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250-240 - Administration of Storage Foundation 4.0 for UNIX - Dump Information

Vendor : Symantec
Exam Code : 250-240
Exam Name : Administration of Storage Foundation 4.0 for UNIX
Questions and Answers : 128 Q & A
Updated On : October 16, 2017
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250-240 Questions and Answers

250-240


  1. Allocation Unit

  2. Relocation Unit

  3. Allocation Policy

  4. Relocation Policy


Answer: C


QUESTION: 119

Which condition is possible using Cross-Platform Data Sharing in Storage Foundation 4.0?


  1. CDS disks and sliced disks in the same sliced disk group

  2. sliced disks and CDS disks in the same CDS disk group

  3. an encapsulated CDS root disk

  4. a version 90 CDS data disk group


Answer: A


QUESTION: 120

Which must be created FIRST in the creation of a multivolume file system?


  1. an Allocation Policy

  2. a new file system

  3. a volume set

  4. a file set


Answer: C


QUESTION: 121

In the QoSS model, the data center and its service accounts typically set service-level agreements that define metrics. Which four metrics are used in the QoSS model? (Choose four.)


  1. System Administrator training

  2. survivability of data

  3. time to recovery

  4. time to capacity

  5. volumes split between disk groups

  6. application performance guarantees


Answer: B, C, D, F


QUESTION: 122

What is an application volume?


  1. a meaningful collection of template sets that define how storage is organized

  2. a volume used to manage two or more hardware paths directing I/O to a single drive

  3. a volume that is created in a storage pool

  4. an image of data at a selected instant


Answer: C


QUESTION: 123

Intelligent storage provisioning provides a method to .


  1. standardize how volumes are created, modified, and managed

  2. reduce the impact of volume synchronization on online performance

  3. disable I/O to a host disk controller

  4. discontinue the use of vxconfigd


Answer: A


QUESTION: 124

Which option to the vxsnap command retakes a space-optimized instant snapshot?


  1. restore

  2. reattach

  3. refresh

  4. reassociate


Answer: C


QUESTION: 125

You can use intelligent storage provisioning to .

  1. recover from an intermittent disk failure by moving data off of the disk and removing the disk from the system

  2. add an additional container in the disk group to hold all the disks to be used for off- host processing

  3. adjust the tuning parameters to optimize system performance

  4. start, stop, and report on Volume Manager I/O daemons


Answer: B


QUESTION: 126

What are two advantages of using a Logical Point-In-Time Copy (PITC)? (Choose two.)


  1. The PITC is initially a complete copy of the primary data.

  2. The PITC is available for use instantaneously.

  3. Potentially, less storage space is required.

  4. The storage space required is the same regardless of volume size.


Answer: B, C


QUESTION: 127

Which level in the device hierarchy does NOT have to provide support for Cross-

Platform Data Sharing?


  1. VERITAS File System

  2. end-user applications

  3. operating system

  4. dynamic multipathing


Answer: D


QUESTION: 128

Which Point-In-Time copy solution provided by VERITAS Storage Foundation 4.0

requires an amount of free disk space equal to that of the original volume?


  1. full file system snapshot

  2. full-sized instant snapshot

  3. full buffer-optimized instant snapshot

  4. storage checkpoint

Answer: B 39


Symantec 250-240 Exam (Administration of Storage Foundation 4.0 for UNIX) Detailed Information

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  • 019 10.0 facets in this question, n=8. here is

