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Super Mario Galaxy 2 ReviewBy Andrew Pfister - Posted May 21, 2010
Super Mario Galaxy 2 is the culmination of over 20 years of Mario gaming into one fantastically-designed and creative platformer. It's also one of 2010's absolutely best games.
The Pros
- Level designer creativity in full bloom
- Yoshi works great in 3D
- Most New Power-Ups Are Winners
The Cons
- Controls get tricky messing with multiple dimensions
- Boo Suit Not Fun
In grade school, my friends and I would sometimes take out our rulers and blank sheets of paper, and draw elaborate corridor paths that would snake around the sheet until it reached an end point on the other side. Filling the white space with giant triangles, wavy lines, black holes, and other devious (to a 4th-grader) traps, the goal of the game was for another person to draw a continuous line from the beginning of the path to the end, without hitting any of the corridor walls or the hazards we concocted. If we did, we'd lose a "life." It should go without saying that all of us were die hard Super Mario Bros. fans, and to us, it wasn't so much about platforming (a term we had no conception of) as it was the sense of running through an obstacle course. So if I were to travel back through time and show my 10-year old self and friends Super Mario Galaxy 2, heads would probably explode.
Building on a Strong Foundation
Having already done the hard work of building the engine in Super Mario Galaxy, and establishing the concepts of spherical navigation and gravitational pull, Galaxy 2 sees the Mario team's creativity in full, unrestrained bloom. The obstacle courses they've assembled within the game's six (plus) worlds are, for the most part, thoroughly honed, wildly varied, and lacking in filler. The variance stems from a large toolbox that's been collected from the Mario games over the years, and because the walls between the traditional "ice/fire/water/space levels" have been completely razed -- there's a galaxy where you turn lava to ice with a flip of a switch -- the designers are constantly throwing change-ups and new combinations of enemies, power-ups, and environments. But it's also done with logic and restraint: never do they throw in nonsensical combinations or repeat level themes just for the sake of padding out an idea.
And, even more so than the first Galaxy, the manipulation of perspective leads to the game's finest moments. In one galaxy, there are pre-determined gravity zones that Mario needs to get through. This involves running upside down, jumping "up" onto shifting platforms (each with their own gravity zones), and then through a gauntlet of Thwomps who are crushing you from the bottom of the screen in a very un-Thwomp-like manner. It's all very complex and intimidating...until you realize that because of your perspective at the start of the level, you can do a backflip on top of the blocks that border the gravity maze and simply run over the top of everything, dropping back in when you get to the Power Star. There are numerous such instances of camera angles, gravity, and planes mixing and matching within the same level that generates this weirdly wonderful mix of 2D and 3D Mario play. It doesn't always lead to perfect platforming, as there'll be times when Mario gets confused about which way is down; particularly frustrating when tasked with staying alive on rotating objects with 90 degree angles ("Clockwork Galaxy" is a rare low point in this regard). There are other legacy control issues as well, including Mario wall jumping to his death when you want him to grab the easily within-reach ledge and making sharp turns while swimming; these are unpleasant -- though thankfully infrequent -- reminders that the more dimensions you add, the more problems you'll have.
Well-Suited Gameplay
Like the mix of 2D and 3D, there's a perfect blending of old franchise mainstays and brand new elements. We're given access to Yoshi right away so that we can get a feel for how he works in 3D. The flutter jump and tongue-lashings via the Wii pointer translate extremely well, and somehow manage to capture the Super Mario World vibe. Before too long, we're turning him into a floating blimp, a pepper-fueled speed demon impervious to gravity, and a flashlight that keeps essential footholds in existence. What's great is that all of these things feel like they've always belonged in the Mario series. The same holds true for the majority of Mario's new power-ups. The Cloud Suit and its three temporary platforms provide 8 seconds of safety, but it also encourages you to attempt long jumps of faith...because it might prove beneficial to hold on to that last cloud. The Rock Suit provides invulnerability at the expense of control; the risk of careening off a ledge is surpassed by the reward of bowling through enemies and harvesting the star bits left behind. The only disappointing new toy is the Boo Suit, which is designed more around player punishment; movement is slow and any surface contact kills momentum. Thankfully (and probably for a reason), it's only prominent in one galaxy. The new powers are scattered smartly throughout the levels, which further creates a sense of variety and that you're always doing something fresh.
Something for Everyone
Super Mario Galaxy 2 is a Mario game for lifelong Mario fans, and as such, it will be challenging. Some Power Stars will naturally be easier to retrieve than others, but on average, the game assumes that you know the differences among Mario's array of jumps and spins, that you can instinctively judge distances across gaps, and that you know how the majority of the game's enemies and environmental hazards behave. It's difficult in the way that a school test is difficult, but we've had the advantage of studying the franchise for about 20 years. There are hand-holding options for those who wish to use them, one that shows you how to do something, and one that actually does it for you, but they are nearly invisible if you already know what you're doing. As expected, some of the Prankster Comet challenges get a little too close to "unfair" territory, especially when they involve both Purple Coins and a timer (or a Chimp), but perseverance eventually pays off.
In conclusion, Super Mario Galaxy 2 culminates over 20 years of Mario gaming -- whether you were around for it all as it happened or you picked it up later -- and distills it into a wonderful experience. The essence of Super Mario games has always been getting from Point A to Point B, being proud that you made it to the end, but then being disappointed because the middle part was so entertaining. This is a magnificent feeling that occurs so often in Super Mario Galaxy 2, I really do want to visit my 10-year old self and give him a sneak peek at what the future holds. (And pray that his/my head doesn't explode).


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#202292 - 09/05/11 02:37 PM made up languages
Registered: 06/11/05
Posts: 131
Loc: Oregon
I thought this was interesting and looked at the dictionary also. Just the existing 'real' languages are enough to keep me guessing on meanings, etc. I don't think I have the imagination to create a new language, but I know that more than several authors have done so.
I could definitely use a few of these words though!
The Right Words
After earning a Ph.D. in linguistics, Suzette Haden Elgin invented the language Láadan for a science fiction novel. What makes the language unique is that its designed particularly to express the perceptions of women:
widazhad: to be pregnant late in term and eager for the end
radiídin: a non-holiday, a holiday more work that its worth, a time allegedly a holiday but actually so much a burden because of work and preparations that it is a dreaded occasion; especially when there are too many guests and none of them help
rathom: a non-pillow, one who lures another to trust and rely on them but has no intention of following through, a lean on me so I can step aside and let you fall person
rathóo: a non-guest, someone who comes to visit knowing perfectly well that they are intruding and causing difficulty
ramimelh: to refrain from asking, with evil intent; especially when it is clear that someone badly wants the other to ask
bala: anger with reason, with someone to blame, which is not futile
bina: anger with no reason, with no one to blame, which is not futile
ab: love for one liked but not respected
doóledosh: pain or loss which comes as a relief by virtue of ending the anticipation of its coming
One word that has no English equivalent is doroledim, which means sublimation with food accompanied by guilt about that sublimation: Say you have an average woman. She has no control over her life. She has little or nothing in the way of a resource for being good to herself, even when it is necessary. She has family and animals and friends and associates that depend on her for sustenance of all kinds. She rarely has adequate sleep or rest; she has no time for herself, no space of her own, little or no money to buy things for herself, no opportunity to consider her own emotional needs. She is at the beck and call of others, because she has these responsibilities and obligations and does not choose to (or cannot) abandon them. For such a woman, the one and only thing she is likely to have a little control over for indulging her own self is FOOD. When such a woman overeats, the verb for that is doroledim. (And then she feels guilty, because there are women whose children are starving and who do not have even THAT option for self-indulgence )_________________________
#202295 - 09/05/11 07:05 PM Re: made up languages [Re: va-vavoom]
Carpal Tunnel
Registered: 06/23/08
Posts: 8532
Loc: Land of the Flat Water
Curious and interesting. Put it next to Elvish created by Tolkien;
and Klingon, in Star Wars; and probably a host of others. Esperanto too.
Makes a novel more interesting, that's for sure.
Edited by LukeJavan8 (09/05/11 07:06 PM)_________________________
----please, draw me a sheep----
#202301 - 09/05/11 11:00 PM Re: made up languages [Re: va-vavoom]
Carpal Tunnel
Registered: 03/15/00
Posts: 11613
Loc: Louisville, Kentucky
a non-pillow, What an interesting concept! It makes you think twice about relaxing, that's for sure!
#202305 - 09/06/11 01:04 PM Re: made up languages [Re: Jackie]
Carpal Tunnel
Registered: 06/23/08
Posts: 8532
Loc: Land of the Flat Water
In the novel is it a Women's world, with no men;
do they not speak the language or have another of their own?
----please, draw me a sheep----
#202323 - 09/07/11 02:54 PM Re: made up languages [Re: LukeJavan8]
Registered: 06/11/05
Posts: 131
Loc: Oregon
I haven't read any of her work, but thought I would look for it in the library, so I don't know if it is solely 'women'.
Jackie, I thought that was an intriguing concept also....I know a few people that would describe and think I will add the word to my vocabulary as a pejorative. they'll never know how badly they are being insulted!_________________________
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I'm currently having flu and cough. Can the expressed milk from this period still be stored and used later (put in freezer)? Will there be germs in the milk that will infect the baby?
