Rabu, 26 Disember 2012

#14 : Sunat.



"Eh, esok hari khamis, mahu puasa sunat?"

Dia angguk.

" Insya-Allah." Bunyinya.

Untuk hari isnin pun, begitulah ragamnya.

Jika dia bangun awal, dia masakkan sahur. Jika saya lebih awal, saya yang akan sediakan.

Sama-sama saling melengkapi. Satu lemah, satu lagi kuatkan. Itulah fungsi menjadi sahabat.

Bukan mudah untuk lakukan berseorangan, perlu berdepan dengan para syaitan dan nafsu-nafsu buas sendirian, lalu mudah tewas dengan segala pujuk rayunya. Terus, jadi lemah.

Harus ada jemaah. Walau berdua, itu sudak ok. Solat sendirian tidak dinamakan jemaah, dua orang barulah boleh.


Bina iman diri, untuk bina iman generasi hadapan.

Hari ini, bergelumang berlawan dengan nafsu fasad, menentang syaitan. Kerana suatu hari nanti, kita, sang lelaki ini, bakal jadi imam kepada keluarga.

Walau nampak lambat, tetapi ianya sudah dekat. Mula sekarang, untuk masa hadapan.

Jangan tunggu mahu kahwin baru mahu bina. Bina sekarang, insya-Allah binaannya bakal jadi binaan yang lebih besar dan nampak lebih bersedia dan matang untuk menghadapi segala cabaran mendatang.

Bukan mudah mahu bina keluarga yang diredhai Allah, perlu kerah segala kekuatan untuk berkorban. Bersedialah.


Sunat.

Lazimnya, orang yang lakukan banyak amalan sunat ini, mereka yang punya jalan juang mujahadah yang tinggi. Mereka bukan sahaja berjaya laksanakan yang wajib, bahkan juga yang sunat.

Mahu dapat redha Allah, apapun onak duri mendatang, sanggup sahaja diredahi.  Jangan mudah mengalah dan kalah. Jangan menyerah, teruskan mujahadah!

Hidup, bukan saja untuk bina badan, tapi juga untuk membina iman.

Tanpa iman, siapalah kita. Siapakah kita untuk dipandang-Nya?

Mari, sama-sama kita kejar mardhaatillah.


Rasa lemah berseorangan? Carilah sahabat baik yang mampu menguatkanmu.



-Mr.Hope-
26.12.2012
11:27 p.m.






Ahad, 25 November 2012

#13 : Beban Yang Terbeban.


Semangat, satu elemen yang sangat penting dalam jalan menuntut ilmu. Walaupun nampak mudah, tetapi tanpanya, membuat sesuatu pekerjaan dirasakan tidak lengkap, istiqamah mudah luntur.

Semangat, kadang-kadang mudah sungguh lari. Jika lari begitu sahaja tidak mengapa, tetapi perginya membawa sakit yang membarah di dalam diri. Sakit. Lelah.

Kini saya sedar, jika hati kotor, semangat juga turut menurun luntur. Tidak kira apa jenis semangat, pasti lari menghilangkan ruh hati.

Oh, ini sesuatu yang berat. Mungkin satu bala, saya kira. Bagaikan satu pakej. Semua terhubung kait. Sakit.

Bagaimana mahu jernihkan kembali? Mudah. Jangan kotori lagi sang hati. Lubuk dan pintu segala ilmu.

Bagaikan salur darah yang tersekat, aliran darah tidak dapat lagi lalu menuju ke destinasi yang hendak dituju. Tersekat dan terhalang. Akhirnya yang perit menanggung, seluruh badan. Pedih menanggung.

Solusinya mudah. Biar hati berpanjangan suci. Walau pahit mujahadah sendiri.


-Mr. Hope-

31.11.2012
 10:13 p.m


Khamis, 25 Oktober 2012

Face Dangerous Area


Triangular Area of Facial Skin


The Triangular Area of Facial Skin including :

- Upper lip

- Nose

- Medial angle of eyes

Are considered as dangerous area of face. If this area became infected, the infection would spread to cavernous sinus and causing its thrombosis.

Deep communication of anterior facial vein in connected with cavernous sinus via two routes.

1st Route :

- Facial vein is connected to superior opthalmic vein which then drains in the cavernous sinus.

 2nd Route :

- Facial vein is connected to pterygoid venous plexus through deep facial vein.

- Then, the pterygoid venous plexus is connected to cavernous sinus via three emissary veins.





Causes of cavernous sinus thrombosis ( from http://www.nhs.uk )

The most common cause of cavernous sinus thrombosis is when an infection in another part of the skull, such as the eye, nose or ears, spreads into the cavernous sinuses.

The two infections most commonly associated with a cavernous sinus thrombosis are:

- Sinusitis, which is an infection of the small, air-filled cavities behind the cheekbones and forehead
a boil, which is a large painful pus-filled swelling or lump that develops on the face

- Attempting to squeeze a boil can sometimes result in an infection spreading into the cavernous sinuses.

The immune system will create a blood clot to prevent the infection from spreading further into the body.

However, the clot will usually block the flow of blood away from the brain through the jugular vein. This blockage increases the pressure on the brain and blood can also flow back up into the brain, both of which can damage the brain, as well as the eyes and the central nervous system.

In addition, the immune system, despite the blood clot, is normally ineffective in preventing the spread of infection out of the skull and into the rest of the body.

So the infection often spreads through the blood stream causing multiple organ failure, which is known as blood poisoning or sepsis.

Other causes


Other less common causes of cavernous sinus thrombosis include:

- A severe head injury that results in a blood clot. This is thought to be the second most common cause.

- An infection spreading from a tooth or gum infection .

- Having a health condition or other underlying factor that makes you more prone to blood clots - the most common being pregnancy.

- People who have conditions that cause inflammation (swelling) inside their body, such as lupus or Behçet’s disease, can occasionally develop blood clots.

- Some types of medication, such as the contraceptive pill or the medications used in hormone replacement therapy, can cause blood clots as a side effect, though this is very rare.



Points to Remember

- Use a clean tissue to clean something from your nose instead of picking it with fingers. Nasal passage can be cleaned using nasal rinses.

- Instead of plucking your nose hair, use a nose trimmer.

- Do not squeeze or pick the pimples or zits in this area. Use emollient jelly instead.

- Facial piercings may also give problems.




Wallahua'lam.



-MrHope-

25 October 2012
11:50 a.m


Favism


Favism.


From Biochemistry Department Book :

- Favism is a type of Congenital Haemolytic Anaemia or Hereditary Haemolyti Anaemia.

- Congenital Hemolytic Anaemia is occurs due to congenital deficiency of Glucose 6 Phosphate Dehydogenase ( G6PD ).

- It is X-linked condition.

- Deficiency of G6PD result in :

 * Decrease in the level of NADPH+H

 * Hence, a decrease in the concentration of Reduced Glutathione ( GSH ), which is the main defense mechanism facing the dangerous effect of Hydrogen Peroxide and other oxidant radicals.

- Hydrogen Peroxide may decrease the life span of Erythrocytes and increase the rate of oxidation of Haemoglobin ( Hb ) into Methaemoglobin.

- The deficiency is manifested only after intake of certain oxidant drugs  like primaquine, the antimalarial drug or after ingestion of fava beans ( broad beans ).