    Unformatted textual content preview: 019 10.0 aspects during this query, n=8. here is because C starts as CH four and turns into CO 2 . If the general free power change for com- bustion of 1 mole of CH 4 (g) is- 818 kJ mol 1 , calculate the usual voltage that may well be bought from a gas mobile the use of this reaction. 1. + 4.24 V 2.- 1.06 V 3. + 8.48 V 4. + 0.53 V 5. + 1.06 V appropriate clarification: 020 10.0 aspects Catalysts work through 1. expanding the exothermicity of the reac- tion, which increases entropy within the encompass- ings, making the reaction extra favorable. 2. expanding the diffusion rates (collision fee) of molecules in answer. 3. increasing the kinetic power of the reac- tant molecules. four. developing a brand new response route with a decrease activation barrier. proper rationalization: Definition 021 10.0 facets here is a BONUS query: get it correct your max features are 250/240; get it wrong and your max elements are 240/240. The common response for the discharge of a nickel/cadmium mobilephone is Cd + NiO 2 + 2 H 2 O Cd(OH) 2 + Ni(OH) 2 Which of here statements is right? 1. Cadmium metallic loses 2 electrons and is converted to Cd 2+ on the cathode. 2. it's unimaginable to recharge a nickel/cadmium cell. 3. The nickel is oxidized right through this reac- tion. four. Insoluble Cd(OH) 2 is deposited on the anode. relevant explanation: looking at the reaction above, Cd Cd 2+ + 2 e is an oxidation response with the intention to occur on the anode. The nickel is not oxidized because we have proven that Cd is being oxidized. Nickel/cadmium batteries are rechargable. Insoluble CD(OH) 2 is deposited on the an- ode considering that Cd is oxidized on the anode. 022 10.0 elements a definite response is found to have a price steady of 1.50 10 8 sec 1 at 0 C and an activation energy of forty five.0 kJ mol 1 . What will be its expense consistent at a hundred C? 1. k = 68 . four s 1 2. not one of the different answers is proper. 3. k = 7 . 37 10 eleven s 1 four. k = 3 . 05 10 6 s 1 relevant 5. ok = three . 10 10 three s 1 explanation: edition 173 examination four 302 sutcliffe (51060) 7 T 1 = 273 k T 2 = 373 ok E A = 45 . 0 kJ k 1 = 1 . 50 10 eight sec 1 ln ok 2 ok 1 = ln ok 2- ln okay 1 = E A R parenleftbigg 1 T 1- 1 T 2 parenrightbigg ln ok 2 = ln ok 1 + E A R parenleftbigg 1 T 1- 1 T 2 parenrightbigg = ln 1 . 50 10 eight + 45000 eight . 314 parenleftbigg 1 273- 1 373 parenrightbigg =- 12 . 699876 ok 2 = three . 05 10 6 s 1 023 10.0 points note: use a = 1 in this query. For the reaction cyclopropane propene a plot of ln[cyclopropane] vs time in seconds offers a straight line with slope- four . 1 10 three s 1 at 550 C. what's the rate constant for this reaction? 1. 1 . eight 10 3 s 1 2. 8 . 2 10 3 s 1 three. 4 . 1 10 3 s 1 proper four. three . 9 10 2 s 1 5. 2 . 1 10 3 s 1 explanation: 024 10.0 points be aware: use a = 1 during this query....View Full document


    (school document playing cards 1996)

    November 14, 1996

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    Your key to analyzing faculty file playing cards

    The 1985 college reform legislations enacted by means of the state legislature dependent the Illinois purpose assessment software as an accountability measure to compel the training neighborhood record to taxpayers on student success.

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    each and every score within the separate, faculty-by-school tables is the typical for college kids at each faculty who took the examine. The percent of seniors who took the ACT also is listed. no longer all take the examination. charge per pupil is the typical can charge to each scholar in a school district. p.c low earnings is the percent of students from families beneath the poverty line in a faculty district. %%

    Suburban cook County

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    Chicago Ridge 127 270 229 226 353 257 246 20.5 23.3 26.5