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I'm currently having flu and cough. Can the expressed milk from this period still be stored and used later (put in freezer)? Will there be germs in the milk that will infect the baby?
This information might help:
You should know, too, that your baby has already been exposed to your illness. By the time you've realized you're sick, your baby has already been exposed. The good news is that your milk will provide your baby with antibodies to the germ you have, which means your baby might not be as ill if he should "catch" would you have, the duration of the illness might be shorter, or he may not come down with the illness at all! :)
I can find nothing in my references that says you cannot freeze milk when you're ill to feed later.
Thanks for the reply. I'm aware that presently, I should breastfeed to pass the antibodies to my baby. What I'm worried about is if I express my milk and store it now, say 2 months down the road, I feed this milk to the baby, will it cause the baby to be sick?
Another matter which I need help on: I presently store my milk in portions of 120ml (my baby is currently drinking this amount). Can I thaw the frozen milk (by immersing it in cool tap water) and then keep it in the fridge for 24 hours? This is so that I can top up the milk in case my baby needs to drink more later. I know the ideal is to store milk in smaller portions so that I can use each portion up in one go, but I have limited storage space.
Hi Seleste,
In LLL's BREASTFEEDING ANSWER BOOK, under the section "Colds, Flu, or Mild Infections" it says that "Illnesses are usually transmitted through skin contact and secretions from the nose and mouth, not through breastfeeding. When a mother is ill, good hygiene can decrease the baby's chances of catching her illness." (Good hygiene meaning regular hand-washing, trying not to breathe face-to-face with the baby.)
The same book (BAB) goes on to say about milk storage that previously frozen milk that was thawed can be safely kept refrigerated for up to 24 hours. It should not be refrozen.
Fresh milk can be added to frozen milk provided it is first cooled and there is less fresh milk than frozen milk. Cool it for about a half an hour before adding it to the frozen milk so it does not thaw the top layer.
Small quantities, 2 to 4 ounces (60 to 120 ml) thaw and warm quickly and less milk will be leftover if the baby doesn't take it all.
Does this help?
Yes. Thks very much for your help


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Topic Contents
- General Information About Childhood Central Nervous System (CNS) Atypical Teratoid / Rhabdoid Tumor
- Tumor Biology of Childhood CNS Atypical Teratoid / Rhabdoid Tumor
- Stage Information for Childhood CNS Atypical Teratoid / Rhabdoid Tumor
- Treatment for Newly Diagnosed Childhood CNS Atypical Teratoid / Rhabdoid Tumor
- Treatment for Recurrent Childhood CNS Atypical Teratoid / Rhabdoid Tumor
- Current Clinical Trials
- Changes to This Summary (10 / 13 / 2014)
- About This PDQ Summary
- Get More Information From NCI
Childhood Central Nervous System Atypical Teratoid/Rhabdoid Tumor Treatment (PDQ®): Treatment - Health Professional Information [NCI]Skip to the navigation
This information is produced and provided by the National Cancer Institute (NCI). The information in this topic may have changed since it was written. For the most current information, contact the National Cancer Institute via the Internet web site at http://cancer.gov or call 1-800-4-CANCER.
General Information About Childhood Central Nervous System (CNS) Atypical Teratoid / Rhabdoid Tumor
Dramatic improvements in survival have been achieved for children and adolescents with cancer. Between 1975 and 2010, childhood cancer mortality decreased by more than 50%.[1] Childhood and adolescent cancer survivors require close follow-up because cancer therapy side effects may persist or develop months or years after treatment. (Refer to the PDQ summary on Late Effects of Treatment for Childhood Cancer for specific information about the incidence, type, and monitoring of late effects in childhood and adolescent cancer survivors.)
Primary brain tumors are a diverse group of diseases that together constitute the most common solid tumor of childhood. The PDQ childhood brain tumor treatment summaries are primarily organized according to the World Health Organization classification of nervous system tumors.[2,3] Brain tumors are classified according to histology, but immunohistochemical analysis, cytogenetic and molecular genetic findings, and measures of mitotic activity are increasingly used in tumor diagnosis and classification. Tumor location and extent of spread are important factors that affect treatment and prognosis. For a full description of the classification of nervous system tumors and a link to the corresponding treatment summary for each type of brain tumor, refer to the PDQ summary on Childhood Brain and Spinal Cord Tumors Treatment Overview.
Central nervous system (CNS) atypical teratoid/rhabdoid tumor (AT/RT) is a rare, clinically aggressive tumor that most often affects children aged 3 years and younger but can occur in older children and adults. About one-half of AT/RTs arise in the posterior fossa. The diagnostic evaluation includes magnetic resonance imaging (MRI) of the neuraxis and lumbar cerebrospinal fluid examination. AT/RT has been linked to somatic and germline mutations of SMARCB1, a tumor suppressor gene. There is no current standard treatment for children with AT/RT. Multimodal treatment consisting of surgery, chemotherapy, and radiation therapy is under evaluation.
Based on present biologic understanding, AT/RT is part of a larger family of rhabdoid tumors. In this summary, the term AT/RT refers to CNS tumors only and the term rhabdoid tumor reflects the possibility of both CNS and non-CNS tumors. Unless specifically noted in the text, this summary is referring to CNS AT/RT.
The exact incidence of childhood CNS AT/RT is difficult to determine because the tumor has been widely recognized for only the last decade.
- In two North American prospective studies performed by the Children's Cancer Group and the Pediatric Oncology Group for children aged 3 years or younger at diagnosis, retrospective review disclosed that approximately 10% of children with brain tumors had AT/RTs.[4]
- A Taiwanese study found that AT/RTs account for 26% of primitive or embryonal tumors in children younger than 3 years.[5]
- The Austrian Brain Tumor Registry, conducted between 1996 and 2006, confirmed that AT/RTs represent the sixth most common malignant brain tumor among 311 newly diagnosed children (6.1%), with a peak incidence during the first 2 years of life.[6]
The incidence in older patients is unknown. However, in the Central Nervous System Atypical Teratoid/Rhabdoid Tumor Registry (AT/RT Registry), 12 (29%) of the 42 patients were older than 36 months at the time of diagnosis.[7]
Anatomy of the inside of the brain, showing the pineal and pituitary glands, optic nerve, ventricles (with cerebrospinal fluid shown in blue), and other parts of the brain. The tentorium separates the cerebrum from the cerebellum. The infratentorium (posterior fossa) is the region below the tentorium that contains the brain stem, cerebellum, and fourth ventricle. The supratentorium is the region above the tentorium and denotes the region that contains the cerebrum.
Clinical Presentation
Childhood AT/RT is a clinically aggressive tumor that primarily occurs in children younger than 3 years, but it also can occur in older children and has been reported in adults.[8,9]
In about one-half of patients, the tumor is located in the posterior fossa, although it can occur anywhere in the CNS.[4] Tumors of the posterior fossa may occur in the cerebellopontine angle or more midline. Involvement of individual cranial nerves has also been noted.
Because AT/RT grows rapidly, patients typically have a fairly short history of progressive symptoms, measured in days to weeks. Signs and symptoms are dependent on tumor location. Young patients with posterior fossa tumors usually present with symptoms related to hydrocephalus, including the following:
- Early morning headaches.
- Vomiting.
- Lethargy.
They may also develop ataxia or regression of motor skills.
Data from the AT/RT Registry suggest that approximately 20% of patients present with disseminated disease.[7] Dissemination is typically through leptomeningeal pathways seeding the spine and other areas of the brain. There are also reports of rare patients with synchronous renal rhabdoid tumor and CNS AT/RT.[10]
Diagnostic Evaluation
All patients with suspected childhood AT/RT should have MRI of the brain and spine. Unless medically contraindicated, patients should also have lumbar cerebrospinal fluid inspected for evidence of tumor. Patients may also undergo renal ultrasound to detect synchronous tumors.
AT/RT cannot be reliably distinguished from other malignant brain tumors based on clinical history or radiographic evaluation. Surgery is necessary to obtain tissue and confirm the diagnosis of AT/RT. Immunostaining for loss of SMARCB1 (INI1, hSNF5) protein expression is used to confirm the diagnosis, especially in children younger than 3 years.[11]
Prognostic factors that affect survival for AT/RTs are not fully delineated.
Known factors associated with a poor outcome include the following:
- Germline mutation.[12]
- Age younger than 2 years.[13]
- Metastases at diagnosis.[13]
- Subtotal resection.[14]
Most published information on outcomes for patients with AT/RT is based on small series and is retrospective in nature. Initial retrospective studies reported an average survival from diagnosis of only about 12 months.[4,8,14,15,16] In a retrospective report, 2-year overall survival was better for patients who underwent a gross-total resection than for those who had a subtotal resection. However, in this study the effect of radiation therapy on survival was less clear.[14]
There are reports of long-term survivors.[17] Notably, improved survival has been reported for those receiving intensive multimodal therapy.