- Oxidizing drugs and sulfa drugs, in absence of reduced glutathione ; may distort the membrane of RBCs resulting in hemolysis.

* The urine turns black

* Jaundice is developed

* Hb contentof blood drops sharply.


- In some cases; massive destruction of RBCs causes death.

- This disease could be treated by :

* Administration of antioxidants

* Regular transfusion of packed RBCs.


Meaning of Favism :


Dorland's Pocket Medical Dictionary 28th Edition.

- An acute hemolytic anemia precipitated by fava beans ( ingestion or inhalation of pollen ), usually caused by G6PD in erythrocytes.


Oxford Medical Dictionary.

- Inherited defect in the enzyme G6PD causing the red blood cells ( RBC ) to become sensitive to a chemical in fava beans.

Eating this bean result in destruction of RBC ( Haemolysis ), which may lead to severe anaemia, requiring blood transfusion. Favism occur most commonly in the Mediterranean and Middle East.


Fava Beans ( Broad Beans )





Wallahua'lam.



-MrHope-

25 October 2012.
7:04 a.m


Ahad, 21 Oktober 2012

# 12 : Dengki Mulia



Mata mendengki.

Entah mengapa, saya secara tidak sengaja wujud satu sifat yang jarang-jarang tumbuh dalam diri. Dengki.

Kala saya terlihat atau terserempak dengan orang yang memegang rekod sebagai pelajar terbaik batch, hati saya pantas melirik dengki. Pendengkian atas kejayaannya itu datang secara tiba-tiba.

Saya faham, itu dengki yang baik dan dibenarkan syarak. Mana tidaknya, berlumba untuk jadi yang terbaik di sisi Allah dan manusia sememangnya digalakkan.

Tapi, dengki bukan setakat mendengki. Dengki mulia itu perlu diiringkan dengan usaha menganjakkan diri semahu dan setinggi yang mampu. Kemudian, serah saja segalanya kepada Yang Maha Mengatur.

Moga harapan besar ini tidak didengki sang malas yang selalu meracun diri. Lawan tetap lawan. Alang-alang mujahadah, biarlah sampai jannah!


Terlanjur mendengki, biarlah dengki mulia. ^^



Wallahua'lam.



-Mr.Hope-

2 Oktober 2012
8:42 p.m


#11 : Yang Tidak Menyukai Jawatan



Kelu. Mahu kata bagaimana pun saya tak tahu.

Saya, apabila semakin dewasa, ada saja perubahan yang berlaku. Kadang-kadang, saya tak tahu, apa punca sebenar saya berubah sebegitu.

Antaranya, yang pertama, saya jadi malu mahu letakkan gambar di laman sosial.  Kedua, saya kini jadi tidak suka berjawatan, tambah-tambah kalau jawatan itu jawatan besar.

Huh.

Tarik nafas dalam-dalam, tahan dan lepaskan kembali.

Sungguh, semua perubahan ini berlaku tanpa saya sedari. Mungkin persekitaran hidup saya yang telah lama mempengaruhi saya.

Dan mungkin juga hati saya yang tak pernah surut merendah diri.  Tak tahu lagi nak buat bagaimana.
Apabila berfikir secara mendalam, saya fikir saya perlu mengorak langkah baharu. Tak perlu takut lagi dengan jawatan. Bahkan gunakannya dengan daya yang terbaik. Jadikan diri lebih bermanfaat dengan jawatan tersebut.

Namun, dari satu sudut, hati haruslah sentiasa dijaga. Agar segalanya dilakukan hanya kerana Allah, bukan kerana jawatan.

Alhamdulillah, satu lagi harapan yang bakal menyinari hidup saya, insya-Allah.


Wallahua'alam.

-MrHope-

20 Oktober 2012
10:04 a.m

Rabu, 26 September 2012

#10 : Leka Insan.



Masa terus berjalan, diri sendiri juga dewasa perlahan-lahan.

Kini, musim baharu kembali dan terus membuka langkah emas. Biar emas pada awalnya, supaya terus sayang langkah pertama itu untuk dibawa ke jauh ke peringkat seterusnya. Saya cuba binakan juga pembukaan lembaran dan harapan baru untuk tahun ini, insya-Allah. Syukur.

Hajat diri mahu jadi orang yang bermanfaat. Jadi, mengapa masih keluar keluhan penat?

Mengurut dada. Duhai hati, adakah kau makin kotor? Sungguh, saya sangat risau. Bagaimana akan saya persembahkan segala ibadah buat Allah, jika datangnya dari hati yang dikotori.

Istighfar.

Astaghfirullahal'azim.

Bangun, bangun, bangun. Jangan redha dengan nafsu keji itu. Biar seletih mana, jangan pernah lelah untuk mengejar Redha Allah, Rahmat Allah. Kerana bukan kerana amalan bergunung kita, yang dapat memasukkan kita ke dalam Syurga Allah nan indah. Tetapi dengan Rahmat-Nya. Serius!


Leka.

Kamu, kalau bermain dengan dunia, sampai bila pun tak akan terkejar. Kerana dunia ini bukan tempat yang mulia, ia hanya diibaratkan Nabi tercinta sebagai bangkai. Can you imagine bangkai? Kalau mahu terus leka bermain di dalamnya, mungkin dengan kamu sekali akan jadi busuk bangkai. Eeeee...

Syaitan itu ada di mana-mana. Tugasnya sudah jelas, mahu rosakkan anak adam. Kamu keturunan siapa?

Hidup jika terus menerus leka, pasti rugi. Tiada apa yang bakal dikenangkan nanti. Hanya sepi. Maka, mahukah kamu leka lagi?

Jangan terus berpatah hati. Tapi, berpatahlah balik kepada Allah.

Jika dirasakan dosa kita terlalu besar untuk diampunkan, maka ingatlah pengampunan Allah itu lebih besar dari itu.

Percayalah.

Kredit


Ingat, 
walau sejauh mana jalannya, 
bersimpang siur simpangnya,
kita tetap dengan aqidah kita. 
Tetap dengan jalan kita. 
Jangan toleh lagi ke jalan pesong yang lain. 
Tepis segala gangguan.
Tolak segala rintangan.



Wallahua'lam.


-Mr.Hope-
26.9.2012
9:36 p.m



Sabtu, 8 September 2012

Alzheimer Disease ( AD )


Alzheimer Disease [ AD ]

Based on textbook.

- Proggresive brain disease.

Characterized by :

- Development of amyloid plaque.

- Loss of connection between nerve cells in the brain and the death of these nerve cell.

Caused by :

- A number of different gene mutations, each of mutation causes abnormal folded proteins to be formed.

Alzheimer disease is identified as protein misfolding disease. Caused by :

- Accumulation of abnormally folded proteins in the brain called Amyloid Precursor Protein (APP), which is critical to the neuron growth, survival dan post-injury repair.

- This abnormal folded protein will the be degraded into smaller fragments called beta-amyloid which form plaques around neuron.


From Wikipedia.

Alzheimer's disease (AD), also known in medical literature as Alzheimer disease, is the most common form of dementia. There is no cure for the disease, which worsens as it progresses, and eventually leads to death. It was first described by German psychiatrist and neuropathologist Alois Alzheimer in 1906 and was named after him.

