case study #3 muscular system

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Health Lesson: Learning About Muscles

Information on this page is mapped to national science and health education standards and is for students in grades 4 through 6 who are learning about the human body. Teachers may also use these resources to inform their lesson plans.

On This Page

• For Students : Find all classroom materials and activities about muscles
• Kahoot! Quiz : Test your knowledge about muscles on your own or as a class!
• Vocabulary : See all of the medical terms in this lesson defined
• Teacher's Corner : See the National Education Standards covered in these lessons

For Students

What are your muscles for? When you think about muscles, you probably think about the ones in your arms, legs, back, or abs. But muscles do more than help you lift heavy things. Did you know that muscles also help you breathe, pump your blood, and move food through your gut?

On this page, you can learn about muscles, what happens when they get hurt, and how to keep them healthy.

What are muscles?

Muscles control all movement in the body. There are more than 650 muscles in the human body.

Muscles work together with bones to help you move. Muscles and bones (your skeleton) are part of the musculoskeletal (muh-skyuh-low-SKEH-luh-tl) system .

Muscle is a type of tissue , a group of cells that work together to accomplish a specific job, like movement.

You control some of your muscles, but others work on their own. Even when you sit perfectly still, muscles in your body are constantly working!

Muscles do a lot to keep your body healthy. They:

• Help you move, sit still, and stand up straight.
• Allow you to move your eyes to look around.
• Push food through your digestive system.
• Pump blood through your heart and blood vessels.

Watch this video to see heart muscles pumping blood.

• Move air in your body so that you can speak and breathe.

A special muscle in your chest called the diaphragm (DAI-uh-fram) helps the lungs fill with air when you breathe. Make a model to see how the diaphragm works.

How do muscles work?

Muscles help you move because they are connected to bones with a special kind of tissue called a tendon (TEN-dn) .

Muscles are made up of thousands of small elastic fibers, similar to rubber bands, that contract and relax to cause movement. When the fibers contract, they get shorter, which pulls the bones they’re connected to closer together. Learn more about bones .

What are the types of muscles?

There are three main types of muscle: skeletal, smooth, and cardiac.

Skeletal muscles

Skeletal (SKEH-luh-tuhl) muscles help you move, sit up straight, and keep your balance. Skeletal muscles are sometimes called voluntary muscles because you can control them.

You can move skeletal muscles just by thinking about it and then doing it. To make skeletal muscle move, the brain sends electrical messages to your skeletal muscles. The messages tell the muscles to do things like contract or relax when you want to raise your hand, move your jaw to chew food, or kick a soccer ball into a goal.

Skeletal muscles lie under the skin. They work with your bones and joints to give your body power and strength.

Did You Know?

Your face is filled with muscles! The muscles in your face allow you to make dozens of different types of expressions. Stick out your tongue! Did you know your tongue is a muscle? It helps you talk and chew your food.

Smooth muscles

Smooth muscles work to keep your body healthy without you having to think about moving them. Because you can’t control these muscles, they are sometimes called involuntary muscles. Smooth muscles help you focus your eyes, move food through your body, and go to the bathroom.

In your eyes, smooth muscles help you focus your vision and adjust to different levels of light.

Smooth muscles help you move food through and out of your body. Waves of smooth muscle contractions called peristalsis (peh-ruh-STAAL-suhs) help move food through your digestive system. Have you heard your stomach growling when you’re hungry or after you eat a meal? Those sounds are created by peristalsis!

Smooth muscles at the end of your digestive system help you push waste out of your body as feces (poop). Smooth muscles in your bladder contract and relax to hold in or push out urine (pee).

Cardiac muscles

Cardiac (KAAR-dee-ak) muscles make up the heart. Like smooth muscles, cardiac muscles are involuntary. They contract and relax automatically to pump blood through your body.

You do not need to think about telling the heart to beat. A special area of muscle in your heart sends electrical messages in a steady rhythm to help your heart beat.

Heart muscles help make sure that your blood flows in the right direction with structures called valves . Try this activity to learn how heart valves work!

What happens when muscles get hurt?

A strain happens when a muscle or tendon stretches too much or tears. Some people describe muscle strains by saying they “pulled a muscle.” If you exercise too much, too intensely, or don’t stretch enough, you may get a strain.

Strains that happen from tearing a muscle or tendon are more serious than strains from overstretching a muscle or tendon. Strains can cause pain, swelling, and bruising. Your body heals strains by creating new muscle fibers to fill in the damaged area.

Tendons—the tissues that connect muscles to bones—can also get hurt. Tendinitis (ten-duh-NAI-tuhs) is a condition in which repetitive or intense motions injure the tendon, causing pain and swelling.

If you think you have a muscle strain or tendon injury, you can try resting, putting ice on the painful area, and asking an adult for over-the-counter pain medication. Go to the doctor if your injury doesn’t get better. Doctors may treat some strains with a splint or temporary cast.