    Cicero 99 182 a hundred and seventy 169 218 209 218 16.four 21.three 23

    Cntry membership

    Hills 160 223 191 209 238 217 239 17.9 21 25.2

    cook County one hundred thirty 215 212 198 227 235 257 17 21.7 22.2

    Des Plaines 62 260 271 255 336 336 300 19 24.four 26.four

    Dolton 148 210 219 195 234 240 222 16.7 23.1 24.1

    Dolton 149 189 198 194 247 223 207 17.5 19.8 22.8

    East Maine 63 264 296 259 303 319 294 19.5 22.7 25.1

    East Prairie 73 246 252 262 323 333 344 18.7 23 26

    Elmwood Park 401 255 265 253 281 283 269 17.7 23.3 26.three

    Evanston sixty five 281 278 274 316 316 331 18.6 23.7 26.7

    Evergreen Park 124 275 294 270 308 317 292 17.6 25.1 26.7

    Flossmoor 161 274 292 279 317 314 331 19 25.7 27.three

    Ford Heights 169 217 163 149 209 191 183 17 19 20.four

    forest Park ninety one 237 257 265 287 301 321 17.1 22 25.3

    woodland Ridge 142 285 258 253 344 307 300 18.3 24.1 25.6

    Franklin Park 84 274 253 258 298 297 295 20.5 23.5 26.9

    Glencoe 35 310 322 337 350 375 409 17.6 25 25.9

    Glenview 34 296 294 273 332 350 341 20.6 25.eight 25.8

    Golf 67 315 277 279 369 300 335 20.7 25.5 27.7

    Harvey 152 191 187 171 230 216 197 15.eight 20 21.7

    Hazel Crest 152 218 195 179 257 219 212 13.2 20.9 21.6

    Hillside 93 280 252 259 332 287 294 21.2 22 26.3

    Homewood 153 308 314 278 353 327 327 20.5 25.2 26.3

    Hoover- Schrum 157 223 214 223 252 247 258 15.6 22.four 23.9

    Indian Springs 109 229 245 216 262 273 285 18.1 22.7 24.1

    Kenilworth 38 334 346 349 362 398 434 20.4 22.3 26.5

    Kirby one hundred forty 290 283 260 342 318 325 19.eight 23.2 24.6

    Komarek ninety four 250 240 213 253 312 287 15.7 23.6 25.3

    La Grange 102 326 291 299 373 328 329 19.4 24.3 26

    LaGrange

    Hilands 106 327 326 339 384 354 362 19.four 24.6 28.5

    LaGrange S. 105 259 300 264 314 340 331 18.three 24.eight 24

    Lansing 158 265 281 246 295 273 296 19 21.5 24

    Lemont-Brombrek 113 282 286 284 308 316 334 18.eight 22.8 25

    Lincoln 156 199 one hundred seventy five 187 233 213 243 sixteen.3 20 21.three

    Lincolnwood 74 275 303 293 322 352 364 20.2 25.four 26.5

    Lindop ninety two 204 217 236 264 247 280 17.5 21.9 25

    Lyons 103 224 234 254 248 262 269 sixteen.eight 20.9 24.three

    Mannheim eighty three 260 242 218 287 287 262 18.1 22.9 23.eight

    Matteson 159 262 278 263 321 293 304 17.7 23 25.6

    Matteson 162 249 237 238 294 263 254 17.7 21.four 24.3

    Maywd-MelPk-

    Brdvw 89 179 180 181 202 205 216 sixteen.5 21.three 23.5

    Midlothian 143 239 242 218 274 242 265 17.4 21.5 24.8

    Morton Grove 70 263 297 278 294 326 338 20.9 23.9 27.four

    Mt Prospect 57 291 307 312 345 336 347 20.2 25.2 28.2

    Niles 71 291 304 269 374 326 339 19.4 23.7 27.7

    Norridge eighty 273 261 264 326 312 323 18.5 23.6 25.4

    North Palos 117 270 255 239 311 287 274 20.5 24.9 26

    Northbrk-

    Glenview 30 321 319 299 374 368 353 19.eight 22.eight 27.6

    Northbrook 27 327 312 298 376 363 395 21.5 25.9 27.8

    Northbrook 28 348 319 301 396 355 391 21.2 26 29

    okayLwn-

    place of origin 123 279 282 279 306 317 300 19.7 24.9 27.2

    alrightPark 97 303 298 269 327 323 306 20.1 24.eight 25.8

    Orland a hundred thirty five 274 279 261 328 328 335 19.eight 25.1 26

    Palatine 15 308 319 290 350 369 342 20.2 25.2 27


    APOPTOSIS, NECROPTOSIS and AUTOPHAGY associate Professor Dr. Alexey Podcheko Spring 2015.

    1

    2 APOPTOSIS, NECROPTOSIS and AUTOPHAGY associate Professor Dr. Alexey Podcheko Spring 2015

    three goals 1. define apoptosis 2. compare and distinction the morphologic adjustments seen in apoptosis versus necrosis three.outline the 4 phases of apoptosis 4. Describe the intrinsic and extrinsic pathways of apoptosis

    four objectives 5. record 4 physiologic examples of apoptosis 6. listing one role of apoptosis in the Pathology of the immune system 7. Describe the function of p53 in carcinogenesis eight. Describe the role of apoptosis in neurodegenerative illnesses 9. outline Autophagy 10. list 2 diseases where Autophagy play role in pathogenesis

    5 stages of the mobile response to emphasize and injurious stimuli

    6

    7 APOPTOSIS  DEFINITION: energy dependent CONTOLLED system OF PROGRAMMED cell dying.

    eight energy stylish CONTOLLED technique OF PROGRAMMED mobilephone loss of life

    9

    10 Apoptosis Why may still I care?

    11

    12 (keeps regular size of the organ) (continual myelogenous leukemia)