Most often, AD is diagnosed in people over 65 years of age, although the less-prevalent early-onset Alzheimer's can occur much earlier. In 2006, there were 26.6 million sufferers worldwide. Alzheimer's is predicted to affect 1 in 85 people globally by 2050.

Although Alzheimer's disease develops differently for every individual, there are many common symptoms. Early symptoms are often mistakenly thought to be 'age-related' concerns, or manifestations of stress. In the early stages, the most common symptom is difficulty in remembering recent events. When AD is suspected, the diagnosis is usually confirmed with tests that evaluate behaviour and thinking abilities, often followed by a brain scan if available.

Characteristics :

Pre-dementia

The first symptoms are often mistakenly attributed to ageing or stress. Detailed neuropsychological testing can reveal mild cognitive difficulties up to eight years before a person fulfils the clinical criteria for diagnosis of AD. These early symptoms can affect the most complex daily living activities. The most noticeable deficit is memory loss, which shows up as difficulty in remembering recently learned facts and inability to acquire new information.

Subtle problems with the executive functions of attentiveness, planning, flexibility, and abstract thinking, or impairments in semantic memory (memory of meanings, and concept relationships) can also be symptomatic of the early stages of AD.Apathy can be observed at this stage, and remains the most persistent neuropsychiatric symptom throughout the course of the disease.The preclinical stage of the disease has also been termed mild cognitive impairment, but whether this term corresponds to a different diagnostic stage or identifies the first step of AD is a matter of dispute.

Early

In people with AD the increasing impairment of learning and memory eventually leads to a definitive diagnosis. In a small portion of them, difficulties with language, executive functions, perception (agnosia), or execution of movements (apraxia) are more prominent than memory problems. AD does not affect all memory capacities equally. Older memories of the person's life (episodic memory), facts learned (semantic memory), and implicit memory (the memory of the body on how to do things, such as using a fork to eat) are affected to a lesser degree than new facts or memories.

Language problems are mainly characterised by a shrinking vocabulary and decreased word fluency, which lead to a general impoverishment of oral and written language. In this stage, the person with Alzheimer's is usually capable of communicating basic ideas adequately.

While performing fine motor tasks such as writing, drawing or dressing, certain movement coordination and planning difficulties (apraxia) may be present but they are commonly unnoticed. As the disease progresses, people with AD can often continue to perform many tasks independently, but may need assistance or supervision with the most cognitively demanding activities.

Moderate

Progressive deterioration eventually hinders independence, with subjects being unable to perform most common activities of daily living. Speech difficulties become evident due to an inability to recall vocabulary, which leads to frequent incorrect word substitutions (paraphasias). Reading and writing skills are also progressively lost.Complex motor sequences become less coordinated as time passes and AD progresses, so the risk of falling increases. During this phase, memory problems worsen, and the person may fail to recognise close relatives.Long-term memory, which was previously intact, becomes impaired.

Behavioural and neuropsychiatric changes become more prevalent. Common manifestations are wandering, irritability and labile affect, leading to crying, outbursts of unpremeditated aggression, or resistance to caregiving. Sundowning can also appear. Approximately 30% of people with AD develop illusionary misidentifications and other delusional symptoms. Subjects also lose insight of their disease process and limitations (anosognosia). Urinary incontinence can develop.
 These symptoms create stress for relatives and caretakers, which can be reduced by moving the person from home care to other long-term care facilities.

Advanced

During the final stage of AD, the person is completely dependent upon caregivers. Language is reduced to simple phrases or even single words, eventually leading to complete loss of speech. Despite the loss of verbal language abilities, people can often understand and return emotional signals.Although aggressiveness can still be present, extreme apathy and exhaustion are much more common results. People with AD will ultimately not be able to perform even the simplest tasks without assistance. Muscle mass and mobility deteriorate to the point where they are bedridden, and they lose the ability to feed themselves AD is a terminal illness, with the cause of death typically being an external factor, such as infection of pressure ulcers or pneumonia, not the disease itself.

Classification and external resources : Comparison of a normal aged brain (left) and the brain of a person with Alzheimer's (right). Differential characteristics are pointed out

PET (positron emission tomography)scan of the brain of a person with AD showing a loss of function in the temporal lobe

Enzymes act on the APP (amyloid precursor protein) and cut it into fragments. The beta-amyloid fragment is crucial in the formation of senile plaques in AD.

In Alzheimer's disease, changes in tau protein lead to the disintegration of microtubules in brain cells.




From Micinenet.

What is Alzheimer's disease?

Alzheimer's disease (AD) is a slowly progressive disease of the brain that is characterized by impairment of memory and eventually by disturbances in reasoning, planning, language, and perception. Many scientists believe that Alzheimer's disease results from an increase in the production or accumulation of a specific protein (beta-amyloid protein) in the brain that leads to nerve cell death.

The likelihood of having Alzheimer's disease increases substantially after the age of 70 and may affect around 50% of persons over the age of 85. Nonetheless, Alzheimer's disease is not a normal part of aging and is not something that inevitably happens in later life. For example, many people live to over 100 years of age and never develop Alzheimer's disease.

Who develops Alzheimer's disease?

The main risk factor for Alzheimer's disease is increased age. As a population ages, the frequency of Alzheimer's disease continues to increase. Ten percent of people over 65 years of age and 50% of those over 85 years of age have Alzheimer's disease. Unless new treatments are developed to decrease the likelihood of developing Alzheimer's disease, the number of individuals with Alzheimer's disease in the United States is expected to be 14 million by the year 2050.

There are also genetic risk factors for Alzheimer's disease. Most patients develop Alzheimer's disease after age 70. However, 2%-5% of patients develop the disease in the fourth or fifth decade of life (40s or 50s). At least half of these early onset patients have inherited gene mutations associated with their Alzheimer's disease. Moreover, the children of a patient with early onset Alzheimer's disease who has one of these gene mutations has a 50% risk of developing Alzheimer's disease.

There is also a genetic risk for late onset cases. A relatively common form of a gene located on chromosome 19 is associated with late onset Alzheimer's disease. In the majority of Alzheimer's disease cases, however, no specific genetic risks have yet been identified.

How is the diagnosis of Alzheimer's disease made?

As of June 2007, there is no specific "blood test" or imaging test that is used for the diagnosis of Alzheimer's disease. Alzheimer's disease is diagnosed when:

1) a person has sufficient cognitive decline to meet criteria for dementia;

2) the clinical course is consistent with that of Alzheimer's disease;

3) no other brain diseases or other processes are better explanations for the dementia.

What other conditions should be screened for?

There are many conditions that can cause dementia, to include the following:

Neurological disorders: Parkinson's disease, cerebrovascular disease and strokes, brain tumors, blood clots, and multiple sclerosis can sometimes be associated with dementia although many patients with these conditions are cognitively normal.

Infectious diseases: Some brain infections such as chronic syphilis, chronic HIV, or chronic fungal meningitis can cause dementia. 

What are risk factors for Alzheimer's disease?

The biggest risk factor for Alzheimer's disease is increased age. The likelihood of developing Alzheimer's disease doubles every 5.5 years from 65 to 85 years of age. Whereas only 1%-2% of individuals 70 years of age have Alzheimer's disease, in some studies around 40% of individuals 85 years of age have Alzheimer's disease. Nonetheless, at least half of people who live past the 95 years of age do not have Alzheimer's disease.