How can I help keep my muscles healthy?

Exercise to work your muscles..

Being physically active keeps your muscles healthy, which helps you work, play, and do other activities without getting hurt or tired.

You don’t need to lift weights to exercise your muscles! You can walk, jog, play sports, dance, swim, and bike. Exercising in different ways helps make sure you work all your muscles.

Remember, your heart is a muscle! Any activity that makes your heart pump blood faster will exercise this important muscle.

Bigger muscles are not necessarily better. Working out helps your muscles get stronger. Sometimes they also get bigger, but your muscles can be strong and healthy without being big.

Avoid muscle injuries.

• Warm up and cool down . Before exercising or playing sports, warm-up exercises, such as stretching and light jogging, may make it less likely that you’ll strain a muscle. They are called warm-up exercises because they make the muscles warmer and more flexible. Cool-down exercises, such as stretching, are also very important to do after exercising. They help you to loosen the muscles that have tightened during exercise or while playing sports.
• Wear the proper protective gear for your sport, such as pads or helmets. This will help reduce your risk of injuring yourself.
• Remember to drink lots of water while you’re playing or exercising, especially in warm weather. Dehydration (dee-hai-DRAY-shn) is when your body’s water level gets too low. If you become dehydrated, you could get dizzy or even pass out. Dehydration can cause many medical problems.
• Don’t try to “play through the pain.” If something starts to hurt, STOP exercising or playing. You might need to see a doctor, or you might just need to rest for a while.
• If you have been inactive, “start low and go slow” by gradually increasing how often and how long you are active. Increase physical activity gradually over time.
• Be careful when you lift heavy objects . Keep your back straight and bend your knees to lift the object. This will protect the muscles in your back and put most of the weight on the strong muscles in your legs. Get someone to help you lift something heavy.
• Don’t try to “bulk up” by using weights that are too heavy for you . This can cause injury. Start with smaller weights and build your way up. You do not need to be able to lift very heavy weights to have healthy muscles. Instead, try doing exercises with smaller weights, but repeat the exercise more times.

Eat a healthy diet.

There is no special diet to keep your muscles healthy. Try to eat a balanced diet with fruits and vegetables, whole grains, low-fat dairy, and lean proteins .

MYTH BUSTED!

Some people think that they need protein shakes and powders to get big muscles. But most kids get plenty of protein just by eating a balanced diet. In fact, eating too much protein can be harmful to your body.

Test your knowledge about muscles with this Kahoot! quiz

This Kahoot! quiz tests your knowledge about what muscles do and how to keep them healthy.

Check out our other webpages to learn about bones , joints , and skin .

Cardiac (KAAR-dee-ak) muscles . These muscles make up your heart. You cannot control these muscles.

Cells . The smallest building blocks of life. Your body is made of trillions of cells!

Contraction . Tightening or shortening of muscle fibers.

Dehydration (dee-hai-DRAY-shn) . When your body’s water level gets too low. If you become dehydrated, you could get dizzy or even pass out. Dehydration can cause many medical problems.

Diaphragm (DAI-uh-fram) . A muscle in your chest that helps the lungs fill with air when you breathe.

Musculoskeletal (muh-skyuh-low-SKEH-luh-tl) system . All the muscles, bones, and other tissues that work together to give your body its basic shape and ability to move.

Peristalsis (peh-ruh-STAAL-suhs) . Waves of smooth muscle contractions that help move food through your digestive system.

Skeletal (SKEH-luh-tuhl) muscles. These are the muscles you can control. They help you move, sit up straight, and keep your balance.

Smooth muscles . You cannot control these muscles. They help you focus your eyes, move food through your body, and go to the bathroom.

Strain . When a muscle or tendon stretches too much or tears. Some people describe a muscle strain by saying they “pulled a muscle.”

Tendinitis (ten-duh-NAI-tuhs) . A condition in which repetitive or intense motions injure the tendon, causing pain and swelling.

Tendon (TEN-dn) . A special kind of tissue that connects muscles to bones.

Tissue . A group of cells that work together to accomplish a specific job, like movement.

Valves . Special structures in your heart that make sure your blood flows in the right direction. 

Teacher’s Corner

The content on this NIAMS webpage aligns with the following national standards:

Next Generation Science Standards

• NGSS Standard 4-LS1-1 “Animals have internal and external structures that serve various functions in growth, survival, behavior, and reproduction.”
• NGSS MS-LS1-1 “All living things are made up of cells , which are the smallest units that can be said to be alive. An organism may consist of one single cell (unicellular) or many different numbers and types of cells (multicellular).”
• NGSS MS-LS1-3 “In multicellular organisms, the body is a system of multiple interacting subsystems. These subsystems are groups of cells that work together to form tissues and organs that are specialized for particular body functions.”