    13 Complexity of Apoptotic pathways

    14 Comparative morphologies of Apoptosis and Necrosis

    15

    sixteen

    17 both important routes to Apoptosis: Intrinsic and Extrinsic

    18

    19 The extrinsic (dying receptor–initiated) pathway of apoptosis

    20 click on here to peer video

    21 The intrinsic or mitochondrial pathway 1.involves Bcl household of proteins 2.each pro and anti apoptotic contributors 3.greatest primary is anti- apoptotic Bcl2 4.construction of Bcl2 can be precipitated by way of increase components (IGF1) deprivation or IR

    22 The mitochondrial pathway of Apoptosis BCL2 antagonists- Bim, Bid, and dangerous Smac/DIABLO (blocks IAPs)

    23 The equilibrium between proapoptotic and antiapoptotic members of the Bcl-2 family of proteins displays binding of antiapoptotic contributors to themselves (homodimers) or to the proapoptotic proteins Bak and Bax

    24 Opening of the mitochondrial permeability transition pore leads to Apaf-1 activation and triggering the apoptotic cascade. CytC- cytochrome c PTP= permeability transition pores ROS = reactive oxygen species

    25 An test introduces a “knockout” gene mutation right into a phone line. The frequency of shrunken cells with chromatin clumping and cytoplasmic blebbing is expanded compared with a telephone line devoid of the mutation. ordinary survival of the mutant cellphone line is reduced. Which of right here genes is absolutely to be littered with this mutation? (A) BAX (B) p53 (C) C-MYC (D) FAS (E) BCL-2

    26 a way to discover or measure apoptotic pursuits in the tissues ?

    27

    28

    29 Poly (ADP-ribose) polymerase (PARP) is a protein concerned in a couple of cellular techniques- exceptionally DNA fix and programmed telephone demise Inducer of Apoptosis - +

    30

    31 Phosphatidylserine publicity all through apoptosis Annexin-V-FITC “devour-me” sign for skilled phagocytes

    32 Phosphatidylserine publicity all through apoptosis Propidium Iodide stains in pink only cells with damaged membranes

    33

    34 DNA condensation and fragmentation of base pair fragments is among the earliest degrees of apoptosis! manner of fragmentation will proceed except fragment size will attain app. 200 base pairs. Why?

    35 DNA Fragmentation accessories of a nucleosome

    36 DNA Fragmentation Nucleosomal Banding pattern

    37

    38

    39

    40

    41 Accumulation of cells in sub-G1 phase of cellphone cycle all the way through apoptosis G1 S G2/M

    forty two How apoptotic cells removed from tissues? Phagocytosis is the leading mechanism alerts for phagocytosis are: 1.Flip of phosphatidylserine from internal to outer leaflet of mobile membrane (ligand for macrophages receptors) 2. Secretion of soluble factors that recruit phagocytes three.construction of thrombospondin on telephone surface of apoptotic cells four.Coating of apoptotic cells with C1q complement

    43 Apoptosis Why may still I care?

    44

    45 role of Apoptosis in the Hand Plate

    forty six A forty y/o male dropped at ED submit-MVA. affected person has a background of fever, headache, chills, and ache in RUQ 5 days ago. Histologic exam suggests liver section w/disruption of usual hepatic lobule. Small shrunken hepatocytes w/severe eosinophilic cytoplasm, fragmented nuclear chromatin, & cytoplasmic bleb formations are referred to. Which procedure is certainly happening within the hepatocytes described? A) apoptosis B) Atrophy C) Caseous necrosis D) Coagulation necrosis E) Dysplasia F) Fatty alternate G) Hetrophagy H)Liquefaction necrosis I) metaplasia

    forty seven CLINICO-PATHOLOGIC CORRELATIONS: APOPTOSIS AND sickness 1.decreased Apoptosis – melanoma, Autoimmune ailments (SLE, Rheumatoid Arthritis, and many others) 2.expanded Apoptosis – Neurodegenerative diseases, Myocardial Infarction, Stroke, Viral illnesses (Hepatitis, AIDS)

    forty eight A 55-yr-historical woman with colon melanoma and a fit fifty five-yr-historic girl are taking part a analyze of colon cancer. Malignant cells are acquired from the tumor in the affected patient, and general colonic epithelial cells are procured from the fit field. After each mobilephone forms are treated with reworking boom component-beta, the number of typical cells decreases, whereas the variety of tumor cells is still unchanged. The tumor cells obviously specific a mutation that inhibits which of right here physiologic strategies? A) Apoptosis B) telephone cycle progression C) DNA fix D) Migration E) Necrosis