- Children aged 3 years and older who received postoperative craniospinal irradiation and high-dose, alkylator-based chemotherapy had improved survival compared with those younger than 3 years with AT/RT. In this report, the incidence of leptomeningeal metastases was also higher in the infant group of patients.[18]
- In one prospective study of 25 children with AT/RT receiving intensive multimodal therapy, including radiation and intrathecal chemotherapy, the reported 2-year progression-free survival rate was 53%, and the overall survival rate was 70%.[19]
- Smith MA, Altekruse SF, Adamson PC, et al.: Declining childhood and adolescent cancer mortality. Cancer 120 (16): 2497-506, 2014.
- Louis DN, Ohgaki H, Wiestler OD, et al., eds.: WHO Classification of Tumours of the Central Nervous System. 4th ed. Lyon, France: IARC Press, 2007.
- Louis DN, Ohgaki H, Wiestler OD, et al.: The 2007 WHO classification of tumours of the central nervous system. Acta Neuropathol 114 (2): 97-109, 2007.
- Packer RJ, Biegel JA, Blaney S, et al.: Atypical teratoid/rhabdoid tumor of the central nervous system: report on workshop. J Pediatr Hematol Oncol 24 (5): 337-42, 2002 Jun-Jul.
- Ho DM, Hsu CY, Wong TT, et al.: Atypical teratoid/rhabdoid tumor of the central nervous system: a comparative study with primitive neuroectodermal tumor/medulloblastoma. Acta Neuropathol 99 (5): 482-8, 2000.
- Woehrer A, Slavc I, Waldhoer T, et al.: Incidence of atypical teratoid/rhabdoid tumors in children: a population-based study by the Austrian Brain Tumor Registry, 1996-2006. Cancer 116 (24): 5725-32, 2010.
- Hilden JM, Meerbaum S, Burger P, et al.: Central nervous system atypical teratoid/rhabdoid tumor: results of therapy in children enrolled in a registry. J Clin Oncol 22 (14): 2877-84, 2004.
- Burger PC, Yu IT, Tihan T, et al.: Atypical teratoid/rhabdoid tumor of the central nervous system: a highly malignant tumor of infancy and childhood frequently mistaken for medulloblastoma: a Pediatric Oncology Group study. Am J Surg Pathol 22 (9): 1083-92, 1998.
- Lutterbach J, Liegibel J, Koch D, et al.: Atypical teratoid/rhabdoid tumors in adult patients: case report and review of the literature. J Neurooncol 52 (1): 49-56, 2001.
- Biegel JA, Fogelgren B, Wainwright LM, et al.: Germline INI1 mutation in a patient with a central nervous system atypical teratoid tumor and renal rhabdoid tumor. Genes Chromosomes Cancer 28 (1): 31-7, 2000.
- Bruggers CS, Bleyl SB, Pysher T, et al.: Clinicopathologic comparison of familial versus sporadic atypical teratoid/rhabdoid tumors (AT/RT) of the central nervous system. Pediatr Blood Cancer 56 (7): 1026-31, 2011.
- Kordes U, Gesk S, Frühwald MC, et al.: Clinical and molecular features in patients with atypical teratoid rhabdoid tumor or malignant rhabdoid tumor. Genes Chromosomes Cancer 49 (2): 176-81, 2010.
- Dufour C, Beaugrand A, Le Deley MC, et al.: Clinicopathologic prognostic factors in childhood atypical teratoid and rhabdoid tumor of the central nervous system: a multicenter study. Cancer 118 (15): 3812-21, 2012.
- Lafay-Cousin L, Hawkins C, Carret AS, et al.: Central nervous system atypical teratoid rhabdoid tumours: the Canadian Paediatric Brain Tumour Consortium experience. Eur J Cancer 48 (3): 353-9, 2012.
- Rorke LB, Packer RJ, Biegel JA: Central nervous system atypical teratoid/rhabdoid tumors of infancy and childhood: definition of an entity. J Neurosurg 85 (1): 56-65, 1996.
- Athale UH, Duckworth J, Odame I, et al.: Childhood atypical teratoid rhabdoid tumor of the central nervous system: a meta-analysis of observational studies. J Pediatr Hematol Oncol 31 (9): 651-63, 2009.
- Olson TA, Bayar E, Kosnik E, et al.: Successful treatment of disseminated central nervous system malignant rhabdoid tumor. J Pediatr Hematol Oncol 17 (1): 71-5, 1995.
- Tekautz TM, Fuller CE, Blaney S, et al.: Atypical teratoid/rhabdoid tumors (ATRT): improved survival in children 3 years of age and older with radiation therapy and high-dose alkylator-based chemotherapy. J Clin Oncol 23 (7): 1491-9, 2005.
- Chi SN, Zimmerman MA, Yao X, et al.: Intensive multimodality treatment for children with newly diagnosed CNS atypical teratoid rhabdoid tumor. J Clin Oncol 27 (3): 385-9, 2009.
Tumor Biology of Childhood CNS Atypical Teratoid / Rhabdoid Tumor
Childhood central nervous system (CNS) atypical teratoid/rhabdoid tumor (AT/RT) was first described as a discrete clinical entity in 1987 [1] based on its distinctive pathologic and genetic characteristics. Before then, it was most often classified as a medulloblastoma, primitive neuroectodermal tumor, or choroid plexus carcinoma. The World Health Organization began classifying AT/RT as an embryonal grade IV neoplasm in 1993.[2]
Histologically, classic AT/RT is morphologically heterogeneous, typically containing sheets of large epithelioid cells with abundant eosinophilic cytoplasm and scattered rhabdoid cells, most often with accompanying components of primitive neuroectodermal cells (small round blue cells), mesenchymal cells, and/or glial cells.[3]
Immunohistochemical staining for epithelial markers (cytokeratin or epithelial membrane antigen), glial fibrillary acidic protein, synaptophysin (or neurofilament), and smooth muscle (desmin) may help to identify the heterogeneity of differentiation, but will vary depending on the cellular composition.[4] Rhabdoid cells, while not present in all AT/RTs, will express vimentin, epithelial membrane antigen, and smooth muscle actin.
Immunohistochemistry for the SMARCB1 protein is useful in establishing the diagnosis of AT/RT. A loss of SMARCB1 staining is noted in neoplastic cells, but staining is retained in non-neoplastic cells (e.g., vascular endothelial cells).[5,6,7]
AT/RT is a rapidly growing tumor that can have an MIB-1 labeling index of 50% to 100%.[2]
AT/RT is the first primary pediatric brain tumor for which a candidate tumor suppressor gene, SMARCB1 (also known as INI1 and hSNF5), has been identified.[8]SMARCB1 loss causes aberrant activation of the sonic hedgehog pathway and may drive tumorigenesis through the expression of GLI1.[9] In one series of six infants, AT/RTs were thought to arise from the superior medullary velum. Sonic hedgehog signaling through expression of GLI1 is critically involved in morphogenesis of the cerebellar midline structures, suggesting, in part, why tumors arise in this region.[10]SMARCB1 has been found to be abnormal in the majority of rhabdoid tumors, including CNS, renal, and extrarenal rhabdoid malignancies.[8] Alterations (mutations as well as gains/losses) in other genes are very uncommon in patients with SMARCB1-associated AT/RT.[11,12,13]
SMARCB1 is a component of a Switch (SWI) and Sucrose non-fermenting (SNF) adenosine triphosphate–dependent chromatin-remodeling complex.[14] The exact function of the SMARCB1 gene is unknown, but it is likely that a mutation results in altered transcriptional regulation of downstream targets. Rare familial cases of rhabdoid tumors expressing SMARCB1 and lacking SMARCB1 mutations have also been associated with germline mutations of SMARCA4/BRG1, another member of the SWI/SNF chromatin-remodeling complex.[7,15]
In addition to somatic mutations, germline mutations in SMARCB1 have been reported in a substantial subset of AT/RT patients.[8,16] A study of 65 children with rhabdoid tumors found that 23 (35%) had germline mutations and/or deletions of SMARCB1.[5] Children with germline alterations in SMARCB1 presented at an earlier age than sporadic cases (median age, approximately 5 months versus 18 months) and were more likely to present with multiple tumors.[5] One parent was found to be a carrier of the SMARCB1 germline abnormality in 7 of 22 evaluated cases showing germline alterations, with four of the carrier parents being unaffected by SMARCB1-associated cancers.[5] This indicates that AT/RT shows an autosomal dominant inheritance pattern with incomplete penetrance.
Gonadal mosaicism has also been observed, as evidenced by families in which multiple siblings are affected by AT/RT and have identical SMARCB1 alterations, but both parents lack a SMARCB1 mutation/deletion.[5,6] Screening children diagnosed with AT/RT for germline SMARCB1 mutations may provide useful information for counseling families on the genetic implications of their child's AT/RT diagnosis.[5]
Rhabdoid Tumor Predisposition Syndrome (RTPS)
RTPS, related primarily to germline SMARCB1 alterations, has been clearly defined.[8,16] RTPS is highly suggested in patients with synchronous occurrence of renal malignant rhabdoid tumor and AT/RT, bilateral malignant rhabdoid tumors of the kidney, or malignant rhabdoid tumors in two or more siblings.
This syndrome is manifested by a marked predisposition to the development of malignant rhabdoid tumors in infancy and early childhood. Up to one-third of AT/RTs are thought to arise in the setting of RTPS, and the majority of these occur within the first year of life. The most common non-CNS malignancy of RTPS is the malignant rhabdoid tumor of the kidney, which is also noted in infancy.