National Health Education Standards

• NHES 2.5.2 “Identify the influence of culture on health practices and behaviors.”
• NHES 1.5.5 “Describe when it is important to seek health care.”
• NHES 1.5.1 “Describe the relationship between healthy behaviors and personal health.”
• NHES 1.5.4 “Describe ways to prevent common childhood/adolescent injuries and health problems.”

CDC Healthy Schools

• CDC Characteristics of an Effective Health Education Curriculum, Characteristic 4: “Address social pressures and influences”

• Case Report
• Open access
• Published: 26 June 2024

Incomplete Kawasaki disease with muscular weakness and bladder retention: a case report

• Yating Sang 1 , 2 ,
• Lili Luo 1 , 2 &
• Lina Qiao 1 , 2 , 3  

BMC Pediatrics volume  24 , Article number:  415 ( 2024 ) Cite this article

10 Accesses

Metrics details

Kawasaki disease (KD) is an acute systemic immune vasculitis affecting multiple organs and systems in children, and is prevalent in children under 5 years of age. Muscular weakness is a rare manifestation of KD, and only 11 pediatric patients with KD combined with muscular weakness have been reported, of which evidence of myositis was found in 2/3 of the patients, and 1/3 could not be explained by myositis, the mechanism of which is still unclear. Cases of KD combined with bladder retention are even more rare, and there has been only 1 case report of KD combined with bladder retention in a child with no previous underlying disease.

Case presentation

We report a 22-month-old Asian child with incomplete Kawasaki disease (IKD) who initially presented with fever and progressive muscular weakness in the lower extremities, followed by the bladder and bowel retention abnormalities and rapid onset of heart failure, respiratory failure and shock. The child developed coronary artery ectasia (CAA) without the main clinical features of KD such as rash, conjunctival congestion, desquamation of the extremity endings, orofacial changes and enlarged lymph nodes in the neck. Creatine kinase and electromyography were normal. Temperature gradually normalized and muscle strength recovered slightly after intravenous immunoglobulin. The child could be helped to walk after 1 week of aspirin combined with steroid therapy.

Conclusions

We present the case of a 22-month-old child with IKD. The child began with progressive muscular weakness in the extremities, followed by the bladder and bowel retention abnormalities, and rapidly developed heart failure, respiratory failure, and shock. Despite early failure to detect the disease, the child recovered rapidly and had a favorable prognosis. KD comorbidities with muscular weakness as the main manifestation are uncommon. This is the first case report of IKD combined with both muscular weakness and bladder and bowel retention, which may provide clinicians with diagnostic and therapeutic ideas, as well as a basis for future exploration of the mechanisms of KD combined with muscular weakness or bladder and bowel retention abnormalities.

Peer Review reports

Introduction

Kawasaki disease is a systemic mesangial vasculitis disease of unknown etiology, commonly seen in children under 5 years of age [ 1 ], with the most important complication being involvement of the coronary arteries and the development of CAA or coronary artery aneurysm (CAE). The diagnosis of KD relies on clinical features, systemic multisystemic vasculitis manifestations, and laboratory tests. The main clinical features include 1) fever; 2) changes in the extremities (reddening, swelling and peeling of the skin) 3) bilateral conjunctivitis; 4) changes of lips and oral cavity: reddening of lips, strawberry tongue, diffuse injection of oral and pharyngeal mucosa; 5) redness of the skin rashes or at the site of BCG inoculation; and 6) nonsuppurative enlargement of the lymph nodes in the neck. Complete Kawasaki disease (CKD) is diagnosed when fever and 4 or more other clinical features are present. Children with fewer than 4 major clinical features may be evaluated for IKD in conjunction with laboratory tests and echocardiography (see guidelines for details  [ 2 ,  3 ]).

Children with KD can be combined with multi-organ and multi-system injuries, including gastrointestinal (vomiting, diarrhea, intestinal obstruction, etc.), neurological injuries (aseptic meningitis, encephalopathy, impaired consciousness, etc.), and urological (aseptic pyuria, urethritis, etc.) [ 4 ]. To date, 11 cases of children with KD have been reported with combined muscular weakness, mainly characterized by difficulty in walking, ptosis, ocular dyskinesia, respiratory failure, dysphonia and dysphagia [ 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 ]. The objective of the study is to report a child diagnosed with IKD combined with Kawasaki disease shock syndrome (KDSS), characterized by muscular weakness of the extremities and the bladder and bowel retention abnormalities, who was effectively treated with gammaglobulin, aspirin, and steroid, which has not been reported previously.

Case report

A 22-month-old boy presented with fever and weakness of the extremities for 3 days. The initial symptoms were decreased activity and abnormal walking gait. he child was treated with a 3-day anti-infection therapy of cefazolin and ceftizoxime at another hospital. Before using antibiotics, they collected the child’s blood for pathogen culture, and the results were negative. However, the child continued to have recurrent temperatures, and developed symptoms such as inability to walk, unsteadiness in holding objects, and choking on drinking water. More importantly he develpoed the bladder and bowel retention abnormalities, and required catheterization. Abdominal CT suggests enlarged gallbladder (See Table 1 for relevant examinations).

