperpigmented (bronzed) and persistent fatigue is a widespread symptom. Importantly, when on account that the natural history of category 1 hemochromatosis, besides the fact that children excessive iron deposition begins from start, scientific indicators only occur in adulthood (around age forty years in men and 50 years in ladies), for this reason, HFE-related hemochromatosis is a genetic sickness it truly is clinically expressed only in adults.

Epidemiological & Therapeutic features

From the epidemiological perspective, class 1 hemochromatosis issues most effective Caucasian populations. likely of Celtic beginning,[21] the C282Y mutation is incredibly usual during this population, affecting more than 10% of Caucasian people. as a minimum one adult in a thousand is homozygous for this mutation, and the regular frequency is approximately three individuals in one thousand, with even enhanced frequency in some areas, akin to Brittany (France) and ireland. Penetrance, in terms of each plasma iron indicators and associated sickness indicators, is partial,[22–25] and analysis pursuits identification of alternative genes/polymorphisms that modulate HFE feature and the interaction among genetic history, C282Y and environmental elements.[26–28]

From a therapeutic perspective, class 1 hemochromatosis is likely one of the infrequent genetic diseases for which there's a good remedy.[29,30] It contains repeated phlebotomies (venesections) on the precept of subtracting pink blood cells, which are normal to be wealthy in iron, therefore obliging the body to atone for this loss of erythrocytes by way of pumping its iron from its storage locations (particularly the liver). provided this remedy is all started before the onset of extreme problems, corresponding to cirrhosis, insulin-elegant diabetes, cardiomyopathy or harmful arthritis, the efficacy is striking, and patients Excellerate each an excellent great of life and general life expectancy.

Diagnostic elements with particular Emphasis on Molecular diagnosis

The diagnosis is in line with a 3-step method. step one is recognizing scientific signals and signs. Many symptoms in numerous combinations may additionally indicate the chance of hemochromatosis, together with chronic fatigue, impotence, joint pains, osteoporosis, gentle hypertransaminasemia, hepatomegaly, cirrhosis, diabetes, cardiac rhythm disturbances, coronary heart failure and dermis pigmentation.

The 2nd step is confirmation of iron overload. This confirmation is in keeping with each biochemical and imaging thoughts. Biochemically, plasma iron and transferrin saturation (proven by a 2nd fasting saturation percent) are extended, reflecting the simple mechanism it is dysregulated in this ailment. There should be an accelerated plasma concentration of ferritin, which reflects intracellular iron excess (ferritin being the intracellular iron storage protein) and represents a key biochemical parameter in diagnosing iron excess, supplied confounding medical instances were dominated out (equivalent to inflammatory syndrome, polymetabolic syndrome, alcoholism, or rarer circumstances, such as those involving L-ferritin mutations with or devoid of cataract[31,32]). MRI is a great tool for confirming visceral iron overload by using displaying a characteristic hyposignal with an depth correlated with the degree of iron extra.[33,34] The T2-star MRI approach has been developed for the evaluation of cardiac iron.[35]

The third and last step is molecular analysis. the usage of blood sampling, cheek brushing or saliva sampling, the genetic test have to be carried out best after the patient has given suggested consent.[36] It has no indication in newborns or in people below 18 years of age (because phenotypic expression is restrained to adults). This verify can detect the presence of C282Y homozygosity, confirming the analysis of category 1 hemochromatosis. This legit molecular look at various makes it possible for for a noninvasive diagnostic system because it has rendered liver biopsy out of date for the prognosis of type 1 hemochromatosis. it can be emphasized that fundamental C282Y heterozygosity can not be regarded to be chargeable for clinically colossal body iron excess, even within the variety of HFE compound heterozygosity (peculiarly C282Y/H63D), that could only clarify a confined and constant boost of plasma transferrin saturation and ferritin.[37] Likewise, H63D homozygosity, regardless of some experimental records[38] and infrequent case stories, isn't frequently regarded to account alone for gigantic iron extra. In apply, the look for the H63D mutation is no longer suggested in France[101] and should be confined to scientific analysis. The identical holds genuine for other HFE mutations, equivalent to S65C, V59M, R66C, G93R, I105T, R224G and V295A.[39] every time a C282Y mutation within the heterozygous state is associated with large visceral iron overload (hepatic iron awareness more than threefold the higher commonplace limit), one ought to search both for an associated rare HFE mutation[40–42] or for linked non-HFE mutations.[43] A homozygous deletion or frameshift mutation of HFE also can produce a phenotype akin to that as a consequence of C282Y/C282Y homozygosity.[44–46] even if haplo-insufficiency of HFE can result in hemochromatosis is still beneath dialogue.[47]

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