    49 increase aspect Deprivation: Lymphocytes that aren't inspired by means of antigens and cytokines, neurons deprived of nerve growth ingredient, endometrial glands in put up menopause DNA damage: Radiation or chemotherapeutic agents induces DNA harm Mechanisms of extended apoptosis:

    50 position of P53 Tumor suppressor protein in apoptosis and cancerogenesis P53 is a 53kDa protein existing by and large in the nuclei of all cells, swiftly accumulates after damage and develop into phosporylated Phosphorylation permits to bind to DNA and set off transcription of cellphone cycle inhibitors or proapoptotic proteins P53 block transition of cells from G1 to S part if DNA damage isn't repaired

    51 P53 mediated apoptosis

    52 If restoration is unsuccessful then P53 will induce expression of BAX. BAX acts in opposition t bcl2 and motives apoptosis Hormonally related cancers seem to specially involve lack of p53 related apoptosis Chemo/rad work highest quality when p53 is undamaged as also act via apoptosis role of P53 Tumor suppressor protein in apoptosis and cancerogenesis

    fifty three Neurodegenerative ailments and Apoptosis  - Withdrawal of growth factors favors movements of professional-apoptotic contributors of Bcl household - For neurons stylish on nerve increase components the loss of this stimulation can lead to neural apoptosis and degenerative neurologic ailments: (Alzheimer's sickness, Amyotrophic lateral sclerosis, Friedreich's ataxia, Huntington's sickness, Lewy physique disease, Parkinson's disorder, Spinal muscular atrophy)

    54 SOD-1 mutations can activate caspase-1 and caspase-three, and could raise free- radical generation, resulting in motor neuron apoptosis. The activation of caspase-1 leads to interleukin-1 construction, that could set off a native microglial inflammatory response and boost the variety of neurons affected. example: SOD-1 mutations prompt mobile death pathways in familial amyotrophic lateral sclerosis

    fifty five Mechanisms of IR prompted mobile death

    56 mobile injury led to by using virus an infection Direct harm: -Depletion of cellular supplies -Activation of Apoptosis Immunologically mediated damage: -Antibodies+complement -T-lymphocytes/Granzyme

    fifty seven Protein Misfolding and unfolded protein response (aka ER-stress) Proteins which called “Chaperones” play crucial function in the suitable folding of newly synthesized proteins constantly misfolded polypeptides are ubiquitinated and centered for proteolysis in proteasomes. Accumulation of misfolded proteins in the ER set off a couple of cellular responses, at the same time called the unfolded protein response If cells are unable to contend with the buildup of misfolded proteins, the mobilephone activates caspases and induces apoptosis. Examples: Alzheimer, Huntington, and Parkinson illnesses, type 2 diabetes

    58 Mechanisms of protein folding and the unfolded protein response

    fifty nine Autophagy What can activate Autophagy: 1.Nutrient Deprivation( low level of a.acids) 2.Accumulation of lengthy-residing proteins What alter Autophagy? 1.MTOR signaling pathway 2.Atgs genes/proteins What Mechanism? 1. Atgs proteins create autophagic vacuoles 2. Autophagic vacuoles fuse with lysosomes and content material is digested Definition: Autophagy is the system by which a cell sequesters and recycles damaged organelles and macromolecules ( eats its personal contents)

    60 Autophagy and ailment 1.cancer: here's a local of energetic investigation, autophagy can both promote melanoma increase and act as a defense towards cancers. 2.Neurodegenerative issues: In Alzheimer disorder, formation of autophagosomes is accelerated. In Huntington ailment, mutant protein huntingtin impairs autophagy. three.Infectious illnesses: Many pathogens are degraded with the aid of autophagy; these include mycobacteria, Shigella spp., and HSV-1. here's a method wherein microbial proteins are digested and dropped at antigen presentation pathways. Macrophage-selected deletion of Atg5 raises susceptibility to tuberculosis 4.Inflammatory bowel diseases: experiences have linked each Crohn sickness and ulcerative colitis to autophagy linked genes.