For more information about RTPS, refer to the Rhabdoid predisposition syndrome section in the PDQ summary on Wilms Tumor and Other Childhood Kidney Tumors Treatment.
- Rorke LB, Packer RJ, Biegel JA: Central nervous system atypical teratoid/rhabdoid tumors of infancy and childhood: definition of an entity. J Neurosurg 85 (1): 56-65, 1996.
- Kleihues P, Louis DN, Scheithauer BW, et al.: The WHO classification of tumors of the nervous system. J Neuropathol Exp Neurol 61 (3): 215-25; discussion 226-9, 2002.
- Kleihues P, Cavenee WK, eds.: Pathology and Genetics of Tumours of the Nervous System. Lyon, France: International Agency for Research on Cancer, 2000.
- McLendon RE, Adekunle A, Rajaram V, et al.: Embryonal central nervous system neoplasms arising in infants and young children: a pediatric brain tumor consortium study. Arch Pathol Lab Med 135 (8): 984-93, 2011.
- Eaton KW, Tooke LS, Wainwright LM, et al.: Spectrum of SMARCB1/INI1 mutations in familial and sporadic rhabdoid tumors. Pediatr Blood Cancer 56 (1): 7-15, 2011.
- Bruggers CS, Bleyl SB, Pysher T, et al.: Clinicopathologic comparison of familial versus sporadic atypical teratoid/rhabdoid tumors (AT/RT) of the central nervous system. Pediatr Blood Cancer 56 (7): 1026-31, 2011.
- Hasselblatt M, Gesk S, Oyen F, et al.: Nonsense mutation and inactivation of SMARCA4 (BRG1) in an atypical teratoid/rhabdoid tumor showing retained SMARCB1 (INI1) expression. Am J Surg Pathol 35 (6): 933-5, 2011.
- Biegel JA, Tan L, Zhang F, et al.: Alterations of the hSNF5/INI1 gene in central nervous system atypical teratoid/rhabdoid tumors and renal and extrarenal rhabdoid tumors. Clin Cancer Res 8 (11): 3461-7, 2002.
- Jagani Z, Mora-Blanco EL, Sansam CG, et al.: Loss of the tumor suppressor Snf5 leads to aberrant activation of the Hedgehog-Gli pathway. Nat Med 16 (12): 1429-33, 2010.
- Tomita T, Frassanito P: Tumors of the superior medullary velum in infancy and childhood: report of 6 cases. J Neurosurg Pediatr 11 (1): 52-9, 2013.
- Lee RS, Stewart C, Carter SL, et al.: A remarkably simple genome underlies highly malignant pediatric rhabdoid cancers. J Clin Invest 122 (8): 2983-8, 2012.
- Kieran MW, Roberts CW, Chi SN, et al.: Absence of oncogenic canonical pathway mutations in aggressive pediatric rhabdoid tumors. Pediatr Blood Cancer 59 (7): 1155-7, 2012.
- Hasselblatt M, Isken S, Linge A, et al.: High-resolution genomic analysis suggests the absence of recurrent genomic alterations other than SMARCB1 aberrations in atypical teratoid/rhabdoid tumors. Genes Chromosomes Cancer 52 (2): 185-90, 2013.
- Biegel JA, Kalpana G, Knudsen ES, et al.: The role of INI1 and the SWI/SNF complex in the development of rhabdoid tumors: meeting summary from the workshop on childhood atypical teratoid/rhabdoid tumors. Cancer Res 62 (1): 323-8, 2002.
- Schneppenheim R, Frühwald MC, Gesk S, et al.: Germline nonsense mutation and somatic inactivation of SMARCA4/BRG1 in a family with rhabdoid tumor predisposition syndrome. Am J Hum Genet 86 (2): 279-84, 2010.
- Biegel JA, Fogelgren B, Wainwright LM, et al.: Germline INI1 mutation in a patient with a central nervous system atypical teratoid tumor and renal rhabdoid tumor. Genes Chromosomes Cancer 28 (1): 31-7, 2000.
Stage Information for Childhood CNS Atypical Teratoid / Rhabdoid Tumor
There is no defined staging system for childhood central nervous system atypical teratoid/rhabdoid tumor. For treatment purposes, patients are classified as having newly diagnosed or recurrent disease with or without neuraxis dissemination.
Treatment for Newly Diagnosed Childhood CNS Atypical Teratoid / Rhabdoid Tumor
There is no established standard treatment for children with central nervous system (CNS) atypical teratoid/rhabdoid tumor (AT/RT). Given the highly aggressive nature of the tumor, most patients have been treated with intensive multimodal therapy. However, the young age of most patients limits the extent of treatment, particularly radiation therapy.
Treatment options for newly diagnosed CNS AT/RT include the following:
- Surgery, chemotherapy, and radiation therapy (multimodal therapy).
Surgery, Chemotherapy, and Radiation Therapy (Multimodal Therapy)
The extent of the surgical resection may affect survival. Data from the Central Nervous System Atypical Teratoid/Rhabdoid Tumor Registry (AT/RT Registry) suggest that patients who have had a complete resection may have a longer median survival, although complete surgical resection is often difficult given the invasive nature of the tumor.[1]
Chemotherapy has been the main adjuvant therapy for very young children with AT/RT. Cooperative group studies that included children younger than 36 months demonstrated poor survival when treated with standard chemotherapeutic regimens alone.[2] The Children's Cancer Group reported a 2-year event-free survival (EFS) of 14% for 28 children younger than 36 months treated with multiagent chemotherapy.[3]
Intensive regimens that utilize varying combinations of high-dose chemotherapy,[4][Level of evidence: 3iA]; [5,6][Level of evidence: 3iiiDi] intrathecal chemotherapy, and radiation therapy have led to prolonged survival for some patients. Thirteen patients in the AT/RT Registry were treated with high-dose chemotherapy with hematopoietic stem cell rescue as part of initial therapy.[1] Four of these patients, two of whom also received radiation, were alive without progressive disease 21.5 to 90 months following diagnosis at last report. Of 15 evaluable children, all younger than 32 months at diagnosis, who were on a chemotherapy Head Start III protocol, 2 survived for more than 47 months.[7][Level of evidence: 3iA]
Radiation therapy appears to have a positive impact on survival for AT/RT patients.
- Of the 42 patients in the AT/RT Registry, 13 patients (31%) received radiation therapy in addition to chemotherapy as part of their primary therapy.[1] The radiation field was to the primary tumor bed in nine children, and the tumor bed and the craniospinal axis in four children. Their median survival was 48 months, while the median survival of all patients on the registry was 16.75 months.
- A retrospective series of 31 patients with AT/RT from St. Jude Children's Research Hospital in which the 2-year EFS for patients older than 3 years was 78%, considerably better than 11% for patients younger than 3 years.[8] All but one of the surviving patients (seven of eight) in the older group received craniospinal irradiation and intensive chemotherapy with hematopoietic stem cell transplant; only 3 of 22 of the younger patients received any form of radiation therapy, two of whom are disease free.
- In a Surveillance, Epidemiology, and End Results registry review, radiation therapy was associated with improved survival in children younger than 3 years.[9]
Evidence (multimodal therapy):
- The Third Intergroup Rhabdomyosarcoma Study (IRS-III) utilized radiation therapy, intrathecal methotrexate, cytarabine, hydrocortisone, and systemic multiagent chemotherapy. The results of small retrospective series were encouraging,[10,11] leading to the first prospective study of multimodality treatment in this group of patients.
- Based on the previous pilot series, a prospective multi-institutional trial was conducted for children with newly diagnosed CNS AT/RT. Treatment was divided into five phases: preirradiation, chemoradiation, consolidation, maintenance, and continuation therapy. Intrathecal chemotherapy was administered, alternating intralumbar and intraventricular routes. Radiation therapy was either focal (54 Gy) or craniospinal (36 Gy, plus primary boost), depending on the child's age and extent of disease at diagnosis.[12]
- Results of the prospective study demonstrated a 2-year progression-free survival of 53% ± 13% and an overall survival of 70% ± 10%, with results most favorable in children who were older, had a gross-total resection, and had no metastatic disease at presentation.
- Six of the eight children without progressive disease at the time of the report had received conformal radiation therapy and two children had received craniospinal radiotherapy; seven children had a gross total resection and only one child had metastatic disease (this child had persistent, stable disease 1.5 years from diagnosis).
Because AT/RT is responsive to radiation therapy, this modality is incorporated into many treatment protocols.[13]
Prospective cooperative group clinical trials for AT/RT are greatly needed to better understand how age and extent of therapy affect survival.
Treatment Options Under Clinical Evaluation
Early-phase therapeutic trials may be available for selected patients. These trials may be available via Children's Oncology Group phase I institutions, the Pediatric Brain Tumor Consortium, or other entities. Information about ongoing clinical trials is available from the NCI Web site.
- Hilden JM, Meerbaum S, Burger P, et al.: Central nervous system atypical teratoid/rhabdoid tumor: results of therapy in children enrolled in a registry. J Clin Oncol 22 (14): 2877-84, 2004.