What are the Symptoms of Alzheimer's disease?

There is no "typical" person with Alzheimer's. There is tremendous variability among people with Alzheimer's in their behaviors and symptoms. At present, there is no way to predict how quickly the disease will progress in any one person or the exact changes that will occur. We do know, however, that many of these changes will present problems for caregivers. Therefore, knowledge and prevention are critical to safety.

People with Alzheimer's disease have memory problems and cognitive impairment (difficulties with thinking and reasoning), and eventually they will not be able to care for themselves. They often experience confusion, loss of judgment, and difficulty finding words, finishing thoughts, or following directions. They also may experience personality and behavior changes. For example, they may become agitated, irritable, or very passive. Some people with Alzheimer's may wander from home and become lost. Others may not be able to tell the difference between day and night—they may wake up, get dressed, and start to leave the house in the middle of the night thinking that the day has just started. People with Alzheimer's also can have losses that affect vision, smell, or taste.

These disabilities are very difficult, not only for the person with Alzheimer's, but for the caregiver, family, and other loved ones as well. Caregivers need resources and reassurance to know that while the challenges are great, specific actions can reduce some of the safety concerns that accompany Alzheimer's disease.


What treatment and management options are available for Alzheimer's disease?

The management of Alzheimer's disease consists of medication based and non-medication based treatments. Two different classes of pharmaceuticals are approved by the FDA for treating Alzheimer's disease: cholinesterase inhibitors and partial glutamate antagonists. Neither class of drugs has been proven to slow the rate of progression of Alzheimer's disease. Nonetheless, many clinical trials suggest that these medications are superior to placebos (sugar pills) in relieving some symptoms.

Cholinesterase inhibitors
In patients with Alzheimer's disease there is a relative lack of a brain chemical neurotransmitter called acetylcholine. (Neurotransmitters are chemical messengers produced by nerves that the nerves use to communicate with each other in order to carry out their functions.) Substantial research has demonstrated that acetylcholine is important in the ability to form new memories. The cholinesterase inhibitors (ChEIs) block the breakdown of acetylcholine. As a result, more acetylcholine is available in the brain, and it may become easier to form new memories.

Four ChEIs have been approved by the FDA, but only donepezil hydrochloride (Aricept), rivastigmine (Exelon), and galantamine (Razadyne - previously called Reminyl) are used by most physicians because the fourth drug, tacrine (Cognex) has more undesirable side effects than the other three. Most experts in Alzheimer's disease do not believe there is an important difference in the effectiveness of these three drugs. Several studies suggest that the progression of symptoms of patients on these drugs seems to plateau for six to 12 months, but inevitably progression then begins again.

Of the three widely used AchEs, rivastigmine and galantamine are only approved by the FDA for mild to moderate Alzheimer's disease, whereas donepezil is approved for mild, moderate, and severe Alzheimer's disease. It is not known whether rivastigmine and galantamine are also effective in severe Alzheimer's disease, although there does not appear to be any good reason why they shouldn't.

The principal side effects of ChEIs involve the gastrointestinal system and include nausea, vomiting, cramping, and diarrhea. Usually these side effects can be controlled with change in size or timing of the dose or administering the medications with a small amount of food. Between 75% and 90% of patients will tolerate therapeutic doses of ChEIs.

General Safety Concerns

People with Alzheimer's disease become increasingly unable to take care of themselves. However, the disease progresses differently in each person. As a caregiver, you face the ongoing challenge of adapting to each change in the person's behavior and functioning. The following general principles may be helpful.

    1) Think prevention.

It is very difficult to predict what a person with Alzheimer's might do. Just because something has not yet occurred does not mean it should not be cause for concern. Even with the best-laid plans, accidents can happen. Therefore, checking the safety of your home will help you take control of some of the potential problems that may create hazardous situations.

    2) Adapt the environment.

It is more effective to change the environment than to change most behaviors. While some Alzheimer's behaviors can be managed with special medications prescribed by a doctor, many cannot. You can make changes in an environment to decrease the hazards and stressors that accompany these behavioral and functional changes.

    3) Minimize danger.

By minimizing danger, you can maximize independence. A safe environment can be a less restrictive environment where the person with Alzheimer's disease can experience increased security and more mobility.








Wallahua'lam.


-Mr.Hope-
8.9.2012
10:35 a.m



Selasa, 4 September 2012

#9 : Risau Sang Ayah.



Berada di luar negara, membuatkan hati sentiasa merindui keluarga. Apabila rindu sampai kemuncaknya, maka Skype lah sebagai wadah utama untuk bersua muka, bertanya khabar, bergurau senda bagi meriangkan suasana.

Namun, kalau mahu cepat, saya terus sahaja telefon mama. Tapi, menefon keluarga bukanlah menggunakan telefon atau handpone, tapi menggunakan laptop kerana kos telefon melalui internet lebih murah berbanding telefon biasa. Hidup mahasiswa perlulah bijak mencatu wang.


Ganggang mama.

Bila rindu bertandang tiba-tiba, perkara pantas yang yang boleh dilakukan ialah telefon. Menelefon terus ke talian rumah lebih murah daripada menelefon talian handphone. Saya selalunya akan bercakap dengan mama, sebab saya memang suka cakap dengan mama dan saya suka dengar suara mama. Suara yang telah lama didengari sejak keluar dari perutnya, hingga kini.

Tapi, hari itu, mama ada cakap sesuatu yang saya tak tahu sebelum ini.

" Ayah risaukan abang...." Mama mula bercerita.

" Kenapa nak risau, abang kat sini selamat saja. Tak payah la risau sangat.." Saya cuba menenangkan mama.

" Bukan risau tu..."

" Habis tu?" Saya naik hairan.

" Ayah risau, kalau abang tinggal solat malam...."

Saya telan air liur. Gulp.

Saya tahu, ayah sangat yakin dengan ibadah-ibadah lain anaknya ini. Tapi, untuk solat malam, mungkin ayah wajar risaukan saya. Kerana saya sendiri pun kadang-kadang risau juga.

" Insya-Allah mama, mama dengan ayah doakanlah juga buat abang, moga sentiasa diberi taufiq untuk buat qiamullail, bermunajat kepada Allah setiap hari. Doa mama dan ayah kan mustajab. Hehe...." Saya beri harapan buat mereka.

" Insya-Allah, mama dengan ayah selalu doakan abang. Abang sabar ya hadapi segala dugaan." Pujuk sang ibu.


Solat malam.

Ayah, seorang yang sangat cakna dalam ibadah qiamullail. Walau dia hanya marhaen biasa, guru biasa dan ayah biasa, dia masih pentingkan perkara itu.

Kalau boleh, walau iman tak boleh diwarisi, dia mahu didik anak-anak dia supaya sentiasa kental iman. Kental menghambakan diri buat Yang Maha Kuasa.

Solat malam, satu ibadah yang benar-benar mendidik jiwa menjadi hamba yang taat. Pada saat kita dapat bersujud dalam lautan malam yang sunyi, ada ketenangan yang tak dapat digambarkan menerjah hati sanubari.