    sixty one Necroptosis Necroptosis become first diagnosed as a caspase- unbiased form of cell loss of life that can be triggered via treatment with TNF simplest in the presence of a pan- caspase inhibitors leading executing molecule of the system is called RIPK3 - receptor-interacting protein kinase three (RIPK3) Necroptosis requires that the feature of caspase 8 be inhibited or disrupted. in contrast to apoptosis, by which a couple of of the totally immunogenic intracellular proteins are sequestered in the dead phone, necroptosis is a strong trigger of innate and adaptive immune responses

    62 Formation of the Necrosome is essential factor in the induction of Necroptosis Molecular mechanism of TNF-mediated necroptosis: cross-linking of TNFR1 by way of TNF factors recruitment of RIP1 and RIP3 together with caspase eight. Inhibition of caspase 8, as may additionally happen in some viral infections, allows RIP1 and RIP3 to initiate alerts that affect mitochondrial technology of ATP and ROS. here is adopted by means of movements typical of necrosis.

    sixty three Key concepts of Necroptosis Necroptosis resembles necrosis morphologically and apoptosis mechanistically as a type of programmed mobilephone death. Necroptosis is caused with the aid of ligation of TNFR1, and viral proteins of RNA and DNA viruses. Necroptosis is caspase-impartial however dependent on signaling by means of the RIP1 and RIP3 complicated. RIP1-RIP3 signaling reduces mitochondrial ATP generation, reasons creation of ROS, and permeabilizes lysosomal membranes, thereby inflicting cellular swelling and membrane damage as occurs in necrosis. liberate of cellular contents conjures up an inflammatory response as in necrosis.

    64 medical implications of the necroptosis Activation of Necroptosis should be advisable to result in mighty anti-viral immune response, e.g. for vaccination or for remedy of viral infections Inhibition of Necroptosis could be a good option for medication of ischemia-reperfusion harm (MI, strokes, transplantation of organs) more particulars:

    sixty five Mediation of Programmed phone dying by way of Apoptosis or Regulated Necrosis mitochondrial permeability transition

    sixty six Necrostatin1, Necrosulfonamide and Cyclosporine are constructive in the prevention of the Ischemia-reperfusion injury

    67 Pyroptosis a further kind of programmed phone demise Accompanied by using the liberate of fever-inducing cytokine IL-1 from ells Has some biochemical similarities with apoptosis Pyroptosis happens in cells infected via microbes (microbes in the cytoplasm of cells)!!! involves activation of caspase-1, generation by cell IL-1 IL-1 recruit leukocytes to the web page of infection

    sixty eight From : cellphone dying within the host response to infection mobilephone loss of life and Differentiation (2008) 15, 1339–1349; doi: /cdd ; published on-line 20 June 2008, okay Labbé1 and M Saleh1,21 2

    sixty nine Pathogen-induced host phone demise The category of loss of life the mobilephone undergoes depends upon the character of the pathogen, pathogen load and placement of infection. Pyroptotic, apoptotic, autophagic or oncotic cells display a definite set of morphological and biochemical traits Apoptosis and autophagy do not set off irritation Apoptosis, pyroptosis and autophagy are generally really useful to the host, oncosis favors pathogen dissemination

    70 Please, take your pen and answer on here questions you have eighty seconds to reply every query

    71 Q1: A forty three-year-ancient man gifts with a scaly, erythematous lesion on the dorsal surface of his left hand. dermis biopsy exhibits odd Keratinocytes and inflammatory cells, as well as a large number of scattered apoptotic our bodies. Which of here proteins plays essentially the most critical position in mediating programmed mobile death in these Keratinocytes? A. Catalase B. Cytochrome c C. Cytokeratins D. Myeloperoxidase E. Superoxide dismutase 2:001:591:581:571:561:551:541:531:521:511:501:491:481:471:461:451:441:431:421:411:401:391:381:371:361:351:341:331:321:311:301:291:281:271:261:251:241:231:221:211:201:191:181:171:161:151:141:131:121:111:one hundred and one:091:081:071:061:051:041:031:021:011:000:590:580:570:560:550:540:530:520:510:500:490:480:470:460:450:440:430:420:410:400:390:380:370:360:350:340:330:320:310:300:290:280:270:260:250:240:230:220:210:200:one hundred ninety:one hundred eighty:one hundred seventy:one hundred sixty:150:a hundred and forty:130:a hundred and twenty:110:100:090:080:070:060:050:040:030:020:01End