- Packer RJ, Biegel JA, Blaney S, et al.: Atypical teratoid/rhabdoid tumor of the central nervous system: report on workshop. J Pediatr Hematol Oncol 24 (5): 337-42, 2002 Jun-Jul.
- Geyer JR, Sposto R, Jennings M, et al.: Multiagent chemotherapy and deferred radiotherapy in infants with malignant brain tumors: a report from the Children's Cancer Group. J Clin Oncol 23 (30): 7621-31, 2005.
- Nicolaides T, Tihan T, Horn B, et al.: High-dose chemotherapy and autologous stem cell rescue for atypical teratoid/rhabdoid tumor of the central nervous system. J Neurooncol 98 (1): 117-23, 2010.
- Gardner SL, Asgharzadeh S, Green A, et al.: Intensive induction chemotherapy followed by high dose chemotherapy with autologous hematopoietic progenitor cell rescue in young children newly diagnosed with central nervous system atypical teratoid rhabdoid tumors. Pediatr Blood Cancer 51 (2): 235-40, 2008.
- Finkelstein-Shechter T, Gassas A, Mabbott D, et al.: Atypical teratoid or rhabdoid tumors: improved outcome with high-dose chemotherapy. J Pediatr Hematol Oncol 32 (5): e182-6, 2010.
- Zaky W, Dhall G, Ji L, et al.: Intensive induction chemotherapy followed by myeloablative chemotherapy with autologous hematopoietic progenitor cell rescue for young children newly-diagnosed with central nervous system atypical teratoid/rhabdoid tumors: the Head Start III experience. Pediatr Blood Cancer 61 (1): 95-101, 2014.
- Tekautz TM, Fuller CE, Blaney S, et al.: Atypical teratoid/rhabdoid tumors (ATRT): improved survival in children 3 years of age and older with radiation therapy and high-dose alkylator-based chemotherapy. J Clin Oncol 23 (7): 1491-9, 2005.
- Buscariollo DL, Park HS, Roberts KB, et al.: Survival outcomes in atypical teratoid rhabdoid tumor for patients undergoing radiotherapy in a Surveillance, Epidemiology, and End Results analysis. Cancer 118 (17): 4212-9, 2012.
- Olson TA, Bayar E, Kosnik E, et al.: Successful treatment of disseminated central nervous system malignant rhabdoid tumor. J Pediatr Hematol Oncol 17 (1): 71-5, 1995.
- Zimmerman MA, Goumnerova LC, Proctor M, et al.: Continuous remission of newly diagnosed and relapsed central nervous system atypical teratoid/rhabdoid tumor. J Neurooncol 72 (1): 77-84, 2005.
- Chi SN, Zimmerman MA, Yao X, et al.: Intensive multimodality treatment for children with newly diagnosed CNS atypical teratoid rhabdoid tumor. J Clin Oncol 27 (3): 385-9, 2009.
- De Amorim Bernstein K, Sethi R, Trofimov A, et al.: Early clinical outcomes using proton radiation for children with central nervous system atypical teratoid rhabdoid tumors. Int J Radiat Oncol Biol Phys 86 (1): 114-20, 2013.
Treatment for Recurrent Childhood CNS Atypical Teratoid / Rhabdoid Tumor
There is no standard treatment for recurrent childhood central nervous system atypical teratoid/rhabdoid tumor.
Treatment Options Under Clinical Evaluation
Early-phase therapeutic trials may be available for selected patients. These trials may be available via Children's Oncology Group phase I institutions, the Pediatric Brain Tumor Consortium, or other entities. Information about ongoing clinical trials is available from the NCI Web site.
Current Clinical Trials
Check for U.S. clinical trials from NCI's list of cancer clinical trials that are now accepting patients with childhood atypical teratoid/rhabdoid tumor. The list of clinical trials can be further narrowed by location, drug, intervention, and other criteria.
General information about clinical trials is also available from the NCI Web site.
Changes to This Summary (10 / 13 / 2014)
The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.
This summary was reformatted.
This summary was comprehensively reviewed.
This summary is written and maintained by the PDQ Pediatric Treatment Editorial Board, which is editorially independent of NCI. The summary reflects an independent review of the literature and does not represent a policy statement of NCI or NIH. More information about summary policies and the role of the PDQ Editorial Boards in maintaining the PDQ summaries can be found on the About This PDQ Summary and PDQ NCI's Comprehensive Cancer Database pages.
About This PDQ Summary
Purpose of This Summary
This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about the treatment of childhood central nervous system atypical teratoid and rhabdoid tumor. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.
Reviewers and Updates
This summary is reviewed regularly and updated as necessary by the PDQ Pediatric Treatment Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).
Board members review recently published articles each month to determine whether an article should:
- be discussed at a meeting,
- be cited with text, or
- replace or update an existing article that is already cited.
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The lead reviewers for Childhood Central Nervous System Atypical Teratoid/Rhabdoid Tumor Treatment are:
- Kenneth J. Cohen, MD, MBA (Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins Hospital)
- Karen J. Marcus, MD (Dana-Farber Cancer Institute/Boston Children's Hospital)
- Roger J. Packer, MD (Children's National Medical Center)
- Malcolm A. Smith, MD, PhD (National Cancer Institute)
Any comments or questions about the summary content should be submitted to Cancer.gov through the Web site's Contact Form. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.
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Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Pediatric Treatment Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.
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National Cancer Institute: PDQ® Childhood Central Nervous System Atypical Teratoid/Rhabdoid Tumor Treatment. Bethesda, MD: National Cancer Institute. Date last modified <MM/DD/YYYY>. Available at: http://www.cancer.gov/types/brain/hp/child-cns-atrt-treatment-pdq. Accessed <MM/DD/YYYY>.
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Dordt College News
Motionpoems creator's visit is rescheduled
April 11, 2013
The community is invited to hear award-winning Poet Todd Boss give a public reading on Thursday, April 18, at Dordt College in the Science and Technology Center Room S101 at 8:30 p.m.
During his visit to the college, Boss will meet with English and graphic design classes to discuss reading and writing poetry and share his work with Motionpoems, a poetry film initiative that turns contemporary poetry into short films.
Boss is the author of two books of original poetry. His debut work, Yellowrocket, was a finalist for the Minnesota Book Award and was named a Midwest Booksellers' Honor Book for Poetry. His latest book, Pitch, was the winner of the Midwest Bookseller's Choice Award and was a finalist in the Minnesota Book Award.
Boss' poems have appeared in Poetry, The London Times, The New Yorker, NPR, Best American Poetry, and Virginia Quarterly Review, which called Yellowrocket "one of the year's 10 best poetry books" and awarded him the Emily Clark Balch Prize.
Along with co-founder and co-director Angella Kassube, Boss developed Motionpoems in an effort to broaden the audience for poetry. What began as a project featuring his own poems has grown to a full-scale production company featuring the work of a variety of poets. To see a sampling of the projects visit http://toddbosspoet.com/motionpoems.
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This Side of Paradise (episode)
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(written from a Production point of view)
|"This Side of Paradise"
|TOS, Episode 1x25
Production number: 6149-25
First aired: 2 March 1967
Remastered version aired: 28 July 2007
|26th of 80 produced in TOS
|24th of 80 released in TOS
|40th of 80 released in TOS Remastered
|24th of 728 released in all
| Teleplay By
D.C. Fontana
Story By
Nathan Butler and D.C. Fontana
Directed By
Ralph Senensky
|3417.3-3417.7 (2267)
The Enterprise crew finds happiness at a colony where alien spores provide total contentment.
The USS Enterprise arrives at the planet Omicron Ceti III, the site of a colony established in 2264. Unfortunately, the Enterprise's mission is only to catalog its destruction under the bombardment of deadly berthold rays, which were discovered after the colonists left Earth.
Captain Kirk, Commander Spock, Doctor McCoy, Lieutenant Sulu, Lieutenant DeSalle, and Lieutenant Kelowitz beam down to the planet's surface and discover to their surprise that Elias Sandoval and the other colonists are not dead after all.
Act OneEdit
Spock encounters Leila Kalomi, a botanist he had met on Earth many years before. She had loved him, but he had been unable to return her love despite being half-Human. McCoy is astounded to discover that every colonist is in perfect physical health, even to the point where childhood injuries have repaired themselves. Sandoval attributes this to their healthy lifestyle that is a plant based diet. Other anomalies are discovered, such as the total lack of any animal life other than the colonists themselves, and no cars or trucks are present as well.
Leila promises to tell Spock their secret, and leads him to a flowering plant, which blasts him with spores. The spores cause Spock's emotional barriers to break down, and he confesses his love for Leila.
Act TwoEdit
When Kirk hails Spock, he does not respond, forcing Kirk to come and find out what is wrong. Spock manages to blast Sulu and Kelowitz with spores while DeSalle, already under their influence as well, infects Dr. McCoy who begins beaming the plants aboard the Enterprise.
As it turns out, the spores not only induce a feeling of total peace and euphoria, but they are also the reason that the colonists have been protected from the berthold rays. Spock explains that the plants traveled through space until they landed on the planet, actually thriving on the berthold rays. The plants act as a repository for thousands of microscopic spores until they find a Human body to inhabit. In return, they give their host complete health and peace of mind: in short, paradise; no wants and no needs. When Kirk hears that, he disagrees, stating that Humans weren't meant for that. He insists that man stagnates if he has no challenge to drive him and motivate him. But Spock says that Kirk simply doesn't understand now, but that he would come around eventually and really comprehend what they mean and join them.