On admission (3th day of illness), the boy was noted to have muscular weakness with diminished patellar tendon reflex. The proximal and distal muscle strength of upper limbs was scaled as grade IV, and lower limbs grade III-IV (See Table 2 for muscle strength scale). Six hours after admission (Day4), the child developed shallow coma, oliguria, decreased blood pressure (85/36 mmHg), respiratory failure (FiO2 50%, PEEP 5 cmH2O), muffled heart tones, hepatomegaly, and a Glasgow score of 6 (E1M4V1). The child required endotracheal intubation for respiratory support, urinary catheterization and other supportive therapy,including continuous pumping of epinephrine, norepinephrine, and furosemide (Day4-6). At the same time, the child was treated with intravenous immunoglobulin (a total of 2 g/kg, infused on Day4 and Day5 respectively) and dexamethasone (0.32 mg/kg, Day 4–7). Because of persistent anemia, coagulopathy, and hypoalbuminemia, multiple transfusions of red blood cells, plasma, and albumin were administered to correct the condition.

On day 7 of illness, he stopped having fever (the last time of fever was 24 h after stopping the immunoglobulin infusion). Circulation was stable. Self-breathing test was passed and he was discharged from invasive ventilator-assisted ventilation therapy. Glasgow coma score improved to10 (E4M4V1).

On day 9 of illness, a repeat echocardiogram suggested coronary artery ectasia (LCA = 2.8 mm, LAD = 2.0 mm, LCX = 1.5 mm, RCA = 2.1 mm, Z value = 2.34, Figs. 1 and 2 ). Combined with other tests and the child's manifestations of inadequate tissue perfusion, he was diagnosed with IKD, combined with severe complication of KDSS. We treated with aspirin (4 mg/kg·d) and dexamethasone (0.16 mg/kg, Day8-9) or prednisone acetate (1 mg/kg, since Day 10). The child was able to pass urine and feces voluntarily. Tendon reflexes were normal. Upper and lower extremity muscle strength was grade IV.

Ultrasound measurement of the left coronary artery and its branches

Ultrasound measurement of the right coronary artery

On day 16 of illness, the child could walk dozens of steps with support. At this time, the electromyography (EMG) was normal. He continued to take aspirin (for 6 months) and prednisone (gradually tapered off in the outpatient clinic over a 4-week period).

Gradually the child regained complete muscle power with normal activity over the next 3 months. Echocardiography showed normal coronary Z-scores and no valvular regurgitation.

Discussion and conclusions

This child was unusual in that he did not have the typical clinical manifestations of KD throughout the course of his illness, except for fever, which began with progressive muscular weakness in the extremities, followed by the bladder and bowel retention abnormalities. Therefore, we initially considered Guillain-Barré syndrome, but cerebrospinal fluid examinations performed on days 3 and 15 of the child’s illness showed no protein cell separation. All four central demyelination tests in the cerebrospinal fluid were negative. Cranial and spinal MRI results were normal. EMG was normal. And the child has persistent bladder and bowl dysfunction. But we did not test for GBS-related antibodies. Subsequently, the child rapidly developed multi-organ dysfunction and shock. So we considered infection-related septic shock. However, the child’s blood and cerebrospinal fluid cultures were negative (Specimens were collected prior to the administration of antibiotics at our hospital), and the efficacy of antibiotics (vancomycin and meropenem, 6 days in total) was inconclusive. No rare pathogens were detected in the his blood and cerebrospinal fluid mNGS, such as Rickettsia, Leptospira and so on. We only detected moderate levels of Haemophilus influenzae and Microbacterium fragilis in the blood mNGS. We believe that these two etiological infections do not explain the severe clinical manifestations and systemic inflammatory responses of the child. No link has been found between Kawasaki disease and Haemophilus influenzae or fragile bacteroides. No nucleic acids of echovirus-11/30, Enterovire-71, Cox-A6/16/10 were detected. Tests for EBV, Cox-IgM, Mycoplasma pneumoniae-IgM, HSV-IgM, fungi and M.tuberculosis were negative. Therefore, we did not consider the possibility of infection by rare pathogens. Fortunately, we used high-dose intravenous immunoglobulin (2 g/kg) at the same time, and the child’s temperature gradually normalized within 36 h. C-reactive protein was essentially normalized within 48 h of normalization of temperature. No further dilation of the coronary arteries. No predisposition for macrophage activation syndrome. Therefore there is no indication for the use of biological agents such as infliximab. We retrospectively diagnosed KDSS until the child developed coronary artery ectasia.