Tika itu juga, kita perlu syukur kerana masih mampu bangun malam untuk mengabdikan diri kepada-Nya. Mungkin ramai yang salah anggap, kita dapat buat ibadah apa sekali pun, sesungguhnya ia bukanlah dengan kekuatan diri kita sendiri, tetapi ia sebenarnya kekuatan atau taufiq yang diberikan oleh Allahu Subhanllah Ta'ala kepada kita.

Maka, andai masih diberi peluang untuk sujud menyembah Yang Esa, bersyukurlah. Kerana, anda hamba-Nya yang terpilih.


-Mr.Hope-

4.9.2012
8:01 a.m






Jumaat, 24 Ogos 2012

# 8 : Mujahadah.



MU.   JA.  HA.  DAH.

Mujahadah, sebutnya sungguh mudah. Walau empat suku kata, ianya tetap mudah disebut.

Saya tak tahu suatu ketika dahulu, berperang dengan nafsu fasad ini suatu yang sangat menyakitkan. Sakit, letih, tension, terbeban. Ah, sungguh berat.

Apa yang saya tahu sekarang, mujahadah itu sungguh tenat, penat dan rasa ralat. Semuanya rasa berat.

Kalau sudah biasa dalam biah tarbiyah, biah orang-orang soleh, biah ilmu, biah menjaga ikhtilat, biah diskusi ilmu dan biah dakwah, tiba-tiba Allah letakkan kita berada keseorangan dan dilimpahkan segala kenikmatan.

Adakah pada masa itu kamu mahu hanyut dalam ketaatan atau memilih hanyut dalam kelam kemaksiatan?

Benarlah, hidup itu hanya untuk diuji, mahu lihat sejauh mana ketaatan kita kepada Allah.

Jika kamu keluar dari biah solehah dalam keadaan kamu dibekalkan oleh segala ilmu yang bermanfaat buat diri dan orang lain, apakah kamu masih mahu kekal dalam ketaatan itu. Mahukah kamu mujahadah?

Saat kita kesunyian, keseorangan, hanya iman yang sudah padu terpasak dalam diri kita yang bakal memandu segala kerja buat kita, sama ada mahu memilih Taqwa atau Leka.

Sesungguhnya, ia suatu ujian yang perit. Sungguh sakit.


Coklat masam.

Suatu ketika, semasa kita kecil, kita rela makan coklat sangat masam. Itu sangat pelik, kerana kemasaman coklat itu masih boleh menarik minat kita untuk makan coklat itu. Bukan kerana apa, tetapi kerana kita sudah tahu yang akhir sekali coklat tadi akan bertukar menjadi manis dan akan bertukar rasa yang sungguh sedap.

Oleh sebab itu, kita masih mampu makan coklat seperti itu. Hanya kerana kita yakin dan sungguh yakin yang segala kemasaman itu akan bertukar menjadi manis di hujungnya.


Manis.

Saya, orang yang dirasakan tidak layak untuk bercerita tentang syurga. Kerana saya sedar diri saya yang terlalu hina ini. Terperosok dalam menembusi hati ini, saya sungguh kerdil di sisi Allah.

Tapi, yang perlu kita tahu, syurga itu bukan sebarangan tempat. Tempat yang tidak murah, yang tak dapat diduduki semua orang. Hanya yang terpilih sahaja akan dapat mengecapinya.

Seakan kita membeli coklat yang mahal-mahal, kita tahu rasanya juga manis seperti coklat-coklat lain. Tetapi, kita juga tahu coklat yang mahal-mahal itu, punya rasa manis yang tiada pada coklat-coklat biasa. Lalu, kita sanggup habiskan duit yang berlipat kali ganda daripada harga coklat-coklat biasa hanya semata-mata mahu beli coklat-coklat yang mahal itu.

Hanya dengan satu kemanisan, kita sanggup untuk berkorban. Kerana kita tahu, pengorbanan kita itu tidak sia-sia dan bakal dibalas dengan rasa manis coklat itu yang sungguh memuaskan.

Jika begitu, mengapa tidak untuk syurga? Bukankah kita sudah dikhabarkan bahawa ianya sungguh manis?

Mujahdahlah. Jangan mudah mengalah. Walau perlu menangis, kuatkanlah jiwa kita.

Pahit dan masam mujahadah kita hari ini, pasti akan dikurniakan Allah suatu yang manis dihujungnya nanti.

Syurga itu maniskan?

Terlalu sangat manis. Undescribable.

Yakinlah. Allah pasti balas dengan apa yang telah kita usahakan.

Pujuklah hati, pujuklah diri.

^^

-Mr.Hope-
24.8.2012
10.24 a.m




Selasa, 21 Ogos 2012

Prion Disease


Prion Disease

Based on textbook of biochemistry :

- It is a neurodegenerative disorder disease.

- Can affect both human and animal.

- Referred as Transmissible Spongiform Encephalopathies ( mad cow disease ).


- Some symptoms :

* Dementia - a chronic and progressive deterioration of behaviour and higher intellectual function due to organic brain disease.

* Loss of coordination.


- Prion Protein is a normal constituent of brain tissue in all mammals.

* present on the surface of neuron and glial cells.

* its role is unknown in detail. But, it appears to have a molecular signalling function.


- PrP ( Prion Protein )

* become infectious when it changes in 3-dementional conformation.

* a number of Alpha-helices in non-infectious PrP are replaced by Beta-sheets in the infectious form.


- Infectious PrP, act as template.

* Because, for converting the normal PrP to the infectious conformation.

* Tend to form insoluble aggregates of fibrils similar to the amyloid found in neurodegenerative disorder.

* These aggregates, damage or destroy nerve cells and create microscopic sponge-like hole in the brain.



Something from wikipedia :

Prions cause neurodegenerative disease by aggregating extracellularly within the central nervous system to form plaques known as amyloid, which disrupt the normal tissue structure. This disruption is characterized by "holes" in the tissue with resultant spongy architecture due to the vacuole formation in the neurons.

 Other histological changes include astrogliosis and the absence of an inflammatory reaction.While the incubation period for prion diseases is generally quite long[vague], once symptoms appear the disease progresses rapidly, leading to brain damage and death. Neurodegenerative symptoms can include convulsions, dementia, ataxia (balance and coordination dysfunction), and behavioural or personality changes.

*Convulsion - an involuntary contraction of the muscles producing contortion of the body and limbs.


All known prion diseases, collectively called transmissible spongiform encephalopathies (TSEs), are untreatable and fatal. A vaccine has been developed in mice, however, that may provide insight into providing a vaccine in humans to resist prion infections. Additionally, in 2006 scientists announced that they had genetically engineered cattle lacking a necessary gene for prion production – thus theoretically making them immune to BSE, building on research indicating that mice lacking normally occurring prion protein are resistant to infection by scrapie prion protein.


Many different mammalian species can be affected by prion diseases, as the prion protein (PrP) is very similar in all mammals. Due to small differences in PrP between different species it is unusual for a prion disease to be transmitted from one species to another. The human prion disease variant Creutzfeldt-Jakob disease, however, is believed to be caused by a prion which typically infects cattle, causing Bovine spongiform encephalopathy and is transmitted through infected meat.