Kirk, however, decides to go back to the ship. However, because Dr. McCoy had ordered some of the plants beamed aboard, the spores are carried throughout the Enterprise by the ship's ventilation system. Uhura, under the spores influence herself, leaves the bridge to beam down, but not before sabotaging the communications station so Kirk cannot contact Starfleet, only to be in contact with the planet. Kirk then discovers that his entire crew is beaming down to the surface and orders them to go back to their stations. Leslie, speaking for the deserting crew, refuses and mutinys against the Captain.
Act ThreeEdit
Alone on the bridge and growing increasingly desperate in his situation and realizing the helpless position he is in as the last person unaffected by the spores, he records a message on the log, confessing to his isolation and his inability to offer something against this alluring paradise, when he is suddenly blasted by a pod plant left on the Enterprise bridge. He becomes just as mindlessly happy as the others and hails Spock to let him know that he finally understands and wants to join them after all. About to beam down on the planet, he suddenly gets a hold of himself and becomes angry, yelling that he cannot leave the Enterprise, and becomes himself again, free of the spores. That is when he realizes that violent emotions and anger are what counteract the spores' euphoria-inducing effects. Noting this cure for the spores in his log, Kirk also realizes that his plan to free his crew and the colonists from the spores' effects comes with one potential danger: Spock. Knowing his first officer to be stronger than a normal human being, and could kill him with his bare hands, Kirk decides to risk it as he successfully tricks him into beaming up, taunting the Vulcan with insults angering him sufficiently enough to destroy the spores, even though Spock came very close to bashing Kirk's head in with a table.
Act FourEdit
When Spock comes to, the two create a subsonic transmitter that induces anger and intense emotions in everyone on the planet's surface, thus eradicating the spores.
When Leila beams up to the ship to find out what happened to Spock, she tells him that she cannot lose him again. But Spock tells her that he has a responsibility to the ship, and to his friend the captain. He goes on to tell her that he is who he is, and that if there are self-made purgatories then we all have to live in them, that his can be no worse than someone else's. Leila cries and then realizes that she lost not only Spock but the feeling the spores induced as well. However, she says that her feelings for Spock still have not changed and that she still loves him.
The transmitter is activated, and fights break out across the colony, destroying the spores' effects. Sandoval expresses regret, noting that they have not really accomplished anything, as any progress they made was purely the result of the spores. He hopes that he and the other colonists can try again on another planet. As the Enterprise leaves Omicron Ceti III for Starbase 27, McCoy cynically states that this is the second time Humans have been thrown out of paradise and Kirk responds jokingly that actually this time they just walked out on their own; maybe they weren't meant for paradise, says Kirk, maybe they were meant to fight their way through, struggle and scratch for every inch of the way. Spock, on the other hand, realizes that his time with Leila on the surface was the first time he had ever been happy.
Log EntriesEdit
Memorable QuotesEdit
"It's like a jigsaw puzzle all one color. No key to where the pieces fit in."
- - Kirk, on Omicron Ceti III
"I have never understood the female capacity to avoid a direct answer to any question."
- - Spock, to Leila
"Emotions are alien to me. I'm a scientist."
- - Spock, to Leila
"It didn't hurt us."
"I am not like you."
- - Leila and Spock, after he gets sprayed with spores
"I love you. I can love you."
- - Spock, before kissing Leila
"I thought you said you might like him if he mellowed a little."
- - Kirk to McCoy, on Spock's spore-induced behavior
"Ah yeah, Jimmy boy. Hey, I've taken care of everything. All you gotta do is just relax - doctor's order."
- - McCoy (spore-influenced) to Kirk
"This is mutiny, mister!"
"Yes, sir. It is."
- - Kirk and Leslie, as Leslie refuses to go back to his station
"Who wants to counteract paradise, Jim boy?"
- - McCoy, to Kirk
"Man stagnates if he has no ambition, no desire to be more than he is."
- - Kirk, to Spock and Sandoval
"I'm beginning to realize just how big this ship really is."
- - Kirk, after the crew has deserted the Enterprise
"No...NO! I...can't...LEAVE!"
- - Kirk, fighting off the effects of the spores
"All right, you mutinous, disloyal, computerized half-breed! We'll see about you deserting my ship!"
- - Kirk, provoking Spock into a fight
"What makes you think you're a man? You're an overgrown jackrabbit; an elf with a hyperactive thyroid!"
- - Kirk, provoking Spock into a fight
"What can you expect from a simpering, devil-eared freak, whose father was a computer and his mother an encyclopedia?"
- - Kirk, provoking Spock into a fight
"Your father was a computer, like his son! An ambassador from a planet of traitors! The Vulcan never lived who had an ounce of integrity!"
- - Kirk, provoking Spock into a fight
"You're a traitor from a race of traitors! Disloyal to the core! Rotten...like the rest of your subhuman race! And you've got the gall to make love to that girl!"
- - Kirk, provoking Spock into a fight
"Does she know what she's getting, Spock? A carcass full of memory banks who should be squatting on a mushroom instead of passing himself off as a man! You belong in a circus, Spock, not a starship! Right next to the dog-faced boy!"
- - Kirk, before Spock strikes him
"It isn't every first officer who gets to belt his captain ... several times."
- - Kirk, after Spock is cured
"I am what I am, Leila. And if there are self-made purgatories, then we all have to live in them. Mine can be no worse than someone else's."
- - Spock to Leila, in the transporter room
"You never told me if you had another name, Mister Spock."
"You couldn't pronounce it."
- - Leila and Spock, as he wipes away her tears
"We don't need you. Not as a doctor."
"Oh, no? Would you like to see how fast I can put you in a hospital?"
- - Sandoval and McCoy, before McCoy punches him
"Maybe we weren't meant for paradise."
- - Kirk, to McCoy
"I have little to say about it, captain. Except that for the first time in my life, I was happy."
- - Spock, about Omicron Ceti III
Background InformationEdit
Production TimelineEdit
- Treatment by Jerry Sohl, 15 June 1966
- Treatment by Jerry Sohl, July 1966
- Treatment by Jerry Sohl, 9 August 1966
- Second draft teleplay by Jerry Sohl, 11 October 1966
- Treatment by D.C. Fontana, 15 November 1966
- First draft teleplay by D.C. Fontana, 7 December 1966
- Final draft teleplay, 15 December 1966
- Revised final draft teleplay, 28 December 1966
- Filmed: 4 January 1967 – 11 January 1967
- Original airdate: 2 March 1967
- Rerun airdate: 10 August 1967
- First UK airdate: 29 November 1969
Story and ScriptEdit
- In Jerry Sohl's original draft (first titled "Power Play," then "The Way of The Spores"), it was Lieutenant Sulu who was infected by the spores and was able to fall in love with the Eurasian beauty Leila. McCoy discovered an internal condition that would have necessitated Sulu's resignation from Starfleet service, had the spores not cured his condition. His illness gave Sulu a will to develop a relationship with Leila just as similar circumstances would later affect McCoy's judgment in "For the World is Hollow and I Have Touched the Sky". (The Star Trek Compendium, p. 59)
- The spores, in the early drafts, were a communal intelligence; when someone was possessed by them, that individual was granted telepathic abilities to link up with other possessed minds. The abilities of the spores to restore health were complete enough to enable them to return the dead to life. The antidotes for the spores were either the possession of a certain blood type or the introduction of alcohol into the affected person. Originally, Kirk leaped onto Spock and forced liquor down his throat to restore him to normal. In a surprise ending, the spores were revealed to be benevolent, conscious entities who never intended to act against anyone's will. (The Star Trek Compendium, p. 59)
- According to Dorothy Fontana, the episode had to be seriously rewritten because Sohl had not quite gotten it right. Gene Roddenberry told her, "If you can rewrite this script, you can be my story editor." She thought about it and eventually realized that the story wasn't really about Sulu, but about Mr. Spock. Nimoy, who was initially taken aback when he was told that they were working on a love story for Spock, later felt that the episode turned out to be a lovely story. (TOS Season 1 DVD feature Kiss 'n' Tell: Romance in the 23rd Century)
- One of the basic aspects that Fontana immediately changed was Sohl's original conception of the spore plants residing in a cave. Thus, to avoid the danger of the plants, the crew merely had to avoid the cave. Fontana put the plants everywhere around the planet, and later the Enterprise to make them a real menace. (Star Trek: The Original Series 365, p. 131)
- Jerry Sohl was unhappy with Fontana's rewrites of his script and credited himself under his pseudynom "Nathan Butler".[1]
- Fontana very much liked the finished episode. She recalled, "It worked out very well because the actors were brilliant for me, and had a very good director, and you know, I really like it." [2]
- The script featured characters named Lieutenant Timothy Fletcher and Crewman Dimont as members of the landing party. When Michael Barrier and Grant Woods were cast in these roles, the names were changed to DeSalle and Kelowitz respectively, to appear constant with the two actors' previous appearances on the series.[3]
Production Edit
- Originally "The Devil in the Dark" was scheduled to be filmed before this episode with Ralph Senensky directing it, and Joseph Pevney directing "This Side of Paradise", but during pre-production the two episodes were switched, and changed directors. [4]
- In a blooper, Leonard Nimoy flubs his line about the plants acting as a repository for thousands of spores. Instead, he says the plants act as a "suppository." The crew cracks up, as does Nimoy, who caps the fun by putting a Tootsie Pop in his mouth. [5]
- The empty shot of the bridge, before the turbolift opens to admit Kirk, was the best available piece of film for TNG: "Relics" to reuse as the holosimulation of the NCC-1701 bridge. The short snippet of film was "looped" several times and bluescreened in behind James Doohan and Patrick Stewart's scenes. Using the stock footage in this way eliminated the need to completely rebuild the bridge – they only built a short section of the computer stations, the door alcove, and the command stations for the TNG-era actors to sit at.