According to the American Heart Association (AHA) guidelines [ 16 ], Kawasaki disease can be diagnosed when a patient meets the following clinical criteria: 1) Persistent high fever ≥ 5 days with at least 4 main characteristics: rash, bilateral bulbar conjunctival congestion, oral mucosal changes, peripheral limb changes, cervical lymph node enlargement, and other similar clinical features were excluded. When a child has an unexplained fever more than 5 days, incomplete or atypical Kawasaki disease should be considered in conjunction with laboratory and echocardiographic results. The child had no major symptoms other than fever for more than 5 days and coronary dilation. Combined with the clinical manifestations of the child and all auxiliary examinations, other evidences supporting the diagnosis of IKD/KDSS include: 1) Cardiovascular system: left ventricular function transient systolic dysfunction, valve regurgitant, shock; 2) Digestive system: gallbladder enlargement and thickening of gallbladder wall, intestinal obstruction; 3) Respiratory system: interstitial changes in both lungs with a small amount of pleural effusion on both sides; 4) Nervous system: aseptic meningitis (CSF nucleated cells number 20 × 10^6/L, and CSF culture and mNGS were negative); 5) Urinary system: sterile pyuria (urine routine leukocytosis, urine culture negative); 6) Laboratory examinations: neutrophilic leukocytosis, anemia and the trend of thrombocytosis; CRP, ESR increase; hypoalbuminemia and hyponatremia; BNP increased significantly.

CAA has a variety of etiologies in childhood, in addition to the most common Kawasaki disease, other etiologies including juvenile idiopathic arthritis, multiple Arteritis, systemic lupus erythematosus, etc. However, with the exception of KD, None of these other diseases could explain the manifestations of systemic inflammatory responses and multisystem involvement. Since this case occurred in the era of covid, we should also consider the possibility of multi-system inflammatory syndrome in children (MIS-C), which may be caused by a state of excessive inflammation that usually occurs in the weeks following infection. MIS-C is a syndrome of multisystem involvement in the context of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) outbreak epidemics, including persistent fever, gastrointestinal symptoms, myocardial injury, shock, and coronary artery aneurysm [ 17 , 18 , 19 ]. Nearly half of the patients with MIS-C will present with neurologic manifestations. The muscle involvement may vary from an asymptomatic elevation of CK to severe rhabdomyolysis [ 20 ]. However, our child did not present with a rash, no acute kidney injury and myoglobinuria, normal CSF results, negative demyelinating antibodies, and normal spinal MRI and EMG. So causes other than viral myositis can be excluded. Musclular weakness can be the first manifestation of COVID-associated viral myositis, the mechanism of which may be direct infiltration of myocytes by the SARS-CoV-2 virus or induced by autoimmunity [ 21 ]. CK may not be elevated, which is consistent with our child. However, our child also showed urinary retention, which has only been reported in patients with MIS-C combined with acute transverse myelitis (ATM) [ 22 ,  23 ]. CSF and spinal MRI were normal in our child. So the diagnosis of ATM was not supported. There was overlap between patients with MIS-C and KDSS compliant clinical presentations and complementary tests. Coronary dilation, myocardial damage, elevated markers of inflammation and cytokines can also be tested in MIS-C. Imaging changes of lung and gastrointestinal symptoms are also common. However, the evidence that does not support MIS-C is as follows: 1) The onset peak of MIS-C is more than 6 years old [ 24 ], and the age of children is younger; 2) The common gastrointestinal symptoms of MIS-C include vomiting, abdominal pain and diarrhea, but no cases of intestinal obstruction have been reported until now, which is inconsistent with our children; 3) Patients with MIS-C often have electrocardiogram changes, such as conduction blocks and arrhythmias, but this child’s electrocardiogram showed only sinus tachycardia; 4) Importantly, the child tested negative for SARS-CoV-2 nucleic acid from the nasopharynx. No history of SARS-CoV-2 infection in last 6 weeks, and no SARS-CoV-2 vaccination. From this point of view, the diagnosis of MIS-C is not valid. The suspicious history is that the child presented with nasal congestion and runny nose in the week before the onset of the disease, but there was no fever or cough. The serological test of COVID-19 that our hospital can perform was SARS-CoV-2 antibody, but unfortunately we did not test for this child. However, the serologic test for SARS-CoV-2 has a low positive rate in the days or weeks after infection. The primarily use is to determine prior exposure, and is very limited in the diagnosis of acute infection [ 25 , 26 ]. Therefore, we continue to analyze the mechanisms of combined muscular weakness and the bladder and bowel retention abnormalities in children, based on the diagnosis of Kawasaki disease, but we must consider the possibility of an atypical MIS-C.