Transmission

It has been recognized that prion diseases can arise in three different ways: acquired, familial, or sporadic. It is often assumed that the diseased form directly interacts with the normal form to make it rearrange its structure. One idea, the "Protein X" hypothesis, is that an as-yet unidentified cellular protein (Protein X) enables the conversion of PrPC to PrPSc by bringing a molecule of each of the two together into a complex.

Current research suggests that the primary method of infection in animals is through ingestion. It is thought that prions may be deposited in the environment through the remains of dead animals and via urine, saliva, and other body fluids. They may then linger in the soil by binding to clay and other minerals.


A University of California research team, led by Nobel Prize winner Stanley Prusiner, has provided evidence for the theory that infection can occur from prions in manure. And since manure is present in many areas surrounding water reservoirs, as well as used on many crop fields, it raises the possibility of widespread transmission. It was reported in January 2011 that researchers had discovered prions spreading through airborne transmission on aerosol particles, in an animal testing experiment focusing on scrapie infection in laboratory mice.

 Preliminary evidence supporting the notion that prions can be transmitted through use of urine-derived human menopausal gonadotropin, administered for the treatment of infertility, was published in 2011.



Sterilization

Infectious particles possessing nucleic acid are dependent upon it to direct their continued replication. Prions, however, are infectious by their effect on normal versions of the protein. Sterilizing prions therefore involves the denaturation of the protein to a state where the molecule is no longer able to induce the abnormal folding of normal proteins. Prions are generally quite resistant to proteases, heat, radiation, and formalin treatments, although their infectivity can be reduced by such treatments. Effective prion decontamination relies upon protein hydrolysis or reduction or destruction of protein tertiary structure.

Examples include bleach, caustic soda, and strongly acidic detergents such as LpH.134°C (274°F) for 18 minutes in a pressurized steam autoclave may not be enough to deactivate the agent of disease. Ozone sterilization is currently being studied as a potential method for prion denature and deactivation. Renaturation of a completely denatured prion to infectious status has not yet been achieved; however, partially denatured prions can be renatured to an infective status under certain artificial conditions.

The World Health Organization recommends any of the following three procedures for the sterilization of all heat-resistant surgical instruments to ensure that they are not contaminated with prions:

Immerse in a pan containing 1N NaOH and heat in a gravity-displacement autoclave at 121°C for 30 minutes; clean; rinse in water; and then perform routine sterilization processes.

Immerse in 1N NaOH or sodium hypochlorite (20,000 parts per million available chlorine) for 1 hour; transfer instruments to water; heat in a gravity-displacement autoclave at 121°C for 1 hour; clean; and then perform routine sterilization processes.

Immerse in 1N NaOH or sodium hypochlorite (20,000 parts per million available chlorine) for 1 hour; remove and rinse in water, then transfer to an open pan and heat in a gravity-displacement (121°C) or in a porous-load (134°C) autoclave for 1 hour; clean; and then perform routine sterilization processes.


From Genetics Home Refence :

 What is prion disease?

Prion diseases belong to group of progressive conditions that affect the nervous system in humans and animals. In people, prion diseases impair brain function, causing memory changes, personality changes, a decline in intellectual function (dementia), and problems with movement that worsen over time. The signs and symptoms of these conditions typically begin in adulthood, and these disorders lead to death within a few months to several years.

Familial prion diseases of humans include classic Creutzfeldt-Jakob disease (CJD), Gerstmann-Sträussler-Scheinker syndrome (GSS), and fatal insomnia (FI). These conditions form a spectrum of diseases with overlapping signs and symptoms.

How common is prion disease?

These disorders are very rare. They affect about one person per million worldwide each year. Approximately 300 cases occur annually in the United States.

What genes are related to prion disease?

Mutations in the PRNP gene cause prion disease.
Only a small percentage of prion disease cases run in families. Most cases are sporadic, which means they occur in people without any known risk factors or gene mutations. Rarely, prion diseases can be transmitted by accidental exposure to prion-contaminated tissues during a medical procedure. This type of prion disease is called iatrogenic.

One type of prion disease in humans, variant Creutzfeldt-Jakob disease (vCJD), is acquired by eating beef products obtained from cattle with prion disease. In cows, this form of the disease is known as bovine spongiform encephalopathy (BSE) or, more commonly, "mad cow" disease. Another example of an acquired human prion disease is kuru, which was identified in the South Fore tribe in Papua New Guinea. The disorder was transmitted when tribe members ate the tissue of affected people during cannibalistic funeral rituals.

Familial forms of prion disease are caused by inherited mutations in the PRNP gene. This gene provides instructions for making a protein called prion protein (PrP). Normally, this protein is likely involved in transporting copper into cells. It may also play a role in protecting brain cells and helping them communicate. In familial cases of prion disease, mutations in the PRNP gene cause cells to produce an abnormal form of the prion protein known as PrPSc. In iatrogenic and acquired cases, an affected person develops prion disease from exposure to this abnormal protein.

In a process that is not fully understood, PrPSc has the ability to convert the normal prion protein, PrPC, into more PrPSc. This abnormal protein builds up in the brain, forming clumps that damage or destroy nerve cells. The loss of these cells creates microscopic sponge-like holes in the brain, which leads to the signs and symptoms of prion disease.


How do people inherit prion disease?


Familial forms of prion disease are inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In most cases, an affected person inherits the altered gene from one affected parent. In some people, familial forms of prion disease are caused by a new mutation in the PRNP gene.

Although such people most likely do not have an affected parent, they can pass the genetic change to their children.

The sporadic, iatrogenic, and acquired forms of prion disease, including kuru and variant Creutzfeldt-Jakob disease, are not inherited.

What other names do people use for prion disease?


-Inherited Human Transmissible Spongiform Encephalopathies
-Prion-associated disorders
-Prion-Induced Disorders
-Prion Protein Diseases
-Transmissible Dementias
-Transmissible Spongiform Encephalopathies
-TSEs



-Mr Hope-

21.8.2012
9.48p.m





# 7 : Sang Jatuh


Kadang-kadang, apa yang kita pernah buat kita lupa. Kita perlukan sesuatu untuk trigger kita untuk mengingat kembali apa yang pernah kita buat.

Namun, buat yang rajin mencatat kerja buat anda, membuat diari, blog dan segala bagai, mungkin ianya merupakan sesuatu yang bermakna setelah kita membacanya kembali dalam masa yang lama selepas itu. Ya, ini serius, anda boleh cuba sendiri kalau nak rasa.

Setelah membaca kembali, dirasakan seperti, ' Eh, akukah yang tulis ni?'.

Huh.

Kita boleh lupa dan lalai dalam mencatat. Namun, dua malaikat di kiri dan kanan kita ini tak pernah lupa mencatat segala amalan kita. Tak pernah. Dari kita baligh, hinggalah meninggal dunia.

Di sana juga, ada malaikat yang mencatat segala percakapan kita, word by word. So, think deeply before speak a word. Hatta, siulan kita sekali pun, dia mencatatnya. Hati-hati.

Terjumpa.

Tadi, saya terbaca sesuatu dalam buku hafaz saya, di kulit bahagian hadapan. Ada sesuatu yang menyentuh. Dan, seperti biasa, saya rasakan ' Eh, akukah yang tulis ni?'.

Silakan baca. Nak duduk bersila pun boleh.

" Buku ini,
aku mahu bina harapan baharu.