- In Leila's first close-up Jerry Finnerman lighted Jill Ireland with a baby spot light from behind, adding an "aura of light" around her face.[6]
- Senensky originally wanted to film the Kirk vs. Spock fight scene from a wider angle, so the stunt doubles wouldn't be so obvious, but the transporter room set was too small to achieve this. [7]
- Gerald Fried's score from "Shore Leave" is heavily featured in this episode, most notably the "Ruth theme", successfully accompanying the lost love between Spock and Leila.
- The large open meadow seen in several sequences is in Malibu State Park in southern California. It is the same spot where the hunt in the corn field took place in Planet of the Apes, and also extensively used in the series Gunsmoke.
- The barn Kelowitz and Sulu investigate can be seen in several episodes of Kung Fu.
- The buildings seen in the teaser, the first scene after and the scene in which DeSalle shows McCoy the Spores are at a different location than the buildings seen in the rest of the episode. The green farm structures were located at the Disney Ranch. The concept of Sandoval's people refusing modern technology was intended to justify the late-19th century Americano style of the ranch. [8]
- According to director Ralph Senensky, the original schedule was that the first three of the six shooting days were to be spent on location, shooting at the Golden Oak Ranch (also known as the Disney Ranch), then the remaining three days indoors, filming the Enterprise scenes. However, after two days of shooting outdoors, Jill Ireland fell ill and couldn't appear on the set. It was in question if she had measles or not. Senensky decided to film all the farm scenes which didn't contain Leila's character and then return to the studio for Enterprise interiors in the remaining of the day, and hope for the actress' return. Ireland appeared the following day, as it turned out that she did not have measles. However, the crew couldn't return to Disney Ranch as it was already booked for another production. They decided to film the remaining scenes at Bronson Canyon. [9]
- In the script, Kirk first spots Spock and Leila kissing passionately by the stream; there is no scene of Spock hanging off the tree limb. That facet of the episode may have been made up on the spot. [10] Indeed, director Ralph Senensky came up with the idea of Spock hanging from the tree on location, when he found the tree and the spot closely to Bronson Canyon. Originally the scene was to be shot on a clearing. [11] Evidence taken from a deleted scene, of Spock and Leila's presence near the stream, appears in the episode's preview trailer.
Sets and PropsEdit
- The food processors in the transporter room, placed there so Kyle could provide chicken soup for the air sergeant in "Tomorrow is Yesterday", disappeared from the room by the end of the first season. In this episode, an enraged Spock destroys one of them.
- There is a piece of equipment attached to the left side of the transporter console. It seems to serve no purpose, other than for Spock to hit when he misses Kirk during their brief dust-up, and was only seen in this episode. In fact, it was not in the scene where six crew members, under the influence of the spores, transport down.
- Similarly, the tray-like metal object that Spock is poised to throw on Kirk at the end of Act III is not seen in the transporter room in any other episode.
- The suitcase in which Kirk packs his belongings, and which he later places on the transporter platform, is a very obvious piece of 20th century Samsonite luggage.
- Omicron Ceti III is M-113 in "The Man Trap", Alfa 177 in "The Enemy Within" dyed a green color.
- James Doohan (Scotty) does not appear in this episode, although he is referenced and asked for by Kirk.
- Stuntman Bobby Bass, whose character tried to break up the fight between the two officers, had his only lines of dialog in the series here.
- Frank Overton died shortly after completing this episode, which was filmed in early January 1967.
- This is the last episode in which Eddie Paskey delivers dialog as Leslie.
Continuity Edit
- Admiral Komack is mentioned in this episode; he is seen in "Amok Time". According to Denise and Michael Okuda, the character was named for James Komack, director of "A Piece of the Action".
- In "The Tholian Web", Chekov asks Spock if there has ever been a mutiny on a starship before. Spock replies that there has never been, despite the fact the events of this episode were specifically called a mutiny.
- As established in The Making of Star Trek, there are only 17 starbases. However, Kirk announces that he has been ordered to take the colonists to Starbase 27.
- Although DeSalle wears a gold uniform top denoting that he is a member of the command division, it is he who is assigned to deliver a biology report on the colony. A more logical choice would have been Kelowitz, a blue-shirted member of the sciences division.
- At one point during his log recording, Kirk refers incorrectly to the planet as "Omicron III."
- An alternate reality version of Kirk would again attempt (and succeed) to provoke Spock to anger in Star Trek.
Video and DVD ReleasesEdit
- Original US Betamax release: 1985
- UK VHS release (two-episode tapes, CIC Video): Volume 14, catalog number VHR 2307, release date unknown
- US VHS release: 15 April 1994
- UK re-release (three-episode tapes, CIC Video): Volume 1.9, 30 December 1996
- Original US DVD release (single-disc): Volume 13, 11 July 2000
- As part of the TOS Season 1 DVD collection
- As part of the TOS Season 1 HD DVD collection
- As part of the TOS Season 1 Blu-ray collection
Links and ReferencesEdit
Guest StarEdit
Special Guest StarEdit
- Grant Woods as Kelowitz
- George Takei as Sulu
- Nichelle Nichols as Uhura
- Michael Barrier as DeSalle
- Dick Scotter as Painter
- Eddie Paskey as a crewman
Uncredited Co-StarsEdit
- Bobby Bass as Crewman #2
- William Blackburn as Hadley
- Frank da Vinci as:
- Walker Edmiston as the Transporter chief (voice)
- John Lindesmith as Engineer #2
- Jeannie Malone as
- a yeoman
- an Omicron colonist
- Sean Morgan as Harper
- Fred Shue as Crewman #1
- Ron Veto as Harrison
Stunt DoublesEdit
- Bill Catching as the stunt double for Leonard Nimoy
- Chuck O'Brien as the stunt double for William Shatner
- William Blackburn as the stand-in for DeForest Kelley
- Frank da Vinci as the stand-in for Leonard Nimoy
- Jeannie Malone as the stand-in for Jill Ireland
- Eddie Paskey as the stand-in for William Shatner
2261; 2263; 2264; admiral; agriculture; ambassador; appendectomy; appendix; bean; Berengaria VII; berthold rays; biochemistry lab; biology; "Bones"; butterfly net; circus; climate; cloud; cow; dog; dog-faced boy; dragon; drum; Earth; Eden; elf; encyclopedia; Georgia; grain; Grayson, Amanda; horse; hyperactive thyroid; insect; itching powder; jackrabbit; jigsaw puzzle; Komack; logic; lute; mechanic; mint julep; mushroom; mutiny; Omicron Ceti III; Omicron colony; Omicron pod plant; Omicron spore; pig; pneumonia; potato; rain; rainbow; rib; Sarek; scientist; soil; Starbase 27; Starfleet Command; Starfleet Medal of Honor; subsonic transmitter; teacher; tonsil; tricorder; vegetarian; ventilation system; Vulcanian; Vulcan (planet)
External linkEdit
- This Side of Paradise at Memory Beta, the wiki for licensed Star Trek works
| Previous episode produced:
"Space Seed"
| Star Trek: The Original Series
Season 1
| Next episode produced:
"The Devil in the Dark"
| Previous episode aired:
"A Taste of Armageddon"
| Next episode aired:
"The Devil in the Dark"
| Previous remastered episode aired:
"The Squire of Gothos"
|TOS Remastered
| Next remastered episode aired:
"The Galileo Seven"
de:Falsche Paradiese es:This Side of Paradise fr:This Side of Paradise ja:TOS:死の楽園 nl:This Side of Paradise pl:This Side of Paradise


text:
Danke Schoen Greenwich
Greenwich United Way
photographs by Susan Ferris
The Greenwich United Way party committee outdid themselves by turning the Loading Dock in Stamford into an Alpine village for the fourth annual Oktoberfest fundraiser. Hundreds of supporters, sponsors and guests enjoyed a special evening of German-inspired foods, regional beers and wines, traditional German music, dancing and a silent auction.
The Greenwich United Way is the largest nongovernmental source of funding for local health and human service programs. Giving to the annual community-wide fundraising campaign is the most effective and efficient way to support critically-needed local services that strengthen children and families, support seniors, foster self-sufficiency and assist individuals in crisis in our community. unitedway-greenwich.org


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Ill Communication
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Berkeley County deputy on administrative leave after alleged inappropriate communication with minor
Helen L. Parrish
Helen L. Parrish, 98, of Inwood, and formerly of Mannington, passed away unexpectedly and peacefully Sunday evening, July 14, 2013, at the Shenandoah Center Nursing Home in Charles Town.