In previous case reports of KD combined with muscular weakness (Table 3 ), evidence of myositis was found in 2/3 of cases ((i) elevated creatine kinase or (ii) EMG or muscle biopsy supportive of myositis). In other 1/3 of cases, the creatine kinase and EMG were normal. They did not seem to be explained by myositis. In our case, no evidence of myositis was found (creatine kinase, myoglobin and EMG were normal) [ 27 ]. All relevant examinations revealed no evidence of neuromuscular disease. The child’s muscle strength consent also returned to normal soon after we gave him gammaglobulin, aspirin and prednisone acetate treatment. A 40-year-old adult patient was diagnosed with Kawasaki disease, associated with significant distal motor and sensory neuropathy, electromyographic abnormalities, and elevated creatine kinase levels. The biopsy of a distal muscle showed immunoglobulin deposition in the sarcolemma. Immunologic evaluation showed high concentrations of cryoglobulins and circulating immune complexes. It is hypothesized that the manifestations of combined musculo-neuropathy in KD may be mediated by immune complexes deposition in vessels and tissues [ 20 ].

The incidence of KD combined with intestinal pseudoobstruction is 2%-3%. The mechanism is thought to be KD-induced mesenteric artery vasculitis, leading to intestinal ischemia and associated intestinal muscular plexus dysfunction [ 28 ]. Only one case of KD combined with bladder retention has been reported previously. Hoon et al. reported a 35-month-old girl diagnosed with refractory KD combined with paralytic bowel obstruction and loose neurogenic bladder. They did not mention creatine kinase and EMG  [ 29 ]. In our case, the child presented with similar bladder and fecal retention. We examined creatine kinase and EMG, and the results were normal. But EMG was performed after the child’s muscle strength had recovered, so the possibility of muscular weakness due to myositis could not be completely excluded. His whole spinal MRI was normal, except for the possibility of tumor compression such as neuroblastoma  [ 30 ]. We hypothesized that the cause of urinary and fecal retention could be ischemic vasculitis of the arteries supplying the pelvic nerves caused by KD, resulting in a dysfunction of the coordination of the internal and external anal sphincters and the bladder-distractor-sphincter-pelvic floor muscles. However, case reports of KD combined with bladder retention are very rare, the mechanisms need to be further explored.

In summary, when a child with persistent fever presents with muscular weakness, urinary or fecal retention, and rapid and critical progression of disease, clinicians must consider the possibility of IKD in combination with rare neurologic disorders. Gammaglobulin, aspirin and steroid treatment is effective.

Availability of data and materials

The datasets used and analyzed during the current study are available from the author Yating Sang ([email protected]) on reasonable request.

Abbreviations

• Kawasaki disease

Electromyography

Multi-system inflammatory syndrome in children

Acute transverse myelitis

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Sang, Y., Luo, L. & Qiao, L. Incomplete Kawasaki disease with muscular weakness and bladder retention: a case report. BMC Pediatr 24 , 415 (2024). https://doi.org/10.1186/s12887-024-04874-0

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  Tanzania Journal of Health Research Journal / Tanzania Journal of Health Research / Vol. 25 No. 3 (2024): Tanzania Journal of Health Research / Articles (function() { function async_load(){ var s = document.createElement('script'); s.type = 'text/javascript'; s.async = true; var theUrl = 'https://www.journalquality.info/journalquality/ratings/2406-www-ajol-info-thrb'; s.src = theUrl + ( theUrl.indexOf("?") >= 0 ? "&" : "?") + 'ref=' + encodeURIComponent(window.location.href); var embedder = document.getElementById('jpps-embedder-ajol-thrb'); embedder.parentNode.insertBefore(s, embedder); } if (window.attachEvent) window.attachEvent('onload', async_load); else window.addEventListener('load', async_load, false); })();  

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Mathew mganga.

Presidents’ Office, Regional Administration and Local Government, Dodoma, Tanzania

Stephen Kibusi

University of Dodoma, Dodoma

Romuald Mbwasi

St. John’s University of Tanzania, Dodoma.

Main Article Content

Understanding implementers' perceptions on the prime vendor system: a case study of tanzania mainland.

Introduction: Access to safe, effective, quality and affordable essential medicines for all is a central component of Universal Health Coverage (UHC). However, the availability of quality medicines in low and middle-income countries is often limited, especially in peripheral health facilities. MSD, as the sole supplier of drugs and medical supplies to all public health facilities, has been facing difficulties that hinder its efficiency in supplying 100% of all facility’s needs. Despite significant reforms, including introducing the Prime Vendor System in 2018, challenges persist, leading to regional disparities in commodity availability at the facility level. Successfully establishing an intervention based on PPPs within the public sector in the health commodities supply chain system mostly requires high acceptability by the Government, implementers, and beneficiaries. Furthermore, the effectiveness of any activity is primarily influenced by the participants' attitudes. While most studies have extensively researched the effectiveness of the prime vendor system in bridging the supply chain gap, none have researched implementers' perceptions of the prime vendor system in complementing health commodities. This study seeks to understand the Implementer's perceptions of the prime vendor system implementation.

Materials and Methods: This was a quantitative cross-sectional study. Data was collected from June to September 2023 using the ODK application from 356 respondents from Dodoma, Morogoro, Mtwara, and Mwanza in Tanzania. The data was analysed using SAS version 9.4. Statistical significance was determined at a 95% confidence level.