    seventy two Q2: You study 250-240 a slide containing a lot of epithelial cells. A colleague looks at the unstained cells beneath the easy microscope and says that many of the cells are present process apoptosis. You seem to be on the slide within the microscope and agree. What modifications within the cellular constitution did you take a look at within the easy microscope that led to the conclusion that the cells had been present process apoptosis? A Plasma membrane turned into intact B Mitochondria had been absent C Plasma membrane showed blebbing D Nucleus was absent E Polysomes had been linked to the endoplasmic reticulum 2:001:591:581:571:561:551:541:531:521:511:501:491:481:471:461:451:441:431:421:411:401:391:381:371:361:351:341:331:321:311:301:291:281:271:261:251:241:231:221:211:201:191:181:171:161:151:141:131:121:111:a hundred and one:091:081:071:061:051:041:031:021:011:000:590:580:570:560:550:540:530:520:510:500:490:480:470:460:450:440:430:420:410:four hundred:390:380:370:360:350:340:330:320:310:300:290:280:270:260:250:240:230:220:210:200:190:180:a hundred and seventy:a hundred and sixty:one hundred fifty:a hundred and forty:one hundred thirty:a hundred and twenty:a hundred and ten:100:090:080:070:060:050:040:030:020:01End

    73 2:001:591:581:571:561:551:541:531:521:511:501:491:481:471:461:451:441:431:421:411:401:391:381:371:361:351:341:331:321:311:301:291:281:271:261:251:241:231:221:211:201:191:181:171:161:151:141:131:121:111:one hundred and one:091:081:071:061:051:041:031:021:011:000:590:580:570:560:550:540:530:520:510:500:490:480:470:460:450:440:430:420:410:400:390:380:370:360:350:340:330:320:310:300:290:280:270:260:250:240:230:220:210:200:one hundred ninety:a hundred and eighty:a hundred and seventy:160:one hundred fifty:140:one hundred thirty:one hundred twenty:one hundred ten:a hundred:090:080:070:060:050:040:030:020:01End Q3: On day 28 of her menstrual cycle, a 23-year-ancient lady experiences onset of menstrual bleeding that lasts for six days. She has had standard cycles for many years. Which of the following techniques is undoubtedly occurring in the endometrium simply before the onset of bleeding? (A) Apoptosis (B) Caseous necrosis (C) Heterophagocytosis (D) Atrophy (E) Liquefactive necrosis

    seventy four this autumn: A mobilephone pathologist performs experiments to verify the biochemical and physiological adjustments that occur in cells undergoing apoptosis. Which of right here qualities is associated with the primary stage of apoptosis of cells? A DNA ladder formation B Nuclear condensation C Blebbing or "boiling" of the cytoplasmic membrane D Chromatin condensation E Fragmentation of DNA into kilobase fragments 2:001:591:581:571:561:551:541:531:521:511:501:491:481:471:461:451:441:431:421:411:401:391:381:371:361:351:341:331:321:311:301:291:281:271:261:251:241:231:221:211:201:191:181:171:161:151:141:131:121:111:a hundred and one:091:081:071:061:051:041:031:021:011:000:590:580:570:560:550:540:530:520:510:500:490:480:470:460:450:440:430:420:410:four hundred:390:380:370:360:350:340:330:320:310:300:290:280:270:260:250:240:230:220:210:200:one hundred ninety:a hundred and eighty:170:one hundred sixty:one hundred fifty:a hundred and forty:a hundred thirty:one hundred twenty:one hundred ten:100:090:080:070:060:050:040:030:020:01End

    75 A male newborn is discovered to have syndactyly of three fingers of his right hand. as the attending resident you're called upon to clarify to the newborn's fogeys as to why this happened to their baby. Which of here cellular tactics is obviously to have failed during development in utero and brought about the malformation? A Apoptosis B Differentiation C Fusion D Fission E Migration F Proliferation V


    Effectiveness of Digital educational materials for establishing Spatial pondering of fundamental college college studentsNo influence discovered, are attempting new key phrase!attainable on-line at www.sciencedirect.com Procedia Social and Behavioral Sciences 21 (2011) 116–119 overseas conference: Spatial thinking and Geographic information Sciences 2011 Effectiveness of Digital tutorial substances for setting up Spatial ...


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