BACKGROUND

Curcumin has been investigated as a potential natural solution to prevent or even treat skeletal muscle decline. There are a number of externally sourced finished products (ie, those imported from other countries) containing curcumin, but high cost limits their usage. The emerging research and development of locally sourced curcumin is an opportunity to produce high-quality oral supplements comparable to existing imported products.

The primary purpose of this study is to determine the effects of oral administration of a local curcumin formulation on skeletal muscle using an animal model that similarly demonstrated the course of human sarcopenia.

Purpose-bred 11- to 12-week-old female Sprague Dawley (SD) rats will be used in this study. SD rats are extensively used in animal models of human diseases and conditions such as diabetes, obesity and sarcopenia. Female rats have been selected because they do not demonstrate more temperature or activity variance and have more stable behavior compared to males. To simulate sarcopenia in this animal model, the tail suspension (TS) method was utilized. The TS method involves decreased hind limb function by suspending the animal’s tail for the duration of treatment. The laboratory animals will be randomized to receive any of the four treatments: (1) low-dose curcumin + vehicle; (2) high-dose curcumin + vehicle; (3) vehicle only; and (4) control (distilled water). The interventions will be subdivided into two: 2-week treatment and 4-week treatment. The gastrocnemius muscles on both sides will be excised and weighed, and the muscle tissues subjected to rapid freezing in acetone-dry ice and sliced into 10 μm-thick sections for staining. Examination of muscle architecture and computation of atrophy factors will be performed. The presence of connective tissue, fat tissue and number of atrophic muscle cells will be determined. Accurate quantitative detection of the rat total AMP (adenosine monophosphate)-Activated Protein Kinase will be performed in the gastrocnemius muscle tissue utilizing the enzyme-linked immunosorbent assay kit.

Human ; Time ; Aging ; Healthy Aging

There are rapid advancements in AI-driven diagnostics and wearable technologies, which are enabling early disease prediction, especially in conditions like Parkinson's disease. Precision medicine, underpinned by molecular biology and genomic data, allows clinicians to tailor treatment based on patient phenotypes, significantly enhancing personalized healthcare. AI complements this by processing vast datasets, from health records to biomarker evaluations, supporting more precise diagnostics and treatment recommendations.

Associated with aging, sarcopenia is characterized by a decline in skeletal muscle mass, muscle strength and physical performance, eventually resulting in reduced physical capability, disability, poor quality of life, mortality in older people and high health care expenditure. The prevalence varies significantly by population characteristics, disease status, diagnostic criteria and measurement tools. It is essential to achieve an accurate diagnosis of sarcopenia for the management plan to be effective. This review briefly discusses the essential steps in diagnosing sarcopenia: Find – Assess – Confirm - Severity.
Sarcopenia ; Muscle Strength

Spinal muscular atrophy (SMA) is the most common inherited lethal disease in children. Confirmatory diagnosis is based on molecular genetic testing of survival motor neuron (SMN) genes. We aimed to describe the phenotypic presentation of Filipino infants and children with SMA based on the copy number analysis of SMN genes. Medical records of 17 Filipino children were reviewed from January 2017 to December 2019. De-identified clinical data fulfilled the diagnostic criteria defined by the International SMA Consortium. Among Filipino children, the predominant SMA type by copy number was type I having two copies of SMN2 gene. The clinical severity based on symptom onset and highest functional motor capacity attained correlated with SMN2 copy number congruent with existing data. A significant time lag between symptom onset to confirmation of genetic diagnosis was noted. Nine out of the 17 (52%) children did not have a family history of the disease, raising the possibility of mutation carriers in these families since the incidence of de novo mutations in literature is about 2%. These data offered the first epidemiological pattern of genetically confirmed SMA among Filipino children; provided additional information for genetic counselling; and an avenue to consider pre-symptomatic newborn screening and carrier testing that would change proactive measures and opportunities for therapy. These measures unavoidably will decrease the incidence and prevalence of disease in the future.
Muscular Atrophy, Spinal

Rationale: Duchenne muscular dystrophy (DMD) is a disease that primarily manifests in the early stages of life and progressively affects muscle strength resulting in quadriparesis and ultimately resulting in premature death secondary to cardiac or respiratory failure. DMD is the most common x-linked genetic disorder in children that is because of an alteration of a protein called “dystrophin” which is responsible for strengthening muscle fibers and protecting them from injury as muscles contract and relax. Objective: To highlight the case of a 19-year-old male who was diagnosed with DMD at 8 years of age and treated with oral corticosteroid and rehabilitation. Case: We present the case of a 19-year-old male who developed difficulty climbing stairs and was diagnosed with DMD at 8 years old with the use of clinical exome sequencing. Corticosteroid therapy was initiated and rehabilitation perpetuated which dramatically improved his life expectancy. Discussion and Summary Clinical exome sequencing was employed on our patient to confirm the diagnosis of DMD from other neuromuscular and neurodegenerative diseases. Most cases of DMD succumb to cardiopulmonary arrest before reaching adulthood; however, this case exemplifies DMD from other cases since our patient was able to prolong his life with continuation of oral corticosteroid and rehabilitation and in the absence of extensive life support.
Dystrophin ; Mortality, Premature

