Sega update

Read me. Developers can now include important notes and information they want users to read. It is a cd image format that uses compression, as well as allows for meta data to be added. More intuitive UI. The UI provides more information a person may want, as well as makes it easier to create or use patches.

You can now customize the experience of the program. Cheat Detection removal patch. Will remove Action replay blocking methods in games. Needs to be added via Settings.

Pseudo Kai Fast Boot patch. If you are a Pseudo Kai user, you can apply this patch to skip the second Sega authorization check. Application is now resizeable. Command line can be used to create CD image formats. This feature will allow for homebrew developers to generate more accurate CD images. Just place the files that need patching into a zip file, and assign the file to SSP in the settings.

There are 2 different drivers that need to be added depending on the online play available. These files do not need to be renamed or placed into any folders. To include your patch at SegaXtreme, go and set up an account if applicable. Head over to the resources page, and click on Add Resource. Fill out the form, but do not add your file yet. Do not worry about the APIKey, this will be provided for you.

Save your SSP. This SSP will now notify users if they are using an older version of your patch. Valid choices:bin,iso,ccd,sscd. Do not mix patching options with generation. Add audio tracks to image. Reactions: saturn32beats. Patcher has been rebuild from the ground up.

If you are a Pseudo Kai Cartridge user, you can apply this patch to skip the second Sega authorization check. Reactions: dibz , saturn32beats and derek ateam. Fix for single file bin images Apr 30, When using a single file bin image, the CUE sheet may contain obscure terms.

This update handles some of those terms. Reactions: linlhutz , dibz and Benjamin Siskoo. Small update to version 1. The risks of surgery include acute morbidity and the permanent need for ventriculoperitoneal shunting, which must be balanced against the adverse effects of mTOR inhibitors, including immunosuppression infections, mouth sores , hypercholesterolemia, and the need for chronic drug monitoring. Some additional benefits of mTOR inhibition in patients with tuberous sclerosis complex, however, may include shrinkage of angiofibromas and angiomyolipomas as well as a possible decrease in seizure burden.

Recent reports of successful nonsurgical treatment of SEGAs are promising, and it is hoped that further specifics on dosing, duration, and long-term outcome will help patients and physicians to make informed therapeutic choices. Present treatment recommendations for SEGAs include routine surveillance neuroimaging and close clinical follow-up, paying particular attention to signs and symptoms of acute hydrocephalus. If symptoms arise, or if serial neuroimaging demonstrates tumor growth, neurosurgical intervention is recommended.

When gross total resection is impossible, rapamycin and everolimus should be considered, but may not offer a durable response. Inactivation of the tumor suppressor genes hamartin TSC1 or tuberin TSC2 are associated with tuberous sclerosis complex TSC , a relatively common autosomal dominant genetic disorder affecting up to one out of 6, people [ 1 ]. Multiple organs are at risk for developing tumors, including the heart, lungs, skin, and kidneys.

The most common findings in the brain of TSC patients include tubers in the cortical parenchyma, which are relatively static.

Cortical tubers are thought to contribute to the high rate of epilepsy in TSC but do not have a high rate of oncologic growth potential. On MRI imaging, most patients with TSC are found to have subependymal nodules that line the ventricles, with a subset of nodules being completely or partially calcified; some show contrast enhancement [ 2 , 3 ].

To date, no radiographic features have been identified that will accurately predict which subependymal nodules will grow and require treatment. Serial neuroimaging demonstrates a continuum from subependymal nodules to SEGAs. Histopathologically, SEGAs are indistinguishable from subependymal nodules, with loosely cohesive clusters of large cells with round to oval nuclei and no or minimal atypia; fine, evenly distributed chromatin; and abundant eosinophilic cytoplasm embedded in abundant thin, hairlike processes [ 5 ].

Formed by three types of cells—fibrillated spindle cells, swollen gemistocytic-like cells, and giant pyramidal cells with a ganglioid appearance—SEGAs show both glial and neuronal features. Some authors have demonstrated that all subependymal nodules are clonal and have the capacity to proliferate [ 6 , 7 ].

SEGAs typically arise from subependymal nodules in the area of the foramen of Monro, and can be unilateral or bilateral. SEGAs are slow-growing tumors and typically have no symptoms until obstructive hydrocephalus develops [ 2 , 3 ]. They are distinguished from subependymal nodules by increasing size on serial neuroimaging, or by signs and symptoms of obstructive hydrocephalus.

Without intervention, SEGAs typically continue to grow slowly over weeks to months, with only sparse evidence of regression or growth stabilization. Rarely, SEGAs can exhibit more aggressive behavior, associated with parenchymal invasion or extensive peritu-moral edema, or they can occur in an atypical location such as the pineal or hypothalamic regions.

They typically project into the ventricle and can produce acute or chronic hydrocephalus. Typically, serial neuroimaging every 1 to 3 years is recommended for pediatric patients with TSC, even in the absence of symptoms [ 8 ]. If a subependymal nodule has grown over the interval of routine imaging, more frequent follow-up imaging is appropriate. Symptoms can be subtle in the early presentation of a SEGA. Complaints in patients with TSC that warrant urgent imaging include positional headache worse in a dependent position , sudden worsening of seizures, or progression to include nausea, vomiting, diplopia, and lethargy.

Clinical series suggest a male predominance, with a mean age at surgery of 11 years [ 3 , 4 ]. In a series of 14 surgical patients, SEGA was identified at a mean of 90 months of age, and surgical intervention occurred at a mean of 38 months after identification. Surgery was performed for evidence of hydrocephalus in nine of 12 patients, and for evidence of tumor growth in five of 12 [ 9 ].

In one series, ten of 21 patients with SEGA died, six as a direct result of tumor growth acute obstructive hydrocephalus in five, and intratu-moral hemorrhage in 1. In this series, death from brain tumor was most common at ages 10 to 19 years [ 10 ]. In patients followed by a neurologist experienced in caring for patients with TSC, deaths from SEGAs are rare, but morbidity including vision loss, chronic ventriculoperitoneal shunting, and headache are still seen.

Surgery was avoided in all five patients, and only mild adverse effects were observed. SEGAs causing significant hydrocephalus and impending herniation should undergo surgical resection for acute management. Severe infections are a contraindication for rapamycin therapy, as rapamycin decreases immune function.

Because epilepsy is a common problem in patients with TSC, and some antiepilepsy drugs utilize CYP3A4 and the P-gp transporter, sirolimus may have complex interactions with antiseizure medications. Known inducers of the CYP3A4 include phenytoin, carbamazepine, phenobarbital, oxcarbazepine, and rufinamide.

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