She was born Jan. 7, 1915, at Dent's Run, Mannington, daughter of the late Henry H. Satterfield and Zella A Batson Sloan Satterfield.
She is survived by her son, James A. Parrish and wife, Martha, of Inwood; one granddaughter, Dawn Denise Parrish, of Inwood; two grandsons, Jeffrey Jay Parrish and wife, Nicole, of Bunker Hill and Mark Allen Parrish and wife, Michele, of San Clemente, Calif.; five great-grand-daughters, Elizabeth Smith and husband Andrew, Emily Parrish, Savanna Parrish, Jessica Parrish and Julia Parrish; two great-great-grandsons; and several nieces and nephews.
In addition to her parents, Helen was preceded in death by her husband, Chester Parrish, who died in 1991; three sisters, Irene Snider, Della Blankenship and Georgia Hibbs; and two brothers, Floyd Sloan and Denzil Satterfield, who died in infancy.
Helen was a very devoted wife, mother and grandmother who cared very deeply for all her family. She enjoyed cooking and family get-togethers.
Friends and family may call from 3 to 5 and 7 to 9 p.m. today at Masters Funeral Home, 209 Main St., Mannington.
Funeral services will be held at 11 a.m. Friday, July 19, 2013, at the funeral home. Burial will follow at Viewpoint Cemetery in Rachel.
Online condolences may be left at www.mastersfuneralhomewv.com.


text:
U.S. hawks dead wrong on Syria war
There are at least two schools of thought regarding President Barack Obama's conduct of U.S. foreign policy. One holds that he knows what he's doing. The other suggests that he's a bull in a china shop.
Last week's White House announcement that the United States will give more military aid, including weapons, to Syrian "rebels" seems to tip the balance toward the latter.
Obama's Syrian problem started with a jerk of the knee two years ago. "Rebels" had launched protests, peaceful and then violent, against the Assad regime, and Obama thought the Arab Spring had returned.
His messianic complex finally got the better of him, and he declared, "The future of Syria must be determined by its people, but President Bashar al-Assad is standing in their way. For the sake of the Syrian people, the time has come for President Assad to step aside."
The death toll at the time was 2,000.
Assad didn't step aside, so Obama doubled down. He helped Saudi Arabia and Qatar arm the "rebels," and he authorized U.S. training for them.
Today, two years later, the death toll stands at an estimated 93,000.
Obama perseveres. He promises more weapons for the "rebels," and Saudi Arabia donates shoulder-fired anti-aircraft missiles and anti-tank guns to the cause.
The death toll a year from now? Hard telling, but it's likely to be much higher.
Obama is as inarticulate as he is undaunted, and U.S. objectives, beyond making good on his vision for Syria, are unclear at best.
He told a sympathetic interviewer the other day that we (you and me) can't understand the Syrian situation because we "haven't been in the Situation Room" at the White House.
Sure. But we can recognize a slippery slope when we see one, and in the view of many, including some on the left, Obama has started to slide down the path to full U.S. involvement in the Syrian civil war
Bob Dreyfuss, a freelance investigative journalist writing in "The Nation," believes Syria could turn into another Vietnam, with Obama making similar mistakes "simply because he won't want to tolerate an Assad victory."
Meanwhile, important questions hang in the air. What vital U.S. interests are on the line in Syria? How much of our national treasure ? blood and money ? is Obama willing to spend? And what makes him, or anyone else, for that matter, think that arming the "rebels" will lead to democracy in Syria and long-term stability in the Middle East?
An overarching question: Who are the "rebels?"
The uprising was sparked by ragtag groups two years ago, but radical Islamists and elements of al-Qaeda are taking over.
Example: Ghurabaa al-Sham, a moderate rebel group, has fallen apart in the last month. The group's leader told a Reuters reporter on Wednesday that his 2,000-man "army" was attacked by radical Islamists. They seized his weapons, ammunition and cars, and his force has fallen to 100 or so men. The Sharia Authority has taken over in the city of Aleppo.
Ban Ki-moon, secretary general of the United Nations, believes more fighting will lead to the disintegration of Syria, and he seems to have a point.
The new "rebels" are not likely to yield. After all, more weapons are on the way, and Sunni clerics in other Arab nations, including Egypt and Saudi Arabia, are calling for "jihad" against Assad and his followers.
Likewise, Assad is not likely to yield. He has the backing of Russia and Iran, and he knows that walking away could subject his 2.7 million Shiite followers (12 percent of Syria's population) to a blood-bath at the hands of the hard-line Sunnis.
Given the circumstances, then, Obama and other U.S. hawks (GOP Sens. John McCain and Lindsey Graham, especially) need to stop feeding the tiger and refocus on real threats to our vital national interests. And a good place to start would be Iran and its nuclear weapons program.


text:
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#128437 - 05/10/04 08:36 AM intelligence vs intellect
Registered: 05/10/04
Posts: 4
What is the difference between the two?
#128438 - 05/10/04 08:54 AM Re: intelligence vs intellect
old hand
Registered: 03/15/00
Posts: 1027
Loc: Switzerland
At the risk of getting lost at sea in metaphor, I suggest: intellect is the motor, and intelligence is the power delivered by this motor (for better or worse).
#128439 - 05/10/04 09:42 AM Re: intelligence vs intellect
Registered: 05/10/04
Posts: 4
Thank You for your reply. It seems to make sense. Where my struggle began from was the usage of the adjectives, i.e. what would be the distinction between say an intelligent person and an intellectual person. How, if at all, does the motor methaphor transfer to that situation?
An intellectual person has the ability(motor) and intelligent person actually uses it(delivering the power)?
(please excuse the overuse of parentheses and question marks)
#128440 - 05/10/04 10:18 AM Re: intelligence vs intellect
Registered: 01/06/04
Posts: 1475
Loc: California
To me, intellectual has a slightly more pejorative connotation to it than intelligent. Interestingly, the etymologies show that both words come from the same verb in Latin: intellect is from the past particple and intelligence is from the present particple. You might want to look at the synonym section of this entry:
#128441 - 05/10/04 10:43 AM Re: intelligence vs intellect
Carpal Tunnel
Registered: 03/15/00
Posts: 6511
Loc: lower upstate New York
Welcome, Reebecca.
"Intellect" suggests to me a type of intelligence. You can be intelligent without being intellectual, but not vice-versa.
#128442 - 05/10/04 12:23 PM Re: intelligence vs intellect
Registered: 06/28/02
Posts: 1624
Loc: Utter Placebo, Planet Reebok
Oh, I dunno, ASp. I've met a lot of intellectuals who didn't seem to be all that intelligent ... an intellectual will think and think about a problem but may well still come to a nonsensical although potentially strictly logical answer.
Welcome, Reebecca. Good question.
#128443 - 05/10/04 04:11 PM Re: intelligence vs intellect
Carpal Tunnel
Registered: 12/24/00
Posts: 2661
Loc: Chicago
...nonsensical althought potentially strictly logical answer.
Just as a *sensical answer may be potentially strictly illogical!
I like wsieber's perspective. Neither function on thier own plane without the operation of the other. What one does with either is not (really) part of the difference between them.
#128444 - 05/10/04 08:06 PM Re: intelligence vs intellect
Carpal Tunnel
Registered: 12/01/00
Posts: 13803
both words come from the same verb in Latin
Speaking of double-dipping.
#128445 - 05/11/04 01:07 AM Re: intelligence vs intellect
old hand
Registered: 03/15/00
Posts: 1027
Loc: Switzerland
intellectual has a slightly more pejorative connotation to it than intelligent - Yeahbut, this is a secondary evolution of the word "intellectual", quite separate from "intellect". I even suspect that "intellectual", as a noun, entered English independently from French, whereupon it was devalued by the pragmatists.
#128446 - 05/11/04 02:51 AM Re: intelligence vs intellect
Registered: 05/10/04
Posts: 4
Thanks for all your replies.
I did try to work from the roots of the word: intelligence coming from the present participle of inter- and legere perhaps denoting the present action of collecting/perceiving 'knowledge', while intellect, from the past participle of the same Latin term, perhaps referring more to the processing of that knowledge that follows its collection/perception... all in all it lead me into a big mental knot and, ultimately, to this board.
I would however have to disagree with jheem-based on gut feeling, I definitely would not name intellectual as the pejorative of the two.
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text: So I was just thinking the other day and thought I would ask..... We have had every problem you could have other than mastitis. I have always had supply issues and take fenugreek and now Dom. My DD is 8 months old and spends 5 min max with multi latches per feeding than refuses. She is very wiggly and impatient when I pump post feeding I get maybe one oz so I think she is getting most of it. Could this fast feeding thing she.has going on be contributing to my low supply? I try supplementing but she refused most times.


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~ Ann Marie
"Build schoolhouses then for the religious education of your children as the best protest against a system of education from which religion has been excluded by law."
~ Bernard J. McQuaid, Bishop of the Diocese of Rochester; in firm command to his flock, after the failure of the State to remedy the injustice to Catholic parents who were forced to pay education taxes to support public schools detrimental to their faith.


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