Background: Resting tremor is a prominent cardinal motor symptom of Parkinson’s disease (PD). In some cases, the tremor may be refractory to dopaminergic and anticholinergic treatment. Multiple studies were previously done to evaluate the effectiveness of Botulinum Neurotoxin A (BoNT/A) with essential tremors and dystonia, but data regarding its use on tremors of PD is still lacking. Objective: This meta-analytic study aims to determine the effectiveness of BoNT/A in treating tremors of patients with PD. Data Sources: Data Sources: Researches were searched at PubMed, ScienceDirect and EBSCO Host. Review Methods: Articles on the effect of BoNT/A on PD hand tremors were searched. Studies and data pertaining to non-PD tremors like essential tremors excluded in the analysis due to difference in pathophysiology. Standardized mean difference was used as the effect measure and was computed with Review Manager version 5.4 software. Results: Three open label studies were used for final analysis in this study. Studies included are those pertaining to tremors due to PD. Pooled estimates showed a significant change in decreasing tremor score after BoNT/A injection. Conclusion Botulinum Toxin A injections can be used to manage PD tremors effectively.
Botulinum Toxins, Type A ; Tremor

POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, M-protein, skin changes) also known as Crow-Fukase syndrome or Takatsuki syndrome is a rare and disabling paraneoplastic syndrome that frequently occurs in the fifth or sixth decade of life without a known standard first-line therapy. A 34-year-old Filipino male nurse, who presented with gradually progressive distal lower extremity weakness and sharp shooting pain in bilateral legs accompanied by mild joint effusion on the left knee, hypertrichosis, bilateral conjunctival injection, and gynecomastia underwent extensive workup and was diagnosed with POEMS syndrome. Complete blood count revealed erythrocytosis and thrombocytosis with elevated serum VEGF (vascular endothelial growth factor) and elevated monoclonal serum free lambda light chains. The electrophysiologic studies revealed chronic demyelinating sensorimotor polyneuropathy while bone marrow core biopsy and bone marrow aspirate smear immunohistochemical staining showed it to be positive for lambda and CD138. He had an initial unsuccessful treatment course with melphalan and prednisone. Hence, bortezomib and dexamethasone were given which gave significant improvement in symptoms from the overall neuropathy limitation score of 5 to 1.

I see clinicians often and when time is kind, a conversation about research ensues. There is always interest but to actually engage in research, many shake their heads and sigh “no time.” I wonder about lost opportunities to learn and study diseases when clinicians are not inclined to or not supported in research. At every stage of medical education, training, and professional practice whether in academia or in clinic or hospital, physicians inevitably encounter a fork in the road. The paths of clinician and/or academician are large lanes in the highway, yet at a junction, the highway becomes two roads, one to remain as clinician or academicians and the other to pursue research and publication. As well-known, many choose to remain in clinic or in classroom.
Research ; Publications

Rationale: Entrapment neuropathies are peripheral nerve disorders at specific anatomical locations. They may be caused by trauma in a manner of sprains or bone fracture, but it is often caused by repetitive insults or compression of nerves as they travel through a narrow anatomic space. Pregnancy and pre-existing comorbidities such as diabetes, obesity, cancer, or autoimmune diseases may also cause nerve entrapment.

Objective: To highlight the case of a 52-yearold female developing right foot dysesthesia and weakness after continuous restraint strapping from her previous hospitalization.

Case: Here we have the case of a 52-year-old Filipino female consulted because of right foot dysesthesia, allodynia, and mild weakness. She had a history of bipolar disorder and recent onset of acute psychosis and overdosing with her irregularly taken maintenance olanzapine tablets. She was put on restraint strapping of the right lower limb in her one-week hospital stay. This resulted in developing restraint marks on her right ankle accompanied by difficulty walking on heels and toes, spontaneous dysesthesia, and touch allodynia of her entire right foot. An electrodiagnosis yielded right lower limb focal neuropathies involving the right fibular nerve, right tibial nerve, right superficial fibular, and right sural nerves. The prescribed amitriptyline and gabapentin for 6 months led to gradual improvement of neuropathic pain.

Discussion and Summary: Our case exemplifies focal limb neuropathies from entrapment due to restraint strapping. Electrodiagnostic confirmation of neuropathies of the same limb sensory and motor nerves was mandated to corroborate clinical neuropathic pain and after ruling out other causes of entrapment neuropathies. Prolonged use of neuropathic pain medications were needed to attain relief in this present case. Restrictive strapping is an iatrogenic cause of entrapment neuropathy that is preventable, had there been proper medical attention applied.