Results: 77.84% of study participants strongly agreed that involving the private sector in health commodities supply chain management is the best approach to solving supply chain problems. Additionally, 81.53% of all study participants believe that the Prime Vendor System has contributed positively to the improved availability of health commodities at the facility level.

Conclusion: Perceptions regarding the prime vendor system vary across different areas, including its impact on the overall availability of health commodities, streamlining of procurement processes, and the role of the private sector in addressing supply chain challenges within the country. Notably, the level of experience in the workplace emerges as a considerable influence on respondents' perceptions regarding the Prime Vendor System and its implementation nationwide.

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Study Finds Israeli Patients With Vitiligo at Lower Risk for Parkinson Disease

Israeli patients with vitiligo exhibit a significantly reduced risk of developing Parkinson disease (PD).

Israeli patients with vitiligo have a decreased risk of subsequent Parkinson disease (PD), according to a study published in Frontiers in Neurology . 1

The researchers explained that PD is a neurodegenerative disorder that is estimated to affect 0.3% of the general population, 1.0% of patients older than 60 years, and 3.0% of people older than 80 years. 2 Also, vitiligo is described as a chronic inflammatory disease, which typically targets the hair, skin, and mucous membranes and manifests as segmental or nonsegmental depigmented patches. 3 It is estimated to be prevalent in 0.1% to 2% of adults and children worldwide.

Past studies discovered that PD coexisted with autoimmune diseases, including bullous pemphigoid, inflammatory bowel disease, and Sjogren syndrome. 4 However, the association of PD with vitiligo has yet to be established. 1 Therefore, the researchers conducted a study to investigate the bidirectional associations between PD and vitiligo; they also aimed to assess PD determinants among patients with vitiligo.

Israeli patients with vitiligo exhibit a significantly reduced risk of developing Parkinson’s disease (PD) | Image Credit: Savory - stock.adobe.com

This large-scale population-based study included 2 different designs. One was a retrospective cohort study design, which was used to longitudinally follow patients with vitiligo and estimate the incidence of new-onset PD. The other was a case-control study design, which the researchers used to estimate the prevalence of preceding PD in patients with subsequent vitiligo.

To conduct their investigation, the researchers used the computerized data set of Clalit Health Services (CHS). CHS is Israel's largest health care provider, with 4,554,343 members as of 2018. Its database is updated continuously as it records each patient interaction with the health care system.

Therefore, the researchers screened the CHS database for incident cases with a vitiligo diagnostic code between 2002 and 2019. They considered patients to have vitiligo if they received a documented vitiligo diagnosis by a board-certified dermatologist or in a discharge letter from a dermatological ward. Conversely, PD diagnosis was solely based on documentation by a certified neurologist.

When constructing their study population, the researchers enrolled a control group, which included up to 5 patients without vitiligo per case; they matched the controls based on sex, ethnicity, and age. Also, the researchers adjusted outcome measures for demographic variables and putative confounding comorbidities, like smoking, hypertension, diabetes mellitus, and body mass index (BMI).

The study population consisted of 123,326 patients. Of these patients, 20,852 had vitiligo, and 102,475 were controls; the mean (SD) age at vitiligo diagnosis was 34.7 (22.4) years. Also, 10,570 (50.7%) patients were female and 15,311 (73.4%) were Jewish.

The researchers estimated the PD incidence rate to be 2.9 (95% CI, 2.1-4.1) and 4.3 (95% CI, 3.8-4.9) cases per 10,000 person-years among patients with vitiligo and controls, respectively. Compared to the controls, patients with vitiligo had a significantly decreased PD risk (HR, 0.68; 95% CI, 0.48-0.98; P = .037).

In sex- and age-stratified analyses, there was only a significantly reduced PD risk in male patients with vitiligo (HR, 0.61; 95% CI, 0.38-0.98; P = .041) and patients aged 32.4 years and older (HR, 0.68; 95% CI, 0.47-0.97; P = .034). However, after adjusting for demographics and comorbidities, the researchers determined that vitiligo was associated with a significantly reduced PD risk (fully adjusted HR, 0.62; 95% CI, 0.43-0.89; P = .009).

Also, the researchers observed preexisting PD in 59 (0.3%) patients with vitiligo and 361 (0.4%) controls. Therefore, the development of subsequent vitiligo was not significantly associated with a PD history (OR, 0.80; 95% CI, 0.61-1.06; P = .116).

Through the age- and sex-stratified analysis, the researchers did not find a significant association between PD history and subsequent vitiligo except in female patients, where an inverse association was found (OR, 0.67; 95% CI, 0.45-0.99; P = .043). After controlling for demographic variables and comorbidities, they determined that the odds of vitiligo remained statistically comparable after PD (fully adjusted OR, 0.80; 95% CI, 0.61-1.06; P = .117).