Walau ianya pahit menimpa,
namun ku tetap setia,
redha kepada yang Maha Esa.

Bangunlah,
kita bersama bina mahligai harapan baharu.

Jatuh sekarang bukan melumpuhkan,
tepi menyempurnakan hidup.

Maka,
sayanglah buat yang pantas mengalah. "



-Mr Hope-

21.8.2012
7.58 p.m






Khamis, 16 Ogos 2012

# 6 : Nenek Tua


Alam ini bukan sahaja dicipta semena-menanya. Adanya alam ini, menunjukkan dalil kewujudan Allah. Maka beruntunglah hamba-Nya yang bijak mentadabbur alam ini.

Sebagai manusia normal, yang tiada kuasa-kuasa super duper seperti super hero yang kacak gagah  bergaya, kita tak mampu untuk mengingati Allah for 24 hours. Kalau pun boleh, itu mungkin buat hamba-hamba-Nya yang terpilih. Oh, sungguh beruntungnya mereka.

Nenek.

Saya, hari ini Allah nikmatkan saya berbuka bersama orang-orang susah. Saya suka tengok mereka, serius!

Bila melihat mereka, hati kita jadi sayu. Hati kita belajar sendiri erti syukur. Walau mereka hanya gelandangan ( homeless ) yang tidak punya apa-apa, namun mereka masih teruskan hidup menempuh segala apa yang mendatang.

Melihat mereka membuka kuncupan kesyukuran dalam diri kita. Dia tak mampu nak makan banyak-banyak, dan dia bawakan tupperware plastik untuk mengisi hidangan yang lebih itu. Mungkin boleh jadi dia mahu jadikan hidangan bersahur, mungkin juga untuk anak-anaknya. Tapi kebanyakan kita hanya buang saja semua makanan yang tak habis. Membazir.

Nenek tua itu, hanya senyum dan tak lokek dan malu untuk ucap 'terima kasih' apabila ada yang memberi. Sungguh menghargai orang di sekeliling. Tak rugi kita melihat alam dan kait segalanya dengan Allah.

Lihatlah diri kamu. Dan sentiasalah jadi insan yang bersyukur.

"Dan juga pada diri kamu sendiri. Maka mengapa kamu tidak mahu melihat serta memikirkan (dalil-dalil dan bukti itu)?"

(Adz-Dzaariyaat 51:21)


-Mr. Hope-

16.8.2012
8.50 a.m

Ahad, 12 Ogos 2012

Hypothalamus

Hypothalamus.


Meaning of Hypothalamus according to Oxford Medical Dictionary 5th Edition :

- The right region of the forebrain, in the floor of the third ventricle, linked with the thalamus above and pituitary gland below.

- It contains several important centres controlling :
# body temperature
# water balance
# sexual function

-It is also closely connected with emotional activity and sleep, and function as a centre for the integration of hormonal and autonomic nervous activity through its control of the pituitary secretions.

Hypothalamus in Chapter Amino Acid & Protein :

- Oxytoxin, is a nonapeptide ( formed 9 amino acids ).

- It is a hormone synthesized by hypothalamus and stored and secreted by the posterior pituitary.


From Wikipedia :

The hypothalamus (from Greek ὑπό = under and θάλαμος = room, chamber) is a portion of the brain that contains a number of small nuclei with a variety of functions. One of the most important functions of the hypothalamus is to link the nervous system to the endocrine system via the pituitary gland (hypophysis).

The hypothalamus is located below the thalamus, just above the brain stem. In the terminology of neuroanatomy, it forms the ventral part of the diencephalon. All vertebrate brains contain a hypothalamus. In humans, it is roughly the size of an almond.

The hypothalamus is responsible for certain metabolic processes and other activities of the autonomic nervous system. It synthesizes and secretes certain neurohormones, often called hypothalamic-releasing hormones, and these in turn stimulate or inhibit the secretion of pituitary hormones.

The hypothalamus controls body temperature, hunger, thirst, fatigue, sleep, and circadian cycles.




Hypothalamus (animation, shown in red)






- Mr. Hope -

12.8.2012
1 : 46 a.m

Jumaat, 10 Ogos 2012

# 5 : Soleh



Sejak membaca satu artikel yang ditulis oleh seorang perempuan, saya renung sebentar.

" Oh, begitu rupanya kebanyakkan wanita."

Ini yang dia tulis.

kredit
" Bukan lelaki sahaja yang bisa tidak tentu arah bila melihat perempuan solehah idamannya, bahkan yang bernama perempuan itu juga bisa bergetar hatinya melihat lelaki yang soleh. Hingga tersemat di sudut hatinya, berdoa dan meminta pada ALLAH agar dipilih oleh lelaki soleh itu.. "


Itu sebuah rasa. Rasa yang jarang-jarang orang lain ungkapkan. Mungkin sebab semua dipagari perasaan malu.

Dan kini, saya rasa, bukan sekadar pihak perempuan sahaja yang merasakan aura lelaki soleh, bahkan seorang lelaki juga bisa bertsunami hatinya apabila terlihat perempuan solehah. Ini serius. Apabila kejujuran itu muncul, begitulah bunyinya. Huh.

 Dahulunya, mendengar lagu 'Isteri Solehah' langsung tiada feeling. Tapi, setelah meninggi dewasa, entah dari mana feeling pelik tiba-tiba muncul. Itu memang pelik, entah dari mana datangnya. Hanya yang rasa, tahu apa feelingnya.^^

Bila meningkat dewasa, pelbagai hormon yang muncul, pelbagai rasa yang dirasa. Tinggal kita sahaja yang mahu memandu semua itu ke lembah yang di redhai-Nya, atau di murkai-Nya!

 Bila terlihat perempuan solehah, bukan sekadar bertsunami hati, tetapi rasa rendah diri dan malu sendiri. Oh, hinanya diri, betapa mulianya dia!

Adakah ini juga satu harapan? Harapan untuk dikurniakan isteri solehah. Ya, sudah semestinya. It's not a crime guys.

Masih terus berharapan.

" Isteri solehah, mengkayakan suami" Ustaz Kazim membaca kitab dalam video di you tube.

 " (Lazimnya) perempuan-perempuan yang jahat adalah untuk lelaki-lelaki yang jahat, dan lelaki-lelaki yang jahat untuk perempuan-perempuan yang jahat; dan (sebaliknya) perempuan-perempuan yang baik untuk lelaki-lelaki yang baik, dan lelaki-lelaki yang baik untuk perempuan-perempuan yang baik. Mereka (yang baik) itu adalah bersih dari (tuduhan buruk) yang dikatakan oleh orang-orang (yang jahat); mereka (yang baik) itu akan beroleh pengampunan (dari Allah) dan pengurniaan yang mulia. "

( an-Nuur 24 : 26)

-Mr. Hope-

10.8.2012
2.05 a.m






Khamis, 9 Ogos 2012

# 4 : Pesan Ayah.


Sejak dulu, saya kurang cakap dengan ayah. Mungkin, pada saya, ayah masih garang, tetap garang hingga kini.

Lalu, segalanya saya luah dan ceritakan kepada mama. Saya anggap mamalah yang terlebih memahami saya, dan mungkin ia juga extraordinary hyper covalent bond yang lang tak dapat di break by any else, even denaturation atau annealing sekalipun!