In particular, the researchers found that the presence of PD in patients with vitiligo was significantly associated with obesity, smoking, older age, and Jewish ethnicity; it was also significantly associated with ischemic heart disease, hypertension, hyperlipidemia, and diabetes mellitus.

As for the risk of all-cause mortality in patients with vitiligo and comorbid PD, the univariate (HR, 14.45; 95% CI, 10.04-20.79; P < .001) and multivariate (adjusted HR, 2.63; 95% CI, 1.82-3.80; P < .001) analyses determined that these patients experienced an elevated risk of all-cause mortality; they also had a greater burden of cardiometabolic comorbidities.

The researchers acknowledged their limitations, which included the relatively homogenous ethnic background of their study population; this may limit the generalizability of their findings. Consequently, the researchers identified areas most pressing for future research.

“Vitiligo patients with comorbid PD are at increased risk of all-cause mortality and cardiometabolic conditions as compared to vitiligo patients without these comorbidities,” the authors concluded. “Additional studies investigating this association in other study populations originating from different ethnic backgrounds are necessary.”

• Kridin K, Ofir L, Weinstein O, Badarny S. Clarifying the association between Parkinson's disease and vitiligo: a population-based large-scale study.  Front Neurol . 2024;15:1387404. doi:10.3389/fneur.2024.1387404
• Lee A, Gilbert RM. Epidemiology of Parkinson disease. Neurol Clin . 2016;34:955-965. doi:10.1016/J.NCL.2016.06.012
• Dahir AM, Thomsen SF. Comorbidities in vitiligo: comprehensive review. Int J Dermatol . 2018;57:1157-1164. doi:10.1111/ijd.14055
• Li M, Wan J, Xu Z, Tang B. The association between Parkinson’s disease and autoimmune diseases: a systematic review and meta-analysis. Front Immunol . 2023;14:14. doi:10.3389/FIMMU.2023.1103053

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Evaluation of coal-seam roof-water richness based on improved weight method: a case study in the dananhu no.7 coal mine, china, 1. introduction, 2. study area and mining conditions, 3. methodology, 3.1. factors influencing the coal-seam roof water richness, 3.2. the determination of indicator weights, 3.2.1. improvement of the entropy method, 3.2.2. improvement of the scatter degree method, 3.2.3. coupled weighting, 4. results and discussion, 4.1. results, 4.2. discussion.

• The middle section of the Xishangyao Group is a water-bearing layer composed of fractured and porous conglomerate sandstone, which directly inundates the roof of the third coal seam, posing a threat to mining safety. Six factors, including the aquifer thickness, recharge index, dip angle of the coal seam, core take rate, sand–mud interbed index, and lithological coefficient of sandstone, were selected as the main indicators for evaluating the water abundance of the roof of the third coal seam;
• To address the limitations of the entropy method, which focuses on local differences and lacks inheritability and transitivity, the indicator conflict correlation coefficient was employed to weigh the information entropy, thus improving the entropy method to obtain the weights of individual indicators;
• Before obtaining the weights of each indicator using the scatter degree method, a subjective optimization method was employed to pre-weigh the original values of each indicator, thereby enhancing the method. The resulting weight coefficients can better differentiate the relative importance of each indicator and their significance in evaluating the target, enabling a more comprehensive assessment;
• The combination weighting of each indicator was performed, and a water-richness zoning model was established using GIS software. The evaluation model predicted a higher water richness in the northeastern part of the mining area. The prediction was validated to be consistent with the actual conditions, thus providing a reference for hydrological measures in other coal-seam roofs.

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Data availability statement, acknowledgments, conflicts of interest.

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Xu, J.; Wang, Q.; Zhang, Y.; Li, W.; Li, X. Evaluation of Coal-Seam Roof-Water Richness Based on Improved Weight Method: A Case Study in the Dananhu No.7 Coal Mine, China. Water 2024 , 16 , 1847. https://doi.org/10.3390/w16131847

Xu J, Wang Q, Zhang Y, Li W, Li X. Evaluation of Coal-Seam Roof-Water Richness Based on Improved Weight Method: A Case Study in the Dananhu No.7 Coal Mine, China. Water . 2024; 16(13):1847. https://doi.org/10.3390/w16131847

Xu, Jie, Qiqing Wang, Yuguang Zhang, Wenping Li, and Xiaoqin Li. 2024. "Evaluation of Coal-Seam Roof-Water Richness Based on Improved Weight Method: A Case Study in the Dananhu No.7 Coal Mine, China" Water 16, no. 13: 1847. https://doi.org/10.3390/w16131847

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• DOI: 10.1007/s42452-024-06007-9
• Corpus ID: 270537995

Performance assessment of large-scale rooftop solar PV system: a case study in a Malaysian Public University

• Logeswaran Govindarajan , Mohd Faizal Bin Mohideen Batcha , Mohammad Kamil Bin Abdullah
• Published in Discover Applied Sciences 14 June 2024
• Environmental Science, Engineering
• Discover Applied Sciences

44 References

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