Kala kesunyian, saya akan telefon atau mesej dengan mama. Rasa tenang hati kalau dapat dengar suara mama, suara seorang ibu yang telah semestinya kita semua telah dengar sejak hari pertama kita keluar melihat dunia, bahkan secara hakikinya sejak pendengaran kita mula berfungsi di dalam rahim ibu kita. It sounds pretty good!

Saya call rumah, walau dah lewat malam waktu Malaysia, saya call juga. Sebab mama selalu tidur lewat gara-gara sibuk dengan pengajian dan kerjanya, tak kurang juga kerja melayan si kecil yang sedang membesar dengan sungguh nakal.

Tapi, mama dan si kecil sudah pun tidur. Ayah yang angkat telefon. Saya seperti biasa, akan kehabisan modal bercakap. Tak tahu lagi mahu bercakap apa. Selalunya memang begitu, sejak di asrama lagi kes seperti sudah berlaku, berlanjutan hingga sudah ke overseas.

Ayah bijak. Dialah yang akan punya modal yang banyak untuk berborak panjang. Nasihatnya, tiada bandingan. Walau dia tinggi terlalu tinggi belajar, namun pengalaman hidup banyak mengajarnya survive dalam hidup. Semestinya, dia kerap berkongsi dengan anaknya.

Walaupun, situasi dahulu dan sekarang sudah jauh berbeza, namun ianya tetap relevan untuk diceritakan. Saya tetap jadi pendengar yang setia. Gaya ayah bercerita memang best, memang layak menjadi seorang guru. Salute ayah tinggi-tinggi.

Satu sahaja, panjang mana ayah bercakap, bercerita, berjenaka, mesej akhirnya tetap sama.

" Walau sesusah atau sesenang mana pun kita, tahajjud jangan tinggal."

Itu sahaja pesan ayah. Satu kekuatan realiti. Sejak zaman-zaman berzaman. Punca keutuhan seorang hamba dengan Tuhannya. Bangun malam dan bertahajjud.

Itu harapa tinggi ayah buat saya. Insya-Allah, itu juga harapan saya dan bakal keluarga saya. Perkara kecil yang membawa seribu keberkatan dalam hubungan hamba hina dan Tuhannya.

Ya, itu harapan besar!


-Mr Hope-

9.8.2012
1:29 a.m




Isnin, 6 Ogos 2012

# 3 : Dua Doktor


Saya tak tahu ini kali ke berapa, tapi kerap sungguh nampak dua kelibat itu. Satu berbaju hijau lengkap, dan satu lagi berbaju biru lengkap. Kadang-kadang di leher mereka ada terselit stethoscope.

Rumah sewa saya amat dekat dengan sebuah hospital. Dan rumah saya juga amat dekat juga dengan sebuah masjid. Masjid itu tak lah terlalu gah besarnya, hanya keluasan biasa.

Sekali imbas, muka mereka sememangnya nampak letih. Itulah kerja doktor, perlu tabah. Setiap kali saya lihat wajah mereka, saya terbayangkan keadaan saya sendiri suatu hari nanti. Andai diberi rezeki dan peluang  oleh Allah, maka itulah pekerjaan saya pada suatu hari nanti.

Walau wajah mereka nampak penat, namun ketika selesai solat, mereka masih mampu tersenyum manis ketika bersalaman dengan jemaah lain. Seolah, riak penat tadi hilang. Orang lain yang lihat juga turut bahaya.

"Ubat paling tinggi harganya, ialah senyuman."

Senyum, ianya memang mudah. Senyuman seolahnya juga memberi pengharapan kepada orang lain. Buat juga insan lain bahagia melihat.

Paling penting, sesibuk mereka, mereka tidak abaikan arahan Sang Pencipta. Masih setia beribadah, kerana ianya mudah, tidak payah.

-Mr. Hope-

6.8.2012
6:44a.m


Ahad, 5 Ogos 2012

# 2 : al-Quran dan Buku Hafaz


Di sini, dia antara sahabat yang memahami saya. Saya akan ceritakan masalah kepadanya. Kalau nak diceritakan kepada orang lain saya segan. Malah, dialah sahabat yang thiqah menjaga rahsia saya. Saya sayang dia.

Ketika saya down, kepada dialah antara tempat pengaduan. Satu ketika saya mengadu yang saya lemah ingatan.

" Sukar nak mengingat itu bukan masalah kamu seorang, tapi masalah biasa semua orang. Sejak datang sini, aku tak tengok sangat movie, tengok pun sikit sangat. Sebab memang melalui itulah akal kita jadi tumpul, payah nak mengingat sesuatu. Ilmu tu tak masuk ke dalam hati pelaku maksiat. Jauhi melihat perkara maksiat insya-Allah Allah pelihara hati kamu. Mudah ilmu masuk.

Aku hanya boleh nasihat. Sebaiknya, kurangkan atau tak payah tengok movie atau drama-drama tu. Kita ni bukan setakat nak menghafaz fakta, al-Quran dan hadis jugak perlu kita hafaz. Itu lagilah berat prasyarat untuk tembus ke dalam hati kita."

Dia seorang yang rajin dan bijak. Pandai bahagi masa dan kenyang hanya dengan ibadah kepada Allah. Kadang-kadang rasa segan sungguh dengan dia. Nasihat dia amat-amat berguna.

Solusi.

Saya ada terfikir, bagaimana mahu atasi semua ini. Saya rasa, lepas ni, saya akan bawa dua benda ini ke mana-mana semampu yang boleh. al-Quran dan buku hafaz.

Dengan al-Quran, moga-moga saya tak jauh daripada Allah.

Dengan buku hafaz, saya akan sematkan apa fakta yang perlu saya hafaz. Moga-moga saya tak akan lupa tanggungjawab saya sebagai seorang pelajar dan akan mudah menghafaz segala fakta yang perlu dihafaz.

Ini satu harapan.

Moga ianya jadi satu kenyataan dan penuh istiqamah.

^^

-Mr. Hope-

5 Ogos 2012.
7.15 p.m.

# 1 : Mula.


Saat tanggal ini. 5 Ogos 2012, 17 Ramadan 1433H.

Saya mula untuk menulis di sini. Mahu tulis apa yang saya rasa, apa yang saya suka dan apa-apa sahaja. Untuk apa, hanya kerana Allah. Sungguh, ia serius. Saya tak tahu perkara lain yang lebih best dari itu.

Apa guna hidup berfoya-foya kalau hidup dalam alam murka-Nya.

Perkara awal yang saya perlu ketengahkan ialah saya tak mahu di kenali. Dan anda semua tak perlu meneka siapa saya. Kerana saya juga insan biasa seperti anda. Bukan batman, superman mahupun keluangman. Huh.

Saya tak pasti ada atau tidak manusia yang akan baca tulisan huduh saya ini, walau ia ditaip menggunakan komputer. Mungkin hari ini tiada. Namun siapa tahu, ada yang terlintas untuk membaca.

Mengapa harus putus harapan kalau kita belum pun menyelam sedalam dalamnya ke dasar kehidupan?

Bina harapan,
bina diri.

Jangan biar kita jatuh tak lagi berdiri.

 -Mr Hope-

5.8.2012